The Feline Patient Fourth Edition
The Feline Patient Fourth Edition
Editor
Gary D. Norsworthy, DVM, DABVP (Feline)
Founding Authors
Gary D. Norsworthy, DVM, DABVP (Feline) Mitchell A. Crystal, DVM, DACVIM (Internal Medicine) Sharon Fooshee Grace, MAgric, MS, DVM, DABVP (Canine-Feline), DACVIM (Internal Medicine) Larry P. Tilley, DVM, DACVIM (Internal Medicine)
A John Wiley & Sons, Inc., Publication
Edition first published 2011 © 2011 Blackwell Publishing Ltd. Blackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell’s publishing program has been merged with Wiley’s global Scientific, Technical, and Medical business to form Wiley-Blackwell. Editorial Office 2121 State Avenue, Ames, Iowa 50014-8300, USA For details of our global editorial offices, for customer services, and for information about how to apply for permission to reuse the copyright material in this book, please see our Website at www.wiley.com/wiley-blackwell. Authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by Blackwell Publishing, provided that the base fee is paid directly to the Copyright Clearance Center, 222 Rosewood Drive, Danvers, MA 01923. For those organizations that have been granted a photocopy license by CCC, a separate system of payments has been arranged. The fee code for users of the Transactional Reporting Service is ISBN-13: 978-0-8138-1848-1/2011. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought. Library of Congress Cataloging-in-Publication Data The feline patient / editor, Gary D. Norsworthy. – 4th ed. p. ; cm. Includes bibliographical references and index. ISBN 978-0-8138-1848-1 (hardback : alk. paper) 1. Cats–Diseases. I. Norsworthy, Gary D. [DNLM: 1. Cat Diseases–diagnosis. 2. Cat Diseases–therapy. SF985.F46 2011 636.8′0896–dc22
SF 985 F3156 2011]
2010020439 A catalog record for this book is available from the U.S. Library of Congress. Set in 8/10pt Palatino by Toppan Best-set Premedia Limited Printed in Singapore 1
2011
Dedications Gary D. Norsworthy The previous editions of this book have been dedicated to my family members who have stood behind me in this effort, to primary care practitioners who are the first deliver care to feline patients, to secondary care practitioners who deliver the next level of care, to researchers who discover the future level of care, and to veterinary students who will deliver the future level of care. For this edition I would like to repeat my appreciation to each of those groups and add to them the externs who have spent time in my practice. You keep me rejuvenated and refreshed with your enthusiasm for the future of feline medicine. I would also like to express appreciation to my staff: Drs. Anderson and Macdonald, Amanda, Linda, Emily, Stephanie, Rachel, Lorenzo, Lewis, Stacey, Veronica, Laura, Melody, and Kelsey. Each of you has contributed to this in ways you may not realize.
Sharon Fooshee Grace Dedicated to: My Lord and Savior, Jesus Christ; My family, Pete, Branion, and Mary; The memory of my parents, Joel and Janie Fooshee; and And Cleopatra, the kitten who continues to inspire me.
Mitchell A. Crystal I dedicate this book to all those who make up the veterinary profession who have treated me so kindly and allowed me to achieve so much. I hope in this book I have given something back to you. I dedicate this book to my family, Sue, Samantha, Matthew, Bunny, Kacy and Heidi, thanks for teaching me to have fun, to try my best, and to be a good sport. I dedicate this book to Gary Norsworthy who keeps all of us on track and on time, who dots all the i’s and crosses all the t’s, and who is the face, heart, and soul of The Feline Patient.
Larry P. Tilley To my wife, Jeri, and my son, Kyle, in honor of that secret correspondence within our hearts; To Tucker, our new grandson who represents the purity of life.
Contents Founding Authors / xiii Contributors / xiv Preface / xvii
Section 1: Diseases and Conditions 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52
Acetaminophen Toxicosis Sharon Fooshee Grace / 5 Acne Christine A. Rees / 7 Acromegaly Sharon Fooshee Grace / 8 Actinomycosis Sharon Fooshee Grace / 10 Adenocarcinoma and Carcinoma Mark Robson / 12 Amyloidosis Andrew Sparkes / 14 Anal Sac Disease Gary D. Norsworthy / 16 Anaplasmosis Sharon Fooshee Grace / 18 Anemia Sharon Fooshee Grace / 19 Anorexia Mitchell A. Crystal / 22 Aortic Stenosis Larry P. Tilley / 24 Arrhythmias Larry P. Tilley and Francis W. K. Smith, Jr. / 26 Ascites Larry P. Tilley / 28 Aspergillosis Sharon Fooshee Grace / 30 Aspirin Toxicosis Sharon Fooshee Grace / 32 Atopic Dermatitis Christine A. Rees / 33 Bartonellosis Mark Robson and Mitchell A. Crystal / 35 Basal Cell Tumor Bradley R. Schmidt and Mitchell A. Crystal / 37 Biliary Cysts Michele Fradin-Fermé / 39 Bite Wounds: Canine Gary D. Norsworthy / 41 Bite Wounds: Feline Gary D. Norsworthy / 44 Blastomycosis Sharon Fooshee Grace / 46 Blindness Karen R. Brantman and Harriet J. Davidson / 48 Bordetella Infection Teija Kaarina Viita-aho / 50 Brachial Plexus Neuropathy Gary D. Norsworthy / 52 Brachycephalic Syndrome Mac Maxwell and Gary D. Norsworthy / 53 Bronchial Disease, Chronic Philip Padrid / 58 Calicivirus Infection Gary D. Norsworthy / 62 Carcinomatosis Bradley R. Schmidt / 65 Cardiopulmonary Arrest Larry P. Tilley / 67 Cataracts Shelby L. Reinstein and Harriet J. Davidson / 70 Ceruminous Gland Disease Mark Robson / 72 Cervical Ventroflexion Mitchell A. Crystal and Paula B. Levine / 74 Chemotherapy for Lymphoma Mitchell A. Crystal and Bradley R. Schmidt / 76 Chlamydophila Infection Teija Kaarina Viita-aho / 81 Chylothorax Gary D. Norsworthy / 83 Cobalamin Deficiency Jörg M. Steiner / 85 Coccidiomycosis Sharon Fooshee Grace / 87 Coccidiosis Mark Robson and Mitchell A. Crystal / 89 Constipation and Obstipation Sharon Fooshee Grace and Mitchell A. Crystal / 91 Corneal Ulcers Gwen H. Sila and Harriet J. Davidson / 93 Coughing Gary D. Norsworthy / 96 Cryptococcosis Sharon Fooshee Grace / 97 Cryptosporidiosis Mark Robson and Mitchell A. Crystal / 100 Cutaneous Markers of Internal Disease Christine A. Rees / 102 Cuterebra Sharon Fooshee Grace / 104 Cytauxzoonosis Mark Robson and Mitchell A. Crystal / 106 Dermatophytosis Christine A. Rees / 108 Diabetes Insipidus Andrew Sparkes / 111 Diabetes Mellitus: Chronic Complications Gary D. Norsworthy / 113 Diabetes Mellitus: Ketoacidosis Jacquie Rand / 115 Diabetes Mellitus: Uncomplicated Jacquie Rand / 118
vii
Contents
53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108 109 110 111 112 113 114 115 116 117 118
viii
Diaphragmatic Hernia Gary D. Norsworthy / 121 Diarrhea Mitchell A. Crystal and Mark C. Walker / 124 Digital Diseases Mitchell A. Crystal and Paula B. Levine / 126 Dilated Cardiomyopathy Larry P. Tilley / 129 Draining Tracts and Nodules Christine A. Rees / 131 Dysautonomia Karen M. Lovelace / 134 Dyspnea Gary D. Norsworthy / 136 Dystocia Gary D. Norsworthy / 138 Dysuria, Pollakiuria, and Stranguria Gary D. Norsworthy / 140 Ear Mites Sharon Fooshee Grace / 143 Envenomization: Arachnids Tatiana Weissova / 145 Envenomization: Insects Tatiana Weissova / 148 Envenomization: Snakes Tatiana Weissova / 151 Eosinophilic Granuloma Complex Christine A. Rees / 154 Eosinophilic Keratitis Gwen H Sila and Harriet J. Davidson / 157 Epilepsy Teija Kaarina Viita-aho / 159 Esophageal Disease Andrew Sparkes / 162 Ethylene Glycol Toxicity Tatiana Weissova and Gary D. Norsworthy / 167 Exocrine Pancreatic Insufficiency Jörg M. Steiner / 169 Eyelid Diseases and Surgery Gwen H. Sila and Harriet J. Davidson / 171 Feline Enteric Coronavirus Infection Amanda L. Lumsden and Gary D. Norsworthy / 175 Feline Idiopathic Cystitis Tatiana Weissova and Gary D. Norsworthy / 176 Feline Immunodeficiency Virus Infection Sharon Fooshee Grace / 179 Feline Infectious Peritonitis Gary D. Norsworthy / 181 Feline Leukemia Virus Diseases Fernanda Vieira Amorim da Costa and Gary D. Norsworthy / 184 Fever Mitchell A. Crystal and Paula B. Levine / 187 Flea Allergy Dermatitis Christine A. Rees / 189 Fleas Sharon Fooshee Grace / 191 Flukes: Liver, Biliary, and Pancreatic Gary D. Norsworthy / 193 Food Reaction Christine A. Rees / 195 Giardiasis Mark Robson and Mitchell A. Crystal / 197 Gingivitis-Stomatitis-Pharyngitis Mark Robson and Mitchell A. Crystal / 199 Glaucoma Shelby L. Reinstein and Harriet J. Davidson / 202 Glomerulonephritis Gary D. Norsworthy / 205 Granulosa Cell Tumor Fernanda Vieira Amorim da Costa and Heloisa Justen Moreira de Souza / 207 Heartworm Disease Jane E. Brunt / 208 Heinz Body and Methemoglobinemia Anemia Sharon Fooshee Grace / 211 Helicobacter Mark Robson and Mitchell A. Crystal / 213 Hemangiosarcoma Bradley R. Schmidt / 215 Hemoplasmosis Sharon Fooshee Grace and Gary D. Norsworthy / 218 Hepatic Lipidosis Gary D. Norsworthy / 220 Hepatitis, Inflammatory Sharon Fooshee Grace / 222 Herpesvirus Infection Sharon Fooshee Grace / 225 High-Rise Syndrome Mitchell A. Crystal / 228 Histoplasmosis Sharon Fooshee Grace / 231 Hookworms Mitchell A. Crystal and Mark C. Walker / 234 Horner’s Syndrome Sharon Fooshee Grace / 235 Hydronephrosis Gary D. Norsworthy / 237 Hyperadrenocorticism Karen M. Lovelace / 239 Hyperaldosteronism Andrew Sparkes / 241 Hypercalcemia Michele Fradin-Fermé / 243 Hypereosinophilic Syndrome Sharon Fooshee Grace / 245 Hyperesthesia Syndrome Amanda L. Lumsden / 246 Hyperkalemia Michele Fradin-Fermé / 247 Hypertension, Systemic Beate Egner / 250 Hypertensive Cardiomyopathy Beate Egner / 254 Hyperthyroidism Mitchell A. Crystal and Gary D. Norsworthy / 256 Hypertrophic Cardiomyopathy Larry P. Tilley / 261 Hypoadrenocorticism Karen M. Lovelace / 265 Hypoalbuminemia Sharon Fooshee Grace / 267 Hypocalcemia Karen M. Lovelace / 270 Hypokalemia Mark Robson and Mitchell A. Crystal / 272 Hypomagnesemia Michele Fradin-Fermé / 274 Hypophosphatemia Stephanie G. Gandy-Moody / 275 Icterus Sharon Fooshee Grace / 277 Idiopathic Ulcerative Dermatitis Christine A. Rees / 280
Contents
119 120 121 122 123 124 125 126 127 128 129 130 131 132 133 134 135 136 137 138 139 140 141 142 143 144 145 146 147 148 149 150 151 152 153 154 155 156 157 158 159 160 161 162 163 164 165 166 167 168 169 170 171 172 173 174 175 176 177 178 179 180 181 182 183 184
Immune-Mediated Hemolytic Anemia Anthony P. Carr / 282 Inflammatory Bowel Disease Mark Robson and Mitchell A. Crystal / 284 Inflammatory Polyps and Masses Gary D. Norsworthy / 287 Intraocular Tumors Karen R. Brantman and Harriet J. Davidson / 290 Ischemic Encephalopathy Sharon Fooshee Grace / 292 Keratitis and Conjunctivitis Shelby L. Reinstein and Harriet J. Davidson / 294 Kidneys, Abnormal Size Gary D. Norsworthy / 297 Laryngeal Disease Andrew Sparkes / 298 Leprosy Syndrome Sharon Fooshee Grace / 302 Linear Foreign Body Gary D. Norsworthy / 304 Lung Parasites Gary D. Norsworthy / 306 Lymphoma Bradley R. Schmidt and Mitchell A. Crystal / 308 Malassezia Dermatitis Christine A. Rees / 313 Mammary Gland Neoplasia Bradley R. Schmidt and Mitchell A. Crystal / 314 Mammary Hyperplasia Gary D. Norsworthy / 317 Manx Syndrome Vanessa Pimentel de Faria / 318 Mast Cell Tumors Bradley R. Schmidt and Mitchell A. Crystal / 320 Megacolon Mitchell A. Crystal / 323 Meningioma Sharon Fooshee Grace / 326 Mesothelioma Fernanda Vieira Amorim da Costa / 328 Metaldehyde Toxicity Tatiana Weissova / 330 Miliary Dermatitis Christine A. Rees / 332 Mitral Valve Dysplasia Larry P. Tilley / 333 Murmurs Larry P. Tilley and Francis W. K. Smith, Jr. / 334 Myasthenia Gravis Paula Schuerer and Sharon Fooshee Grace / 336 Mycobacterial Diseases, Rapidly Growing Sharon Fooshee Grace / 338 Myiasis Elizabeth Macdonald / 340 Nasal Discharge Gary D. Norsworthy / 342 Nasal-Frontal Sinus Infection Gary D. Norsworthy / 344 Nasal Myiasis Sarah M. Webb / 347 Nasopharyngeal Disease Arnold Plotnick / 349 Neonatal Isoerythrolysis Sharon Fooshee Grace / 352 Neurogenic Bladder Sharon Fooshee Grace / 354 Nocardiosis Sharon Fooshee Grace / 356 Obesity Mark Robson, Mitchell A. Crystal, and Debra L. Zoran / 358 Oral Neoplasia Bradley R. Schmidt and Mitchell A. Crystal / 361 Organophosphate and Carbamate Toxicosis Gary D. Norsworthy / 364 Osteoarthritis Andrew Sparkes / 366 Otitis Externa Gary D. Norsworthy / 369 Otitis Media and Interna Sharon Fooshee Grace / 374 Pancreatitis, Acute Jörg M. Steiner / 377 Pancreatitis, Chronic Jörg M. Steiner / 380 Panleukopenia (Feline Parvovirus Infection) Sharon Fooshee Grace / 382 Panniculitis Mark Robson and Mitchell A. Crystal / 384 Paraneoplastic Syndromes Mark Robson / 386 Patent Ductus Arteriosis Larry P. Tilley / 388 Pectus Excavatum Sharon Fooshee Grace / 390 Pemphigus Foliaceus Christine A. Rees / 392 Perinephric Pseudocysts Fernanda Vieira Amorim da Costa / 394 Peritonitis, Septic Sharon Fooshee Grace / 397 Plague (Yersiniosis) Sharon Fooshee Grace / 400 Plant Toxicities Karen M. Lovelace / 402 Pleural Effusion Gary D. Norsworthy / 412 Pneumothorax Gary D. Norsworthy / 414 Pododermatitis: Lymphoplasmacytic Richard Malik and Gary D. Norsworthy / 416 Polycystic Kidney Disease Gary D. Norsworthy / 418 Polydactylism Sharon Fooshee Grace / 420 Polyphagic Weight Loss Mitchell A. Crystal and Paula B. Levine / 422 Polyuria and Polydipsia Mark Robson and Mitchell A. Crystal / 424 Portosystemic Shunt Mark Robson and Mitchell A. Crystal / 426 Pulmonary Fibrosis Sharon Fooshee Grace / 428 Pulmonic Stenosis Larry P. Tilley / 430 Pyelonephritis Gary D. Norsworthy / 432 Pyometra and Mucometra Gary D. Norsworthy / 434 Pyothorax Gary D. Norsworthy / 436 Pyrethrin and Pyrethroid Toxicosis Gary D. Norsworthy / 439
ix
Contents
185 186 187 188 189 190 191 192 193 194 195 196 197 198 199 200 201 202 203 204 205 206 207 208 209 210 211 212 213 214 215 216 217 218 219 220 221 222 223 224 225 226 227 228 229 230
Rabies Mark Robson and Mitchell A. Crystal / 440 Recreational Drug Toxicosis Tatiana Weissova / 442 Rectal Disease Heloisa Justen Moreira de Souza / 446 Refeeding Syndrome Karen M. Lovelace / 449 Renal Failure, Acute Sharon Fooshee Grace / 452 Renal Failure, Chronic Gary D. Norsworthy / 455 Renal Insufficiency Gary D. Norsworthy / 457 Restrictive Cardiomyopathy Larry P. Tilley / 460 Retinal Disease Karen R. Brantman and Harriet J. Davidson / 462 Rodenticide Toxicosis Mitchell A. Crystal / 466 Roundworms Mitchell A. Crystal and Mark C. Walker / 468 Salmonellosis Mark Robson and Mitchell A. Crystal / 470 Sarcomas, Injection Site Sharon Fooshee Grace / 472 Sarcomas, Other Mark Robson / 475 Scottish Fold Osteochondrodysplasia Sharon Fooshee Grace / 478 Seizures Sharon Fooshee Grace / 480 Skin Parasites Christine A. Rees / 483 Sporotrichosis Vanessa Pimentel de Faria / 487 Squamous Cell Carcinoma, Cutaneous Bradley R. Schmidt and Mitchell A. Crystal / 489 Stomach Worms Mitchell A. Crystal and Mark C. Walker / 492 Stud Tail Christine A. Rees / 493 Tail Injuries Sharon Fooshee Grace / 494 Tapeworm Infections Mitchell A. Crystal and Mark C. Walker / 496 Tetanus Sharon Fooshee Grace / 498 Tetralogy of Fallot Larry P. Tilley / 500 Thiamine Deficiency Gary D. Norsworthy / 502 Third Eyelid Diseases Gwen H. Sila and Harriet J. Davidson / 503 Thromboembolic Disease Larry P. Tilley / 506 Thymoma Bradley R. Schmidt / 509 Toxoplasmosis Gary D. Norsworthy and Sharon Fooshee Grace / 512 Tracheal Disease Andrew Sparkes / 515 Triad Disease Anthony P. Carr / 519 Trichobezoars Mitchell A. Crystal / 521 Tritrichomoniasis Mark Robson and Mitchell A. Crystal / 523 Ureteral Obstruction Rhett Marshall / 526 Urethral Obstruction Rhett Marshall / 530 Urinary Bladder Tumors Bradley R. Schmidt / 535 Urolithiasis Gary D. Norsworthy / 538 Uveitis Gwen H. Sila and Harriet J. Davidson / 543 Ventricular Septal Defect Larry P. Tilley / 546 Vestibular Syndrome Mitchell A. Crystal / 548 Viral Dermatitis Christine A. Rees / 550 Vitamin A Toxicosis Gary D. Norsworthy / 552 Vitamin D Toxicosis Gary D. Norsworthy / 553 Vomiting Mitchell A. Crystal and Paula B. Levine / 555 Weight Loss Mitchell A. Crystal and Mark C. Walker / 558
Section 2: Behavior 231 232 233 234 235 236 237 238 239
Aggression towards Humans Debra F. Horwitz / 563 Catnip Effects Sharon Fooshee Grace / 566 Environmental Enrichment in the Home Debra F. Horwitz / 567 Environmental Enrichment in the Hospital Gary D. Norsworthy and Linda Schmeltzer / 571 Housesoiling Debra F. Horwitz / 577 Intercat Aggression Debra F. Horwitz / 581 Marking Debra F. Horwitz / 584 Psychogenic Alopecia Debra F. Horwitz / 587 Behavioral Pharmaceuticals Debra F. Horwitz / 591
Section 3: Dentistry 240 241 242 243
x
Dental Examination R. B. Wiggs and B. C. Bloom / 597 Dental Prophylaxis R. B. Wiggs, S. L. Ruth, and B. C. Bloom / 599 Endodontics and Restorations R. B. Wiggs, S. L. Ruth, and B. C. Bloom / 602 Extractions R. B. Wiggs, B. C. Bloom, and S. L. Ruth / 606
Contents
244 245
Dental Resorption R. B. Wiggs, B. C. Bloom, and S. L. Ruth / 608 Oral and Dental Radiography R. B. Wiggs, B. C. Bloom, and S. L. Ruth / 610
Section 4: Surgery 246 247 248 249 250 251 252 253 254 255 256 257 258 259 260 261 262 263 264 265 266 267 268 269 270 271 272 273 274 275 276 277 278
Anesthesia: Local Ludovic Pelligand / 617 Anesthesia: Sedation and General Ludovic Pelligand / 620 Bulla Osteotomy: Ventral Approach Don R. Waldron / 626 Colectomy Don R. Waldron / 631 Corneal Surgery Gwen H. Sila / 636 Cranial Cruciate Ligament Rupture Mac Maxwell / 638 Cryptorchidism Surgery Mac Maxwell / 640 Esophagostomy Tube Placement Gary D. Norsworthy / 642 Frontal Sinus Obliteration Gary D. Norsworthy / 646 Gastrostomy Tube Placement Don R. Waldron / 649 Jejunostomy Tube Placement Don R. Waldron / 651 Laser Surgery, CO2 John C. Godbold, Jr. / 655 Lip Avulsion Replacement Gary D. Norsworthy / 660 Luxating Patella Otto Lanz / 662 Mandibular Symphyseal Separation Don R. Waldron / 664 Mastectomy Don R. Waldron / 666 Nasopharyngeal Polyp or Mass Removal Gary D. Norsworthy / 667 Nephrolith Removal Don R. Waldron / 670 Onychectomy Don R. Waldron / 673 Oronasal Fistula Repair Heloisa Justen Moreira de Souza / 676 Pain Management Sabine Tacke / 682 Perivulvar Skin Fold Removal Gary D. Norsworthy / 685 Physical Therapy and Rehabilitation Barbara Bockstahler and David Levine / 687 Rhinotomy Gary D. Norsworthy / 691 Sliding Skin Flaps Mac Maxwell / 693 Subcutaneous Fluid Catheter Placement Gary D. Norsworthy / 696 Thoracostomy Tube Placement Don R. Waldron / 698 Thyroidectomy Gary D. Norsworthy / 701 Total Ear Canal Ablation and Lateral Bulla Osteotomy Don R. Waldron / 704 Ureterolith Removal Don R. Waldron / 707 Urethrostomy, Perineal Don R. Waldron / 709 Urethrostomy, Prepubic Don R. Waldron / 712 Urinary Bladder Marsupialization Gary D. Norsworthy / 715
Section 5: Cytology 279 280 281 282 283 284 285 286 287 288 289 290
Sample Staining Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 719 Inflammation versus Neoplasia: Differentiation Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 721 Adenocarcinoma Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 728 Atypical Bacterial Infections Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 730 Fibrosarcoma Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 732 Hepatic Lipidosis Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 734 Lymph Node Disease Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 736 Lymphoma Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 738 Mast Cell Tumors Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 740 Pleural Effusions Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt / 742 Systemic Fungal Disease Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 746 Transtracheal Wash Hemosiderosis Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano / 749
Section 6: Imaging 291 292 293 294
Imaging: The Thorax Merrilee Holland and Judith Hudson / 753 Imaging: The Abdomen Merrilee Holland and Judith Hudson / 784 Imaging: The Head and Spine Merrilee Holland and Judith Hudson / 828 Imaging: Cardiovascular Disease Merrilee Holland and Judith Hudson / 849
Section 7: Clinical Procedures 295 296
Blood Transfusion Sharon Fooshee Grace / 879 Bone Marrow Aspiration Mitchell A. Crystal / 882
xi
Contents
297 298 299 300 301 302 303 304 305 306 307 308 309 310 311 312
Central Venous Catheter Placement Mitchell A. Crystal / 885 Cerebrospinal Fluid Collection Mitchell A. Crystal / 888 Eye Examination Karen R. Brantman and Harriet J. Davidson / 890 Euthanasia Amanda L. Lumsden and Gary D. Norsworthy / 893 Fine-Needle Biopsy Mitchell A. Crystal / 896 Fluid Therapy Sharon Fooshee Grace / 898 Jugular Blood Collection Gary D. Norsworthy / 902 Lung Aspiration Karen M. Lovelace / 904 Nasal Sampling Gary D. Norsworthy / 906 Necropsy of Kittens Michele Fradin-Fermé / 908 Neurologic Examination Stephanie G. Gandy-Moody / 910 Orogastric Tube Feeding Gary D. Norsworthy / 913 Polymerase Chain Reaction Testing Christian M. Leutenegger / 915 Restraint Devices and Techniques Gary D. Norsworthy / 920 Testing Procedures Mitchell A. Crystal and Gary D. Norsworthy / 924 Therapeutic Laser Applications Ronald J. Riegel / 928
Section 8: Appendices 313 314 315 316 317 318 319 320 321 322 323 324 325 326 327 328 329
Age Approximation Karen M. Lovelace / 933 Anatomical Differences in Cats and Dogs Clay Anderson and James E. Smallwood / 937 Body Surface Area Conversion Gary D. Norsworthy / 939 Breed Specific Diseases James K. Olson / 940 Cattery Hygiene Suvi Pohjola-Stenroos / 943 Echocardiographic Tables Larry P. Tilley and Francis W. K. Smith, Jr. / 945 Electrocardiographic Tables Larry P. Tilley and Francis W. K. Smith, Jr. / 947 Feral and Free-Roaming Cats Christine L. Wilford / 948 Grief Response by Cat Owners Larry A. Norsworthy, Kacee Junco, and Brooke Woodrow / 954 Hospital Hygiene Suvi Pohjola-Stenroos / 957 Life Stage Guidelines AAFP/AAHA / 960 Normal Laboratory Values Gary D. Norsworthy and Teija Kaarina Viita-aho / 977 Pregnancy, Parturition, and Lactation Teija Kaarina Viita-aho / 979 Purring Sharon Fooshee Grace / 982 Renal Transplantation Daniel A. Degner / 984 Vibrissae Sharon Fooshee Grace / 987 Zoonotic Diseases Suvi Pohjola-Stenroos / 989
Section 9: Formulary 330
Drug Formulary Gary D. Norsworthy, Linda Schmeltzer, Sharon Fooshee Grace, and Mitchell A. Crystal / 999
Index / 1034
xii
Founding Authors Gary D. Norsworthy, DVM, DABVP (Feline) Chief of Staff Alamo Feline Health Center San Antonio, TX Adjunct Professor College of Veterinary Medicine Mississippi State University
Mitchell A. Crystal, DVM, DACVIM (Internal Medicine) North Florida Veterinary Specialists, P.A. Jacksonville, FL Larry P. Tilley, DVM, DACVIM (Internal Medicine) President, VetMed Consultants Consultant, New Mexico Veterinary Referral Center Santa Fe, NM
Sharon Fooshee Grace, MAgric, MS, DVM, DABVP (Canine-Feline), DACVIM (Internal Medicine) Mississippi State University College of Veterinary Medicine Mississippi State, MS
xiii
Contributors Fernanda Vieira Amorim da Costa, DVM, MSc, PhD Founder and President, Brazilian Academy of Feline Practice Florianopolis, Brazil Clay Anderson, DVM Alamo Feline Health Center San Antonio, TX Tara Arndt, DVM, DACVP Ontario Veterinary College Department of Pathobiology Guelph, ON, Canada Bonnie. C. Bloom, DVM Fellow, Academy of Veterinary Dentistry Dallas Dental Service Animal Clinic Dallas, TX Barbara Bockstahler, DVM, CCRP Specialized Veterinarian in Physiotherapy and Rehabilitation University of Veterinary Medicine Vienna, Austria Karen R. Brantman, DVM Michigan Veterinary Specialists Grand Rapids, MI Jane E. Brunt, DVM Owner and Founder Cat Hospital at Towson Cat Hospital Eastern Shore Baltimore, MD Anthony P. Carr, DVM, DACVIM (Internal Medicine) Professor Small Animal Clinical Sciences Western College of Veterinary Medicine University of Saskatchewan Saskatoon, SK, Canada Rick L. Cowell, DVM, MS, MRCVS, DACVP IDEXX Laboratories Stillwater, OK Harriet J. Davidson, DVM, DACVO Michigan Veterinary Specialists Grand Rapids, MI Daniel A. Degner, DVM, DACVS Michigan Veterinary Specialists Auburn Hills, MI Beate Inge Egner, Doctor med. vet., Board Certified Freelance specialist for cardiovascular disease Kleintierzentrum Hörstein (Clinical Center for Small Animals) Hoerstein, Germany
xiv
Michele Fradin-Fermé, DVM Vincennes, France Stephanie G. Gandy-Moody, DVM The Cat Hospital of Madison Madison, AL John C. Godbold, Jr. DVM Stonehaven Park Veterinary Hospital Laser Surgery Center Jackson, TN Merrilee Holland, DVM, DACVR Associate Professor, Radiology Section Department of Clinical Science College of Veterinary Medicine Auburn University Auburn, AL Debra F. Horwitz, DVM, Diplomate, ACVB Owner, Veterinary Behavior Consultations St. Louis, MO Judith Hudson, DVM, DACVR Professor, Radiology Section Department of Clinical Sciences College of Veterinary Medicine Auburn University Auburn, AL Kacee Junco, BS QMHP-CS, M.S., LPC-I Texana Center Brookshire, TX Heloisa Justen Moreira de Souza, DVM, PhD Professor Feline Medicine and Surgery Department of Medicine and Surgery Institute of Veterinary Medicine University Federal Rural of Rio de Janeiro Rio de Janeiro, RJ, Brazil Otto Lanz, DVM, DACVS Associate Professor, Surgery Department of Small Animal Clinical Sciences Virginia-Maryland Regional College of Veterinary Medicine Virginia Tech Blacksburg, VA Christian M. Leutenegger, Dr. Vet. Med., PhD, FVH Regional Head of Molecular Diagnostics (MDx) IDEXX Reference Laboratories West Sacramento, CA
Contributors
David Levine, PT, PhD, DPT, OCS, CCRP Walter M. Cline Chair of Excellence in Physical Therapy Department of Physical Therapy The University of Tennessee at Chattanooga Chattanooga, TN Paula B. Levine, DVM, DACVIM (Internal Medicine) North Florida Veterinary Specialists, P.A. Jacksonville, FL Karen M. Lovelace, DVM The Cat Doctor (Thousand Oaks) Thousand Oaks, CA Amanda L. Lumsden, DVM Cat and Bird Clinic Santa Barbara, CA Elizabeth Macdonald, DVM Alamo Feline Health Center San Antonio, TX Richard Malik, DVSc DipVetAn, MVetClinStud, PhD, FACVSc, FASM Centre for Veterinary Education Veterinary Science Conference Centre The University of Sydney Sydney, NSW, Australia Rhett Marshall, BVSc, MACVSc (Small Animal Surgery) Member, Australian College of Veterinary Scientists in Small Animal Surgery Senior Feline Practitioner and Principle The Cat Clinic, Mt. Gravatt, QLD, Australia Mac Maxwell, DVM, DACVS Medvet Veterinary Specialists Cordova, TN Larry A. Norsworthy, PhD Professor of Psychology Licensed Clinical Psychologist Department of Psychology Abilene Christian University Abilene, TX James K. Olson, DVM, DABVP (Feline) Cat Specialist, PC Castle Rock, CO
Vanessa Pimentel de Faria, DVM, MSc Specialized in Feline Medicine Owner, Só Gatos Brasilia-DF, Brazil Arnold Plotnick MS, DVM, DACVIM (IM) Manhattan Cat Specialists New York, NY Suvi Pohjola-Stenroos, DVM, PhD, DABVP (Feline) Clinivet Oy, Cat Clinic Felina Founder, Practitioner Helsinki, Finland Jacquie Rand, BVSc, DVSc, Diplomate ACVIM (Internal Medicine) Professor of Companion Animal Health Director, Centre for Companion Animal Health School of Veterinary Science The University of Queensland St. Lucia, QLD, Australia Christine A. Rees, DVM, DACVD Veterinary Specialists of North Texas Dallas, TX Shelby L. Reinstein, DVM, MS Research Veterinarian Retinal Disease Studies Facility School of Veterinary Medicine University of Pennsylvania/NBC Kennett Square, PA Ronald J. Riegel, DVM Independent Consultant, Author, Manufacturer Marysville, OH Mark Robson, BVSc (Distinction), DACVIM, Registered Veterinary Specialist Veterinary Specialist Group Auckland, New Zealand Sunny L. Ruth, DVM Dallas Dental Service Animal Clinic Dallas, TX Linda Schmeltzer, RVT Head Technician Alamo Feline Health Center San Antonio, TX
Philip Padrid, DVM Southwest Regional Medical Director VCA Associate Professor of Molecular Medicine (Adjunct) University of Chicago Pritzker School of Medicine Associate Professor of Small Animal Medicine (Adjunct) The Ohio State University School of Veterinary Medicine Corrales, NM
Bradley R. Schmidt, DVM, Diplomate ACVIM (Oncology) Staff Oncologist North Florida Veterinary Specialists, P.A. Jacksonville, FL
Ludovic Pelligand, Dr. Med. Vet., MRCVS, Dipl. ECVAA Royal Veterinary College North Mymms, Hatfield Hertfordshire, UK (England)
Gwen H. Sila, DVM Michigan Veterinary Specialists Southfield, MI
Paula A. Schuerer, DVM, MBA Animal Ark Animal Hospital, LLC Franklin, TN
xv
Contributors
Andrew H. Sparkes, BVetMed, PhD, DECVIM, MRCVS Head of Small Animal Studies Animal Health Trust Lanwades Park Kentford Newmarket Suffolk United Kingdom (England) James E. Smallwood, DVM, MS Alumni Distinguished Professor of Anatomy Director of CVM Alumni Relations Department of Molecular Biomedical Sciences North Carolina State College of Veterinary Medicine Raleigh, NC Francis W.K. Smith, Jr., DVM, DACVIM (Cardiology and Small Animal Internal Medicine) Lexington, MA Vice-President, VetMed Consultants, Inc. Clinical Assistant Professor Tufts University Cummings School of Veterinary Medicine North Grafton, MA Jörg M. Steiner, DVM, PhD, Dipl. ACVIM, Dipl. ECVIM-CA Associate Professor and Director of Gastrointestinal Laboratory Department of Small Animal Clinical Sciences College of Veterinary Medicine and Biomedical Sciences Texas A&M University College Station, TX PD Dr. Sabine Tacke Anesthesia, Pain Therapy, Perioperative Intensive Care Animal Protection Officer of the Department of Veterinary Clinical Sciences Consultant Veterinary Anesthetist Consultant Veterinary Surgeon Treasurer EVECCS Department of Veterinary Clinical Sciences Clinic for Small Animals, Surgery Justus-Liebig-University Giessen Giessen, Germany Amy C. Valenciano, DVM, MS, DACVP IDEXX Reference Laboratories Veterinary Clinical Pathologist Dallas, TX
xvi
Teija Kaarina Viita-aho, DVM Helsinki, Finland Don Waldron, DVM, DACVS Director of Specialty Services VCA Veterinary Care Animal Hospital and Referral Center Albuquerque, NM Mark C. Walker, BVSc, DACVIM (Internal Medicine) North Florida Veterinary Specialists, P.A. Jacksonville, FL Sarah M. Webb, BVSc, MACVSc Specialist Small Animal Surgeon Surgical Referral Services Gungahlin, ACT Australia Tatiana Weissova, DVM, PhD The Small Animal Clinic Department of Internal Diseases University of Veterinary Medicine Slovak Republic R. B. Wiggs, DVM, DAVDC, deceased Fellow, Academy of Veterinary Dentistry Adjunct Professor, Baylor College of Dentistry Texas A&M University Systems Dallas Dental Service Animal Clinic Dallas, TX Christine L. Wilford, DVM Cats Exclusive Veterinary Center Shoreline, WA Brooke Woodrow, M.S., LPC-I Academic Counselor Academic Development Center Abilene Christian University Abilene, TX Debra L. Zoran, DVM, PhD, DACVIM-SAIM Associate Professor and Chief of Medicine Department of Small Animal Clinical Sciences College of Veterinary Medicine and Biomedical Sciences Texas A&M University College Station, TX
Preface In the real world of veterinary practice, diagnosis and treatment of feline diseases are usually done at a rapid pace. The primary goal of this book is to resolve the conflict between the need for accurate and relevant information and the urgency demanded by a patient on your examination table while others are waiting for your care. I have designed this book like I would want it for my use in the primary care setting. Knowing that primary care practitioners are the ones who will use it most, I hope
that The Feline Patient, Fourth Edition, will prove itself to be a valuable resource for thousands of veterinary practitioners around the world to the betterment of feline health. Gary D. Norsworthy, DVM, Diplomate, ABVP (Feline) Alamo Feline Health Center, San Antonio, Texas
xvii
The Feline Patient Fourth Edition
SECTION
1 Diseases and Conditions
CHAPTER 1
Acetaminophen Toxicosis Sharon Fooshee Grace
Overview Acetaminophen toxicosis usually occurs when well-intentioned owners, unaware of the significant toxicity of this drug in cats, administer the drug for a variety of reasons. Most case reports indicate that owners give acetaminophen to individual cats as a pain reliever. Ingestion of as little as 10 mg/kg of acetaminophen may be fatal for cats. This amounts to less than one regular-strength tablet (325 mg) for a 4- to 5-kilogram (8.8to 11-pound) cat. One case report described fatal toxicosis in a kitten that had played with an empty acetaminophen bottle. Acetaminophen attacks several metabolic peculiarities of the feline species. Once the cat’s limited ability to produce nontoxic drug metabolites via sulfate and glucuronide conjugation has been exceeded, the hepatic cytochrome P450 oxidase system converts acetaminophen to the reactive electrophilic intermediate N-acetyl-para-benzoquinoneimine (NAPQ1). The toxic effects of acetaminophen are a direct result of formation of NAPQ1 and its assault on cellular macromolecules. Following depletion of glucuronide and sulfate, supplies of the next available line of defense—the cellular antioxidant, glutathione—become exhausted by rising levels of NAPQ1. As NAPQ1 continues to accumulate, hemoglobin is oxidized from its normal ferrous state (+2) to a ferric state (methemoglobin, +3) and becomes unable to effectively deliver oxygen to tissues, with catastrophic consequences for the patient. Notably, even under normal circumstances, the feline erythrocyte is always vulnerable to oxidative stress because of the relatively large number of sulfhydryl groups present in cat hemoglobin. Further, precipitation of damaged hemoglobin on the erythrocyte membrane leads to the second significant event: development of Heinz body hemolytic anemia. The feline spleen is relatively ineffective at removing Heinz bodies from erythrocyte membranes so they persist, with the net effect of increased erythrocyte membrane fragility, decreased deformability, and development of hemolytic anemia. Whereas methemoglobinemia is potentially reversible, Heinz body formation (and damage to the red blood cell membrane) is not. Finally, acetaminophen toxicosis may cause liver necrosis in cats via oxidative damage to hepatocyte membranes and reaction with hepatocellular proteins, but hepatic damage is usually minimal when compared with that typically seen in dogs. Earliest signs of toxicosis include anorexia, vomiting, and ptyalism. The appearance of cyanotic or brown-colored mucous membranes (usually within 24 hours of drug ingestion) heralds the onset of significant methemoglobinemia. Edema of the face and paws is common, though the precise cause for these findings remains unclear. As Heinz body hemolytic anemia develops within hours to a few days of drug ingestion, the mucous membranes become pale and sometimes icteric.
• Clinical Signs: The appearance of cyanotic or brown-colored mucous membranes and facial and paw edema are noteworthy. Other findings may include vocalization, tachycardia, dyspnea, depression, and weakness. Icterus may occur 24 to 48 hours after drug ingestion. • Complete Blood Count (CBC): Submitted blood will often have a dark brown color (see Diagnostic Notes for more information). Typical findings include anemia and the appearance of Heinz bodies on the red cell membrane. See Figure 1-1. Reticulocytes may appear several days later if the cat survives. Heinz bodies and reticulocytes are more easily recognized if a drop of new methylene blue stain is applied to an air-dried blood smear, which is then coverslipped and examined microscopically. See Figure 89-2 and Chapter 311. • Chemistry Profile: Hepatocellular leakage enzymes (serum alanine aminotransferase and serum aspartate aminotransferase) may be mildly to severely elevated. Because acetaminophen does not commonly cause significant hepatic necrosis in cats, these elevations could be due to hepatocyte hypoxia. Serum bilirubin is sometimes increased. • Urinalysis: Chocolate- or red-colored urine may be seen due to methemoglobinuria or hematuria.
Diagnostic Notes • In healthy, nonanemic cats up to 5% of erythrocytes may contain Heinz bodies. As such, detection of occasional Heinz bodies should be considered normal in cats. • Methemoglobinemia is the usual cause of death. It appears when more than 20 to 30% of hemoglobin is in the form of methemoglobin. • Methemoglobinemia is sometimes difficult to discern in a blood sample because venous blood is normally dark. As a clinical screening test, one drop of patient blood can be placed on a white paper towel or filter paper next to a drop of normal “control” blood. If the methemoglobin content is greater than 10%, the patient’s blood
Diagnosis Primary Diagnostics • History: Because the clinical signs are not always distinctive, a history of acetaminophen administration or potential exposure to the drug is critical to help confirm a diagnosis.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 1-1 Heinz body formation (arrow) on the red blood cells is one of the diagnostic features of acetaminophen toxicity.
5
SECTION 1: Diseases and Conditions
is expected to be noticeably brown when compared to the brighter red of the control blood. • Acetaminophen serum concentration may be measured and is maximally increased 2 to 3 hours post-ingestion. In most cases, it is unnecessary and impractical to measure blood levels of the drug.
Treatment Primary Therapeutics • Removal of the toxin: Acetaminophen is rapidly absorbed from the gastrointestinal tract so emesis should be induced only if drug ingestion has occurred within the previous 1 to 2 hours. Emesis may be induced by apomorphine or xylazine. Use of activated charcoal is controversial; it should be given only if acetaminophen ingestion has occurred within the preceding 2 hours. Because of the risk for aspiration pneumonia, activated charcoal should be used cautiously if the cat is vomiting or if emesis has been induced. If acetylcysteine is given orally, charcoal may bind the drug. • Acetylcysteine (Mucomyst®): This drug is recommended as a specific antidote. It supplies precursors for replenishment of glutathione stores. The available solutions are in 10 and 20% concentrations and should be appropriately diluted to a 5% solution with 5% dextrose. An initial oral or intravenous dose of 130 to 140 mg/kg should be followed by 70 mg/kg q6h PO, IV for five to seven treatments. It is recommended that intravenous treatments be administered through a 0.2-µm Millipore filter over 60 minutes. Some have suggested that oral administration may be superior to the intravenous route because of the higher concentration of drug available to the liver via portal circulation. It has been shown that therapy is less effective when started more than 8 hours after ingestion of acetaminophen, though there may still be some benefit appreciated when treating up to 80 hours post-ingestion.
Secondary Therapeutics • Cimetidine: This drug may have an additive effect with Nacetylcysteine because of its ability to inhibit the cytochrome P450 oxidase system and thus limit formation of toxic metabolites and limit hepatotoxicity. It should be used as adjunctive therapy only. The true efficacy of cimetidine in the setting of acetaminophen toxicosis remains unknown. The dose is 5 mg/kg q6 to 8 h IV for 48 hours. • Ascorbic acid (vitamin C): Vitamin C is an antioxidant which, through nonenzymatic means, is proposed to assist in reduction of methemoglobin back to hemoglobin, though the process is slow. This is an adjunctive therapy and should not be substituted for acetylcysteine administration. Give 30 mg/kg q6h IV until methemoglobinemia resolves. Consult a formulary before mixing ascorbic acid with other solutions due to a high likelihood of incompatibility. If intravenous ascorbic acid is not available, an oral formulation may be given at 125 mg/kg q6h for six treatments. • S-Adenosylmethionine (SAMe): SAMe, currently marketed as Denosyl® and Denamarin®, demonstrates hepatoprotective and
6
systemic antioxidant properties. SAMe has been shown to increase the cat’s resistance to oxidative stress and thus appears beneficial as an adjunct therapy for acetaminophen toxicity. In one placebocontrolled feline study evaluating oxidant injury caused by acetaminophen, SAMe-treated cats had reduced Heinz body formation and erythrocyte destruction as compared to cats receiving only acetaminophen. However, additional studies need to be done, especially with regard to its effect on methemoglobinemia, which did not appear to improve with SAMe therapy in the aforementioned study. At this time, it should be considered an adjunctive treatment because N-acetylcysteine is a proven therapy. • Transfusion with blood or hemoglobin solutions: Administration of whole blood or Oxyglobin® (5–15 ml/kg IV) may be useful in cats with severe hemolytic anemia and should be considered if the hematocrit falls below 20%. Signs of hypoxemia would also warrant a transfusion, even with a normal hematocrit because the hematocrit is not a true reflection of the oxygen-carrying capacity of the blood. Oxyglobin is currently limited in availability and its use is controversial in this setting. It has the potential to cause volume overload in cats so slow infusion rates of 0.5 to 5 ml/kg per hour are recommended. • Supportive therapy: This may include intravenous fluids, electrolytes, and limited handling of the patient.
Therapeutic Notes • Corticosteroids are of no value in treating acetaminophen toxicosis. • The literature contains varied opinions about the benefit of oxygen therapy because methemoglobin is unable to bind oxygen. However, it is reasonable to consider oxygen support, being mindful that oxygen administration may further stress the patient. • Though opinions vary, most consider that methylene blue is contraindicated in treatment of this disorder because of the potential to worsen the hemolytic anemia. • A positive response to therapy is indicated by improvement within 48 hours.
Prognosis A grave prognosis is indicated when methemoglobinemia and Heinz body hemolytic anemia are severe and unresponsive to appropriate therapy. For cats that recover, no long-term effects have been reported.
Suggested Readings Allen AL. 2003. The diagnosis of acetaminophen toxicosis in a cat. Can Vet J. 44(6):509–510. El Bahri L, Lariviere N. 2003. Pharm profile: N-Acetylcysteine. Compend Contin Educ Pract Vet. 25(4):276–278. Savigny M, Macintire DK. 2005. Acetaminophen toxicity in cats. Compend Contin Educ Pract Vet. 7(3):8–11. Webb CB, Twedt DC, Fettman MJ, et al. 2003. S-adenosylmethionine (SAMe) in a feline acetaminophen model of oxidative injury. J Fel Med Surg. 5(2):69–75.
CHAPTER 2
Acne Christine A. Rees
Overview Acne is a common dermatologic condition in cats. Feline acne is a follicular keratinization and glandular proliferation of tissue and glands of the chin area. Other areas that can also be affected include the lower and upper lips. The usual age of onset is 6 months to 14 years of age (median age 4 years old). One study evaluating 22 cats with acne found that a variety of skin lesions are present with feline acne. The most common skin lesions noted with acne are comedones (73%), alopecia (68%), crusts (55%) papule (45%), and erythema (41%). In severe cases edema, cysts, and scars can be present. The most common body location is the chin. Pruritus is infrequent (35% of 22 cats). Malassezia pachydermatitis is uncommon (18%) of affected cats. Bacteria is present almost half of the patients (45%). The bacteria that are isolated include coagulase-positive staphylococci and alpha-hemolytic streptococci. Histopathologic findings in cats with acne include lymphoplasmacytic periductal inflammation, sebaceous gland duct dilatation, follicular keratosis with plugging and dilatation, folliculitis, pyogranulomatous adenitis, and furunculosis. See Figures 2-1 and 2-2.
Diagnosis Primary Diagnostics • History and Clinical Signs: These are so distinct that they are usually used to formulate the diagnosis. • Histopathology: Histologic signs for feline acne are classic (see description).
Figure 2-2 Advanced acne can result in severe folliculitis, pyogranulomatous adenitis, and furunculosis. At this stage, aggressive cleansing under anesthesia and antibiotic therapy are indicated. Image courtesy Dr. Gary D. Norsworthy.
Treatment Primary Therapeutics • Secondary infections should be treated with systemic antibiotics for 3 weeks or 1 week beyond when the skin appears normal. • Topical medications are useful for treating feline acne. The chin should be clipped and cleaned prior to applying these topical medications. Examples of topical medications that have been used include salicylic acid pads (i.e., Stridex® pads), benzoyl peroxide 5% gel, 0.01 to 0.025% tretinoin cream or lotion, 0.75% metronidazole gel, clindamycin ointment, and mupiricin ointment.
Therapeutic Notes • Hot packing of the chin prior to treatment often makes the treatment more effective. A warm, moist cloth can be held on the chin for 30 seconds to open the pores and allow the medication to penetrate better.
Prognosis The prognosis is good for feline acne. Intermittent lifelong symptomatic treatment is often necessary. Feline acne is primarily a cosmetic concern. The exception is when a secondary infection is present. Bacterial skin infections often require systemic therapy to achieve control. Figure 2-1 Early acne is characterized by the presence of comedones. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Suggested Readings Jazic E, Coyner KS, Loeffler DG, et al. 2006. An evaluation of the clinical, cytological, infectious and histopathological features of feline acne. Vet Derm. 17(2):134–140.
7
CHAPTER 3
Acromegaly Sharon Fooshee Grace
Overview Acromegaly is a well-recognized but rare disorder of cats caused by a functional growth hormone (GH) secreting tumor of the anterior pituitary. The disease is characterized by overgrowth of bone, viscera, and soft tissue and insulin-resistant diabetes mellitus. Most acromegalic cats are middle-aged to older males; a breed predisposition has not been recognized. Severe insulin-resistant diabetes mellitus is the most common and important clinical manifestation. GH exerts significant diabetogenic activity through its ability to create peripheral insulin resistance. Some acromegalic cats require 30 to 130 units of insulin per day to control concurrent diabetes. Historical and clinical findings include polyphagia, polyuria, polydipsia, weight gain despite poorly controlled diabetes, enlargement of the head, widened interdental spaces, inferior prognathism, large paws, rapid growth of toenails, thickened skin, degenerative arthritis, thickening of pharyngeal tissues, and organomegaly (especially cardiac, hepatic, and renal). Cats presented late in the course of disease may show signs of heart disease or failure (i.e., systolic murmur, pulmonary edema, pleural effusion) and chronic renal failure.
Diagnosis Primary Diagnostics • Change in Physical Appearance: Owners often fail to recognize gradual changes in their cat’s appearance. When possible, it is helpful to compare the appearance of the cat to a photograph taken several years before onset of signs to evaluate for changes consistent with acromegaly. • Minimum database (complete blood count, chemistry profile, and urinalysis): Hyperglycemia and glucosuria are consistent findings. Other common findings include hyperphosphatemia, hyperproteinemia, hypercholesterolemia, and mild increases in liver enzymes. Proteinuria can precede development of azotemia, which usually occurs late in the course of disease. • Insulin-Like Growth Factor-I (Somatomedin C) Levels: This is a commercially available test that provides an indirect assessment of GH levels. It is currently available through the endocrine laboratory at Michigan State University (phone 1-517-353-1683). The laboratory reports a sensitivity of 84% and specificity of 92%. The normal range is 12 to 92; a value greater than 200 is strongly suggestive of acromegaly. • Growth Hormone Assay: Measurement of serum GH can provide a definitive diagnosis. This test is offered at the University of Minnesota Veterinary Diagnostic Lab. See www.vdl.umn.edu. • Computed Tomography (CT) or Magnetic Resonance Imaging (MRI): At present, advanced imaging techniques are the most reliable means for detecting a pituitary mass. Pituitary imaging is also helpful in defining the size and progression of the tumor. See Figure 3-1. The presence of a mass is not diagnostic of a GH-secreting tumor because other types of pituitary tumors occur in cats (e.g., adrenocorticotropic hormone [ACTH]-secreting pituitary tumor). However,
Figure 3-1 A large pituitary mass can be seen at the tip of the arrow. This computerized tomography scan is typical for a cat with acromegaly. Image courtesy of Linda Abraham BSc, BVetMed, MRCVS, PhD, FACVSc and Steven Holloway, BVSc, DACVIM, PhD, The University of Melbourne, Australia. the likelihood that a pituitary tumor is secreting GH rises significantly if clinical signs of acromegaly are present, and if hyperadrenocorticism is ruled out via lack of clinical signs and results of adrenal testing. See Chapter 101.
Secondary Diagnostics • Radiographs: Survey radiographs of the chest, abdomen, and bones may reveal cardiomegaly, pulmonary edema, pleural effusion, hepatomegaly, splenomegaly, renomegaly, degenerative arthropathy, and a periarticular periosteal reaction. • Echocardiography: This may reveal hypertrophic changes in the septum and left ventricular free wall. • Adrenal Function Testing: Adrenal function should be evaluated to eliminate hyperadrenocorticism as a cause of insulin-resistant diabetes mellitus. Available tests include ACTH stimulation, dexamethasone suppression, endogenous plasma ACTH concentrations, and urinary cortisol-to-creatinine ratio. See Chapter 101 for details. • Thyroid Testing: Hyperthyroidism is common in elderly cats and may be a cause of insulin resistance in cats with naturally occurring diabetes mellitus. All geriatric cats should be evaluated with a total T4 value. However, the presence of unregulated diabetes often results in lowered total T4 values.
Diagnostic Notes th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
8
• GH assays that have been designed for humans will not accurately assess feline GH levels.
Acromegaly
• Hypertension is a common attendant problem in humans with acromegaly but has not been evaluated in affected cats.
Treatment Primary Therapeutics • Radiation Therapy: Radiation therapy offers the best chance for control of the disease. Results have varied from minimal to dramatic shrinkage of the tumor. Unfortunately, it is common for the tumor to regrow and signs to recur after cessation of therapy (6–18 months). • Medical Therapy: Drugs that lower circulating GH levels (e.g., dopamine agonists or somatostatin analogues) have been tried with mixed results; most cats fail to demonstrate a positive response. Therapy is not generally recommended unless other management techniques (i.e., high dose insulin, managing other secondary conditions, or radiation therapy) have been attempted and are not successful.
Secondary Therapeutics • Insulin: Increasing doses of insulin will be required to manage insulin-resistant diabetes mellitus.
Therapeutic Notes • Monitoring for secondary conditions (e.g., renal disease or cardiac disease) and provision of appropriate therapy will be necessary in most cases of feline acromegaly.
• Cryosurgical ablation of the pituitary gland has been reported in two cats; one had a positive outcome and the other was euthanized several months later.
Prognosis Many cats will do well for 1 to 2 years without specific treatment for acromegaly if the diabetes is managed reasonably well. One study of 14 acromegalic cats reported a mean survival time of 22 months and a median survival time of 21 months. Most cats will eventually die or are euthanized from secondary conditions (i.e., congestive heart failure, renal disease, and so on).
Suggested Readings Berg RIM, Nelson RW, Feldman EC, et al. 2007. Serum insulin-like growth factor-I concentration in cats with diabetes mellitus and acromegaly. J Vet Intern Med. 21(5);892–898. Dunning MD, Lowrie, CS, Bexfield NH, et al. 2009. Exogenous insulin treatment after hypofractionated radiotherapy in cats with diabetes mellitus. J Vet Intern Med. 23(2):243–249. Hurty CA, Flatland B. 2005. Feline acromegaly: A review of the syndrome. J Vet Intern Med. 41(5):292–297. Mayer M, Greco DS, LaRue SM. 2006. Outcomes of pituitary tumor irradiation in cats. J Vet Intern Med. 20(5):1151–1154. Niessen SJM, Petrie G, Gaudiano F, et al. 2007. Feline acromegaly: An underdiagnosed endocrinopathy. J Vet Intern Med. 21(5):899–905. Peterson ME, Taylor RS, Greco DS, et al. 1990. Acromegaly in 14 cats. J Vet Intern Med. 4(4):192–201.
9
CHAPTER 4
Actinomycosis Sharon Fooshee Grace
Overview Feline actinomycosis is a suppurative to pyogranulomatous disease caused by infection with the filamentous, gram-positive, non-acid-fast bacterium Actinomyces spp. It is an anaerobic or facultative anaerobic organism found as a saprophytic inhabitant of mucous membranes, most notably the oral cavity. Endogenous species are not normally considered highly pathogenic. Typically, disease will not develop until the organism is inoculated into a wound in association with other bacteria, usually other commensal organisms from the oral cavity. Though it is occasionally seen in cats, few cases have been detailed in the literature. However, several different species of the organism have been recovered from cats. Establishment of infection in cats is thought to most commonly occur through bite wounds, although other modes are possible. It spreads locally by dissection through local tissue planes; hematogenous dissemination is thought rare. This disease has a variety of presentations that are clinically indistinguishable from other infectious diseases, particularly nocardiosis. Affected cats most often have cutaneous/subcutaneous and thoracic disease (i.e., empyema or pyothorax). Cutaneous/subcutaneous lesions may appear acutely or peracutely and are often around the head or neck. One case had local extension of a subcutaneous abscess into the spinal canal. Wounds are often non-healing and may be abscessed or fistulous with a serosanguinous to purulent exudate that is yellow to reddishbrown in color. See Figure 4-1. Abscesses may have a foul odor that is suggestive of an anaerobic infection. Drainage sometimes contains grossly visible clusters of bacterial macrocolonies called “sulfur granules.” Occasionally, cutaneous lesions are nodular in appearance and devoid of drainage. The lung and pleural space may become involved by
aspiration or inhalation of infected material, direct extension from more superficial disease, or perhaps through a bite wound to the chest. Respiratory infection may involve the lung itself or only the pleural space, and clinical signs are consistent with pulmonary or pleural disease. Important differential diagnoses for actinomycosis include but are not limited to nocardiosis (Chapter 152), mycobacteriosis (Chapter 144), leprosy (Chapter 127), plague (Chapter 169), sporotrichosis (Chapter 202), dermatophyte kerion (Chapter 48), dermatophilosis (Chapter 48), and panniculitis (Chapter 162). No cases of human actinomycosis have been reported from direct contact with an infected cat, although it may feasibly be transmitted through the bite wound of an animal.
Diagnosis Primary Diagnostics • Cytology and Gram Staining: Specimens for cytology may be collected by aspiration of abscesses, nodules, or body cavity fluid; impression smears may be made from the discharge of draining tracts. The organisms, easily visualized microscopically, are filamentous and occasionally branched; neutrophils are present, but macrophages may or may not be present. (See Chapter 282.) A polymicrobial infection is usually noted. In contrast, exudate from lesions of nocardiosis does not usually contain a mixed bacterial population. Fibrous masses without drainage may yield little diagnostic material. On Gram stain, the organisms are gram-positive. • Culture: Because actinomycosis (variably anaerobic or facultative anaerobic) is clinically indistinguishable from nocardiosis, which is an aerobe, (Chapter 152), both aerobic and anaerobic cultures of should be submitted. Most diagnostic laboratories can provide supplies for anaerobic submission of a sample. Culture for actinomycosis is often unrewarding because anaerobes are difficult to grow in culture, although some species are facultative anaerobes and may grow aerobically. Other organisms are likely to grow in addition to Actinomyces because it is usually a mixed bacterial infection. Presence of these other organisms may complicate isolation of Actinomyces. • Biopsy/Histopathology: Histologic study of tissue reveals a suppurative to pyogranulomatous reaction. There may be a core of neutrophils encapsulated by granulation tissue containing macrophages, plasma cells, and lymphocytes. Organisms may not be evident with routine hematoxylin/eosin stain and special stains may be needed. • Acid-fast Staining: A small amount of exudate can be smeared onto a microscope slide and submitted for acid-fast staining with ZiehlNiessen stain. Actinomyces is a non-acid-fast organism.
Secondary Diagnostics
Figure 4-1 Multiple draining fistulas are seen on the ventral abdomen of this cat with actinomycosis. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
10
• Complete Blood Count, Chemistry Profile, and Urinalysis: There are no laboratory abnormalities specific for actinomycosis. However, this information is helpful in evaluating overall health of the cat. • Retroviral Testing: All cats with nonhealing wounds or pyothorax should be tested for feline leukemia virus and feline immunodeficiency virus. • Diagnostic Imaging: Radiographs are indicated if pleural or peritoneal involvement is suspected. Abdominal ultrasound may be needed to investigate possible abdominal abscesses.
Actinomycosis
Diagnostic Notes • It is important to distinguish actinomycosis from nocardiosis because different antibiotics are required to treat the two diseases.
Treatment Primary Therapeutics • Antibiotics: Antibiotics must be administered for weeks to months beyond clinical resolution of disease to prevent relapse. Preferred protocols include amoxicillin (20–40 mg/kg q6h IM, SC, or PO) or clindamycin (5 mg/kg q12h PO, SC). Oral medication may be given if the patient is not anorexic or vomiting; it should be given on an empty stomach. Other drugs reported to have efficacy include doxycycline, tetracycline, erythromycin, and first-generation cephalosporins. Antibiotics are not a substitute for drainage of free fluid and abscesses. • Surgery: When possible, focal lesions should be surgically debrided and adequate drainage established. • Thoracic or Abdominal Drainage: Pyothorax should be addressed with a thoracic drainage system and saline lavage twice daily. This therapy should be continued until the thoracic fluid is clear and no organisms are found on cytologic examination of the fluid. This normally requires 4 to 10 days. Some have advocated thoracic lavage
with fluids containing sodium penicillin (not potassium penicillin). Surgical exploration of the abdomen will likely be required for abdominal infections.
Therapeutic Notes • Penicillin was considered the drug of choice, but poor absorption makes it less effective than once thought. • Drug penetration into granulation tissue can be problematic. • In some cases, the course of therapy has extended beyond a year.
Prognosis Prognosis is variably reported from guarded to good in cats with actinomycosis.
Suggested Readings Edwards DF. 2006. Actinomycosis and nocardiosis. In C Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 451–456. Philadelphia: Saunders Elsevier. Thomovsky E, Kerl ME. 2008. Actinomycosis and nocardiosis. Compend Contin Educ. 10(3):4–10.
11
CHAPTER 5
Adenocarcinoma and Carcinoma Mark Robson
Overview Carcinomas are malignant tumors of epithelial origin. If the tumor forms glands and ducts and has therefore arisen from glandular tissue it is termed an adenocarcinoma (AC). Therefore, these malignancies can arise from any epithelial or glandular tissue at any location in the body. The cytological features of these tumors are outlined in Chapters 281 and 288. With a few exceptions, there is a relative paucity of peer-reviewed literature specifically concerning carcinomas and ACs of cats when compared to the canine and human body of knowledge. Hence, a great deal of our approach to these tumors in cats is extrapolated from similar lesions in dogs and to a lesser extent people. Commonly recognized carcinomas include squamous cell carcinoma (SCC; see Chapter 203) and transitional cell carcinoma (TCC). AC is well recognized in the nasal cavity, lung, gastrointestinal tract, pancreas, liver, and mammary gland (see Chapter 132). Clinical signs of carcinomas and ACs are highly variable and related to their location. The nasal cavity of cats can give rise to SCC, AC, and undifferentiated carcinomas. In one study 60% of 320 cats with nasal tumors had carcinomas of various types, and males were more commonly affected than females. Nasal SCC or AC may cause sneezing, nasal discharge, and abnormal respiratory noises. Primary lung tumors are rare in cats but 70 to 85% of them are ACs, and the terminology can vary depending on whether site of origin (difficult to confirm in many cases) or cellular morphology is used to classify them. They may be described as an AC, an undifferentiated carcinoma, an SCC, or a bronchoalveolar carcinoma. Other similar terms may also be used. These tumors can be advanced before any clinical signs are seen. Cats do not cough as readily as dogs and humans so this sign can be variable. Weight loss, reduced appetite, and lethargy are more likely but are, of course, non-specific. Wheezing, cyanosis, fever, and hemoptysis are occasionally seen, along with lameness if musculoskeletal metastasis has occurred. Lung tumors in cats are often discovered incidentally after radiographs have been taken for other reasons. Metastasis to digits is discussed in Chapters 55 and 163. Epithelial tumors of the pancreas are termed carcinomas if they arise from the ductal epithelium and AC if they arise from acinar cells. Metastasis and local spread is common, with the liver often being the first tissue affected. Any gastrointestinal or pancreatic carcinoma or AC may result in anorexia, weight loss, vomiting, diarrhea, lethargy, and dyschezia, but none of these signs are specific; and the disease can be advanced before any signs are seen. Sometimes these tumors will be discovered in the abdomen serendipitously when ultrasound is performed for other reasons. Primary tumors of the liver are rare in cats, but cholangiocellular carcinoma and hepatocellular carcinoma have been well described, with a mean age at diagnosis of 11 years. Clinical signs include detection of an abdominal mass, polyuria/polydipsia, anorexia, and vomiting. Icterus may not be a common finding. Intestinal ACs are well recognized in cats but are less common than lymphoma. In contrast to the dog, most of these tumors occur in the ileum and jejunum rather than the colon. Mean age at time of diagnosis
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
12
is 11 years, and most have metastasized at the time of surgery. Despite this, survival times can be prolonged, and in one study 11 of 32 cats that survived more than 2 weeks postoperatively showed a mean survival time of 15 months. Prostatic neoplasia is rare in the cat and, as in the dog, may be classed as AC or TCC depending on the precise appearance of the cells. Epithelial tumors of the reproductive tract of female cats are extremely rare. Renal carcinomas and ACs are rare in the cat. In contrast to dogs, lymphoma is the most common renal tumor in the feline. In the few reports that exist in cats the mean age at diagnosis was 9.3 years, the tumors metastasized widely, and clinical signs were variable and nonspecific. A case report documenting the resolution of paraneoplastic polycythemia after surgical resection of a renal AC in two cats has been published, though one cat died 8 months later from metastatic lesions. The biological behavior of a carcinoma or AC is highly variable with regard to metastasis, but they all show local invasion. Nasal carcinomas and ACs usually metastasize quite late if at all, whereas pancreatic, hepatic, and intestinal tumors often metastasize, and in many cases this will have already occurred at the time of diagnosis. Pancreatic tumors often metastasize to the liver, and clinical signs may be more obvious from liver involvement than from the pancreas. Any abdominal carcinoma or AC can spread locally across abdominal structures and the peritoneum, leading to the phenomenon of carcinomatosis (see Chapter 29). The actual tissue of origin may be difficult to define in these cases. The differential diagnosis of any particular carcinoma or AC will depend on the location. For instance, in the nasal cavity an AC could present in a similar way to lymphoma, deep fungal diseases, or a foreign body. In the gastrointestinal tract an AC needs to be distinguished from lymphoma, foreign body, or a leiomyosarcoma.
Diagnosis Primary Diagnostics • Cytology and Histology: These are the cornerstones of diagnosis. Lesions that are visible or palpable will be more amenable to sampling, but ultrasound-guided aspiration/biopsy, laparoscopy, or exploratory laparotomy may be required for abdominal lesions. See Chapter 281. • Imaging: Radiography will often be the first step in diagnosing pulmonary neoplasia, but ultrasonography will likely be the primary modality in the abdomen. Computerized tomography (CT) may be useful in some cases. Assessment of metastasis to local nodes, distant nodes, lung, and liver must be performed if surgery is considered, using ultrasound, radiography, advanced imaging, and guided aspiration. • Pancreatic Tumors: These can be difficult to distinguish from the lesions of pancreatitis. The ultrasound appearance, blood changes (including pancreatic lipase immunoreactivity [PLI]) and cytology of these two diseases can be similar. Often it requires biopsy by ultrasound guidance, laparoscopy, or laparotomy to reach a firm diagnosis. In one study comparing cats with pancreatic neoplasia with cats with nodular hyperplasia the existence of a single mass that exceeded 2 cm (3/4 inch) in any dimension was predictive of neoplasia. • Pulmonary Tumors: Diagnosis of pulmonary tumors may require bronchoscopy with bronchoalveolar lavage, lung aspiration, or
Adenocarcinoma and Carcinoma
lobectomy (complete or partial) via thoracoscopy or thoracotomy. Significant risk is involved with all pulmonary diagnostic procedures in the cat, and these should be discussed with the owner. • Prostatic Neoplasia: This rare tumor may be classed as carcinoma or AC, and lesions can be so undifferentiated that it is impossible for the pathologist to be sure. Cells from the urinary tract are notoriously difficult for cytologists to define accurately, with dysplasia and neoplasia having a large overlap in appearance. Histopathology will almost always be needed for a definitive diagnosis.
dipitously at laparotomy exist. At my practice partial remission of a biopsy-confirmed pancreatic AC was achieved using carboplatin and piroxicam. Survival time thus far has been 10 months. • Radiation Therapy: This may be appropriate, especially for lesions in accessible regions such as the nasal cavity, and consultation with a radiation oncologist is encouraged. • Nasal AC: A single case report exists of the treatment of a nasal AC with long-term oral piroxicam and then chemoembolization with carboplatin. This cat lived 744 days after first presentation.
Diagnostic Notes
Therapeutic Notes
• When considering ultrasound-guided aspiration or biopsy of abdominal structures, thought must be given to the undesirable possibility of “seeding” the abdominal cavity or needle track with neoplastic cells.
• Because surgery for cancer is a field filled with possible pitfalls, consultation with or referral to a specialist surgeon should be considered. • There is little peer-reviewed information concerning medical treatment of carcinoma and AC in the cat other than TCC and mammary carcinoma. Anecdotally, many internists will try a combination of carboplatin and a nonsteroidal anti-inflammatory drug (NSAID) such as piroxicam or meloxicam. The use of NSAIDs in this setting is extrapolated from their original use in TCC of dogs.
Treatment Primary Therapeutics • Surgical Feasibility Decision: The clinician must first consider whether surgery is appropriate and possible for the individual patient. The presence of metastasis may make surgery a poor option, but in some cases resection of a tumor can result in dramatic improvement in clinical signs even if metastasis is known to have occurred. An example is AC of the intestine in which functional obstruction can be relieved and the patient may have many months of good quality life even if metastasis to nodes is detected. • Pancreatic Tumors: These are generally regarded as resistant to treatment, even in humans. Isolated reports of prolonged survival time after surgical resection of a lesion that was discovered seren-
Prognosis The outlook for cats with carcinoma and AC is guarded overall but highly variable and dependent on the location and tissue of origin of the tumor. Lesions that are amenable to surgical resection carry a much better prognosis.
Suggested Readings Kosovsky JE, Matthiesen DT, Patnaik AK. 1988. Small intestinal adenocarcinoma in cats: 32 cases. J Am Vet Med Assoc. 192:233–235.
13
CHAPTER 6
Amyloidosis Andrew Sparkes
Overview Amyloidosis is a diverse group of diseases characterized by deposition of inert, insoluble extracellular protein fibrils (amyloid) that have a distinctive three-dimensional conformation. Although more than 25 chemical types of amyloid have been identified in man and animals, they all share the morphology of being composed of non-branching fibrils, approximately 7- to 10-nm thick and of variable length. Histologically, amyloid deposits in tissues are amorphous and demonstrate apple-green birefringence when stained with Congo red. Amyloid fibrils have the potential to form when there is an accumulation of an amyloidogenic protein (increased synthesis or decreased degradation). Some normal proteins may have the ability to form amyloid fibrils if present in high enough concentrations; other proteins may become amyloidogenic as a result of genetic mutation (leading to production of an abnormal, amyloidogenic protein) or as a result of posttranslational events that affect the protein. Over time, accumulation of amyloid in tissues can lead to interference with their structure and function and thus lead to development of disease. A variety of amyloid-related diseases have been identified and described in cats. Importantly, these include: • Diabetes Mellitus: Many, although not all, diabetic cats have an accumulation of amyloid in their pancreas, which is derived from the hormone amylin that is co-secreted with insulin from β cells. Amylin is an amyloidogenic protein in a few species including man and cats, and pancreatic amyloidosis is an important part of the pathogenesis of humans with type-2 diabetes and also in many cats with diabetes. • Alzheimer-like Pathology in the Brains of Aging Cats: Studies have demonstrated amyloid plaques and fibrils in the brains of aging cats, which bear close resemblance to the changes seen in humans with Alzheimer ’s disease and related conditions. The clinical significance of these changes in cats is yet to be determined but may, for example, be related to cognitive dysfunction. • Prion Diseases: These are a form of amyloidosis, and although no longer recognized in cats, the emergence of bovine spongiform encephalopathy led to its spread to cats in the form of feline spongiform encephalopathy. • Immunoglobulin Light-Chain Associated Amyloidosis: As in other species, cats with plasmacytomas may produce excessive quantities of immunoglobulin light chain fragments, and these may be amyloidogenic. Generally the amyloid appears to be deposited locally and predominantly within the neoplastic tissue. • Reactive Amyloidosis (AA-amyloid): This is the most commonly described form of amyloid in veterinary medicine and is well recognized in cats. The amyloid is derived from serum amyloid-A (SAA), an acutephase protein produced in the liver as part of the inflammatory process. In this disease, amyloid deposits have been found in the liver, spleen, adrenals, small intestine, stomach, endocrine and exocrine pancreas, thyroids, parathyroids, heart, tongue, and kidneys. Despite the generalized nature of the deposits, the heaviest deposits usually occur in the liver (leading to spontaneous hepatic rupture)
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
14
or the kidneys (leading to chronic renal disease as the deposits are primarily in the medullary interstitial space). Reactive amyloidosis may occur sporadically secondary to inflammatory or neoplastic diseases in any breed of cat, but predispositions have been described in Abyssinian cats and in Oriental Shorthair cats. Familial amyloidosis in Abyssinian cats has been well characterized in the United States, where AA-amyloid accumulates in a wide variety of tissues but clinical signs relate to accumulation in the renal medullary interstitium that leads to chronic renal disease. Affected cats have typically developed renal disease at around 1 to 5 (average 3) years of age, but some older cats that die of other causes have also been found to have subclinical renal amyloidosis. It has been suggested that this might be inherited as an autosomal dominant trait with incomplete penetration. A number of publications have now appeared identifying systemic amyloidosis in Siamese and Oriental cats. In contrast to Abyssinians, in many of these cats the liver is most severely affected, although widespread amyloid deposits are typical; this may include renal amyloidosis and thus concomitant chronic renal disease may also be present. Heavy amyloid accumulation in the liver leads to dramatic friability of the liver with spontaneous or easily induced rupture, evidenced by recurrent or catastrophic bleeding episodes into the abdomen. Current research suggests that affected Siamese and Oriental Shorthair cats have genetic mutations resulting in amino acid substitutions in the serum AA protein that renders it more amyloidogenic, but similar to the situation in Abyssinians, for the disease to develop there probably also needs an inflammatory process(es) to increase the production of SAA in most cases. Further studies are necessary to clarify the heritability of the disease in these breeds.
Diagnosis Primary Diagnostics • Histopathology: Examination of biopsies stained with Congo red is usually sufficient for a diagnosis to be made, but additional investigations, including the use of immunostains, are necessary for characterising the nature of the amyloid. Due to the friable nature of the liver, if biopsy is being contemplated and amyloidosis is suspected, it is preferable to perform surgical biopsies with laparotomy rather than ‘blind’ or ultrasound-guided needle biopsies in which the risk of significant haemorrhage is high.
Secondary Diagnostics • Clinical Signs: These may be diverse in cats with systemic amyloidosis. There may be progressive chronic renal disease (that may develop at a relatively young age), although the rate of progression is variable. When hepatic amyloidosis predominates there may be mild to profound elevations in liver enzymes, and cats often present with recurrent bouts of lethargy associated with acute onset anemia (due to abdominal hemorrhage) or acute death or life-threatening anemia due to a catastrophic hemorrhagic event. Clotting times are prolonged in some affected cats.
Amyloidosis
Figure 6-1 Lateral radiograph of a cat with severe hepatic amyloidosis. Irregular hepatomegaly is evident.
Figure 6-2 Hepatic ultrasound of the same cat showing that the normally homogenous echogenic pattern has been replaced by a mixed echogenic pattern.
• Radiographs: Abdominal radiographs may show an irregular enlargement of the liver. See Figure 6-1. • Ultrasound: The hepatic parenchyma may display a diffuse increase in echogenicity on ultrasound, and there may be a speckled or “sparkling” appearance. See Figure 6-2. Following acute episodes of hemorrhage, ascites (hemoperitoneum) may also be detectable by ultrasound.
ments should be considered. See Chapters 190 and 191. When liver hemorrhage occurs, blood transfusion should be considered. These cats should have a lifestyle that will minimize the risk of even mild abdominal trauma.
Diagnostic Notes • Although biopsy material is preferable for confirmation, in some cases a diagnosis of amyloidosis may be possible from fineneedle aspirates from affected tissues.
Treatment Primary Therapeutics • Amyloidosis is not a curable disease. • Efforts should be made to identify and treat any other concomitant diseases that may be predisposing to amyloid deposition (e.g., infectious/inflammatory diseases) or may be the result of amyloidosis.
Secondary Therapeutics • Medical Treatment: Treatments that have been attempted include vitamin K therapy (e.g., 10 mg/cat q7d PO), especially if there is evidence of prolonged clotting times, and prednisolone at antiinflammatory doses (1–2 mg/kg q24–48h PO). However, it is unclear whether either of these approaches produces genuine clinical benefit. Colchicine (0.03 mg/kg q24–48h PO) has been suggested because it may reduce SAA production in other species and thus reduce the accumulation of amyloid, but its efficacy (if any) in cats is unknown. • Supportive Therapy: This is important in cats with amyloidosis. When chronic renal disease develops, the usual supportive treat-
Therapeutic Notes • Prevention of systemic amyloidosis may be possible through selective breeding programs. Because many cats with systemic amyloidosis develop disease at a relatively young age, breeding from older healthy cats may be beneficial. Further work is needed to identify underlying genetic abnormalities (and thus diagnostic tests) in affected breeds/lines of cats.
Prognosis The prognosis for cats with clinical systemic amyloidosis is grave. Currently there is no known effective treatment, and the disease is progressive, usually leading to death from renal disease or liver rupture.
Suggested Readings Beatty JA, Barrs VR, Martin PA, et al. 2002. Spontaneous hepatic rupture in six cats with systemic amyloidosis. J Small Anim Pract. 43(8): 355–363. Godfrey DR, Day MJ. 1998. Generalised amyloidosis in two Siamese cats: spontaneous liver haemorrhage and chronic renal failure. J Small Anim Pract. 39(9):442–447. Gunn-Moore DA, McVee J, Bradshaw JM, et al. 2006. Ageing changes in cat brains demonstrated by beta-amyloid and AT8-immunoreactive phosphorylated tau deposits. J Fel Med Surg. 8(4):234–242. Rand J. 1999. Current understanding of feline diabetes: part 1, pathogenesis. J Fel Med Surg. 1(3):143–153.
15
CHAPTER 7
Anal Sac Disease Gary D. Norsworthy
Overview The anal sacs are located lateral to the anus in the 4- to 5-o’clock and 7- to 8-o’clock positions. They are positioned between the internal and external anal sphincters and contain sebaceous and apocrine tubular anal glands, which secrete a malodorous substance that is used for scent marking, individual recognition, and defense purposes. This substance is temporarily stored in the paired anal sacs (paranal sinuses), which empty voluntarily when the cat feels threatened or involuntarily with bowel movements. If the sacs are not emptied periodically, the anal gland secretion desiccates and thickens. See Figure 7-1. At this stage, the anal sacs are said to be impacted; the cat exhibits pain when defecating and may experience tenesmus. The cat responds by licking or biting at the tailhead region. If infection occurs within the sacs, pain will increase. Abscess formation may follow resulting in expulsion of purulent material through a draining tract over one or both anal sacs. See Figure 7-2. Thus, the three stages of anal sac disease are impaction, infection, and abscessation. An unrelated anal sac condition is incompetence of the anal sac sphincters. When affected, cats spontaneously release normal anal sac material involuntarily. Although uncommon and of no health threat to the cat, this condition is not well tolerated by owners of indoor cats.
Diagnosis
Figure 7-2 The left anal sac of the cat in Figure 7-1 was abscessed. It was surgically opened with an incision over the abscess. Blood tinged purulent material drained freely.
release of anal sac material is characteristic of anal sac sphincter incompetence.
Primary Diagnostics • Clinical Signs: The signs of tenesmus, licking at the perineal region, and a draining tract are characteristic of anal sac disease. Spontaneous
Diagnostic Notes • Anal sac disease of dogs usually produces scooting. Scooting is not a common finding in cats with anal sac disease. • Some cats with anal sacculitis may lick the perineal area and the caudal thighs, producing a symmetrical pattern of alopecia.
Treatment Primary Therapeutics • Manual Expression: This procedure should permit removal of thickened secretions. Anesthesia or sedation is required in many cats because of the cat’s tight anal sphincter and small anal size. The first phalanx of one’s index finger or thumb is inserted into the anus. The anal sac is squeezed between it and the other mentioned digit. See Figure 7-1. • Irrigation: An antiseptic solution, such as dilute chlorhexidine, is used to flush remaining dried debris from the anal sacs. Sedation of the cat generally is required. • Antibiotic Instillation: Local treatment with antibiotics is indicated. Drugs expected to be effective against Escherichia coli, Streptococcus fecalis, and Clostridium spp. should be considered. • Systemic Antibiotics: Systemic antibiotics with the characteristics above speed recovery and should be given for 7 to 14 days. Figure 7-1 Desiccated, thick anal sac material was expressed from the right anal sac of the cat in Figure 7-2. This is a predisposing factor to anal sac abscessation.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
16
Secondary Therapeutics • Surgical Drainage: Anal sac abscesses that have not drained spontaneously should be opened surgically to establish drainage through the skin.
Anal Sac Disease
• Anal Sacculectomy: This procedure should be considered in recurrent cases but should not be performed until infection is resolved. It is the treatment of choice for incompetent anal sphincter disease. Fecal incontinence is a possible sequel, but it occurs infrequently if careful dissection is performed. If it occurs, it usually resolves spontaneously in 7 to 21 days.
Suggested Readings Zoran DL. 2005. Rectoanal Disease. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1408–1420. St. Louis: Elsevier Saunders.
Prognosis The prognosis is good; however, aggressive therapy as outlined should occur.
17
CHAPTER 8
Anaplasmosis Sharon Fooshee Grace
Overview Although molecular technology has greatly expanded our understanding of bacterial organisms in recent years, it has also created confusion as large numbers of bacteria have been reclassified and renamed. In 2001, the families Rickettsiaceae and Anaplasmataceae, members of the order Rickettsiales, underwent major reorganization. The genera Ehrlichia and Wolbachia were moved from the family Rickettsiaceae to the family Anaplasmataceae. The genus Rickettsia remained in the family Rickettsiaceae. Additionally, species within the genus Ehrlichia were significantly reorganized: E. phagocytophila, E. equi, and E. platys now reside in the genus Anaplasma; E. risticii and E. sennetsu have been moved to the genus Neorickettsia. Feline ehrlichiosis continues to be an area of active research, but little is known about this disease in cats. The family Anaplasmataceae contains gram-negative obligate intracellular organisms that parasitize leukocytes, erythrocytes, platelets, and endothelial cells. Ehrlichia phagocytophila, the granulocytic Ehrlichia, has been renamed Anaplasma phagocytophilum. This is a tick-borne organism found in many parts of the world, including the United States. Cats are not infected with tick-transmitted diseases as often as dogs, a finding which has been attributed to the fastidious grooming behavior of cats. Ticks are likely removed by cats before the 24- to 48-hour time frame required for transmission of most tick-transmitted diseases. A. phagocytophilum is transmitted transtadially by nymph and adult forms of Ixodes scapularis (the deer tick or black-legged tick) or Ixodes pacificus (the western black-legged tick). The deer tick is common in the eastern, southeastern, and midwestern United States, and depending upon geographic location, it feeds primarily on mammals, birds, or lizards. The western black-legged tick is found in the western United States. Larval forms feed on the white-footed mouse and other small rodents whereas nymphs and adults have a diverse range of hosts, including white-tailed deer, dogs, cats, and humans. The disease, formerly called ehrlichiosis, is now called feline granulocytotropic anaplasmosis or simply anaplasmosis. At present, little is known about the pathogenesis of the disease, although it is likely similar to infection in other species. In the limited number of cases described in the literature, clinical findings have included acute onset fever, lethargy, weight loss, vomiting, lameness (polyarthritis), and ocular discharge. Most cats have vague, nonspecific signs of illness. This organism has public health significance because humans are known to be susceptible to the organism. However, there is no evidence that human infection has resulted from contact with a cat.
Diagnosis Primary Diagnostics • History: The few cats reported with disease have had access to the outdoors. • Complete Blood Count, Biochemical Profile, and Urinalysis: Thrombocytopenia, the presence of morulae in neutrophils, mild hyperglycemia, and hyperglobulinemia have been reported in
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
18
infected cats. The organism has been found to rarely infect eosinophils.
Secondary Diagnostics • Serology: Published studies have used immunofluorescent assays and enzyme-linked immunosorbent assay (ELISA) methodology to detect antibodies against the organism. • Polymerase Chain Reaction (PCR) Test: PCR testing is available at several commercial veterinary laboratories. Consult the diagnostic lab prior to sample submission for additional details on sample collection and shipping.
Diagnostic Notes • Clinical illness may develop prior to seroconversion. Therefore, a single negative antibody test does not exclude infection.
Treatment Primary Therapeutics • Antibiotics: Reported cases have appeared to improve when treated with doxycycline (5–10 mg/kg q24h PO) for 28 to 30 days.
Therapeutic Notes • Inadequate duration of therapy or selection of antibiotics without efficacy against A. phagocytophilum may result in incomplete response to treatment or relapse. • Antibodies may persist beyond the end of treatment, in some cases for months.
Prevention The disease can be prevented if tick-control measures are implemented. Cats going outdoors should be treated with topical acaricidal products approved for cats.
Prognosis Little is known about the disease in cats, but based on cases reported to date, prognosis is generally good if the cat is treated with doxycycline.
Suggested Readings Billeter SA, Spencer JA, Griffin B, et al. 2007. Prevalence of Anaplasma phagocytophilum in domestic felines in the United States. Vet Parasitol. 147(1–2):194–198. Lappin MR, Bjoersdorff, Breitschwerdt EB. 2006. Feline granulocytic ehrlichiosis. In C Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 227–229. Philadelphia: Saunders Elsevier. Lappin MR, Breitschwerdt EB, Jensen WA, et al. 2004. Molecular and serologic evidence of Anaplasma phagocytophilum infection in cats in North America. J Am Vet Med Assoc. 225(6):893–896. Magnarelli LA, Bushmich SL, Ijdo JW, et al. 2005. Seroprevalence of antibodies against Borrelia burgdorferi and Anaplasma phagocytophilum in cats. Am J Vet Res. 66(11):1895–1899. Stuen S. 2007. Anaplasma phagocytophilum—the most widespread tickborne infection in animals in Europe. Vet Res Comm. 31(1):79–84.
CHAPTER 9
Anemia Sharon Fooshee Grace
Overview Anemia is a reduction below normal of the number of circulating red blood cells (RBCs) and hemoglobin. It is important to note that the cat’s RBC count is normally lower than that of dogs, and they tend to have a less vigorous marrow response to anemia. There are numerous causes of anemia in the cat. Historical findings depend on the chronicity of the anemia with acute, rapidly progressing anemias causing more severe signs than chronic, slowly progressing anemias. Cats may demonstrate mild or severe decreases in activity or tolerance for exercise and mild or severe increases in respiratory effort; pica is often present. Physical examination may reveal pale mucous membranes, increased ventilatory effort (especially with stress), a soft systolic heart murmur, tachycardia, and weakness. In examining the feline patient with anemia, particular attention should be given to the size of the peripheral lymph nodes and the spleen because common neoplastic, infectious, and immune causes of anemia often lead to enlargement of these organs. The initial step in the evaluation of any anemia involves defining the anemia as regenerative or nonregenerative. Circulating reticulocytes (immature RBCs) should be counted whenever the hematocrit is less than 20% to assess bone marrow responsiveness. The cat is unique in that two types of reticulocytes may be present. Aggregate reticulocytes are more
reflective of a recent regenerative response and contain numerous darkstaining clumps of ribosomes, whereas punctate reticulocytes contain small clumps or specks of ribosomal material. The presence of aggregate reticulocytes is the most reliable indicator of a regenerative response. Regenerative anemias are associated with three main categories of causes: blood loss, hemolysis, or sequestration. Nonregenerative anemias are caused by decreased production of erythrocytes; the underlying cause may be a disease of the bone marrow or may be secondary to an extramedullary disorder.
Diagnosis Differential Diagnoses There are many known diseases that cause anemia in cats. They are classified and listed in Table 9-1.
Primary Diagnostics • Complete Blood Count (CBC): A CBC should be performed if anemia is suspected. Diagnosis of anemia requires identification of erythrocyte numbers or a hematocrit lower than normal for the individual
TABLE 9-1: Known Causes of Anemia in Cats Regenerative
Hemolysis Erythrocyte parasites: Mycoplasma hemofelis and Candidatus Mycoplasma hemominutum (formerly known as Hemobartonella felis) Cytauxzoon felis, and Babesia spp. Immune-mediated destruction (i.e., drug-induced, idiopathic, paraneoplastic, or toxicity) Microangiopathic hemolysis (DIC) Oxidative injury (i.e., zinc, methylene blue, acetaminophen, benzocaine, phenazopyridine, or onions) Neonatal isoerythrolysis Blood Loss Trauma or surgical loss Coagulopathy External loss (i.e., urinary tract, trauma, or epistaxis) Internal or poorly visualized loss (i.e., gastrointestinal, peritoneal, or pleural) Sequestration Splenic disease with splenomegaly
Non-Regenerative
Intramedullary Hematopoietic neoplasia with or without feline leukemia virus or feline immunodeficiency virus infection Lymphoproliferative neoplasia Myelodysplasia Myeloproliferative neoplasia Red blood cell aplasia Extramedullary Chronic inflammatory disease (e.g., fungal disease, Feline Infectious Peritonitis, and so on) Chronic renal disease Neoplasia Poor nutrition or starvation
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
19
SECTION 1: Diseases and Conditions Corrected reticulocyte count = ( reticulocyte % ) × ( patient′s HCT normal HCT* ) *Normal hematocrit = 37.5%
MacroC
• Feline Retroviral Screen: The cat should be evaluated with an antigen test for feline leukemia virus (FeLV) and an antibody test for feline immunodeficiency virus (FIV).
Secondary Diagnostics
MetaR
Figure 9-1 Signs of a regenerative anemia include the presence of nucleated red blood cells and reticulocytes. A metarubricyte (MetaR) and several macrocytes (MacroC) are shown. Macrocytes are reticulocytes stained with a modified Wright’s stain that demonstrate increased cell diameter but do not show the reticulum. The organisms on the red blood cells are Mycoplasma haemofelis.
A
P
• Serum Chemistry Profile: A serum chemistry profile is indicated to detect underlying diseases, especially in cases of nonregenerative anemia. Particular attention should be given to serum color (look for hemolysis or icterus), blood urea nitrogen (BUN), creatinine, alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin, and total protein. • Bone Marrow Examination: With unexplained nonregenerative anemia, bone marrow aspiration and cytology are indicated. Several sites are available for aspiration: the humeral head, femoral shaft, or wing of the ilium is commonly used sites. See Chapter 296. The bone marrow slides should be submitted to a veterinary clinical pathologist, along with a tube of EDTA-anticoagulated blood drawn at the time of marrow aspiration. In some cases, a core biopsy of the marrow may be indicated. • Coombs’ Test: A Coombs’ test may be performed when an immunemediated cause of anemia is suspected. It should be remembered that a positive test is not diagnostic of immune-mediated hemolysis; a variety of disorders may produce a positive Coombs’ test. An EDTA-anticoagulated tube of blood should be submitted to a veterinary diagnostic laboratory. See Chapter 119. • Radiography: Thoracic and abdominal radiographs may be a useful component of the minimum data base in cats with unexplained anemia. • Coagulation Tests: If a coagulopathy is suspected, clotting tests and a manual platelet count are indicated.
Diagnostic Notes
Figure 9-2 When stained with new methylene blue stain, reticulocytes demonstrate the reticulum as either younger aggregate reticulocytes (A) or more mature punctuate reticulocytes (P). Aggregate reticulocytes are counted to generate the reticulocyte count.
laboratory. The blood smear should be evaluated for the presence of young RBC types (see Figure 9-1), RBC parasites, Heinz bodies and other morphologic changes, and cytopenias. Because of the small size of feline erythrocytes, spherocytosis (indicative of immune-mediated destruction) is not detectable on feline blood smears. • Reticulocyte Count: Equal parts of ethylenediaminetetra-acetic acid (EDTA) anticoagulated blood and new methylene blue stain are gently mixed, and the solution allowed to incubate at room temperature for 10 to 15 minutes. A smear is made, and then 500 to 1,000 red cells are examined. The percentage that is aggregate reticulocytes is recorded (see Figure 9-2). After 5 or 6 days and with sufficient anemia to stimulate erythrocyte production, the percentage of aggregate reticulocytes should be 1 to 5%. The feline regenerative response is more subtle than that of the dog with a comparable anemia. Additionally, some peculiarities of the feline erythron occasionally make it difficult to interpret the significance of a response; a veterinary clinical pathologist should be consulted, as needed. The reticulocyte count should be corrected for the hematocrit (HCT):
20
• Mucous membrane color is a poor indicator of anemia in cats because normal feline mucous membranes are relatively pale, especially when compared with those of dogs, and excitement or stress may raise blood pressure and increase the color in the mucous membranes. • Circulating nucleated RBCs do not indicate a regenerative response unless accompanied by an increase in reticulocytes. Causes of circulating nucleated red bloods in the absence of a regenerative anemia include neoplasia, hypoxic or toxic bone marrow injury, lead toxicity, and splenic disease. • Regenerative anemias may take 5 to 6 days to respond with an appropriate peripheral reticulocytosis. This timeframe should be taken into consideration when the initial hemogram and reticulocyte count are consistent with nonregenerative anemia, but blood loss, hemolysis, or sequestration is likely. • Mycoplasma haemofelis and Candidatus Mycoplasma haemominutum (previously known as Hemobartonella felis) organisms may detach from red blood cells after incubating in EDTA anticoagulant. A fresh blood smear should accompany the anticoagulated blood when hemotrophic Mycoplasma spp. are suspected. • Whole blood or bone marrow may be submitted for PCR detection of Mycoplasma haemofelis and Candidatus Mycoplasma haemominutum circulating DNA. The receiving laboratory should be contacted for sample requirements. • New methylene blue stain, as described for the reticulocyte count, will allow Heinz bodies to be identified easily.
Anemia
• Increased numbers of Heinz bodies have been associated with hyperthyroidism, lymphoma, and diabetes mellitus.
Treatment Primary Therapeutics • Transfusion with Blood or Hemoglobin Solutions: Administration of whole blood or hemoglobin solutions (e.g., Oxyglobin®) may be useful in cats with severe anemia (see Chapter 295); however, Hct alone is a poor indicator of the need to transfuse because cats with chronic severe anemia (packed cell volume as low as 10%) may often be relatively stable. Acute hemolysis or hemorrhage would warrant transfusion if the Hct falls below 20%. Transfusion in cats with chronic anemia should be assessed on a case-by-case basis, though transfusion is usually needed when the Hct is less than 12%. Oxyglobin (maximum dose 5–15 ml/kg), a hemoglobin-based oxygen carrier solution derived from bovine hemoglobin, is available but is expensive. It has the potential to cause volume overload in cats so slow infusion rates of 0.5 to 5 ml/kg per hour are recommended.
Secondary Therapeutics • Erythropoietin: Feline recombinant erythropoietin is not commercially available for veterinary use at this time. Human recombinant erythropoietin may be used in cases of nonregenerative anemia owing to renal failure. See Chapter 190. For other causes of anemia, this treatment is not indicated because serum erythropoietin levels are already elevated.
• Initial blood samples for diagnostic testing should be collected pre-transfusion. • A standard reference should be consulted for details of managing the donor cat, performing blood typing and cross-matches, and specific information on transfusion protocols. See Chapter 295. • For cats with anemia of chronic disease, specific treatment of the anemia is rarely indicated. The practitioner should focus on identification and treatment of the underlying cause. If this treatment is successful, the anemia should resolve.
Prognosis Prognosis is dependent upon identification and successful management of the underlying cause of anemia. Generally, the prognosis is better for acute and regenerative than for chronic and nonregenerative anemias.
Suggested Readings Cotter SM. 2003. A diagnostic approach to anemic patients. Vet Med. 98(5):420–430. Haldane S, Roberts J, Marks S, et al. 2004. Transfusion medicine. Compend Contin Educ Pract Vet. 26(7):502–518. Loar AS. 1994. Anemia: Diagnosis and treatment. In JR August, ed., Consultations in Feline Internal Medicine, 2nd ed., pp. 469–487. Philadelphia: WB Saunders. Webb CB, Twedt DC, Fettman MJ, Mason G. 2003. S-adenosylmethionine (SAMe) in a feline acetaminophen model of oxidative injury. J Fel Med Surg. 5(2):69–75.
Therapeutic Notes • Emphasis should be placed on stabilizing the patient while aggressively pursuing the underlying disesase process.
21
CHAPTER 10
Anorexia Mitchell A. Crystal
Overview Anorexia is the loss of appetite for food. Anorexia can result from numerous pathologic and nonpathologic conditions, including metabolic, gastrointestinal, oropharyngeal, cardiopulmonary, or neurologic disorders, inflammatory/infectious diseases, reactions to drugs/toxins, neoplasia, fever, pain, environmental stress, and lack of diet palatability. Because so many conditions may lead to anorexia, other accompanying clinical signs are variable. Some cats will demonstrate anorexia or anorexia/lethargy/weight loss as the only presenting complaint of a disease process. Unlike many other animals, cats are obligate carnivores with special nutritional requirements. This is due to the cat’s persistent use and loss of some nutrients and inadequate synthesis of others (see Table 10-1). As a result, persistent or prolonged anorexia can lead to serious metabolic derangements, complicating a pre-existing condition. An additional concern in prolonged anorexia is the cat’s potential to develop hepatic lipidosis. See Chapter 93. Therefore, anorexia in the cat warrants prompt diagnostic investigation and therapeutic intervention.
Diagnosis
• History: Question the owner about the cat’s environment (i.e., indoor versus outdoor, any recent moves, any new or departed pets or members of the household), travel history (i.e., to areas endemic for infectious diseases), recent drug therapy (i.e., prescription, nonprescription, otic, ophthalmic, topical), exposure to toxins, foreign bodies or other animals, signs of other disease processes (e.g., polyuria/polydipsia, vomiting, diarrhea), or change in diet. Review the cat’s vaccination history. • Physical Examination: Examine closely for wounds and abscesses, internal or external masses, organ size (enlargement or reduction), lymphadenopathy, abnormal cardiopulmonary auscultation, and pain. A complete oral examination is warranted to look for gingival
TABLE 10-1: Special Nutrient Requirements of the Cat Nutrient
Clinical Signs of Deficiency
Arginine
Ptyalism, hyperesthesia, vomiting, tremors, and ataxia; signs can develop within hours to days. Retinal degeneration, dilated cardiomyopathy, reproductive problems, and decreased growth in kittens; signs develop over weeks to months Dermatitis, dry hair coat, anemia, reproductive problems, and decreased growth in kittens; signs develop over weeks to months Retinal degeneration, weakness, dry/unkempt hair coat, and decreased growth in kittens; signs develop over weeks to months
Arachidonic Acid
Vitamin A
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
22
Secondary Diagnostics • Thoracic Radiography or Ultrasound: Abnormalities may suggest inflammatory/infectious, neoplastic, or cardiopulmonary disease. • Abdominal Radiography or Ultrasound: Abdominal imaging may reveal abnormalities in organ size and architecture, gastrointestinal obstruction, or neoplasia.
Diagnostic Notes
Primary Diagnostics
Taurine
or dental disease and to look under the tongue for a linear foreign body. A complete ophthalmologic examination (anterior chamber and retina) will sometimes disclose evidence of inflammatory/ infectious diseases, or lymphoid neoplasia. See Chapter 299. • Database (Complete Blood Count, Chemistry Profile, and Urinalysis): Abnormalities may suggest metabolic disorders, inflammatory/ infectious diseases, or neoplasia. • Retroviral Tests: Positive results are not confirmatory but strongly support illnesses related to feline leukemia virus (FeLV) or feline immunodeficiency virus (FIV) as the source of anorexia.
• Dental disease is a rare cause of anorexia except for painful resorptive lesions. A complete evaluation of any cat with anorexia is indicated prior to anesthesia and dental prophylaxis, despite the presence of dental tartar. A complete evaluation will rule out the more common causes of anorexia and will determine if anesthesia is safe. • If a foreign body is suspected and a complete oral (including sublingual) examination cannot be completed in the awake cat, sedation is recommended.
Treatment Primary Therapeutics • Treat Underlying Disease: This is essential in restoring appetite. • Fluid Support: Fluids may be administered orally or parenterally if needed to correct or maintain hydration. See Chapter 302. • Nutritional Support: Indications for nutritional support include weight loss of greater than 10% of body weight (greater than 5% in kittens), anorexia persisting more than 3 to 5 days (longer than 1–2 days in kittens), hypoalbuminemia, lymphopenia, anemia, increased nutrient losses (i.e., vomiting, diarrhea, burns, large wounds, intestinal malassimilation, protein-losing nephropathies, peritonitis, pleuritis), diseases associated with high metabolic demand (e.g., neoplasia), and inability to eat because of a disease or therapy (e.g., oropharyngeal disease, chemotherapy). Each cat must be individually evaluated when deciding whether one or several of the aforementioned criteria should be present before initiating nutritional support. Nutrients may be provided via enteral tube (i.e., gastrostomy, esophagostomy, jejunostomy, or nasoesophageal tube placement or intermittent orogastric intubation), forced hand feeding or parenterally (total or partial parenteral nutrition). See Chapters 253, 255, 256, and 308. • Therapy for Nausea: This should be attempted if there are signs or suspicion that nausea may be present (e.g., dolacetron, metoclopramide, maropitant, and so on; see Chapter 229).
Anorexia
Secondary Therapeutics • Appetite Stimulants: Appetite stimulants should only be used to help promote voluntary eating in cases in which a diagnosis has been achieved, specific therapy has been instituted, and immediate nutritional support is not feasible. Prior to using chemical agents, an attempt to stimulate eating should be made by offering a variety of foods of different flavors, odors, and textures, by warming foods, by placing foods in a wide shallow bowl to prevent the sides of the bowl from contacting the cat’s whiskers, and by stroking and petting the cat at the time of feeding (or providing a quiet environment for the stressed cat such as a covered cage or a cardboard box). Chemical appetite stimulants reported effective in the cat include mirtazapine (3.75 mg/cat q48–72h PO), vitamin B12 (2000 mcg/cat SC), cyproheptadine (1–2 mg/cat 5–20 minutes prior to feeding up to q12h PO), diazepam (0.1–0.2 mg/kg immediately prior to feeding up to q12h IV), and oxazepam (1.25–2.5 mg/cat 5–20 minutes prior to feeding up to q12h PO).
as a 5% solution contains 0.17 kcal per milliliter which, when delivered at maintenance for 24 hours for a 5-kg cat, provides only 50 kcal or about one-fifth of the daily caloric need. Providing a fraction of the caloric need via a carbohydrate source can contribute to muscle wasting by promoting protein over fat catabolism. • Glucocorticoids (prednisone or prednisolone 1–2 mg/kg up to q12h PO or dexamethasone 0.1–0.2 mg/kg up to q12h PO) may be helpful in stimulating appetite in some cats; however, undesirable catabolic and immunosuppressive side effects may occur. • If no significant response is seen after chemical appetite stimulants have been used for 24 hours, chemical appetite stimulants should be discontinued and nutritional support started. • Mirtazapine dosing should be decreased by 50% in cats with hepatic disease.
Prognosis The prognosis varies depending on the underlying disorder causing the anorexia.
Therapeutic Notes • It is best to provide nutrition via the enteral route. This maintains gastrointestinal mucosal health, is less expensive, and provides a more natural means of nutrient absorption and utilization. If the gastrointestinal tract is unable to absorb and digest food, total or partial parenteral nutrition can be used. • Forced hand feeding is a less optimal means of enteral nutrition than tube feeding because it significantly increases patient stress and generally cannot deliver the volumes necessary to meet the patient’s nutritional requirements. • Intravenous fluids with 2.5 or 5% dextrose do not supply significant calories when delivered at rates at or moderately above maintenance; thus, they are only indicated in patients with hypoglycemia or in patients that require hypotonic fluids (e.g., heart disease). Dextrose
Suggested Readings Case LP, Carey DP, Hirakawa DA, Daristotle D. 2000. Canine and Feline Nutrition. A Resource for Companion Animal Professionals, 2nd ed. St. Louis: Mosby. Marks SL. 1998. Demystifying the anorectic cat. In Proceedings of the Sixteenth Annual Veterinary Medical Forum, pp. 62–64. Sanderson S, Bartges JW. Management of anorexia. 2000. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIII. Small Animal Practice, pp. 69–74. Philadelphia: WB Saunders Company. Streeter EM. 2007. Anorexia. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult: Canine and Feline, 3rd ed., pp. 86–87. Ames, IA: Blackwell Publishing Professional.
23
CHAPTER 11
Aortic Stenosis Larry P. Tilley
Overview Congenital narrowing of the left ventricular outflow tract, aortic valves, or supravalvular aorta has been reported in the feline. Although there are several acquired abnormalities that cause left ventricular outflow obstruction, most notably hypertrophic cardiomyopathy, congenital aortic stenosis in the cat is rare. Of the different types of aortic stenosis noted in the cat, supravalvular stenosis appears to be most commonly encountered lesion. Aortic stenosis may be seen concurrently with other congenital defects such as mitral valve dysplasia. Left ventricular concentric hypertrophy occurs when significant outflow obstruction is present. The elevated left ventricular pressures may eventually result in left-sided congestive heart failure in severely affected cats. Physical examination reveals a left basilar systolic ejectiontype murmur and potentially late-rising femoral pulses, which are difficult to note at high heart rates.
Diagnosis Primary Diagnostics • Echocardiography: Left ventricular concentric hypertrophy, left atrial enlargement, high-velocity turbulent systolic flow in the left ventricular outflow tract as demonstrated by spectral or color-flow Doppler echocardiography, systolic anterior movement of the anterior mitral valve leaflet, mitral regurgitation, aortic regurgitation, and premature closure of the aortic valves may be present. A pressure gradient can be estimated from the flow velocity (pressure gradient = 4 × flow velocity squared) with variable accuracy.
Secondary Diagnostics • Electrocardiography: Increased R-wave amplitude and wide QRS complexes, suggestive of left ventricular enlargement; wide P-waves, suggestive of left atrial enlargement; and atrial and ventricular tachyarrhythmias may be present. • Thoracic Radiography: Left atrial and ventricular enlargement, dilation of the ascending aorta, and signs consistent with left-sided congestive heart failure, such as pulmonary edema, may be present. Heart enlargement is usually not seen because myocardial hypertrophy from pressure overload usually does not increase the size of the cardiac silhouette (concentric hypertrophy). • Advanced Imaging: Cardiac catheterization and selective angiocardiography may be used for definitive diagnosis but often is unnecessary. See Figure 11-1.
Diagnostic Notes • This congenital abnormality is rare in the cat.
Figure 11-1 Angiography can be used to diagnose aortic stenosis. A catheter (open arrows) is passed through the carotid artery into the left ventricle. Contrast material is injected and lateral thoracic radiographs are made. The supravalvular stenotic area (closed arrow) is seen in the outflow of contrast from the left ventricle into the aortic outflow tract.
Treatment Primary Therapeutics • Medical management of left-sided congestive heart failure consists of the use of diuretics, vasodilators (such as angiotensin-converting enzyme [ACE] inhibitors) and moderate dietary salt restriction. • Surgical intervention or balloon valvuloplasty of the stenotic lesion is not recommended in cats.
Secondary Therapeutics • Atenolol: Giving 6.25 mg q12–24h PO may be effective in reducing ventricular and supraventricular arrhythmias, slowing the heart rate, and limiting myocardial oxygen requirements. • Diltiazem: Giving 1.75–2.4 mg/kg q8h PO may have benefits in this disease if atenolol not effective.
Therapeutic Notes • Medical management of this abnormality often is unrewarding, especially if significant aortic regurgitation is present. • Prophylactic antibiotic therapy is indicated at times of potential bacteremia (i.e., dental procedures) because these patients (even those with mild stenosis) are predisposed to valvular endocarditis.
Prognosis th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
24
The prognosis of aortic stenosis is directly related to the severity of the outflow obstruction. Patients with significant pressure gradients across
Aortic Stenosis
their outflow tract (i.e., 75–100 mmHg) have a guarded-to-poor prognosis. As with other causes of ventricular concentric hypertrophy, there is an increased risk of sudden cardiac death. Considering the genetic potential, breeding of affected cats should be discouraged.
Oyama MA, Sleeper MM, Strickland K. 2008. Congenital Heart Disease. In LP Tilley, ed., Manual of Canine and Feline Cardiology, 4th ed., pp. 223–227. St. Louis: Elsevier.
Suggested Readings Brown DJ. 2007. Aortic Stenosis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5 Minute Veterinary Consult, 4th ed., pp. 96–97. Ames: Blackwell Publishing.
25
CHAPTER 12
Arrhythmias Larry P. Tilley and Francis W. K. Smith, Jr.
Overview The essentials of electrocardiography include the assessment of heart rate, heart rhythm, and the P-QRS-T wave forms. The electrocardiogram (ECG) is needed to accurately diagnose cardiac arrhythmias because it is extremely sensitive for this purpose. The ECG should be a standard part of the systemic disease workup, as well as part of the database in cats with suspected heart disease. An arrhythmia can be defined as (a) an abnormality in the rate, regularity, or site of origin of the cardiac impulse, or (b) a disturbance in conduction of the impulse such that the normal sequence of activation of atria and ventricles is altered. It is important to establish the causes of arrhythmias because such information affects prognosis and therapy. The possible sources of arrhythmias in dogs and cats can be divided into three basic categories: (a) autonomic nervous system; (b) cardiac sources; and (c) extracardiac sources. A classification of cardiac arrhythmias is listed in Table 12-1. See Figure 12-1.
Normal sinus rhythm
Sinus tachycardia
Sinus bradycardia
TABLE 12-1: Classification of Cardiac Arrhythmias Sinus Rhythm
Normal sinus rhythm Sinus tachycardia Sinus bradycardia Sinus arrhythmia Wandering pacemaker
Abnormalities of Impulse Formation
Supraventricular Sinus arrest Atrial premature complexes (APC) Atrial tachycardia Atrial flutter Atrial fibrillation Atrioventricular (AV) junction AV junctional escape rhythm (secondary arrhythmia) Ventricular Ventricular premature complexes (VPCs) Ventricular tachycardia Ventricular flutter, fibrillation Ventricular asystole Ventricular escape rhythm (secondary arrhythmia)
Abnormalities of Impulse Conduction
Sinoatrial (SA) block Atrial standstill (i.e., hyperkalemia or sinoventricular conduction) AV block: first degree, second degree, or third degree (complete heart block)
Abnormalities of Both Impulse Formation and Impulse Conduction
Pre-excitation (Wolff-Parkinson-White) syndrome and reciprocal rhythm (re-entry) Parasystole
Sinus arrhythmia
Figure 12-1
Examples of different rhythms from the sinoatrial node.
Diagnosis Differential Diagnoses There are several physiologic and pathologic conditions that must be considered. They are listed in Table 12-2.
Primary Diagnostics • Thoracic Auscultation: A markedly irregular cardiac rhythm on auscultation with an arterial pulse deficit may implicate arrhythmias such as ventricular premature complexes and atrial fibrillation, but it will require an ECG to differentiate among them. • Electrocardiography: A systematic method for an accurate ECG analysis of a rhythm strip (usually lead II) should always include the following steps: (a) general inspection of the rhythm strip; (b) identification of P-waves; (c) recognition of QRS complexes; (d) relationship between P-waves and QRS complexes; and (e) summary of findings and final classification of the arrhythmia.
Secondary Diagnostics th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
26
• Vagal Stimulation: This includes the mechanical application of pressure to receptors that cause a reflex increase in vagal tone (either by
Arrhythmias
TABLE 12-2: Differential Diagnoses of Feline Cardiac Arrhythmias Autonomic Nervous System
Excitement, exercise, pain, or fever (sympathetic influence) Respiratory influences on vagal tone (not as pronounced in cats as in dogs) Organic brain disease causing sympathetic or vagal stimulation
Cardiac Sources
Hereditary (rare) Acquired damage to the conduction system, hypertrophic cardiomyopathy, or neoplasia Diseases of the atria and ventricles; arrhythmias occurring in neoplasia, hypertrophic cardiomyopathy, and myocarditis (many causes)
Extracardiac Sources
Hypoxia Disturbances of acid-base balance Electrolyte imbalance Drugs Endocrine disease: hyperthyroidism, diabetes mellitus
ocular pressure or carotid sinus massage). The effects of increasing vagal tone are mainly supraventricular, causing a slowing of the heart rate and a decrease in conduction through the atrioventricular (AV) junction. • Long-Term Ambulatory Recordings: A Holter™ Monitor records the ECG for extended periods of time. The long-term ECG recording technique is the most sensitive noninvasive test to demonstrate transient arrhythmias. • Echocardiography: Arrhythmias can often be picked up as an incidental finding during an ultrasound study, or in some cases, can affect the hemodynamics.
used in the specific treatment of arrhythmias in the cat. Diltiazem (1.75–2.4 mg/kg PO q8h) and atenolol (6.25 mg/cat q12–24h PO) are currently the drugs of choice in cats because of their broad antiarrhythmic effects.
Secondary Therapeutics • Treat the Underlying Disease: Specific treatment for many of the arrhythmias present in cats often is not required. In the majority of cases, arrhythmias disappear when the underlying disease is brought under control. For example, the correction of hyperkalemia resulting from urethral obstruction by relieving the obstruction and restoring normal acid-base status and fluid volume may eliminate the associated arrhythmias. See Chapters 106 and 220. • Digoxin: Because of the recent use of angiotensin-converting enzyme (ACE) inhibitors in the cat and the side effects of digoxin, digoxin is used infrequently. Digoxin (0.008–0.01 mg/kg [approximately one-quarter of a 0.125 mg tablet] q48–72h PO) is used mainly to control the ventricular rate in atrial arrhythmias and for its inotropic effect in the improvement of cardiac performance in dilated cardiomyopathy.
Therapeutic Notes • Other antiarrhythmic drugs, including quinidine, procainamide, and lidocaine, have been shown to be dangerous in the cat. These drugs have not been used extensively in the cat because of their high risk of reactions and because ventricular arrhythmias are not common in the cat. Lidocaine could be used as an emergency ventricular antiarrhythmic drug in the cat, but very low doses should be used and only if the arrhythmia has not resolved by the treatment of the underlying cause.
Prognosis Diagnostic Notes • A pronounced sinus arrhythmia, normally auscultated in dogs, is rare in cats. Therefore, an irregular cardiac rhythm auscultated in the cat is generally an abnormal finding. • It should be emphasized that severe, life-threatening arrhythmias, such as ventricular tachycardia or atrial tachycardia, may easily be missed on auscultation as the cardiac rhythm is often regular on auscultation. An ECG is the only way to accurately make this diagnosis.
Treatment
The prognosis is variable depending upon the exact cause of the arrhythmia. In the majority of cases, arrhythmias disappear when the underlying disease is brought under control.
Suggested Readings Tilley LP. 1992. Essentials of Canine and Feline Electrocardiography. Interpretation and Treatment, 3rd ed. Ames, IA: Blackwell Publishing. Tilley LP, Smith FWK, Jr., Oyama MA, Sleeper MM. 2008. Manual of Canine and Feline Cardiology, 4th ed. St. Louis: Elsevier.
Primary Therapeutics • Antiarrhythmic Drugs: Beta-blockers (i.e., atenolol, propranolol) and calcium channel blockers (i.e., diltiazem) are different drug groups
27
CHAPTER 13
Ascites Larry P. Tilley
Overview Ascites is the accumulation of fluid within the peritoneal cavity. Ascites is indicative of an underlying disease process (exception: overzealous fluid administration) and may be clinically significant if it restricts diaphragmatic excursions, impeding respiration.
•
• •
Diagnosis Differential Diagnoses The most common causes of ascites in the cat are listed in Table 13-1.
Primary Diagnostics • Mucous Membrane Color and Capillary Refill Time (CRT): Pallor and delayed CRT may be present in cases of congestive heart failure or hemorrhage. • Thoracic Auscultation: In most cases of cardiomyopathy, a murmur or a gallop rhythm is present. Heart sounds are muffled when pericardial effusion is present. • Abdominal Palpation: This technique helps to confirm the presence of ascites and grades severity. Organomegaly is suggestive of con-
TABLE 13-1: Differential Diagnosis List for Ascites in Cats Abdominal Neoplasia (This is the most common cause of ascites in adult cats.)
Carcinomatosis; carcinomas and adenocarcinomas in abdominal organs.
Peritonitis
Feline infectious peritonitis (This is the most common cause of ascites in cats less than 1 year of age.) Chylous peritonitis Bacterial peritonitis
Congestive Heart Failure
Dilated cardiomyopathy Hypertrophic cardiomyopathy Congenital cardiac anomaly (i.e., tricuspid dysplasia or cor triatriatum dexter) Pericardial effusion
Hypoalbuminemia
Chronic hepatic disease Urinary loss (glomerulonephritis) Protein-losing enteropathy Malnutrition (parasitic or dietary)
Hemorrhage
Anticoagulant (i.e., warfarin and so on) toxicity Trauma Surgery
•
gestive heart failure or neoplasia. It is important to rule out pregnancy, bladder distension, and obesity. Peritoneal Fluid Analysis: Determine whether fluid is a transudate, exudate, hemorrhage, or chyle. Transudates are suggestive of congestive heart failure or hypoalbuminemia. Modified transudates are suggestive of feline infectious peritonitis and other infectious diseases or neoplasia. Complete Blood Count (CBC): This is to evaluate for anemia. Chemistry Profile: These tests may reveal hypoalbuminemia, elevation of liver enzymes, or low blood urea nitrogen (BUN), which are suggestive of hepatic insufficiency. Radiography: This is usually unrewarding when ascites is present other than to confirm the presence of ascites. See Figure 292-1.
Secondary Diagnostics • Bile Acids: Elevation of prepandial and postprandial bile acids is supportive of chronic liver disease. • Abdominal Ultrasonography: Ultrasound is indicated if abdominal disease is suspected. It is more diagnostic of ascites than radiography. See 292-4. • Echocardiography: An echocardiogram is indicated if cardiac disease is suspected. • Coronavirus Test: This is one of several tests indicated when feline infectious peritonitis (FIP) is suspected. See Chapter 76. FIP is uncommon in cats over 2 years of age and an unlikely disease in older cats with ascites. • Urinalysis: This test is used to detect proteinuria.
Diagnostic Notes • The first condition to be ruled out when ascites is present in cats less than 2 years of age is FIP; neoplasia should be highly suspected in older cats. • Analysis of peritoneal fluid should always be performed when ascites is present. • Conditions that may mimic ascites include hepatomegaly, splenomegaly, obesity, large neoplasms, pyometra, hydrometra, pregnancy, and advanced obstipation.
Treatment Primary Therapeutics • Primary Disease: The goal of diagnostics is to confirm ascites and diagnose the underlying disease. Successful treatment of the underlying disease is paramount to a successful outcome. • Abdominocentesis: This is essential when effusion is interfering with respiration. Approximately 50 to 75% of the ascites may be removed with minimal risk if a moderately sized (18-–22-gauge) catheter is used.
Secondary Therapeutics th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
28
• Furosemide: This drug is indicated only if ascites is secondary to congestive heart failure. A dose of 0.25 to 0.50 mg/kg q24h IV, IM,
Ascites
SC, PO is usually effective, although the dose can be increased. Using furosemide in noncardiogenic ascites will do little to remove the ascites and will dehydrate the patient.
Therapeutic Notes
Suggested Readings Thornhill JA. 2007. Ascites. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5 Minute Veterinary Consult, 4th ed., pp. 108–109. Ames, IA: Blackwell Publishing.
• Periodic abdominocentesis is better tolerated than long-term aggressive diuretic use.
Prognosis The prognosis is variable depending upon the exact cause of the ascites. Most cats with respiratory distress can be stabilized with abdominocentesis.
29
CHAPTER 14
Aspergillosis Sharon Fooshee Grace
Overview Aspergillosis is a relatively uncommon fungal disease of cats. A large number of cats with disseminated disease have been described in the literature; however, until recent years, there have been few published reports of localized infection involving the nasal, sinus, or orbital cavities. It is unclear why localized infections are being reported with increased frequency. Aspergillosis is caused by a saprophytic fungus, which is ubiquitous in the environment. The most important species in small animal medicine are Aspergillus fumigatus and Aspergillus terreus, with the former being most common. Infection is established through inhalation of airborne conidia, spores that are released from the free-living asexual form of the organism. Aspergillus is considered an opportunistic invader, which, once inside the host, adheres to and penetrates respiratory epithelium. Both host factors (i.e., immune competence, concurrent disease) and fungal characteristics (i.e., virulence of the invading species and size of inoculum) determine whether the infection will become established. The role of immunosuppression in facilitating infection remains unclear, although it does appear more common in cats with disseminated disease. One retrospective study reported that aspergillosis was more common in young adult cats and another found a higher prevalence in middleaged to older cats. The observed duration of illness reported by owners is typically a few weeks to a few months. No sex or breed predisposition has been noted, but brachycephalic breeds (Persians) have been suggested to have a marginally higher incidence of sino-nasal infection compared to other breeds. One report speculated that this could be due to disrupted nasal airflow and abnormal mucociliary clearance in Persians. Though not a consistent finding in all cases, a number of cats have been reported to have various diseases and infections concurrent with aspergillosis, including diabetes mellitus, feline infectious peritonitis (FIP), feline leukemia virus (FeLV), and panleukopenia. One review of 40 cases found an association with administration of glucocorticoids, long-term antibiotics, or both. Two distinct forms of aspergillosis have been described in cats: localized sino-nasal/orbital disease and disseminated disease. Localized disease is much less common than disseminated disease and involves the nasal cavity and frontal sinus. Local extension into the orbit may cause exophthalmos, although orbital disease has been described in one cat with no evidence of sino-nasal or disseminated disease. Sinonasal infection is associated with extensive and irreversible turbinate destruction. Clinical signs of nasal and sinus involvement include inspiratory dyspnea and stertor, sneezing, chronic mucopurulent nasal discharge, epistaxis, facial swelling, and mandibular lymphadenopathy. A mass lesion may be visualized within the nasal cavity. Localized infection has also been described in the urinary bladder of a cat with cystitis. Cats with disseminated disease have nonspecific signs of lethargy, fever, anorexia, and depression; vomiting and diarrhea have been reported in a few cats. Necropsy of cats with disseminated disease has demonstrated fungal hyphae in the lungs, heart, bladder, kidney, liver, and brain.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
30
Diagnosis Primary Diagnostics • Diagnostic Imaging: Radiographs of the nasal cavity and paranasal sinuses demonstrate increased soft-tissue density (sometimes with areas of mineralization) and bone destruction. See Figure 14-1. Computerized tomography (CT) is superior to conventional radiography in determining extent of disease and degree of bone destruction (including turbinates) because it can provide cross-sectional images. See Figure 14-2. Thoracic radiographs should be taken to evaluate the patient for pulmonary involvement. • Rhinoscopy: Rhinoscopy can be used to obtain tissue for histopathology, cytology, and culture. White-to-yellow masses, copious white-to-gray discharge, mucosal erythema, and turbinate destruction have been observed in cats with nasal infection. • Histopathology: Biopsy specimens may be placed in 10% formalin for submission. The cellular infiltrate contains lymphocytes, plasma cells, and neutrophils. Microscopic study demonstrates large mats of branching septate fungal hyphae consistent with Aspergillus. Superficial biopsies may be inconclusive.
Secondary Diagnostics • Complete Blood Count, Biochemical Profile, Urinalysis, and Retroviral Testing: Aspergillosis does not produce any pathognomonic changes in routine bloodwork, but the information gained is
Figure 14-1 The bony destruction caused by aspergillosis in the nasal cavity can be seen on this radiograph (arrow).
Aspergillosis
may be of potential use, although pharmacokinetic data is unavailable; it has been used at 10 mg/kg q24h PO. It is unknown how long therapy should continue, but a minimum of 6 months has been suggested. • Topical Therapy: Noninvasive infusion of clotrimazole through the nasal cavity over a period of 1 hour is the treatment of choice for nasal aspergillosis in dogs; results have been promising. Contact time of 1 hour seems to be critical in allowing the drug adequate time to damage the fungal cell membrane. The technique has had limited use in the cat but shows promise. The reader is referred to Suggested Readings section (Tomsa, Glaus, Zimmer, and Greene and Furrow and Groman) for more information. Potential complications include fatal aspiration of clotrimazole, laryngeal edema, leakage of medication across a disrupted cribriform plate, neurologic deficits, and death. Topical enilconazole therapy has been used in dogs, but it requires placement of indwelling catheters and repeated administration of the drug over 1 to 2 weeks.
Figure 14-2 This computerized tomography image shows aspergillosis in the frontal sinuses (small arrow) and the nasal cavity (large arrows). Images courtesy of Dr. Carolyn O’Brien, The Cat Clinic, Melbourne, AU.
helpful in assessing overall health of the cat and the potential for concurrent disease. Feline immunodeficiency virus (FIV) and FeLV testing should be performed in all debilitated cats. See Chapters 75 and 77. • Fungal Culture: Culture material should be taken directly from fungal colonies within the respiratory passage. Because fungal culture may yield false-positive or false-negative results, it is considered unreliable as the sole basis of diagnosis and should be used in conjunction with other tests. Urine culture is reported to have a high yield in cases of disseminated disease. • Serology: Several serologic tests are available for detection of Aspergillus-specific antibodies. It should not be used as the sole basis for ruling in or ruling out a diagnosis. It is unclear how prevalent these antibodies might be in the general population of uninfected, healthy cats. • Polymerase Chain Reaction (PCR) Testing: PCR tests have been developed, but their value in documenting disease in cats is still under investigation.
Diagnostic Notes • Aspergillus and Penicillium appear grossly and histologically similar. Culture is required to distinguish the two organisms.
Treatment Primary Therapeutics • Systemic Therapy: Effective therapy for aspergillosis has been elusive. Itraconazole has been used (10 mg/kg q24h PO) but has not been effective in all cases. In many cats, it appears to offer improvement but not resolution of disease. Posaconazole (5 mg/kg q24h PO, 40 mg/ml suspension) resulted in cure of one cat; disease had not recurred 20 months after therapy ended. Fluconazole has been used successfully to treat Aspergillus in the urinary bladder (7.5 mg/kg q12h PO). Voriconazole is another antifungal, which
Secondary Therapeutics • Nutritional Support: A feeding tube should be placed while the cat is under anesthesia if nutritional support is not needed. See Chapter 253 for placement of an esophagostomy tube.
Therapeutic Notes • Erosion of the cribriform plate is a contraindication for infusion of topical medications under pressure. • Rhinotomy and turbinectomy were used in the past, but these procedures are no longer considered of benefit in treating aspergillosis and may be detrimental to the patient. They cause additional pain and distress and do not appear to improve the success rate.
Prognosis Aspergillosis generally carries a poor prognosis, regardless of whether the disease is disseminated or localized.
Suggested Readings Adamama-Moraitou KK, Paitaki CG, Rallis TS, et al. 2001. Aspergillus species cystitis in a cat. J Fel Med Surg. 3(1):3–34. Day MJ. 2006. Feline disseminated aspergillosis. In C Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 626–627. Philadelphia: Saunders Elsevier. Furrow E, Groman RP. 2009. Intranasal infusion of clotrimazole for the treatment of nasal aspergillosis in two cats. J Amer Vet Med Assoc. 235(10):1188–1193. Hamilton HL, Whitley RD, McLaughlin SA. 2000. Exophthalmos secondary to aspergillosis in a cat. J Amer Anim Hosp. 36(4):343–347. Mathews KG, Sharp NJH. 2006. Feline nasal aspergillosis-penicilliosis. In C Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., p. 620. Philadelphia: Saunders Elsevier. McLellan GJ, Aquino SM, Mason DR, et al. 2006. Use of posaconazole in the management of invasive orbital aspergillosis in a cat. J Amer Anim Hosp. 42(4):302–307. Tomsa K, Glaus TM, Zimmer C, et al. 2003. Fungal rhinitis and sinusitis in three cats. J Am Vet Med Assoc. 222(10):1380–1384. Whitney BL, Broussard J, Stefanacci JD. 2005. Four cats with fungal rhinitis. J Fel Med Surg. 7(1):53–58.
31
CHAPTER 15
Aspirin Toxicosis Sharon Fooshee Grace
Overview The cat has a slow rate of drug metabolism compared to other species because of a relative deficiency of some hepatic glucuronyl transferases, enzymes that are important for drug conjugation and excretion. This group of enzymes participates in the most common phase II reaction of drug metabolism—glucuronidation. Glucuronidation adds a water soluble glucuronide molecule to either the parent drug or a phase I metabolite, enhancing renal elimination. Delayed drug conjugation renders the cat sensitive to a variety of drugs and compounds, including phenols and phenolic derivatives, amines, and aromatic acids. As a phenol, aspirin falls into the category of drugs that have delayed elimination in the cat. Aspirin may be safely given at a dose of 10 to 20 mg/kg with a dosing interval of 48 to 72 hours. The increased dosing interval is required because the half-life of aspirin is approximately 40 hours in the cat as compared to 7.5 hours in the dog. Failure to adhere to recommended dosages and dosing intervals may lead to salicylate toxicity in the cat. Also, because the drug is highly-protein bound, cats with hypoalbuminemia may be more at risk for toxicity with aspirin administration. With aspirin toxicosis, nonspecific signs such as anorexia, depression, vomiting, tachypnea, and hyperthermia may initially occur. It is difficult to make a specific diagnosis of aspirin toxicosis if a history of aspirin ingestion is unrecognized. The likelihood of respiratory distress, acid-base disturbances, seizures, generalized bleeding tendencies, and gastrointestinal hemorrhage (with potential perforation) is increased with repeated dosing of the drug. Drug-induced hepatitis may lead to icterus. Muscle weakness, ataxia, seizures, coma, and death may follow within days.
Diagnosis Primary Diagnostics • History: Because the clinical signs are non-specific, it is important to question the owner about the administration of aspirin. The presence of a condition requiring analgesic or antithrombotic medication may prompt the clinician to suspect aspirin toxicosis in the patient. • Complete Blood Count (CBC): Anemia due to bone marrow suppression and the presence of Heinz bodies are occasionally noted on the CBC, especially with chronic exposure. Thrombocytopenia and leukocytosis with a left shift are also reported. • Acid-Base Evaluation: An initial respiratory alkalosis with subsequent high anion gap metabolic acidosis may be noted.
Secondary Diagnostics • Serum Salicylate Levels: Commercial laboratories may be equipped to measure salicylate levels in the blood, but toxic concentrations are not well defined for dogs and cats. • Ethylene glycol toxicity is an important differential diagnosis.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
32
Treatment Primary Therapeutics • Removal: If early intervention is possible, emesis may be induced or gastric contents removed by lavage. Activated charcoal should be given orally at 2 g/kg followed by an appropriate cathartic or as directed on the product label. Some activated charcoal products contain a cathartic. • Gastrointestinal Ulceration: This should be treated with appropriate protectants (sucralfate [0.25 g (one-fourth of 1-g tablet) q8–12h PO] or H2-receptor antagonists).
Secondary Therapeutics • Supportive Care: This should include fluid and electrolyte therapy as needed and attention to the patient’s body temperature. • Acid-Base Management: The patient should be monitored and treated for ongoing acid-base disturbances. Sodium bicarbonate therapy (based on blood gas results or, if these are unavailable, 0.5– 1.0 mEq/kg total dose delivered over 30 minutes to several hours depending on severity of lab changes/signs) may combat metabolic acidosis and hasten elimination of the drug.
Therapeutic Notes • No specific antidote is available for aspirin toxicity. • Therapy with sodium bicarbonate can exacerbate or lead to hypokalemia. • Aspirin should always be used with caution in young or old cats and in those suffering from renal or liver dysfunction, asthma, coagulation disorders, gastrointestinal ulceration, or hypoalbuminemia. It may delay parturition so should not be used in late gestation. Aspirin should be discontinued 1 week prior to elective surgery because of the impact on bleeding time.
Prognosis The prognosis should be favorable with early intervention and the cessation of aspirin administration. Chronic administration of aspirin to cats may lead to bone marrow suppression, which is life-threatening.
Suggested Readings Groff RM, Miller JM, Stair EL, et al. 1993. Toxicoses and Toxins. In GD Norsworthy, ed., Feline Practice, pp. 551–569. Philadelphia: JB Lippincott. Kore AM. 1997. Over-the-counter analgesic drug toxicosis in small animals. Vet Med. 92(2):158–165. Rumbeiha WK, Oehme FW, Reid FM. 1994. Toxicoses. In RG Sherding, ed., The Cat: Diseases and Clinical Management, pp. 215–249. Philadelphia: WB Saunders.
CHAPTER 16
Atopic Dermatitis Christine A. Rees
Overview Atopic dermatitis, or atopy, is an exaggerated response to one or more environmental allergens. These allergens are thought to be inhaled or absorbed percutaneously into the skin. This allergy is an immediate or immunoglobulin E-mediated disease that is thought to be inherited. Although the genetics of atopy in cats have not been determined, the familial predisposition suggests a genetic component to feline atopy. Feline atopy is currently thought to be the second most common allergy in cats. The exact pathogenesis has not been determined, but an inappropriate T helper-2 response, ultimately leading to allergic inflammation in the skin, is the most widely accepted theory. More recently, Langerhans cells have been found to be important in feline atopy. These are antigen presenting cells found in the skin. Therefore, percutaneous absorption of allergens may be more important than previously thought.
some cats will have nonseasonal atopy or respiratory signs associated with their allergies. • Progression: Many patients’ symptoms will become perennial as the duration progresses. • Intradermal Allergy Testing: Most veterinary dermatologists agree that the intradermal allergy testing is the method of choice. • Diagnose Secondary Infections: Secondary infections may be present and must be identified and treated to get a true picture of the underlying baseline allergic symptoms. Tape cytology to evaluate for presence of secondary bacterial or Malassezia spp. is indicated. Dermatophytosis must be ruled out by direct hair examination and dermatophyte test media (DTM®) culture.
Secondary Diagnostics • Serology: In vitro serologic testing is controversial at this time.
Diagnosis Primary Diagnostics • Dermatologic History: History is extremely important. Diagnosis begins by exclusion of other pruritic diseases such as other hypersensitivities, parasitic infections, dermatophytosis, neoplastic conditions, and immune-mediated conditions. • Clinical Appearance: The clinical signs for feline atopy are variable. Recurrent otitis externa, pruritus, miliary dermatitis, eosinophilic plaque, and other forms of eosinophilic granuloma complex, excessive grooming, and seasonal waxing and waning dermatitis are typical clinical findings. See Figure 16-1. Although not as common,
Treatment Primary Therapeutics • Immunotherapy: The only specific therapy available at this time is allergen-specific immunotherapy based on intradermal allergy testing or serologic in vitro testing. This is the therapy of choice by dermatologists for moderately-to-severely affected patients due to low therapeutic risk and the ability to potentially interrupt the sensitization and elicitation phases of the atopic state, thus offering the potential of more complete allergy control. • Technique: An allergy test is performed, either by intradermal or in vitro means. Specific allergens are selected to which the patient appears to be to allergic. An allergen-based serum is formulated and injected subcutaneously according to various protocols. If the patient responds, injections must be continued for life. • Disadvantage: The primary drawback is the delayed therapeutic response (1–3 months, range of 1–12 months). Symptomatic management may be needed during the first 3 months of the immunotherapy. Potential risks include worsening of symptoms, which can be controlled by modification of injection protocol, and immediate adverse reaction to the injection, manifested as diarrhea, vomiting, weakness, or collapse. Severe reactions are rare when the immunotherapy is administered properly.
Secondary Therapeutics
Figure 16-1 Atopic dermatitis can have many presentations. This cat exhibits patchy alopecia due to licking and scratching. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Treat Secondary Causes of Pruritus: Secondary infections of the skin or ears need to be treated. In addition, exposure to external parasites, such as fleas, can cause an increase in pruritus. Therefore, cats should be on flea control products during immunotherapy. • Control Pruritus Pharmacologically • Corticosteroids: Corticosteroids are typically effective in reducing atopic pruritus, but long-term side effects are a concern. Prednisolone given at anti-inflammatory doses (2.2–4.4 mg/kg q12h PO for 1 week then taper) is the drug of choice because some cats have difficulty metabolizing prednisone to prednisolone. Triamcinolone (0.15%; Genesis Spray®) has been used as an extra-label adjunct in some cats. This medication appears to have relatively
33
SECTION 1: Diseases and Conditions
TABLE 16-1: Antihistamines for Cats Drug
Dose
1. Chlorpheniramine 2. Clemastine 3. Amitriptyline
1. 0.4–0.6 mg/kg q12h PO 2. 0.05–0.1 mg/kg q12h PO 3. 5–10 mg/cat/day q24h or divided q12h PO; initial trial of 3 weeks; Note: This is a tricyclic antidepressant that has antihistaminic properties in some cats. 4. 0.5–1.0 mg/kg q8–12h PO 5. 1–2 mg/kg q8–12h PO 6. 2.2 mg/kg q8–12h PO 7. 5 mg q24h PO
4. 5. 6. 7.
Cyproheptadine Hydroxyzine Diphenhydramine Cetrizine
minimal systemic absorption and may be of benefit in some patients. However, it is not completely without potential steroid side effects. Furthermore, the spray contains alcohol, which some cats find objectionable. • Modified Cyclosporine (Atopica®): Modified cyclosporine is not labeled for use in cats, but it may be useful for symptomatic management of some cats with atopy. Drug-to-drug interactions are of significant clinical importance; many drugs can potentially raise or lower cyclosporine blood levels. Interactions should be doublechecked for each patient before prescribing. This drug appears to ultimately inhibit T-cell function and can interrupt the symptoms of atopic dermatitis. There is currently no labeled indication for cats, but it is used for cats by dermatologists at 4 to 7 mg/kg q24h PO initially, then tapered to the least frequent effective dose. There is usually a lag phase before pruritus reduction is noted (2–3 weeks). Cyclosporine suppresses the immune system and may predispose patients to opportunistic infection and neoplasia. Therefore, its use is strictly contraindicated in patients with a history of malignant neoplasms or in patients infected with a retrovirus, and it should not be used without careful thought. In addition, a case of fatal toxoplasmosis has been reported in a cat administered cyclosporine. The serostatus for Toxoplasma should be checked in cats that are on cyclosporine and develop respiratory signs. Gastrointestinal upset is the primary clinical side effect noted and, in my
34
experience, approximately 25 to 30% of patients will experience some form of transient upset (i.e., decreased appetite, vomiting, loose stools, or diarrhea) during the first 1 to 2 weeks of therapy. Little is known about the validity of cyclosporine blood levels in the cats. • Prevent Secondary Pruritus: Antihistamines combined with omega3 fatty acids supplemented at high doses (5–10 mg/kg based on eicosapentaenoic acid [EPA®] content) may benefit patients with less intense itching. These medications are better suited to prevent allergic itching than actually stopping it. It is typically better to start at the upper end of the antihistamine dosage and frequency to see if the cat responds because it can be difficult to convince an owner to repeat an antihistamine that has been tried previously with little success. See Table 16-1.
Prognosis Most cats with atopy can be reasonably controlled with corticosteroids. The long-term prognosis depends upon one’s ability to either restrict the patient’s contact with the allergen or one’s ability to desensitize the patient.
Suggested Readings Barrs VR, Martin P, Beatty JA. 2006. Antemortem diagnosis and treatment of toxoplasmosis in two cats on cyclosporine therapy. Aust Veter J. 84(1):30–35. Roosje PJ, van Kooten PJ, Thepen T, et al. 1998. Increased numbers of CD4+ and CD 8+ T cells in lesional skin of cats with allergic dermatitis. Vet Pathol. 25(4):268–273. Moriello KA. 2001. Feline Atopy in Three Littermates. Vet Dermat. 12(3):177–181. Last RD, Suzuki Y, Manning T, et al. 2005. Veterinary Drug Handbook, 5th ed. Ames, IA: Blackwell. Reedy LM, Miller WH, Willemse T. 1997. Atopy. In LM Reedy, ed., Allergic skin diseases of dogs and cats. 2nd ed., pp. 116–149. Philadelphia: WB Saunders. Last RD, Suzuki Y, Manning T, et al. 2004. A case of fatal systemic toxoplasmosis in a cat being treated with cyclosporin A for feline atopy. Vet Dermat. 15(3):194–198.
CHAPTER 17
Bartonellosis Mark Robson and Mitchell A. Crystal
Overview Bartonella spp. (previously named Rochalimaea spp.) are fastidious, arthropod-transmitted, hemotropic, intraerythrocytic, facultative, gramnegative bacteria. These coccobacilli or rod bacteria are 1 to 2 µm in length, appear slightly curved in shape, and stain positive with silver stain. Although Bartonella organisms are most well known as the causative agent of the human ailment cat-scratch disease (CSD), they are also associated in people with bacillary angiomatosis (proliferations of blood vessels), visceral bacillary peliosis (extravasation of blood), septicemia, granulomatous hepatitis or splenitis, meningitis, encephalitis, endocarditis, retinitis and optic nerve swelling, osteolysis, and granulomatous pneumonia. Immunocompetent individuals tend to contain infection to local or regional lymph nodes resulting in pyogranulomatous lymphadenitis; immunocompromised individuals often develop bacteremia and disseminated disease. Although over 20 species of Bartonella have been recognized, only four species have been identified in cats: B. henselae, B. clarridgeiae, B. koehlerae, and B. bovis (formerly B. weissii); currently, only B. henselae and B. clarridgeiae have clinical or zoonotic significance. There are two main genotypes of B. henselae. The Marseille genotype is the most common in the western United States, Australia, and western Europe, whereas in the eastern United States the Houston-1 genotype is equally prevalent. Arthropod vectors, especially the cat flea Ctenocephalides felis, play a major role in the cat to cat transmission of Bartonella spp. Transmission may occur via contact with flea excrement rather than by bites. Direct transmission from cat to cat in a flea-free environment and vertical transmission from queen to kitten have not been detected. Transmission of Bartonella spp. from cat to human occurs primarily via contact with cats (i.e., scratches, bites). A small number of human Bartonella cases (5%) lack feline exposure, suggesting that insect transmission may play a role in human transmission as well. Cat saliva/ bites seem to be a less common means of Bartonella transmission compared to scratches. Prevalence of Bartonella antibodies in cats is variable from region to region. Overall prevalence in North America is 28%. Climates that support the flea life cycle have higher prevalence rates than do those where fleas are less common (i.e., Southeast 60%, Hawaii 53%, Pacific Coast 40%, Midwest 7%, and Rocky Mountain region 4%). Japan has a prevalence of 6 to 22%. Kittens and possibly feral cats have a higher prevalence than do adult cats. Feline leukemia virus (FeLV) status does not appear to influence the prevalence of Bartonella. The role of Bartonella as a disease-causing organism in cats is uncertain. Experimental infections in cats have resulted in inoculation swelling, lymphadenopathy, febrile episodes lasting from 2 days to a few weeks, reproductive disorders (i.e., infertility and stillbirths), and splenic hyperplasia. Inflammatory lesions have been documented in the liver, spleen, myocardium, and kidney of chronic experimentally infected cats. It has been suggested that naturally infected cats (based on serology) have a higher incidence of stomatitis/gingivitis and some urologic diseases. Intracellular Bartonella-like organisms have been demonstrated in some cats with idiopathic peripheral lymphadenopathy. Recent studies have failed to demonstate a correlation between Bartonella infection and disease in cats with anemia, uveitis, and neu-
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
rological disease. A Japanese study has shown that coinfection with feline immunodeficiency virus (FIV) and Bartonella was more likely to result in gingivitis or lymphadenopathy than either agent alone. There has been a report of a single cat in which B. henselae deoxyriboneucleic acid (DNA) was found in an aortic valve damaged by endocarditis; however, a causal relationship was not proven. In a recent study by Lappin and colleagues it was found that afebrile control cats were significantly more likely to be antibody positive than febrile cats with clinical illness. There was found to be no significant difference in frequency of detection of Bartonella DNA in blood between afebrile and febrile cats. The authors concluded that “in cats Bartonella species antibody tests cannot predict whether fever is due to Bartonella species infection and should not be used to determine the Bartonella species infection status.” Bartonella vinsonii subsp berkhoffii has been identified as a cause of endocarditis, myocarditis, granulomatous lymphadenitis, and granulomatous rhinitis in dogs. It should be emphasized that although large numbers of cats have been exposed to Bartonella and might be positive on serology, polymerase chain reaction (PCR), or even culture, there is almost no evidence that clinical disease will ensue. A sick cat that is positive for Bartonella is far more likely to be suffering from another illness, and many clinicians doubt the wisdom of testing for Bartonella at all. Clinical signs of CSD in humans include lymphadenopathy, fever, malaise, myalgia, anorexia, weight loss, and headache. Bartonella is considered of zoonotic importance to humans, regardless of immune status. Any person demonstrating clinical signs consistent with CSD or other Bartonella-induced diseases should be referred to a physician for confirmation. If Bartonella is confirmed, discontinuation of exposure to and contact with the affected animal should be recommended.
Diagnosis Primary Diagnostics • PCR: Amplification of Bartonella DNA from whole blood, fresh tissues, and frozen tissues via PCR is sensitive and specific. See Table 17-1 for testing laboratories. • Culture and Sensitivity of Blood or Tissues: Blood or tissue cultures are performed using blood agar media in a 5% carbon dioxide and high humidity environment at 35°C and may require up to 56 days to grow visible colonies.
Secondary Diagnostics • Western blot, indirect immunofluorescent antibody (IFA) or enzymelinked immunosorbent assay (ELISA) for antibodies to Bartonella: These may be helpful in screening cats prior to adoption by immunocompromised individuals. Serologic testing provides helpful epidemiologic information but is of limited clinical utility for identifying actively infected cats. Serologic testing is used to confirm cat scratch disease in people. • Other Disease Tests: Because an illness in a cat is highly unlikely to be due to Bartonella infection, testing for diseases with a higher likelihood of being the causative agent is indicated. These would include feline leukemia virus (FeLV), FIV, Toxoplasma, Histoplasma, and so on.
35
SECTION 1: Diseases and Conditions
TABLE 17-1: Laboratories Performing Polymerase Chain Reaction Testing for Bartonella Antech Diagnostics
Colorado State University
IDEXX Reference Laboratories
University of California, Davis
Galaxy Diagnostics
VCA ANTECH, 12401 West Olympic Blvd., Los Angeles, CA 90064; Phone: 1-800745-4725; www.antechdiagnostics.com Veterinary Diagnostic Laboratory, 300 West Drake, Fort Collins, CO 80523. Phone: 1-970-297-1281 Fax: 1-970-297-0320, www.dlab.colostate.edu 2825 KOVR Drive, West Sacramento, CA 95605 Phone: 1-916-267-2454 Fax: 1-916-267-2413 www.idexx.com/ animalhealth/laboratory/realpcr/tests/ vectorbornedisease.jsp Lucy Whittier, Molecular and Diagnostic Core Facility, Department of Medicine and Epidemiology, School of Veterinary Medicine, 2108 Tupper Hall, University of California, Davis, CA 95616. Phone: 1-530-752-7991 Fax: 1-530-754-6862 www.vetmed.ucdavis.edu/vme/ taqmanservice/diag_home Animal Health Division, 2 Davis Drive, Durham, NC 27709; Phone: 1-919-3541056; Fax: 1-919-287-2476; www. galaxydx.com
• Bartonella culture in humans and dogs is typically unsuccessful; PCR has proven more successful in these species.
Treatment Primary Therapeutics • Antibiotics: Antibiotic therapy in cats may reduce bacteremia but is unlikely to eliminate infection. Therapy is not indicated unless significant illness is present, which is unlikely. There is no definitive proof that any drug is effective, but antibiotics that have been reported to be helpful in the cat include azithromycin (10 mg/kg q24h PO for 7 days then q48h for 5 weeks) doxycycline (10 mg/kg q12h PO), rifampin (10 mg/kg q24h PO), and enrofloxacin (5 mg/kg q24h PO; note the possibility of retinal damage especially at higher doses) for 2 to 4 weeks. Follow-up screening 3 weeks post-treatment may be indicated. For humans, azithromycin, rifampin, ciprofloxacin, and trimethoprim-sulfamethoxazole are recommended. Immunocompetent patients are treated for 2 weeks, immunocompromised patients are treated for a minimum of 6 weeks. • External Parasite Control: This will help prevent bartonellosis.
Therapeutic Notes • The treatment of choice in humans remains controversial as a result of limited clinical studies.
Prognosis Diagnostic Notes • The potential infectivity of a cat cannot be definitively predicted by serology because cats may be serologically positive and culture negative, although higher titers are frequently associated with bacteremia. A negative antibody IFA titer has a high predictive value and may be of use when assessing the risk of infection from a cat to an immunocompromised owner. • Culture is often accurate in cats but bacteremia may be intermittent and repeated cultures may be necessary. A negative result is not, therefore, definitive. Using special collection tubes and at least 1.5 mL of blood will aid in recovery of bacteria. It is advisable to check with the laboratory for submission requirements.
36
Cats with Bartonella usually have inapparent infections and thus have an excellent prognosis. They will rarely develop any serious illness as a result of the infection. CSD in humans is usually self-limiting or responds well to antibiotic therapy, although relapses requiring prolonged treatment may occur in immunocompromised individuals.
Suggested Readings L Guptill-Yoran. Bartonellosis. 2006. In C Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 510–524. St Louis: Saunders-Elsevier. Lappin MR, Breitschwerdt E, Brewer M, Hawley J, Hegarty B, Radecki S. 2009. Prevalence of Bartonella species antibodies in the blood of cats with and without fever. J Fel Med Surg. 11:141–148.
CHAPTER 18
Basal Cell Tumors Bradley R. Schmidt and Mitchell A. Crystal
Overview Basal cell tumors are common, making up 11 to 30% of feline skin tumors. Basal cell tumors occur in older adult cats (mean age 10–11 years) and may be benign (i.e., benign basal cell tumor, basal cell epithelioma, basaloid tumor, basaloma) or malignant (basal cell carcinoma). As most basal cell tumors are benign (>90%) and carcinomas are generally of low-grade malignancy with a low metastatic potential, the preferred nomenclature is “basal cell tumor” for both benign and malignant tumors. Basal cell carcinomas are more common in the cat than in the dog. Tumors arise from epidermal basal cells and usually affect the head, neck, limbs, and thorax. See Figure 18-1A. Basal cell carcinomas more commonly arise from the nasal planum and eyelids. See Figure 18-1B. They appear as well circumscribed, solitary, 0.5- to 10.0-cm (0.25- to 4-inch) raised, ulcerated, hairless, lesions, which are occasionally melanotic or cystic. Occasionally multiple tumors may be found in the same patient. Tumors are typically fixed to the overlying skin and are freely movable. Tumors are often slow growing and may be present for months prior to diagnosis. All breeds are affected, although Siamese (carcinoma) and Himalayan and Persian (benign basal cell tumor) breeds may be predisposed to basal cell tumor development. There is no known etiology, although a strong correlation exists in humans between ultraviolet light exposure and tumor formation. Clinical signs are limited to the presence of the mass. Differential diagnoses include squamous cell carcinoma, melanoma, mast cell tumor, cutaneous hemangioma or hemangiosarcoma, hair follicle tumors, and sebaceous gland tumors.
(A)
Diagnosis Primary Diagnostics • Surgical Removal or Biopsy/Histopathology: This is the most accurate means of diagnosis.
Secondary Diagnostics • Fine-Needle Aspiration/Cytology: This may reveal the diagnosis prior to surgery. • Fine-Needle Aspiration/Cytology of the regional lymph nodes: may be indicated in cases of basal cell carcinoma; however, metastasis is rare. • Thoracic Radiographs: Metastasis is extremely rare; however, thoracic radiographs may be indicated in cases of basal cell carcinoma and to evaluate for other cardiopulmonary disorders. • Minimum Data Base: The complete blood count, serum chemistry profile, urinalysis, retrovirus tests are generally unremarkable; however, they are recommended to evaluate the overall health of the patient.
(B) Figure 18-1 Although benign, some basal cell tumors can be large (A) or in difficult surgical locations (B). Photos courtesy Dr. Gary D. Norsworthy.
Treatment Primary Therapeutics • Surgical Excision: Complete removal of the tumors is curative in most cases of both benign and malignant tumors.
Diagnostic Notes
Secondary Therapeutics
• Basal cell tumors usually behave in a benign manner even if assessed as a carcinoma by histopathology or cytology.
• Laser Ablation, Cryotherapy, Electrosurgery: These methods have been successful in treating small lesions. • Radiation Therapy: This may be indicated for incompletely resected malignant basal cell tumors. • Chemotherapy: Efficacy of chemotherapy has not been determined but may be considered in the rare metastatic event.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
37
SECTION 1: Diseases and Conditions
Prognosis The prognosis for cure is excellent with complete surgical excision in nearly all cases, regardless if the tumor is classified as malignant or benign. In the rare event of metastasis, the prognosis would be guarded to poor. The effectiveness of chemotherapy in treating metastatic lesions is unknown.
Suggested Readings Elmslie RE. 2004. Basal cell tumor. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 3rd ed., p. 147. Baltimore: Williams & Wilkins.
38
Moore AS, Ogilvie GK. 2001. Skin Tumors. In Moore AS, Ogilvie GK, eds., Feline Oncology, pp. 398–428. Trenton: Veterinary Learning Systems. Scott DW, Miller WH, Griffin CE. 2001. Miller & Kirk’s Small Animal Dermatology, 6th ed., pp. 1260–1263. Philadelphia: WB Saunders. Vail DM, Withrow SJ. 2007. Tumors of the skin and subcutaneous tissues. In SJ Withrow, DM Vail, eds., Small Animal Clinical Oncology, 4th ed., pp. 375–401. Philadelphia: Elsevier Saunders.
CHAPTER 19
Biliary Cysts Michele Fradin-Fermé
Overview Biliary cysts are cystic lesions delineated by thin walls and filled with serous or mucoid fluid; they can be observed either at the surface of the liver or within the hepatic parenchyma. They arise from primitive bile ducts (intra- or extrabiliary ducts) but develop into retention cysts lacking a connection with the biliary tree. They grow by expansion and bulge at the surface of the liver although they may remain intrahepatic. Their number, color, degree of lobulation, and size are variable. Cyst walls are composed of connective tissue lined by flattened or cuboidal biliary epithelium. Biliary cysts can be acquired or congenital. Acquired cysts are usually solitary and contain bile or blood. They are initiated by an inflammatory process such as trauma, chronic cholangiohepatitis, or neoplasia. Congenital cysts are usually multiple and may be associated with cysts in other organs (i.e., pancreas, kidneys, and so on). Congenital cysts are often seen in Persian cats and Himalayans, but they are not always related to polycystic kidney disease (PKD). Their content is usually clear and acellular. As they develop, they can create compression on the adjacent parenchyma leading to secondary inflammation and fibrosis. Most biliary cysts are asymptomatic; they are incidental findings on ultrasound or necropsy. In some cases they may become large and can produce increasing pressure on abdominal organs leading to reduced appetite and vomiting. See Figure 19-1. Acquired cysts accompanying cholangiohepatitis may produce symptoms that are rather related to the affected parenchyma rather than the cysts. Congenital cysts tend to be multiple; therefore, extensive fibrosis can occur leading to portal hypertension and hepatic dysfunction with encephalopathy and ascites.
Diagnosis Primary Diagnostics • Ultrasound: It is used to identify, enumerate, and confirm their connection with the liver. Cysts have usually thin, well-defined walls with anechoic contents causing distal acoustic enhancement. See Figure 19-2. Cysts with thicker, irregular walls and internal echoes are more likely to be clinically significant. Percutaneous aspiration with ultrasound guidance of a cyst for cytology and bacterial culture may be indicated. Serial ultrasound examinations also may be helpful in following cyst progression over time; generally, benign lesions do not change over time. The common bile duct may be compressed but typically remains patent even though it may become tortuous. • Radiographs: Biliary cysts are radiolucent, but, in cases of large cysts, displacement of abdominal organs by a fluid-density mass can be observed.
Secondary Diagnostics • Complete Blood Count and Chemistry Profile: These tests are usually unremarkable unless the cysts are linked to chronic cholangiohepatitis or they are numerous and associated with extensive fibrosis. • Analysis of the Contents of the Cyst: Congenital cysts usually have a clear, acellular content. Acquired cysts often contain blood or bile. • Computerized Tomography (CT): This imaging modality may be helpful in confirming the connection of the cyst to the liver. It also permits an assessment of cyst numbers and size prior to surgery. • Histopathology: Histologic examination is useful because it allows identification of the lesion and permits the differentiation between a cyst and a malignant tumor. However, there are some difficulties for the pathologist. When inflammation is associated with the cyst,
Figure 19-1 A large, solitary biliary cyst is seen attached to the periphery of one lobe of liver. At this size, biliary cysts may cause pressure on nearby viscera. This cyst was surgically excised. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 19-2 A large biliary cyst is seen in the parenchyma of the liver. Image courtesy Dr. Gary D. Norsworthy.
39
SECTION 1: Diseases and Conditions
a determination should be made of primary inflammation as an etiology, as in chronic cholangiohepatitis, versus secondary inflammation due to adjacent organ impingement by the cyst. A large biliary cyst compressing hepatic parenchyma will create inflammation of the surrounding parenchyma. The pathologist must also differentiate between a biliary cyst and a cystadenoma, benign tumor. However, even with histopathology, distinction between the two may not be assured. The main difference is the amount of supporting stroma around the lesion. Biliary cysts have scant stroma; moderate stroma occurs around a cystadenoma. The fibrovascular stroma surrounding the epithelium of a cystadenoma may contain frequent islands of entrapped hepatocytes and occasional muscle fibers and inflammatory cells. This benign tumor arises primarily in cats over 10 years of age. It is a slow-growing tumor that requires surgical excision, if possible. In humans it can undergo malignant transformation; however, this has not been documented in cats. The histologic examination will also permit differentiation of a biliary cyst from an abscess, a parasitic cyst, cystadenocarcinoma, and hemangiosarcoma. • Liver Biopsy: Biopsy of the liver should also be performed at the time of surgery to rule in or out cholangiohepatitis or lymphoma. If the former is suspected, intestinal biopsy is also recommended to look for concurrent inflammatory bowel disease.
performed during a laparotomy to avoid bile spillage into the abdomen and to permit abdominal lavage if this occurs. Ultrasoundassisted drainage followed by alcoholization can also be used with success.
Secondary Therapeutics • Cystectomy: If a cyst is drained but the fluid reforms quickly, laparotomy and cyst removal should be considered. If the cyst cannot be completely removed, partial excision accompanied by marsupialization and possible omentalization may be considered. • Lobectomy: In case of numerous biliary cysts located on the same liver lobe, partial lobectomy may be indicated. • Biliary Diversion Surgery: If biliary cysts impinge bile flow of the extrahepatic ducts, biliary diversion surgery should be considered.
Prognosis The prognosis is generally good for congenital biliary cysts as most of them are asymptomatic. For acquired cysts, the prognosis is guarded as cysts are often associated with cholangiohepatitis or neoplasia.
Suggested Readings Treatment Primary Therapeutics • No Treatment: This is appropriate for biliary cysts if they are asymptomatic. • Drainage: In the case of a large cyst compressing other organs and inducing vomiting, ultrasound-guided aspiration to empty the cyst is indicated. However, if the cyst content is bile, aspiration should be
40
Maxie MG. 2007. The Liver and Biliary System. In MG Maxie, ed., Jubb, Kennedy, Palmer ’s Pathology of Domestic Animals, 5th ed., pp. 301–302. Philadelphia: Saunders Elsevier. Zatelli A, D’Ipollito P, Bonfanti U, et al. 2007. Ultrasound-assisted drainage and alcoholization of hepatic and renal cysts: 22 cases. J Am Anim Hosp Assoc. 43(2):112–116. Laurence HJ, Erb HN, Harvey HJ. Nonlymphomatous Hepatobiliary Masses in Cats: 41 Cases (1972–1991). Vet Surg. 23:365–368.
CHAPTER 20
Bite Wounds: Canine Gary D. Norsworthy
Overview Cats are frequently the victims of bite wounds from dogs. Most cats are attacked by stray or free-roaming dogs, and often by more than one dog. Occasionally, a cat will stray into a fenced yard that contains a dog, and an attack will occur. Although dogs and cats frequently coexist in amiable relationships, if a cat suddenly runs from a dog, hunting instincts may override the previously friendly relationship, resulting in a seemingly inappropriate attack. When a cat bites a dog, a relatively small hole is made in the skin. However, dogs frequently hold their prey and shake their heads, resulting in much more severe damage to underlying tissues, including bones and thoracic or abdominal walls. The canine jaw is capable of applying 150 to 450 psi of crushing force. Wounds that penetrate thoracic or abdominal organs occur frequently. In addition to the physical trauma that occurs, canine oral bacteria and environmental contamination frequently occur. Dirt and plant material may contaminate the superficial and deep aspects of the wound. Wound healing has four stages: (a) The inflammatory phase lasts about 5 days. In addition to hemorrhaging and clotting, inflammatory mediators, including histamine, serotonin, proteolytic enzymes, kinins, and prostaglandins, contribute to inflammation; (b) during the debridement phase, an exudate composed of white blood cells, dead tissue, and wound fluid forms. Neutrophils infiltrate, releasing enzymes that facilitate the breakdown of extracellular debris and necrotic material. Monocytes enter tissue and transform to macrophages for removal of necrotic tissue, bacteria, and foreign material. Lymphocytes stimulate or inhibit protein synthesis and migration of other cells; (c) the repair stage begins 3 to 5 days after the injury. Fibroblasts migrate along fibrin strands to synthesize and deposit collagen, elastin, and proteoglycans that mature into fibrous tissue. Capillaries invade wounds to increase oxygen tension and augment fibroplasia. Granulation tissue begins to form at the wound edges about 3 to 5 days post-injury. Healthy granulation tissue is highly resistant to bacterial colonization. Granulation tissue proliferates and matures as wound contraction begins; (d) The maturation phase results in scar tissue formation and final healing. Cats that are bitten by dogs often have widespread tissue necrosis that will prevent primary wound healing. Therefore, these wounds must close by second intention healing that involves the healing phases described above.
Diagnosis Primary Diagnostics • History: The owner will often witness the attack and describe the head-shaking of the dog and the wounds sustained by the cat. In some cases, the cat is able to return home on its own despite the injuries; in other cases, the cat is found at or near the attack scene. • Physical Examination: The cat is often non-ambulatory and in pain; it is often non-responsive. The cat’s hair is often wet with canine saliva and the cat’s blood. Open wounds may be observed although they usually appear less serious than the deeper wounds. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Treatment Primary Therapeutics • Stabilization: The cat must be stabilized. These measures will vary depending on the degree of injury. Some cats need intravenous fluids for shock. If a penetrating chest wound or tracheal injury has occurred, oxygen therapy may be needed. • Emergency Surgery: Immediate surgery is needed if penetrating chest or tracheal wounds have occurred. If abdominal dehiscence has occurred, surgery is needed immediately to replace, repair, or remove damaged abdominal organs. Surgery may be needed to control hemorrhage. See below regarding closing contaminated wounds. • Analgesics: An analgesic, such as buprenorphine, at 0.005 to 0.01 mg/ kg IV, q4 to 8 h IM or SC should be started at presentation. • Antibiotics: Injectable broad-spectrum antibiotics (cefovecin) or antibiotic combinations (fluoroquinolone plus ampicillin or amoxicillin) should be started at presentation and given until the time of discharge from the hospital. • Circulation Assessment: Wounds to an extremity may compromise or destroy circulation, making amputation necessary. Blood pressure determination at the level of the foot can be helpful in assessing circulatory viability. • Wound Cleaning: If thoracic or abdominal injuries do not necessitate emergency surgery, wound cleaning should be done after the cat is stabilized. This may occur on the day of hospital admission or the next day. Sedation or generally anesthesia is usually required. Hair should be removed from the wound and should be clipped from the cat’s skin near the wound. Copious, vigorous flushing with sterile saline or tap water is used to remove environmental debris, canine saliva, and contamination. Flushing with dilute (0.05%) chlorhexadine solution is advised due to its broad spectrum of activity and residual activity; 1 or 0.1% povidone-iodine is acceptable. Deep and contaminated wounds should either be not sutured or should be closed with loosely applied sutures just to approximate skin apposition. Drain tubes should be considered if the skin is closed.
Secondary Therapeutics • Tissue Viability Assessment: Skin circulation may deteriorate for about 5 days. If skin closure is performed prior to 5 days, the owner should be told that skin sloughing and future surgery are likely. Nonviable skin becomes black, bluish-black, or white during those 5 days, at which time it will slough. • Open Wound Phase: About 3 to 5 days post-injury, granulation tissue begins to form. Depending on the size of the wound, it may take several more days to weeks for all nonviable tissue to slough. Final closure should not occur prior to that. See Figures 20-1A, 20-1B, and 20-1C. • Final Wound Closure: Clinical judgment is used to determine when the open wound phase appears completed. The wound should be filled with pink granulation tissue with no or minimal nonviable skin or deeper tissue. Surgical closure is performed even though drain tubes may still be needed to prevent seroma formation when the wounds are deep or extensive. Any nonviable tissue is excised prior to closure. See Figure 20-1D.
41
(A)
(B)
(C)
(D)
(E) Figure 20-1 A 7-year-old, female, spayed, domestic short-hair cat was pulled from a tree by two dogs as she tried to escape. Extensive bite wounds occurred on the ventral abdomen. A, At 7 days post-trauma sloughing and granulation are underway. B, At 9 days, most of the necrotic tissue had sloughed. C, At 16 days a clean bed of granulation tissue is present. The cat is ready for primary closure (D), which was performed the next day. By 3 months post-trauma healing was complete, hair had regrown, and the cat was clinically normal (E).
42
Bite Wounds: Canine
• Skin Grafting: Extensive wounds may require closure using various reconstructive techniques such as V-to-Y plasty, Z plasty, and pedicle flaps. • Buprenorphine (at 0.01 to 0.02 mg/kg q8 to 12h PO) or meloxicam (0.05–0.1 mg/kg q24 to 48h PO) should be dispensed to be given by the owner for 3 to 7 days. • Antibiotics: Broad-specturm antibiotics should be given at home until it is obvious that primary healing without wound drainage is occurring.
Therapeutic Notes • Many cats will not eat until most of the necrotic tissue sloughs. Anorexia may last for 2 or more weeks. Placement of an esophagostomy or gastrostomy tube may be needed to prevent non-healing and the onset of hepatic lipidosis. See Chapters 253 and 255.
days, the prognosis is good. See Figure 20-1E. Owners should be prepared for a healing period of several weeks that may include two or more surgeries.
Selected Readings Fossum TW. 1997. Surgery of the Integumentary System. In TW Fossum, ed., Small Animal Surgery, pp. 91–152. St. Louis: Mosby. Griffin GM, Hold DE. 2001. Dog-Bite Wounds: Bacteriology and Treatment Outcome in 37 cases. J Am Anim Hosp Assoc. 37:453–460. Waldron DR, Zimmerman-Pope N. 2003. Superficial Skin Wounds. In D Slatter, ed., Textbook of Small Animal Surgery, 3rd ed., pp. 259–273. Philadelphia: Saunders Elsevier. Trout NJ. 2003. Principles of Plastic and Reconstructive Surgery. In D. Slatter, ed., Textbook of Small Animal Surgery, 3rd ed., pp. 274–292. Philadelphia: Saunders Elsevier.
Prognosis Dog bites to cats can be a fatal event depending on the extent of the injuries. If the cat is successfully stabilized and survives the first few
43
CHAPTER 21
Bite Wounds: Felines Gary D. Norsworthy
Overview The territoriality of the cat is largely responsible for its fighting behavior, whether it is the aggressor or the territory defender. The typical feline bite wound is due to a tooth that penetrates the skin and underlying tissue, leaving a lesion of minimal diameter but substantial depth. Within a few hours, the skin puncture closes, entrapping bacteria from the cat’s mouth and debris, which were carried into the wound. Aerobic and anaerobic bacterial infections are common. The three stages are preabscess (swelling and pain), abscessation (focal pocket of pus), and postabscess (abscess drains spontaneously through the skin). Abscessation occurs about 3 to 5 days after the bite. If not surgically opened, it will usually rupture and drain spontaneously by 5 to 7 days. See Figure 21-1. Some cats develop chronic draining tracts due to resistant bacteria, Mycoplasma, Mycobacterium, or fungal infections, the presence of foreign bodies or bone sequestra within the wound, or immunosuppressive states associated with the feline immunodeficiency virus (FIV) or the feline leukemia virus (FeLV).
Diagnosis Cellulitis is a variant of this process. See Figure 21-2. If a bite wound occurs in a location that does not have loose skin, such as a distal extremity, infection will dissect through fascial and muscle planes, resulting in diffuse swelling instead of an abscess. Lethargy, inappetence, fever, and lameness are the early signs.
Diagnosis There are specific body regions that are more likely to be bitten based on the cat being the aggressor or the defendant. See Figure 21-3. Areas of swelling anywhere on the body of a cat showing the appropriate
Figure 21-2 This cat’s right foreleg was bitten by another cat. Because there is minimal loose skin in this location, cellulitis developed.
clinical signs should arouse suspicion of a bite wound abscess. Draining tracts, especially if the material has a putrid odor, indicates an advanced stage of the process and usually the presence of anaerobic bacteria.
Diagnosis Primary Diagnostics • History: Outdoor cats or cats in multicat households with a history of fighting are at highest risk. • Clinical Signs: The presence of a painful swollen area or a draining tract, accompanied by fever, should arouse one’s suspicion for a bite wound abscess.
Secondary Diagnostics
Figure 21-1 Two bite wounds occurred on this cat’s head about 5 days prior. The abscesses had ruptured and were draining at the time of presentation.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
44
• Culture and Sensitivity: This is generally not necessary as most infections are due to Pasturella multocida; however, chronic draining wounds should be cultured for aerobes, anaerobes, fungi, and Mycobacterium. In addition to Pasturella, commonly isolated organisms include Fusobacterium, Bacteroides, Eubacterium, Peptococcus, Peptostreptococcus, Corynebacterium, Actinomyces, and Micrococcus. • Complete Blood Count: Marked neutrophilic leukocytosis with a left shift is typical. • Retroviral Tests: Cats with recurrent or nonresponsive abscesses should be tested for FeLV and FIV. Although the FeLV antigen test will usually be positive within a few days after the bite occurs, the FIV antibody test may take up to 8 weeks to turn positive. Testing at 8 weeks post-presentation is recommended because it is unlikely to miss incubating infections. However, testing at the time of initial presentation has been recommended due to poor owner compliance for testing at 8 weeks. If both tests are negative retesting at 8 weeks should still be recommended.
Bite Wounds: Felines
Figure 21-3 Certain body regions are more likely to sustain fight wounds. These are largely influenced by whether the cat is the aggressor or the defendant. Adapted drawing courtesy of Journal Feline Medicine and Surgery and Dr. Richard Malik.
Diagnostic Notes • Because of the high incidence of this disease, a bite wound infection should be suspected first when draining tracts are present, especially if fever and outdoor exposure are present.
Treatment Primary Therapeutics • Antibiotics: The high incidence of Pasturella multocida makes penicillins and cephalosporins the drug families of choice. If begun within the first 24 hours after the bite, they may abort abscess formation and be curative. Antibiotic therapy is the treatment of choice for cellulitis. • Surgical Drainage: Surgically opening an abscess enhances rapid resolution. A drainage hole should be made in the ventral aspect of the abscess to facilitate drainage of purulent material. Flushing or swabbing the abscess with an antibacterial solution is appropriate. Placement of a drain tube is optional; if it is used, it should be placed so it exits the skin in the ventral aspect of the abscess. Suturing should not occur for 3 to 4 days; however, an abscess will generally granulate and close within 2 to 5 days without suturing. Surgical drainage is not appropriate for cellulitis.
Secondary Therapeutics • Surgical Exploration and Excision: Abscesses that do not heal promptly should be surgically explored to identify and remove foreign material. Chronic fistulous tracts should be excised, if surgically feasible. • Alternative Antibiotics: Bite wound infections that are not responsive to penicillins may be due to unusual organisms, including Mycobacterium or bacterial L-forms. Culture of the lesion and antibi-
otic sensitivity testing are recommended. Doxycycline or enrofloxacin may be effective for abscesses resistant to other antibiotics. These should be tried if culture is not feasible or while culture and sensitivity results are pending. • Cefovecin: The third-generation cephalosporin cefovecin (Convenia®, Pfizer) has proven efficacy for abscesses and cellulitis and avoids the use of oral antibiotics; dosage is 8 mg/kg q14d SC. One injection lasts about 2 weeks which is typically long enough for infection resolution. Client acceptance is good for cats that are resistant to oral administration of medications.
Therapeutic Notes • Castration should be recommended because the nature of the tom cat is to enlarge his territory by fighting. Fighting often leads to abscesses and FeLV or FIV infections. • If further fighting activity is likely, vaccination with FeLV and FIV vaccines is recommended.
Prognosis The prognosis for fight wound infections is excellent with proper diagnosis and antibiotic therapy. Cats with nonhealing wounds should have the wound exudate cultured and should also be tested for FeLV and FIV. These viral organisms make the cat susceptible to repeated and resistant infections.
Suggested Readings Dowers KL, Lappin MR. 2006. The pyrexic cat. In R. Jacquie, ed., ProblemBased Feline Medicine, pp. 364–392. Philadelphia: Elsevier Saunders. Greene CE. Feline abscesses. 2006. In CE Greene, ed., Infectious diseases of the dog and cat, 2nd ed. pp. 328–330. Philadelphia: WB Saunders.
45
CHAPTER 22
Blastomycosis Sharon Fooshee Grace
Secondary Diagnostics
Overview Blastomyces dermatitidis, the etiologic agent of feline blastomycosis, is a dimorphic, saprophytic fungus. The disease is uncommon in the cat. Most reports indicate no breed, age, or sex predisposition in cats, although one study found a preponderance of cases in young adult males. To date, an association between blastomycosis and feline retroviral infections has not been made. The organism is worldwide in distribution. In North America, it is endemic in the Mississippi, Ohio, and Missouri River valleys, near the Great Lakes, and in Ontario, Manitoba, and Southern Saskatchewan. Attempts to isolate the organism from soil have met with only limited success. Increased risk has been demonstrated for dogs living near water with soil that is moist, acidic, and enriched with organic matter. The disease has been identified in cats confined to the indoors. Inhalation of infective conidia is the primary means for establishment of infection. Once in the lung, the conidium transforms to a thick-walled yeast, with dissemination by hematogenous and lymphatic routes. Reproduction in the host animal occurs asexually by budding from the parent organism. Disseminated disease is common in the feline cases reported, and the course of illness has ranged from weeks to months. Vague signs such as anorexia, fever, weight loss, and depression are expected. Pulmonary involvement appears to provide the most organ-specific findings (i.e., coughing, dyspnea, tachypnea, and increased lung sounds). Also reported are inflammatory ocular lesions (i.e., anterior uveitis and chorioretinitis), central nervous system (CNS) signs (i.e., ataxia and circling), lymphadenopathy, draining tracts/nodules, and osteomyelitis. The yeast (tissue) phase is not considered contagious to humans or other pets though caution should be exercised with open draining tracts. Public health risk is derived from a shared environmental exposure.
• Complete Blood Count (CBC), Biochemical Profile, Urinalysis, and Retroviral Tests: Nonregenerative anemia has been reported. Other changes reflective of specific organ involvement may be seen. • Radiography: The most common radiographic finding is a diffuse miliary or nodular interstitial lung pattern. Pleural and peritoneal effusions and perihilar lymphadenopathy have been reported. See Figure 291-39. • Urine Antigen Assay: MiraVista Labs (Indianapolis, IN, www. miravistalabs.com) has developed a urinary antigen test for Blastomyces in humans that also appears quite sensitive for diagnosis of canine blastomycosis. Because few cases of the disease have been reported in cats, use of the test has been limited, but it shows promise. • Serologic and Intradermal Skin Testing: These tests are not reliable indicators of infection in the cat.
Diagnostic Notes • The broad-based bud attachment that is present during reproduction is helpful in distinguishing Blastomyces from Cryptococcus neoformans. • Respiratory signs are not a reliable indicator of degree of pulmonary involvement. Therefore, thoracic radiographs should be taken prior to initiation of therapy. If lung disease is severe, worsening of respiratory signs should be anticipated following initiation of treatment. Supportive care may be needed. • Blastomyces may not stain reliably with routine histopathologic stains. If blastomycosis is suspected, the pathologist should be advised so that other stains (periodic acid-Schiff reaction [PAS], Gomori’s methenamine silver, or Gridley’s) may be used. • Travel history and prior geographic residence should always be obtained for any sick cat. Cats housed exclusively indoors are still at risk for infection.
Treatment
Diagnosis Primary Diagnostics • Clinical Signs: Respiratory signs, ocular disease (especially posterior chamber), draining tracts and nodules, and evidence of systemic disease in cats residing or traveling in the endemic area should raise one’s index of suspicion for blastomycosis. • Cytology: Identification of the organism is essential for definitive diagnosis. The organism is easily recognized in samples collected from exudative lesions and infected organs via impression smears or fine-needle aspirates. With Wrights-type stains, the organism appears as a moderate to large (5–20 µm) basophilic yeast with a characteristic thick, refractile double-contoured wall. Budding organisms are attached to the parent organism by a broad base. The associated inflammatory response is usually pyogranulomatous in nature. See Figure 289-5.
Primary Therapeutics • Itraconazole: At present, this is the antifungal drug of choice, although fluconazole is being increasingly utilized. Itraconazole is dosed at 5 mg/kg q12h PO and given with a meal to promote absorption of the drug. The capsule may be opened and the contents divided into gelatin capsules or mixed into canned food. The oral solution has better bioavailability than the capsules. Treatment duration should be a minimum of 60 days. If clinical signs are still present, continue for 2 months beyond resolution of signs. • Fluconazole: This newer azole has superior penetration of the ocular and CNS tissues compared to itraconazole. It is gaining in popularity since its release in generic form. One recent report showed recovery of several cats with 3 to 5 months of treatment at 5 mg/kg q12h PO. • Placement of a feeding tube, when needed, permits the owner to administer proper nutritional support at home.
Secondary Therapeutics th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
46
• Fluconazole and Amphotericin B are alternative treatments if the cat does not respond to itraconazole. A subcutaneous protocol has
Blastomycosis
become available for administration of amphotericin B; this protocol appears to reduce associated nephrotoxicity. See Chapter 43 for the protocol. • Affected cats should be periodically monitored after therapy is discontinued for possible relapse.
Therapeutic Notes • Although itraconazole is usually well tolerated, serum chemistries should be periodically checked during itraconazole therapy to assess for hepatotoxicity. For cats with clinical evidence of hepatotoxicity (i.e., anorexia, jaundice), the drug should be discontinued, at least temporarily. Asymptomatic cats with increased liver enzymes do not necessarily need cessation of therapy but should be closely monitored.
those severely debilitated by pulmonary disease must be given a guarded prognosis.
Suggested Readings Bromel C, Sykes JE. 2005. Epidemiology, diagnosis, and treatment of blastomycosis in dogs and cats. J Small Anim Pract. 20(4):233–239. Gilor C, Graves TK, Barger AM, et al. 2006. Clinical aspects of natural infection with Blastomyces dermatitidis in cats: 8 cases (1991–2005). J Am Vet Med Assoc. 229(1):96–99. Legendre A. 2006. Blastomycosis. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 569–576. Philadelphia: Saunders Elsevier.
Prognosis In general, the prognosis for infected cats has improved with the introduction of itraconazole and fluconazole. Cats with CNS involvement or
47
CHAPTER 23
Blindness Karen R. Brantman and Harriet J. Davidson
Overview Loss of vision may be caused by various diseases involving the eyes or the brain. It is important to determine the cause of the blindness to treat any serious or painful conditions. In some cases, vision may be restored, whereas in others the cat and owner must learn to adapt. Owners may bring their cats in for examination of acute blindness or gradual vision loss. Cats that have slowly lost vision frequently learn to compensate so well that the owner may be unaware of any change. As a result, the veterinarian may be the first person to detect vision loss during a routine examination. Visually impaired or blind cats still make wonderful house pets; however, some minor adaptations to the environment may be helpful.
Diagnosis Primary Diagnostics • History: A complete medical history is vital. It should include current diseases, all medications the cat has taken recently, and the patient’s overall status at home. Because owners frequently use several veterinarians, it is necessary that information be taken with each visit. Direct questions regarding vision should focus on changes in the patient’s behavior, navigation of surroundings, and the general appearance of the eyes. What the owner first noticed about the cat’s vision, the duration of the problem, any changes over time, and changes to the cat’s environment, such as a new home, new furniture, or recent rearrangement of furniture should be noted. Initially, ask questions in an open manner to prevent leading the owner to a particular answer. Direct questions should come at the end to confirm or deny particular findings. • Vision Assessment, Observation: Measuring vision is a challenge in the cat, and at its best, is a subjective test. The best method of assessing vision takes behavioral observations, physical manipulation of the cat, as well as ophthalmic examination results into account. Proceed first with simply observing how the cat holds itself, how its eyes appear without manipulation, and how it maneuvers within the examination room. Placing the cat in a new environment may help. Blind animals are more reluctant to walk, will bump into objects, and will not be able to jump onto elevated objects. They will sometimes walk with an accentuated gait of the forelegs, as if they are using their legs to test for objects. Keep in mind that if the cat does not move, it does not necessarily mean the cat is blind. Attempt to test the ability of the cat to see and track objects by tossing an object, such as a cotton ball. Again, be aware that the cat may choose to simply ignore the object and not move its eyes or head even though vision is intact. Likewise, maze testing is another challenge if the cat does not wish to walk. • Vision Assessment, Hands On: To test a cat’s visual placing, hold the cat with its chest supported and approach a flat surface. Animals with normal vision and normal proprioception will hold their paws out in anticipation of standing. A blind animal may not hold its paws out until they touch the surface. Next, assess the cat’s menace The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
48
and palpebral responses. The menace response is a learned response and does not become fully developed until about 10 to 16 weeks of age. It is important to note, however, that cats are able to override the menace response; they may not blink or respond even when they see an object coming toward them. In addition, take caution when menacing not to move air currents at the corneal surface. Air current sensation tests the corneal-palpebral reflex and not necessarily vision. If a negative menace is detected, touch the face near the eyelids to be certain that the cat is able to blink (palpebral reflex). If there is no palpebral reflex, the facial nerve is affected. When the facial nerve is not functional, any positive menace response will be subtle, such as retraction of the globe or pulling the face away. • Ophthalmic Examination: Due to the variable types of ocular diseases that can cause vision loss, a thorough ophthalmic examination should be completed including pupillary light and dazzle reflexes, measurement of intraocular pressures, and pupillary dilation for a complete lenticular and fundic examination. Stimulating a dazzle reflex involves shining a bright light into the eye and watching for a blink, narrowing of the palpebral fissure, or turning away of the head. Pupillary light and dazzle reflexes are subcortical responses and do not alone determine vision. A cat may have a cortical brain lesion and be blind, yet still maintain a positive pupillary light reflex (PLR) and dazzle response. In this instance, it is also likely that there will be other neurologic lesions. Thus, all cranial nerves should be assessed following PLR, dazzle, and menace.
Secondary Diagnostics • Electroretinogram: Measurement of the electrical activity of the retina may be used to determine retinal function. This is a specialized test performed by an ophthalmologist. The test can be done in the awake animal to determine mass retinal effect; specialized testing for subtle changes frequently requires general anesthesia. • Visual-Evoked Potentials: This is another form of electrodiagnostics and tests the integrity of the optic nerve, optic tracts, and the occipital cortex. • Brain Imaging: Magnetic resonance imaging (MRI) is the best method for evaluation of the soft tissues of the eyes, optic nerves, optic tracts, and the brain. This evaluation should be considered when no specific form of ocular disease can be identified.
Treatment Primary Therapeutics • Specific Treatments: The exact form of treatment is based on the particular disease. Uveitis, glaucoma, cataracts, and retinal disease can result in blindness and, in many instances, are treatable. See Chapters 31, 85, 223.
Secondary Therapeutics • Adaptation: If vision cannot be returned, it is important that the owner realize the cat may need some adjustments to its care and environment.
Blindness
• Environment: When a blind cat is placed into a new environment, it may experience a temporary change in behavior. Not knowing its surroundings may result in aggression or extreme timidity and hiding. A blind cat needs to be given time to adjust to its surroundings. To prevent problems, a cat’s food and water bowls, as well as litter pan, should be kept in the same location and on the ground floor of the home. Most blind cats become accustomed to their surroundings; they easily adapt and memorize where objects can be found. Cats that have learned their environment rarely bump into objects unless they have recently been moved. Due to their extraordinary senses, cats can learn to jump and climb, although this ability varies from cat to cat. • Playtime: The use of objects with a sound or scent may enhance the blind cat’s quality of life by allowing it to play, but playing is not necessary. Some cats are able to compensate for their lack of vision and may resume normal activity, including jumping on furniture and chasing objects. Blind cats have been observed “gazing” out windows. It is always hard to tell what is really in the mind of a cat.
• Outdoors: A blind cat should never be left outdoors unrestricted. Although its other senses remain alert and potentially greater than normal, allowing it to sense aspects of its environment. It can easily be lead astray by a scent or a sound and not have the ability to find its way home. • Enucleation: Cats that have suffered ocular trauma with possible lens capsule rupture and those with intraocular tumors or intractable glaucoma are candidates for enucleation. Sarcomas are usually malignant with local invasion along the optic nerve See Chapter 122.
Suggested Readings Martin CL. 2001. Evaluation of patients with decreased vision or blindness. Clin Tech Small Animal Pract. 16(1):62–70.
49
CHAPTER 24
Bordetella Infection Teija Kaarina Viita-aho
Overview Bordetella bronchiseptica is an aerobic, gram-negative bacterium that causes respiratory tract infections in many mammals. In dogs it causes infectious tracheobronchitis, also known as kennel cough. B. bronchiseptica is considered to be a primary pathogen of cats, but it also may act as a secondary pathogen or co-pathogen with other respiratory tract pathogens such as the feline herpesvirus (FHV-1), feline calicivirus (FCV), and Chlamydophila felis. Exposure to the organism is common, and infection is widespread in the cat population. The prevalence of B. bronchiseptica is 3 to 14% in cats with respiratory tract disease, and 1 to 10% in clinically healthy cats. It has been isolated in 21% of cats with history of respiratory tract disease. Seroprevalence is reported to be much higher, up to 60% in diseased cats and up to 40% in clinically healthy cats. Seroprevalence is highest in high population density conditions such as rescue shelters and multicat households. Overcrowding, stress, and poor hygiene predispose to infection. The bacterium is shed in oral and nasal secretions. The primary route of infection is via the oronasal cavity. Transmission occurs primarily with direct contact because the organism does not survive long periods of time outside the host. However, in a heavily contaminated environment the organism can survive long enough outside the host to allow it to be transmitted indirectly with infected oral or nasal secretions. The bacterium is easily killed by many common disinfectants and by extremes of pH and temperature. The incubation time is 2 to 5 days. The most common clinical signs are sneezing, ocular and nasal discharge, and coughing. However, coughing is not as usual in cats than in dogs with kennel cough. Nevertheless, infection should be considered in any coughing cat. See Chapter 42. Other clinical signs include increased lung sounds, fever, and lymphadenopathy. Usually the clinical signs resolve after about 10 days. Poor hygiene and overcrowding may contribute to a heavy burden of infection and increase the severity of clinical signs. Severe signs such as pneumonia, dyspnea, and cyanosis may occasionally occur. Pneumonia, which may be generalized or localized, is usually seen in kittens younger than 10 weeks old, but older cats may be affected as well. Many of the clinical signs of B. bronchiseptica infection in cats mimic those observed with other respiratory pathogens (with the exception of coughing). Therefore, the disease cannot be determined solely by a visual or physical examination. Cats living in direct proximity with dogs have shown to have elevated prevalence of B. bronchiseptica. Therefore, it is believed that the infection can be transmitted between dogs and cats. Additionally, cats with B. bronchiseptica infection may act as reservoirs to the dog population, especially in an animal shelter setting. Because B. bronchiseptica is also a human pathogen, there is a potential for B. bronchiseptica to transmit between cats and their owners. Immunocompromised people are suggested to be in the highest risk of zoonotic infection. Some cats may become carriers of B. bronchiseptica after recovering from the acute disease and continue to shed the organism for several weeks after infection. The infection may also be clinically asymptomatic.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
50
Long-term asymptomatic carriage has been reported, and carrier cats only shed the bacterium during periods of stress.
Diagnosis Primary Diagnostics • Polymerase Chain Reaction (PCR) Testing: Some laboratories offer a PCR test for diagnosis of B. bronchiseptica. PCR is rapid, and it has high sensitivity and specificity. Samples are collected from the oropharynx or nasal cavity using sterile cotton swabs. • Bacterial Isolation: Samples for isolation can be obtained from the oropharynx with a sterile cotton swab or through transtracheal wash or bronchoalveolar lavage. If there is a nasal discharge, a nasal swab can also be obtained. The swab is placed immediately in charcoal transport medium. The sample is cultured on selective charcoal-cephalexin agar.
Diagnostic Notes • Serology is of limited diagnostic value due to the high seroprevalence in the cat population. • Isolation of B. bronchiseptica from oropharyngeal swabs should be interpreted with caution because many cats are asymptomatic carriers. However, the identification of B. bronchiseptica from bronchoalveolar lavage samples of cats with lower respiratory tract signs is diagnostic. • Chronic carrier cats often shed relatively few organisms and may require repeated oropharyngeal culturing. Furthermore, isolation does not confirm that the bacterium is the only causative agent of the respiratory disease.
Treatment Primary Therapeutics • Doxycycline: This is the drug of choice. It is dosed at 5 mg/kg q12h PO or 10 mg/kg q24h PO for 4 weeks. Doxycycline has been reported to cause esophageal strictures and esophagitis. To minimize the risk, doxycycline suspension is preferred over tablets. Alternatively, water should be syringed into the cat’s mouth or the tablet lubricated with butter or similar. Doxycycline, as other tetracyclines, may cause discoloration of teeth if used in pregnant queens or young kittens. Nevertheless, doxycycline is safer than other tetracyclines. I have used doxycycline in kittens of 4 to 5 months of age without dental problems.
Secondary Therapeutics • Fluoroquinolones: This group of drugs is also effective. Enrofloxacin is dosed at 5 mg/kg q24h PO. Overdosing should be avoided because enrofloxacin may cause blindness if higher doses are used. In contrast to dogs, cats treated with enrofloxacin are not predisposed to developing chondrotoxic side effects. Marbofloxacin has not shown to have adverse ophthalmic effects. It is dosed at 2.75 to 5.55 mg/kg q24h PO.
Bordetella Infection
• Clavulanic Acid-Potentiated Amoxicillin: Give at 20 mg/kg q12h PO for 4 weeks. It can be safely used in young kittens and pregnant queens. However, B. bronchiseptica is not as susceptible to it as to doxycycline and another course of treatment with doxycycline may be needed later to ensure that the organism is eliminated from the body. • Cats with severe signs may require supportive treatment such as intravenous fluid administration to correct the dehydration and restore electrolyte and acid-base balance.
Therapeutic Notes • Asymptomatic or mild disease does not usually require antimicrobial therapy. Treatment is indicated for cats with more severe or persistent signs. However, it has been suggested that antibacterial therapy should be used even in mild cases because B. bronchiseptica may colonize the lower respiratory tract and lead to more severe disease.
Prevention • An avirulent live intranasal vaccine for B. bronchiseptica is available in some European countries and in the United States. Because the infection is usually mild, it is not considered a core vaccine. Vaccination should be considered for cats living in or moving into high-density populations with a history of bordetellosis, such as shelters with endemic B. bronchiseptica. The intranasal vaccination is easy to perform and is well tolerated. After vaccination, cats may exhibit mild transient sneezing or clear ocular discharge. • Vaccination does not prevent the infection but significantly reduces clinical signs. The protection starts within 72 hours after the administration of vaccine. Such rapidly induced protection is particularly valuable if an outbreak of disease occurs. The immunity lasts for at
least a year and annual vaccination should provide continuous protection. • Cats receiving live vaccines will shed the bacteria for 4 to 5 days. Therefore, vaccination must be avoided if the owner is immunocompromised because B. bronchiseptica may transmit to humans. Alternatively, if vaccination is indicated, isolation of the cat for 1 week following vaccination should prevent any transmission to susceptible individuals. Additionally, immunocompromised cats should not be vaccinated.
Prognosis The prognosis is good in mild cases, but it can be poor in severe pneumonia occurs, which is more likely in young kittens.
Suggested Readings Binns SH, Dawson S, Speakman AJ, et al. 1999. Prevalence and risk factors for feline Bordetella bronchiseptica infection. Vet Record. 144:575–580. Egberink H, Addie D, Belák S, et al. 2009. Bordetella bronchiseptica infection in cats ABCD guidelines on prevention and management. J Fel Med Surg. 11:610–614. Helps CR, Lait P, Damhuis A, et al. 2005. Factors associated with upper respiratory tract disease caused by feline herpesvirus, feline calicivirus, Chlamydophila felis, and Bordetella bronchiseptica in cats: experience from 218 European catteries. Vet Record. 156:669–673. Speakman AJ, Dawson S, Binns SH, et al. 1999. Bordetella bronchiseptica infection in the cat. J Small Anim Pract. 40:252–256. Williams J, Laris R, Gray AW, et al. 2002. Studies of the efficacy of a novel intranasal vaccine against feline bordetellosis. Vet Record. 150:439–442.
51
CHAPTER 25
Brachial Plexus Neuropathy Gary D. Norsworthy
Overview Brachial plexus neuropathy is a disease that affects the motor, and to some degree, sensory nerves that make up the brachial plexus. Etiology is unknown; an immune-mediated response directed at epitopes specific to nerves derived from the brachial plexus is postulated to play a role. The typical clinical presentation is paresis or paralysis of only the thoracic limbs with depressed spinal reflexes. Conscious proprioception (CP) is lacking in the thoracic limbs; however, it is normal in the pelvic limbs. See Figure 25-1. Muscle atrophy of the thoracic limbs may occur if the duration is sufficient. Although the affected nerves and muscles appear to be solely those of the thoracic limbs, other peripheral nerves are likely to be involved but less or not noticeable clinically. Spontaneous remission in 7 to 14 days was noted in the two cats and three dogs reported and in the one case treated by the author. Relapse occurred in one of the reported cats 13 months later, but spontaneous recovery occurred again.
Diagnosis Primary Diagnostics • Clinical Signs: Affected cats exhibit paresis or paralysis of the thoracic limbs. In limited cases studied, this is the only clinically observed clinical sign.
• Electromyographic Testing: Nerve conduction studies are abnormal in the affected peripheral nerves. This form of testing permits identification of affected nerves that are not associated with clinically apparent signs.
Diagnostic Notes • A tentative diagnosis can be made based on clinical signs. Other nontraumatic diseases causing paresis of the thoracic limbs but not the pelvic limbs are unreported.
Treatment Primary Therapeutics • Spontaneous remission has occurred in the observed cases. Within 7 days improvement is apparent. The cat may be normal within 14 days.
Secondary Therapeutics • Analgesics are indicated if pain is present.
Therapeutic Notes • Other forms of therapy have not been reported.
Prognosis The prognosis appears to be good with the possibility of relapse and subsequent recovery.
Suggested Readings Freeman PM, Harcourt-Brown TR, Jeffery ND, et al. 2009. Electrophysiologic evidence of polyneuropathy in a cat with signs of bilateral brachial plexus neuropathy. J Am Vet Med Assoc. 234(2):240–244.
Figure 25-1 Brachial neuropathy is characterized by neurological deficits, including loss of conscious proprioception (CP) in the front legs with normal CP in the rear legs.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
52
CHAPTER 26
Brachycephalic Syndrome Mac Maxwell and Gary D. Norsworthy
Overview The brachycephalic syndrome in dogs is a recognized constellation of conditions directly related to shortening of the nasal and oral cavities. One or more of the components may be found in brachycephalic dogs, with the English bulldog being the most consistently and severely affected. The canine components are stenotic nares, elongated soft palate, and hypoplastic trachea. Secondary changes that may occur are laryngeal edema, laryngeal collapse, tonsillar eversion, tracheal collapse, and laryngeal saccule eversion. Respiratory compromise is the overall net result. The clinical signs can vary from stridorous breathing or exercise intolerance to cyanosis and collapse. The brachycephalic syndrome in cats is not just a respiratory syndrome; it includes some of these respiratory components (i.e., stenotic nares, elongated soft palate), but it also affects the tongue, eyes, and teeth. Tonsillar, laryngeal, and tracheal induced respiratory compromise is rare in cats. Persians and Himalayan cats are the most consistently affected. Longevity of Persians is significantly less than eight other breeds studied in Sweden. It is likely that the conditions described in this chapter contribute to that.
Brachycephalic Corneal Disease Overview The feline cornea encompasses about 30% of the eyeball. Brachycephalism results in rostral protrusion of the eyeball resulting in more corneal contact with environmental factors than with other cats. Recurrent or chronic keratitis, corneal ulcers, corneal scarring, and corneal sequestra result. These are discussed in detail in Chapters 41 and 124.
Diagnosis
Prognosis The prognosis for treating brachycephalic corneal disease is good although the need for repeated treatment is likely because the facial conformation that underlies this disease cannot be changed. The recurrent nature often results in permanent scarring to significant portions of the cornea.
Idiopathic Facial Dermatitis of Persians Overview This is a facial dermatitis found in Persian and Himalayan cats that is also known as the Persian Dirty-face Syndrome. Because of its strong breed predilection, it is presumed that brachycephalism or other breedrelated genetic factors are involved. However, the nasolacrimal duct system of brachycephalic cats is usually inoperative so epiphora can keep the face moist. The characteristic finding is an accumulation of black waxy debris that mats in the hair principally around the eyes but also around the mouth and on the chin. See Figure 26-1. Otitis externa is also common. Initially it is not pruritic, but pruritus may develop if an inflammatory component develops. Exudative and erythematous facial folds and mucoid ocular discharge may occur. Erythema of the preauricular skin or ceruminous otitis externa with black, waxy debris in the ear canals may also be present. Secondary bacterial and Malassezia dermatitis may occur, but even if they are treated successfully the syndrome persists.
Diagnosis Primary Diagnostics • Clinical Appearance: The occurrence of the lesions described previously in a Persian or Himalayan cat is diagnostic. It is more difficult to detect in Himalayans due to the dark hair color in the affected areas.
Primary Diagnostics • Ophthalmic Examination: The corneal portion of the ophthalmic examination described in Chapter 299 should be employed. Fluorescein staining is essential for identifying active corneal ulcers. A corneal sequestrum is a focal, black, hard cicatrix usually located near the center of the cornea. See Figure 124-2.
Diagnostic Notes • The chronic or recurrent nature of the keratitis, corneal scarring, and corneal ulceration are what makes these events characteristic of brachycephalism.
Treatment Primary Therapeutics • See Chapters 41 and 124. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 26-1 A buildup of dark, waxy material ventral to the eyes is typical of the idiopathic facial dermatitis of Persian cats.
53
SECTION 1: Diseases and Conditions
(B)
(A)
(C)
Secondary Diagnostics • Cultures and Cytology: Fungal and bacterial cultures and cytology preps may identify secondary infections that need to be treated.
Treatment Primary Therapeutics • Successful treatment for the primary disease has not been found; it is, at this time, incurable.
Secondary Therapeutics • Seborrhea: Antisecorrheic products to reduce the waxy buildup may be of some benefit. Chlorhexidine (3%) wiping pads (Douxo, chlorhexadine 3% PS Pads; Sogeval, Coppell, TX) are helpful for some cats, but the owner should not get chlorhexidine in the eyes. • Antifungal Drugs: An azole antifungal drug (itraconazole, fluconazole) is indicated for Malassezia. • Others: One report documents promising results using oral cyclosporine. Steroids, doxycycline, hyposensitization, and food trials have been inconsistently effective in some cats.
54
Figure 26-2 A, The nares are so stenotic in this cat that they nearly closed during inspiration. B, The nares are open so airway impairment is not a problem at 2 months post-operatively. A CO2 laser was used to sculpt the nares. Notice that this cat also has diverging strabismus. C, Stenotic nares can also be corrected using this surgical technique. A vertically oriented wedge-shaped incision is made (arrow) so tissue can be removed. When the wedge is closed with sutures, the naris is pulled open.
Stenotic Nares Overview Stenotic nares are the most common respiratory component of the feline brachycephalic syndrome. It results in nares that are minimally open during expiration and almost closed during inspiration. See Figure 262A. If exercise occurs the cat may be forced to breathe through its mouth.
Diagnosis Primary Diagnostics • Physical Examination: This disease is diagnosed by observing the narrow nasal openings. When the respiratory rate or the depth of respiration increases, the nares may be even more stenotic.
Treatment Primary Therapeutics • Surgery: The treatment for this condition is surgical reconstruction of the nares. A CO2 laser can be used to sculpt the nares. See Figure
Brachycephalic Syndrome
26-2B. Alternatively, a wedge of tissue can be removed lateral to each naris as will be described.
Surgical Procedure • See Figure 26-2C. Grasp the naris with forceps, and make a vertically oriented wedge-shaped incision using a No. 11 blade. The medial incision should be made first followed by the lateral aspect. • Appose the cut edges of the nostril using 3-0 or 4-0 polydiaxanone. • Repeat on the opposite nostril taking care to excise a similarly shaped wedge.
Malocclusion Overview Malocclusion is defined as faulty contact between the upper and lower teeth when the jaw is closed. When brachycephalism occurs, the teeth often become rotated dorsally and displaced due to crowding. Any of the teeth may be affected, but the canines are affected most commonly.
Figure 26-3 Malocclusion, usually involving the canine teeth, is common in brachycephalic cats.
Prognosis Diagnosis Primary Diagnostics • Oral Examination: An examination of the oral cavity will easily reveal the presence of malocclusion. See Figures 26-2A and 26-3.
The prognosis is good because it is unlikely that ocular perception is hindered significantly.
Elongated Tongue Overview
Treatment • No Treatment: In most cases, the mouth remains functional so treatment is not needed. In these cases, the condition is strictly cosmetic. • Orthodontics: In some cases the misdirected teeth may be returned to their normal position with orthodontics. Consult a veterinary dental textbook for technique or consider a referral to a veterinary dentist. • Extractions: Teeth that interfere with chewing or closing of the mouth or that cause the owner personal concern are candidates for extraction. See Chapter 243.
Prognosis Generally the prognosis is excellent because most affected cats have no trouble with prehension of food. The prognosis is also excellent if extraction or orthodontia is employed.
Diverging Strabismus Overview Strabismus is a disorder of vision due to a deviation from normal orientation of one or both eyes so that both cannot be directed at the same object at the same time. It occurs as a converging abnormality (cross eyes) or a diverging abnormality (walleyed).
Diagnosis Primary Diagnosis • Physical Examination: On physical examination the lines of sight of the two eyes diverge. See Figure 26-2A and 26-2B.
Treatment Primary Therapeutics • None: There is no treatment for this disorder.
Occasionally the tongue will not experience the same degree of shortening as the mandible and maxilla. This results in protrusion of the tongue from the mouth. This is common in brachycephalic cats, but it is usually not severe enough to justify treatment. When it is severe, the tongue is so long that it protrudes 1 cm (3/8 inch) or more, and it cannot be withdrawn into the mouth. This results in drying of the tip of the tongue. See Figure 26-4A. Infection or ulceration of the tongue may result.
Diagnosis Primary Diagnostics • Physical Examination: Observation of the tongue with the mouth closed is diagnostic. If there are signs of chronic desiccation near the tip, treatment should be recommended.
Treatment Primary Therapeutics • Surgery: Surgical excision of the rostral 1- to 2-cm (3/8- to 3/4-inch) of the tongue (partial glossectomy) is curative. Surgical Procedure • With the cat under general anesthesia, mark the portion of the tongue that extends rostral to the incisor teeth. • Place a noncrushing clamp (e.g., Doyen) across the rostral aspect of the tongue just proximal to the area to be resected. See Figure 26-4B. • Excise the rostral aspect of the tongue using a No. 10 scalpel blade. See Figure 26-4B. • Control hemorrhage as needed with electrocautery, digital pressure, or ligation. • Appose the epithelial edges with 4-0 or 3-0 polydiaxanone in a simple interrupted pattern. • Healing generally takes about 10-14 days. See Figure 26-4C.
55
SECTION 1: Diseases and Conditions
(A)
(A)
(B) (B) Figure 26-5 A, This lateral radiograph shows the caudal aspect of the soft palate (arrow) overlying the epiglottis. B, Note the length of a normal soft palate (arrow) in another brachycephalic cat.
Elongated Soft Palate Overview
(C) Figure 26-4 (A) More than 1 cm (3/8 inch) of this elongated tongue protrudes from the mouth. The tip shows signs of constant drying. (B) A Doyen-type clamp is used to control hemorrhage during amputation of the tip of the tongue. (C) One month following surgery the tongue is healed and retracts normally into the mouth.
56
Elongated soft palate in a brachycephalic dog can be severe enough to create significant respiratory impairment. The brachycephalic cat may also have a soft palate that is elongated enough to cause snoring sounds, especially when it is asleep, or that causes respiratory impairment similar to affected dogs. The decision to treat should be based on the severity of the clinical signs.
Diagnosis Primary Diagnostics • History and Clinical Examination: If the owner reports snoring the cat should be examined to determine if the soft palate is the cause. • Examination Under Anesthesia: The use of a laryngoscope will permit visualization of whether or not the caudal aspect of the soft palate contacts the epiglottis during inspiration.
Brachycephalic Syndrome
• Radiography: A lateral view of the cervical region using high quality radiographic equipment and technique will permit visualization of how far caudal the soft palate extends. See Figure 26-5.
Treatment Primary Therapeutics • None: If the clinical signs are mild (snoring) and the owner is tolerant of the snoring sounds, no treatment is needed. • Surgery: If the soft palate is so long that it interferes with unobstructed passage of air into the larynx or if the owner is intolerant of the snoring, surgery is indicated. A CO2 laser can be used to simultaneously cut and cauterize the caudal (elongated) portion of the soft palate. Alternatively, conventional surgery can be used; however, surgical access is limited. Surgical Technique: Soft Palate Resection • Place the patient in sternal recumbency and elevate the head. The endotracheal tube should be secured to the lower jaw to allow visualization of the soft palate. • Identify the landmarks for resection: the rostral tip of the epiglottis and the caudal aspect of the tonsillar crypts. • Place stay sutures on the lateral aspects of the soft palate just rostral to the anticipated site of resection. • Transect the soft palate using Metzenbaum scissors at the point where it touches the tip of the epiglottis. • Appose the dorsal and ventral aspects of the mucosa with 3-0 or 4-0 polydiaxanone in a simple continuous pattern. Alternatively, the palate may be partially transected and sutured to minimize hemorrhage.
Prognosis For mild cases causing snoring, the prognosis is excellent as long as the owner can tolerate the snoring and respiratory impairment does not occur. For severe cases the prognosis is excellent with surgical resection of the soft palate.
Suggested Readings Bond R, Curtis CF, Ferguson EA, et al. 2000. An idiopathic facial dermatitis of Persian cats. Vet Dermatol. 11:35–41. Egenvall A, Nodtvedt A, Haggstrom J, et al. 2009. Mortality of lifeinsured Swedish cats during 1999–2006: Age, breed, sex, and diagnosis. J Vet Intern Med. 23:1175–1183. Fontaine J, Heimann M. 2004. Idiopathic facial dermatitis of the Persian cat: three cases controlled with cyclosporine. Vet Dermatol. 15:64. Griffon DJ. 2000. Upper airway obstruction in cats: Pathogenesis and clinical signs. Compendium. 22(9):822–829. Griffon DJ. 2000. Upper airway obstruction in cats: Diagnosis and treatment. Compendium. 22(9):897–906. Malik R, Sparkes A, Bessant C. 2009. Brachycephalia—a bastardisation of what makes cats special (editorial). J Fel Med Surg. 11:889–890. Ordeix L, Galeotti, F, Scarampella F, et al. 2007. Malassezia spp overgrowth in allergic cats. Vet Dermatol. 18(5):316–323. Schlueter C, Budras KD, Ludewig E, et al. 2009. Brachycephalic Feline Noses: CT and anatomical study of the relationship between head conformation and the nasolacrimal drainage system. J Fel Med Surg. 11:891–900.
57
CHAPTER 27
Bronchial Disease, Chronic Philip Padrid
Overview Chronic bronchial disease in cats occurs most commonly in two forms: chronic bronchitis and asthma. Chronic bronchitis is defined as an inflammatory disorder of the lower airways that causes a daily cough, for which other causes of cough (i.e., heartworm disease, pneumonia, lungworms, neoplasia, and so on) have been excluded. Asthma is more loosely defined as a disorder of the lower airways that causes airflow limitation that may resolve spontaneously or in response to medical treatment. Airflow limitation is generally the result of some combination of airway inflammation and airway smooth muscle contraction. The symptoms of asthma can be dramatic, including acute wheeze and respiratory distress. Sometimes however, the only symptom of asthma-induced airflow limitation is a daily cough, and in human patients, this is referred to as “cough-variant” asthma. Clinical signs are variable. Bronchitic cats have a daily cough and may be absolutely symptom free in between episodes of cough. Alternatively, cats with bronchitis may be tachypneic at rest. Asthmatic cats may cough, wheeze, and struggle to breathe on a daily basis. In mild cases, symptoms may be limited to occasional and brief coughing. Some cats with asthma may be asymptomatic between occasional episodes of acute airway obstruction. Severely affected cats may have a persistent daily cough and experience many episodes of life-threatening acute bronchoconstriction. The pathogenesis of asthmatic airway inflammation and hyperreactivity is clearly multifactorial. Numerous investigations suggest that the interaction between T lymphocytes and eosinophils within airways may play an important role in the generation of airway inflammation and airway hyperreactivity in human asthma. Most of the recent research in asthma pathogenesis includes the notion that effector lymphocytes may be broadly defined in terms of the pattern of cytokine secretion that they demonstrate, with the Th2-lymphocyte subtype generating the cytokines that drive asthmatic inflammation. Importantly, a Th2-driven cytokine profile has been demonstrated in antigen-induced asthma models in the feline species. There are no other disorders besides asthma that cause acute reversible, nonprogressive wheezing and tachypnea. Other causes of cough and tachypnea in the feline species include:
chitis from asthma in the feline patient. Nevertheless, the diagnosis, prognosis, and treatment options for both diseases overlap with great frequency.
Diagnosis Primary Diagnostics • History: The cat’s history should include of one or more of these clinical signs: cough (most consistent), acute wheeze, tachypnea, or respiratory distress including labored, open mouth breathing. These signs are usually relieved quickly with some combination of oxygen, bronchodilators, and corticosteroids. • Radiographs: Radiographic evidence of bronchial wall thickening, usually described as “doughnuts” and “tramlines.” See Figure 291-23. Air trapping may be assumed if the lungs are hyperinflanted. This is seen most prominently on the lateral view and can be appreciated by recognizing the position of the diaphragmatic crus at approximately the level of L1-L2. See Figure 27-1. Radiographs may also demonstrate atelectasis, most commonly of the right middle lung lobe. It is usually easier to see this pattern on a dorsal-ventral or ventral-dorsal exposure because the right middle lung lobe silhouettes with the cardiac silhouette on the lateral view. Atelectasis most commonly occurs in the right middle lung lobe because of mucus accumulation within the bronchus, and this airway is most commonly involved because it is the only airway that has a dorsal-ventral orientation within the bronchial tree and, therefore, subject to the effects of gravity (see Figure 27-2). In more extreme cases, you may appreciate fluffy illdefined heavy interstitial infiltrates in multiple lung lobes. The cause of these changes in cats with lower airway disease may be multiple small areas of atelectasis in multiple lung lobes resulting from multiple diffuse small mucus plugs. This presents a diagnostic challenge because this radiographic change is consistent with a number of disorders including neoplasia and diffuse interstitial pneumonitis.
• • • • • •
Chronic noninfectious bronchitis. Parasitic tracheobronchitis including Aelurostrongylus. Viral or bacterial tracheobronchitis. Infectious pneumonia (i.e., bacterial, viral, or parasitic). Interstitial lung disease (usually idiopathic). Cardiac disease (i.e., hypertrophic and congestive cardiomyopathy); few cats have a cardiac-generated cough, in contrast to dogs. • Primary or metastatic lung neoplasia; tracheobronchial neoplasia is uncommon. • Heartworm infestation. Definitive diagnosis of asthma is usually based on specific pulmonary function studies that require patient cooperation. Because both disorders, bronchitis and asthma, can cause a daily cough as the only clinical sign, there are many times when it is not possible to distinguish bronThe Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
58
Figure 27-1 Air trapping may be assumed if the lungs are hyperinflated. This is seen most prominently on the lateral view and can be appreciated by recognizing the position of the diaphragmatic crus at approximately the level of L1–L2.
Bronchial Disease, Chronic
bacteria does not by itself confirm airway infection. If a positive culture truly reflects infection, bacteria may be found intracellularly, or the bacteria should have grown on a primary culture plate without the need for enrichment broth; the bacteriology report will state this.
Treatment Primary Therapeutics Emergency Treatment
Figure 27-2 Lateral radiograph of a cat with asthma demonstrating right middle lung lobe collapse. The increased density of the atelectatic lung lobe is not readily apparent because the lung (arrow) silhouettes over the heart shadow.
Chest radiographs can also rule out other common causes of cough and tachypnea. See Figure 291-22. • Response to Therapy: Cats with asthma may stop coughing or wheezing within 10 minutes after administration of a bronchodilator (terbutaline [0.01 mg/kg IM, SC] or albuterol [2 puffs followed by 7–10 breaths from a spacer and mask]). The great majority of cats with bronchitis or asthma respond to high dose corticosteroid therapy within 5 to 7 days, and a patient with a diagnosis of bronchitis or asthma that responds poorly should be reevaluated and the diagnosis revisited.
Secondary Diagnostics • Heartworm Testing: An antibody test should be performed in regionally selected cases. If the antibody test is positive follow it with an antigen test and echocardiography. • Echocardiography: This to rule out cardiomyopathy or to demonstrate adult heartworms in endemic areas. Note that many cats with cardiomyopathy do not cough as a primary clinical sign. See Chapters 88 and 110. • Bronchoalveolar Lavage (BAL) with Cytology and Culture: Common cytologic findings include large numbers of eosinophils found in the recovered tracheobronchial secretions in asthmatic airways and nonseptic neutrophils in bronchitic airways of some cats. BAL eosinophilia is consistent with but not a good marker for asthma because of the large number of eosinophils found the recovered fluid from cats with normal pulmonary function and quiescent airways. The primary indication for bronchoscopy is when there is not an otherwise predictable cessation or minimization of clinical signs after 7 to 10 days of aggressive corticosteroid treatment.
Diagnostic Notes • Bronchoscopy is rarely required to make an accurate diagnosis of asthma in feline patients. Bronchoscopy in healthy cats is not a trivial undertaking. In cats with cough and respiratory compromise, bronchoscopy may be a life-threatening procedure and should only be performed by persons adequately and formally trained in the technique. • Cats with asthma do not generally have airway infection with bacteria. In fact, one well designed study showed that cats with signs of bronchial disease had fewer positive airway cultures than a cohort population of healthy cats. Thus, BAL fluid that harbors
• Oxygen: An oxygen cage with 100% ambient oxygen will deliver less than 40% inspired oxygen to patients; this is nevertheless effective, safe, and is the least stressful method of delivering oxygen to these unstable patients. • Parenteral Corticosteroids: Dexamethasone sodium phosphate is effective with a wide dose range; I recommend 0.2 to 0.5 mg/kg IV. The best understood effect of corticosteroid treatment in asthmatic patients is to inhibit cytokine and inflammatory protein expression the level of mRNA transcription. This process takes hours and days. Clearly then, we do not fully understand why intravenous corticosteroids work quickly, but they do. • Inhaled Bronchodilators: Albuterol sulfate (Ventolin™, Proventil™) is the drug of choice. Two puffs into a spacer are followed by 7 to 10 breaths through a mask connected to the spacer. In emergency cases, albuterol can be used q30m for up to 6 hours without serious side effects; it will last for 2 to 4 hours • Systemic Bronchodilator: If an inhaled bronchodilator is not available or possible, give terbutaline (0.01 mg/kg IM). Terbutaline is a selective beta2-receptor agonist that produces relaxation of bronchial smooth muscle. It is available as a 1-mg/ml suspension. For a 5-kg (11-lb) cat, dilute terbutaline with sterile saline in a 1:9 ratio to produce terbutaline 0.1 mg/ml. Administer 0.5 ml of this concentration (0.05 mg) to achieve a dose of approximately 0.01 mg/kg.
For the Stable Asthmatic • Oral Corticosteroids: Newly diagnosed patients should receive prednisolone 1.0 mg/kg q12h PO for 5 days. If there are positive therapeutic effects begin to wean to lowest effective dose that controls >75% of the clinical signs. • Inhaled Corticosteroids: Fluticasone (Flovent™) is dosed as a 110 µg inhaler. Give two puffs into the spacer followed by 7 to 10 breaths. This is an excellent replacement for oral corticosteroids once the oral medications have been used and found to be effective. Because inhaled fluticasone may take 10 days to reach peak effectiveness begin inhaled steroid therapy while the patient is receiving oral corticosteroids and wean off the oral steroid over a 10- to 14-day period. See Figure 27-3. • Oral Bronchodilator: Terbutaline can be given at 0.1 to 0.2 mg/kg per 8 hours PO q8 to 12h. • Injectable, Long-Acting Corticosteroids: Parenteral administration of long acting corticosteroids is limited to patients for whom no other method of drug administration is feasible. In this setting, injection of a Depo-Medrol™ (10–20 mg IM total dose) once every 2 to 8 weeks may be effective. This therapy is likely to result in significant/serious side effects including weight gain, diabetes mellitus, and reduced immunity, and represents the treatment of last resort.
Therapeutic Notes • Albuterol only comes in a single strength (90 µg per acuation). Albuterol usually results in relaxation of airway smooth muscles within 1 to 5 minutes, so the effect is almost immediate. This drug
59
SECTION 1: Diseases and Conditions
be relatively unaffected by their disease most weeks of every month and most months of every year. • It is critically important to understand that human (and perhaps feline) asthmatic and bronchitic airways show evidence of chronic ongoing inflammation whether the patient is symptomatic or not. Therefore, treatment strategies are most successful if they are directed toward decreasing the underlying inflammatory component of the disease in addition to addressing the acute clinical signs of cough, wheeze, and increased respiratory effort. • Patients with symptoms that occur less than once weekly (without medication) are generally not considered to have chronic active inflammatory airways. These patients may be safely treated with bronchodilators when needed.
Secondary Therapeutics Figure 27-3 with asthma.
•
•
•
•
60
Proper position of spacer device to deliver inhaled medications to cat
should be used in cats with bronchoconstriction. Symptoms that may indicate bronchoconstriction include wheezing, noisy lower airway breathing, prolonged expiratory phase of ventilation, and coughing. Albuterol can be used once or twice daily prior to administering fluticasone or as needed for acute coughing and wheezing. Flovent comes in three strengths: 44 µg, 110 µg, and 220 µg per actuation. Dosing with the 44 µg q12h does not consistently result in acceptable clinical responses. For cats with mild/moderate disease 110 µg q12h frequently results in clinical responses equivalent to that achieved by administration of 5 mg of prednisone q12h PO. Cats with more serious disease may require 220 µg inhaled q12h. Administration of fluticasone more than twice daily has not resulted in clinical benefit in my experience. Administration of inhaled medications requires special technique. Fluticasone and albuterol are administered using a small, aerosolholding chamber (spacer; AeroKat™, Trudell Medical, Ontario CA) attached to a metered dose inhaler (MDI) on one end and a face mask on the other. The spacer is approximately the size of the inner cardboard roll used with toilet paper. The MDI supplies precise doses of the aerosol drug, and the holding chamber contains the aerosol so it can be inhaled when the patients inspires. The mask is designed to cover the nose of the cat. The choice of spacer is relevant as cats have a tidal volume of between 5 and 10 mL of inspired air per pound of body weight. Currently, only the AeroKat brand spacers have been designed specifically based on the tidal volume characteristics of the cat. Using these spacer devices, cats will inhale the majority of drug propelled into the spacer by breathing 7 to 10 times through the spacer-mask combination after actuation of the MDI. It is important to teach the owner to observe the pet actually breathing because cats may initially hold their breaths when introduced to this form of treatment. The procedure is not time consuming, but it can be helpful to acclimate the cat to the mask. When administering inhalation therapy, the MDI is first shaken to open an internal valve within the canister, and then it is attached to the spacer. The mask attached to the other end of the spacer is placed snuggly on the animal’s nose or muzzle, and the MDI is pressed to release the medication into the spacer. Patients with asthma may have clinical signs once a month, once a week, or multiple times every day. The frequency of signs may be stable for months and then suddenly worsen without obvious cause. This does not necessarily reflect a nonreversible worsening of disease. In contrast, asthmatic patients may have signs that wax and wane for many years without a predictable pattern. Therefore, drug doses and frequency of administration must be tailored to the individual patient. The goal of course is to make the patient symptom free. Realistically, the goal is for patients to cough less than daily and to
• Antibiotics: A fluoroquinolone, such as enrofloxacin (3–5 mg q24h PO for 10 days) should be given for documented bacterial infection or if a previously stable asthmatic patient suddenly becomes unstable. Because 25% of cats with signs of lower airway disease have Mycoplasma spp., enrofloxacin, doxycycline, and azithromycin are good antibiotic choices. • Cyproheptadine: This drug comes in both tablet and liquid form and is dosed at 2 to 4 mg q12h PO. The primary indication for this drug is a trial in the symptomatic asthmatic cat already receiving maximal doses of bronchodilators and corticosteroids. It has antiserotonin properties. Serotonin is a primary mediator released from activated mast cells into feline airways and causes acute smooth muscle contraction (bronchoconstriction) in cats but not in humans. A beneficial therapeutic response may not be seen for 4 to 7 days, but depression, the primary side effect of this drug, may be observed 24 hours after administration. Depression is not lifethreatening but may cause the owner to discontinue cyproheptadine therapy. • Anti-leukotrienes: Zafirlukast, montelukast, and zileuton have been recommended; however, there is no evidence that drugs that affect leukotriene synthesis or receptor ligation play a significant role in the treatment of feline or canine respiratory disease. Having said that, there is at least one undocumented claim of efficacy using zafirlukast (1–2 mg/kg q12h PO) or montelukast (0.5–1.0 mg/kg q24h PO) for treatment of feline asthma. • Methylxanthines: Theophylline and aminophylline (5–6 mg/kg q12h PO; sustained release: 25 mg/kg q24h PO) are purported to relax smooth muscle, particularly bronchial smooth muscle, as well as stimulate the central nervous system and act as a weak cardiac and diaphragmatic stimulant and diuretic. However, I do not use this class of drugs to treat feline patients with asthma; both inhaled albuterol and oral and injectable terbutaline are more effective bronchodilators in cats.
Prognosis Chronic bronchitis and asthma cause a constellation of symptoms in the feline patient, including cough, wheeze, and variable amounts of disability at rest. Other nonairway disorders can cause similar signs in these patients, and there are only a small number of diagnostic tests available to distinguish one disorder from another. Therefore, the clinician in general practice must rely on careful history taking, physical examination skills, and accurate interpretation of thoracic radiographs to insure that a proper diagnosis is made. Asthma may resolve spontaneously or become a lifelong disorder with a variable clinical presentation. In general, cats with asthma can be well controlled with aggressive treatment. The use of inhaled medications to treat asthma and bronchitis is considered the standard of care in humans and is now widely recommended for cats with chronic bronchial disease. This approach avoids
Bronchial Disease, Chronic
many of the side effects previously seen in patients treated with systemic medications.
Suggested Readings Boothe DM. 2006. Drugs affecting the respiratory system. In LG King, ed., Textbook of Respiratory Disease in Dogs and Cats, pp. 236–245. St. Louis: Elsevier. Chandler1 JC, Lappin MR. 2002. Mycoplasma respiratory infections in small animals: 17 cases (1988–1999). J Am Anim Hosp Assoc. 38(2):111–119. Johnson LR, Drazenovich, TL. 2007. Flexible bronchoscopy and bronchoalveolar lavage in 68 cats (2001–2006). J Vet Intern Med. 21(2): 219–225.
Kirchvink N, Leemans J, Delvauz F, et al. 2006. Inhaled fluticasone reduces bronchial responsiveness and airway inflammation in cats with mild chronic bronchitis. J Fel Med Surg. 8(1):45–54. Norris CR, Decile KC, Berghaus LJ, et al. 2003. Concentrations of cysteinyl leukotrienes in urine and bronchoalveolar lavage fluid of cats with experimentally induced asthma. Am J Vet Res. 64(11):1449–1453. Padrid PA. 2000. Feline Asthma. Diagnosis and Treatment. Vet Clin North Am Small Anim Pract. 30(6):1279–1293. Reinero CR, Byerly JR, Berghaus RD, et al. 2005. Effects of drug treatment on inflammation and hyperreactivity of airways and on immune variables in cats with experimentally induced asthma. Am J Vet Res. 66(7):1121–1127.
61
CHAPTER 28
Calicivirus Infection Gary D. Norsworthy
Overview The causes of feline upper respiratory infections (URIs) include bacteria, fungi, and viruses. This chapter will concentrate on those diseases caused by the various strains of the feline calicivirus (FCV), a small, noneveloped single-stranded RNA virus of which there is wide antigenic variability. However, currently all strains are classified as a single serotype. The FCV and the feline herpesvirus-1 (FHV-1) account for about 80% of all feline URIs. These viruses are contagious and often endemic to multicat households and facilities. Both are likely to produce a carrier state in which stress-induced intermittent viral shedding (FHV-1) or continuous viral shedding (FCV) occurs. Maternal antibodies wane at about 5 to 7 weeks of age, so kittens in these environments are usually exposed before vaccine-induced immunity occurs. The clinical signs are based on the fact that the FCV replicates in epithelial cells of the upper respiratory tract, conjunctiva, tongue, and in pneumocytes in the pulmonary alveoli. The most consistent clinical sign of an FCV infection is sneezing; other common signs include fever, nasal discharge, oral ulceration, and hypersalivation. See Figure 28-1. Anorexia occurs due to fever, oral ulceration, or nasal congestion and can lead to dehydration and death. Less frequently, various strains of FCV cause polyarthritis, ulceration of the nasal planum, or interstitial pneumonia. The FCV can be isolated from the mouths of the vast majority of cats with lymphoplasmacytic stomatitis-gingivitis. If it is etiologically involved it is due to an immune response to the virus and not the virus itself. Transmission primarily occurs by direct contact between cats involving oral and nasal secretions. Indirect transmission via infectious discharges and fomites is also possible. Infection occurs via the nasal,
oral, or conjunctival routes. Sneezed macrodroplets are unlikely to be infectious beyond 2 meters (6 feet) from a sneezing cat, but they may persist in the environment for up to one month. The incubation period is typically 3 to 4 days; a transient viremia occurs at that time. The FCV is not transmissible to humans. Recently, a highly virulent strain of FCV, called the virulent systemic feline calicivirus (VS-FCV), has been reported to cause severe disease with a mortality rate of more than 40% of affected cats. It causes high fever, facial and paw edema, ulceration and hair loss on the face, feet, and ears, icterus, and hemorrhage from the nose and in the feces, in addition to the more typical respiratory signs. See Figure 28-2. It affects adult cats more than kittens; affected cats may die within 24 hours of the onset of clinical signs. When introduced into a naïve household,
(A)
Figure 28-1 The signature sign of an feline calicivirus infection is lingual ulceration. The ulcers typically affect the anterior or lateral margins of the tongue as seen in this cat.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
62
(B) Figure 28-2 A, The virulent systemic feline calicivirus (VS-FCV) causes a vasculitis resulting in swelling, edema, local alopecia, and ulcerative dermatitis as seen in this 10-week-old kitten. B, Other manifestations of the VS-FCV include icterus and lingual ulceration as seen in this 6-year-old cat that died of the disease.
Calicivirus Infection
hospital, or shelter, disease can spread rampantly directly between cats or via fomites and cause death in a large number of the affected cats. Newer vaccines include this strain.
Diagnosis Primary Diagnostics • History and Clinical Signs: Although there are several causes of sneezing in cats, sneezing that persists over 48 hours is highly suggestive of URI. Some or many of the other aforementioned clinical signs are usually present.
Secondary Diagnostics • Viral isolation: Many veterinary reference laboratories can isolate and identify the FCV in cell culture from oropharyngeal or conjunctival swabs. However, because of the asymptomatic carrier state, interpretation of a virus isolation result in terms of active infection versus carrier must not be misinterpreted. The presence of virus and clinical signs are poorly correlated. False-negative results are a problem. • Polymerase Chain Reaction (PCR) Testing: PCR testing can be used to identify the FCV. The same interpretation limitations as virus isolation apply. False-negative results are a problem.
Diagnostic Notes • The clinical signs of all viral URIs are similar. When secondary bacterial infections occur, these diseases are indistinguishable based on clinical signs except for the severe signs caused by the VS-FCV.
Diagnostic Notes • Virus neutralizing antibody titers are not reliable for diagnosing active respiratory viral infections due to natural infection and vaccination.
Treatment Primary Therapeutics • Antibiotics: An FCV infection can become complicated by bacteria. Although most strains of FCV produce a self-limiting disease of a few days duration, the bacterial infections can become lifethreatening if not treated. The drugs of choice for mild-to-moderate disease are amoxicillin (12.5 mg/kg q12h PO) or amoxicillinclavulanic acid (15 mg/kg q12h PO). If severe disease occurs, either azithromycin (10 mg/kg q24h PO for 10 days) or clavulanic acid/ amoxicillin plus a fluoroquinolone is preferred for outpatients; if the cat resists oral medications, cefovecin injectable (8 mg/kg q24h SC) can be used. Amoxicillin (12.5 mg/kg q12h SC) or ampicillin (10–20 mg/kg q12h SC) plus enrofloxacin (2 mg/kg q12h SC) is preferred for hospitalized cats. • Hydration: Nasal and ocular secretions thicken when dehydration occurs. To prevent this added discomfort, cats should receive rehydrating and maintenance doses of balanced electrolyte fluids IV or SC. • Nutritional Support: Anorexia is common and is the most serious common complication of URIs. Nutritional support using orogastric or nasoesophageal tubes should begin as early as possible. Contraindications include dyspnea and severe depression. Nasal secretions should be softened with water and removed before an orogastric tube is passed as cats with nasal blockage tend to panic when an orogastric tube is passed. Severe nasal congestion and irritation contraindicates the use of nasoesophageal tubes. See Chapters 253 and 308.
Secondary Therapeutics • Ophthalmic Antibiotics: These are indicated when conjunctivitis exists. Do not to use products containing corticosteroids if a corneal ulcer is present. • Nasal Decongestants: Oxymetazoline hydrochloride (Afrin Pediatric Nasal Drops®) is advocated by some. One drop is placed in one nostril once daily. However, most cats object to nasal drops; aftercongestion (also called “rebound congestion”) may develop, and efficacy has not been clearly demonstrated.
Therapeutic Notes • Antiviral drugs currently available are only effective against DNA viruses and retroviruses. There is not a proven antiviral drug that is effective against the FCV and that is safe. Ribavirin inhibits RNA viruses in vitro, but it is toxic to cats. • Cats should be treated in a hospital with isolation facilities when anorexia occurs or to prevent exposure of others cats in the household. If cats are treated at home, they should be isolated from other cats, if possible. • Cats infected with the VS-FCV should be treated aggressively with intravenous fluids, parenteral antibiotics, and nutritional support and strictly isolated from other cats. • Treatment of chronic gingivitis/stomatitis is discussed in Chapter 84.
Prevention • A vaccine containing FHV-1 and FCV should be considered a core vaccine to be given to all cats. However, neither antigen produces sterilizing immunity; they are only able to mute the severity of clinical signs rather than prevent infection, disease, and virus shedding. Their duration of immunity must be defined in terms of the expected outcome of vaccination. Most FCV-containing vaccines in the United States contain only one strain of FCV that was chosen over 30 years ago. Due to frequent mutation, there are many vaccine-resistant strains present in the feline population. • Newer vaccines contain a common FCV strain and the VS-FCV strain. Dual strain vaccines offer broader cross-protection to more strains of FCV. • Kittens should be vaccinated about every 3 to 4 weeks beginning at about 8 weeks of age. The last vaccine should not be administered before 16 weeks of age. Kittens in breeding colonies and catteries with endemic FCV should be vaccinated initially at 4 weeks of age then every 2 weeks until 12 weeks of age then at 16 weeks of age. • Intranasal vaccination has not been shown to shorten clinical infection or to terminate the carrier state. However, immunity develops more quickly with intranasal vaccines than with injectable vaccines, so they have merit in situations in which exposure is likely. Intranasal vaccines may also prevent the carrier state. Some cats receiving intranasal vaccine develop chronic sneezing. • Disinfection of premises is important in multicat situations. Effective disinfecting agents include sodium hypochlorite (5% bleach diluted 1:32), potassium peroxymonosulfate, chlorine dioxide, and commercial products approved for FCV inactivation. Note that bleach is only effective for 24 hours after dilution. • In a cattery situation queens should be boostered prior to mating. Vaccination during pregnancy is discouraged. • Vaccination of feline immunodeficiency virus (FIV) infected, feline leukemia virus (FeLV) infected, and chronically ill cats should continue as long as these cats are not febrile or showing signs of immunosuppression. However, immunity may be delayed and less than that produced in a normal cat so more frequent vaccinations should be considered. Inactivated vaccines are preferred over modified-live vaccines.
63
SECTION 1: Diseases and Conditions
Prognosis The prognosis is good except for cats infected with the VS-FCV if anorexia and dehydration do not occur or if they are treated aggressively. Cats that fail to respond to appropriate therapy within 4 to 6 days should be tested for the FeLV and the FIV, two viruses that can be immunosuppressive and prevent response to therapy. Cats infected with the VS-FCV have a much more guarded prognosis due to the aggressive nature of the virus.
Suggested Readings Gaskell RM, Dawson S. 2006. Other Feline Viral Diseases. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 5th ed., pp. 667–671. St. Louis: Elsevier Saunders.
64
Pedersen NC, Elliot JB, Glasgow A, et al. 2000. An isolated epizootic of hemorrhagic-like fever in cats caused by a novel and highly virulent strain of feline calicivirus. Vet Microbiol. 73:281–300. Radford D, Addie D, Belak S, et al. 2009. Feline calicivirus infection: ABCD guidelines on prevention and management. J Fel Med Surg. 11:556–564. Sykes JE. 2001. Feline upper respiratory tract pathogens. Herpesvirus-1 and calicivirus. Compend Contin Educ. 23:166–167.
CHAPTER 29
Carcinomatosis Bradley R. Schmidt
Overview Carcinomatosis (effusions containing malignant epithelial cells) is generally associated with the presence of a carcinoma of any organ in the thoracic or abdominal cavity and can be cytologically difficult to distinguish from a mesothelioma. As with mesothelioma, malignant epithelial effusions may develop secondary to exudation from the primary tumor, inflammation associated with the primary tumor, and diffuse lymphatic metastasis/obstruction. Malignant effusions are generally present within the body cavity where the primary tumor is identified but may also develop in other body cavities secondary to lymphatic metastasis. Solid metastasis to other organs may also be seen. See Figure 29-1A and Figure 29-1B. Reported cancers associated with carcinomatosis in the cat include, but are not limited to, carcinoma of the lung, pancreas, intestinal tract, and liver as well as aortic body tumors. See Chapter 5 for patient signalment associated with the various tumors. Clinical signs associated with pleural and pericardial effusion are related to respiratory compromise and cardiac tamponade and may include dyspnea, coughing, and progressive effusions resulting from right-sided heart failure. Nonspecific signs of malignant effusion arising in any body cavity include lethargy, anorexia, and intermittent vomiting. In addition to these clinical signs, clinical signs related to the primary and metastatic tumors may also be seen. Differential diagnoses for carcinomatosis includes lymphoma, malignant effusion secondary to a sarcoma, and benign effusions secondary to cardiac disease, protein-losing enteropathy and nephropathy, liver disease, heartworm disease, feline infectious peritonitis (FIP), and other infectious processes.
(A)
Diagnosis Primary Diagnostics • Fluid Analysis and Cytology: Fluid analysis and cytology may aid in the diagnosis of malignant effusion. Confirming and differentiating carcinomatosis or mesothelioma cytologically may be difficult as reactive mesothelial cells associated with benign effusions may also display marked atypia. Furthermore, mesothelioma and malignant epithelial cells may cytologically appear similar, further complicating the diagnosis. • Fine-Needle Aspiration and Cytology: Fine-needle aspiration of masses or enlarged organs may help determine the origin of the malignant pleural effusion. • Tissue Biopsy and Histopathology: Tissue biopsy of masses or enlarged organs via a surgical or laparoscopic approach may determine the origin of the malignant pleural effusion if fine-needle aspirations are negative.
Secondary Diagnostics • Immunohistochemistry: Immunohistochemical staining may aid in the diagnosis of carcinomatosis because these tumors generally stain positive for cytokeratin whereas most sarcomas do not.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
(B) Figure 29-1 Carcinomatosis often produces solid metastasis the mesentery (A) and to other organs (B). Photo courtesy of Dr. Gary D. Norsworthy.
• Fibronectin: Elevations in fluid fibronectin is reported to be a sensitive but nonspecific test for malignant effusions in dogs and cats. Normal levels in effusion would help to rule out mesothelioma. • Thoracic Imaging: Thoracic radiographs or computerized tomography (CT) scan of the thorax should be performed to evaluate for the presence of pleural thickening or masses as well as pulmonary or mediastinal masses. Thoracocentesis prior to performing thoracic radiographs or CT scan may aid in the interpretation. • Ultrasound: Abdominal ultrasound should be performed in all cases of abdominal effusions, as well as in cases with malignant pleural effusion, to evaluate for tumors that may have metastasized to the thoracic cavity. Although radiographs or CT scans are the diagnostics of choice for the thoracic cavity, thoracic ultrasound may be performed when pleural fluid is present. Carcinomatosis
65
SECTION 1: Diseases and Conditions
•
•
•
•
generally appears as a diffuse, hyperechoic thickening or as a nodular thickening of the pleural or peritoneal lining. Lymph Node Fine-Needle Aspiration and Cytology: A fine-needle biopsy should be performed if lymphadenopathy is present. Benign mesothelial cells have been reported within lymph nodes in dogs with nonmalignant pericardial effusions; therefore, interpret results with caution. Echocardiogram, Electrocardiogram (ECG), and Thyroid Tests: A cardiac evaluation and thyroid evaluation should be performed in all cats where hyperthyroidism or cardiac disease is suspected to be the cause of effusion, especially in cases of pericardial effusion. Minimum Data Base: A complete blood count, serum biochemistry profile, urinalysis, feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) serology, and heartworm antigen and antibody testing should be performed to evaluate the overall health of the patient and for nonneoplastic causes for effusion development. Fluid Culture and Sensitivity: This should be performed if primary or concurrent sepsis is suspected cytologically.
Diagnostic Notes • Carcinomatosis should be considered over mesothelioma when a mass lesion is identified in thoracic or abdominal organs and when histopathology or cytology distinguishes it as a primary tumor. • Effusion pH: One study suggested that fluid pH may be helpful in differentiating benign from malignant pericardial effusions; however, a subsequent study suggested that the pH values overlapped too much to be of any clinical use.
Treatment
these drugs appears to be minimal, the use of intracavitary chemotherapy alone may not be indicated when larger mass lesions are present.
Secondary Therapeutics • Intravenous Chemotherapy: Intravenous chemotherapy is indicated when larger nodules or masses are present or when nodal or organ metastasis is present. Responses to intravenous chemotherapy in most cases appear to be limited and short in duration. Common chemotherapy agents include doxorubicin (1 mg/kg or 25 mg/m2 q3w IV), mitoxantrone (6.0–6.5 mg/m2 q3w IV) and carboplatin (225–240 mg/m2 q3–4w IV). Careful monitoring of the white blood cell counts is recommended. Carboplatin is excreted by the kidneys; therefore, use with caution in cats with renal compromise. • Pericardectomy for Pericardial Effusion: In the rare event of malignant pericardial effusion, pericardectomy may be performed to alleviate signs related to cardiac tamponade. Adjunctive intravenous chemotherapy as above may also be considered. • Surgery: Surgery to remove a primary tumor (e.g., primary lung tumor or small intestinal tract tumor) may be palliative; however, survival times are generally short when malignant effusions or metastasis is present. • COX-1/COX-2 Inhibitors or COX-2 Inhibitors: These agents have been reported in the treatment of squamous cell carcinoma and other tumors in the cat. Although use of these drugs either as a single agent or in combination with carboplatin has been reported, no studies exist on the benefits of the use of these agents in the treatment of carcinomatosis. • Prednisone/Prednisolone: Corticosteroids may be used to palliate clinical signs.
Primary Therapeutics • Centesis: Thoracocentesis, pericardiocentesis, or abdominocentesis should be performed to alleviate potentially life-threatening clinical signs and discomfort associated with fluid accumulation. A 21- or 23-gauge butterfly catheter or 20- or 22-gauge over-the-needle catheter attached to an extension set and three-way stopcock may be used. Sedation may be indicated in some cats but must be used with caution if respiratory or cardiac compromise is present. • Intracavitary Chemotherapy: Intracavitary chemotherapy (pleural or peritoneal cavities only) delivers a higher concentration of chemotherapy to the tumor while minimizing systemic effects and may relieve lymphatic obstruction resulting in the resolution or slowing of fluid accumulation. Commonly used drugs include carboplatin (225–240 mg/m2) or mitoxantrone (6.0–6.5 mg/m2). Carboplatin is further diluted with 5% dextrose in water or sterile water and mitoxantrone with 0.9% sodium chloride to a total volume of 15 to 30 mL, depending upon the residual fluid volume present in the body cavity post-centesis, to aid in the diffusion of the drug into the body cavity. The chemotherapy drug is infused into the body cavity with a 21- or 23-gauge butterfly catheter or 20- or 22-gauge over-the-needle catheter attached to an extension set and three-way stopcock. In cases of pleural effusion, the dose may be divided and administered into the right and left pleural cavity. After infusion is complete, the patient is gently rolled to aid in the diffusion of the chemotherapy. Mild sedation may be indicated. Systemic absorption of these drugs is reported to be minimal; therefore, neutropenia and other adverse effects are generally not seen. However, monitoring the while blood cell count is recommended. Furthermore, carboplatin is excreted by the kidneys, and caution should be used in administering to cats with renal compromise. Because penetration of carboplatin and, most likely, mitoxantrone is only 2 to 3 mm or less and the systemic absorption of
66
Therapeutic Notes • Radiation therapy has not been critically evaluated in the treatment of malignant effusions in the cat. • Intracavitary chemotherapy may be considered in cases where larger nodules or masses are not present. When larger tumor burdens are present, surgery or intravenous chemotherapy should be incorporated in the treatment. Some advocate dividing the chemotherapy and administering 50% intravenously and 50% intracavitary when treating malignant effusions with concurrent larger tumor burdens. • Pleurodesis: Pleurodesis with agents such as doxycycline or talc has generally been unsuccessful.
Prognosis The prognosis for most cats with carcinomatosis is generally poor due to the metastatic nature of most tumors and the inability of intracavitary or intravenous chemotherapy to result in durable remissions. Removal of effusion or the use of prednisone may be palliative for 1 to 5 months.
Suggested Readings Fine DM, Tobias AH, Jacob KA. 2003. Use of pericardial fluid pH to distinguish between idiopathic and neoplastic effusions. J Vet Intern Med. 17:525–529. Hirschberger J, Pusch S. 1996. Fibronectin concentrations in pleural and abdominal effusions in dogs and cats. J Vet Intern Med. 10:321–325. Monteiro CB, O’Brien RT. 2004. A retrospective study on the sonographic findings of abdominal carcinomatosis in 14 cats. Vet Radiol Ultrasound. 6:559–564.
CHAPTER 30
Cardiopulmonary Arrest Larry P. Tilley
Overview
Diagnosis
Cardiopulmonary arrest (CPA) is an immediately life-threatening condition that requires prompt recognition and appropriate intervention to restore circulatory function. In CPA, cessation of effective cardiac contractions and ventilation quickly lead to widespread hypoxia, with cerebral death occurring within 4 to 5 minutes. CPA is usually a grave development, with survival rates of 2 to 5% reported even with optimal therapy. Considering this, the clinician should place a major emphasis on the recognition of impending CPA. Reversal of abnormalities placing the cat at risk of CPA is generally much more successful than cardiopulmonary resuscitation itself. Signs of CPA include loss of consciousness, dilated pupils, agonal or absent respiration, absent heart sounds and arterial pulsations, cyanosis, and often opisthotonos. These signs may be abrupt and dramatic in a previously healthy cat or may occur rather subtly in a moribund case.
• Mucous Membrane Color and Capillary Refill Time (CRT): Look for pallor or cyanosis. CRT may be delayed. • Thoracic Auscultation: Look for absence of respiratory or heart sounds. In some cases, extreme bradycardia may be detected. • Electrocardiography: Look for asystole (absence of complexes), slow ventricular escape rhythm, and idioventricular rhythm.
Secondary Diagnostics • Blood Gas Analysis: Look for severe hypoxemia, hypercapnia, and acidosis.
Diagnostic Notes
Diagnosis Differential Diagnoses Virtually any pathophysiologic state can deteriorate to the point at which CPA occurs. The most common clinical disorders predisposing cats to CPA are listed in Table 30-1.
TABLE 30-1: Differential Diagnoses for Cardiopulmonary Arrest Cardiopulmonary Disease
Primary Diagnostics
Congestive heart failure (secondary to cardiomyopathy or other primary cardiac disease) Obstructive airway disease Heartworm disease Trauma (i.e., myocardial contusions and traumatic myocarditis) Pleural effusion Neoplasia Hemorrhage Trauma, surgery
Systemic Abnormalities
Severe acid-base disturbances Severe electrolyte disturbances (e.g., hyperkalemia secondary to urethral obstruction) Overwhelming sepsis or endotoxemia
Other
Drugs, particularly anesthetic agents Surges in parasympathetic tone (as may occur with tracheal intubation and manipulation of ocular, laryngeal, or pharyngeal areas)
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Intensive monitoring (i.e., vital signs, mucous membrane color, electrocardiograph) of cats with conditions predisposing them to CPA and during anesthesia is essential.
Prevention • Correct Hypoxemia: For anesthetized cats, discontinue anesthetic, increase oxygen flow, and confirm proper endotracheal tube placement. For cats with pulmonary edema, administer diuretics and supplemental oxygen. • Thoracocentesis: This should be performed if significant pleural effusion is present. • Intravascular Abnormalities: Correct fluid deficits and electrolyte or acid-base disturbances. • Correct Cardiac Arrhythmias: See Chapter 12.
Treatment Primary Therapeutics (see Figure 30-1) for Cardiopulmonary Resuscitation, follow ABCD • A = Airway: Clear the airway of any obstructive material. Endotracheal intubation should be performed, and tracheostomy should be considered if complete obstruction exists. • B = Breathing: Provide respiratory support if spontaneous respiration is absent or insufficient. Provide 100% oxygen with an Ambu® bag, through the reservoir bag of an anesthesia machine, or via a mechanical ventilator. Institute artificial ventilation; administer two short breaths of about 2 seconds duration each and reassess. If no spontaneous respiration occurs, continue ventilations at a rate suitable for this cat (normal respiratory rate 10–24 breaths per minute). Peak airway pressures should not exceed 20 cm H2O. • C = Circulation: External cardiac massage provides at best about 30% of normal cardiac output; internal cardiac massage is two to three times more effective in improving cerebral and coronary perfusion. Perform chest compressions rapidly, at a rate of between 80 and 100 compressions per minute; the chest should be displaced about 30%. With the patient in right lateral recumbency, perform compressions
67
Cardiopulmonary Arrest Begin Basic Life Support Airway
Assess for airway obstruction. assess for breathing Perform intubation
Breathing
Ventilate with 100% oxygen. avoid hyperventilation Provide 10–24 breaths/minute
Circulation
Assess for heart beat and pulses If absent, begin chest compressions Provide 100–120 compressions/minute Minimize interruptions
Begin Advanced Life Support Place ECG and Determine Arrest Rhythm Obtain Access for Drug Therapy
VF/Pulseless VT Defibrillate
Drug Therapy
Asystole/Bradycardia/PEA
2–10 joules/kg (external) 0.2–1 joule/kg (internal) Provide up to 3 consecutive shocks before resuming CPR for 1–2 min.
Drug Therapy
Epinephrine (0.01–0.1 mg/kg IV) or Vasopressin (0.8 units/kg IV)
Atropine (0.04 mg/kg IV) Use lower dose if palpable pulse or suspected vagal arrest Epinephrine (0.01–0.1 mg/kg IV) May be repeated @ 3–5 min. intervals or Vasopressin (0.8 units/kg IV) Given one time only
Lidocaine (2 mg/kg IV) or Amiodarone (5 mg/kg IV) Repeat Defibrillation (escalating dose)
Anesthesia-Related Arrest Turn off vaporizer, flush circuit Administer specific drug reversal agent Low-dose epinephrine (0.01 mg/kg) where indicated
During CPR Consider Interposed Abdominal Compression Consider Open-Chest CPR Especially with prolonged arrests or in large patients. Transdiaphragmatic approach during laparotomy Consider Sodium Bicarbonate (1–2 mEq/kg IV) Indicated in patients with significant pre-existing metabolic acidosis, hyperkalemia, or with prolonged (>10 min.) CPA Consider Calcium Gluconate (50–100 mg/kg IV)
Indicated in patients with hyperkalemia or ionized hypoca/cemia
Consider Magnesium Sulfate (30 mg/kg IV)
Indicated in patients with hypomagnesemia
Monitor Ongoing Resuscitating
Use end-tidal CO2 monitoring available
Search for Underlying Causes of Arrest Figure 30-1
68
Run ‘stat’ bloodwork (PCV/TS/BG/Blood Gas/Electrolytes)
Algorithm for performing cardiopulmonary resuscitation in veterinary patients.
Cardiopulmonary Arrest
directly over the heart (intercostal spaces 3–5); this can be performed using one hand. Different compression and ventilation regimes have been reported. The goals are to (a) provide appropriate compressions (80–100 per minute) and (b) provide appropriate ventilations (10–24 per minute) without stopping compressions for ventilations and without trying to synchronize ventilations with compressions. • D = Drugs: Administer atropine (0.02–0.05 mg/kg IV or 0.2– 0.5 mg/kg intratracheally [IT]) if asystole or severe bradycardia is present. Give epinephrine (0.01–0.1 mg/kg IV [1 mL per 5 kg or 11 lbs of the 1:1000 concentration] IV, or 2 ml per 5 kg [11 lb] IT). This may be repeated every 3 to 5 minutes. Give bicarbonate (1–2 mEq/kg IV) if acidosis or severe hyperkalemia present or if arrest duration has exceeded 10 minutes. Another agent to consider is vasopressin (0.8 mg/kg IV [or 0.8 units/kg IV]; can repeat at 5 minute intervals.)
• Defibrillation is rarely achieved with drugs. A defibrillator should be available for CPR, especially in critical care and emergency clinics. • A flowchart of ABCD steps should be placed in surgery and the intensive care area. Organization of efforts is essential. Prepare technicians with mock arrest situations. All technicians should be familiar with basic cardiopulmonary resuscitation (CPR). Establish a mobile “crash cart” of supplies and drugs needed for CPR.
Prognosis The prognosis is best when CPA is unexpected (e.g., during elective anesthesia), not associated with significant underlying disease, and promptly detected. Otherwise, the prognosis is poor.
Therapeutic Notes • Intracardiac administration of emergency drugs is not recommended. If a central venous catheter is not available, administer drugs (i.e., atropine, epinephrine, or lidocaine) intratracheally. Dilute the drugs with 5 to 10 mL of sterile saline and administer them through a catheter placed within the endotracheal (ET) tube. The tip of the catheter should be at the level of the carina. The IT dose of emergency drugs is twice the IV dose.
Suggested Readings Mark SL. 2007. Cardiopulmonary Arrest. In CE Greene, FWK Smith, Jr., eds., Blackwell’s 5 Minute Veterinary Consult. 4th ed., pp. 218–219. Ames, IA: Blackwell Publishing. Cole SG, Drobatz KJ. 2008. Cardiopulmonary resuscitation. In LP Tilley, ed., Manual of Canine and Feline Cardiology. 4th ed., pp. 333–341. St. Louis: Elsevier Saunders.
69
CHAPTER 31
Cataracts Shelby L. Reinstein and Harriet J. Davidson
Overview The lens is an avascular, transparent tissue that functions to refract light onto the retina. When the lens is diseased, a loss of transparency often manifests as an opacity, or cataract, within the lens. Nuclear sclerosis is a normal aging change and should be differentiated from cataracts. Nuclear sclerosis results from an increased density of the central portion of the lens as it ages; it is visible as a bluish opacity in the center of the lens. Nuclear sclerosis does not affect vision unless advanced; however, cataracts can progress and cause blindness. Additionally, cataracts often induce a secondary uveitis (see Chapter 223), which can lead to glaucoma (see Chapter 85). There are many methods used to classify cataracts. It is helpful to determine the age of onset, stage of progression, location, and cause of a cataract.
Diagnosis Primary Diagnostics • Examination: Examining the lens is achieved following full dilation of the pupil, in a darkened room. The examination can be performed using a transilluminator with or without magnification, or a direct ophthalmoscope. The transilluminator may be held approximately 12 inches from the cat’s face. The normal tapetal reflex is seen, which creates back lighting, or retroillumination, of the lens. This helps to identify opacities within the lens, seen as dark spots in the tapetal reflex. If the entire lens is opaque (cataractous), no reflex is seen. Close examination of the lens with magnification will allow determination of the location and size or stage of the cataract. A slit beam of light can be used to examine a cataract and help determine size and location. When the slit beam is shone into the eye, three beams of light are visualized; called the pyrkinje reflexes. The first beam of light is seen as a convex reflex off the cornea, a second convex beam is seen reflecting off of the anterior lens surface, and lastly a concave beam is seen reflecting off of the posterior lens surface of the lens. By moving the slit beam of light across the lens, the reflected lights will also move, allowing identification of the location and size of the cataract. • Classification: Many methods exist to classify a cataract. Often, it is fitting to use multiple schemes to accurately describe the cataract. • Age of Onset: Cataracts may be described as congenital, juvenile, or senile. Differential diagnoses will differ based upon the age of onset, and it may suggest an etiology. • Stage of Progression: The size of a cataract is described based upon the percentage of the total lens it occupies. An incipient cataract involves <10 to 15% of the lens, an immature cataract involves 15 to 99% of the lens (see Figure 31-1), and a mature cataract involves 100% of the lens, which completely obscures a fundic reflection. Mature cataracts can progress to become hypermature, at which time the lens begins to resorb and clear in areas. A Morgagnian cataract is a late stage change describing a situation in which the nucleus of the lens
Figure 31-1 Cataracts secondary to trauma are common in the cat, and therefore often occur unilaterally. This one is classified as immature. Photo courtesy Dr. Gary D. Norsworthy.
•
•
•
•
•
is all that remains and has fallen to the inferior aspect of the lens capsule. Location: Terms commonly used to describe the location of a cataract include anterior or posterior capsular, anterior or posterior cortical, nuclear, axial, and equatorial. Cause: Cataracts can be classified as primary or secondary, based on the underlying cause. As opposed to dogs, primary and inherited cataracts are rare in the cat. Most cataracts occur secondarily to anterior uveitis, trauma, glaucoma, or lens luxation. The most common cause of secondary cataracts in the cat is anterior uveitis. Inflammation in the anterior segment affects the nutritional health of the lens, which leads to cataractous change. Chronic uveitis is most often associated with causing cataract formation; however, acute or subclinical uveitis may lead to the condition as well. These cataracts progress slowly and are associated with evidence of chronic inflammation. Traumatic cataracts are usually a result of penetrating injury to the eye. These cataracts are usually focal and associated with regional inflammation (i.e., fibrin strands or posterior synechia). It is important to note that the development of intraocular neoplasia has been shown to be associated with severe lens damage in cats. See Chapter 122. Lens luxation occurs when there is disruption of the zonular lens fibers resulting in a shifting of the lens. Lens luxation may also occur as a result of chronic glaucoma with buphthalmous. Secondary cataracts from lens luxations form presumably from abnormal lens metabolism. These cataracts are often more diffuse.
Secondary Diagnostics th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
70
• Electroretinogram: This procedure measures the electrical activity of the retina in response to light stimulus. It is critical to insure proper
Cataracts
functioning of the retina if it cannot be properly visualized prior to cataract surgery to achieve a good visual outcome. • Ocular Ultrasound: Ocular ultrasound may be used prior to cataract surgery to look for retinal detachments or other lesions within the eye when the cataract obscures fundic examination.
Secondary Therapeutics • Uveitis is commonly associated with cataracts. Anterior uveitis may cause cataract formation, and cataracts may induce a secondary uveitis. See Chapter 223. Treating concurrent uveitis is critical and will limit secondary changes and vision loss.
Diagnostic Notes • Anterior uveitis is the most common cause of feline cataracts, so remember to examine the eye thoroughly for any evidence of inflammation. See Chapter 223. • Arginine deficiency has been documented as the cause of cataracts in kittens fed a milk replacer, although is considered rare due to today’s commercial diets. • Radiation therapy on the head or facial region can result in both focal and generalized cataracts. • In contrast to dogs, diabetes mellitus does not cause cataracts in the cat.
Treatment Primary Therapeutics • Phacoemulsification: Removal of the cataract is the only option to restore vision following formation of a mature cataract. Phacoemulsification is performed by a veterinary ophthalmologist. It involves the use of an intraocular instrument with an ultrasound probe used to break up the lens material, while aspirating the lens fragments. The entire lens cortex and nucleus is removed, leaving only the lens capsule intact. Placement of an intraocular lens (IOL) within the capsular bag improves the cat’s ability to see near objects; however, there has been no definitive evidence that cats are impacted greatly without the lens placement. Cataract surgery has a high success rate and improves the quality of life for the cat. Complications include severe uveitis, glaucoma, retinal detachment, and endophthalmitis.
Therapeutic Notes • Cataract surgery is an expensive elective procedure. Not all owners will be able to make the financial or personal commitment necessary for surgery. • Cataracts with associated uveitis should be monitored regularly (every 2–6 months), and treatment should be adjusted if clinical signs are present. • Untreated uveitis resulting from cataracts may develop into glaucoma and blindness. See Chapter 85.
Prognosis The prognosis for vision will be determined based partly upon the classification of the cataract. The presence of uveitis and response to medications will affect visual prognosis. The result of cataract surgery is generally good.
Suggested Readings Gelatt KN, Gelatt JP. 2001. Surgical Procedures for the Lens and Cataracts. In KN Gelatt, JP Gelatt, eds., Small Animal Ophthalmic Surgery: Practical Techniques for the Veterinarian, pp. 286–335. Philadelphia: Elsevier Health Sciences. Zeiss CJ, Johnson EM, Dubielzig RR. 2003. Feline Intraocular Tumors May Arise from Transformation of Lens Epithelium. Vet Pathol. 40: 355–362.
71
CHAPTER 32
Ceruminous Gland Disease Mark Robson
Overview Ceruminous glands are modified apocrine glands that exist throughout the deeper connective tissue of the external ear canal extending onto the pinna. Their oily secretions are combined with those of sebaceous glands to result in the formation of cerumen. The ducts of ceruminous glands often open into the infundibulum of hair follicles but may also open directly to the epidermal surface, a feature not seen with apocrine glands. Disease of these glands can be described as hyperplastic, cystic, or neoplastic. Ceruminous gland neoplasia (i.e., benign and malignant) in cats is not common, but it is the most frequently seen tumor of the ear canal in the feline. See Figures 32-1 and 32-2. In one study of 176 tumors the ratio of adenomas-to-carcinomas was 45:55. Neoplasia appears to be more common in cats than dogs and also tends to be more aggressive when it occurs. Otitis externa is frequently stated to be a cause of ceruminous gland disease, particularly hyperplasia and cystic change. A link has been stated between the sequential development of otitis externa, ceruminous gland hyperplasia, or cyst formation, and subsequent neoplastic transformation. This link is unproven. See Chapter 157.
Figure 32-2 They may extend down into the external ear canal as seen in this cat that required a total ear canal ablation. It can be difficult or impossible to tell the difference on visual examination between different forms of ceruminous gland disease and to determine whether the lesion is of ceruminous gland origin or represents another lesion such as an inflammatory polyp, melanoma, or squamous cell carcinoma. Ceruminous gland lesions can appear as single or multiple masses and can be darkly pigmented. Ceruminous gland disease can occur anywhere within the canal and can penetrate the tympanum and enter the middle ear. Any patient with chronic otitis externa should be suspected of having a neoplasm, and strenuous efforts should be made to properly examine the entire ear canal and tympanum. Examination of the feline ear canal can be difficult due to the presence of exudate, tissue swelling, hyperplasia, and pain. Proper evaluation will often involve general anesthesia. Treating the infection first may permit visualization without anesthesia. Ear swabs alone are a poor method of diagnosing a mass as the cytology will be dominated by inflammation and infection. Fine-needle aspiration (FNA) has been shown to be quite accurate in differentiating inflammatory polyps from neoplastic change but much less accurate at differentiating a ceruminous gland adenoma from a carcinoma or ceruminous gland neoplasia from other forms of cancer. Histopathology remains the most accurate means of diagnosis and can be achieved with incisional biopsy pending decisions on wider resection and possible ear canal ablation. The clinical signs of ceruminous gland disease are similar to other inflammatory, infectious, or neoplastic syndromes. They include head shaking, ear pawing or scratching, otic odor, pain, pruritus, head tilt, folding over of the pinna, malaise, and anorexia.
Figure 32-1 Multiple ceruminous gland adenomas are found on the concave side of the pinna.
Diagnosis Primary Diagnostics
th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
72
• Otoscopic Examination: Thorough visual examination of the entire ear canal bilaterally is essential. This will probably require deep
Ceruminous Gland Disease
sedation or general anesthesia. Assisted viewing using a video otoscope may be useful, especially if a working channel is available for flushing, suction, and biopsy. • Cytology and Culture: An ear swab for cytology and culture will be helpful in managing the otitis externa that may be primary or secondary. Diagnosis of a lesion will require FNA or more reliably biopsy. • Biopsy and Histopathology: Proliferative lesions can be sampled using an incisional technique or skin punch biopsy. Lesions deeper in the ear canal may be more difficult to sample, especially if they are not exophytic. A video otoscope is the ideal tool for biopsy. Alternatively, initial cytology may have to be used to guide decisions on more aggressive surgery, and, as always, dialogue with your cytologist about equivocal results can be helpful. Grasping forceps may allow sufficiently large tissue samples to be obtained from deep lesions. • Skull Radiographs: Skull radiographs with emphasis on views that highlight the bullae are indicated to assess the level of middle ear involvement.
Secondary Diagnostics • Thoracic Radiographs: Metastasis is rare with ceruminous gland neoplasia, but because many of the patients will be older, thoracic radiographs may be prudent to assess for a second disease. • Advanced Imaging: In certain patients, especially with biopsy proven malignancy, advanced imaging such as computerized tomography (CT) may be helpful for surgical planning. • Minimum Data Base: Routine checking for feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV) status as well as complete blood count (CBC), blood chemistries, and urinalysis will be appropriate, especially in older cats before general anesthesia.
lesions is surgical. Appropriate textbooks and articles should be consulted (see Suggested Readings), and the approach may vary from a simple marginal excision for a benign lesion to total ear canal ablation for larger or malignant masses. See Chapter 274. • Middle Ear Surgery: If the lesion has entered the middle ear or if chronic infection and inflammation have resulted in middle ear changes, a lateral or ventral bulla osteotomy may be required in conjunction with management of the soft tissue changes. See Chapter 248 and 274.
Secondary Therapeutics • Chemotherapy: This has not been reported in the context of malignant ceruminous gland disease. • Radiation: The use of radiation therapy has been reported, but case numbers are too small for drawing conclusions on outcome.
Prognosis The prognosis for appropriately treated benign lesions is excellent. For malignant tumors, the survival times are less than 1 year.
Suggested Readings Fossum TW. 2002. Surgery of the Ear. In TW Fossum, MD Willard, CS Hedlund, et al., eds., Small Animal Surgery, 2nd ed., pp. 229–253. St. Louis: Mosby Elsevier. Krahwinkel DJ. 2003. External Ear Canal. In TW Fossum, CS Hedlund, AL Johnson, eds., Small Animal Surgery, 3rd ed., pp. 1746–1756. St. Louis: Mosby Elsevier. White RAS. 2003. Middle Ear. In TW Fossum, CS Hedlund, AL Johnson, eds., Textbook of Small Animal Surgery, 3rd ed., pp. 1757–1766. St. Louis: Mosby Elsevier.
Treatment Primary Therapeutics • Tumor Surgery: Once pain relief, local inflammation, and infection have been considered, the primary treatment for ceruminous gland
73
CHAPTER 33
Cervical Ventroflexion Mitchell A. Crystal and Paula B. Levine
Overview Cervical ventroflexion is a syndrome characterized by muscle weakness or rigidity of the neck, causing an inability to raise the head. See Figure 33-1. The neck may be so ventroflexed that the top of the head rests near or on the ground, and the chin rests near the thoracic inlet. Other muscles of the body may also demonstrate weakness. The clinical signs are often acute in nature. The mechanism of cervical ventroflexion is variable depending on the etiology. It is uncertain why cervical muscles demonstrate greater weakness than other muscles in this syndrome; the speculation has to do with the weight of the head. The differential diagnoses include hypokalemia, hyperthyroidism, chronic organophosphate toxicity, thiamine-responsive myopathy, diabetes mellitus, idiopathic polymyositis (immune mediated), myasthenia gravis, hypernatremia polymyopathy, portosystemic shunt and encephalopathy, and ammonium chloride toxicity (which causes acidosis, which leads to intracellular potassium depletion). Hypokalemia is the most common cause of cervical ventroflexion. Organophosphate intoxication, thiamine-responsive disease, and hyperthyroidism are moderately common causes of this syndrome.
hyperthyroidism, hypokalemia, or portosystemic shunt), increased appetite with concurrent weight loss (i.e., diabetes mellitus or hyperthyroidism), neurologic signs (i.e., hypernatremia, organophosphate toxicity, portosystemic shunt, or thiamine-responsive disease), ptyalism (i.e., portosystemic shunt), and muscle pain or rigidity (i.e., hypokalemia, idiopathic polymyositis, or thiamine deficiency). • Chemistry Profile: Evaluate for abnormalities in glucose (i.e., diabetes mellitus), sodium (i.e., hypernatremia), potassium (i.e., ammonium chloride toxicity or hypokalemia), liver enzymes (i.e., hyperthyroidism or portosystemic shunt), albumin (i.e., portosystemic shunt), creatine kinase (i.e., hypernatremia, hypokalemia, or idiopathic polymyositis), and blood urea nitrogen and creatinine (hypokalemia secondary to renal disease). • Urinalysis: Evaluate for glucosuria (i.e., diabetes mellitus) and decreased specific gravity (i.e., renal disease, diabetes mellitus, hyperthyroidism, hypokalemia, or portosystemic shunt). • Total T4: This hormone is increased with hyperthyroidism.
Secondary Diagnostics Diagnosis Primary Diagnostics • History: Investigate the possibility of exposure to ammonium chloride (such as urinary acidifiers) and organophosphates. Investigate the presence of other clinical signs that might suggest an etiology, such as polyuria and polydipsia (i.e., diabetes mellitus,
Figure 33-1 Muscle weakness results in this cat’s cervical ventroflexion or inability to lift its head.
• Thoracic Radiography: Megaesophagus or cranial mediastinal masses are occasionally seen in cats with myasthenia gravis. See Chapter 143. • Administer Thiamine: Clinical response, typically within 2 days, to thiamine therapy (vitamin B1 25–50 mg/cat q24h for 3 days IM) along with a nondefinitive diagnostic evaluation is supportive of thiamineresponsive cervical ventroflexion. See Chapter 210 and Primary Therapeutics in this chapter. • Edrophonium Chloride Challenge: 0.25 to 0.5 mg IV results in resolution of cervical ventroflexion and muscle weakness in most cats with myasthenia gravis. See Chapter 143. • Acetylcholine Receptor Antibody Titer: An increased titer is diagnostic for acquired myasthenia gravis. See Chapter 143. • Serum Cholinesterase Activity: This is reduced more than 50% in cats with organophosphate toxicity. See Chapter 155. • Fasting and Postprandial Serum Bile Acids: These are significantly increased (2-hour postprandial samples are typically greater than 100 mmol/L) in cats with portosystemic shunt. See Chapter 178. • Abdominal Imaging: Survey radiographs and abdominal ultrasound can demonstrate abnormalities in the kidneys (i.e., renal disease), adrenal glands (i.e, adrenal tumor leading to hyperaldosteronism and subsequent hypokalemia, also known as Conn’s syndrome; see Chapter 102) or liver (i.e., portosystemic shunt). Rectal technetium scintigraphy (99mTc pertechnetate) and positive contrast portography often demonstrate abnormalities in cats with portosystemic shunts. • Electromyography and Repetitive Nerve Stimulation: Abnormalities can be seen in cats with hypokalemia, idiopathic polymyositis, myasthenia gravis, organophosphate toxicity, and ammonium chloride toxicity.
Diagnostic Notes th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
74
• Primary diagnostic tests should be performed in all cats with cervical ventroflexion along with a total T4 in cats over 7 years of age.
Cervical Ventroflexion
• Secondary diagnostic tests should be performed if indicated by history, clinical signs, or chemistry abnormalities or if primary tests are nondiagnostic.
Treatment
• Intravenous potassium administration should not exceed 0.5 mEq/ kg per hour. • Oral potassium supplementation is more effective in correcting hypokalemia than is therapy with potassium containing IV fluids. See Chapter 114.
Primary Therapeutics • Treat Underlying Disease: This is the key to resolution of the problem. • Administer thiamine (vitamin B1 25–50 mg/cat q24h for 3 days IM): All cats with cervical ventroflexion in which a definitive diagnosis cannot be made should receive thiamine since there is no diagnostic test available for thiamine deficiency, there are no side effects to this dosage, and cats on normal diets can occasionally develop thiamine-responsive cervical ventroflexion. Improvement is usually seen within 2 days (see Chapter 210). • Fluid Support: Administer fluid therapy if dehydration or renal disease is present or if prolonged lack of fluid intake is anticipated. See Chapter 302. If hypokalemia is present, potassium chloride should be added to the fluids at the rate of 40 to 60 mEq/L (for fluids not containing potassium) because fluid therapy not supplemented with potassium will worsen hypokalemia. See Chapter 114. • Nutritional Support: Administer nutritional therapy if prolonged anorexia is anticipated.
Therapeutic Notes • Creatine kinase should be assessed prior to administration of any intramuscular medications.
Prognosis The prognosis is excellent if the underlying disease can be identified and treated. Idiopathic polymyositis and myasthenia gravis carry less favorable prognoses, as they are difficult to treat and may not respond to therapy. Severe hypernatremia (>180 mEq/L [180 mmol/L]) is often associated with neurologic damage that can be residual or can result in coma or death.
Suggested Readings Gaschen FP, Jones BR. 2005. Feline Myopathies. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 906–912. St. Louis: Elsevier Saunders. Joseph RJ, Carrillo JM, Lennon VA. 1988. Myasthenia gravis in the cat. J Vet Intern Med. 2(2):75–79. Podell M. 2000. Neurologic Manifestations of Systemic Disease. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 5th ed., pp. 548–552. Philadelphia: WB Saunders. Shelton D. 2007. Myasthenia gravis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult. Canine and Feline, 4th ed., pp. 908–909. Ames, IA: Blackwell Publishing.
75
CHAPTER 34
Chemotherapy for Lymphoma Mitchell A. Crystal and Bradley R. Schmidt
Overview In the cat, lymphoma is broadly categorized into two histopathological categories based on behavior and response to chemotherapy: the more common large cell (lymphoblastic) lymphoma that arises from any anatomic location and is usually associated with rapid disease progression, and the less common small cell (lymphocytic) to intermediate cell lymphoma that has been described in the small intestinal tract as well as in other organs and may be associated with a more indolent course of progression. Although lymphoma is considered a chemosensitive malignancy, drug resistance has likely developed by a variety of genetic and cellular pathways by the time the neoplasm becomes clinically detectable. Combination chemotherapy attempts to overcome chemotherapy resistance and maximize tumor cell kill by using drugs with different mechanisms of action and minimize side effects by avoiding the use of drugs with overlapping toxicities. Chemotherapy drugs are administered by injection or orally on an outpatient basis or orally at home. Minimally, a complete blood cell count (CBC) assessment and a complete physical examination should be performed prior to and 1 week after each therapy until a pattern is established that indicates each agent is safe and well tolerated. If a serious side effect occurs, subsequent dose reduction, delay in therapy, or change in chemotherapy drugs used may be indicated.
TABLE 34-1: Cyclophosphamide, Vincristine, Prednisone (COP) Week 0 Week 1 Week 2 Week 3 Week 6
Reported first remission rate Reported median first remission duration Median survival time
Vincristine 0.75 mg/m2 IV and cyclophosphamide 300 mg/m2 PO Vincristine 0.75 mg/m2 IV Vincristine 0.75 mg/m2 IV Vincristine 0.75 mg/m2 IV and cyclophosphamide 300 mg/m2 PO Vincristine 0.75 mg/m2 IV and cyclophosphamide 300 mg/m2 PO Prednisone: 2 mg/kg per day PO given continuously for 1 year beginning week 0 Treatment is continued with vincristine and cyclophosphamide at 3-week intervals for 1 year 79 to 100% 84 to 180 days Not reported
Combination Protocols with Author’s Notes • Combination chemotherapy protocols are considered the mainstay in therapy of feline lymphoma and are generally associated with higher remission rates and longer remission times when compared to single agent protocols. Four combination chemotherapy protocols that have been successfully used in the treatment of feline lymphoma are listed in Tables 34-1, 34-2, 34-3, and 34-4. The overall first remission rates, durations, and survival times (when available) are listed. Variations of the aforementioned protocols are also described with similar response rates and survival times. • We commonly use one the following protocols to treat cats with large cell (lymphoblastic) and some forms of intermediate cell lymphoma of various anatomic locations: • cyclophosphamide, Oncovin® (vincristine), prednisone (COP) • L-asparaginase, Oncovin® (vincristine), cyclophosphamide, chlorambucil, Adriamycin® (doxorubicin), prednisone (CHOP) • cyclophosphamide, Oncovin® (vincristine), prednisone, Adriamycin® (doxorubicin) (COPA). • Whereas responses may vary, remission rates associated with these protocols are generally high, however survival times are typically less than 1 year. • The chlorambucil/prednisone protocol is generally reserved for the treatment of cats with small to intermediate cell lymphoma of the small intestinal tract, small cell lymphoma of other anatomic locations, and chronic lymphocytic leukemia. These cats may enjoy prolonged survival times with this less aggressive protocol (11 months or more).
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
76
• L-asparaginase may be used in the first week of therapy in many of the combination protocols described; however, when used concurrently with vincristine, myelosuppression may occur anecdotally. Some advocate the use of L-asparaginase only in critical cases or as part of a rescue protocol. Efficacy of L-asparaginase in the cat is coming under question, as a recent study reported only a 30% response rate in feline lymphoma. • Vincristine and cyclophosphamide doses reported in the combination protocols may result in toxicities that are not acceptable to the cat owner. Dose reduction may be indicated initially and may be increased in subsequent administrations if the patient is tolerating therapy well. See Commonly Used Drugs in the Therapy of Lymphoma listed in this chapter.
Single-Agent Protocols • Doxorubicin: In contrast to dogs, doxorubicin has demonstrated poor efficacy when used as a single-agent therapy for feline lymphoma (26% complete response, median first remission duration 92 days, median survival time 84 days). It has been demonstrated, however, that the addition of doxorubicin to a combination chemotherapy protocol such as COP may significantly prolong remission times. Doxorubicin is generally administered at 1 mg/kg or at 25 mg/m2 diluted with saline, IV every 21 days. A recent study comparing these two dosages reported that the latter dose was associated with a lower posttreatment neutrophil count but not associated with more clinical toxicities. It was not determined if there was a difference in tumor response between the two dosages. In cats, renal toxicity is more of a concern than cardiomyopathy. Monitor blood urea nitrogen (BUN) and creatinine prior to each administration for evidence of evolving renal disease.
Chemotherapy for Lymphoma
TABLE 34-2: Modified Wisconsin—L-asparaginase, Vincristine, Cyclophosphamide, Chlorambucil, Doxorubicin, Prednisone (Modified CHOP) Week 0 Week Week Week Week Week Week Week Week Week Week Week Week Week Week Week
1 2 3 5 6 7 8 10 12 14 16 18 20 22 24
First remission rate Median first remission duration Median survival time
2
Vincristine 0.5–0.7 mg/m IV and L-asparaginase 400 u/kg SC Cyclophosphamide 200 mg/m2 PO or IV Vincristine 0.5–0.7 mg/m2 IV Doxorubicin 25 mg/m2 IV Vincristine 0.5–0.7 mg/m2 IV Cyclophosphamide 200 mg/m2 PO Vincristine 0.5–0.7 mg/m2 IV Doxorubicin 25 mg/m2 IV Vincristine 0.5–0.7 mg/m2 IV Cyclophosphamide 200 mg/m2 PO or IV Vincristine 0.5–0.7 mg/m2 IV Doxorubicin 25 mg/m2 IV Vincristine 0.5–0.7 mg/m2 IV Cyclophosphamide 200 mg/m2 PO or IV Vincristine 0.5–0.7 mg/m2 IV Doxorubicin 25 mg/m2 IV Prednisone: 2 mg/kg per day PO weeks 0 and 1, then 1 mg/kg/day PO weeks 2 and 3, then discontinue unless clinically indicated. If sterile hemorrhagic cystitis occurs, substitute chlorambucil at 1.4 mg/kg PO. For renal or central nervous system lymphoma, substitute cytosine arabinoside (Cytosar®, 600 mg/m2 SC) every 8 weeks beginning at week 6. 68% 273 days
225 days
TABLE 34-3: Cyclophosphamide, Vincristine, Prednisone, Doxorubicin (COP Induction + Doxorubicin Maintenance; COPA) Week 0 Week Week Week Week Week Week Week Week Week Week
1 2 3 6 9 12 15 18 21 24
First remission rate Median first remission duration Median survival time
Vincristine 0.75 mg/m2 IV and Cyclophosphamide 300 mg/m2 PO Vincristine 0.75 mg/m2 IV Vincristine 0.75 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Doxorubicin 25 mg/m2 IV Prednisone: 2 mg/kg per day PO beginning week 0 and ending at onset of week 3. Treatment ends week 24. 47% 281 days
TABLE 34-4: Chlorambucil + Prednisone for Lymphocytic Alimentary Lymphoma (Chlorambucil, Prednisone) Day 0 Day 1 Day 2 Day 3 Prednisone Chlorambucil Protocol end point not reported First remission rate Median first remission duration Median survival time
Chlorambucil 15 mg/m2 PO Chlorambucil 15 mg/m2 PO Chlorambucil 15 mg/m2 PO Chlorambucil 15 mg/m2 PO 10 mg/cat per day PO beginning day 0 4-day pulse treatment is repeated every 3 weeks
69% 615 days 510 days
• Idarubicin: Idarubicin is an oral anthracycline agent that has been shown to have efficacy in feline lymphoma (2 mg q24h PO for 3 consecutive days, repeated every 21 days). Furthermore, the addition of idarubicin as a single agent in 18 cats that achieved remission with COP induction resulted in median remission times of 183 days. • CCNU (CeeNU®, Lomustine®): This oral alkylating agent is being investigated for use in feline lymphoma. It is renally and hepatically metabolized and crosses the blood-brain barrier. Limited information is available regarding the use of CCNU in cats. Dogs with resistant lymphoma demonstrate a 20% response rate to CCNU. CCNU can be considered as a rescue agent for cats with resistant lymphoma. It is dosed at 50 to 60 mg/m2 (typically 10 mg/average to large-sized cat) q4 to 6w PO. Acute dose limiting toxicity is neutropenia, which can occur 7 to 28 days after treatment; gastrointestinal toxicity can also occur. Cumulative dose limiting toxicity is thrombocytopenia, which can occur 14 to 21 days after treatment. Further chronic effects of CCNU have not yet been evaluated in the cat; delayed liver damage has been documented in the dog (9 of 228 dogs receiving chronic therapy). Monitoring of the CBC (prior to and 7 to 10 days following each treatment) and chemistry profile (prior to every other treatment) is indicated if CCNU is used. • Miscellaneous Notes: Single agent use of cyclophosphamide, chlorambucil, vincristine, vinblastine, L-asparaginase, and prednisone have all anecdotally resulted in prolonged survival times; however, their use is generally reserved to combination protocols.
Commonly Used Drugs in the Therapy of Lymphoma Chlorambucil • Supplied as 2 mg tablets. • Drug type: Alkylating agent. • Dosage: 0.1 mg/kg q24h PO or 6 to 8 mg/m2 q24h PO. Because the tablets should never be split, this usually translates to 2 mg q24h PO to q3d PO days depending upon the weight of the cat. Also, it may be dosed as indicated in combination chemotherapy protocols. It is generally used as a substitute for cyclophosphamide if hemorrhagic cystitis occurs or in the treatment of small cell lymphoma or chronic lymphocytic leukemia. • Toxicities: It is generally well tolerated; however, gastrointestinal side effects and myelosuppression may occur.
Not reported
Cyclophosphamide • Supplied as 25- and 50-mg tablets; 100-, 200-, and 500-mg and 1- and 2-g vials.
77
SECTION 1: Diseases and Conditions
• Drug type: Alkylating agent. • Dosage: 50 mg/m2 orally in the morning q48h PO or 200 to 300 mg/m2 q21d PO. Do not split the tablet; adjust the actual dose based on tablet size. For example, if a dose is calculated at 12 mg q48h with the cumulative 2-week dose being 84 mg divided over 7 doses, administer 25 mg tablets in 3 doses equally spaced in that 2-week interval. The intravenous dose is 200 to 300 mg/m2 mixed with any volume of 0.9% saline, administered over 20 to 30 minutes. Cyclophosphamide is eliminated by the kidneys; reduce the dose if renal disease is present. • Toxicities: Anorexia, vomiting, or diarrhea is seen more commonly with intravenous administration. Neutropenia may occur uncommonly to occasionally with the nadir being 7 to 14 days after therapy; it usually returns quickly to normal. The low count does not cause signs of illness unless infection or sepsis occurs. Decrease the dose by 20% if severe neutropenia (<1,000/µL) occurs. Cyclophosphamide may rarely cause a chemical irritation of the bladder, leading to a sterile hemorrhagic cystitis. This is not an infection and must be differentiated from infectious cystitis by a urine culture. Cyclophosphamide-induced cystitis can be prevented in some cases by giving the drug in the morning, allowing opportunity for urination during the day, and maintaining adequate fluid intake. Prednisone will also help prevent this condition. If a sterile hemorrhagic cystitis should occur, discontinue immediately and substitute chlorambucil into the protocol. Loss of hair is unusual in cats because their hair does not grow continuously throughout their life (as in humans); however, shaved hair is slow to regrow. Also, whisker loss may be noted. Anaphylaxis, pulmonary fibrosis or infiltrates, and hyponatremia are rarely reported.
Doxorubicin • Supplied as 10-, 20-, 50-, 150-, and 200-mg vials. • Drug type: anthracycline antibiotic. • Dosage: 25 mg/m2 or 1 mg/m2 IV, diluted with 30 mls of 0.9 % saline, administered over 15 to 30 minutes. Do not use heparin because this will cause precipitation of the drug. Doxorubicin is metabolized by the liver and excreted in the bile; therefore, reduce the dose by 50% if the serum bilirubin is greater than 2 mg/dL. • Toxicities: Anorexia, and less commonly vomiting or diarrhea, may occur. Neutropenia may occur, with the nadir being 7 to 10 days after therapy; it usually quickly returns to normal. Neutropenia does not cause signs of illness unless infection or sepsis occurs. Decrease the dose by 20% if severe neutropenia (< 1,000/µL) occurs. Severe tissue necrosis at the injection site (about 100% occurrence if any amount of this drug is administered extravascularly) may occur; this should be prevented by administering the drug via a secure, cleanly placed over-the-needle intravenous catheter. Nephrotoxicity is the dose-limiting toxicity in cats (versus cardiotoxicity in dogs). Cumulative doses over 200 mg/m2 should be avoided. Urine specific gravity, creatinine, and BUN should be assessed in cats prior to administering therapy. A few cats may itch or develop hives as the drug is being given. This is a transient event. Drug administration should be stopped for 15 to 30 minutes and, after that time, administered at a slower rate. Red discoloration of the urine may occur after the drug is given. This is not abnormal and is merely from the color of the drug. Mild hair loss including loss of whiskers (more common) may occur.
L-asparaginase • • • •
78
Supplied as a 10,000-Unit vial. Drug type: enzyme. Dosage: 10,000 U/m2 or 400 U/kg q7d or less frequently SC, IM. Toxicities: Hypersensitivity reactions may occur, especially if multiple doses are administered. Do not give IV because the risk for an
anaphylactic reaction is high. Cats that have received the drug before should be observed at home or in the hospital after the injection. Reactions usually occur immediately, but delayed hypersensitivity reactions may occur. Other less common side effects include vomiting and fever. Myelosuppression may occur if given concurrently with vincristine.
Methotrexate • Supplied as 2.5-mg tablets; 5-, 20-, 50-, 100-, 200-, and 250-mg and 1-g vials. • Drug type: antimetabolite. • Dosage: 2.5 mg/m2 q24h or per indication in combination protocols. Methotrexate is eliminated in the urine, and dose reduction should be performed in patients that are azotemic. • Toxicities: Anorexia, vomiting, and diarrhea may be seen and are the most common side effects. Neutropenia is not common in cats. High doses may be used in the treatment of lymphoma followed by reversal with leucovorin; however, this is rarely performed in the treatment of feline lymphoma.
Prednisone or Prednisolone • Supplied as 1-, 2.5-, 5-, 10-, and 20-mgtablet: 1-mg/mL syrup (vanilla flavor); 50-mg/mL injection. • Drug type: corticosteroid. • Dosage: 1 to 2 mg/kg q24h or as indicated in a combination protocol. • Toxicities: Few side effects occur as a result of prednisone therapy in the cat, although some risk of diabetes mellitus exists. Weight gain, diabetes mellitus dysregulation, iatrogenic hyperadrenocorticism are common in dogs. Some advocate the use of prednisolone over prednisone because it has been suggested that prednisone is not efficiently converted to prednisolone by the liver. Prednisone and prednisolone are equivalent based on tumor response to either of these drugs.
Vincristine • Supplied: 1-, 2,- and 5-mg vial. • Drug type: plant derived vinca alkaloid. • Dosage: 0.5 to 0.75 mg/m2 q7d IV. Higher doses may result in increased risk of toxicities. Vincristine is excreted in bile; therefore, decrease the dose by 50% of the bilirubin is greater than 2 mg/dL. • Toxicities: This drug can cause neurotoxicity resulting in paresthesia but more commonly constipation and paralytic ileus. Anorexia and vomiting may occur and may be prolonged and severe in some cats; these signs may be as a result of paralytic ileus. Neutropenia is not common but may be seen when higher doses are administered or if L-asparaginase is used concurrently. Severe tissue necrosis at the injection site can occur if the drug is administered extravascularly. Because of the small volumes administered (typically 0.1–0.3 mL) and ability to administer rapidly, use of a butterfly catheter is appropriate unless the cat cannot be restrained; then, a more secure catheter is necessary. Thrombocytosis may occur; this is not a clinical concern.
Vinblastine • Supplied as a 10-mg vial. • Drug type: plant derived vinca alkaloid. • Dosage: 1.5 to 2.0 mg/m2 q2 to 3w. Vinblastine is excreted in bile; therefore, decrease the dose by 50% if the bilirubin is greater than 2 mg/dL. • Toxicities: In contrast to vincristine, vinblastine can result in severe neutropenia with the nadir being at 4 to 7 days after administration. As with vincristine, vinblastine can result in paralytic ileus, vomiting,
Chemotherapy for Lymphoma
and constipation; however, these effects are less severe than with vincristine. Vinblastine may be used as a substitution for vincristine if severe anorexia is noted; however, as neutropenia is commonly seen with vinblastine, use with caution when other myelosuppressive drugs are concurrently administered. Severe tissue necrosis at the injection site can occur similarly to that seen with vincristine.
Approach to Common Chemotherapy Side Effects Many chemotherapy reactions are listed in the literature and drug inserts. There are three notable side effects. • Sepsis: life-threatening; the most serious. • Gastroenteritis: self-limiting with supportive care. • Neutropenia without sepsis: a mild problem of limited clinical concern.
Sepsis Clinical Aspects • Onset: 6 to 14 days following a chemotherapy dose. • Clinical signs: Anorexia, lethargy, vomiting, diarrhea, collapse, fever, or hypothermia. • Diagnosis: Clinical signs, timing of clinical signs, neutropenia on a CBC, and possible hypoglycemia. • Treatment: Intravenous catheter; intravenous fluids (usually requires shock fluids [50 mL/kg per hour] initially, then 1.5 times the maintenance fluid rate for 1–3 days); intravenous antibiotics (broad-spectrum, such as cephalosporins or ampicillin with fluoroquinolone), aminoglycosides can be added but only after dehydration and shock have been treated and resolved; nothing by mouth (NPO) if vomiting, withhold food but not water if diarrhea occurs without vomiting. G-CSF (Filgrastim, 3–5 µg/kg q24h SC), is a cytokine that results in the production and differentiation of neutrophils and may be beneficial in increasing the neutrophil count in neutropenic patients, however antibody production against G-CSF may develop over time preventing future responses to this drug. • Prognosis: Good if detected and treated early; guarded to poor if severe. • Prevention: Delay/do not administer any chemotherapy if the pretreatment CBC reveals neutropenia of <2000/µL; if neutropenia occurs, decrease the dose of the chemotherapy agent that caused the neutropenia by 20% for all subsequent doses of that drug.
Client Communication and Patient Management • If the owner calls with a sick cat in the 6- to 10-day postchemotherapy window, instruct the client to bring in the patient immediately. This is a potentially life-threatening condition. • Once the cat is at the hospital, collect blood for a CBC, chemistry profile, and urinalysis. • Place an intravenous catheter, and begin intravenous fluid and intravenous antibiotic therapy. • Adjust fluids for electrolyte abnormalities if indicated; length of intravenous therapy should be based on hydration, general condition, neutropenia, and presence or absence of fever. Oral antibiotics should be dispensed if neutropenia is present or gastrointestinal mucosal compromise is suspected.
Gastroenteritis Clinical Aspects • Onset: 2 to 5 days following a chemotherapy dose. • Clinical signs: Anorexia, lethargy, vomiting, diarrhea, and mild fever.
• Diagnosis: Clinical signs, timing of clinical signs, and lack of neutropenia. • Treatment: NPO if vomiting (withhold food but not water if the cat has diarrhea without vomiting); if there is suspicion of dehydration (severity of vomiting/diarrhea), subcutaneous fluids on an outpatient basis or hospitalization with intravenous fluids is appropriate, as well as the administration of antiemetics if indicated. • Prognosis: Good. • Prevention: There is no need to decrease the dose of the chemotherapy agent causing the gastroenteritis unless the episode is severe or unless this has occurred from the same agent previously. Pretreatment with an anti-emetic is recommended to reduce the incidence and severity of clinical signs.
Client Communication and Patient Management • If the owner calls with a sick cat in the 2- to 5-day post-chemotherapy window, determine the severity of illness (i.e., how much vomiting/ diarrhea, what is the patient’s attitude and appetite, and so on); if there is concern for the patient’s hydration status, request that the patient be brought in for examination. • If the patient is not dehydrated (decision by phone or examination), instruct the client to make the patient NPO if the cat is vomiting or withhold food but not water if the cat has diarrhea without vomiting. • Slowly (with small amounts frequently) reinstitute water and an easily digestible diet. • Return to normal diet gradually over 1 to 2 days. • Sepsis may be a consideration for the borderline cases (4–7 days). Therefore, when a client calls have the client take the cat’s body temperature. If there is fever, the cat should be seen immediately. If there is fever or hypothermia the cat should be seen immediately. If the body temperature is normal conservative therapy can be attempted if the illness is of limited severity. Oral antibiotics should be used in these cases, along with conservative therapy.
Neutropenia without Illness Clinical Aspects • • • •
Onset: 6 to 10 days following a chemotherapy dose. Clinical signs: None unless sepsis occurs. Diagnosis: Neutropenia. Treatment: None if WBC >2,000/µL, oral antibiotics if WBC < 2,000/µL. • Prognosis: Excellent when sepsis does not occur.
Client Communication and Patient Management • Assess the degree of neutropenia and administer antibiotics, if indicated. • Decrease the dose of the chemotherapy agent that caused the neutropenia by 10 to 15% for all subsequent doses of that drug.
Suggested Readings Carreras JK, Goldschmidt M, Lamb M, et al. 2003. Feline epitheliotropic intestinal malignant lymphoma: 10 cases (1997–2000). J Vet Intern Med. 17:326–331. LeBlanc AK, Cox SK, Kirk CA, et al. 2007. Effects of L-aparaginase on plasma amino acid profiles and tumor burden in cats with lymphoma. J Vet Intern Med. 12(4):760–763. Moore AS, Cotter SM, Frimberger AE, et al. 1996. A comparison of doxorubicin and COP for maintenance of remission in cats with lymphoma. J Vet Intern Med. 10:372–375.
79
SECTION 1: Diseases and Conditions
Moore AS, Ogilvie GK. Lymphoma. 2001. In AS Moore, CK Ogilvie, eds., Feline oncology: a comprehensive guide to compassionate care. pp. 191–219, 423–428. Philadelphia: Veterinary Learning Systems. Pohlam LM, Higginbotham ML, Welles EG, et al. 2009. Immunophenotypic and histological classification of 50 cases of feline gastrointestinal lymphoma. Vet Pathol. 46(2):259–268. Reiman RA, Mauldin GE, Mauldin GN. 2008. A comparison of toxicity of two dosing schemes for doxorubicin in the cat. J Fel Med Surg. 10(4):324–331. Simon D, Eberle N, Laacke-Singer L, et al. 2008. Combination chemotherapy in feline lymphoma: Treatment outcome, tolerability, and duration in 23 cats. J Vet Intern Med. 22(2):394–400.
80
Vail DM, Moore AS, Ogilvie GK, et al. 1998. Feline lymphoma (145 cases): Proliferation indices, cluster of differentiation 3 immunoreactivity, and their association with prognosis in 90 cats. J Vet Intern Med. 12:349–354. Vail DM, Withrow SJ. 2007. Feline Lymphoma and Leukemia. In SJ Withrow, DM Vail, eds., Small Animal Clinical Oncology, 4th ed., pp. 773–756. Philadelphia: Elsevier Saunders.
CHAPTER 35
Chlamydophila Infection Teija Kaarina Viita-aho
Overview Chlamydophila felis (formerly known as Chlamydia psittaci var. felis) is an intracellular gram-negative bacterium. It causes mainly ocular infections but also upper respiratory tract infections in cats. Serological studies suggest that multiple strains of C. felis exist, which may differ in virulence. The organism is relatively unstable outside the body. It survives less than 48 hours at room temperature, and it is easily inactivated with lipid solvents and detergents. The prevalence of C. felis infection is highest in cats aged 5 weeks to 9 months, and it is most common in multicat environments where the cats are in close contact, particularly in breeding catteries and animal shelters. In one study, males and Birman cats were predisposed to infection. About 5 to 10% of unvaccinated cats have antibodies against C. felis. The prevalence of C. felis in cats with ocular or upper respiratory tract infection ranges from 11 to 32%. In clinically healthy cats, the prevalence of C. felis is reported to be up to 13%. Cats can be asymptomatic carriers of the infection, but as a result of stress or immunosuppression, the latent infection can be reactivated and clinical signs develop. Transmission of infection requires close contact with infected cats and their aerosols, but the infection may also be transmitted via fomites. Ocular secretion is probably the most important body fluid for infection. Conjunctival shedding usually ceases at around 60 days after infection, but cats with persistent infections may excrete the infectious agent for up to 8 months. C. felis may occur simultaneously with other upper respiratory tract pathogens, such as the feline herpesvirus (FHV-1) and feline calicivirus (FCV). Both Mycoplasma felis and Bordetella bronchiseptica can complicate C. felis infection. Chlamydophila felis is not solely an ocular and respiratory tract pathogen. Instead, it may become systemic. It has been isolated from the rectum and vagina of cats. Therefore, intestinal and reproductive tracts are suggested to be sites of persistent infection. Following an infection, immunity is generally weak and short in duration. There is age-related resistance of cats to C. felis infection suggesting that some form of protective immunity eventually develops. Cats are susceptible to recurrent infections within the first 1 to 2 years of life. Cats older than 2 years are much more resistant to recurrent disease. Recurrent infections are rarely as severe as the primary infection and usually last no longer than 5 to 10 days. Recurrent disease can be due to reactivation of a persistent asymptomatic infection or from reinfection. Clinical disease most commonly occurs in cats less than 1 year old and in cats kept in colonies. The incubation time is 2 to 5 days. The course of primary disease is 2 to 6 weeks in kittens and 2 weeks or less in older cats. Ocular signs predominate; respiratory signs beyond mild rhinitis and sneezing are minimal. Cats with respiratory signs but no ocular signs are very unlikely to have C. felis infection. Table 35-1 lists the clinical signs associated with Chlamydophila felis infection. Ocular signs usually start in one eye and appear in the second eye 5 to 7 days later. See Figure 35-1. Ocular discharge is initially watery but becomes mucoid or mucopurulent later. Transient fever, inappetence,
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
TABLE 35-1: Clinical Signs of Chlamydophila Infections Ocular Signs
Nonocular Signs
Conjunctivitis Conjunctival congestion Chemosis Blepharospasm Third eyelid prolapse Hyperemia of third eyelids Ocular discharge Ocular discomfort Eyelid swelling Conjunctival follicles
Rhinitis and Nasal Discharge Sneezing Lymphadenopathy Depression or lethargy Transient fever Inappetence Weight loss
Figure 35-1 In the early stages of disease one eye is often affected. The ocular discharge is initially watery but becomes mucoid or mucopurulent later. Photo courtesy of Dr. Gary D. Norsworthy.
and weight loss may occur shortly after infection, although usually cats remain well and continue to eat. In chronic infection clinical signs can persist for more than 2 months. Chronic infection usually shows mild signs in one or both eyes including conjunctival hyperemia, serous ocular discharge, and mild blepharospasm. Lameness has been reported to occur in some cats a couple of weeks after the onset of ocular signs. C. felis has also been associated with reproductive diseases such as abortion, infertility, and neonatal mortality. It can infect neonates and cause conjunctivitis that develops behind the closed eyelids. The first noticeable sign of conjunctivitis in neonates is a delay in opening the eyelids at the normal age of seven to ten days. Bulging of the closed eyelids is often seen and is due to accumulation of exudate. Affected kittens appear otherwise normal and grow at a normal rate. Other organisms causing sneezing, rhinitis, and conjunctivitis include FHV-1, FCV, and Mycoplasma felis. As Chlamydophila felis is primarily
81
SECTION 1: Diseases and Conditions
a conjunctival pathogen, it is highly unlikely that C. felis is the primary pathogen in the presence of upper respiratory tract signs without conjunctivitis. Keratitis and corneal ulcerations are not generally associated with C. felis but are commonly seen in FHV-1 infection. Oral ulcers are typical for FCV infection. Diagnosis cannot be confirmed based on clinical signs only; diagnostic tests are required.
Diagnosis Primary Diagnostics • Polymerase Chain Reaction (PCR) Testing: Many laboratories offer a PCR test for diagnosis of C. felis. PCR is rapid, and it has good sensitivity and specificity. Samples are collected from the conjunctival sac using cotton swabs. Because the organism is intracellular, good swabbing technique is important to obtain sufficient number of cells. In cats with obvious conjunctivitis, swabbing of the affected eye should be sufficient, but in more chronic cases and with mild clinical signs swabbing of both eyes is preferred.
Secondary Diagnostics • Bacterial Isolation: Cell culture has previously been widely used for diagnosis, but because it is technically demanding, time consuming, and expensive its use has decreased because of PCR testing. • Serology: Antibody detection in unvaccinated cats can confirm the diagnosis. Low titers are generally considered to be negative. Active or recent infections are often associated with relatively high titres. Serology has the disadvantage of indicating exposure to an organism rather than whether an active infection is still present.
Diagnostic Notes • Conjunctival Smears: Examination of Giemsa-stained conjunctival smears for C. felis inclusions is possible but no longer recommended as a reliable means of diagnosis. Intracytoplasmic inclusions may be seen during the first few days of an acute infection but are unlikely to be found in chronic cases. Additionally, C. felis inclusion bodies are easily confused with other basophilic inclusions.
Treatment Primary Therapeutics • Doxycycline: This is the drug of choice (5 mg/kg q12h PO or 10 mg/ kg q24h PO for 4 weeks). Doxycycline reaches high local concentrations in tears and saliva, and response is rapid. Doxycycline has been reported to cause esophageal strictures and esophagitis. To minimize the risk, doxycycline suspension is preferred over tablets. Alternatively, water should be syringed into the cat’s mouth or the tablet lubricated with butter or similar. Doxycycline, as other tetracyclines, may cause discoloration of teeth if used in pregnant queens or young kittens. Nevertheless, doxycycline is safer than other tetracyclines. Doxycycline has been used in kittens of 4 to 5 months of age without problems.
Secondary Therapeutics • Clavulanic Acid-Potentiated Amoxicillin: It can be safely used in young kittens and pregnant queens (20 mg/kg q12h PO for 4 weeks).
82
However, another course of treatment with doxycycline may be needed later to ensure that the organism is eliminated from the body. • Fluoroquinolones: This group of drugs are also effective. They have been used successfully in humans against C. trachomantis and C. psittaci infections. Enrofloxacin is dosed at 5 mg/kg q24h PO. Overdosing should be avoided because enrofloxacin may cause blindness if higher doses are used. In contrast to dogs, cats treated with enrofloxacin are not predisposed to developing chondrotoxic side effects. Marbofloxacin has not shown to have adverse ophthalmic effects. It is dosed at 2.75 to 5.55 mg/kg q24h PO. • Azithromycin: It has also been used to treat C. felis infections. However, it may not clear the infection. Its advantage is a longer half-life and, therefore, less frequent administration. Different dose regimens have been used including 5 mg/kg q24h PO for 5 days followed by 5 mg/kg q72h PO for 5 doses or 10 mg/kg q24h for 3 days followed by 10 mg/kg q48h for 3 to 4 weeks. • Topical antibiotic ointments or artificial tear supplements provide lubrication and surface protection to the eye and may relieve discomfort of the eyes.
Therapeutic Notes • Topical therapy alone is not effective due to the systemic nature of C. felis infections in cats. Systemic therapy is required to eliminate the organism from the body. • All the cats in the household should be treated simultaneously due to the high rate of asymptomatic carriers. • Infected cats receiving doxycycline continue shedding the bacterium as long as 10 days after initiation of treatment. Therefore, they are risk for other cats almost for two weeks of treatment. • For catteries a minimum of eight weeks of treatment has been suggested.
Prevention Vaccines for C. felis are available, but because the disease is not considered to be severe, it is not considered a core vaccine. However, it should be considered for cats at risk for infection such as cats living in shelters and catteries with endemic C. felis. In those situations, all cats should be treated with doxycycline for four weeks before vaccination. • Both modified-live vaccine and inactivated cell culture vaccines are used. Vaccination generally begins at 8 to 10 weeks of age, with a second injection 3 to 4 weeks later, followed by boosters annually. C. felis vaccines have been associated with adverse reactions in some cats consisting of fever, lethargy, anorexia, and lameness 7 to 21 days after vaccination.
Suggested Readings Gruffydd-Jones T, Addie D, Belák S, et al. 2009. Chlamydophila felis infection ABCD guidelines on prevention and management. J Fel Med Surg. 11:605–609. Sparkes AH, Caney SMA, Sturgess CP, et al. 1999. The clinical efficacy of topical and systemic therapy for the treatment of feline ocular chlamydiosis. J Fel Med Surg. 1:31–35. Sykes JE, 2005. Feline Chlamydiosis. Clin Tech Small Anim Pract. 20: 129–134. Sturgess CP, Gruffydd-Jones TJ, Harbour DA, et al. 2001. Controlled study of the efficacy of clavulanic acid-potentiated amoxicillin in the treatment of Chlamydia psittaci in cats. Vet Record. 149:73–76.
CHAPTER 36
Chylothorax Gary D. Norsworthy
Overview Chyle is transported through the lymphatic system to the cysterna chili from which it travels through the thoracic duct, which terminates at the lymphaticovenous junction, and then into vascular circulation. Rupture or leakage from thoracic drainage results in accumulation of chylous fluid in the pleural space creating chylothorax. Chylothorax may be trauma related, but this accounts for only a small percentage of feline cases. Most cases of feline chylothorax have no identifiable cause and, after a complete diagnostic evaluation, are deemed idiopathic in origin. The remainder of cases is associated with either mechanical or functional (relative) obstruction of the cranial vena cava or the thoracic duct itself. Lymphatic hypertension develops as a consequence of the obstruction, allowing the lymphatic vessels to become dilated and tortuous (lymphangiectasia). Therefore, chyle is able to exude from enlarged but intact lymphatics. In some cases, increased lymphatic flow or volume may be contributory. Initially, the chylous effusion is reabsorbed through the pleura; however, it is a pleural irritant. After a few days to weeks of exposure to chyle, the pleural surfaces no longer permit reabsorption, and the effusion collects in the pleural space. The most common underlying causes are right-sided heart failure (i.e., heartworm disease, pericardial effusion, and cardiomyopathy) and mediastinal masses (especially lymphoma, but also fungal granulomas and thymoma). It has also been documented secondary to an indwelling jugular catheter. Cats with chylothorax are usually presented with a reported sudden onset of dyspnea. They are lethargic, often anorectic, and may cough. Coughing is notable as there are only a few diseases that cause coughing in cats. They are usually reluctant to lie in lateral or dorsal recumbency. Heart sounds are typically muffled.
• Thoracentesis: A few milliliters of fluid may be removed to confirm the presence of pleural effusion and to obtain fluid for laboratory analysis. • Pleural Fluid Analysis: The fluid is usually milky white in color; if hemorrhage has occurred, it may be pink. Color and clarity of the fluid is affected by nutritional status. Pleural fluid of anorectic cats may lack the characteristic milky opalescence of chyle. The nucleated cell count is typically less than 10,000 cells/mL. The protein content is unreliable due to interference of the refractive index by the high lipid content of the fluid. Fluid should be placed in red top and purple top blood tubes for these tests. See Chapter 288. • Pleural Fluid Cytology: Cells may be more than 80% small mature lymphocytes, having approximately the same diameter as erythrocytes. See Figure 36-1 and Chapter 288. If the disease is chronic, there will be a large number of non-degenerate neutrophils and macrophages. Bacteria are absent unless a secondary bacterial infection exists; this is usually the result of thoracocentesis without proper sterile technique. • Pleural Fluid Chemistry: Chylous fluid has higher triglyceride content than serum and lower cholesterol level than serum. Pseudochylous fluid has greater cholesterol content than serum and a triglyceride content less than or equal to serum. Though mentioned in the literature, it is likely that pseudochylous fluid may not exist in the cat; therefore, any milky white pleural effusion should be considered chylous until proven otherwise. • Heartworm Tests: A positive antibody test is suggestive of heartworm infection, and a positive antigen test is confirmatory. However, heartworm antigen and antibody tests have relatively low sensitivities. See Chapter 88.
Diagnosis Primary Diagnostics • Clinical Signs: Dyspnea with systemic signs will occur. Coughing may also occur. Affected cats typically demonstrate forced inspiration with delayed expiration, as though they are holding their breath. • Auscultation: Muffled heart and lung sounds are found. • Radiography: Radiographic signs of pleural effusion include visualization of pleural fissure lines and scalloping of the lung borders. Atelectic lung lobes should not be mistaken for a thoracic mass. Radiographs are most meaningful following thoracentesis. Note the caudal pulmonary arteries as an indication of heartworm disease and observe for an anterior mediastinal mass. Note the presence of rounded lung lobes as an indication of fibrosing pleuritis. • Ultrasound: This should be performed before fluid is removed from the pleural space if the cat’s respiratory status permits. It may be helpful in establishing the presence of an anterior mediastinal mass or detecting pericardial or cardiac disease. Occasionally, heartworms can be visualized in the right side of the heart or in the pulmonary trunk.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 36-1 Small lymphocytes (dark cells), having about the same diameter as erythrocytes (light cells), are the predominant cell in chylous fluid. The presence of neutrophils indicates chronicity. Bacteria should be absent.
83
SECTION 1: Diseases and Conditions
Secondary Diagnostics • Complete Blood Count (CBC) and Serum Chemistries: These are usually normal, although anemia of chronic disease and lymphopenia would not be unexpected findings. • Aerobic and Anaerobic Cultures: Although most chylous fluids are sterile, some have had growth on cultures, and infection may be introduced by poor thoracentesis technique.
Diagnostic Notes • Dyspneic cats should be handled carefully because increased stress may be fatal. Extreme care should be taken when doing the physical examination, radiographs, and thoracentesis. It may be necessary to place the cat in an oxygen cage for several minutes prior to diagnostics and between diagnostic procedures. If that is not successful, thoracentesis of 30 to 90 mL can greatly improve ventilatory capacity. The least stressful radiographic view is usually the dorsoventral view; it may be the only view that is practical in some cases and is usually sufficient to diagnose the presence of pleural effusion. In some cats, the lateral view is better tolerated. • Chyle is irritating to the pleura. When chronic, chylothorax causes fibrosing pleuritis, a thickening of the pleura by fibrous connective tissue (FCT). Sheets of FCT form between the thoracic organs. Radiographs will reveal rounded or collapsed lung lobes, and degenerate neutrophils and macrophages will be present in the effusion. See Figure 36-2. Ventilation will be compromised because the lung capacity is reduced. If chylothorax is resolved, the resulting reduced pulmonary volume may be well tolerated by indoor-only cats. Fibrosing pleuritis can also be caused by pyothorax and feline infectious peritonitis.
Treatment Primary Therapeutics • Thoracentesis: The least amount of sedation should be employed. Aspirate both sides of the chest because pockets of fluid form as fibrosing pleuritis occurs. Remove as much fluid as possible. Aspirate below the costochondral junction in multiple locations beginning at
the fourth to sixth intercostal space with the cat in ventral recumbency. Repeat as needed. • Rutin: This drug is in the benzopyrone family and is a bioflavanoid and derivative of vitamin C. It and appears that at least 25% of cats with chylothorax will have resolution of the effusion after two months of treatment. It is dosed at 50 to 100 mg/kg q8h PO and is available as 500-mg tablets that are tasteless. They may be crushed and mixed in food. • Octreotide (Sandostatin™): This naturally-occurring substance that inhibits gastric, pancreatic, and biliary secretions and prolongs gastrointestinal transit time. It is dosed at 10 µg/kg q8h SC for 2 to 3 weeks and may resolve the pleural fluid.
Secondary Therapeutics • Thoracostomy Tube: This permits continuous or intermittent chest drainage without the repeated stress of restraint and the pain of needle placement into the chest during thoracentesis. Generally, one tube will drain both sides of the chest; however, some cases require bilateral tube placement. The chest should be aspirated q12 to 24h until less than 1 to 2 mL/kg per day of fluid is removed. (This amount usually is due to the presence of the tube.) Some authorities discourage the use of thoracostomy tubes; the author prefers their use to reduce the trauma of repeated thoracentesis and because they seem to achieve better drainage in the presence of fibrosing pleuritis. • Intravenous Fluids: Placement of an intravenous catheter and fluid administration should be delayed until thoracentesis has been performed because of the stress involved. • Thoracotomy: Cats that do not respond to 1 to 2 months of chest drainage and medical management are candidates for surgical ligation of the thoracic duct or pleuroperitoneal or pleurovenous shunts and pericardectomy. The latter is recommended because thickening of the pericardium may prevent formation of lymphaticovenous communications. Success is reported to be 25 to 50%. • Rutin can be used alone when finances prohibit more conventional forms of therapy. However, it has no efficacy in resolving fibrosing pleuritis.
Therapeutic Notes • Fat binders, such as chitin and chitosan, have been proposed to decrease fat-induced chyle flow. Efficacy is unproved. • Low-fat diets and medium chain triglycerides (MCT) have been used in an attempt to reduce chyle formation. The former has some efficacy, and its use is justified. The efficacy of MCT oil has come into question, and it is no longer recommended. Most cats reject food with MCT oil because of the bitter taste.
Prognosis This is a serious and potentially fatal disease. However, with aggressive diagnostics and therapeutics many of these cats will recover as long as (a) an underlying cause can be identified and treated, (b) the idiopathic form resolves with appropriate supportive care, and (c) fibrosing pleuritis has not occurred. The presence of fibrosing pleuritis reduces the chance for a good outcome.
Suggested Readings
Figure 36-2 Rounded lung lobes, as seen in this dorsoventral thoracic radiograph, are characteristic of fibrosing pleuritis.
84
Fossum TW. 2006. Chylothorax. In JR August, ed., Consultations in Feline Internal Medicine, 5th ed., pp. 369–375. St. Louis: Elsevier Saunders. Fossum TW. 2007. Chylothorax. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 250–251. Ames, IA: Blackwell Publishing. Mason, RA. 2006. The cat with hydrothorax. In J Rand, ed., Problem-Based Feline Medicine, pp. 71–89. Philadelphia: Elsevier Saunders.
CHAPTER 37
Cobalamin Deficiency Jörg M. Steiner
Overview Cobalamin (vitamin B12) is a water-soluble vitamin that is plentiful in most commercial feline diets. Ultimately, cobalamin is of bacterial origin, but in animals with a high count of bacterial organisms in the proximal gastrointestinal tract (e.g., cows) bacterial cobalamin is absorbed and stored in the body. In contrast, in cats the load of bacterial organisms is quite low in the proximal gastrointestinal tract, and cobalamin must be supplied through meat-based protein. Dietary cobalamin is tightly bound to dietary protein and cannot be absorbed in this form. In the stomach, dietary protein is digested by pepsin and hydrochloric acid, and cobalamin is released. Free cobalamin is immediately bound by the so-called R protein (also known as haptocorrin), which is mostly secreted in gastric secretions and saliva. Cobalamin bound to R-protein is also not available for absorption. In the small intestine, R-protein is digested by pancreatic proteases, and the released cobalamin is bound by intrinsic factor. It has been estimated that in cats, 99% of intrinsic factor is secreted by the exocrine pancreas. This is different from humans, where most intrinsic factor is secreted by the stomach. Intrinsic factor-cobalamin complexes are absorbed by specific receptors in the ileum (also known as cubilin). Distal small intestinal disease, if severe, leads to destruction of cobalamin receptors in the ileum and can thus be associated with cobalamin malabsorption. If cobalamin malabsorption occurs for a long time, cobalamin stores are depleted and cobalamin deficiency ensues. In one study 49/80 cats with clinical signs of chronic gastrointestinal disease were shown to have a decreased serum cobalamin concentration. Also, these cats were shown to have a much shorter half-life for cobalamin compared to normal cats. Diffuse small intestinal disease also can lead to cobalamin malabsorption as long as the ileum is involved in the disease process. Finally, exocrine pancreatic insufficiency almost invariably leads to cobalamin deficiency in cats because most of the intrinsic factor is synthesized by the exocrine pancreas in this species. Cobalamin malabsorption in itself does not lead to cobalamin deficiency. Only if cobalamin malabsorption is long-standing are cobalamin stores of the body being depleted, ultimately leading to cobalamin deficiency. Cobalamin is essential for several crucial biochemical reactions, related to the generation of energy, metabolism of fatty acids and amino acids, protein-synthesis, and cell division. Virtually all tissues need cobalamin for proper function. Thus clinical signs of cobalamin deficiency can vary. Some cats may just show lethargy, anorexia, and weight loss, whereas others may show diarrhea, intermittent septic episodes, or even severe neurological signs, resembling those of hepatic encephalopathy. Experimentally induced cobalamin deficiency in cats leads to progressive anorexia, weight loss, and an unkempt hair coat. Pica has been reported in some cats. Additionally, humans with cobalamin deficiency have been shown to develop intestinal abnormalities, such as villous atrophy, infiltration of the intestinal mucosa with inflammatory cells, further cobalamin malabsorption, and malabsorption of other nutrients. Similar gastrointestinal signs have not been proven in cats with cobalamin deficiency, but the author believes that there is strong evidence that they do occur. Cats with small intestinal disease or exo-
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
crine pancreatic insufficiency and concurrent cobalamin deficiency may not appropriately respond to therapy unless they are supplemented with cobalamin.
Diagnosis Primary Diagnostics • Serum Cobalamin Concentration: Measurement of serum cobalamin concentration is diagnostic for cobalamin deficiency in most cases. The current reference range for serum cobalamin concentration used by the GI Lab at Texas A&M University is 290-1,500 ng/L. An undetectable serum cobalamin concentration is clear evidence of cobalamin deficiency. However, cats with detectable but subnormal or low-normal serum cobalamin concentrations may be cobalamin deficient and should be preemptively supplemented with cobalamin to avoid further complications.
Secondary Diagnostics • Serum or Urinary Methylmalonic Acid Concentration: Ultimately, cobalamin concentrations on a cellular level determine whether cobalamin deficiency is present. Serum or urinary methylmalonic acid concentrations are indicators of metabolic derangements due to cobalamin deficiency on the cellular level. Unfortunately, the measurement of methylmalonic acid in serum or urine requires sophisticated technology and is currently not feasible for routine testing.
Diagnostic Notes • In a recent study, 49 of 80 cats with clinical signs of chronic gastrointestinal disease had a decreased serum cobalamin concentration. Also, cats with exocrine pancreatic insufficiency (EPI) commonly have cobalamin deficiency. This underscores the importance of evaluating cats with hypocobalaminemia for evidence of EPI or gastrointestinal disease, especially if they do not respond to parenteral cobalamin supplementation alone. Conversely, serum cobalamin concentration should be measured in every cat with clinical signs of chronic gastrointestinal disease.
Treatment Primary Therapeutics • Cobalamin Supplementation: Cobalamin supplementation is the mainstay of therapy for cobalamin deficiency. As cobalamin deficiency leads to clinical signs of chronic gastrointestinal disease and further cobalamin malabsorption, a vicious cycle can ensue that maintains cobalamin deficiency even if the primary cause of the gastrointestinal disease has subsided. Thus, if the cat does not have EPI (i.e., serum feline trypsin-like immunoreactivity [fTLI] concentration >12 µg/L), cobalamin supplementation alone or together with a dietary trial is a rational first approach for cats with cobalamin deficiency. Depending on the size of the cat 100 to 250 µg/cat of cobalamin (most commonly cyanocobalamin) are injected subcutaneously q7d for 6 weeks, followed by 100 to 250 µg/
85
SECTION 1: Diseases and Conditions
cat q14d SC for 6 weeks, and another injection of the same dose four weeks later. Serum cobalamin concentration should be rechecked 4 weeks after the last dose of cobalamin to evaluate the patient’s need for further cobalamin supplementation.
Prognosis
Therapeutic Notes
The overall prognosis for cats with cobalamin deficiency is dependent on the underlying cause. However, once cobalamin deficiency has been diagnosed and appropriately addressed therapeutically, cobalamin deficiency does not continue to contribute to the overall morbidity and mortality of the patient.
• If the cat does not respond to cobalamin supplementation alone, it is crucial to carefully evaluate the patient for the underlying cause for the cobalamin deficiency. This involves evaluation of the cat for chronic small intestinal disease and may include fecal examination for intestinal parasites and treatment with a broadspectrum anthelmintic agent, feeding trials, abdominal ultrasound, endoscopic or surgical biopsy with histopathological evaluation, and other diagnostic tests that may be deemed necessary in a specific case. Then, the underlying cause of the cobalamin deficiency can be addressed therapeutically in addition to cobalamin supplementation. • It has also been speculated that cobalamin may have a direct pharmacologic effect on appetite. Many cats with cobalamin deficiency have a poor appetite and start eating well after cobalamin supplementation has been instituted. In some of these patients the poor appetite recurs as soon as cobalamin supplementation is discontinued even though serum cobalamin concentration may be well within the reference range. In these patients cobalamin supplementation should resume and may need to be continued long term.
Ruaux CG, Steiner JM, Williams DA. 2001. Metabolism of amino acids in cats with severe cobalamin deficiency. Am J Vet Res. 62:1852–1858. Ruaux CG, Steiner JM, Williams DA. 2005. Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia. J Vet Int Med. 19:155–160. Ruaux CG, Steiner JM, Williams DA. 2009. Relationships between low serum cobalamin concentrations and methlymalonic acidemia in cats. J Vet Int Med. 23:472–475. Simpson KW, Fyfe J, Cornetta A, et al. 2001. Subnormal concentrations of serum cobalamin (Vitamin B12) in cats with gastrointestinal disease. J Vet Int Med. 15:26–32. Thompson KA, Parnell NK, Hohenhaus AE, et al. 2009. Feline exocrine pancreatic insufficiency: 16 cases (1992–2007). J Fel Med Surg. 11(12): 935–940.
86
Suggested Readings
CHAPTER 38
Coccidioidomycosis Sharon Fooshee Grace
Overview Of all the deep (systemic) mycotic agents, Coccidioides has the most limited geographic distribution. Cats and dogs are infrequently infected outside the endemic areas of the dry, southwestern United States, Mexico, and Central and South America. This ecologic niche, the Lower Sonoran life zone, is well suited to support growth of the organism. C. immitis is found in the San Joaquin Valley, whereas C. posadasii is found in other areas. Endemic areas are characterized by sandy alkaline soil, low annual rainfall, and high summer temperatures. During periods of high temperature and scant rainfall, the organism survives below the soil surface. When a period of heavy rainfall follows such a dry spell, the organism replicates in the upper soil surface and sporulates, and the infective arthrospores are dispersed through the environment by wind or any activity that creates dust. Increased numbers of human cases have occurred in endemic areas following dust storms and earthquakes. Cats appear relatively immune to the disease as compared to dogs, though cats are often more debilitated than dogs at the time of initial presentation. Although only a limited number of cases have been described in cats, the primary route of infection appears to be inhalation of airborne arthrospores, as occurs in other species. Infection of cats by direct inoculation of the organism has been rarely reported. Dissemination occurs through hematogenous and lymphatic routes. A competent cellmediated immune response must be present to contain infection. Infection with the feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) does not appear to predispose cats to coccidioidomycosis. Traditionally, it has been considered that humans are not at risk for the disease from contact with infected cats but that they may become infected because of shared environmental exposure. A recent report described an unusual case of direct transmission of the disease from a cat to a human via a bite wound. This case represents an uncommon scenario for disease transmission. The incubation period from inhalation of the organism until respiratory signs appear is presumed to be a few weeks, as it is in dogs. Nonspecific signs of fever, anorexia, and weight loss are common. Dermatologic abnormalities, such as draining tracts and abscesses, with regional lymphadenopathy are the most common findings in infected cats. Though the lungs are often subclinically involved, overt lower respiratory signs (i.e., coughing or dyspnea) are not frequently observed. Ocular inflammation and lameness due to bone involvement have been reported. Pericardial infection was seen at necropsy in 26% of infected cats in one study, although there were no antemortem signs of heart disease. Hyperesthesia, seizures, behavior changes, and ataxia are reported but nervous system involvement appears uncommon.
Diagnosis Primary Diagnostics • Clinical Signs: Clinical signs are non-specific; however, cats from the endemic area with signs of systemic disease should be suspected of being infected.
• Cytology: This disease typically has low numbers of organisms in lesions, making cytological diagnosis a challenge. Negative findings do not rule out the disease, but visualization of organisms will confirm it. Samples may be obtained by aspiration of cutaneous nodules, lung parenchyma, or lymph nodes; performing impression smears from draining tracts; or by making slides from bronchioalveolar lavage specimens, though airway washing is considered a lowyield procedure. See Chapter 289. The associated inflammatory response is usually pyogranulomatous. Routine in-office stains will sometimes fail to stain the organism. The organism is basophilic and has a thick cell wall which shrinks during fixation, giving it a folded appearance. • Histopathology: Histological identification of organisms confirms infection. Routine hematoxylin and eosin stains may detect the organism, but special stains will sometimes be needed. GrocottGomori methenamine silver and periodic acid-Schiff (PAS) stains are often useful. The pathologist should be alerted when coccidioidomycosis is a differential diagnosis.
Secondary Diagnostics • Minimum Data Base: The minimum data base will not provide a diagnosis but is useful as a general health screen for the patient. Nonregenerative anemia and hyperproteinemia have been reported in a number of cases. • Radiography: Hilar lymphadenopathy, interstitial lung disease, and pleural disease may be present. See Figure 291-39. Hilar lymphadenopathy appears to be a useful indicator of canine disease in endemic areas, but this relationship has not been established for cats. Bone lesions are infrequent but are a mixture of osteoproductive and osteolytic lesions. • Serologic Testing: Though experience with serologic testing in cats is limited, there is increasing evidence that serology is more valuable than previously thought. Precipitin antibodies and complement-fixing antibodies were present in most infected cats tested in one study, and both persisted for a long period of time. Although further evaluation is needed to assess the usefulness of serologic testing, at present, seropositivity does seem to correlate well with the disease in cats. However, serology is a questionable tool for detecting progression of disease and response to therapy.
Diagnostic Notes • The organism is not always present in large numbers so cytological identification sometimes requires an extended microscopic search. • A thorough travel history should be obtained for any sick cat. • Culture should not be attempted in clinic. Infectious arthroconidia are easily aerosolized, placing personnel at risk. In endemic areas, a veterinary diagnostic lab should be contacted before culturing material from any draining lesion.
Treatment Primary Therapeutics
th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Azole drugs: Itraconazole and fluconazole have both been used to treat the disease. Itraconazole is safely dosed at 5 mg/kg q12h PO
87
SECTION 1: Diseases and Conditions
and should be given with a meal; an acid environment in the stomach enhances absorption of the drug. The capsule may be opened and the contents divided into gelatin capsules or mixed into canned food. An oral solution is available and has greater bioavailability than the capsule. Itraconazole becomes concentrated in the skin and may be especially useful for cutaneous involvement. Fluconazole has the added benefit of superior penetration into the CNS and eye and is now available in relatively inexpensive generic form. Several dosing protocols are published with a recent review article suggesting 25 to 50 mg/cat q12-24h PO. Unlike itraconazole, fluconazole does not need to be administered with food for enhanced absorption.
• Recovery confers lifelong immunity in people, but it is unknown whether recovered animals have the same ability. • Although itraconazole is usually well tolerated, serum chemistries should be periodically checked during therapy to assess for hepatotoxicity. For cats with clinical evidence of hepatotoxicity (i.e., anorexia, jaundice), the drug should be discontinued, at least temporarily. Asymptomatic cats with increased liver enzymes do not necessarily need cessation of therapy but should be closely monitored.
Prognosis The long-term prognosis for cats with coccidioidomycosis is guarded.
Secondary Therapeutics • The imidazole drugs are considered fungistatic, not fungicidal. Treatment duration should be long term (i.e., 2 months past resolution of clinical signs). • Amphotericin B is an alternative treatment if the cat does not respond to itraconazole or fluconazole. A subcutaneous protocol has become available for administration of amphotericin B; this protocol appears to significantly reduce the nephrotoxic potential of the drug. See Chapter 43 for the protocol. • At diagnosis, many cats are debilitated due to prolonged anorexia. Placement of a feeding tube permits the owner to administer proper nutritional support.
Therapeutic Notes • Relapse is fairly common following cessation of therapy, even with long-term therapy.
88
Suggested Readings Gaidici A, Saubolle MA. 2009. Transmission of coccidioidomycosis to a human via a cat bite. J Clin Microbiol. 47(2):505–506. Graupmann-Kuzma A, Valentine B, Shubitz LF, et al. 2008. Coccidioidomycosis in dogs and cats: A Review. J Am Anim Hosp Assoc. 44(5):226–235. Greene RT, Troy GC. 1995. Coccidioidomycosis in 48 cats: A retrospective study (1984–1993). J Vet Intern Med. 9(2):86–91. Shubitz LF. 2007. Comparative aspects of coccidioidomycosis in animals and humans. Ann NY Acac Sci. 111(10):395–403.
CHAPTER 39
Coccidiosis Mark Robson and Mitchell A. Crystal
Overview Coccidia are obligate intracellular parasites usually found in the small intestine. There are several genera of coccidia that infect cats, most commonly Isospora (see Table 39-1; for information regarding Toxoplasma gondii, refer to Chapter 214; for information regarding Cryptosporidium spp., refer to Chapter 44). Coccidia are acquired via ingestion of monozoic cysts in intermediate host tissue or sporulated oocysts from infected feces. There is generally no extra-intestinal involvement in the cat, and transplacental and transmammary infection does not occur. Cats are the definitive host for Isospora felis and Isospora rivolta, and infection with these species rarely causes disease. Kittens younger than 1 month old, and cats that are stressed, immunosuppressed, or in crowded (e.g., catteries) or unsanitary conditions are at a higher risk of developing clinical signs. Physical examination may be normal or reveal evidence of diarrhea, hematochezia, weight loss, and dehydration. Death may occur in severely affected animals. Cats are also the definitive host for Hammondia hammondi, Besnoitia wallacei, B. darlingi, and B. oryctofelisi. Cats become infected from ingesting tissue cysts in the intermediate host, commonly rodents. Infection is generally limited to the gastrointestinal tract; however, Besnoitia may be found in extra-intestinal organs. These species are considered to be non-pathogenic. Cats are an intermediate host for Sarcocystis neurona of which the definitive host is the opossum. Infection is acquired by direct ingestion of sporocysts shed in opossum feces. S. neurona can cause a fatal encephalomyelitis in kittens, although limited studies have found serum antibodies in 5% of domestic and 13% of feral cats indicating that exposure is not uncommon. Many other Sarcocystis spp. have been identified in the intestinal tract of cats and, rarely, skeletal and cardiac muscle; however, these species appear to be non-pathogenic.
Diagnosis
Figure 39-1 Coccidiosis: The top image is an oocyst of Isospora felis. The bottom image is a sporulated oocyst. Both were found in a fecal flotation and measure approximately 40 µm longitudinally. For comparison, Toxicara cati (ascarid) eggs are about 75 µm in diameter.
Primary Diagnostics
• Histopathology and Immunohistochemistry: S. neurona schizonts and merozoites can be seen in the brain and spinal cord.
• Fecal Flotation: Oocysts are seen on microscopic examination (51% false-negatives without centrifugation, 6% false-negatives with centrifugation). See Figure 39-1.
Secondary Diagnostics
TABLE 39-1: Coccidia Found in the Cat Coccidia Organism
Intermediate Host
Besnoitia spp. Cryptosporidium spp. Hammondia hammondi Isospora felis, Isospora rivolta Sarcocystis spp. Toxoplasma gondii
Rodents, opossum, rabbits, and lizards None Goats and rodents Various mammals Cat and various mammals Various mammals
• Direct Saline Smear: Oocysts are sometimes seen on microscopic examination (95% false-negatives).
Diagnostic Notes • Oocysts found in a cat without diarrhea are most likely an incidental finding. • Oocysts in an immunocompetent cat with diarrhea may be an incidental finding or indicate other concurrent disease. • Oocysts may be shed intermittently, so multiple fecal samples are recommended in cats with diarrhea.
Treatment Primary Therapeutics
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Trimethoprim-sulfonamide: Dose at 15 to 30 mg/kg PO for cats less than 4 kg (8.8 pounds). Dose at 30 to 60 mg/kg PO for cats greater than 4 kg (8.8 pounds). Give q24h for 6 days.
89
SECTION 1: Diseases and Conditions
• Sulfadimethoxine: Administer 50 to 60 mg/kg PO, SC once, followed by 27.5mg/kg q24h PO for 14 to 21 days. • Ponazuril: Administer 50 mg/kg q24h PO for 1 to 5 days. Repeat in 10 days if needed. This drug is extra-label for use in cats but appears to be safe in kittens. Some authors believe it is more effective than the sulfonamides. (Add 10 mL [10g] paste to 20 mL water to make a 50-mg/mL solution.)
Secondary Therapeutics • Furazolidone: Administer 8 to 20 mg/kg q24h PO for 7 to 10 days. • Toltrazuril: Administer 15 mg/kg q24h PO for 3 to 6 days. • Nitrofurazone: Available as a 4.59% soluble powder that can be added to drinking water (up to 1g/2L) for 7 days. • Amprolium: Administer 60 to 100 mg/cat q24h PO for 7 to 12 days. • Supportive Care: Fluid, electrolyte and blood product therapy may be needed if dehydration, electrolyte derangements, or anemia from gastrointestinal hemorrhage are present. Nutritional requirements should be managed.
Therapeutic Notes • Infections are often self-limiting, and therapeutic decisions should be based on clinical signs. • Recurrent or persistent infections warrant investigation of underlying disease or re-evaluation of the environment.
90
• Infections can be avoided by preventing predatory behavior, maintaining appropriate sanitation, avoiding stress/overcrowding, insect control, and cooking all meat fed to cats. • Runs, cages, and food utensils should be disinfected with 10% ammonia solution or boiling water. • Queens should preferably be treated for coccidiosis prior to parturition. • Sarcocystis-associated encephalomyelitis has only been diagnosed post-mortem; thus, treatment has never been attempted. Ponazuril has been effective in the treatment of S. encephalomyelitis in horses.
Prognosis The prognosis for coccidiosis is excellent for most infected cats. The prognosis for Sarcocystis-associated encephalomyelitis is grave.
Suggested Readings De Santis-Kerr AC, Raghavan M, Glickman NW, et al. 2006. Prevalence and risk factors for Giardia and coccidia species of pet cats in 20032004. J Fel Med Surg. 8(5):292–301. Dubey JP, Greene CE. 2006. Enteric coccidiosis. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 775–784. St. Louis: Saunders-Elsevier. Dubey JP, Higgins RJ, Barr BC, et al. 1994. Sarcocystis-associated meningoencephalomyelitis in a cat. J Diagnos Investig. 6:118–120.
CHAPTER 40
Constipation and Obstipation Sharon Fooshee Grace and Mitchell A. Crystal
Overview Constipation is defined as infrequent or difficult evacuation of hard or dry feces. It may be acute or chronic and is characterized by excessive straining to defecate in conjunction with a reduced volume of passed feces. Obstipation represents a state of intractable constipation that results from prolonged fecal retention; it is considered more refractory to therapy than constipation. There are many causes of constipation and obstipation. See Table 40-1. Both constipation and obstipation may eventually lead to development of acquired megacolon, a condition of extreme colonic dilation with colonic muscle dysfunction. See Chapter 136. Note that owners may confuse constipation and dysuria based on positioning in the litter box. The differentials for dysuria should also be considered. See Chapter 61.
TABLE 40-1: Causes of Constipation and Obstipation Environmental
Pain induced
Extraluminal colonic obstruction
Diagnosis Primary Diagnostics • History: A detailed history should record information related to defecation habits (often out of the litter box), over-the-counter or prescription medications given, recent or past trauma, tendency to eat foreign objects, propensity to engage in fights, recent weight loss or evidence of systemic illness, and changes in appetite. • Physical Examination: Careful attention should be given to inspection of the perineal area and anal sacs, as well as an assessment of neurologic status of the lumbar and sacral spinal cord. Pain upon lifting the tail, an easily expressible bladder, and poor anal tone could point to lumbosacral neurologic disease. Dysautonomia would present with signs of diffuse autonomic dysfunction (i.e., decreased lacrimation, pupillary dilation, regurgitation or vomiting, megaesophagus, or nictitans prolapse). See Chapter 58. Megacolon can usually be detected during abdominal palpation as an enlarged, firm, feces-distended colon. • Abdominal, Pelvic, and Hind Limb Radiographs: These help to confirm constipation, to assess the severity of colonic distension, and may identify predisposing factors, such as pelvic or limb fractures, luxations, or arthritis, mass lesions, rectal foreign bodies, and spinal column abnormalities and injuries. See Figures 40-1 and 1361. Megacolon is defined as a colonic diameter equal to or greater than twice the length of the body of L7. See Figures 136-2 and 292-36. Lumbosacral radiographs (with or without an epidurogram), computerized tomography (CT), or magnetic resonance imaging (MRI) may be helpful to further define neurologic disease caused by spinal column or cord abnormalities. • Minimum Data Base (Complete Blood Count [CBC], Biochemical Profile, Urinalysis): The database can give an assessment of the overall health of the cat. The CBC may suggest inflammation or infection (e.g., anal sacculitis or abscess) and may support dehydration (elevated hematocrit). The biochemical profile may reveal abnormalities that cause impaired motility (e.g., hypokalemia, hypercalcemia, evidence of dehydration, and disorders that predispose to dehydration).
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Intraluminal colonic obstruction
Neuromuscular Disease
Drugs or Medications
Metabolic and Endocrine
Lack of exercise No litter box, dirty litter box, or change of litter brand Unfamiliar environment Anorectal disease or stricture Pelvic or hind limb fractures, dislocations, arthritis, or other joint disease (i.e., torn Anterior Cruciate Ligament (ACL) and such) Perianal bite wound or abscess Rectal foreign body Neoplasia Pelvic fracture Pseudocoprostasis (i.e., extreme perineal matting of hair, usually including feces, so stool cannot pass) Atresia ani Hair, bone, plant material, or foreign body Neoplasia Perineal hernia Colonic smooth muscle disease; idiopathic megacolon Spinal cord disease: cauda equina, sacral spinal cord deformations (Manx breed), lumbosacral disease, dysautonomia, or sacral nerve disorders (i.e., tail pull injury and so on) Antacids Anticholinergics Antihistamines Barium sulfate Diuretics Narcotic analgesics Sucralfate Vincristine Dehydration Generalized muscle weakness Hypercalcemia Hypokalemia Hypothyroidism (rare) Obesity
Secondary Diagnostics • Advanced Imaging: In some cases advanced imaging (CT or MRI) of the spinal cord and vertebrae may be necessary. • Digital Rectal Examination: This can be carefully performed under general anesthesia to identify pelvic fractures, masses, perineal hernias, anal sac disease, and strictures. • Colonoscopy: Fiberoptic examination of the rectum and colon can identify polyps, masses, foreign bodies, and strictures. Colonic evacuation and preparation with oral cathartic solutions (polyethyleneglycol solutions [GoLYTELY, Colyte] at 30 mL/kg PO via orogastric or nasogastric tube 18 to 24 and 8 to 12 hours prior to colonoscopy) are needed for good visualization.
91
SECTION 1: Diseases and Conditions
Treatment Primary Therapeutics
(A)
• Fluid Therapy: Fluid therapy is essential to aid in softening the stool in dehydrated cats. Intravenous or subcutaneous administration is preferred to oral rehydration therapy. See Chapter 302. • Enemas: This is indicated as the initial step in the medical management of constipation/obstipation. This is best performed following fluid administration and with the cat under anesthesia. The enema should utilize 15 to 20 mL/kg of warm water without soap or other additives (to minimize mucosal irritation and damage). The volume delivered should be repeated several times to completely empty the colon. Manual evacuation via abdominal palpation and rectal digital manipulation should be performed in conjunction with enema administration for maximal colonic evacuation. A small amount of water-soluble lubrication will help in removing feces. In cats with mild constipation, dioctyl sodium sulfosuccinate enemas may be sufficient. • Prokinetics: Cisapride has proven beneficial in managing constipation in cats. It has been removed from the human market because of side effects but is still available through veterinary compounding pharmacies. For cats up to 10 pounds, the dose is 2.5 mg/cat q8h PO given 30 minutes before feeding. Cats heavier than 10 pounds may receive a dose up to 5 mg/cat q8h PO given 30 minutes before feeding. • Diet: Easily digestible, low-bulk diets are indicated. Supplementation with small amounts of fiber (e.g., psyllium [Vetasyl, Metamucil]) at 2.5–5 mL (1/2–1 teaspoons or 1.7–3.4 g) q12 to 24h PO with food or canned pumpkin at 2.5 to 5 mL (1–2 teaspoons) q12 to 24h PO with food may help soften the stool and stimulate defecation; however, diets high in fiber often create excessive fecal bulk and may complicate or worsen colonic distention. • Lactulose: This is an osmotic stool softener that may help in managing constipation when used in combination with cisapride. The dose is 0.5 to 1.0 ml/kg q8 to 12h PO.
Secondary Therapeutics • Subtotal Colectomy: This is an effective therapy for megacolon and should be recommended if obstipation has occurred more than two or three times despite medical and dietary management or if medical and dietary management are not possible See Chapters 136 and 249.
(B) Figure 40-1 A, This radiograph confirms constipation by the presence of segmented fecal balls in the colon. It also shows potential causes of pain when positioning to defecate. There is spondylosis at T12–T13, L1–L2, L2–L3, and L7–S1. B, A ventral-dorsal view of the pelvis and rear legs also reveals degenerative joint disease of both coxofemoral joints. Radiographic assessment of the knees should also occur because this is another source of pain to the defecating cat. Images courtesy of Dr. Gary D. Norsworthy.
Therapeutic Notes • Phosphate-containing enemas should not be used in cats. Severe hyperphosphatemia may lead to rapid development of severe hypocalcemia and seizures or death. • Enemas given too rapidly may cause nausea and vomiting. Cats receiving enemas for colon evacuation should be under anesthesia with a cuffed endotracheal tube in place.
Prognosis
• Total Thyroxin (TT4): Hypothyroidism is rare in the cat, but it has been associated with obstipation and megacolon.
Diagnostic Notes • Barium enemas are sometimes helpful in identifying mural/intraluminal masses, but colonoscopy is preferred over this technique because more information is typically achieved (i.e., direct visualization of the lesion, tissue biopsy collection for histopathology).
92
Constipation has a better prognosis than obstipation and megacolon, though typically all can be successfully managed.
Suggested Readings Jergens AE. 2007. Constipation and obstipation. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult. Canine and Feline, 4th ed., pp. 294–295. Ames, IA: Blackwell Publishing. Washabau RJ, Hasler AH. 1997. Constipation, obstipation, and megacolon. In JR August, ed., Consultations in Feline Internal Medicine, 3rd ed., pp. 104–112. Philadelphia: WB Saunders.
CHAPTER 41
Corneal Ulcer Gwen H. Sila and Harriet J. Davidson
Overview A corneal ulcer is defined as loss of epithelial tissue from the surface of the cornea due to instantaneous or progressive erosion and necrosis of the tissue. Any trauma to the corneal surface may result in ulceration. In a normal cat a simple superficial ulcer heals quickly. During the initial stage of healing epithelial cells spread and slide across the ulcer to rapidly cover the defect. The next stage is replication and maturation of these cells as the epithelial layers thicken to fill in the defect. Finally, the basement membrane is replaced completing the healing process. If the ulcer is deeper and the stroma is affected the ulcer will take longer to heal because the keratocytes of the stroma must replicate new collagen. Tears and epithelial cells are a significant barrier to infective organisms in a healthy eye. Whenever the corneal epithelium is disrupted the underlying stroma is at risk for infection by opportunistic bacteria. Stromal degradation may occur through enzymatic breakdown of the collagen fibers once the bacteria begin to colonize. The most common bacterial organisms resulting in infection are Staphylococcus spp., Streptococcus spp., Corynebacterium spp., and Pseudomonas spp. Corneal fungal infections are extremely uncommon in the cat. Sources of corneal trauma may be external to the cat or secondary to facial conformation or eyelid abnormalities. External injury may be as simple as a grass stem or weed whipped across the eye or severe injuries, such as a cat fight. Although the eyelid reflexes are normally quick, the cornea can be damaged. Entropion, distichia, trichiasis, and ectopic cilia are uncommon conditions in the cat, but they should be ruled out prior to treatment. Untreated chronic, irritating conditions will prevent a corneal ulcer from healing. Nasal folds and lagophthalmos (incomplete eyelid closure) with exposure keratitis are seen in certain brachycephalic breeds. These conditions more commonly result in conjunctivitis and keratitis rather than direct corneal ulceration. If the cat develops an ulcer from another cause, these concurrent conditions may slow healing and predispose to infection. Keratoconjunctivitis sicca may predispose the cornea to ulceration and prevent normal healing. These conditions need to be treated concurrently with the corneal ulcer. Feline herpesvirus-1 (FHV-1) is an extremely common ocular disease in cats. Cats are frequently exposed to the virus at birth. Although vaccination against herpesvirus is common, the vaccine does not produce sterilizing immunity. Therefore, infection and ocular disease may still occur in vaccinated cats. The virus has a propensity for the corneal epithelium but may replicate within the conjunctiva. The virus may become latent and establish itself within the trigeminal ganglia. After an initial corneal infection, nearly 80% of cats will have latent infections, with upward of 45% of those cats having reoccurrence of clinical disease. Cats can develop keratitis at anytime in their life cycle, but kittens and elderly cats are most likely to become symptomatic as they have a lower immune defense. Cats that are latently infected are prone to re-ulceration during the juvenile state at the onset of estrus and under stress. Stress of any type or systemic steroid administration can allow viral recrudescence resulting in development of clinical signs.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Diagnosis Primary Diagnostics • Clinical Appearance: Corneal ulceration usually causes blephrospasm, epiphora, and accompanying conjunctivitis. A transilluminator held close to the eye while looking across the corneal surface may help to establish the depth of the ulcer. The surrounding cornea should be evaluated for cellular infiltrate, marked edema, or collagenolysis (melting). Any of these findings suggests an infected cornea. Examine the entire eye including the lids, conjunctiva, and anterior chamber to ensure no other abnormalities or causative lesions are present. • Schirmer Tear Test: This is done prior to staining to insure normal tear production. • Fluorescein Stain: This is used to confirm the presence of an ulcer. The cornea should be evaluated after placement of the stain to access the size and depth of the ulcer. Ulcers with a dendritic pattern are considered pathognomonic for herpesvirus infection. See Figures 41-1 and 124-4. Herpesvirus should be suspected in any case of superficial ulcers or those that are recurrent in nature. • Laboratory Testing: Polymerase chain reaction (PCR), enzymelinked immunosorbent assay (ELISA), virus isolation, and so on may be helpful to confirm the diagnosis of FHV-1 infection; however, none of the current tests are sensitive or specific for predicting clinical disease. Due to the variability in testing, many veterinary ophthalmologists recommend treatment for cats suspected of having FHV-1 despite negative test results. See below.
Secondary Diagnostics • Bacterial Culture and Sensitivity: An aerobic swab should be collected for initially severe or complicated ulcers or ulcers that fail to respond to standard therapy. The sample should be collected from
Figure 41-1 Feline cornea: Note pale linear streaks on the corneal surface that are typical of feline herpesvirus lesions.
93
SECTION 1: Diseases and Conditions
the ulcer margin and not the conjunctiva. Care should be taken to touch only the cornea with the swab and not to rupture the eye if the ulcer is deep. • Cytology/Gram Stain: This may be used to help identify any bacteria present. • Topical Anesthetics: These can be an important aspect of the diagnostic process. However, they should not be used prior to a Schirmer Tear Test because they will alter the test results. The use of topical anesthetics can be a diagnostic tool that may provide direction on determining the etiology. Corneal pain from an external stimulus, such as a foreign body, will be greatly reduced when a topical anesthetic is applied. If the cat is significantly improved following topical anesthetic application, the eye and eyelids should be inspected for the source of corneal irritation. Corneal ulcer pain is a combination of direct simulation of the corneal nerve and the axonal reflex. Corneal nerve stimulation results in release of prostaglandins within the ciliary body. A topical anesthetic will not eliminate this intraocular inflammatory response so the eye may remain painful.
Diagnostic Notes • Prior to taking a sample for PCR testing for FHV-1 the diagnostic laboratory that will perform the test should be contacted for instructions on sample collection. A Dacron swab is usually used to sample the cornea or conjunctiva. Unvaccinated clinically normal cats may test positive for the virus and modified live FHV-1 vaccine strains can cause false-positives. Known infected cats may also test negative. • The majority of cats will have an ELISA or serum titer. A recent study found no correlation between FHV-1 disease status (i.e., acute, chronic, and asymptomatic) and magnitude of FHV-1 titer. • Sample collection is crucial to the success of virus isolation of FHV-1. The reference laboratory should be contacted prior to sample collection.
Treatment Primary Therapeutics • Ophthalmic Antibiotics: These are the most essential part of the treatment regime. If used to prevent infection, they should be administered every 6 to 8 hours. If they are being used to eliminate an infection, they should be used at a minimum of every 6 hours and may be needed as often as every 2 hours in the initial phase of treatment. Ophthalmic antibiotics include combination antibiotics (i.e., polymyxin, gramicidin, or bacitracin), tetracycline, erythromycin, gentamicin, tobramycin, ciprofloxacin, ofloxacin, and levofloxacin. Oral antibiotics do not take the place of topical medications. The use of oral antibiotics is generally only helpful if there is extensive corneal vascularization or corneal perforation. • Ophthalmic Atropine: This is used once or twice daily to control ciliary spasm due to the axonal reflex. It has the additional effect of preventing synechia (iris adhering to lens or cornea) in severe ulcers. The ointment causes less salivation than the solution because it does not travel down the tear duct and into the cat’s mouth as easily. However, in cases of imminent corneal perforation ointments should be avoided because they are toxic to the tissues within the eye. • Other Analgesics: Systemic non-steroidal anti-inflammatory medications will also aid in the reduction of pain and uveitis from the axonal reflex. Meloxicam (0.1 mg/kg q24h PO) is recommended on a short term basis (<1–2 weeks) as long as there is no underlying renal insufficiency or dehydration. • Antiviral Medications: Confirmed or suspected FHV-1 infections are best treated with some form of antiviral medication in addition to other forms of therapy.
94
• Topical ophthalmic antivirals include trifluorothymidine (Viroptic®) and idoxuridine. Initially these medications should be used q2 to 4 h; the frequency is decreased as the clinical symptoms regress. Treatment is continued for a minimum of 1 week following secession of all clinical signs. In some cases these medications may be compounded by a pharmacist. Cidofovir 0.5% is a promising antiviral for topical use in cats. A recent study showed improvement in clinical disease scores related to herpesvirus after administration of the drug every 12 hours. Due to the less frequent dosing this may be a more realistic alternative for many owners. It is currently a more expensive option than some of the older drugs; however, up to 20% of cats experience pain on application. • Oral antiviral medications include acyclovir (Zovirax®, 200 mg/cat q12h PO). Acyclovir must be used with caution because it has been reported to be hepatotoxic and bone marrow suppressive. Repeated blood tests should identify problems early. Famciclovir (Famvir®) is another oral antiviral currently in use. In vitro testing has shown it to have superior effectiveness compared to acyclovir against FHV-1. There is no documented dosage for use in cats; however, veterinary ophthalmologists use a range of dosages (31.25 mg/cat q12h PO to 125 mg/cat q24h PO). This is an empirical dosage that may need to be adjusted depending on the size of the cat. Famciclovir appears to be a safer choice than acyclovir, although there are no published reports on its long-term use. A recent study found variable absorption and serum concentrations of the drug among cats following a 62.5 mg dose given at 24-, 12-, and 8-hour intervals. This study also suggested that even at the most frequent dosage (q8h) serum levels of famciclovir do not reach levels predicted to be efficacious by in vitro testing. This is in contrast to many ophthalmologists’ clinical impression that famciclovir does improve symptoms associated with active FHV-1 infection. Careful monitoring is strongly recommended during treatment to avoid severe systemic effects. Treatment should continue for 1 week following secession of clinical signs. • L-lysine is used to prevent viral replication at 250 to 500 mg q1224h PO. L-lysine has been shown to be safe for cats, and there is in vitro evidence that it helps prevent viral replication. One study has found significantly less FHV-1 associated conjunctivitis in cats that were treated with L-lysine, but more recent studies in shelters question that. In humans, it is recommended that the patient begin the use of L-lysine whenever he or she feels the symptoms of an ulcer developing. Because it is not possible to determine when the cat is becoming symptomatic, it is recommended for the cat to remain on L-lysine for life to prevent reoccurrence. Lysine is available on the veterinary market as a palatable paste or hard chewable treats.
Treatment Plan The following are general treatment plans that should be modified to fit the individual cat and clinical disease.
Superficial, Noninfected Ulcer • Clinical Appearance: A superficial defect is present in the corneal surface and is surrounded by clear or minimally edematous cornea. The pupil is normal or can be miotic. These are frequently painful and usually have an acute onset. • Treatment: Remove the cause if one can be identified. Broadspectrum ophthalmic antibiotics (see Therapeutic Notes) as a prophylactic against bacterial infection, ophthalmic atropine q12 to 24 h, and, possibly, systemic anti-inflammatory medications such as meloxicam to make the eye more comfortable are indicated. Re-examination should be performed in 5 to 7 days to access healing.
Corneal Ulcer
Severe, Suspected, or Confirmed Bacterially Infected Ulcer • Clinical Appearance: A large or deep corneal defect is present; the surrounding cornea may have a whitish to yellowish appearance. The cornea may also be swollen or melting with a rapid onset or deterioration. Deep or superficial blood vessels may be present extending from the limbus toward the ulcer. The pupil is usually miotic. There is likely to be concurrent uveitis. If the cornea has ruptured, the iris may prolapse through the hole. • Diagnostics: They should include cytology and culture/sensitivity. • Treatment: The treatment goal is to identify the infective organism and kill it. Any irritating cause should be removed. Ophthalmic antibiotics should be used q2h initially; good choices include aminoglycosides or fluoroquinolones. Ophthalmic atropine should be used q12h. Systemic anti-inflammatory medications such as meloxicam will aid with concurrent uveitis, making the cat feel better. If the cornea is ruptured or rupture is imminent broad spectrum systemic antibiotics should be administered. Re-examination should occur in 1 to 2 days. Surgical referral should be considered in ulcers greater than half thickness or those that fail to improve with therapy. Surgical options may include superficial keratectomy, conjunctival grafts, corneal advancement grafts, artificial corneal materials, or corneal transplants.
Herpetic Ulcer • Clinical Appearance: These ulcers are commonly chronic or recurrent. There is no set time limit to the reoccurrence rate. Dendritic (i.e., superficial, branching, map-like) ulcers are pathognomonic for FHV-1. Cats with conjunctivitis with or without concurrent corneal ulceration should be suspect for FHV-1 infection. Cats with historical upper respiratory tract disease that have reoccurrence of the conjunctivitis are even more suspect. • Diagnostics: FHV-1 testing should be considered when clinical signs are not consistent with a specific disease. The methodology employed by the testing laboratory may influence the outcome of the test. For best results the testing laboratory should be contacted for instructions prior to sample collection. • Treatment: Trifluorothymidine (Viroptic®, q4h) or famciclovir (Famvir®, 31 mg q12h PO) and L-lysine (500 mg q24h PO) with reexamination in 1 to 2 weeks. If there is no improvement, consider increasing the frequency or concentration or switching to another
form of antiviral treatment. If the ulcer is severe add topical ophthalmic antibiotic q6h, topical ophthalmic atropine ointment q12h, and systemic nonsteroiadal anti-inflammatory medication. The owners should be counseled on removing stress from the cat’s life, although identifying the cause of stress may be difficult. Neutering should be considered, if applicable, to decrease reproductive stress.
Therapeutic Notes • There have been reports of severe anaphylactic reactions and death with use of triple antibiotic ointment topically in cats. At this time it is suspected that anaphylaxis is related to the neomycin component in the formulation. Use of triple antibiotic in cats should be avoided due to this risk. • Do not use topical steroids or topical anesthetic as treatments because these potentate infection and slow the healing process. • Do not grid any ulcer in a cat; this has been associated with a higher incidence of sequestrum development. • Ophthalmic atropine solution may drain into the cat’s mouth, and the bitter taste can cause excessive salivation. Ointments are less likely to cause this problem.
Suggested Readings Galle LE. 2004. Antiviral therapy for ocular viral disease. Vet Clin N Amer. 34(3):639–654. Fontenelle JP, Powell CC, Veir JK, et al. 2008. Effect of topical ophthalmic application of cidofovir on experimentally induced primary ocular feline herpesvirus-1 infection in cats. Am J Vet Res. 69(2):289–293. Kern TJ. 2004. Antibacterial agents for ocular therapeutics. Vet Clin N Amer. 34(3):655–668. Maggs DJ, Lappin MR, Reif JS, et al. 1999. Evaluation of serologic and viral detection methods for diagnosing feline herpesvirus-1 infection in cats with acute respiratory tract or chronic ocular disease. J Am Vet Med Assoc. 214(4):502–507. Townsend WM, Stiles J, Guptill-Yoran L, et al. 2004. Development of a reverse transcriptase-polymerase chain reaction assay to detect feline herpesvirus-1 latency-associated transcripts in the trigeminal ganglia and corneas of cats that did not have clinical signs of ocular disease. Am J Vet Res. 65:314–319.
95
CHAPTER 42
Coughing Gary D. Norsworthy
Overview Coughing is an action to free the airway of foreign material. It may originate from the pharynx, larynx, trachea, bronchi, or small airways. Unlike dogs, it is not a common occurrence in the cat because is it not typically associated with feline cardiac disease. When coughing, cats often assume a characteristic crouched position with the neck extended. See Figure 42-1.
pulmonary arteries and lung parenchyma), lungworms, and tracheal disease. • Heartworm Antibody and Antigen Tests: These tests should be performed when the thoracic radiographs reveal enlarged or tortuous pulmonary arteries; they should be considered in all coughing cats. Although specific for heartworm larvae or adults, neither is sensitive enough to rule out heartworms. See Chapter 88.
Secondary Diagnostics Diagnosis Differential Diagnoses: Common • • • •
Asthma. See Chapter 27. Heartworm disease. See Chapter 88. Chylothorax. See Chapter 36. Bordetella tracheobronchitis. See Chapter 24.
Differential Diagnoses: Less Common to Uncommon • Pulmonary roundworm larval migration. See Chapter 195. • Lungworm disease. (May be common in endemic areas.) See Chapter 129. • Tracheal disease, collapse, or foreign bodies. • Idiopathic pulmonary fibrosis. See Chapter 179. • Aspiration of fluids or thick liquids (food). • Inhalation of noxious fumes.
Primary Diagnostics • Thoracic Radiograph: This should be the first diagnostic test performed to determine the presence of or likelihood of asthma, pleural effusion (including chylothorax), heartworm disease (note caudal
• Complete Blood Count (CBC): Many cats with asthma and some cats with heartworm disease and pulmonary parasites have a peripheral eosinophilia. • Bronchoalveolar Lavage: This can be a meaningful way to collect samples for cytologic examination. However, eosinophils can be found in significant numbers in the airways of normal cats. • Echocardiography: Adult heartworms are occasionally visualized as two parallel lines in the right side of the heart or in the pulmonary outflow tract. • Lung Aspiration: The finding of large numbers of eosinophils is strongly suggestive of asthma. Heartworm disease also produces a transient pulmonary eosinophilia. This procedure is not without some risk of lung laceration and pneumothorax. See Chapter 304. • Thoracic Fluid Analysis: When pleural effusion is present, this is an important test. • Fecal Flotation and Baermann Sedimentation: These will detect the presence of metastrongyle (Aelurostrongylus abstrusus) larvae, trichurid (Eucoleus aerophila; sometimes called Capillaria aerophila) and ascarid ova, and lung flukes (Paragonimus kellicotti) ova; however, one negative sample does not rule out their presence. • Tracheal Endoscopy: This procedure will evaluate the trachea for the presence of abnormal secretions, stricture, or collapse. The use of a brush can provide meaningful cytologic samples.
Treatment Therapeutic Notes • Typically, coughing is not a life-threatening or debilitating problem for cats, although it may be a sign of serious disease. • In general, it is not necessary or even desirable to suppress the cough. One’s efforts should be directed at determining and treating the underlying cause. Response to steroids in a coughing cat has been used as an indirect test for asthma. However, cats with heartworms will also have a cough that responds to steroids and may be more common than asthma in heartworm endemic areas.
Prognosis The prognosis is variable depending upon the underlying disease. Figure 42-1 When cats assume this crouched position with the neck extended coughing usually originates from the pulmonary level.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
96
Suggested Readings Ettinger SJ. 2000. Coughing. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed. 162–166. Philadelphia: Saunders. Mason RA, Rand J. 2006. The coughing cat. In J. Rand, ed., Problem-Based Feline Medicine, pp. 90–108. Philadelphia: Elsevier Saunders.
CHAPTER 43
Cryptococcosis Sharon Fooshee Grace
Overview Infection with Cryptococcus is observed regularly in cats. At present, this genus includes two species important to veterinary medicine: C. neoformans, which has a global distribution, and C. gattii, which has a more limited distribution and is associated with cases reported in Australia, British Columbia, and the Pacific Northwest of the United States. Cryptococcosis is the only systemic fungal infection observed more commonly in cats than in dogs. C. neoformans is associated with decaying bird feces (especially the alkaline, nitrogen-enriched droppings of pigeons), although many infected cats have no known contact with pigeon excreta. Birds rarely become infected because of their high body temperature. Environmental exposure and risk factors for C. gattii are still being determined, but disease risk appears linked to the presence of trees (both eucalyptus, as well as other species) or proximity to commercial soil disruption or logging. The exact mode of infection is unknown but probably occurs through inhalation of airborne organisms since the upper respiratory tract is the most common primary site of infection. The age range of affected cats is broad. Some studies have found male cats at increased risk, but other reports have failed to support this observation. It has been suggested that the Siamese, Birman, and Ragdoll breeds may be over-represented. Cryptococcus has several identified virulence factors, a number of which are related to its thick mucopolysaccharide capsule. The capsule may induce some degree of immunosuppression in the host cat. Also, antigens hidden beneath the capsule can evade recognition by and stimulation of the immune system. Opportunistic infection by C. neoformans in patients with human immunodeficiency virus (HIV) infection or other immune-deficient states is well documented; in contrast, several reports have found that immunosuppression is not required for C. gattii infection. These findings suggest that, at least in humans, C. gattii should be considered a primary pathogen because of its potential to infect immunocompetent hosts. Although cats infected with the feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) represent states of cell-mediated immune deficiency comparable to HIV, potential for retroviruses to predispose to infection by either C. neoformans or C. gattii has not been clearly established. Most published reports have evaluated only C. neoformans and findings have been inconsistent, though there is some evidence that FeLV-infected cats may not respond as well to treatment as healthy cats and that they are more prone to relapse. Further clarification is needed regarding the roles of risk factors and underlying disease in feline cryptococcosis. The organism appears to have the greatest affinity for the upper respiratory system, with the nervous and integumentary systems also commonly involved. Unlike in humans, the lower airways usually remain clinically normal in cats, although gross lesions may be found in the lungs on necropsy. Sneezing, snuffling, and progressive inspiratory distress are common; nasal discharge is variably present. Some cats may have a fleshy mass protruding from one or both nostrils, swelling across the bridge of the nose (see Figure 43-1), or facial distortion. Others have respiratory stridor when a fungal mass is present in the nasal cavity or nasopharynx (see Figure 43-2). The mandibular lymph nodes are
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 43-1 The draining lesions on the nose and left ear were cause by cryptococcosis. A diagnosis was made by cytology. Photo courtesy Dr. Richard Malik.
Figure 43-2 A cryptococcal mass is present in the nasopharynx and was seen on radiographs. The cat had a reverse sneeze. The mass (arrow) was approached via a transpalatine incision on the midline. The mass can be seen through the incision. Following surgery, the cat was treated for 8 months with itraconazole and recovered. Photo courtesy Dr. Gary D. Norsworthy.
commonly enlarged. In many cases of central nervous system (CNS) cryptococcosis, respiratory signs are known to precede those of the nervous system. Neurologic abnormalities include behavioral changes, ataxia, paresis, seizures, circling, or head pressing. Infection of the skin and subcutaneous tissues is regarded as a manifestation of disseminated
97
SECTION 1: Diseases and Conditions
useful as a general health screen for the patient and help refine the prognosis. • Radiography: Skull and thoracic radiographs may be useful to detect respiratory involvement but will not offer a definitive diagnosis.
Diagnostic Notes
Figure 43-3 Multiple ulcerated nodules in this cat were caused by Cryptococcus neoformans. Photo courtesy Dr. Richard Malik. disease. Signs include solitary or multiple nodules that are sometimes ulcerated or draining gelatinous material; open lesions are nonhealing. See Figure 43-3. Inflammatory lesions in both anterior and posterior chambers of the eye are common and may involve one or both eyes. Dilated, nonresponsive pupils, chorioretinitis, retinal hemorrhage, and optic neuritis are reported. Anterior uveitis is present in some cats. Fever is uncommon and, when present, is usually mild. Infected cats do not represent a health hazard to humans or other pets but serve as a sentinel to raise awareness of the presence of the organism in the environment.
Diagnosis Primary Diagnostics • Clinical Signs: Cryptococcosis should be of particular concern when inspiratory dyspnea; nasal mass or discharge; or, a facial mass, swelling, or distortion are present. Other clinical signs are described previously. • Cytology: Cytologic inspection of aspirates, swabs, or exudative material is usually sufficient to make a diagnosis. See Figure 289-2. With modified Wright’s or new methylene blue stain, organisms appear as small (3.5–7 µm) light to dark blue yeasts with an outer, thick clear capsule; with Gram stain, the organism is crystal violet with a light red capsule. One to two narrow-based buds are often present. India ink preparations are sometimes useful as the organism appears unstained in a dark background, although organisms may be confused with fat droplets or lymphocytes, especially if budding is not present. • Serologic Testing: The latex agglutination test (LAT) is considered a sensitive and highly specific test for antigens associated with the fungal capsule. When the test is properly performed, a positive result is usually regarded as diagnostic of cryptococcosis, even titers of 1 : 2. False-negative results may occasionally be obtained in cats with transient or localized infection, or when there is a significant antigen excess (prozone effect). LAT testing may also be performed on cerebrospinal fluid when CNS involvement is suspected. See Diagnostic Notes for precautions.
Secondary Diagnostics • Complete Blood Count, Biochemical Profile, Urinalysis, FeLV, FIV: This minimum database will not provide a diagnosis but is
98
• The narrow-based bud attachment that is present during reproduction is helpful in distinguishing Cryptococcus neoformans from Blastomyces. • Histopathology is usually not needed to make a diagnosis; routine hematoxylin-eosin stains may fail to demonstrate the capsule. • Culture is rarely necessary but may be indicated for identification of unusual variants. • If CNS cryptococcosis is suspected, serum testing for cryptococcal antigen should be performed prior to anesthesia for brain imaging or cerebrospinal fluid (CSF) collection. General anesthesia and collection of CSF have been associated with fatal deterioration of the patients with CNS disease. Increased intracranial pressure caused by the fungal mass can cause brain herniation following a CSF tap. • Reactivation of previously arrested infections has been reported.
Treatment Primary Therapeutics • Surgical debulking of large fungal masses or fungal-infected tissues (including lymph nodes) should be performed at the time therapy is initiated to improve the chance for successful treatment. • Itraconazole: Itraconazole has historically been considered the antifungal drug of choice for cats with mild to moderate disease without CNS involvement. It is dosed at 5 mg/kg q12h PO and given with a meal; an acid environment in the stomach enhances absorption of the drug. The capsule may be opened and the contents divided into gelatin capsules or mixed into canned food. Malik suggests that when using capsules, medium-to large sized cats may receive 100 mg (1 capsule) q24h, whereas cats weighing <3.5 kg (7.75 pounds) may receive 50 mg (one-half of capsule contents) q24h or 100 mg q48h PO. An oral solution is available; this formulation has greater bioavailability than the capsule form. Although itraconazole is usually well tolerated, serum chemistries should be periodically checked during therapy to assess for hepatotoxicity. For cats with clinical evidence of hepatotoxicity (i.e., anorexia, jaundice), the drug should be discontinued, at least temporarily. Asymptomatic cats with increased alanine aminotransferase (ALT) do not necessarily need cessation of therapy but should be closely monitored clinically and biochemically. • Fluconazole: Now that a generic formulation of fluconazole is available, it is finding increased use as an alternative to itraconazole. It has superior ocular, CNS, and urinary tract penetration and much less hepatotoxicity than itraconazole and ketoconazole. It generally considered a highly effective therapy, though its efficacy for CNS cryptococcosis is still being evaluated. It does achieve therapeutic concentrations in the CNS and CSF, even in the absence of inflammation, though cats with CNS involvement and disseminated disease appear to respond more quickly to amphotericin-B (AMB). The dose is 30 to 50 mg per CAT q12-24h PO for small and large cats, respectively, and should be given for a minimum of 1 month beyond resolution of signs. • AMB or AMB combined with 5-fluorocytosine (5FC): AMB is fungicidal and stands as the most effective anti-cryptococcal drug available. Like fluconazole, AMB and 5FC are able to penetrate the blood-brain barrier. AMB or AMB-5FC should be used in cases with severe disseminated disease, CNS involvement, or with demonstrated failure to respond to azole drugs. AMB administration via the intravenous route has greater potential for nephrotoxicity
Cryptococcosis
TABLE 43-1: Protocol for Subcutaneous Administration of Amphotericin B 1. Preparation of suspension: Add 10 mL sterile distilled water to a 50-mg vial of amphotericin B deoxycholate (Fungizone, Bristol Myers Squibb, Princeton, NJ) to produce a 5-mg/ml colloidal suspension. 2. Storage: The vial may be frozen for storage for up to 4 weeks. When the drug is needed, the vial may be thawed and the needed amount aseptically withdrawn from the vial. Return to freezer for refreezing and storage. 3. Preparation of subcutaneous infusion: Take a 500-mL bag of 0.45% sodium chloride in 2.5% dextrose, warm to 40°C in a microwave oven, and then connect to an administration set. Discard 100 to 50 ml of the bag. Add the calculated dose of amphotericin B stock suspension via the injection port on the bag. The calculated dose is 0.5 to 0.8 mg/kg (typically, 0.4–0.8 mL). Aspirate fluid into syringe and inject back into the bag several times to ensure transfer of all drug to the bag. 4. Administration of drug: Attach a 19- or 21-gauge to the administration set, then insert the needle into the subcutaneous space between the scapulae (roughly on the midline). Allow the fluid to flow as fast as gravity will permit; elevating the bag will facilitate delivery. It usually takes 10 to 15 minutes to deliver the entire volume (350–400 mL). The entire volume is given in one site unless the cat is visibly uncomfortable after half the solution is delivered. The fluid tends to move extensively throughout the subcutaneous space, with ventral pooling several hours after delivery. 5. Treatment schedule: This formulation is typically administered two to three times per week. 6. Cumulative dose: The cumulative dose appears more important than the time period over which treatments are given. The typical cumulative dose required to effect improvement is 10 to 20 mg/kg. Do not exceed a weekly cumulative dose of 1.6 mg/kg. 7. Notes: (a) Do not substitute other fluids for the recommended fluid because the saline has a protective effect on the kidneys. Adding small amounts of salt to the diet may also be renoprotective. (b) Monitor blood urea nitrogen (BUN) and creatinine closely and at least temporarily discontinue therapy if azotemia develops.
than subcutaneous administration (See Table 43-1). Outcome for disseminated cases is improved if flucytosine is given concurrently. Flucytosine is dosed at 250 mg per cat (one-half tablet) q8h PO for small-to-normal size cats. It is generally well tolerated by cats, except those with impaired renal function. Duration of therapy is 1 to 9 months.
Therapeutic Notes • In some studies, therapy has been relatively unsuccessful in immunosuppressed cats; other studies have failed to support this observation. However, older reports have not distinguished between infection with C. neoformans and C. gattii. Further clarification is needed on the relationships between cryptococcal species, immunosuppression, and response to therapy. • Cats should be periodically re-evaluated with the LAT during treatment. A falling titer has value in determining a favorable response to therapy. Many cats maintain a positive titer for months after clinical resolution of signs. Although it is unknown whether the LAT continues to detect dead organisms, continuation of treatment for 1 to 2 months beyond resolution of clinical signs or beyond confirming a negative LAT (whichever is longer) is recommended. • Lipid-based formulations of AMB have been developed in an effort to reduce toxicity. While they are less nephrotoxic, they are not necessarily more effective. In most cases, the cost of these formulations is prohibitive. • Placement of a feeding tube permits the owner to administer proper nutritional support at home. Placement of an esophagostomy or gastrostomy tube should be considered at the time of diagnosis.
Prognosis In general, the prognosis for infected cats is good with itraconazole, fluconazole, AMB, or AMB-5FC. However, severely debilitated cats with advanced systemic disease and cats with CNS involvement should be considered to have a guarded prognosis.
Suggested Readings Duncan CG, Stephen C, Campbell J. 2006. Evaluation of risk factors for Cryptococcus gattii infection in dogs and cats. J Am Vet Med Assoc. 228(3):377–382. Hector RF. 2005. An overview of antifungal drugs and their use for treatment of deep and superficial mycoses in animals. Clin Tech Small Anim Pract. 20(4):240–249. Lester SJ, Kowalewich NJ, Bartlett KH, et al. 2004. Clinicopathologic features of an unusual outbreak of cryptococcosis in dogs, cats, ferrets, and a bird: 38 cases (January to July 2003). J Am Vet Med Assoc. 225(11):1716–1722. Malik R, Jacobs GJ, Love DN. 2001. Cryptococcosis: New perspectives on etiology, pathogenesis, diagnosis and clinical management. In JR August, ed., Consultations in Feline Internal Medicine, 4th ed., pp. 39–50. Philadelphia: WB Saunders. Malik R, Krockenberger M, O’Brien C, et al. 2006. Cryptococcosis. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 584–598. Philadelphia: Saunders Elsevier.
99
CHAPTER 44
Cryptosporidiosis Mark Robson and Mitchell A. Crystal
Overview Cryptosporidiosis is a disease caused by a ubiquitous coccidian parasite that colonizes the microvillous border of epithelial cells of the intestinal tract of a wide range of mammals. Although Cryptosporidium parvum is the most common other biologically and genetically different species exist: C. felis is primarily found in cats, C. canis in dogs, and C. hominis in humans. Cats become infected by the fecal-oral route, most commonly by ingestion of sporulated oocysts within feces or contaminated food or water. The organism penetrates the intestinal microvilli where it undergoes asexual and sexual reproduction, eventually producing thin-walled (autogenous re-infection) or thick-walled (shed in feces) oocysts. There is no extra-intestinal involvement, and transplacental and transmammary infection do not occur. The prepatent period in cats is 5 to 10 days. The fecally shed oocysts are resistant to environmental damage, chlorination, and standard cleansers. Extreme temperatures and prolonged ammonia contact destroys Cryptosporidium spp. oocysts. Most cats that excrete Cryptosporidium spp. oocysts do not have clinical disease. Surveys using polymerase chain reaction (PCR), immunofluorescent antibody (IFA), and fecal-based tests indicate that up to 38.5% of cats have been exposed to or are excreting Cryptosporidium spp. PCR appears to be much more sensitive than IFA, and there seems to be increased detection of Cryptosporidium spp. in late autumn and early winter. Common clinical signs when present include diarrhea (chronic or intermittent), anorexia, weight loss, dehydration, and weakness. Young and immunocompromised cats (e.g., those with alimentary lymphoma, inflammatory bowel disease, or feline leukemia virus [FeLV] or feline immunodeficiency virus [FIV] infections) are at higher risk of infection and illness. There is no breed or sex predilection. Co-infection with other intestinal parasites such as Giardia (see Chapter 83) and Tritrichomonas foetus (see Chapter 218) may occur leading to more severe clinical disease. Physical examination may be normal or reveal evidence of diarrhea, weight loss, or dehydration. Cryptosporidium spp. is of zoonotic potential. C. felis is relatively host specific, and C. felis infections in humans are rare unless associated with human immunodeficiency virus (HIV) or other immunosuppressive conditions. Most human infections are due to C. parvum or C. hominis. Clients owning pets identified as infected with Cryptosporidium spp. should be advised about appropriate handling of feces and the zoonotic potential of the disease. Recommendations from the U.S. Public Health Service and Infectious Disease Society of America state that HIV-infected humans should not take into their homes stray dogs or cats, animals with diarrhea, or dogs and cats younger than 6 months of age; if any dog or cat younger than 6 months of age is acquired by an HIV-infected person, the animal should be tested for Cryptosporidium spp.
• Direct Fecal Enzyme-linked Immunosorbent Assay (ELISA) or IFA Tests: These methods can detect Cryptosporidium oocysts in feces; IFA sensitivity is reported to be 11.3% and specificity to be 100%. • Special Staining of Feces: Ziehl-Neelsen acid fast staining and other special staining techniques are used by diagnostic laboratories to identify Cryptosporidium oocysts.
Secondary Diagnostics • Fecal Flotation: Oocysts are sometimes seen on high power microscopic examination after fecal flotation in Sheather ’s sugar solution. The oocysts appear as circular, sometimes concave, discs just beneath the cover slip. • Serologic Testing: An ELISA assay for identifying feline anti-Cryptosporidium immunoglobulin G can be performed. This test indicates exposure but does not necessarily indicate infection or oocyst shedding and, thus, is more useful for prevalence studies rather than confirming clinical cases. Not all cats with Cryptosporidium develop positive circulating antibody titers. • Tissue Biopsy: Villous atrophy, reactive lymphoid tissue, and inflammatory infiltrates are seen within the intestinal mucosal lamina propria. Organisms can be seen at the microvillous border. The distal small intestine is most affected.
Diagnostic Notes • Cryptosporidium spp. are not typically seen on routine fecal flotation because of the transparent nature and extremely small size of these organisms (slightly smaller than an erythrocyte, one-tenth the size of Isospora spp.). • False-negatives can occur on histopathology.
Treatment Primary Therapeutics • No Treatment: Most infections are self-limiting and require no therapy. • Azithromycin: Administer 7 to 15 mg/kg q12h PO for 5 to 7 days. Some authors recommend at least 14 days of treatment. • Tylosin: Administer 11 mg/kg q12h PO for 28 days. • Paromomycin: Administer 125 to 165 mg/kg q12h PO for 5 days.
Secondary Therapeutics Diagnosis Primary Diagnostics • Fecal PCR: This method can detect Cryptosporidium spp. DNA in fecal samples and has been shown to be 10 to 100 times more sensitive than immunofluorescence. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
100
• Supportive Care: Address fluid, electrolyte, and nutritional needs. Treat underlying disease. • Nitazoxanide: Administer 25 mg/kg q12h PO for 28 days.
Therapeutic Notes • Prevent infections by maintaining appropriate sanitation. • Caution should be used when using paromomycin in cats with suspected mucosal compromise as renal failure and deafness from aminoglycoside toxicity can occur.
Cryptosporidiosis
• Nitazoxanide therapy may cause vomiting and dark brown-black, foul-smelling diarrhea.
Prognosis The prognosis is usually good for immunocompetent cats (and humans) as infection is usually asymptomatic or self-limiting. Immunocompromised cats (and humans) have a good prognosis if a predisposing illness or cause of immunosuppression can be identified and treated.
Kaplan JE, Masur H, Holmes KK. 2002. Guidelines for preventing opportunistic infections among HIV-infected persons. MMWR 51(RR08): 1–46. (www.cdc.gov/mmwr/preview/mmwrhtml/rr5108a1.htm) Lindsay DS, Zajac AM. 2004. Cryptosporidium infections in cats and dogs. Compend Contin Ed Pract Vet. 26(11):864–874. Tzannes S, Batchelor DA, Graham PA, et al. 2008. Prevalence of Cryptosporidium, Giardia and Isospora species infections in pet cats with clinical signs of gastrointestinal disease. J Fel Med Surg. 10(1):1–8.
Suggested Readings Barr SC. 2006. Cryptosporidiosis and cyclosporiasis. In JR August, ed., Infectious Diseases of the Dog and Cat, 3rd ed., 518–524. St. Louis: Saunders Elsevier.
101
CHAPTER 45
Cutaneous Markers of Internal Disease Christine A. Rees
Overview Skin reaction patterns in cats can provide useful clues that an internal disease may be present. The most prominent of these reaction patterns are exfoliative skin disease, an unusual alopecia with a glistening appearance, and fragile skin. The three feline skin disease, which cause these problems include exfoliative dermatitis associated with thymoma, paraneoplastic syndrome associated with pancreatic carcinoma, and hyperadrenocorticism (spontaneous versus iatrogenic, with or without diabetes mellitus). Each of these conditions will be discussed individually.
Exfoliative Dermatitis Associated with Thymoma Overview Exfoliative dermatitis associated with thymoma most commonly occurs in older cats. It is non-pruritic with white scaling or dandruff, which initially starts on the head and pinna but eventually progresses to the rest of the body. Primary differentials include poor grooming associated with age or obesity, hyperthyroidism, dermatophytosis, epitheliotropic T-cell lymphoma (mycosis fungoides), and cheyletiellosis.
Diagnosis Primary Diagnostics • Clinical Appearance: Although not diagnostic, nonpruritic dermatitis with white scaling or dandruff starting on the head and pinna should raise the index of suspicion. • Cytology: Skin impression cytology should be performed to look for secondary infection (i.e., bacteria or Malassezia spp.). Scotch tape preps or the use of special slides (Durotak® Adhesive Slides, Delasco, Council Bluffs, IA) are the best methods for effectively being able to detect yeast. In addition, direct hair examinations with either potassium hydroxide or chlorphenolac and dermatophyte cultures are used to rule out dermatophytosis. • Histopathology: Skin biopsy for dermatohistopathology is diagnostic. Histopath reveals a cell-poor interface dermatitis with hydropic changes and variable hyperkeratosis. • Thoracic Radiographs: Thoracic radiographs are necessary for detecting the underlying cause for the dermatitis. Radiographs show the presence of a mediastinal mass. • Histopathology of the Chest Mass: Biopsy with histopath of the mediastinal mass is necessary to definitively diagnose thymoma.
Treatment Primary Therapeutics • Chemotherapy or surgical removal of the thymoma resolves symptoms in early cases. See Chapter 213.
Prognosis The prognosis for exfoliative dermatitis due to thymoma is usually grave. Very rarely can the thymoma be successfully treated.
Paraneoplastic Syndrome Associated with Pancreatic Carcinoma Overview Most patients with paraneoplastic syndrome are older cats. These cats typically have weight loss, inappetence, lethargy, and alopecia. Alopecia occurs acutely and is most commonly found on the legs and ventrum. The alopecic areas tend to have an unusual glistening appearance and may have multifocal erythema or scales.
Diagnosis Primary Diagnostics • Clinical Appearance and History: The clinical appearance is not diagnostic, but when seen as described above it should raise the index of suspicion. • Histopathology: Dermatohistopathology shows severe atrophy and miniaturization of the hair follicles. Focal areas of hyperplasia with alternating orthokeratosis and parakeratosis are usually present. In addition, areas of hypokeratosis are prominent. The dermis contains a mild superficial lymphocytic perivascular infiltrate with severe adenexal atrophy. • Abdominal Radiographs: An abdominal mass may be noted (especially if metastasis has occurred). • Abdominal Ultrasonography: This diagnostic test may reveal some hypoechogenicity around the pancreas due to inflammation. Metastasis to the liver and mesentery are possible and may be detected with an ultrasound examination. • Feline Pancreatic Lipase Immunoreactivity: This test is often elevated from the inflammation which results secondary to the presence of the pancreatic neoplasia. See Chapter 159.
Secondary Diagnostics • Exploratory Celiotomy: This may be needed to confirm pancreatic neoplasia.
Treatment Primary Therapeutics • No successful treatment exists for pancreatic carcinomas.
Prognosis The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
102
The prognosis for paraneoplastic syndrome is grave. This pancreatic tumor is aggressive and tends to metastasize early in the course of the disease.
Cutaneous Markers of Internal Disease
Acquired Fragile Skin Syndrome Overview Acquired fragile skin syndrome tends to occur in older cats with either hepatic neoplasia, hyperadrenocorticism (spontaneous or iatrogenic) with or without diabetes mellitus, or hepatic lipidosis. The skin becomes extremely thin and fragile. The skin has been known to tear with even minimal manipulation (i.e. holding the scruff to restrain the cat). Wounds which are sutured do not heal easily and frequently dehisce. See Figure 45-1. Because the skin tears so easily, scruffing cats with this condition is strongly discouraged.
Diagnosis Primary Diagnostics • Clinical Appearance: One or more large tears in thin skin are typical. • Clinical Signs of Diabetes or Hyperadrenocorticism: Symptoms of hyperadrenocorticism, diabetes mellitus, and often hepatic lipidosis may be present. See Chapters 50, 51, 93, and 101.
Secondary Diagnostics • Skin Biopsy: Dermatohistopathology shows a markedly thin epidermis with severe atrophy.
Diagnostic Notes • Megestrol acetate and repository methylprednisolone injections have been indirectly associated with this syndrome due to their insulinantagonistic properties. • This is a distinct syndrome from Ehler-Danlos syndrome, which is inherited/congenital collagen defect that occurs in young cats.
Treatment Primary Therapeutics • Hyperadrenocorticism: See Chapter 101. Medical and surgical treatment options exist. • Diabetes: See Chapter 52.
Secondary Therapeutics • Surgical Wound Management: Primary closure when skin tears occur is desirable, though often not possible. Suturing affected skin is difficult, so tissue gluing may be more effective.
Prognosis This condition carries a guarded prognosis unless the primary disease can be identified and managed. It may take months for the skin to return to nearly normal after the underlying condition is corrected.
Suggested Readings
Figure 45-1 Multiple tears in the skin (fragile skin syndrome) can be seen in this cat with diabetes mellitus and hyperadrenocorticism. Image courtesy Dr. Gary D. Norsworthy.
Angarano DW. 1995. Erosive and ulcerative skin disease. Veter Clin N Amer. Sm Anim Pract. 25:871–885. Neiger R, Witt AL, Noble A, et al. 2004. Trilostane Therapy for treatment of pituitary-dependent hyperadrenocorticism in 5 cats. J Vet Int Med. 18(2):160–164. Rottenberg S, VonTscharner C, Roosje PJ. 2004. Thymoma-associated exfoliative dermatitis in cats. Vet Path. 41:429–433. Turek MM. 2003. Cutaneous paraneoplastic syndromes in dogs and cats: a review of the literature. Vet Derm. 14:279–296.
103
CHAPTER 46
Cuterebriasis Sharon Fooshee Grace
Overview Myiasis, or invasion of the body by fly larvae, is a common finding in feline medicine. Cuterebriasis is a form of facultative myiasis caused by larvae of the bot fly, Cuterebra spp. Dogs are occasionally affected. Cuterebra larvae are sometimes referred to as “wolves” or “warbles.” Another form of myiasis is caused by the larvae of the blowfly, Calliphora spp. Most cases of cuterebriasis occur during the summer and early fall in cats with outdoor access, often in a rural environment. Debilitated kittens, young adults, and older cats are most often affected. It is common in areas along the Gulf Coast and the Eastern Seaboard, although it can occur elsewhere. Adult bot flies are not parasitic on animals because they lack functional mouth parts. The flies are large, bee-like, and have a short life span. The female fly lays hundreds of eggs on vegetation surrounding burrows of rabbits and rodents. With suitable environmental conditions, the eggs hatch into infective first-stage larva. When a host is encountered, the larva attaches and crawls onto the animal, seeking a satisfactory spot to burrow. The larva can directly penetrate the subcutis (a feat made possible by its tissue-digesting proteases) or may find a natural body opening with a mucous membrane, such as the nasal cavity, in which to establish itself. Once beneath the mucosal surface, the larva develops to the third stage, later to emerge through the entry hole, drop to the ground, and pupate through the winter. It emerges in the spring as an adult fly. Within host tissues, the larva produces enzymes which cause local tissue necrosis and inflammation, with eventual development of a fistula or furuncle. See Figure 46-1. Lesions are typically found on the head, neck, and trunk during late summer. Presence of a larva within the nasal cavity often causes upper respiratory signs (especially persistent sneezing and nasal discharge) and sometimes leads to obstructive breathing. Occasionally, a larva is identified in the paranasal sinuses.
In addition to local tissue trauma, an aberrant larva can cause lifethreatening complications when it migrates to unusual locations (i.e., brain, trachea, thoracic cavity, pharynx, or eye). In many reported cases of central nervous system (CNS) cuterebriasis, neurologic signs were preceded by upper respiratory signs. CNS entry by a larva is speculated to occur via erosion of the cribriform plate. CNS signs associated with cuterebriasis are often lateralizing and include rapid onset of CNS dysfunction (i.e., disorientation, seizures, hysteria or depression, aggression or marked behavior changes toward the owner), blindness, and coma. Feline ischemic encephalopathy (FIE) has been attributed to aberrant larva traveling in the CNS, possibly inducing vasospasm which culminates in infarction of a cerebral vessel. (Notably, FIE does not occur in countries without the Dipteran parasite Cuterebra.) A fatal case with an intrathoracic larva has been described. Cuterebra larvae have been found within the eyelid, conjunctiva, or either chamber of the eye, causing severe conjunctivitis, anterior/posterior uveitis, retinal hemorrhage, chorioretinitis, and optic neuritis. One review of 11 cats with a Cuterebra larva found in the CNS suggested that feline idiopathic vestibular syndrome might be related to migration of a larva through the ear canal to the peripheral vestibular apparatus. Although the signs are distinct from those of CNS cuterebriasis, idiopathic vestibular syndrome typically occurs during the summer months in outdoor cats.
Diagnosis Primary Diagnostics • Clinical Signs: A fistulated, nonpainful, nodular swelling on the head, neck, or trunk that is suspicious. Other signs are referable to the organ affected by an aberrant larva.
Secondary Diagnostics • Rhinoscopy is helpful for identifying a nasal larva.
Diagnostic Notes • A history of upper respiratory signs followed 1 to 2 weeks later by abrupt CNS changes, especially in the summer, is important.
Treatment Primary Therapeutics
Figure 46-1
A Cuterebra larva can be seen in the open lesion on this kitten’s face.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
104
• Larva Removal: Removal of accessible larva is curative. The hole is enlarged and the larva carefully extracted so as not to rupture it. A broken larva will cause a severe inflammatory reaction or anaphylaxis. If any part of the larva is left in the wound, it will form a draining tract requiring surgery. • Medical Treatment for CNS Cuterebriasis: Ivermectin is effective against Cuterebra at 0.1 mg/kg and is well tolerated up to 0.3 mg/ kg. One protocol utilizes diphenhydramine (4 mg/kg IM), followed in 1 to 2 hours with ivermectin (0.3 mg/kg SC) and dexamethasone (0.1 mg/kg IV). Another protocol suggests ivermectin (0.3 mg/kg SC) on alternate days for three treatments, to include glucocorticoids.
Cuterebriasis
Unfortunately, there is no proven treatment protocol for CNS involvement. A broad-spectrum antibiotic should be considered ad adjunctive therapy.
Therapeutic Notes • It may be life-saving to treat cats with upper respiratory signs in late summer/early fall with a dose of ivermectin if a nasal larva is suspected but cannot be visualized or extracted. This could prevent CNS access through the cribriform plate.
Suggested Readings Glass EN, Cornetta AM, deLahunta A, et al. 1998. Clinical and clinicopathologic features in 11 cats with Cuterebra larvae myiasis of the central nervous system. J Vet Intern Med. 12:3624–368. Harris BP, Miller PE, Bloss JR, Pellitteri PJ. 2000. Ophthalmomyiasis interna anterior associated with Cuterebra spp. in a cat. J Am Vet Med Assoc. 216(3):352–355.
Prognosis The prognosis for Cuterebra spp. myiasis is good if the cutaneous larva is removed uneventfully. However, aberrant migrations can be difficult to treat effectively.
105
CHAPTER 47
Cytauxzoonosis Mark Robson and Mitchell A. Crystal
Overview Cytauxzoonosis is caused by the small protozoan hemoparasite Cytauxzoon felis. A tissue or schizogenous phase in which schizont replication occurs within tissue macrophages leads to vascular obstruction and severe clinical disease or death. There is also an erythrocytic phase in which pyriform or signet ring-like bodies (merozoites, also known as piroplasms) are released by schizont fission and rupture of infected macrophages, which leads to infection of erythrocytes often causing hemolytic anemia. Cytauxzoon infection is most common in the south central and southeastern United States, but there is some evidence that the organism is spreading to other regions. Infection is acquired from tick vectors; Dermacentor variabilis and (experimentally) Amblyomma americanum are proven vectors and other tick species are suspected. Bobcats serve as an asymptomatic reservoir host. Outdoor cats with exposure to tick vectors are more at risk of developing the disease. Infection is most common in the spring and early summer when tick vectors are most active. Clinical signs of cytauxzoonosis include depression, anorexia, fever, pallor, icterus, dehydration, tachypnea or dyspnea, and hypothermia 1 to 2 days prior to death. Some cats may demonstrate altered mentation, vocalization, seizures, or coma in the later stages of the disease. The tissue (schizont) phase is responsible for the most severe clinical signs and is largely responsible for death of the cat. Physical examination may also reveal hepatosplenomegaly and lymphadenopathy, and an anemic murmur may be present. Without therapy cats usually die within 1 week of demonstrating clinical signs. There have been isolated reports of apparently asymptomatic cats carrying red cell piroplasms, which would imply that they have survived infection without treatment. These cats could represent a reservoir for infection of naïve ticks, as could captive felids in zoos. Recent studies have suggested that there are different genotypes of Cytauxzoon felis and that some may be less pathogenic than others. These variations may be geographical. This may explain the discovery of apparently healthy infected cats and the variable response to treatment seen. Differential diagnosis includes Mycoplasma haemofelis, other infectious agents such as histoplasmosis, immune-mediated hemolytic anemia, and neoplasms, such as lymphoma.
Diagnosis Primary Diagnostics • Complete Blood Count (CBC): Abnormalities include a mild to moderate anemia, which may or may not be regenerative. Leukocyte counts vary but are more often decreased and accompanied by occasional left shifts and thrombocytopenia. Cytauxzoon piroplasms may be seen within erythrocytes and appear as either signet ringshaped, bipolar oval safety pin-shaped, or anaplasmoid round dot-shaped bodies. Figure 47-1. Piroplasms occur near the time of pyrexia, but only 1 to 5% of erythrocytes are affected until near death, when up to 25% of erythrocytes contain piroplasms. There is usually only one piroplasm per erythrocyte, although multiples
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
106
Figure 47-1 Cytauxzoon piroplasms may be seen within erythrocytes and appear as either signet ring-shaped, bipolar oval safety pin-shaped, or anaplasmoid round dotshaped bodies. There are an unusually large number of organisms in this blood sample.
and chains of piroplasms are occasionally seen. Rarely, large mononuclear phagocytes containing schizonts of developing merozoites are seen.
Secondary Diagnostics • Chemistry Profile and Urinalysis: These may demonstrate increased bilirubin or hepatic transaminases and a prerenal azotemia. Hypokalemia, hyperglycemia, and hypoalbuminemia are sometimes present. • Spleen, Lymph node, Liver, or Bone Marrow Aspiration and Cytology: These often reveal large mononuclear phagocytes containing schizonts in various stages of development. • Polymerase Chain Reaction (PCR) Tests: These tests are now available from a variety of diagnostic laboratories. Speed of submission and reporting will be crucial due to the rapid progression of the disease.
Diagnostic Notes • C. felis must be differentiated from Mycoplasma haemofelis. C. felis organisms are single, usually signet ring-shaped bodies within the erythrocyte, whereas M. haemofelis organisms are usually coccoid or rod-shaped bodies seen on the external periphery of the erythrocyte. The degree of anemia tends to be milder in cytauxzoonosis and likely to be normochromic, normocytic and mildly or non-regenerative. The cat will probably appear much more ill than the degree of anemia suggests. With M. haemofelis the anemia tends to be more severe and strongly regenerative. See Chapter 92. • CBCs should be repeated if Cytauxzoon is suspected, as parasitemia may be undetectable one day, then large numbers of organisms may be present the next day.
Cytauxzoonosis
• In cats that die, confirmation of the diagnosis can be made as schizonts will be seen histopathologically if tissue samples are submitted.
Treatment Primary Therapeutics • Recent reports have suggested that the combination of the anti-protozoal drug atovaquone (Mepron®, GlaxoSmithKline) at 15 mg/kg q8h PO for 10 days and the antibiotic azithromycin (Zithromax®, Pfizer) at 10 mg/kg q24h PO for 10 days may result in much improved survival of affected cats. In one study 14 of 22 cats survived to discharge and of the 8 that died, 6 did so within several hours of admission. These results did not seem to be influenced by factors such as genotype of the organism, as the survival rate was much better than previously obtained in the same region. • Supportive Care: Administer fluids, nutritional support, blood products, and/or prophylactic antibiotics as needed. As disseminated intravascular coagulation (DIC) is a frequent complication, management with plasma and heparin may be helpful. The safety and efficacy of nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids has not been evaluated.
Secondary Therapeutics • Previous reports have suggested that antiprotazoal therapy, diminazene aceturate (2 mg/kg IM, repeat in 3–7 days (or imidocarb dipropionate (pre-treat with atropine sulfate 0.05 mg/kg SC to reduce drug reactions then give 2 mg/kg IM, repeat in 3–7 days), has been helpful in a few cases.
Therapeutic Notes • Cats may still die despite therapy, but the combination of atovaquone and azithromycin seems to offer much better chances than previous drug regimes. If the cat survives there seems to be no long-term sequalae. • Tick control is important in prevention, but as most tick control drugs do not kill ticks immediately, transmission of C. felis may still occur in a cat treated with tick preventatives.
Prognosis The previous guarded to grave outlook for these cats may now be improved, but some cats will be too ill at the time of presentation to be successfully treated.
Suggested Readings Birkenheuer AJ, Le JA, Valenzisi AM, et al. 2006. Cytauxzoon felis infection in cats in the mid-Atlantic states: 34 cases (1998–2004). J Am Vet Med Assoc. 228(4):568–571. Birkenheuer AJ, Cohn LA, Levy MG, et al. 2008. Atovaquone and azithromycin for the treatment of Cytauxzoon felis (abstract). Proceedings of the ACVIM Forum, San Antonio; p. 774. Brown HM, Berghaus RD, Latimer KS, et al. 2009. Genetic variability of Cytauxzoon felis from 88 infected domestic cats in Arkansas and Georgia. J Vet Diagn Invest. 21(1):59–63. Greene CE, Meinkoth J, Kocan AA. 2006. Cytauxzoonosis. In CE Greene, ed., Infectious Diseases of the Dog and Cat, pp. 716–722. St Louis: Saunders-Elsevier.
107
CHAPTER 48
Dermatophytosis Christine A. Rees
Overview Dermatophytes are keratophilic fungi that can invade hair, skin and nails. Dermatophytes are frequently classified according to their preferred host or habitat. The two most common species of dermatophyte that affect domestic animals are Microsporum and Trichophyton. These genera are divided up into three groups on the basis of their natural habitat: geophilic, zoophilic, and anthropophilic. The geophilic dermatophytes are fungi that inhabit the soil. The most common geophilic dermatophyte in cats is Microsporum gypseum. Zoophilic dermatophytes have become adapted to animals and only rarely are found in the soil. The most common zoophilic dermatophyte in cats is Microsporum canis and is the most common dermatophyte isolated in the cat. Anthrophilic fungi (i.e. Microsporum audouinii) are adapted to humans and not found in the soil. These fungi do not commonly affect cats. Transmission of dermatophytes occurs through direct contact, a contaminated fomite, or a contaminated environment. This transmission can occur in a variety of ways including animal to animal, human to animal, environment to animal or human). The source for the dermatophyte infection varies according to the species involved. Trichophyton mentagrophytes involves exposure to infected rodents or an immediate contact in the environment. M. gypseum is a soil borne fungus so infection involves exposure to contaminated soil. M. canis is the dermatophyte that is host adapted to cats. For a cat to become infected with dermatophytes some mild skin trauma, such as brushing, grooming, maceration, concurrent skin disease, or ectoparasites, is usually present. Other predisposing factors for a cat developing dermatophytosis are listed in Table 48-1. Dermatophytes invade growing hairs (i.e., anagen stage of the hair cycle) and cause damage. The hair falls out causing alopecia, and the fungus moves on to the peripheral hairs. This results in the development of a ring-like hair loss lesion; hence, the name “ringworm” is commonly used. Dermatophytes have been reported to be able to survive in the environment for 12 to 24 months. If the source of the infection is not found, it will be more difficult to treat the dermatophyte problem.
Diagnosis Primary Diagnostics • Clinical Signs: Clinical signs are extremely variable and reflect the host’s immune response to the fungus. In species-adapted dermatophyte infection, little inflammation occurs, such as in many feline infections with M. canis. See Figure 48-1. If little host response occurs, lesions may be minimal or absent, and these hosts may serve as asymptomatic carriers. On the other hand, dermatophytes that are less well host-adapted may evoke marked inflammatory responses that may be mistaken for a tumor. Dermatophytic fungi produce toxins and allergens that damage skin and elicit an inflammatory response. Erythema and follicular papules or pustules occur secondary to epidermal and follicular inflammation. See Figure 48-2. Fungal hyphae invade the hair shaft and cause breakage and loss. As the inflammatory response expels the fungus from the infected hair follicles, the infection spreads peripherally toward uninvolved hairs, leading to the classic lesion of a circular patch of alopecia with broken, stubby hair, scaling, crusts, and folliculocentric papules and pustules. Therefore, dermatophytosis must be on the differential list for any cat with skin disease. See Table 48-2. • Wood’s Lamp Examination: A Wood’s lamp is an ultraviolet light filtered through a nickel or cobalt filter. M. canis is the only dermatophytes of veterinary importance to produce tryptophan metabolites as they invade hair shafts, which fluoresce. For proper examination, warm up the light for 3 minutes, then hold it over the suspect lesion for a minimum of 3 minutes because some strains are slow to fluoresce. Fluorescence is noted as apple-green color along the hair shaft. Fluorescence of scale and crust is not diagnostic. Positive Wood’s lamp fluorescence is suggestive of a dermatophyte infection and must be confirmed by fungal culture. • Fungal Culture: This is the only reliable method for diagnosing and identifying the causative agent of a dermatophyte infection. Dermatophyte test media (DTM™) and Sabouraud’s dextrose agar
TABLE 48-1: Factors That May Predispose the Feline Patient to Dermatophyte Infection 1. 2. 3. 4. 5. 6.
Lack of previous exposure, usually meaning young age Traumatic (even mild) injury to the skin or concurrent skin disease Poor nutrition or overall health Poor environmental conditions Hot, humid climate Depressed cell-mediated immunity (i.e., retroviral infection, chemotherapy, or corticosteroid therapy)
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
108
Figure 48-1 Although this case of dermatophytosis is generalized, there is little skin reaction; alopecia and mild crusting are the primary clinical signs.
Dermatophytosis
Figure 48-2 If the cat’s immune system is robust, a marked inflammatory response occurs resulting in erythema and follicular inflammation as seen in this cat.
TABLE 48-2: Specific Host Considerations for the Cat with Dermatophytosis 1. The most common clinical presentation is patchy alopecia with scaling, primarily on head, ears, and face. 2. Pruritus is variable and can range from mild to intense. 3. Microsporum canis is responsible for >90% of feline infections. It is a zoophilic dermatophyte with the cat as a likely reservoir. It is an important zoonotic organism. It is endemic in many catteries, especially Persian and Himalayan catteries. 4. Infected catteries may have kittens with clinical symptoms, but many adults are asymptomatic carriers. 5. Dematophytic pseudomycetomas are subcutaneous to cutaneous nodules resulting from marked inflammatory reaction to fungal hyphae within the dermis. They are uncommon and mostly seen in Persians. They may be seen concurrently with “classic” lesions. M. canis and Trichophyton spp. have been reported to cause them. There is a poor prognosis with medical therapy alone; surgery is indicated.
are the most commonly used media. Dermatophytes use protein in the DTM media first, which creates an alkaline metabolite resulting in red color change as the colony grows. See Figure 48-3. Saprophytes use carbohydrates first, then use protein, resulting in red color change after the colony has grown for several days. A media color change on DTM is suggestive of a dermatophyte, but direct microscopic examination of the colony from the culture plate with the presence of macroconidia is the only way to confirm the diagnosis.
Secondary Diagnostics • Direct Examination of the Hair and Scale: These evaluate for the presence of dermatophytic arthrospore invasion into the hair shaft. Collect hair and scale form the margin of an active lesion and place it in mineral oil for direct microscopic evaluation. A clearing solution of 10 to 20% potassium hydroxide (KOH) may be used to help destroy hair and keratin, making the hyphae and arthrospores more visible. This is a good test but has a high learning curve; results are highly operator-dependent. Direct examination is difficult to interpret for inexperienced examiners. Dermatophyte infected hairs are usually broken and appear swollen, frayed, fuzzy, and irregular. Hyphae are of uniform diameter, septate, and variable length. Arthroconidia present as bead-like chains of rounded cells attached to the hair shaft. See Figure 48-4. Dermatophytes do not form mac-
Figure 48-3 A positive fungal culture results in a color change of the medium to red accompanied by a white, cottony growth.
Figure 48-4 Direct microscopic evaluation looks for the presence of dermatophytic arthrospore invasion into the hair shaft. Arthroconidia present as bead-like chains of rounded cells attached to the hair shaft.
roconidia in tissue; any macroconidia seen represent saprophytes and have no significance. Positive examination is diagnostic and should be followed by DTM culture.
Treatment Primary Therapeutics Elimination of Infection from the Host • Systemic Antifungal Medication: Systemic antifungal mediations are most always required to eliminate infection from the host in persistently infected individuals or patients with widespread disease. Griseofulvin and itraconazole are the most commonly employed systemic antifungals. Griseofulvin (microsize) is used at 30 to 60 mg/
109
SECTION 1: Diseases and Conditions
kg q12h PO, given with a high fat meal. Check for pregnancy and feline immunodeficiency virus (FIV) status prior to administration as it is teratogenic and can cause profound leukopenia in cats infected with FIV. Griseofulvin may result in liver or bone marrow toxicity so it is wise to perform a complete blood count (CBC) and chemistry panel regularly during treatment. Itraconazole is also used at 10 mg/ kg q24h PO, which may also result in liver toxicity and is teratogenic. Therapy is continued until there are two consecutive negative DTM cultures at three week intervals.
Prevent Dissemination of Spores • Prevention of further dissemination of infectious spores entails clipping (if long haired) and topical application of products, such as lime sulfur dip or enilconazole to decrease the contagious nature of the arthrospores in the hair and help prevent spread and reinfection. Some patients will worsen clinically after topical therapy is instituted due to minor skin trauma and actual spreading of the infection. Culture-negative cats within the household should be physically quarantined from the infected individuals. Fomites, such as clothing and grooming equipment, may also spread infected spores.
Environmental Decontamination • Removal of infective spores from the environment is best accomplished by vigorous vacuuming of all exposed areas. Bleach and water solution (1 : 10 to 1 : 30 dilution) may be used to cleanse and
110
disinfect all bleachable surfaces. Sheets or towels that can be washed frequently may be used to cover bedding areas.
Therapeutic Notes • Omission of any of the above three steps is likely to result in therapeutic failure for most cases of feline dermatophytosis. • Lufenuron therapy and fungal vaccines do not appear to be an effective way of treating feline dermatophytosis.
Prognosis The prognosis is good with appropriate therapy. However, clinical resolution can be extremely difficult in multiple cat households and catteries. Therefore, the prognosis will vary according to the situation.
Suggested Readings Moriello KA, DeBoer DJ, Schenker R, et al. 2004. Efficacy of pre-treatment with lufenuron for the prevention of Microsporum canis infection in a feline direct topical challenge model. Vet Derm. 15:357–362. Moreillo KA. 2004. Treatment of dermatophytosis in dogs and cats: review of published studies. Vet Derm. 15:99–107. Plumb DC. 2005. Plumb’s veterinary drug handbook, 5th ed. Ames, IA: Blackwell. Scott DW, Miller WH, Griffin CE. 2001. Dermatophytosis. In DW Scott, WH Miller, CE Griffin, eds., Small Animal Dermatology, 6th ed., pp. 5–9. Philadelphia: WB Saunders.
CHAPTER 49
Diabetes Insipidus Andrew Sparkes
Overview Diabetes insipidus (DI) is a disease characterized by severe polyuria (PU) with compensatory polydipsia (PD) with the production of hyposthenuric urine and an inability of the kidneys to concentrate urine through either an absolute deficiency of arginine vasopressin (AVP) synthesis or secretion from the pituitary (central or neurogenic DI) or a lack of responsiveness to vasopressin at the level of the renal tubules (renal or nephrogenic DI). These defects may be either partial or complete. DI is a rare disease in cats, although several cases have been well documented in the literature. Central DI can be either primary (idiopathic and congenital) or secondary (usually as a result of head trauma or pituitary neoplasia). Both primary and secondary central DI has been reported in cats. Primary nephrogenic DI (lack of vasopressin receptors or postreceptor signaling) has not been reported in cats, but secondary partial nephrogenic DI is relatively common and cause or contribute to the PU and PD seen in a variety of renal disorders (e.g., renal failure), metabolic disorders (e.g., hypercalcemia, hypokalemia, hepatic disease, and hyperthyroidism) and also drug therapy. Secondary (acquired) DI is the form that has been most commonly described in the literature. Primary central DI usually occurs in kittens (generally apparent at 2 to 6 months of age); no obvious sex predisposition has been reported. The major clinical sign is severe PU/PD, usually in excess of 100 ml/kg per 24 hours (and often in excess of 200 ml/kg per 24 hours); this is a consistent feature. The severity of the PU/PD will vary depending on whether the defect is partial or complete. If there is secondary inappetence there may be weight loss, and dehydration may occur with the obligatory PU. Onset of disease in older cats usually indicates secondary causes such as head trauma or pituitary neoplasia. History, physical examination, and routine laboratory work will normally differentiate most other causes of PU/PD in the cat (i.e., diabetes mellitus, hyperthyroidism, chronic renal failure, hyper- or hypoadrenocorticism, pyometra, hepatic disease, and so on). Unlike dogs, psychogenic PD has not been reliably reported in cats, and this is not, therefore, a major differential. In DI, routine blood tests are usually normal, or simply reflect dehydration (i.e., prerenal azotemia, hypernatremia, elevated packed cell volume). Urinalysis will reveal persistent hyposthenuria to isosthenuria depending on the severity of the DI; the urine specific gravity is usually in the range of 1.003 to 1.012.
Diagnosis Primary Diagnostics • Rule Out: Eliminate other major differential diagnoses that cause PU/PD. • Water Deprivation Test: This test confirms DI. • Vasopressin Response Test: This test differentiates central and renal disease.
Protocol: Water Deprivation Test • This test is contraindicated in the face of pre-existing azotemia.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• The cat is weighed accurately and confined to a cage without water or food. • Blood and urine samples are collected at the start, and the bladder is emptied via cystocentesis or catheterization. • The cat is accurately weighed at 1- to 2-hour intervals and monitored closely. If a urinary catheter is in place, the bladder is emptied at each monitoring time point. If cystocentesis is being performed, it may be prudent to perform the cystocentesis every 4 hours to minimize the risk of iatrogenic damage to the bladder. • The end point of the test is when body weight has reduced by 5% (i.e., significant dehydration), if physical or neurological deterioration occurs due to dehydration, or if intermittent urine sampling indicates a urine specific gravity (USG) greater than about 1.030.
Interpretation • If 5% weight loss is achieved, repeat urine sampling is carried out at this point. A urine SG of >1.030 (or osmolality >1,000 mOsm/l) is regarded as an adequate renal response. If this is not achieved, DI is confirmed in the absence of any other identified cause. It is imperative that the patient is monitored closely during a water deprivation test as life-threatening dehydration may occur. • Vasopressin Response Test: The modified water deprivation test simply assesses whether vasopressin is produced or responded to in the face of challenge with dehydration.
Protocol: Vasopressin Response Test • Immediately following the water deprivation test, a vasopressin response test is performed. • Urine concentration is determined, and the bladder emptied of urine. • Aqueous vasopressin (DDAVP®, desmopressin) is given by intramuscular injection (about 0.5–1.0 µg/kg). • Urine concentration is assessed 1 to 2 hours post-injection. • Following the test, water is reintroduced gradually (in small amounts).
Interpretation • An appreciable increase in USG (>1.015) following administration of vasopressin is indicative of central DI. • Failure to concentrate suggests nephrogenic DI. • Due to the presence of partial disease or renal medullary washout, results of testing are not always straightforward to interpret. In some cases repeat DDAVP injections over 2 to 5 days may be required to achieve a good response.
Secondary Diagnostics • Gradual Water Deprivation Test: Some clinicians prefer a gradual water deprivation test in the first part of this trial with water intake being restricted from approximately 150 ml/kg down to 70 ml/kg over 2 to 3 days prior to the abrupt water deprivation. The theory of this is that severe PU/PD may cause medullary washout in the kidneys and the gradual water deprivation may reverse this, permitting appropriate responses to the abrupt water deprivation. The disadvantage is that if there is significant obligatory PU there may be significant dehydration prior to beginning the abrupt water deprivation study.
111
SECTION 1: Diseases and Conditions
• Therapeutic Trial: To avoid the potential hazards of a water deprivation test, or where equivocal results are obtained, a therapeutic trial may be given with vasopressin. Other diseases should again be eliminated first (limiting the diagnosis to DI or psychogenic PD) and DDAVP can then be administered for 3 to 5 days with response being carefully monitored by measuring water intake and USG. In theory this is a less satisfactory test than a water deprivation test, as nonspecific responses are possible, but in some situations this may be the most appropriate course of action, and a good response is generally good evidence of the presence of DI.
Treatment • Thiazide Diuretics: Hydrochlorothiazide or chlorothiazide can reduce the polyuria (and hence polydipsia) by as much as 30 to 50% in DI cases through reducing proximal tubular sodium and water resorption and thus reducing the volume of urine reaching the distal tubule. It is the only form of therapy suitable for nephrogenic cases. Doses of the thiazides have to be titrated to the individual, and monitoring is required to ensure hypokalemia does not develop. Initial doses of 1 to 2 mg/kg of hydrochlorothiazide q12h PO or 10 to 20 mg/kg of chlorothiazide q12h PO have been recommended. • DDAVP: DDAVP is a synthetic analogue of AVP with a longer halflife. It is available in human-licensed preparations and can be given by injection, by conjunctival drops, or orally in tablet formulation for the treatment of complete or partial central DI. DDAVP injection is usually given at a dose of 2 to 5 µg/cat q12 to 24h SC. The nasal spray (100 µg/ml) can be administered as conjunctival drops. One to four drops are given q12 to 24h. Conjunctival reaction can occur limiting
112
the value of this route of administration. DDAVP is absorbed after oral administration but relatively poorly. Tablets are available and can be used successfully to treat cats at 25 to 50 µg/cat q8 to 12h PO as a suggested starting dose. This needs to be adjusted according to response, and some cats may need a higher dose. • Chlorpropamide: This drug has the ability to potentiate the effect of vasopressin in the renal tubules. It is only of value in the treatment of partial central DI, but success has been reported in at least one cat when given at 40 mg q24h PO. Care is necessary as this is a sulfonylurea and can cause hypoglycemia as well as hepatotoxicity.
Prognosis The prognosis in most cases is good as clinical signs can usually be controlled well enough to manage the condition effectively. The prognosis must be downgraded with some underlying conditions, such as pituitary neoplasia.
Suggested Readings Aroch I, Mazaki-Tovi M, Shemesh O, et al. 2005. Central diabetes insipidus in five cats: clinical presentation, diagnosis and oral desmopressin therapy. J Feline Med Surg. 7(6):333–339. Campbell FE, Bredhauer B. 2008. Trauma-induced central diabetes insipidus in a cat. Aust Vet J. 86(3):102–105. Campbell FE, Bredhauer B. 2005. Trauma-induced central diabetes insipidus in a cat. Aust Vet J. 83(12):732–735. Court MH, Watson AD. 1983. Idiopathic neurogenic diabetes insipidus in a cat. Aust Vet J. 60(8):245–247.
CHAPTER 50
Diabetes Mellitus: Chronic Complications Gary D. Norsworthy Overview Cats are relatively free of chronic complications of diabetes. Unlike dogs, they do not get diabetic cataracts and their sequela, lens-induced uveitis. They do not have peripheral vascular disease which causes necrosis and sloughing of extremities, as occurs in humans. However, three chronic complications are possible. (a) Diabetic neuropathy occurs in about 10% of diabetic cats. (b) Diabetic nephropathy occurs infrequently in diabetic cats. (c) Specific foot diseases have been reported infrequently.
Diabetic Neuropathy Overview Diabetic neuropathy is thought to be due to polyols (sorbitol and fructose) that collect excessively in Schwann cells. Several differences have been noted in the nerves of diabetic versus normal cats. In diabetic cats, the nerve water content, glucose (8-fold), and fructose (12-fold) are increased, and nerve myoinositol is decreased as compared to normal cats. The latter results in decreased nerve conduction velocity.
Diagnosis
Secondary Diagnostics • Electrodiagnostics: Electrophysiologic testing reveals motor and sensory nerve conduction changes typical of demyelination. Electromyographic testing is normal or reveals abnormalities consistent with denervation. • Histopathology: This reveals Schwann cell injury and axonal degeneration.
Treatment Primary Therapeutics • No specific therapy is known. • Good control of hyperglycemia over several weeks to months usually results in improvement or a return to a near normal state. However, not all cats respond due to permanent peripheral nerve damage.
Secondary Therapeutics • Anecdotally, the use of Vitamin B12 seems to hasten recovery. Injections of 250 µg are given q3 to 4d SC.
Primary Diagnostics • Clinical Signs: Hindlimb weakness often preventing jumping, a plantigrade posture, muscle atrophy of the hindlimb, and depressed limb reflexes and postural reaction tests. Affected cats usually walk with their hocks touching the floor. See Figure 50-1. Rarely, weakness progresses to the forelimbs.
Diagnostic Notes • The use of an oral sulfonylurea, such as glipizide or glyburide, frequently does not control hyperglycemia as well as it controls clinical signs. This will delay or prevent recovery from diabetic neuropathy.
Prognosis The prognosis for cats with diabetic neuropathy is variable. Some cats have a return to normal leg function. Others show no response even with good regulation of the diabetes.
Diabetic Nephropathy Overview
Figure 50-1 A plantigrade stance, in which the cat’s hocks touch the floor when it is walking or standing, is characteristic of diabetic neuropathy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Diabetic nephropathy is thought to occur in diabetic cats; however, its detection is complicated by the fact that most diabetic cats are geriatric, and most geriatric cats have chronic renal deterioration. Diabetic nephropathy results in membranous glomerulonephropathy, glomerular and tubular basement membrane thickening, and an increase in mesangial matrix material, subendothelial deposits, glomerular fibrosis, and glomerulosclerosis. Some of these changes overlap with some of the changes of geriatric renal deterioration so it is difficult to attribute chronic renal failure directly to diabetes. In humans, diabetic nephropathy develops and becomes clinically significant over several decades. Diabetic cats rarely live more than 10 years after diagnosis, principally because they are typically geriatric at the time of diagnosis; therefore, the relatively shorter life span of diabetic cats may preclude sufficient time to develop, or at least recognize, diabetic nephropathy.
113
SECTION 1: Diseases and Conditions
Diagnosis Primary Diagnostics • Biochemical Profile and Urinalysis: Diabetic nephropathy results in azotemia then uremia. Laboratory changes are not different from those of chronic renal insufficiency and failure. Serum creatinine and blood urea nitrogen (BUN) are elevated above normal, and urine specific gravity is decreased below 1.020. Hyperphosphatemia and hypokalemia are common sequels.
Diagnostic Notes • It is not possible to distinguish diabetic nephropathy from geriatric chronic renal disease without renal biopsy, and even then there are many overlapping features that may make diagnosis unsure. Therefore, renal biopsy is not recommended.
Prognosis The prognosis for cats with diabetic nephropathy is good as long as azotemia remains controlled.
Diabetic Foot Disease Overview There are two foot diseases that occur in diabetic cats in increased frequency: overgrown toe nails and cutaneous xanthomatosis. Overgrown toe nails occur in older cats and in sick cats that do not sharpen their nails. Because diabetic cats are usually over 10 years of age and suffering the ill effects of this disease, they are predisposed to nail overgrowth. Nail trimming should be performed on an as-needed basis. Cutaneous xanthomatosis present as whitish, waxy nodules in the skin of the feet. Their association with diabetes is somewhat presumptive. They usually resolve when diabetes is controlled.
Treatment Suggested Readings Primary Therapeutics • Renal Treatment: Affected cats are treated no differently than cats in chronic renal insufficiency (Chapter 191) or chronic renal failure (Chapter 190), depending on the level of renal dysfunction. • Diabetic Regulation: Good regulation of the cat’s diabetes is very important.
Secondary Therapeutics • Hypertension Control: Systemic blood pressure should be checked. Uncontrolled hypertension can be additionally detrimental to the kidneys. See Chapter 107.
114
Bagley RS, Rand J, King T, et al. 2006. The cat with generalized weakness. In J Rand, ed., Problem-Based Feline Medicine, pp. 941–975. Philadelphia: Elsevier Saunders. Nelson RW. 2005. Diabetes Mellitus. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1563–1591. St. Louis: Elsevier Saunders.
CHAPTER 51
Diabetic Ketoacidosis Jacquie Rand
Overview Diabetic ketoacidosis (DKA) in its severe clinical form is a medical emergency requiring prompt treatment to correct dehydration, electrolyte disturbances, and acidosis. In its mild form, cats with DKA appear as “healthy” diabetics. DKA is the result of marked insulin deficiency, and if uncomplicated by precipitating conditions, ketonemia and ketoacidosis can occur approximately 12 and 16 days, respectively, after insulin concentrations are suppressed to fasting levels. Marked insulin suppression occurs on average four days after blood glucose concentrations reach 30 mmol/L (540 mg/dL). However, many cats with DKA appear to have other intercurrent precipitating conditions including infection, pancreatitis, or renal insufficiency. Severe lack of insulin secretion results in accelerated breakdown of fat that releases free fatty acids into the circulation. Free fatty acids are oxidized in the liver to ketones that are used by many tissues as an energy source instead of glucose. This occurs when intracellular glucose concentrations are insufficient for energy metabolism as a result of severe insulin deficiency. In the liver, when insulin is deficient, instead of conversion to triglycerides, free fatty acids are oxidized to acetoacetate, which is converted to behydroxybutyrate or acetone. Ketones are acids that cause central nervous system (CNS) depression and act in the chemoreceptor trigger zone to produce nausea, vomiting, and anorexia. They also accelerate osmotic water loss in the urine. Dehydration results from inadequate fluid intake in the face of accelerated water loss secondary to glycosuria and ketonuria. Dehydration and subsequent reduced tissue perfusion compounds the acidosis through lactic acid production. In the severe form, cats with DKA have marked dehydration, hypovolemia, metabolic acidosis, and shock. There is whole body loss of electrolytes including sodium, potassium, magnesium, and phosphate, and some of these plasma deficiencies are compounded by the intracellular redistribution of electrolytes occurring after insulin therapy. Cats with severe DKA often present recumbent and may have hyperviscosity, thromboembolism, severe metabolic acidosis, and renal failure which may result in death. Differential diagnoses are in three categories. (a) Diabetic cats with another intercurrrent condition. For example, cats with acute necrotizing pancreatitis, sepsis, and acute renal failure need to be differentiated from those with DKA uncomplicated with other life-threatening conditions. Cats with DKA which do not respond within 1 to 2 days to fluid, electrolyte and insulin therapy should be suspected of having underlying disease. Acute necrotizing pancreatitis was a frequent cause of death in one study. (b) Nonketotic hyperosmolar diabetes. These cats have extreme hyperglycemia (>600 mmo/L [10,900 mg/dl]), hyperosmolality (>350 mOsm/L), severe dehydration, and severe depression but are not ketotic or acidotic. (c) Any severe illness resulting in severe depression, recumbency, and dehydration especially if there has been preceeding polyuria, and polydipsia, for example, acute renal failure superimposed on pre-existing chronic renal failure. These cats are easily differentiated from cats with DKA on the basis of the absence of ketonuria, glucosuria, and marked hyperglycemia.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Diagnosis Primary Diagnostics • Clinical Signs: Clinical signs of polydipsia, polyuria, and weight loss for several weeks prior to presentation of an acutely ill cat. However, in some cats, owners do not report polyuria and polydipsia. Ketone odor may be evident on the breath. Cats with mild DKA may have the same preceeding history but appear bright and alert on presentation. • Biochemistry and Urinalysis: Marked hyperglycemia (usually >24 mmol/L [436 mg/dl] and often over 30 mmol/L [540 mg/dl]), glucosuria, and ketonuria. Some cats have ketonemia without significant acidosis and usually present as “healthy” diabetic cats. In cats with blood glucose around 30 mmol/L (540 mg/dL), urine ketones appear at sufficient levels to result in a positive dipstick reaction approximately 5 days after beta-hydroxybutyrate is detectable in the urine and 11 days after beta-hydroxybutyrate is above the reference range in plasma (0.5 mmol/L). This is because the predominant ketone in plasma and urine in cats is beta-hydroxybutyrate, but the urinary test sticks detect mainly acetoacetate. Dipsticks and portable meters for measuring beta-hydroxybutyrate are available and are more sensitive for detecting ketosis in cats. However cats presenting with clinical signs of DKA typically are ketonuric. • Lipemia: This is visible approximately 1 week before ketonuria is evident
Secondary Diagnostics • Other Blood Values: Initially measure packed cell volume, total protein, potassium, phosphorus, total carbon dioxide, blood urea nitrogen (BUN), creatinine, and calcium as a minimum data base for guiding treatment. Serum electrolyte concentrations, particularly potassium and phosphate, and bicarbonate must be measured on admission and at least two to three times a day in the first 1 to 2 days. Although concentrations of potassium and phosphate may be elevated or normal (or subnormal) on admission, they need to be monitored two to three times daily in the first 24 to 48 hours because plasma concentrations of these electrolytes can drop rapidly once fluid and insulin therapy is begun. • Ultrasonography: Depending on signs of other intercurrrent disease, radiography and ultrasonography or other diagnostics may be indicated, for example, to assist in identifying pancreatitis. • Urinalysis: Urine sediment should be examined for signs of infection.
Diagnostic Notes • Diagnosis is rarely a problem in the severe form of DKA. • Using a cut-point of 1.5 mmol/L for urinary ketones, the sensitivity and specificity of urine dipsticks for detecting DKA in cats were reported to be 82% and 95%, respectively; when used with a cut-point of 4 mmol/L in plasma, sensitivity/specificity were 100% and 88% for detecting DKA. • Addition of hydrogen peroxide to urine does not improve the sensitivity of urine dipsticks to detect urinary ketones.
115
SECTION 1: Diseases and Conditions
Treatment Primary Therapeutics • Fluid Therapy: Fluids are essential treatment and are lifesaving. Most cats are moderately to severely dehydrated (7–12%) on initial presentation. • Fluid Type: Both 0.9% or 0.45% saline are used, although 0.9% is more common. Use of hypotonic solutions (0.45%) are advocated by some because of the hyperosmality of the plasma but are controversial. Lactated Ringer ’s solution or Normosol-R are also used as a first choice of fluid type by some. • Fluid Volume: Typically fluid deficits are corrected over 12 to 18 hours with flow rates of 60 to 150 mls/kg per 24 hours. For cats with severe signs of dehydration and poor perfusion, use doses appropriate for shock therapy; however if depression worsens, suspect cerebral edema and reduce fluid rate. Approximately one-third of sick diabetic cats in one study were hyperosmotic (>350 mOsm/kg). Although sodium is the major contributor to osmolality, and whole body hyponatremia helps to protect many DKA cats from marked hyperosmolality, the magnitude of the glucose increase is much greater than the decrease in sodium, as can be seen from the equation: Osmolality = 2 (Na + K mE/L) + 0.05 (glucose mg/dL) + 0.33 (BUN mg/dL). The normal range is from 290 to 310 mOsm/kg. • Monitoring: Diabetic cats have high continuing fluid losses until urinary glucose and ketone loss is substantially reduced; therefore, they have relatively high maintenance fluid requirements. The cat must be monitored carefully to assess adequacy of hydration and urine output; weighing the cat is an important guide for detecting over- and under-hydration during hospitalization. (Use percentage of dehydration on admission as a guide to calculating target body weight and account for 0.5 to 1% body weight loss per day associated with fasting.) • Nonketotic Hyperosmolar Diabetes: Cats with this condition should have cautious fluid replacement; replace 60 to 80% of the deficit over 24 hours and avoid decreasing serum osmolarity by more than 0.5 to 1.0 osmol/hr. • Electrolytes: Supplement fluids with potassium if it is normal or decreased. If elevated, monitor carefully and supplement as soon as in the normal range. If potassium concentrations are not available initially, supplement at 30 to 40 mmol/L; otherwise, supplement fluids using standard dosing protocols. See Chapter 114. Depending on the potassium concentration and rate at which it is falling, 40 to 80 mEq/L or more may be required. • Phosphorus: Tissue phosphorus is usually depleted and plasma levels may be normal, decreased, or increased on presentation. Hypophosphatemia results in Heinz body formation and hemolytic anemia, which may be life-threatening. Supplement phosphate as potassium phosphate, if phosphorus is normal or subnormal, and monitor serum for hemolysis. Because potassium is also depleted, one method is to divide potassium equally as potassium chloride and potassium phosphate. Alternatively correct phosphorus by adding it to calcium-free fluid and infusing at 0.01 to 0.03 mmol/L per kilogram per hour. Provide a matched blood transfusion if hemolysis is evident in the face of a decreasing packed cell volume. Excessive phosphorus supplementation can cause hypocalcemia and resultant signs. • Acidosis: Fluid expansion, provision of sodium chloride containing fluids, and insulin administration rapidly correct acidosis. Generally mild to moderately severe acidosis (HCO3 ≥ 7 mmol/L) resolves with fluid and insulin therapy, and bicarbonate administration is only recommended when HCO3 is less than 7 mmol/L. Although severe acidosis is associated with depression, decreased cardiac contractility, and peripheral vasodilatation, the disadvantages of bicarbonate therapy outweigh the advantages, including accelerated
116
development of hypokalemia and hypophosphatemia. If bicarbonate is being administered, add to fluids at the rate of HCO3(mEq) = body weight (kg) × 0.4 × (12 − patient’s HCO3-) × 0.5. If the patient’s HCO3- or total CO2 concentration is unknown, use 10 for the patient’s HCO3- value in the equation. • Insulin: Insulin therapy is needed to switch off excessive ketone formation and provide insulin sensitive tissues with glucose for energy metabolism. Because insulin therapy will worsen hypokalemia and hypophosphatemia, sometimes precipitously, commence fluid and electrolyte replacement first because severe electrolyte disturbances can be fatal. Generally wait 1 to 2 hours before beginning insulin. If potassium concentration is within the normal range after 2 hours of fluid and electrolyte therapy, begin insulin. If potassium is still below 3.5 mmol/L, insulin therapy can be delayed another 1 to 2 hours, but it should commence no longer than 4 hours after initiation of fluids. The goal with insulin treatment is to stimulate glucose uptake into cells for energy metabolism, and gradually decrease blood glucose concentrations by approximately 4 mmol/L/hr (75 mg/dL per hour) until 12 to 14 mmol/L (216–250 mg/dL). Several protocols for insulin therapy are available. Most intensive-care hospitals use continuous intravenous protocols, whereas for many practitioners, intramuscular protocols may be easier to manage. Once glucose is 10 to 14 mmol/L (180–250 mg/dL) and the cat is rehydrated, swap to subcutaneous regular insulin every 6 to 8 hours or subcutaneous maintenance insulin, which is preferred (glargine, detemir or PZI; or where a legal requirement, porcine Lente insulin) or maintain on regular insulin IM (q4–6h) until eating. • Intravenous Protocol: Add 25 units of soluble (regular or crystalline insulin; do not use Lente or NPH) to a 500-ml bag of fluids. This produces a concentration of 50 mU/mL which is infused at 1 ml/kg per hour and adjusted up or down as indicated by hourly blood glucose measurements to achieve a decrease in blood glucose concentration of 2.8 to 4.2 mmol/L per hour (50–75 mg/dL per hour). Alternatively add 1.1 U/kg body weight to a 250-ml bag of saline and infuse at 10 ml/hr to provide approximately 0.05 U/ kg per 24 hours and adjust as indicated based on blood glucose concentration. Administer insulin using an infusion or syringe pump via a second infusion line attached by a Y piece to the maintenance fluid line, or alternatively, through two separate catheters, to provide both insulin and adequate fluids. Let first 50 mL run out of the line and discard because insulin binds to plastic. Infuse insulin until glucose concentration falls to 12 to 14 mmol/L (216–250 mg/dL), then halve the rate of flow or switch to regular insulin given intramuscularly every 4 to 6 hours. Alternatively, if hydration status is good, switch to regular insulin SC every 6 to 8 hours or standard maintenance insulin SC. Glucose should be added to the fluids to prevent blood glucose concentration decreasing further, while enabling insulin therapy to be maintained to reverse ketone production. Add 50% dextrose to the fluids to create a 5% dextrose solution (e.g., 100 mL of 50% dextrose in 1 liter of fluids). • Intramuscular: There are several protocols, including regular insulin every hour or 4 hours and glargine. The advantage of the 4-hour protocol is that it is less time consuming for the staff; however, glucose concentration can drop precipitously presumably due to depots of insulin that are absorbed from previously poorly perfused muscles. • Regular Insulin; Hourly Intramuscular Protocol: Give a loading dose of 0.2 U/kg followed by 0.1 U/kg hourly, and, once blood glucose is 12 to 14 mmol/L (216–250 mg/dL), change to subcutaneous insulin (either regular insulin every 6 to 8 hours or standard maintenance insulin every 12 hours). Add dextrose to the fluids to maintain blood glucose concentration in the 12 to 14 mmol/L (216–250 mg/dL) range for the first 24 hours. • Four-Hour Intramuscular Protocol: Regular insulin or glargine can be administered every 4 hours.
Diabetic Ketoacidosis
• Glargine Protocol: Glargine administered IV or IM has the same pharmacodynamic and pharmokinetic effect as regular insulin. A simple and effective protocol in cats is to initially give glargine 2 U/ cat subcutaneously and 1 U/cat intramuscularly regardless of body weight, and repeat the intramuscular dose 4 or more hours later if the blood glucose concentration is greater than 14 to 16 mmol/L (250–290 mg/dL); repeat the subcutaneous dose every 12 hours. More than half the cats are on subcutaneous insulin only by 24 hours after admission. Add glucose to the fluids once blood glucose is 12 to 14 mmol/L (216–250 mg/dL). This protocol is simple and less time-consuming and costly for the client. Most cats are eating within 1 to 2 days if there is no other intercurrent condition. Recent research demonstrated that subcutaneous glargine twice daily and a simplified regime of intramuscular regular insulin resulted in a significantly faster time to resolution of metabolic acidosis than a constant rate infusion (CRI) of regular insulin in cats with DKA. • Nonketotic Hyperosmolar Diabetes: Reverse hyperglycemia slowly (eg. 1.1 U/kg per 24 hours regular insulin) and delay insulin for 2 to 4 hours after initiation of fluid therapy. • Food: Encourage cats to eat using palatable food or force feed, preferably low carbohydrate food; however, ingestion of food is more important than the kind of food.
Therapeutic Notes • Fluids are the number one priority together with supplementation of potassium and phosphorus. Careful monitoring of electrolytes during treatment is essential. • Insulin should be given starting 1 to 2 hours (occasionally 3–4 hours if the cat is severely hypokalemic) after fluid and electrolyte therapy.
• Other intercurrent disease is often present and needs an appropriate diagnostic and management plan.
Prognosis The prognosis for recovery from DKA to discharge from tertiary referral hospitals is reported to range from 75 to 82%, and varies depending on coexisting disease. Underlying conditions, delay in seeking treatment and inability to provide intensive care may all affect survival. One study reported that cats with DKA are no less likely to achieve remission than cats without DKA. Another study reported that cats with DKA were more likely to achieve remission than to die of DKA.
Suggested Readings DiBartola S, Panciera DL. 2006. Fluid therapy in endocrine and metabolic disorders. In S DiBartola, ed., Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice, 3rd ed., pp. 478–489. Nelson R. 2005. Diabetes Mellitus. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1563–1591. St. Louis, MO: Elsevier Saunders. Feldman EC, Nelson RW. 2004. Diabetic Ketoacidosis. In EC Feldman, RW Nelson, eds., Canine and Feline Endocrinology and Reproduction, 3rd ed., pp. 580–615. Philadelphia: Elsevier Saunders. Hume DZ, Drobatz KJ, Hess RS, et al. 2006. J Vet Intern Med. 20: 547–555. Koenig A, Drobatz KJ, Beale AB, et al. 2004. Hyperglycemic, hyperosmolar syndrome in feline diabetics: 17 cases (1995–2001). J Vet Emerg Med Crit Care. 14:30–40. www.uq.edu.au/ccah. Maintenance protocols for insulin administration are available.
117
CHAPTER 52
Diabetes: Uncomplicated Jacquie Rand
Overview Diabetes mellitus is defined as persistent hyperglycemia, regardless of cause. In primary care practice, approximately 1 in 200 cats are diabetic, with domestic shorthair cats the most commonly affected. In the United States, Maine Coon, Domestic Longhair, Russian Blue, and Siamese are overrepresented, and Burmese cats are at increased risk in the United Kingdom and Australasia. Peak age of onset is 10 to 13 years of age, and males outnumber females by 2 : 1. Risk factors include obesity, physical inactivity, confinement indoors, and administration of glucocorticoids or progestins. Multiple etiologies cause diabetes in cats, and the relative frequency depends on whether the practice is primary care or a referral hospital. In primary care practice, 85 to 95% of diabetic cats appear to have type 2 diabetes mellitus, previously called adult-onset diabetes or noninsulin dependent diabetes. Type 2 diabetes is characterized by decreased insulin secretion, insulin resistance, and amyloid deposition in the pancreatic islets. Other specific types of diabetes account for approximately 5 to 15% of cases in primary care practice, whereas in referral practice they may account for the majority of cases. Other specific types of diabetes result from disease causing either decreased insulin secretion or impaired insulin action (insulin resistance). Acromegaly causes marked insulin resistance and appears to be the most common other specific type of diabetes in cats (approximately 25–30% in referral institutions in the United Kingdom and United States). See Chapter 3. Less common specific types of diabetes include hyperadrenocorticism, chronic end-stage pancreatitis, and pancreatic adenocarcinoma (reported to account for as many as 18% in tertiary referral practice in the United States). Regardless of the cause of diabetes, at diagnosis, endogenous insulin secretion is usually very low. This is likely the result of β cell failure from the underlying cause of the diabetes, combined with suppression of insulin secretion by glucose toxicity. Glucose toxicity is defined as suppression of insulin secretion by persistently high blood glucose greater than 24 hours duration. Insulin secretion is suppressed to minimal concentrations after 3 to 7 days of blood glucose concentrations of approximately 30 mmol/L (approximately 540 mg/dL); the severity of suppression is dose dependent. Good glycemic control is essential to reverse glucose toxicity. Suppression of insulin secretion by glucose toxicity is initially functional and reversible; however over weeks and months it causes irreversible damage to β cells and β cell loss. This largely explains why cats with poorly controlled diabetes for more than 6 months have significantly reduced probability of remission, even after good glycemic control is achieved.
Diagnosis Primary Diagnostics • Clinical Signs: Classical clinical signs are polyuria, polydipsia, and weight loss. These signs are combined, at least initially, by polyphagia; however, at diagnosis many cats have reduced appetite. Signs are
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
118
usually present for weeks to months, but may be missed by some owners. Cats are often overweight initially, and then lose weight secondary to the disease. Muscle wasting and diffuse peripheral neuropathy are commonly reported, and result in weakness, difficulty jumping, and unsteadiness of gait. A plantigrade stance is less common, but likely indicative of more longstanding diabetes. See Chapter 50. Depression, anorexia and dehydration are present in about 50% of cats, whereas many others are otherwise healthy at initial presentation. • Laboratory Data: Persistent hyperglycemia is the hallmark of diabetes. Clinical signs are present once glucose concentrations exceed the renal threshold (14–16 mmol/L [250–290 mg/dL]). Acute stress, particularly if associated with struggling, can increase blood glucose by 10 mmol/L [180 mg/dL], but usually resolves within 3 to 4 hours. Transient illness-associated hyperglycemia may persist for several days. If blood glucose is <20 mmol/L [<360 mg/dL] with no or minimal glucosuria, and typical clinical signs are absent, it is advisable to repeat blood glucose measurements four or more hours later to confirm diagnosis. • Urinalysis: Glucosuria in the presence of persistent hyperglycemia is considered diagnostic of diabetes.
Secondary Diagnostics • Sick dehydrated diabetic cats often have prerenal azotemia, and electrolyte disturbances including increased or decreased potassium and phosphorus concentrations. See Chapter 51. • Urine Culture: Urine culture is indicated because many cats have secondary urinary tract infection. • Fructosamine: Fructosamine concentration provides limited additional information to glucose concentration for diagnosis, but when increased, is consistent with hyperglycemia of at least 20 mm/L (360 mg/dL) for a minimum of 4 days. • Other Screening Tests: Diabetic cats are typically 8 years of age or older. Tests for renal disease and hyperthyroidism should be performed. See Chapters 109, 190, and 191.
Diagnostic Notes • Additional diagnostic tests to identify other specific types of diabetes, such as acromegaly, hyperadrenocorticism, and pancreatic neoplasia are not usually performed unless clinical signs are suggestive, there is poor response to treatment, or there is evidence of insulin resistance. • Stress hyperglycemia rarely results in blood glucose >16 mmol/L (>290 mg/dL), and more often glucose concentrations range from 7 to 12 mmol/L (126–216 mg/dL). Cats with blood glucose of ≥20 mmol/L (≥360 mg/dL) should be treated as diabetic until proven otherwise, even if the owner has not reported any signs. • Fructosamine concentration is not sufficiently sensitive for differentiating cats with stress hyperglycemia from diabetes. • Although 60 to 80% of diabetic cats are ketonemic based on betahydroxybutyrate measurements, ketonuria is present in a smaller percentage of cats. • Any diabetic cat with visible lipemia should be considered ketotic and treated with insulin because a diabetic ketoacidosis crisis can occur within days.
Diabetes: Uncomplicated
Treatment Primary Therapeutics • Cats with marked depression and dehydration, with or without ketoacidosis, should be initially treated as for cats with diabetic ketoacidosis until they are stable. See Chapter 51. • In newly diagnosed cats with type 2 diabetes and correctable causes of other specific types of diabetes, the primary goal of therapy should be diabetic remission or noninsulin dependence. The primary goal of therapy in cats with long-term diabetes (>12–24 months) and uncorrectable causes of other specific types of diabetes is control of clinical signs and avoidance of clinical hypoglycemia. • Remission is defined as euglycemia without the need for insulin or oral hypoglycemic agents. The most important positive predictive factors for remission are early institution of rigorous glycemic control (delaying diligent management of blood glucose concentration reduces the frequency of remission significantly), and prior use of glucocorticoid treatment. Negative predicative factors are the presence of neuropathy including weakness and inability to jump, and a high maximal insulin dose required to achieve glycemic control. • Insulin Therapy: The aim of insulin therapy is to obtain blood glucose concentrations that are 4 to 11 mmol/L (72–200 mg/dL) throughout the day. In newly diagnosed diabetic cats, remission rates of ≥85% can be obtained using a protocol designed for tight glycemic control using glargine or detemir, diligent monitoring and appropriate dose adjustment, and an ultra-low carbohydrate diet. Because of the short duration of lente action, there is usually no exogenous insulin action several hours before each insulin injection. Therefore, preinsulin blood glucose is typically ≥20 mmol/L (≥360 mg/dL), and the goal of achieving glucose concentrations between 4 and 11 mmol/L (72 and 200 mg/dL) is not usually achievable throughout the day, except for cats going into remission. Remission rates are typically only 25 to 30% for lente. Published remission rates for PZI are less than for determir and glargine. • There are three phases of insulin dose adjustments. Initially there is a phase of increasing dose every 5 to 7 days by (0.25) 0.5 to 1 U, depending if on a low (<3 U) or high (≥3 U) dose of insulin, and the degree of hyperglycemia. The aim is to increase the dose until the blood glucose concentration is within 4 to 11 mmol/L (70–200 mg/ dL) throughout the day. Then hold the dose once blood glucose concentrations throughout day are 4 to 11 mmol/L (70–200 mg/dL). Decrease the dose when preinsulin blood glucose is <10 mmol/L (<180 mg/dL), or if the nadir glucose concentration is <4 to 5 mmol/L (<70–90 mg/dL). To determine if remission has occurred, stop insulin if the cat is on a minimal dose (e.g., 0.5 unit once or twice a day), and preinsulin blood glucose is <10 mmol/L (<180 mg/dL). Reassess 12 hours later; if glucose concentrations are <10 mmol/L (<180 mg/dL), recheck again in a week (have the owner measure blood glucose or urine glucose at home). Immediately reinstitute insulin if glucose concentration increases to ≥10 mmol/L (≥180 mg/dL) by 12 hours after insulin was withheld. It is important to promptly reinstate insulin as soon as a cat in remission has persistent glucose concentrations above 10 mmol/L (180 mg/dL). • Oral Hypoglycemic Agents: Oral hypoglycemic drugs that stimulate insulin secretion have limited usefulness in the management of diabetic cats. If used as a sole agent without insulin, they will substantially decrease the probability of remission. However, using oral hypoglycemic agents can be life-saving for cats when the owner would elect euthanasia rather than inject insulin, and may serve as a conduit to eventual insulin administration. The αglucosidase inhibitors (e.g., acarbose) reduce intestinal glucose absorption and, when used alone, are generally not effective in the treatment of feline diabetes. Acarbose is most useful in cats on a high carbohydrate diet that eat all of their food in one or
•
•
•
•
two daily meals. Its usefulness is minimal in cats eating multiple times in a day. Feeding an ultra-low carbohydrate diet (6% ME) has the same effect as acarbose to decrease postprandial blood glucose, but without the side effects. Dietary Management: A complete and balanced low (<15% metabolizable energy [ME]) or ultra-low (<6% ME) carbohydrate diet should be used for diabetic cats, including cats requiring weight loss. Low carbohydrate diets are associated with increased remission rates and minimize the need for β cells to secrete insulin; they are vital for effective management of diabetic cats. It is generally recommended that cats be fed twice daily at the same time as the insulin injection. Monitoring Response to Therapy: Diligent monitoring and appropriate dose adjustment are cornerstones of achieving good glycemic control. First and foremost, good monitoring involves looking at the cat and talking with the owner. Water consumption, urine output (e.g., amount of clumping in cat litter), and body weight are essential to monitor, as are signs of neuropathy and hypoglycemia. Home monitoring of glucose concentrations can provide more accurate blood glucose measurements. Daily home testing provides data to make more frequent insulin adjustments, which is advantageous because early optimization of blood glucose concentration increases the probability of remission. Home monitoring also allows immediate blood glucose assessment by the owner when vague signs are suggestive of hypoglycemia. Clients still require frequent veterinary visits so the veterinarian can review the homelog of glucose concentrations and insulin dose and examine the cat. Blood Glucose Measurement: Portable glucose meters are ideal for monitoring blood glucose concentration in the clinic and at home. With human-use meters, accuracy decreases substantially when used for feline blood; in the euglycemic range they typically measure 1 to 2 mmol/L (18–36 mg/dL) lower than actual blood glucose. It is advantageous to use a meter calibrated for feline blood and one which requires only 0.3 uL of blood. This facilitates obtaining an adequate sample from the paw or ear for glucose measurement. It is critical that staff and clients understand the difference between meters calibrated for human and cat blood, especially for interpreting readings in the low and normal range. Target glucose concentrations are dependent on the meter used. Typically blood is taken from ear or paw pad using a lancing device. Some owners prefer to draw blood “freehand” using only a lancet needle or syringe needle. Fructosamine: This is sometimes useful for monitoring, especially when clinical signs and blood glucose concentrations are conflicting, for example, if blood glucose concentrations measured in the hospital are high, but the owner reports signs of good control at home. Change in fructosamine lags behind glucose concentrations by a week and is much inferior to home monitoring in the early stages, when aiming for remission. It is more useful once the patient is stable and clinic revisits are only every 3 to 6 months.
Therapeutic Notes • Three factors are crucial in achieving high remission rates in newly diagnosed diabetic cats: (a) use of long-acting insulin (i.e., glargine or detemir), (b) diligent monitoring of blood glucose concentrations with appropriate adjustment of insulin dose, and (c) feeding a low or ultra-low carbohydrate diet.
Prognosis The prognosis for cats that achieve diabetic remission is the same as age-matched healthy cats. For cats that do not achieve remission, prognosis depends on the underlying cause of their diabetes.
119
SECTION 1: Diseases and Conditions
Editor ’s Note: The editor strongly endorses the use of long-acting insulin products in cats. His preferred insulin is protamine zinc, which he was used almost exclusively for over 30 years. The author of this chapter also endorses the use of long-acting insulin products and prefers glargine or detemir. However, the author does not have access to protamine zinc insulin. Protamine zinc insulin is not available in her homeland, Australia, and most of Europe.
Suggested Readings Marshall R, Rand JR, Morton JM. 2009. Treatment with glargine insulin improves glycemic control and results in a higher rate of non-insulin
120
dependence than protamine zinc or lente insulins in newly-diagnosed diabetic cats. J Fel Med Surg. 11(4):683–691. Nelson RW. 2000. Diabetes mellitus. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 5th ed. pp. 1438–1489. Philadelphia: Saunders. Roomp K, Rand J. 2009. Intensive blood glucose control is safe and effective in diabetic cats using home monitoring and treatment with glargine. J Fel Med Surg. 11(4):668–682. www.uq.edu.au/ccah. Maintenance protocols for insulin administration and information on home monitoring are available.
CHAPTER 53
Diaphragmatic Hernia Gary D. Norsworthy
Overview A diaphragmatic hernia (DH) is a rent in the diaphragm through which one or more abdominal organs may pass. The most common cause is trauma, usually associated with an automobile-related injury or a fall from several stories. A sudden increase in abdominal pressure directed cranially can tear the diaphragm at any point. DH may also occur in a congenital form with communication between the abdomen and the pleural space or between the abdomen and the pericardium. Other congenital defects involving the heart may also occur with congenital DH. Clinical signs may include tachypnea and orthopnea, especially if accompanied by pulmonary contusion, bleeding, or marked lung compression, and pain, especially if accompanied by rib fractures. Cats may become dyspneic immediately or a few hours later as more viscera enter the pleural space. Without treatment, some cats will stabilize in a few days, as adhesions form between the viscera and the diaphragm, and clinical signs will only be associated with increased activity. This is the chronic form. These cats often become sedentary but may live for many years without surgical correction. The acute traumatic form produces dyspnea, which may increase over 1 to 2 days as more abdominal organs are displaced into the thorax. The congenital form is often diagnosed incidentally (see Figure 53-1), but gaseous distention of organs within the pericardium may produce acute signs of dyspnea. The chronic form may produce only marked lethargy and shortness of breath upon exercise.
Diagnosis Primary Diagnostics • Clinical Signs: Dyspnea or tachypnea should cause one to consider DH, especially if there are other clinical signs or a history of trauma. • Auscultation: Muffled lung and heart sounds occur on one or both sides of the chest. • Radiography: Typical findings are loss of the diaphragmatic line and presence of abdominal viscera in the thoracic cavity, including gastrointestinal gas patterns. See Figure 53-2. The abdomen will appear smaller in size if several organs are displaced into the thorax. See Figures 291-15 and 291-16.
Secondary Diagnostics • Abdominal Palpation: Palpation may reveal an “empty” feeling due to organ displacement. • Ultrasound: This may reveal abdominal viscera within the pleural space or pericardium. See Figure 53-1C. • Celiogram: Positive contrast organic iodine material is injected into the abdomen, and the cat is gently tilted to encourage flow of contrast into the thorax. If the contrast agent is found in the thorax on a lateral radiograph, a DH is present. This procedure may be non-diagnostic for chronic or peritoneopericardial hernias. See Figure 59-1.
• Positive Contrast Study of the Gastrointestinal Tract: Barium is instilled in the stomach, and a series of radiographs are taken. The stomach or loops of the bowel may be visualized in the pericardium if a congenital peritoneopericardial DH is present. If the liver but not the stomach has herniated, the stomach will be in close proximity to the diaphragm. See Figure 53-3. • Electrocardiogram: Myocardial trauma often produces arrhythmias, especially ventricular tachyarrhythmias. • Thoracentesis: Chronic DH may produce pleural effusion classified as a modified transudate or nonseptic exudate. The fluid typically contains 25 to 60 g/L (2.5–6.0 g/dl) of protein, fibrin, nondegenerate neutrophils, macrophages, and mesothelial cells. This type of fluid can be confused with that of feline infectious peritonitis or chronic heart failure. See Chapter 288.
Diagnostic Notes • Radiographs made immediately after trauma will not be diagnostic for DH unless abdominal viscera have been displaced into the thorax. If a DH is suspected, the cat should be re-radiographed in 12 to 24 hours, or a celiogram should be performed. Owners of cats sustaining abdominal trauma should be warned of possible onset of dyspnea within 24 hours post-trauma. • Dyspneic cats should be handled carefully because increased stress may be fatal. Extreme care should be taken when doing the physical examination, radiographs, and thoracentesis. It may be necessary to place the cat in an oxygen cage or tent for several minutes prior to diagnostics and between diagnostic procedures. The least stressful radiographic view is the dorsal-ventral (DV) view; it may be the only view that is practical in some cases and often is sufficient to diagnose the presence of DH. Alternatively, some cats are more cooperative for a lateral view.
Treatment Primary Therapeutics • Stabilization: In cases involving trauma, treat for shock, improve cardiac output and ventilation, and manage concurrent injuries. Failure to do this prior to surgery may result in anesthetic death. Cage confinement for several hours, especially in an oxygen-enriched atmosphere, can be a useful part of patient stabilization. • Surgery: Repair of the diaphragm should be attempted after patient stabilization unless one or more of the following occur: (a) persistent hypotension in spite of intravenous fluid therapy; (b) severe lung compression; (c) liver failure due to entrapment; or (d) enlarging stomach or bowel due to gas entrapment. The death rate is greater if surgical repair is attempted within the first 24 hours following trauma. It is most desirable to perform surgery within the first 2 to 4 days. Following that time, adhesions develop that make the surgery more difficult.
Secondary Therapeutics th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Thoracentesis: This procedure may improve respiration, especially if pneumothorax is present. The cat’s forequarters should be elevated
121
SECTION 1: Diseases and Conditions
(A)
(B)
(C) Figure 53-1 A thoracic radiograph of a peritoneopericardial diaphragmatic hernia reveals a large cardiac silhouette (A), which if often global; however, it may be irregular, depending on the organs present and their location as seen in (B). Ultrasound can be used to identify abdominal organs that have herniated into the pericardium. It is most commonly the liver as seen in this image (C).
and the chest aspirated in the dorsal two-thirds of the thorax in the seventh to ninth intercostal spaces. The needle is inserted just deeply enough to enter the pleural space so as to avoid penetrating the lungs or the displaced abdominal viscera.
Therapeutic Notes • Arrhythmias associated with DH are usually seen 24 to 72 hours after trauma and are difficult to control with anti-arrhythmics. They usually resolve spontaneously within 5 days. • Surgical repair of congenital and chronic DH may be more difficult due to adhesions present between entrapped organs and the diaphragm or pericardium.
Prognosis Figure 53-2 Two of the most common radiographic signs of diaphragmatic hernia are lack of a complete diaphragmatic line and presence of intestinal gas in the thorax (dorsal to sternum). Both are seen in this lateral radiograph.
122
The prognosis for all forms of DH is good as long as shock and arrhythmias resolve and successful surgical repair can be accomplished. However, cats with traumatic DH may be poor surgical risks, especially if other traumatic injuries are present.
Diaphragmatic Hernia
(A)
(B)
Figure 53-3 A, Another common radiographic finding is the presence of the small bowel in the thorax. The small bowel can be easily identified when barium is placed in the stomach and allowed to pass into the small bowel. B, If the liver is herniated into the thorax but the stomach and intestines are not, the stomach and intestines will be displaced cranially but remain caudal to the diaphragm.
Suggested Readings Gibson TW, Brisson BA, Sears W. 2005. Perioperative survival rates after surgery for diaphragmatic hernia in dogs and cats: 92 cases. J Am Vet Med Assoc. 224:105–109. Mertens MM, Fossum TW, MacDonald KA. 2005. Pleural and Extrapleural Diseases. In SJ Ettinger, EC Feldman, eds., Textbook of
Veterinary Internal Medicine, 6th ed. pp. 1272–1283. St. Louis: Elsevier Saunders. Williams J, Leveille R, Myer CW. 1998. Imaging modalities used to confirm diaphragmatic hernia in small animals. Compend Cont Ed. 20:1199–1210.
123
CHAPTER 54
Diarrhea Mitchell A. Crystal and Mark C. Walker
Overview Diarrhea is best defined as an increased liquidity or decreased consistency of stools. Passage of abnormally liquid or unformed stools at an increased frequency is usually noted. There are four pathophysiologic types of diarrhea: osmotic, secretory, altered permeability (exudative), and altered motility. Osmotic diarrhea is caused by an increase in unabsorbed, osmotically active solutes within the gastrointestinal lumen. An increase in unabsorbed solutes may result from diet, maldigestion/malabsorption (e.g., exocrine pancreatic insufficiency [EPI], lymphangiectasia), and small intestinal mucosal disease (e.g., inflammatory bowel disease [IBD]). Secretory diarrhea is caused by abnormal ion transport in intestinal epithelial cells resulting in excessive secretion of fluid into the gastrointestinal lumen. Causes include enterotoxigenic bacteria, fungal and parasitic disease, IBD, cholinergic agonists, and fatty acid and bile acid malabsorption. Altered permeability is caused by disruption of the integrity of the intestinal mucosa by inflammation or ulceration leading to loss of serum proteins, blood, or mucus into the bowel lumen. Causes include nonsteroidal anti-inflammatory drugs, liver disease, infectious enteritis, IBD, and lymphoma. Altered motility leads to diarrhea as a result of decreased fluid absorption owing to decreased contact time between the intestinal absorptive epithelium and the luminal contents (decreased gastrointestinal [GI] transit time). Deranged GI motility is difficult to identify/prove in a patient because estimates of transit time are inconclusive. The cause is most often a decrease in rhythmic segmentation and, much less commonly, an increase in peristalsis. Altered motility may contribute to other mechanisms of diarrhea and is uncommonly the primary disorder causing diarrhea, such as irritable bowel syndrome and dysautonomia. Determining the pathophysiologic mechanism causing the diarrhea helps to determine the best initial supportive care for the patient. Classifying diarrhea based on chronicity, severity, and anatomical site is clinically helpful in determining the etiologic/specific cause of the problem. This directs the initial diagnostic approach and is also helpful in selecting the initial therapeutic management. Diarrhea should be categorized as acute versus persistent versus chronic, serious versus nonserious, and small bowel versus large bowel. Diarrhea is considered acute if it is less than 2 weeks in duration, persistent if it is between 2 to 4 weeks in duration, and chronic if it is greater than 4 weeks in duration. Parameters indicating serious diarrhea include loss of 10% or more of body weight, dehydration, mental depression, evidence of significant mucosal compromise (i.e., hemorrhagic diarrhea), severe electrolyte disturbances, neutrophilia or neutropenia or changes in body temperature (i.e., hypothermia or pyrexia). Features of small and large bowel diarrhea are listed in Table 54-1. It should be noted that cats with diarrhea usually have large bowel disease or significant small intestinal disease. This explains why chronic vomiting is the most common presenting sign in cats with IBD. The remainder of the assessment of the diarrhea patient includes listing specific diseases considered likely based on the aforementioned criteria. Both GI and extra-GI diseases should be included because many metabolic, neoplastic, and infectious/inflammatory diseases may manifest GI signs despite lacking primary GI involvement. Differential diagnoses for diarrhea are listed below under Diagnosis.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
124
TABLE 54-1: Differentiating Features of Small and Large Bowel Diarrhea Characteristic Frequency: Volume: Type of blood if present: Presence of mucus: Dyschezia: Urgency: Weight Loss:
Small Bowel Diarrhea
Large Bowel Diarrhea
Two to three times normal Increased Melena
More than five times normal Normal to decreased Frank
Absent
May or may not be present Present Increased
Absent Normal to mildly increased Common
Occasional
TABLE 54-2: Differential Diagnoses for Diarrhea Extra-gastrointestinal – Exocrine pancreatic insufficiency – Extra-gastrointestinal neoplasia – Diseases related to feline leukemia virus or feline immunodeficiency virus – Hepatic disease – Hyperthyroidism – Renal failure Gastrointestinal – Food allergy – Food intolerance – Infectious diseases (i.e., Salmonella or Campylobacter) – Inflammatory bowel diseases – Motility disorders (i.e., dysautonomia or irritable bowel syndrome) – Neoplasia (lymphoma, carcinoma, mast cell tumor, and others) – Nonspecific enterocolitis – Parasites (i.e., nematodes, Giardia, Cryptosporidium, Isospora, or Tritrichomonas) – Toxins and drugs
Diseases of the GI tract and extra-GI diseases must be considered in one’s differential diagnosis list. The differential list is found in Table 54-2.
Diagnosis Primary Diagnostics • Database (Complete Blood Count, Chemistry Profile, and Urinalysis): A data base should be submitted to evaluate for liver disease (i.e., hyperbilirubinemia, decreased blood urea nitrogen [BUN], increased liver enzymes, bilirubinuria), renal disease (elevated BUN and creatinine with a decreased urine specific gravity), signs of hyperthyroidism (increased liver enzymes, a mild increase in packed cell volume, low urine specific gravity), and signs of lymphoma
Diarrhea
(occasionally cats demonstrate circulating lymphoblasts and anemia). Protein-losing enteropathy from a variety of causes is an uncommon finding in cats with diarrhea (hypoalbuminemia, hypoglobulinemia). Eosinophilia is sometimes seen with parasitism, eosinophilic enterocolitis, hypereosinophilic syndrome, and mast cell tumors. Neutropenia or panleukopenia may be present in young cats with panleukopenia, cats with retrovirus diseases, and cats with salmonellosis. • Fecal Testing: A zinc sulfate flotation should be performed to evaluate for nematodes and coccidia. See Chapter 311. Zinc sulfate floatation or SNAP® Giardia testing should be performed to evaluate for Giardia. A fresh fecal smear should be evaluated for coccidia, Giardia, and Tritrichomonas. • Total T4: This test is indicated in all cats over 10 years of age with diarrhea to evaluate for hyperthyroidism. • Feline Leukemia Virus and Feline Immunodeficiency Virus Tests: These tests are not confirmatory for specific disease but are good indicators that secondary diseases are likely to be present.
Secondary Diagnostics • Fecal or Rectal Mucosal Cytology: Fecal or rectal mucosal smears are made by inserting a moistened cotton tip applicator into the rectum, rolling the swab against the rectal mucosa, withdrawing the swab from the rectum, and rolling the swab onto a glass microscope slide. Cytological evaluation of stained (Diff-Quick® or other Wright’stype stains) fecal or rectal mucosal smears may demonstrate leukocytes or a homogenous bacterial population (supporting infectious or inflammatory GI disease, prompting consideration for fecal culture) or neoplastic cells. Occasionally, a specific infectious agent such as Clostridium spp. (diagnosis is supported by greater than five spores per high power oil immersion field; spores resemble safety pins, appearing as oval structures with a dense body at one end) or Histoplasma (Chapter 97) may be seen. • Feline-Specific Trypsin-Like Immunoreactivity (fTLI): A 12-hour fasting serum sample can be submitted to evaluate for EPI in cases of chronic diarrhea. See Chapter 71. • Serum cobalamin (Vitamin B12): Hypocobalaminemia is a marker for GI disease because distal small intestinal disease decreases cobalamin absorptive capacity and cobalamin half-life is diminished in GI disease. See Chapter 37. • Fecal culture for Salmonella and Campylobacter: Fecal samples can be submitted for Salmonella and Campylobacter culture and sensitivity. Submission criteria vary from laboratory to laboratory; special media (selenite or tetrathionate media for Salmonella; Campylobacter media for Campylobacter; check with laboratory prior to sample acquisition and submission) may be required because high numbers of normal enteric bacteria present in feces tend to overgrow and mask Salmonella and Campylobacter growth. A positive culture without evidence of other disease processes supports a diagnosis. A negative culture does not necessarily eliminate the possibility of infection. See Chapter 196. • Fecal Polymerase Chain Reaction (PCR) Analysis: PCR analyses can be performed to detect the presence of Giardia spp., Cryptosporidium spp., Clostridium perfringens enterotoxin A gene, feline coronavirus, feline panleukopenia virus, Toxoplasmosis gondii, Salmonella spp., and Tritrichomonas foetus. T. foetus can be cultured using a commercially available T. foetus culture system. See Chapters 44, 83, 161, 196, 214, and 219. • Intestinal Biopsy or Histopathology: This procedure should be performed in cases of chronic diarrhea to investigate for primary intestinal diseases after other noninvasive procedures have been completed. Biopsies may be collected via endoscopy, exploratory laparotomy, or, in the case of diffuse or focal intestinal thickening greater than 2 to 3 cm (3/4–1 1/8 inch), by ultrasound guidance.
Diagnostic Notes • A complete diagnostic workup is indicated in cats with chronic diarrhea and in cats with acute or persistent serious diarrhea. Cats with acute or persistent nonserious diarrhea can be treated with supportive care without an extensive workup if fecal and quick assessment tests (i.e., packed cell volume, total protein, glucose test strip, BUN strip, urine dipstick and specific gravity) are unremarkable.
Treatment Primary Therapeutics • Treat Underlying Disease: This is the key to long-term cure. • Deworming: Anthelmintic therapy is indicated in indoor/outdoor cats even if a negative fecal is obtained. Fenbendazole at 25 mg/kg PO q24h for 3 days, repeating in 2 to 3 weeks, is the drug of choice because it is effective against nematodes and Giardia spp. • Water Only for 24 to 48 hours: Osmotic diarrhea will resolve and altered permeability will improve. Removing food will not affect secretory diarrheas. • Oral Isotonic Glucose, Amino Acid, and Electrolyte Solutions: These solutions will improve secretory diarrheas and may help with other types of diarrhea.
Secondary Therapeutics • Motility Modifiers: Diarrhea with a significant functional component may improve with opioid motility modifiers such as loperamide (0.08–0.16 mg/kg q12h PO), diphenoxylate (0.05–0.1 mg/kg q12h PO), or paregoric-containing solutions (0.05–0.06 mg/kg q12h PO). • Fluid and Electrolytes: Fluid and electrolyte therapy IV, SC, or PO should be administered based on the degree of dehydration and the amount of fluid loss in the feces. • Probiotic Therapy: Administration of live bacteria in the diet. Enterococcus (FortiFlora®, Purina), Lactobacillus and Bifidobacterium are commonly used. Anecdotal data suggests beneficial results. • Prebiotic Therapy: The feeding of complex carbohydrates (e.g., fructooligosaccharides and xylooligosaccharides) selectively alter bacterial populations in the GI tract stimulating “beneficial” bacteria (e.g., Lactobaccilli) and inhibiting “detrimental” bacteria (e.g., Clostridium). Fructooligosaccharides can be found as part of some balanced commercial cat foods. • Cobalamin (Vitamin B12): This can be administered to cats with chronic diarrhea to correct deficiencies. Supplementation has been shown to increase weight gain and decrease diarrhea. It is dosed at 250 µg q7d SC for 6 weeks, then 250 µg q14d SC for 6 weeks. Serum levels should be measured one month later. See Chapter 37.
Prognosis The prognosis varies depending on the cause of the diarrhea.
Suggested Readings Grooters AM. 2007. Diarrhea, chronic–cats. In LP Tilley, FWK Smith, Jr., Blackwell’s 5-Minute Veterinary Consult. Canine and Feline, 4th ed., pp. 384–385. Ames, IA: Blackwell. Guilford WG, Strombeck DR. 1996. Classification, pathophysiology, and symptomatic treatment of diarrheal diseases. In WG Guilford, SA Center, DR Strombeck, et al., eds., Strombeck’s Small Animal Gastroenterology, 3rd ed., pp. 351–366. Philadelphia: WB Saunders. Hall EJ, German AJ. 2005. Diseases of the small intestine. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1332–1378. St. Louis: Elsevier Saunders. Washabau RJ, Holt DE. 2005. Diseases of the large intestine. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1379–1408. St. Louis: Elsevier Saunders.
125
CHAPTER 55
Digital Diseases Mitchell A. Crystal and Paula B. Levine
Overview Disorders of the feline digit are infrequent. Potential causes (listed in Table 55-1) can include trauma (i.e., broken nail, fracture, or wound), infectious diseases (i.e., bacterial infection, fungal infection, feline leukemia virus [FeLV]/feline immunodeficiency virus [FIV]–related infection), cardiovascular disease (leading to thromboembolism), immunemediated disease, neoplasia (primary or metastatic), or metabolic disorders (i.e., hyperthyroidism, hepatocutaneous syndrome also known as necrolytic migratory erythema, superficial necrolytic dermatitis, and metabolic epidermal necrosis). The breed, age, and sex of affected cats are variable depending on the specific disease process, and cats may have single or multiple digits affected on one or more paws. Clinical signs in cats with digital disease include lameness, excessive grooming of the foot/feet, noticeable discharge or wound, digital swelling, crusting lesions, deformity or loss of a nail, or deformity of the foot. Cats with an underlying systemic illness (e.g., pulmonary neoplasia, cardiovascular disease, hyperthyroidism, or hepatocutaneous syndrome) may present only for digital disease without other signs observed by the owner. A few conditions are of special note. Digital swelling, ulceration, discharge, nail loss or deviation, or lameness due to metastatic neoplasia to the digit from primary pulmonary carcinoma (lung-digit syndrome) is occasionally seen in older cats (mean age 12.7 years, range 5–20 years). See Figure 55-1. Respiratory signs are typically absent in these patients. These lesions are often misdiagnosed as infected or nonhealing wounds. Cats with hyperthyroidism often demonstrate long, curved nails as a result of rapid nail growth. Geriatric cats that do not sharpen their nails can also develop similar problems. See Figure 55-2. Plasma cell podo-
TABLE 55-1: Causes of Digital Diseases Inflammatory or Infectious Diseases
Trauma Hereditary Disorders Immune-Mediated Disease Cardiovascular Disease Metabolic Disorders Poor Grooming Habits Neoplasia Miscellaneous
Wound or abscessation Dermatophytosis or other mycoses Declaw complications Infections related to feline leukemia virus or feline immunodeficiency virus Fractures Luxations Syndactyly Polydactyly Plasma cell pododermatitis Pemphigus Thromboembolism Hyperthyroidism Hepatocutaneous syndrome Nail Overgrowth Metastatic (lung-digit syndrome) Primary Drug eruption Eosinophilic granuloma complex
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
126
dermatitis is an infrequent condition in which heavy infiltrations of plasma cells into the tissues of the paws lead to a soft, nonpainful swelling of the footpads that can progress to ulceration and granulation. Lameness and fever may accompany the more advanced stages of the disease. The condition is believed to be immune mediated in nature. See Chapter 173.
Diagnosis Primary Diagnostics • Antibiotic Trial: A therapeutic trial with antibiotics is indicated in wound lesions known or suspected to be caused by a primary bacterial infection and in cases of secondary digital bacterial infection. • Thoracic Radiographs: Radiography is indicated in middle-aged to older cats with digital disease to evaluate for a primary pulmonary carcinoma. They can also be useful to evaluate for evidence of cardiac disease (causing secondary thromboembolic digital disease). • Biopsy for Histopathology with or without Culture: Histopathology will definitively determine the cause, aside from cases of thromboembolism/cardiac disease and the rare cases of hepatocutaneous syndrome and drug eruption where secondary lesions will be identified. These secondary lesions may suggest the causative condition. • FeLV/FIV testing: Infectious disease testing should be performed in cats that have cat bite/fight-induced digital disease or in cats with poorly healing digital wounds that are not from primary pulmonary carcinoma.
Secondary Diagnostics • Cytology of Exudates/Wound Imprints: This test is a simple means of evaluating for bacteria, inflammation, or neoplasia. However, feet lesions are often secondarily infected, and neoplastic and fungal disease might be overlooked. • Minimum Data Base (Complete Blood Count [CBC], Chemistry Profile, and Urinalysis): Screening for systemic disease is recommended if evaluation for local disease is non-diagnostic, if treatment of local disease does not result in resolution of the problem, or in cases in which systemic disease is suspected (e.g., multiple feet affected or the patient appears to have generalized illness). • Digit Radiographs: Radiographs are helpful in the evaluation of digital trauma. If treatment of local disease does not result in resolution of the problem or in cases where neoplastic disease is suspected, digital radiographs should be performed to evaluate for bone lesions. Pulmonary radiographs should accompany digital radiographs, as digital neoplasia is usually metastatic. • Fungal Culture: Testing for digital dermatophytosis is indicated if prior evaluation for local disease is non-diagnostic, if treatment with antibiotics does not result in resolution of the problem, and once primary pulmonary carcinoma has been excluded. • Total T4: Thyroid testing is suggested in older cats to evaluate for a cause of nails that demonstrate excessive growth or curving. • Echocardiogram: Cardiac evaluation is indicated to evaluate for cardiac/thromboembolic disease if evaluation for local disease is non-diagnostic, if treatment of local disease does not result in resolution of the problem, or in cases in which cardiac disease is suspected (cardiac auscultation abnormalities are present).
(A)
(B)
(C) Figure 55-1 The lung-digit syndrome occurs because the microcirculation of the toes efficiently filters circulating neoplastic cells resulting in metastasis to the ends of the digits. A, The digital lesion presents as an open wound or draining tract at the end of the digit, often from the nail bed. B, Radiographs usually reveal bony involvement. C, Thoracic radiographs reveal a lung mass, usually due to pulmonary carcinoma.
Figure 55-2 Overgrown nails occur in hyperthyroid cats due to increased metabolism and in geriatric cats due to poor grooming habits. These nails will frequently grow into the adjacent toe pad causing lameness and infection.
127
SECTION 1: Diseases and Conditions
Diagnostic Notes • Primary pulmonary carcinoma should be considered in any middleaged to older cat with digital disease. • In some cases, digit amputation may be needed to get a representative biopsy sample. This approach may eliminate the need for further surgery.
Treatment Primary Therapeutics • Antibiotic Therapy: Treatment is indicated in primary or secondary digital bacterial infections.
Secondary Therapeutics • Digital Amputation: Removal of the effected digit may help alleviate pain and secondary infection in cats with digital metastatic disease from pulmonary carcinoma. However, survival time is not improved, and lesions in other digits may still develop. Amputation can also be considered for other causes of non-healing digital wounds. • Antifungal Therapy: In cases of dermatophytosis or other digital mycotic infection, antifungal therapy is indicated. Itraconazole (5 mg/kg q12–24h PO), fluconazole (50 mg/cat q24h PO), ketoconazole (5 mg/kg q12h PO), or griseofulvin (25–50 mg/kg q12h PO) may be used. See Chapter 48. • Immunosuppressive Therapy: Immune-mediated disease, such as pemphigus (Chapter 166), eosinophilic granuloma complex (Chapter 66), and plasma cell pododermatitis (Chapter 173), will require immunosuppressive therapy. Begin the prednisone dose at 1 to 2 mg/kg q12h PO. Taper the dose gradually over 4 to 6 months to the lowest effective dose. If oral therapy is difficult, methylprednisolone acetate may be used at 2 to 5 mg/kg q14d IM, SC until a response is seen, then decreased to q4 to 8w as needed. Other agents to consider if corticosteroids are not effective include azathioprine (0.3 mg/
128
kg q48h PO until a response is seen, thereafter every 3 days), chlorambucil (0.1–0.2 mg/kg q24h PO until a response is seen, then q48h), cyclophosphamide (repeated cycles of 50 mg/m2 PO 4 days on, followed by 3 days off), or aurothioglucose or gold sodium thiomalate (gold salts, chrysotherapy; 1 mg/kg q7d IM for 16–20 weeks until a response is seen, then reduce the dose to q14d for 2 months, then monthly for 8 months, then discontinue therapy). • Manage Underlying Systemic Disease: If an underlying causative condition is identified (e.g., cardiac disease, hepatic disease, hyperthyroidism, FeLV/FIV), appropriate therapy is indicated.
Prognosis Cats with most forms of digital disease generally have an excellent prognosis for complete recovery. Prognosis for cats with neoplastic disease or systemic disease is variable depending on the condition. Cats with pulmonary carcinoma and digital metastasis have a median survival time of 67 days (range 6–122 days). Cats with plasma cell pododermatitis have a variable response to therapy. Hepatocutaneous syndrome has been rarely recognized in the cat, and prognosis is likely poor. Thromboembolic/cardiac disease-induced lesions usually heal, although the cardiac disease is typically advanced and associated with poor longterm survival.
Suggested Readings Gottfried SD, Popovitch CA, Goldschmidt MH, et al. 2000. Metastatic digital carcinoma in the cat: A retrospective study of 36 cats (1992– 1998). J Am Anim Hosp Assoc. 36:501–509. Murphy KM. 2007. Pododermatitis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult. Canine and Feline, 4th ed., pp. 1094–1095. Ames, IA: Blackwell Publishing. Rosychuk RAW. 1995. Diseases of the claw and claw fold. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XII, Small Animal Practice. pp. 641–647. Philadelphia: WB Saunders.
CHAPTER 56
Dilated Cardiomyopathy Larry P. Tilley
Overview Dilated cardiomyopathy (DCM) is characterized by severe left and right ventricular dilatation and poor systolic function, resulting in backward (i.e., pulmonary edema, pleural effusion, and ascites) and forward (decreased cardiac output) heart failure. After the discovery in 1987 that taurine deficiency was a significant cause of DCM, the incidence of this disease decreased dramatically following provision of adequate taurine in commercial foods. Dietary taurine supplementation reverses the pathology if cardiomyopathy is secondary to taurine deficiency. Currently, most cases of feline DCM are primary or idiopathic. Siamese, Abyssinian, and Burmese cats have a reported increased incidence. Familial patterns have been identified in some families of cats. A diagnosis of idiopathic DCM is made only after other causes of myocardial failure (such as nutritional or taurine deficiency, longstanding congenital or acquired left ventricular volume overload, toxic, ischemic, or metabolic-induced myocardial failure) have been ruled out. DCM results in heart failure secondary to severe left and right ventricular volume overload and poor systolic function. Typical physical examination abnormalities include weak femoral pulses, cardiogenic shock, increased respiratory sounds, cardiac murmurs, gallop rhythms, jugular distention or pulses, and ascites.
Diagnosis
Figure 56-1 Thin left ventricular walls, increased left ventricular diameter in diastole, and low fractional shortening are characteristic of dilated cardiomyopathy. All are seen in this short-axis echocardiogram. Image courtesy of Dr. Gary D. Norsworthy.
Primary Diagnostics • Echocardiography: Typical findings include severe left and right ventricular dilation, left and right atrial dilation, and left ventricular systolic dysfunction, as demonstrated by a reduced fractional shortening, due to thin left ventricular walls. See Figure 56-1. • Thoracic Radiography: Expected findings are moderate-to-severe cardiomegaly, patchy mixed interstitial-alveolar pulmonary patterns, and pulmonary venous congestion. See Figures 56-2A and 56-2B. • Electrocardiography: This reveals increased R-wave amplitude, suggesting left ventricular enlargement, and arrhythmias, such as sinus tachycardia, atrial premature complexes, and ventricular tachyarrhythmias.
Secondary Diagnostics • Taurine Analysis: Decreases in plasma and whole blood taurine levels may be seen. Plasma taurine concentrations less than 40 nmoles/L or whole blood taurine concentrations less than 250 nmoles/L are subnormal and suggestive of taurine-deficiency dilated cardiomyopathy. • Chemistry Profile and Urinalysis: Concurrent renal and hepatic dysfunction should be ruled out prior to initiation of drug therapy. • Fundic Examination: This may reveal evidence of central retinal atrophy, another possible manifestation of taurine deficiency.
Diagnostic Notes • Ascites seems to be more commonly associated with DCM than with other forms of cardiomyopathy. • Hyperthyroidism should be ruled out in all cats with DCM, even though this is uncommon. • Cats with severe left atrial enlargement are more likely to form thrombi resulting in thromboembolism.
Treatment Primary Therapeutics • Diuretic Therapy: Give furosemide at 1 to 4 mg/kg q1hr IV as needed or q2hr IM as needed for pulmonary edema. When pulmonary edema has resolved, continue furosemide at 1 to 2 mg/kg q12 to 24h PO for 1 to 2 weeks then taper further if continued diuresis is needed. • Thoracentesis: This should be considered if pleural effusion is present. • Oxygen: Supplement as needed. • Stress: Provide a low-stress environment. • Pericardiocentesis: Perform if significant pericardial effusion is present (rare).
Secondary Therapeutics The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Vasodilator Therapy: Use (a) topical nitroglycerin (3–5 mm [1/8–1/4 inch] q6–8h for 24–36 hours) in selected cases with severe acute congestive heart failure; (b) angiotensin-converting enzyme inhibitor
129
SECTION 1: Diseases and Conditions
(A)
• Pimobendan: This inodilator is also recommended to strengthen contractility and provide some vasodilation. Recommended dose range is 0.1 to 0.3 mg/kg q12h PO. Pimobendan is not currently licensed in the United States for use in cats. • Taurine Supplementation: Give to maintain normal plasma taurine levels (60–120 µmol/L). The normal dose is 250 to 500 mg q24h. • Anticoagulation: Give aspirin (10 mg/kg PO twice weekly) to possibly prevent blood clots. In one study though, no significant difference was found in survival or recurrence rate between cats receiving the traditional dose and cats receiving low-dose aspirin (5 mg q72h). Recurrence of thrombi occurs at a high rate (43.5%) even with anticoagulation. Cats with left atrial enlargement, especially greater than 20 mm in diameter, are at greatest risk for aortic thromboembolism. Consider also antithrombotic agents such as clopidogrel (18.75 mg [one-fourth of 75-mg tablet]) q24h PO; unfractionated heparin (200 units/kg q8h SC); low molecular weight heparin (daltaperin [100 units/kg q12–24h SC] or enoxaparin [1 mg/kg q12–24h SC]). • Spironolactone: This drug is used at subdiuretic dose for congestive heart failure. It is dosed at 0.5 to 1.0 mg/kg q12 to 24h PO.
Therapeutic Notes • Aggressive diuretic therapy is continued until respiratory distress resolves and is followed by a reduction in dose to maintain a normal respiratory rate (usually less than 40 breaths per minute). • Maintenance furosemide doses usually range from 6.25 mg q24h PO to 12.5 mg q8h PO. • Diuretic therapy should not precede pericardiocentesis if significant pericardial effusion is present. • Taurine supplementation may be discontinued once echocardiographic values return to within normal limits and dietary taurine intake is deemed satisfactory. However, the serum taurine level should be rechecked 30 to 60 days after discontinuing taurine supplementation.
Prognosis
(B) Figure 56-2 Cardiomegaly with pulmonary edema is seen on the (A) lateral and (B) dorsal-ventral radiographs of the same cat in Figure 56-1 that was presented with labored breathing, cyanosis, and hypothermia. Images courtesy of Dr. Gary D. Norsworthy.
Cats with a taurine–deficiency-induced DCM have a good to excellent prognosis with taurine supplementation if they survive the congestive heart failure crisis. Cats with congestive heart failure secondary to idiopathic DCM have a guarded to poor prognosis. They may survive 1 to 3 months; therapy should stabilize the patient but probably does not alter the progression of the failure. Recent use of angiotensin-converting enzyme inhibitors and spironolactone may extend survival times. More studies are needed to know the optimum therapy.
Suggested Readings therapy (enalapril, 0.25–0.50 mg/kg PO q24h or benazepril, 0.2– 0.5 mg/kg PO q24h). • Positive Inotropic Agents: Consider an intravenous agent, such as dobutamine (0.5–2.0 µg/kg per minute intravenous infusion), as needed for cardiogenic shock.
130
DeFrancisco TC. 2003. Dilated Cardiomyopathy, Feline. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 208–209. Ames, IA: Blackwell Publishing. Kienle RD. 2001. Feline cardiomyopathy. In LP Tilley, FWK Smith, Jr., M Oyama, et al., eds., Manual of Canine and Feline Cardiology, 4th ed., pp. 161–163. St. Louis: Elsevier Saunders.
CHAPTER 57
Draining Tracts and Nodules Christine A. Rees
Overview Nodules are a small, focal accumulation of cells that can be rounded or irregular in shape. A nodule is palpable in the skin and feels like a knot or lump. Focal accumulations of cells can be neoplastic cells, benign accumulation of normal cells, or cells associated with inflammation or infection. Some of the more common skin tumors that may ulcerate and ooze are squamous cell carcinoma (SCC), cutaneous lymphoma, and mast cell tumor (MCT). Each of these tumors has its own individual characteristics and is discussed in Chapters 130, 135, and 203. Melanomas are not common but occur in older cats; the average age is 10 to 11 years. No sex or breed predisposition exists for cats developing melanomas. Melanomas in cats are most commonly solitary lesions which tend to occur on the head (especially on the pinna, eyelids, and lips) and neck. Melanomas are variably circumscribed and shaped (e.g., polypoid, dome, plaque) and brown or black in color. Ulceration is frequently associated with melanomas in cats. Cutaneous lymphoma tends to affect cats that are older; the average age is 9 to 11 years. No sex or breed predisposition is reported. This tumor can look like any other skin lesion. It can be solitary or have multiple nodules or plaques, and ulcers. Some of the ulcers may have tract like lesions associated with them. Cutaneous lymphoma is usually not associated with the feline leukemia virus (FeLV) infection. Subcutaneous nodules due to infection most commonly occur secondary to bites, wounds, or scratches. Infection below the skin leads to the development of cellulitis or a subcutaneous abscess. These infectious nodules are more likely to be bite wound infections if the cat has developed swelling, focal pain, discomfort, or limping on one limb or other parts of the body. See Chapter 21. Draining tracts commonly occur secondary to these infections, but other medical conditions can also cause draining tracts. Differentials for poorly healing or relapsing subcutaneous abscesses should include atypical bacterial such as Rhodococcus equi, fast-growing Mycobacteria spp., Actinomyces spp., Nocardia spp., or systemic opportunistic fungal organisms such as Sporothrix schenckii, Histoplasma capsulatum, or Cryptococcus neoformans. Examples of additional causes for draining tracts include tumors or immune-mediated disorders. Nodules and draining tract-type lesions in cats can be associated with an underlying infection. Abscesses are likely to be infected with Pasturella multicocida, Staphylococcus spp., Bacteroides spp., Fusobacterium spp., and Peptostreptococcus spp. Wounds infected with these organisms are typically drained, flushed, and treated with appropriate antibiotics. Nodules and draining tract lesions can also be caused by higher bacteria and fungi, organisms frequently difficult to treat successfully. The clinical appearances of bacterial granulomas are varied. See Figure 57-1. Four higher bacteria that most commonly cause draining tracts are atypical mycobacteria, Nocardia spp., Actinomyces spp., and L-form bacteria. Each of these has a different source and clinical appearance. Therefore, each will be addressed individually. Atypical mycobacteria are acid-fast, rod-shaped opportunistic bacteria found in soil and water (i.e., water tanks or ponds, swimming pools, streams, creeks, rivers, and so on). The bacteria enters the skin from
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
a site of trauma resulting in a granuloma or nodular swelling (usually multiple but may be solitary) under the skin that will open and drain. Ulcers and fistulae develop as the wound becomes more chronic. Although skin lesions can occur anywhere on the body, the most common lesion locations are the inguinal or lumbar areas. The infected cat may have enlarged regional lymph nodes, and the affected area may be painful. See Chapters 144 and 282. Actinomyces spp. causes nodules and draining tracts. It is a grampositive, non-acid-fast, catalase-positive, filamentous anaerobic rod that is a commensal, opportunistic bacterium of the oral cavity and bowel. Cats are also infected by trauma from bite wounds, foreign bodies, or other types of penetrating wounds. A swelling, nodule, or draining tract may develop in the area of this wound. The most common body locations are the head, neck, paralumbar, and abdominal regions. See Chapter 4. Nocardia spp. is another bacterium that can develop nodules with or without draining tracts. This bacterium is most commonly found in the soil. Modes of transmission for Nocardia spp. include inoculation of wounds, inhalation, and ingestion. The clinical features of Nocardia spp. are indistinguishable from Actinomyces spp. See Chapter 152 and 282. L-form bacteria are partially cell wall deficient bacteria that resemble Mycoplasma spp. Cats with this type of infection most commonly have abscesses and are febrile. In addition, infected cats are depressed and have more than one draining tract lesion. The area around joints is most commonly affected. Many fungal organisms exist in the cat. The three fungal organisms that most commonly cause nodules and draining tracts in cats are Sporothrix, Cryptococcus, and Histoplasma. S. schenckii is a saprophytic fungus found in soil and organic debris. This organism enters the body through a wound; it is an uncommon problem in the United States. This fungus causes abscesses, draining tracts, cellulitis, crusted nodules, ulceration, and tissue necrosis. The areas most commonly affected are the head, distal limbs, and tail region. Systemic signs, such as lethargy, depression, anorexia and fever may be noted. This dermatologic problem is of zoonotic concern. If sporotrichosis is suspected gloves should be worn when handling the cat. See Chapter 202. Cryptococcus neoformis is a saprophytic yeast-like fungus that is associated with pigeon bird droppings. Male cats are overrepresented. Abyssinians and Siamese are thought to be at increased risk of developing cryptococcosis. A variety of different clinical signs can be seen. Abnormalities in the upper respiratory, cutaneous, central nervous system and ocular system have been reported with cryptococcosis. The types of skin lesions most commonly seen are multiple papules, nodules, abscesses, ulcers and draining tracts. The most common lesion locations are the face, pinnae, and paws. See Chapter 43. Histoplasmosis is caused by H. capsulatum. It is a dimorphic, saprophytic soil fungus most commonly seen in bird and bat excrement. Histoplasmosis is most commonly seen in the Ohio, Missouri, and Mississippi River Valleys and in Texas. Most cats that are infected with histoplasmosis are under 4 years of age. The clinical signs most commonly seen in cats with histoplasmosis include anorexia, fever, weight loss, icterus, coughing, dyspnea, ocular disease, gastrointestinal disease, and dermatologic disease. The skin lesions are nodules, ulcers, draining tracts, and papules. They are most commonly located on the face, nose, and pinnae, but they can be anywhere on the body. See Chapter 97.
131
SECTION 1: Diseases and Conditions
(a)
(b)
(c)
(d)
Figure 57-1 Subcutaneous nodules usually result in draining tracts. Although their locations differ, they all result in moist, irregular draining lesions on the skin. A, These lesions are due to Mycobacteria spp. B, These lesions are due to Actinomyces spp. C, These lesions are due to Nocardia spp. D, This image shows widespread sporotrichosis. Images A, B, and C courtesy Dr. Gary D. Norsworthy. Image D courtesy Dr. Vanessa Pimentel.
Diagnosis Primary Diagnostics • Antibiotic Therapy: Response to appropriate antimicrobial therapy is usually good if started early or if cellulitis is present. If the diagnosis is presumptive choose drugs that are likely to be effective against Pasturella multocida or staphylococcal organisms. Amoxicillin, amoxicillin-clavulanic acid, or a cephalosporin are recommended pending culture and sensitivity. See Chapter 21. • Drainage: Surgical drainage of a suspected abscess can provide confirmation. • Cytology: Aspiration cytology may help determine if the lesion is suppurative, pyogranulomatous, sterile, or septic. Special stains such as Gram stain or Brown-Brenn are required to visualize Nocardia spp., and Actinomyces spp. Nocardia’s appearance is like filamentous rods that branch at right angles (i.e., appear like Chinese letters). Fungal organisms can also be seen on cytology. In the case of sporotrichosis, the organisms can be seen on cytology (rarely, if at all, in dogs). Sporotrichosis spp. are pleomorphic yeast that appear as round, oval, or cigar-shaped organisms and are 2 to 10 µm in
132
length. Cryptococcus is similar except it can be larger (2–20 µm in diameter) and have a narrow budding base with a large mucinous capsule that has variable thickness. The capsule is clear or has a refractory halo appearance to it. Histoplasma is much smaller being 2 to 4 µm in diameter, round in shape, and having a basophilic center and a lighter halo. See Chapter 289. • Culture: Bacterial culture is usually not needed, but it is recommended when the initial antibiotic therapy is not successful. Aerobic and anaerobic cultures are recommended. Inform the laboratory if you suspect atypical mycobacteria, Nocardia spp., or Actinomyces spp. because these organisms have special growth requirements. • Histopathology: Biopsy for histopathology with special stains is indicated for draining tracts that do not respond to primary antibiotics or that produce no significant growth on culture. Suspected organisms include fungal or acid-fast organisms. One of the special stains for identification of Nocardia is modified Fite-Faraco stain. Gomori’s methamine silver stain aids in identifying sulfur granules in about 50% of the Actinomyces spp. samples. It can be used to see fungal organisms, too. S. schenckii will appear as pleomorphic yeast that are round, oval or cigar-shaped. Mayer ’s mucicarmine stain is useful to aid in visualization of the large capsule seen in Cryptococcus spp.
Draining Tracts and Nodules
Secondary Diagnostics • Fungal Serology: Fungal serology may be a helpful adjunct investigation. See Chapters 22, 38, 43, and 97. • Retroviral Serology: An FeLV antigen test and feline immunodeficiency virus (FIV) antibody test are indicated in cats with nonhealing or poorly healing wound or draining tracts.
Treatment Primary Therapeutics • Antimicrobial Therapy: Appropriate antimicrobial drugs based on culture or histopathology if primary antibiotics are not successful. In cases where the bacteria are suspected but culture and sensitivity are not available, antibiotic selection can be made based on previous reports and response to therapy. Antibiotics reported to be effective against Nocardia spp. include sulfa antibiotics, azithromycin, amikacin, enrofloxacin, chloramphenicol, tetracyclines, and clarithromycin. Cats should be supplemented with folic acid when sulfa drugs are used. Actinomyces spp. is commonly responsive to high dose penicillins. Other antibiotics that may be effective to treat Actinomyces spp. are clindamycin, erythromycin, cephalosporins, chloramphenicol, and tetracycline. Atypical mycobacteria should be surgically excised or debulked if possible. Antibiotics that have been reported effective against atypical mycobacteria are doxycycline, enrofloxacin,
clofazimine. Cats should be treated for 4 to 8 weeks beyond when the skin appears normal (i.e., no palpable nodules or draining tracts). • Antifungal Therapy: Antifungal therapy varies depending on the fungal organism present. Sporotrichosis responds the best to supersaturated solution of potassium iodide. Cryptococcosis responds to fluconazole and itraconazole. Histoplasmosis also responds to amphotericin-B, itraconazole, and fluconazole. See Chapters 22, 38, 43, and 97.
Prognosis The prognosis for abscesses and cellulitis related to bite wounds is good. The prognosis for draining tracts is variable depending on one’s ability to identify the organism, the pathogenicity of the organism, the degree and duration of infection, and the cat’s response to specific therapy. The prognosis is guarded for infections with higher bacteria.
Suggested Readings Scott DW, Miller WH, Griffin C. 2001. Small animal dermatology, 6th ed. Philadelphia: WB Saunders. Greene CE. 2006. Infectious diseases of the dog and cat, 4th ed. Philadelphia: WB Saunders. Love DN, Jones RF, Bailey M, et al. 1979. Isolation and characterization of bacteria from abscesses in the subcutis of cats. J Med Microbio. 12:207–212.
133
CHAPTER 58
Dysautonomia Karen M. Lovelace
Overview Dysautonomia, also called Key-Gaskell syndrome, was first described in 1982 by Key and Gaskell in the United Kingdom. Originally reported only in Europe, the syndrome now occurs worldwide, but cases are primarily reported in the United Kingdom and Scandinavia. In the United States, it has a regional prevalence in Kansas and Missouri but has also been reported in Oklahoma, Indiana, and California. A rare disease, the incidence of reported cases of this autonomic polyneuropathy in cats has declined significantly from the 1980s. The syndrome is characterized by diffuse autonomic dysfunction and tends to affect cats 5 years of age and under with no known sex predilection. Clinical onset is usually acute, with signs developing over 2 to 3 days. Rarely, the onset of clinical signs will take a week or longer. Initial signs are usually nonspecific, such as lethargy, depression, anorexia, and rarely fever. Signs relevant to the gastrointestinal (GI) tract usually follow, including vomiting and regurgitation, and diarrhea or constipation. Pulmonary aspiration may be a secondary complication of vomiting. Additional signs may include dysuria with a distended urinary bladder, dry mucus membranes or a dry nose, mydriasis with depressed pupillary reflexes, keratoconjunctivitis sicca (KCS), prolapsed third eyelids, dysphagia, bradycardia that is non-responsive to exercise or stress, and weight loss. See Figure 58-1. Less common findings include loss of anal tone and mild postural reaction deficits especially in the hind limbs. No cause has been discovered for feline dysautonomia. The epidemic history of the disease has led researchers in search of an infectious or
toxic agent. Due to the concentration of cases in the United Kingdom and in Kansas and Missouri, an environmental agent was suspected. Autoantibodies against ganglionic acetylcholine receptors have been demonstrated in dogs with the disease, but it is still unknown whether this finding represents a cause or an effect of the pathophysiology of the disease. The Clostridium botulinum type C neurotoxin was successfully isolated from the feces, ileal contents, serum, and the dry cat food of a group of affected cats from a closed colony of eight in the United Kingdom, but the definitive cause is still unknown.
Diagnosis Primary Diagnostics • Clinical Signs: The constellation of clinical signs including vomiting, diarrhea, constipation, ileus, decreased GI motility, KCS, mydriasis with depressed pupillary light reflexes, prolapsed third eyelids, weight loss, dysuria or urine dribbling, distended bladder, and possible bradycardia, dilated anal sphincter, or decreased to absent spinal reflexes should raise the suspicion for feline dysautonomia. • Pilocarpine Test: Denervation of the iris muscle renders it hypersensitive to cholinergic drugs. In normal animals, administering dilute (0.05–0.1%) pilocarpine ophthalmic solution should cause eventual miosis (approximately 30 minutes). Symptomatic animals will exhibit rapid papillary constriction. • The Schirmer Tear Test: This is also consistently decreased in affected cats, with tear production under <5 mm/min. • Wheal and Flare Test: Histamine at a concentration of 1 : 1000 is administered intradermally side by side with a saline control. Normal animals show a wheal and flare within several minutes. Affected cats will show no response or will show a slight wheal without a flare. • Atropine Challenge Test: Atropine (0.04 mg/kg SC) is administered, causing tachycardia in the normal animal. In cats with dysautonomia, there will be no increase in heart rate.
Secondary Diagnostics • Radiographs: Megaesophagus (with or without aspiration pneumonia), distended urinary bladder, generalized ileus, and delayed transit time or gastric emptying after barium administration support the diagnosis of dysautonomia. • Enzyme-Linked Immunosorbent Assay (ELISA): Feces may be tested for Immunoglobulin A by ELISA to test for recent exposure to C. botulinum type C toxin. • Histopathology: Tissue samples may be submitted to look for degenerative lesions in the axons and nerve cell bodies of sympathetic and parasympathetic ganglia. Multiple samples are recommended. Figure 58-1 This cat is showing typical signs of dysautonomia including mydriasis, photophobia, protrusion of nictitating membranes, and xerostomia with dried, crusted nasal secretions. Photo courtesy Dr. Andrew Sparkes.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
134
Diagnostic Notes • Blood pressure tests are available to confirm the diagnosis, but these tests are dangerous, difficult to administer, or unreliable in feline patients and, therefore, are not routinely performed. • Cases of autonomic dysfunction originating from Kansas, Missouri, or the United Kingdom should evoke a suspicion of dysautonomia.
Dysautonomia
• There are no consistent clinical pathology findings for dysautonomia cases.
• In cases of megaesophagus, antibiotics should be administered if aspiration pneumonia is suspected.
Treatment Therapeutic Notes Primary Therapeutics • Supportive: Treatment is largely supportive and is aimed at supporting body functions. Symptomatic care is provided as necessary. • Metoclopramide: Metoclopramide (0.5 mg/kg q8h SC or PO) will enhance the activity of any viable acetylcholine on muscarinic receptors. Cisapride (2.5–5.0 mg/cat q8–12h PO) may also be effective at improving GI motility and gastric emptying. • Bethanechol: Bethanechol (1.25–5.0 mg q8h PO) is used to stimulate bladder contraction as well as to stimulate gastric and intestinal motility. • Pilocarpine: Pilocarpine 1% ophthalmic drops are used to stimulate lacrimation and salivation and may improve mydriasis. • Artificial Tears: Artificial tears, or a product with hydroxymethylcellulose, are used to prevent ophthalmic ulceration and improve the cat’s comfort.
Secondary Therapeutics • Frequent manual expression of the bladder or intermittent urinary bladder catheterization will help maintain bladder evacuation. Urine cultures and antibiotics should be used as appropriate to prevent and treat secondary urinary tract infection.
• Pharmacological effects on muscarinic receptors may be temporary only.
Prognosis Prognosis for dysautonomia is poor. Clinical signs are usually persistent. Fewer than 25% of affected cats survive, and survivors may take more than a year to recover.
Suggested Readings Ettinger SJ. 2005. Peripheral Nerve Disorders. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed. p. 899. St. Louis: Saunders. Kidder AC, Johannes C, O’Brien DP, et al. 2008. Feline dysautonomia in the Midwestern United States: A retrospective study of nine cases. J Fel Med Surg. 10(2):130–136. Nunn F, Cave TA, Knottenbelt C, et al. 2004. Association between KeyGaskell Syndrome and infection by Clostridium botulinum Type C/D. Vet Rec. 155:111–115.
135
CHAPTER 59
Dyspnea Gary D. Norsworthy
Overview Dyspnea is defined as difficulty breathing. The term is frequently used to describe polypnea or tachypnea, two terms that mean rapid breathing, which is more common than true dyspnea in cats. Although the cat’s normal respiratory rate is about 20 to 60 breaths per minute, a rate over 50 is suspicious for disease. The causes of dyspnea are numerous; they are often divided into categories according to the part of the respiratory system that is involved in their pathogenesis. Clinical signs are varied and determined by the location of the abnormality. They include panting, increased abdominal effort, nasal flaring, neck extension, elbow abduction, nasal stertor, upper airway stridor, coughing, expiratory wheezing, pulmonary crackles, and hyperthermia. Because many dyspneic cats are fragile patients, initial care and assessment must be performed quickly and judiciously.
TABLE 59-1: Classification of Causes of Dyspnea Oxygen Deprivation
Anemia Methemoglobinemia Central nervous system disease and shock Congestive heart failure
Upper Airway Disease
Laryngeal paralysis or obstruction Obstructive rhinitis Nasal airway obstruction Nasopharyngeal masses or stenosis Tracheal obstruction, collapse, or compression Inhaled irritant
Lower Airway Disease
Pulmonary edema (i.e., cardiac or pulmonary disease) Pneumonia (i.e., viral, bacterial, fungal, foreign body, or parasitic) Pulmonary trauma (i.e., contusion, torsion, or cysts) Thoracic wall trauma (i.e., open pneumothorax or flail segment) Heartworm disease or Heartworm Associated Respiratory Disease Bronchial asthma Emphysema Pulmonary neoplasia (primary or metastatic) Pulmonary compression from obesity, ascites, or abdominal organomegaly Pulmonary thromboembolism
Pleural Space Disease
Chylothorax (primary or secondary) Pyothorax Hemothorax (i.e., trauma, coagulopathy, bleeding disorder, or torsion) Pneumothorax (i.e., trauma, parasitic, or iatrogenic) Diaphragmatic hernia (i.e., trauma or congenital) Neoplasia (i.e., lymphosarcoma, mesothelioma, thymoma, or pulmonary neoplasia) Hydrothorax (i.e., cardiogenic, pericardial disease, mediastinal mass, Feline Infectious Peritonitis, diaphragmatic hernia, or lung lobe torsion)
Diagnosis Differential Diagnoses The diseases that cause dyspnea have been classified and are shown in Table 59-1.
Primary Diagnostics • Mucous Membrane and Tongue Color: The presence of cyanosis or pallor indicates that a respiratory crisis is present and dictates that emergency therapeutic measures are taken before further diagnostics are considered. • Auscultation: The rate and depth of respiration should be determined. Lung and heart sounds should also be assessed. • Radiographs: The most meaningful diagnostic test is a set of high resolution radiographs of the chest. Including the cervical area or skull is desirable but usually not essential in a crisis situation. The presence of pleural effusion must be determined because it is frequently present in dyspneic cats. Radiographs of the skull are indicated if upper airway obstruction is likely. • Thoracentesis: Aspiration of the pleural space can determine the presence of air or fluid. The most common findings include dull lung sounds, murmurs, tachycardia, and pounding heart sounds. • Pleural Fluid Analysis: If fluid is recovered from the pleural space, the following minimal number of tests should be performed: (a) Total protein content or specific gravity; (b) white blood cell count; and (c) cytology. If bacteria are found on cytology, aerobic and anaerobic cultures should be performed. See Chapters 171 and 288.
Secondary Diagnostics • Laryngopharyngoscopy: Observation of the pharynx and larynx with a laryngoscope or endoscope may reveal masses or other airway obstructions. Observe the function of the larynx. See Chapter 126.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
136
• Nasopharyngoscopy: An endoscope less than 2 mm in diameter and capable of reflexing 160 degrees or more can be passed orally and retroflexed into the nasopharynx to see masses, stenosis, and discharge. • Celiogram: If diaphragmatic hernia is suspected, but the chest radiographs are inconclusive, 5 mL of an intravenous contrast material are injected into the abdomen to see if it will migrate into the thorax. See Figure 59-1. • Feline Leukemia Virus (FeLV) Antigen Test: If the cytology is suggestive of lymphoma, this test should be performed. It will not rule this disease in or out, but it will document a contagious state. • Complete Blood Count (CBC): Eosinophilia is an inconsistent finding in bronchial asthma and heartworm disease. • Heartworm Antibody and Antigen Tests: These tests are useful in confirmation but have a significant number of false-negatives. Other tests are indicated if heartworms are suspected and these tests are negative. See Chapter 88.
Dyspnea
can help to stabilize the cat. This confinement may be necessary between various diagnostic procedures. • Thoracentesis: The removal of 60+ mL of air or fluid can stabilize the cat. Removal of 200+ mL is often achieved. • Body Temperature: Dyspneic cats are prone to hyperthermia. One should monitor body temperature closely and use appropriate means to maintain normal body temperature.
Secondary Therapeutics
Figure 59-1 To confirm the presence of a diaphragmatic hernia, inject 5 mL of an intravenous contrast material into the abdominal cavity (celiogram). A hernia is present if the contrast material migrates through the hernia into the thoracic cavity. Note that the diaphragmatic line is not intact. Prior to making the radiographs, cautiously elevate the cat’s rear quarters to encourage cranial migration of the contrast material.
• Bronchoalveolar Lavage and Transtracheal Wash: These can be helpful in determining the presence of asthma, parasites, and pneumonias. • Echocardiography: This should be performed when cardiac disease, heartworm disease, or an intrathoracic mass is suspected. • Coronavirus Titer: This should be performed when feline infectious peritonitis (FIP) is suspected. See Chapter 76 for interpretation.
Diagnostic Notes • If a radiograph is not feasible because of the critical condition of the cat or due to financial limitations, thoracentesis that removes fluid or air can stabilize the patient; if fluid is recovered, it can be analyzed as part of the diagnostic workup. • In a 4-kg (8.8-lb) cat, a minimum of 50 mL of pleural effusion must be present for it to be radiographically discernible. However, a cat this size may accommodate up to 150 mL of pleural fluid without being significantly dyspneic. • It is important to distinguish whether respiratory distress is more associated with inspiration or expiration. Expiratory dyspnea (prolonged or difficult expiration) is usually attributed to lower airway disease, and inspiratory distress (prolonged or difficult inspiration) is usually linked with upper airway or pleural space disorders.
Treatment Primary Therapeutics • Oxygen: Placing the cat in an oxygen cage or oxygen tent can be life-saving. • Cage Confinement: Even if an oxygen cage is not available, placing the cat in a cage away from the sight or sound of dogs or other cats
• Emergency Treatment: The administration of all three of the following can be life-saving to cats with heart failure, heartworm disease, or severe bronchial asthma. One dose of each is unlikely to be harmful to a cat with any of the diseases causing severe dyspnea. This approach should be considered when the cat is so dyspneic that diagnostic procedures could be fatal. • Furosemide: One 3 mg/kg intravenous dose. Contraindications include dehydration and renal failure. If an intravenous dose is not feasible, use the intramuscular route if possible. • Corticosteroids: One dose of a short-acting steroid (i.e., 1 mg/kg of dexamethasone sodium phosphate) can be helpful for cat with bronchial asthma, heartworm disease, and laryngeal edema. Because cats with bronchial asthma are likely to have secondary bacterial pneumonia, steroids should not be repeated until antibiotics are started. • Nitroglycerin: Topical application of 2 to 4 mg (approximately 0.6 cm [1/4 inch] of ointment) to the inside of the pinna. Gloves should be worn when applying this medication.
Therapeutic Notes • The administration of intravenous fluids should be done cautiously or not at all if catheter placement is too stressful. Fluid overload can be fatal to cats with pulmonary edema or other serious lung disease. • Dyspneic cats have increased distress in ventrodorsal and lateral recumbency. Try to maintain them in a dorsoventral position. • Intubation or temporary tracheostomy should be employed when airway compromise is life-threatening. • Drainage of 100+ mL of ascitic fluid can take pressure off the diaphragm and aid respiration. • Surgical repair of a traumatic diaphragmatic hernia is indicated. In some cases, survival is better if surgery is delayed for 12 to 24 hours. See Chapter 53.
Prognosis The prognosis is variable depending on the condition at the time of presentation, the response to emergency treatment, and the primary disease.
Suggested Readings Hopper K. 2007. Dyspnea, tachypnea, and panting. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 402–403. Ames, IA: Blackwell Publishing. Mason RA, Rand J. 2006. Cat with lower respiratory tract or cardiac signs. In J Rand, ed., Problem-Based Feline Medicine, pp. 47–69. Philadelphia: Elsevier Saunders.
137
CHAPTER 60
Dystocia Gary D. Norsworthy
Primary Diagnostics
Overview Dystocia is difficulty during parturition. Causes can generally be classified into one of two categories: maternal or fetal. There are three stages of labor: (a) onset of uterine contractions and dilation of the cervix, (b) delivery of the fetuses (lasting 4–24 hours), and (c) delivery of the fetal membranes. Dystocia occurs during Stage 2. However, with multiple births, there is alternation between Stage 2 and Stage 3 so dystocia may be intermittent.
Diagnosis Differential Diagnoses Several diseases and disorder must be considered. See Table 60-1.
TABLE 60-1: Causes of Dystocia Maternal
Fetal
Geriatrics Abrupt change in environment at or near parturition time Obesity Narrowed birth canal due to old fracture or other abnormality Insufficient cervical dilation Uterine inertia Hypocalcemia Hypoglycemia Inadequate oxytocin production Placentitis, endometritis Ineffective abdominal pressure Exhaustion Diaphragmatic hernia Chronic or acute pain Fear Uterine torsion Uterine rupture Uterine neoplasia Abnormal vaginal vault Stricture Cyst or neoplasia Small or strictured vaginal opening Ectopic pregnancy
Secondary Diagnostics • Ultrasound: Fetal viability can be determined most accurately by observance of fetal movement and cardiac contraction. Fetal stress is indicated by fetal heart rates <195 or >260 beats per minute. Response to oxytocin therapy for uterine inertia can also be determined.
Diagnostic Notes • The use of radiographs or ultrasound frequently results in underestimation of litter size. Radiographs are the more accurate of the two.
Excessive fetal size (especially litters of one or two kittens) Excessive fetal head size (especially brachycephalic breeds) Fetal death Fetal morphologic abnormalities Abnormal fetal presentation, position, or posture in the birth canal
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
138
• Clinical signs: Dystocia should be suspected when there is (a) more than 2 hours between the passage of a greenish-black discharge (uteroverdin) and the birth of a kitten, (b) diminished or absent Ferguson reflex (feathering of the dorsal vaginal wall), (c) more than 30 minutes of continuous strong abdominal contractions without birth, (d) more than 4 hours of intermittent abdominal contractions without birth, (d) more than 10 minutes of continuous contractions with a kitten in the birth canal, (e) more than 2 hours between delivery of kittens, (f) crying and constant licking of the vulva when contractions are occurring, (g) acute depression during Stage 2 (usually associated with uterine rupture), (h) fresh vaginal bleeding of more than 10 minutes duration, or (i) gestation that lasts more than 68 days from breeding. • Palpation: This is the least accurate test, but it can permit one to make some determination of fetal size. • Radiology: Fetal size, number, and position can be assessed. In some cases, fetal death can be determined by the presence of intrauterine gas or the collapsing of fetal cranial bones or other osseous malposition. See Figure 60-1. The size and shape of the birth canal can be assessed.
Figure 60-1
Intrauterine gas is a sign of fetal death in this term kitten.
Dystocia
• Cesarean Section: Surgical removal of the kittens is recommended when (a) oxytocin and calcium are not effective, (b) if uterine disease is present (i.e., inertia, torsion, or rupture), or (c) if the pelvic : fetal ratio prohibits fetal passage. Premedication with glycopyrrolate (10 µg/kg IM) or atropine (0.04 mg/kg IM) is recommended. Atropine is preferred for fetal bradycardia. The use of rapidly eliminated anesthetics (propofol for induction [4–6 mg/kg IV] and sevoflurane or isoflurane for maintenance) is highly recommended for the benefit of the queen and the kittens.
Therapeutic Notes • Cesarean section can be a life-saving procedure for both the queen and kittens. It should not be delayed unnecessarily. • The queen can voluntarily control parturition so environmental stress can prolong it or delay its onset. Figure 60-2 Head lock occurs when the diameter of the fetal head is greater than the diameter of the pelvic canal. A prompt Caesarean section is needed to save this kitten.
Treatment Primary Therapeutics • Calcium: For hypocalcemia give 10% calcium gluconate (0.2–1.5 mL/ kg [5–15 mg/kg] or 0.5–1.0 ml slowly IV) while monitoring for arrhythmias, especially bradycardia. • Oxytocin: This drug is given (0.5–5.0 U IM q20–30m) for two or three injections. Additional doses are not recommended. It can be repeated 60 minutes or more past the birth of a kitten.
Prognosis The prognosis is excellent for the queen and kittens if medical or surgical intervention occurs quickly.
Suggested Readings Johnson SD, Root Kustritz MV, Olson PNS. 2001. Female parturition. In SD Johnson, MVR Kustritz, PNS Olson, eds., Canine and Feline Theriogenology, 2nd ed., pp. 431–437. Philadelphia: WB Saunders. Lopate C, Archbald LF. Dystocia. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 404–405. Ames, IA: Blackwell Publishing.
139
CHAPTER 61
Dysuria, Pollakiuria, and Stranguria Gary D. Norsworthy
Overview Diseases of the lower urinary tract (i.e., urinary bladder and urethra) are common in male and female cats. The basic mechanisms are damage to the bladder wall and stimulation of sensory nerve endings in the bladder or urethra. Either can result in increased urethral outflow resistance or lower urinary tract pain or inflammation. Affected cats are generally presented with dysuria (difficulty urinating), pollakiuria (urinating small quantities of urine with increased frequency), and stranguria (slow and painful urination with a narrow urine stream). These signs are often accompanied by hematuria or urination out of the litter box (inappropriate urination). The signs are present in several disease states; they are not specific to any one disease as urinary tract disease of almost any cause is manifested with a limited number of clinical signs. Therefore, the presence of these signs should not result in a diagnosis but a diagnostic workup. Polyuria and urine spraying or marking may cause behavior that some owners may report as dysuria. Macroscopic vesicourachal diverticula have been associated with dysuria and pollakiuria; however, they are considered a consequence not a cause. The differential diagnoses are: • • • • • • • • • • • •
Feline idiopathic (sterile) cystitis. Bacterial or fungal cystitis. Urethral obstruction. Urolithiasis (bladder or urethral). Bladder or urethral tumors (benign or neoplastic). See Figure 61-1. Soft tissue strictures at the neck of the bladder or of the urethra. See Figure 61-2. Neurogenic bladder. Cyclophosphamide cystitis. Urethral inflammation or stricture. Traumatic cystitis or urethritis. Iatrogenic bladder or urethral trauma (catheterization, palpation, reverse flushing, urohydropropulsion, surgery, etc.) See Figure 61-3. Prostatitis in intact male cats
Note that owners may confuse constipation and dysuria based on positioning in the litter box. The differentials for constipation should also be considered. See Chapter 40.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
140
Diagnosis Primary Diagnostics • Urinalysis: Pay attention to the presence of crystals, noting the type and number. The preferable sample is collected by cystocentesis with a 22-gauge needle; this procedure may cause or increase hematuria especially when the bladder wall is inflamed. • Bladder Ultrasound: Uroliths in the bladder, kidneys, and sometimes urethra can be seen. Masses in the bladder are also readily seen. See Figures 61-1, 292-60, 292-72, and 292-75 through 292-78. • Survey Radiographs of the Bladder and Urethra: Radiopaque renal, ureteral, bladder, and urethral uroliths may be visualized with radiographs. See Chapter 222. • Urine Culture: Bacterial cystitis is not common in cats under 8 years of age; only about 2% of cats less than 8 years of age with cystitis have positive urine cultures. Dysuric cats 10 years old and older should have their urine cultured. Some cats with quiet urine sediment will have bacteria recovered on a urine culture.
Secondary Diagnostics • Double Contrast Radiographs of the Bladder: Radiolucent uroliths that are not seen on scout radiographs can be seen with this procedure. They are also seen with ultrasound. See Figure 292-76. • Positive Urethrogram: Urethral stricture, due to soft tissue lesions or uroliths, can often be diagnosed with this procedure. See Figures 61-2, 61-3, and 292-80. • Bladder Endoscopy and Biopsy: This procedure may be helpful when neoplasia is suspected. However, equipment limitations make this procedure of limited value.
Diagnostic Notes • Bacteria recovered from a urine culture may originate from the kidney. Pyelonephritis is more prevalent than bacterial cystitis in young cats. • Feline idiopathic cystitis is the most common cause of dysuria/pollakiuria in cats. Although it is a diagnosis of exclusion, it is a nonlife-threatening disease as long as it does not lead to urethral obstruction. It is also self-limiting in most cats in 7 to 14 days. Therefore, it is common practice to diagnose this disease based on clinical signs alone and delay an in-depth workup until the signs persist for more than 14 days. See Chapter 74. • Care should be taken when palpating a distended bladder. Excessive digital pressure can cause bladder rupture. • The minimum data base for a first-occurrence dysuric young cat consists of urinalysis and bladder ultrasound. If the cat is 10 years of age or older, a urine culture is added.
(A) (B)
(C) Figure 61-1 A, A mass is seen attached to the dorsal wall in this transverse view of the bladder. The cat was presented for hematuria and dysuria. B, The mass is seen following excision. It was identified histologically as a transitional cell carcinoma. C, Another transitional cell carcinoma (TCC) is seen as a mass attached to the cranioventral wall of the bladder. Unlike dogs, TCCs in cats usually do not occur at the neck of the bladder.
Figure 61-2 This cat has several urethral obstructions. Repeated catheterizations resulted in a stricture seen in this retrograde urethrogram.
Figure 61-3 This cat had a urethral obstruction due to a calcium oxalate urolith. An overzealous attempt to achieve catheterization resulted in urethral laceration, which further compounded the obstruction as seen in this retrograde urethrogram. The filling defect in the bladder is an air bubble.
141
SECTION 1: Diseases and Conditions
Treatment Primary Therapeutics • The key to resolving dysuria and pollakiuria is to diagnose and remedy the underlying disease.
Secondary Therapeutics • Several drugs have been found to or thought to offer symptomatic relief from dysuria. These include the antispasmodics flavoxate and dantrolene; the anti-inflammatories amitriptyline, Dasuquin® (Nutramax Laboratories, Edgewood, MD), and meloxicam; the progestin megestrol acetate; piroxicam for transitional cell carcinoma; and propantheline, tolterodine, and oxybutynin for urge incontinence. The self-limiting nature of idiopathic cystitis makes evaluation of these difficult. See Chapter 74.
142
Prognosis The prognosis depends on the underlying disease. Most of the common diseases causing dysuria and pollakiuria have a good prognosis.
Suggested Readings Filippich LJ. 2006. Cat with Urinary Tract Signs. In J Rand, ed., ProblemBased Feline Medicine, pp. 173–192. Philadelphia: Elsevier Saunders. Kruger JM, Osborne CA. 2007. Dysuria and Pollakiuria. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 406–407. Ames, IA: Blackwell Publishing. Westrop JL, Buffington CA, Chew D. 2005. Feline Lower Urinary Tract Diseases. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp 1828–1850. St. Louis: Elsevier Saunders.
CHAPTER 62
Ear Mites Sharon Fooshee Grace
Overview Otoacariasis, infestation by the ear mite Otodectes cynotis, is common in cats and is responsible for at least half of all cases of feline otitis externa. Kittens most frequently become infested by contact with the queen or other infested kittens. These highly contagious mites live on the skin surface and are nonburrowing. They irritate the ceruminous glands of the ear, causing the canal to fill with cerumen, blood, and mite excreta. As the mite feeds on the host’s epidermal debris and tissue fluid, the cat is exposed to mite salivary antigen; some cats eventually become sensitized. In one study, wheal and flare reactions (Type I hypersensitivity) and Arthus-type reactions (Type III hypersensitivity) were noted in large numbers of random cats following exposure to mite antigen. Sensitized cats may develop intense otic pruritus with the presence of only a few mites, although the immune system is normally able to limit the severity of infestations in healthy mature cats. The mites are not host specific. Also, because humans are occasionally infested, O. cynotis must be considered a possible zoonotic ectoparasite. The presence of a brownish or blackish ear discharge, shaking the head, and scratching at the ears are highly suggestive. See Figure 62-1. Some cats have significant ear debris with no apparent signs. Ectopic mites can colonize the periaural area, neck, rump, and around the tail. Hypersensitive cats may develop miliary or eosinophilic granuloma complex lesions in response to the mites and may engage in self-mutilation due to intense pruritus involving the head and neck. Aural hematomas may develop as a consequence of this trauma. See Figure 62-2. Differential diagnoses for otoacariasis should include flea bite hypersensitivity, food hypersensitivity, atopy, scabies, otodemodicosis (Demodex cati), pediculosis, and chiggers.
Figure 62-2 An aural hematoma may occur in response to shaking that accompanies head shaking. Photo courtesy of Dr. Gary D. Norsworthy.
Diagnosis Primary Diagnostics • Clinical Signs: Clinical signs are described in the Overview. • Otic Examination: The white mites are often seen moving in response to the warmth of the otoscope light. Although they are relatively large in comparison to some other mites, they cannot be seen in the ear canal without magnification. The canals should be thoroughly examined; when possible, patency of the tympanic membrane should be determined. • Cytology: Some of the debris from the ear canal may be rolled onto each of two microscope slides with a cotton swab. Two or three drops of mineral oil can be applied to the first slide. On scanning (4×) or low (10×) power, mites will be observed “swimming” in the oil. Mite eggs can sometimes be found, even when adult mites are not present. The second slide may be stained with a modified Wright’s stain to determine the presence of yeasts or bacteria.
Diagnostic Notes • Although some cats have an extreme response to the presence of ear mites, others are relatively asymptomatic. • A dark ear discharge is also common in yeast infections. Cytology is needed to differentiate otoacariasis from yeast otitis. Figure 62-1 Ear mites can be intensely pruritic to the external ear canals resulting in scratching that may cause a wound caudal to the pinna. Photo courtesy of Dr. Gary D. Norsworthy.
Treatment Primary Therapeutics
th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Topical: Several topical parasiticides are available for treatment of ear mites, with some administered directly into the ear canal and
143
SECTION 1: Diseases and Conditions
others applied on the dorsal cervical skin. Available approved products contain ivermectin, selamectin, milbemycin, or pyrethrins; also available are combinations of neomycin sulfate-dexamethasonethiabendazole or imidacloprid-moxidectin. Depending upon the product used, retreatment may be required. Though not approved, 10% fipronil solution has shown demonstrated efficacy with placement of 2 to 3 drops of solution into each ear canal and the remainder of the product applied to the skin over the neck. A follow-up treatment should be given 2 to 4 weeks later. • Systemic: Ivermectin (1% injectable = 10 mg/ml) may be administered systemically, although it is not approved for use in cats. It is dosed at 0.2 to 0.3 mg/kg orally every 7 days for three to four treatments. Alternatively, the same dose may be given subcutaneously every 14 days for a three to three treatments. These routes of administration may be the only ones possible for aggressive, uncooperative, or feral cats. The likelihood of cure increases with the number of treatments. Always seek owner ’s consent prior to administration.
Therapeutic Notes • Because ear mites are known to harbor on the body in various locations, systemic therapy is increasingly recommended, especially with cases which are difficult to resolve. • Ear mites are contagious. All exposed animals should be identified and treated regardless of whether they exhibit clinical signs. • Ear mites have a 21-day life cycle and a 2-month life span. Recent work demonstrates off-host survival for at least 12 days. These factors should be considered when planning the most appropriate course of treatment. • Insecticidal collars have shown little utility in preventing ear mite infestation. • Erythema and scratching may persist for up to 2 weeks after all mites are eliminated.
Prognosis With appropriate treatment, the prognosis is good. Most cured cats never are infected again.
Secondary Therapeutics • Cleaning: If the ear canal is full of dried debris, thorough irrigation and cleaning of the external canal will improve penetration of topical medication. The newer parasiticides and systemic therapy will not remove the waxy debris from the ear canals. A wax solvent [Wax-OSol™, Jorgensen Laboratories, Loveland, CO] can be used for this purpose. • Premises: Cleaning and insecticidal treatment of the premises may be appropriate as mites can live off the host for at least 12 days.
144
Suggested Readings Merchant SR. 1993. The skin: parasitic diseases. In GD Norsworthy, ed., Feline Practice, pp. 511–517. Philadelphia: JB Lippincott. Otranto O, Milillo P, Mesto P, et al. 2004. Otodectes cynotis (Acari: Psoroptidae): Examination of survival off-the-host under natural and laboratory conditions. Exp App Acarol. 32(3): 171–179. Scott DW, Miller WH, Griffin CE. 2001. Muller and Kirk’s Small Animal Dermatology, 6th ed., pp. 450–452. Philadelphia: WB Saunders.
CHAPTER 63
Envenomization: Arachnids Tatiana Weissova
Overview Spiders are characterized by a two-segmented body consisting of a head/thorax and an abdomen and the presence of eight segmented legs. Venom is stored in two glands that empty through fangs (chelicerae) located at the rostral end of the head. There are at least 30,000 species of spiders distributed throughout the world, but fewer than 100 spider species can inflict a bite of medical significance. All spiders are capable of inflicting an envenomating bite, but they usually cause only local swelling and pain.
Black Widow Spiders Overview Spiders of the genus Latrodectus are found throughout the world. They are identified by a red, yellow, or orange hourglass-shaped marking on the ventral abdomen of the female. Males and immature females are brown. Females can be 20 times larger than males and are capable of lifethreatening envenomizations. Males are of little medical importance because their mouthparts are unable to penetrate mammalian skin. Immature females are fully capable of delivering a severe envenomization. When hatching, these spiders are red. With the exception of protecting an egg sac, they are usually not aggressive and bite only defensively when the web is disturbed. Widow spiders prefer to be outside or inside dark, rarely disturbed spaces. Adult spiders are most active in the warm months and die during the colder months if not in a heated environment. In the United States, there are five major species of widow spider: Latrodectus mactans (throughout the United States, especially in the southern states), Latrodectus hesperus (western states), Latrodectus variolus (northern states), Latrodectus bishopi (red, red-legged, central and southern Florida), and Latrodectus geometricus (brown, the hourglass is orange, mainly in Florida). The venom of a widow spider is extremely potent. It is a complex mixture of about six neuroactive proteins; the principle toxin for mammals is the polypeptide α-latrotoxin that causes a large release and then depletion of acetylcholine and norepinephrine at postganglionic sympathetic synapses. Acetylcholine, dopamine, noradrenaline, glutamate, and enkephalin systems are all susceptible to the toxin. The venom of L. geometricus is the most potent of the five species. Its LD50 is 0.43 mg/ kg, and the LD50 of L. mactans is 1.39 mg/kg. Also there are antigenic differences in these venoms although the toxic fraction appears to be the same. Latrodectus bites do not necessarily indicate envenomization (socalled latrodectism) because black widow spiders control the amount of inflicting venom. On the other hand, a single bite is fully capable of delivering a lethal dose of venom. The venom has increased toxicity in spiders living in areas with higher temperatures and is highest in autumn and lowest in spring. Following a widow spider bite the venom is taken up by lymphatics then enters the bloodstream. Cats are extremely susceptible to Lactodectrus venom. Small puncture wounds with mild erythema are difficult to see because of skin pigmentation and the hair coat. Systemic manifestation depends on spider
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
size, motivation, and quantity of venom it decides to inject. The time of year is also a factor. Other factors are the victim’s size and age, the location of the bite, and underlying health problems. Moderate to severe envenomizations are extremely painful. Paralysis occurs early and is marked. Severe pain is manifested by howling and loud vocalizations. Hypersalivation, restlessness, and vomiting are common, and diarrhea may occur. Cats often vomit up the spider. Muscle tremors, cramping, ataxia, and inability to stand precede complete paralysis. The body becomes adynamic and atonic. A Cheyne-Stokes respiratory pattern may develop prior to death. Very young, old, and cats with systemic hypertension are under increased risk. Differential diagnoses include acute abdomen, back pain from disk disease, and rabies.
Diagnosis Primary Diagnostics • History: Potential contact with this spider in a risk area (i.e., garden, basement, and bedding) is important. It is helpful if the owner can identify the spider or if a spider is found within or by the cat’s vomitus. • Clinical Signs: Sudden onset of pain and neurological signs are typical. • Minimum Data Base: There are no specific changes. Possibilities include leukocytosis, hyperglycemia (stress), high creatine kinase (severe muscle spasm); urine production can be decreased with elevated specific gravity and albuminuria.
Treatment Primary Therapeutics • Treatment should be aggressive, and the patient should be hospitalized for a minimum of 48 hours. • Lyovac® Antivenin (Latrodectus): This equine-origin specific antivenin is available. One vial is mixed with 100 mL of saline solution and given slowly IV over 30 minutes. • Analgesics: To control pain. • Diazepam: Given IV to control muscle spasms. • Antihistamines: Diphenhydramine (2–4 mg/kg SC) will help control an allergic reaction. • Nitroprusside: 1 to 10 µg/kg per minute intravenous constant rate infusion is given for marked hypertension. • Ice or Cold Compresses: These can be used to quickly relieve pain and swelling, if wounds are identified.
Secondary Therapeutics • Allergic Reaction to the Antivenin: Observe the pinnae; if hyperemia occurs, stop the infusion and give a second dose of diphenhydramine; after 5 to 10 minutes restart the administration of antivenin at a slower rate. • Cardiac: If hypertension occurs, be careful with administration of intravenous fluids to avoid cardiac failure. • Respiratory: Intubation, oxygen administration, and ventilatory support may be necessary for respiratory distress.
145
SECTION 1: Diseases and Conditions
• Wounds: If visible, treat locally until they healed. • Delayed allergic reactions: These are rare but possible.
Diagnostic Notes • Laboratory Tests: There are no specific tests. • The anemia is usually Coombs’ negative.
Prognosis The prognosis is guarded for several days. Weakness, fatigue, and insomnia may persist for months. Death is common in cats that do not receive antivenin.
Brown Spiders Overview Few members of the 50-plus species of Loxesceles are capable of inflicting envenomization, known as loxoscelism. In the United States the only one of medical importance is the brown recluse spider1 (Loxesceles reclusa). It is found from the southern Gulf states and southern Atlantic States through Indiana and Illinois. Loxesceles laeta and Loxesceles gaucho are associated with severe loxoscelism in Brazil, Chile, Argentina, Peru, and Uruguay. Loxesceles laeta is found in the Los Angeles area in California. Brown recluse spiders are nocturnal, non-aggressive, and are active from spring through fall. They are often found in and around human habitations and prefer warm, undisturbed locations. They bite only when threatened. These spiders are recognizable by the “fiddle”-shaped marking on the dorsal surface of cephalothorax. The venom contains several necrotizing enzymes including hyaluronidase, esterases, lipases, and alkaline phosphatases. The most important component in the venom is sphingomyelinase D (a phospholipase), which binds to cell membranes and causes migration and activation of polymorphonuclear leucocytes. The toxin depletes serum hemolytic components, prolongs the activated partial tromboplastin time, and depletes clotting factors VIII, IX, XI, and XII. The venom induces rapid intravascular coagulation and occlusion of small capillaries, leading to tissue necrosis. In the presence of calcium and C-reactive protein, sphingomyelinase D can cause hemolysis. A calcium-dependent platelet aggregation can occur. Lipases can cause free lipids in the blood, which may act as inflammatory mediators or cause embolization. A single bite can inflict a lethal envenomization. Initially, the bite may cause little pain or local reaction. After 3 to 8 hours, the bite site becomes red, swollen, and tender; this creates a so-called “bull’s-eye” lesion. Hemorrhagic bulla may develop within 24 to 72 hours with an eschar developing below. The eschar sloughs in 2 to 5 weeks, leaving an indolent ulcer, which usually does not penetrate into the muscle. Healing is slow and may take months, often leaving a large scar. Systemic signs occur less commonly within 24 hours after envenomization and include hemolysis with anemia and hemoglobinuria, which may cause renal failure. Disseminated intravascular coagulation (DIC) and thrombocytopenia are possible sequelae. Other clinical signs are fever, vomiting, weakness, tachycardia, dyspnea, myalgia, maculopapular rash, leukocytosis, and coma. Differential diagnoses include bacterial or mycobacterial infection, decubital ulcer, third-degree burn, hemolytic anemia, jaundice, thrombocytopenia, and red blood cell parasitism.
Diagnosis Primary Diagnostics • History: Potential contact with the spider is important. • Clinical Signs: The bull′s eye lesions, nonhealing ulcers, black scabs, and eschars are typical. • Minimum Data Base: Likely abnormalities include leukocytosis, anemia, abnormal coagulation values, elevated creatinine, and hemoglobinuria.
146
Treatment Primary Therapeutics • Antidote: A specific antidote is available.1 Symptomatic and supportive care is also important, especially if the antivenin is not available. • Local Wound Care: Several daily cleanings with Burrows solution or hydrogen peroxide help to prevent infection. • Antihistamines: Diphenhydramine can be use to control pruritus. • Analgesics: For mild pain, nonsteroidal anti-inflammatories are used; opioids should be used for severe pain. • Antibiotics: Give to prevent secondary infection. • Cool Compresses: They are helpful in pain management.
Secondary Therapeutics • Debridement: This may become necessary because local tissue necrosis occurs. • Blood Transfusion: Consider this if anemia is severe. • Corticosteroids: Give only in the first few days to aid in minimizing hemolysis. • Wounds: Monitor these weekly until healed, especially looking for infection and the need for debridement. • Hematological Parameters: Monitor frequently because of the possible onset of hemolysis or hemoglobinuria, which indicates progression of the syndrome.
Therapeutics Notes • Antivenins are available for South American Loxesceles spp.1 Experimental antivenins for L. reclusa have been developed but are not commercially available at this time. • Do not use local heat; it may exacerbate the condition. • Avoid drugs that affect clotting. • Early surgical excision may cause a larger defect than supportive care alone. • Dapsone, hyperbaric oxygen, and electric shock were used in the past, but they are currently considered ineffective.
Prognosis Prognosis is guarded.
Redback Spider This spider, Latrodectus hasselti,1 is the main spider in Australia that causes envenomization in cats. The clinical signs are primarily variable disturbances of the autonomic nervous system and muscular paralysis. They include hyperexcitability, salivation with mucoid ropey or frothy saliva, muscle fasciculation, sporadic protrusion of the tongue, and ataxia. Diagnosis is difficult, and there are no methods to detect the venom. Treatment with antivenin during acute stages of envenomization effectively abolishes clinical signs quickly. Cats may recover without antivenin, but recovery can take weeks.
Funnel Web Spiders Spiders from the genera Atrax and Hadronyche are found in Australia. The most dangerous is the Sydney funnel web spider,1 Atrax robustus. It is a large, aggressive black spider. The toxic component of its venom
Envenomization: Arachnids
is the neurotoxin, robustoxin, which binds to the presynaptic neuron inhibiting central nervous system-mediated neurotransmitter release. The toxin affects both the autonomic nervous system and skeletal muscles. Cats are unaffected by the bite of the female spider, but the male funnel web spider ’s venom appears to be four to six times more potent than the female’s and may cause mild transient effects. Therapy is symptomatic; atropine and diazepam may ameliorate the toxic effects of the venom.
Tarantulas There are about a dozen genera of tarantulas that may deliver a potentially life-threatening bite. These spiders occur in the tropical regions of South America, Africa, and Australia. The venom contains a neurotoxin; there may also be a necrotoxin and a hemolytic toxin. These spiders are considered highly poisonous for cats. After envenomization, muscle spasm, edema, hemoglobinuria, jaundice, circulatory shock, apnea, cardiac arrhythmias, and death may occur. Species of tarantula living in the United States are not capable of delivering serious envenomization, but when threatened they can flick their urticating hairs at attacker. The hair can cause severe inflammation of the skin, eyes, mouth, and respiratory tract, but there is no associated toxin so the
effect is purely mechanical. Urticaria, edema, and vasodilatation may occur in the skin. Swelling of the eyelids and corneal abrasions are common. Cats attempting to ingest tarantulas may gag or vomit. Treatment is only symptomatic and supportive with analgesics, topical steroids, and antihistamines.
Suggested Readings Gwaltney-Brant SM, Dunayer EK, Youssef HY. 2007. Terrestrial zootoxins. In RC Gupta, ed., Veterinary Toxicology: Basic and Clinical Principles, pp. 785–807. New York: Academic Press/Elsevier. Peterson ME. 2006. Black widow spider envenomization. Clin Tech Small Anim Pract. 21(4):187–190. Peterson ME. 2006. Brown spider envenomization. Clin Tech Small Anim Pract. 21(4):191–193. Peterson ME. 2007. Spider venom toxicosis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult. 4th ed., pp. 454–455. Ames, IA: Blackwell Publishing. 1. Antivenim available at: Miami-Dade Fire Rescue, Venom Response Unit, 9300 N.W. 41st Street, Miami, Florida 33178-2414, Envenomation Emergency Phone number: 1-786-336-6600.
147
CHAPTER 64
Envenomization: Insects Tatiana Weissova
Overview There are three medically important groups of insects from order Hymenoptera: superfamily Apoidea (bees and bumblebees), and Vespoidea (wasps, hornets, and yellow jackets) and family Formicidae (ants). These insects deliver their venom by stinging their victims. Honeybees can only sting once; then they lose their barbed stinger and die. Wasp, hornet, and yellow jacket stinger are not barbed, and they are capable of delivering multiple venom-injecting stings without dying. Vespids are much more aggressive than bees. However, the aggressive behavior of Africanized honeybees increases the likelihood of multiple stings. Cats are stung accidentally when they step on or otherwise disturb the insect by playing or hunting. Clinical signs may vary from local reactions to anaphylaxis and death. Anaphylactic reactions are not dose related; death can occur after a single sting. Hymenoptera (i.e., bees, wasps, and ants) envenomation may create four primary reactions. First, and the most common, is a local reaction, which consists of swollen, edematous, and erythematous plaques at the site of the sting. These are painful. Small local reactions resolve spontaneously within 24 hours. Second is a larger, regional reaction that often causes edema of the oropharynx. Fatalities can result from airway occlusion from stings inside the oral cavity. Third, and a more severe reaction, is a systemic, anaphylactic response with urticaria, angioedema, nausea, vomiting, diarrhea, hypotension, and dyspnea that is caused by an immediate hypersensitivity reaction; this occurs within few minutes of the sting. Anaphylaxis in cats is immunoglobulin E-(IgE-) mediated and may be manifested by pruritus, salivation, incoordination, and collapse. The shorter the interval between the sting and the onset of signs, the more severe the anaphylactic reaction will be. The majority of fatalities result from severe respiratory compromise. The fourth reaction is an uncommon delayed hypersensitivity reaction due to circulating immune complexes. Symptoms may occur within 3 days to 2 weeks after envenomation and consist of skin rashes and serum sickness-like symptoms (i.e., vasculitis, glomerulonephritis, nephropathy, arthritis, disseminated intravascular coagulopathy, and disseminated intravascular coagulation [DIC]). In case of massive envenomation (multiple stings) cats are usually febrile and visibly depressed with neurological signs such as facial paralysis, ataxia, or seizures. Dark brown or red urine, bloody feces, or bloody or dark brown vomitus may also be seen. Differential diagnoses for insect stings are infection, trauma, cat fight abscess, neoplasia, allergy, foreign object, and abscessed tooth.
component of bee venom. Melittin with phospholipase and peptide 401 (mast cell degranulating peptide) triggers the release of histamine and serotonin. Hyaluronidase (spreading factor) causes changes in cell permeability and disrupts collagen. It allows penetration of venom components into the tissue and is an allergenic agent. Bee venom also contains vasoactive amines, such as histamine, dopamine, and norepinephrine, and other unidentified proteins. The neurotoxin apamin acts on the spinal cord. Adolapin inhibits prostaglandin synthetase and has anti-inflammatory effect. In cats, bee venom can cause contraction of bronchiolar muscles, and hornet venom causes hepatic injury. The venom of vespids contains peptides, enzymes, and amines. The intense pain is causing by kinins, acetylcholine, and serotonin. The major allergen is called antigen 5. Some vespid venom contains neurotoxins or alarm pheromones that alert the swarm to an intruder. The estimated lethal dose is about 20 stings per kilogram in most mammals. The European honeybee injects 147 µg of venom per sting and most wasps about 17 µg of venom each sting.
Diagnosis Primary Diagnostics • History: A potential contact with stinging insects (i.e., garden or balcony exposure, a household with blooming flowers, or garbage contact) is important. It is helpful if the owner can identify the insect. • Clinical Signs: Most patients present with facial, periorbital, or aural edema, pain, and intense pruritus. Most often stings occur in areas that are free of hair or have short hair. For bee stings, the site should be examined to determine if any part of the stinger remains. • Minimum Data Base: There are no specific changes. Possibilities include leukocytosis, thrombocytopenia, myoglobinuria, granular casts (due to massive envenomation, DIC, or renal tubular damage), regenerative anemia secondary to immune-mediated hemolytic anemia, and elevation of blood urea nitrogen (BUN) and alanine transaminase (ALT).
Secondary Diagnostics • Other Diagnostic Aids: These tests include isolation of specific IgE or immunoglobulin G (IgG) antibodies, skin testing, assay for histamine release, and actual sting challenges.
Bee and Vespid (Wasps, Hornets, and Yellow Jackets) Stings Treatment Overview Honeybee venoms are complex mixtures of allergic proteins, peptides, and small organic molecules. The major component is melittin. It is a protein which hydrolyses cell membranes, alters cellular permeability, and causes histamine release. It is the most responsible agent for local pain and can trigger intravascular hemolysis (i.e., DIC) and increase capillary blood flow. Phospholipase A2 is the major allergenic or antigen
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
148
Primary Therapeutics Solitary Stings • No specific treatment exists. Treatment is supportive. • Retained stingers may be gently scraped away with a credit card. This is better than tweezers, which may squeeze the venom sacs and injects more venom in the victim. • Cold: Ice or cold compresses can be used to quickly relieve pain and swelling. • Antihistamines may be helpful. Dose diphenhydramine at 2 to 4 mg/ kg q6 to 12h IM, SC, or PO.
Envenomization: Insects
Regional Reactions • Cold: Ice or cold compresses can be analgesic. • Corticosteroids: Dose prednisolone sodium succinate at 10 mg/kg IV, followed by 1 mg/kg q12h PO for 2 days then tapered over 3 to 5 days. • Saline Solution: Given IV if hypotension is present. • Other Fluids and Electrolytes: Use to correct hypovolemia. Multiple Stings • Early Aggressive Stabilization: Give intravenous fluids and corticosteroids; topical corticosteroids may be helpful.
For Anaphylaxis • Epinephrine: Use the 1 : 1000 concentration. Give 0.1 to 0.5 mL immediately SC; it can be repeated every 10 to 20 minutes. When epinephrine is given IV, it must be diluted to 1 : 10,000; 0.5 to 1 mL is administered cautiously and slowly infused. • Crystalloid Solutions: Give 60 mL/kg to prevent vascular collapse. It should be given rapidly in an anaphylactic patient. • Corticosteroids and Antihistamines: They may need to be administered.
Secondary Therapeutics • Monitoring: Monitor cardiac, respiratory, hematologic, and renal parameters for several days. • Respiratory: Intubation, oxygen administration, and ventilatory support may be necessary. • Diazepam: Given IV to effect for seizures. • Broad-Spectrum Antibiotics: They are indicated if septicemia is a possible sequel to massive envenomation (secondary infection because of scratching).
Prognosis The prognosis is excellent for most uncomplicated bee and vespid stings. Most of these are self-limiting and will resolve within 24 hours. If anaphylactic signs are not apparent within 30 minutes of the sting, they are unlikely to occur. In case of anaphylactic reaction the prognosis is guarded.
Figure 64-1 Fire ant bites are circular and intensely pruritic. Multiple bites often occur simultaneously.
pholipase; there is possible antigenic cross-reactivity with fire ant venom and vespid venom, especially yellow jackets. Reactions range from local pustules to anaphylaxis and death. A wheal forms within 1 minute, papules within 2 hours, and vesicles within 4 hours. Initially the content of vesicles is clear. After 8 hours it is cloudy, then vesicles develop into sterile pustules by 24 hours. These are almost pathognomonic for the sting of imported fire ants. Superficial pustules are infiltrated with activated neutrophils and platelets; necrosis occurs at the base in 24 hours. The wheal and flare are followed by immediate pain and intensive pruritus which usually resolves within 30 to 60 minutes. Sterile pustules may last up to 2 to 3 weeks. Occasionally they become secondarily infected, usually by scratching, and can progress from cellulitis to sepsis. Regional reactions are rare and consist from erythematous, edematous, indurated, and extremely pruritic lesions. They may lead to enough tissue edema to compromise blood flow to an extremity. Systemic or anaphylactic reactions are IgE mediated. The signs include urticaria, cutaneous or laryngeal edema, bronchospasm, and vascular collapse. In general, deaths caused by anaphylaxis occurs a short time after the sting; whereas, deaths caused by venom toxicity occur greater than 24 hours after the sting. The differential diagnoses are trauma, infection, allergy, neoplasia, self-trauma, and other causes of anaphylaxis.
Fire Ants Overview There are two species of fire ants of major medical importance that have been imported to the United States: Solenopsis richteri (black) and Solenopsis invicta (red). The former originated in Argentina and Uruguay and now lives in small areas of Alabama and Mississippi. The latter originated in Brazil and now lives in 12 southern states. Red imported fire ants (RIFA) are living also in Australia, Philippines, China, and Taiwan. The both species of fire ants are aggressive and venomous. After the first sting, while still secured to the victim by its mandibles, the ant withdraws its stinger, rotates one step sideways, and stings again. Typically, they sting six to seven times in a circular pattern while injecting their venom slowly (20–30 seconds). See Figure 64-1. Each sting contains about 0.11 µL of venom; the onset of pain is delayed. Fire ant venom differs from the venoms of bees; it contains water-insoluble alkaloids (95%), solenopsins, and piperidines. It causes dermal necrosis and has cytotoxic, hemolytic, antibacterial, and insecticidal properties and is responsible for pain; however, it does not induce an IgE response. The aqueous phase of fire ant venom contains four major allergenic proteins that are responsible for the specific IgE response of allergic animals. The small protein fraction (less than 1%) contains hyaluronidase and phos-
Diagnosis Primary Diagnostics • History: Potential contact with imported fire ants, actual identification of the stinging ants, and the presence of fire ant mounds are important components of the history. • Clinical Signs: The lesions are typically in a circular pattern. There is a wheal and flare appearance, immediate pain, inflammation, intense pruritus, and pustules present after 24 hours.
Diagnostic Notes • Laboratory Tests: There are no specific tests.
Treatment Primary Therapeutics • Treatment is only symptomatic and supportive. • Cold: Ice or cool compresses (water or alcohol) can be analgesic.
149
SECTION 1: Diseases and Conditions
• Antihistamines: They are given orally or applied topically. They may be combined with corticosteroids, lidocaine, camphor, and menthol (Sarna lotion). • See Overview for anaphylactic shock and severe regional reactions.
Prognosis Simple local reactions resolve with supportive measures and time. Regional reactions require more aggressive therapy but typically resolve. Anaphylactic reactions to fire ant stings can be fatal, if untreated. Older, debilitated, and very young animals are at higher risk.
150
Suggested Readings Fitzgerald KT, Flood AA. 2006. Hymenoptera stings. Clin Tech Small Anim Pract. 21(4):194–204. Fitzgerald KT, Vera R. 2006. Insects—Hymenoptera. In ME Peterson, PA Talcott, eds., Small Animal Toxicology, 2nd.ed., pp. 744–767. St. Louis: Saunders. Gfeller RW, Messonnier SP. 1998. Handbook of Small Animal Toxicology & Poisonings. pp. 154–156. St. Louis: Mosby. Gwaltney-Brant SM, Dunayer EK, Youssef HY. 2007. Terrestrial zootoxins. In RC Gupta, ed., Veterinary Toxicology: Basic and Clinical Principles, pp. 785–807. New York: Academic Press/Elsevier.
CHAPTER 65
Envenomization: Snakes Tatiana Weissova
Overview Venomous snakes, approximately 400 species, are widely distributed around the world (with the exception of certain islands, such as Hawaii, Ireland, and New Zealand). They come from superfamily Colubroidea with families Atractaspidae (Africa), Colubridae (Africa, Asia, and Central and South America), Elapidae (worldwide except Alaska and Antarctica), and Viperidae1 (worldwide except Australia, Alaska, and Antarctica).
Family Elapidae—Coral Snakes
Diagnosis Primary Diagnostics • History: A potential contact with a coral snake is suggestive; it is helpful if the owner saw a bite, heard a snake hiss, or retrieved a dead snake for identification. • Clinical Signs: Evidence of puncture wounds, neurological signs, or respiratory distress. • Minimum Data Base: There are no specific changes. Possibilities include moderate leukocytosis, elevated creatine phospokinase, hyperfibrinogenemia, and myoglobinemia with myoglobinuria.
Overview In North America there are two species of venomous elapid snakes: Sonoran coral snake (Micruroides euryxanthus1; central and southeastern Arizona and southwestern New Mexico) and several subspecies of Micrurus fulvius, including the Texas coral snake (Micrurus fulvius tenere1; southern Arkansas and Louisiana, throughout eastern and west central Texas); the eastern coral snake (M. f. fulvius1; eastern North Carolina south to central Florida and west through Alabama and Mississippi); and the south Florida coral snake (Micrurus fulvius barbouri; southern Florida and the northern Florida Keys). These coral snakes are nocturnal, non-aggressive, and shy. They are brightly colored with alternating bands of black, red, and yellow. The head is small with a black snout and round pupils. Coral snakes have short, fixed front fangs that are partially covered by a membrane. During a bite, the membrane is pushed away, and the snake holds onto the victim and chews, delivering venom to the wound. Bites by coral snakes are relatively rare; occasionally, the snake remains attached to the victim. About 60% of coral snake bites are non-envenomating. Coral snake venom is neurotoxin with little tissue reaction and pain at the bite site. The venom is composed mostly from small peptides and enzymes, which may cause nondepolarizing postsynaptic neuromuscular blockade similar to the effects of curare. This binding appears to be irreversible. The venom induces central nervous system (CNS) depression, muscle paralysis, and vasomotor instability. Other venom components can cause local tissue destruction. The amount of venom injected depends on the duration of the bite, the intensity of chewing, and the reason for the bite (offensive or defensive). The onset of clinical signs may be delayed up to 12 hours. Cats are often presented in several clinical conditions because they usually run and hide following a bite. The clinical signs are primarily neurologic with progressive ascending flaccid paralysis, decreased nociperception, CNS depression, and diminished spinal reflexes. Anal tone and micturition are typically normal. If the cranial motor nerves are affected bulbar dysfunction with palpebral hyporeflexia are observed. Other signs include hypotension, anisocoria, respiratory depression, myoglobinemia, and hypothermia. Potential complications as dysphagia, hypersalivation, trismus, and pharyngeal spasm may lead to aspiration pneumonia. Death is result of respiratory paralysis. Differential diagnoses are myasthenia gravis, botulism, polyradiculoneuritis, trauma, tick paralysis.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Secondary Diagnostics • Thoracic Radiograph: Look for signs of aspiration pneumonia.
Treatment Primary Therapeutics • Emergency Care: If a coral snake bite is likely do not wait for the onset of clinical signs to initiate treatment. The patient must be hospitalized for a minimum a 48 hours and closely monitored. • Ventilatory Support: This is done if antivenin is unavailable or if its administration is delayed; the goal is prevention of aspiration pneumonia. • Specific Antivenin for Micrurus fulvius1: The antivenin is effective against the venom of all North American coral snakes except Sonoran coral snake.1 The earlier the antivenin is administered the more effective it is. One vial is gently mixed with 100 mL crystalloid fluids and administered IV over 20 to 30 minutes. Hyperemia of the inner pinna is an indicator of a possible allergic reaction. If it occurs, stop administration of the antivenin, give diphenhydramine (2–4 mg/kg IV or SC), wait 5 to 10 minutes, and restart the antivenin infusion at slower rate. Repeated doses should be administered as indicated by response.
Secondary Therapeutics • Saline Solution: Given IV if hypotension is present. • Other Fluids and Electrolytes: Use to prevent potential tubular necrosis and renal failure secondary to hypoxemia and myoglobinuria. If myoglobinemia or myoglobinuria occur, treat aggressively for acute renal failure. See Chapter 189. • Wound Care: Treat symptomatically. • Antibiotics: They are indicated if aspiration pneumonia occurs or the bite wound becomes infected.
Therapeutics Notes • Monitor respiratory function and renal biochemical parameters for several days. • Avoid wound incision, application of ice or hot packs, electroshock treatment, and aspiration of the wound. • Corticosteroids are ineffective.
151
SECTION 1: Diseases and Conditions
• Dimethyl sulfoxide (DMSO) is contraindicated because it enhances the uptake and spread of venom. • The use of β-blockers is discouraged because their administration may mask the onset of anaphylaxis.
Clarence River Snake (Tropidechis carinatus), Small-eyed Snake (Cryptophis nigresens), Whip Snake (Demansia spp.), Tasmanian and Chappell Island Black Tiger Snake (Notechis ater). • Diazepam: Give in small doses if the patient is agitated and for immobilization. This procedure helps to delay the systemic absorption of venom. Do not use morphine, pethedine, or other depressants.
Prognosis The prognosis for coral snake envenomation is generally good after prompt and aggressive therapy. The expected recovery period is 7 to 10 days with or without antivenin therapy.
Subfamily Hydrophiinae Overview This subfamily includes six species which are the most deadly snakes in the world. All of them live in Australia. They are usually divided into three groups: Brown snakes, Black snakes, and others. The most significant Brown snakes are from genus Pseudonaja: Common Brown Snake (Pseudonaja textilis)1 and Western Brown Snake1 or Gwardar1 (Pseudonaja nuchalis). The Black snake group consists from genus Pseudechis; the most significant is the Mulga1 or King Brown Snake1 (Pseudechis australis). It is the largest Australian venomous snake and has the largest recorded venom output of any snake. It is mistakenly called the King Brown Snake; doing so may cause one to use brown snake antivenin. It is active at night, mostly in hot weather. It can be aggressive and will strike repeatedly. Other venomous snakes in Australia are from the genuses Oxyuranus, Notechis, and Acantophis. They are dangerous and include the Inland Taipan (Oxyuranus microlepidotus), the Taipan1 (Oxyuranus scutellatus), the Tiger Snake1 (Notechis scutatus), and the Death Adder1 (Acantophis antarcticus). The venom of these snakes consists of pre- and postsynaptic neurotoxins, procoagulants, hemolysins, mycotoxins, and cytotoxins. Neurotoxins cause paralysis, which results in death from respiratory failure. The effect of procoagulants is a consumptive coagulopathy. The hemolytic activity is less important. The onset of clinical signs may take more than 24 hours. Cats often initially show weakness and ataxia. Other signs are often inconsistent or transient and include intermittent weak struggling, lethargy, mydriasis, absent pupillary light reflex, hematuria, posterior paresis, generalized paresis, ataxia, salivation, bleeding from the bite site and coma. Despite paralysis there is often movement in the tail.
Diagnosis • See Diagnosis for coral snake bites.
Treatment Primary Therapeutics • AVSL Multi Brown Snake Antivenom™ (Pseudonaja spp.), or Summerland Serums’ Multi-Brown Snake Antivenom (Pseudonaja spp.). The principle of administration is the same as for coral snakes. These antivenoms should not be used to treat the bite of the King Brown Snake (P. australis), which is member of Black Snake genus. The antivenom should be gently warmed to room temperature. • Summerland Serums’ Tiger/Multi-Brown Snake Antivenom™: This product includes antivenins against the Tiger Snake (N. scutatus); three species of Brown snakes (Pseudonaja spp.): Black snakes (Pseudechis spp.), including the Mulga or King Brown Snake (P. australis) and the Red-bellied Black Snake (Pseudechis porphyriaceus); and others: Copperhead Snake (Austrelaps superbus), Rough Scaled or
152
Prognosis See Prognosis for coral snakes bites.
Family Crotalidae—Rattlesnakes Overview Rattlesnakes are also known as pit vipers because of their heat-sensing pits between the nostrils and eyes. They have triangular-shaped heads, elliptical pupils, retractable and hollow front fangs, and some snakes of this family have special keratin “rattles” on the end of tail. Crotalids of North America are members of genuses Crotalus, Sistrulus (both groups rattlesnakes), and Agkistrodon (without rattles). They are responsible for most envenomation in animals and humans in the United States. The rattlesnake group includes at least 29 subspecies, including the Eastern and Western diamondback rattlesnake1 (Crotalus adamanteus, C otalus atrox), Mojave rattlesnake1 (Crotalus scutulatus), Massasauga1 (Sistrurus catenatus) and Pygma snake1 (Sistrurus miliarius barbouri). Other crotalids are cottonmouth water moccasins1 (Agkistrodon piscivorus) and copperheads1 (Agkistrodon contortrix). The crotalid venom is complex of enzymes, cytotoxins, neurotoxins, hemolysins, coagulants/anticoagulants, lipids, and other components. In North America, rattlesnakes have three general venom types: (a) Classic (diamondback venom) that causes marked tissue destruction, coagulopathy, and hypotension, (b) Neurotoxic (Mojave A venom) that causes severe neurotoxicosis, and (c) a combination of the other two. The enzymes hyaluronidase and collagenase help to spread venom into interstitial spaces; proteases lead to coagulopathies (hypo- or hypercoagulation), and necrosis. Phospholipases cause cytotoxic effects resulting in inflammation and endothelial cell damage. This leads to edema and ecchymosis in the lungs, kidneys, myocardium, peritoneum, and occasionally central nervous system, resulting in hypotension, hypovolemic shock, and lactic acidosis. Myotoxin causes an increase in intracellular calcium, leading to myonecrosis. The venom of some diamondback rattlesnakes contains cardiotoxic agents that cause profound hypotension that is unresponsive to fluid therapy. Neurotoxic components are responsible for paralysis. The mechanism of coagulopathy is pure defibrination without disseminated intravascular coagulation (DIC). Prolonged clotting tests result from defibrination and the presence of thrombin-like enzymes; there is a failure to activate factor XIII. This is the reason that standard treatments for coagulopathies (i.e., heparin and blood transfusion) are ineffective and often harmful. The toxicity of the bite depends on both snake factors (i.e., species, size, age, the time of year, defensive or offensive bite) and victim factors (i.e., size, age, site of bite, pre-existing health conditions). Toxicity ranked by severity is: rattlesnakes, cottonmouths, and copperheads. Clinical signs begin with localized pain and swelling within 30 to 60 minutes after envenomation; tissue necrosis follows. Cats are often presented with advanced clinical signs because they often hide after the bite so treatment is delayed. Bite locations are often on the thorax or abdomen; these locations are more dangerous than the head or legs. Systemic signs include lethargy, weakness, hypotension, hyperthermia, ataxia, arrhythmias, bleeding, vomiting, diarrhea, respiratory distress, and shock. Differential diagnoses are angioedema secondary to insect or spider envenomation, animal bite, penetrating wound, blunt trauma, draining abscess, and penetration of a foreign body.
Envenomization: Snakes
Diagnosis Primary Diagnostics • History: Potential contact with snake is likely. • Clinical Signs: They may be delayed for up to 8 hours after envenomation. The hair coat or swelling may mask the bite wounds. It is necessary to carefully examine the cat. Evidence of puncture wounds, pain, local tissue swelling, bruising, and ecchymoses and petechia in the tissue or mucous membranes are important signs. • Minimum Data Base: This is likely to reveal anemia, thrombocytopenia, leukocytosis, echinocytes (burr cells; resolve in 48 hours), prolonged clotting tests, hypoproteinemia, hypoalbuminemia, hypofibrinogenemia, hypokalemia, azotemia, elevated fibrin degradation products, elevated creatine kinase, elevated hepatic enzymes, myoglobinuria, and possibly hematuria.
• • • •
•
and measured every 15 minutes looking for progression of local tissue involvement. The affected area should be treated like an open wound until healed. Crystalloids and Colloids: These are given to correct hypovolemia and oncotic pressure. Diphenhydramine: Give in case of an allergic reaction. Analgesics: Give for pain. Withhold treatment when neurological signs are present. Antibiotics: Generally, they are not necessary because venom has some antibacterial properties; give only in case of secondary infection. Monitoring: Monitor respiratory, cardiac function, hematology, and biochemistry values; monitor urine output for several days.
Therapeutic Notes See Therapeutic Notes for coral snakes bites.
Secondary Diagnostics • Electrocardiogram: This may detect ventricular arrhythmias.
Treatment Primary Therapeutics • Antivenin: Antivenin (Crotalidae, Polyvalent [ACP™] Fort Dodge Animal Health), can neutralize venom from North, Central and South American crotalids. This antivenom is often ineffective in treating venom-induced neurotoxicity. • Antivenin: CroFab (Crotalidae, Polyvalent Immune Fab-ovine™, Fort Dodge Animal Health). It is considered five times more potent than ACP™ and appears to be effective in treating crotalid-induced neurotoxicity. Antivenom administration is recommended for worsening local injury, clinically significant coagulopathy, or systemic signs. Ideally, it should be administered within the first 4 hours, but antivenin can still have clinically positive effects for up to 24 hours after envenomation. Local tissue necrosis cannot be stopped by its administration. The principle of administration is the same as coral snake antivenin. If local swelling continues to worsen, administration of another vial of antivenin should be considered.
Secondary Therapeutics • Wound Care: Gently clip nearby hair, clean the wound with antiseptic solution, and keep it dry. The extent of swelling should be marked
Prognosis The prognosis for snake envenomation is dependent on the type of snake, the severity of envenomation, and the rapidity and aggressiveness of medical intervention. If death does not occur during the first 2 hours, and the untreated animal is not in shock or depressed, the prognosis is usually favorable.
Suggested Readings Gwaltney-Brant SM, Dunayer EK, Youssef HY. 2007. Terrestrial zootoxins. In RC Gupta, ed., Veterinary Toxicology: Basic and Clinical Principles, pp. 785–807. New York: Academic Press/Elsevier. Najman L., Seshadri R. 2007. Rattlesnake envenomation. Comped Contin Educ Pract Vet. 29(3):166–175. Peterson ME. 2007. Snake venom toxicosis. In LP Tilley, FWK Smith, Jr., eds.,Blackwell’s 5-Minute Veterinary Consult. 4th ed., pp. 1273–1275. Ames, IA: Blackwell Publishing. Peterson ME. 2006. Snake bite: Coral snakes. Clin Tech Small Anim Pract. 21(4):183–186. Valenta J. 2008. Jedovati hadi. Intoxikace, terapie [The venomous snakes. Intoxication, Therapy], p. 401. Galen: Praha.
1. Antivenim available at: Miami-Dade Fire Rescue, Venom Response Unit, 9300 N.W. 41st Street, Miami, Florida 33178-2414, Envenomation Emergency Phone number: 1-786-336-6600.
153
CHAPTER 66
Eosinophilic Granuloma Complex Christine A. Rees
Overview Eosinophilic granuloma complex (EGC) is a type of skin reaction pattern with a variety of different underlying etiologies. The types of skin lesions that can be seen with EGC include: eosinophilic ulcer, eosinophilic plaque, and linear granuloma. Eosinophilic plaque lesions are intensely pruritic. The most common underlying etiology is allergy (i.e., insect allergies, atopy, food allergies, and contact allergies), but idiopathic cases also exist. A diagnosis of idiopathic ECG is made only after an underlying allergic cause has been ruled out. One report suggests that these idiopathic ECG cats may be genetically predisposed to developing these skin lesions. The lesion location and clinical signs can vary depending on the type of skin lesion present See Table 66-1. Regardless of the type of skin lesion present, EGC skin lesions can be secondarily infected. If an infection is present, it needs to be treated.
noted. Feline eosinophilic plaque lesions appear as superficial hyperplasia, deep perivascular dermatitis with eosinophilia histologically. See Figure 66-3A, 66-3B, and 66-3C. Flame figures are also possible. Diffuse spongiosis of the outer root sheaths of hair follicles may also be noted. The histopathologic findings for eosinophilic granuloma lesions are more dramatic than the other two types of skin lesions. See Figure 66-4. The eosinophilic granuloma lesion reveals nodular to diffuse granulomatous dermatitis with flame figures. Eosinophils and multinucleated histiocytic giant cells are common cells also found on biopsy.
Diagnosis Primary Diagnostics • Allergy Work-Up: Allergies are most commonly associated with cats developing EGC. Allergies that can cause EGC include flea allergy dermatitis, food allergy, atopic dermatitis, and contact dermatitis. Flea combing, flea or mosquito antigen intradermal skin tests, or response to flea control aid in determining whether flea allergy dermatitis is an underlying cause. (See Figures 66-1A, 66-1B, and 66-1C) An 8- to 12-week food elimination diet with a food rechallenge to prove or disprove food allergies is present is also a useful diagnostic tool. See Chapter 82. Intradermal allergy testing is a sensitive and useful test for diagnosing atopic dermatitis. Contact allergies rarely cause EGC and are difficult to diagnose. The diagnosis of contact allergy is most commonly performed by history and distribution pattern. Patch testing exists, but the veterinarian needs to select contact allergens in the environment that may be causing this problem. No predetermined contact allergy panels exist for patch testing. • Biopsy: Skin biopsies of affected lesions are useful for diagnosing EGC. If ulcerative lesions are present, the biopsy sample should be collected at the junction between the normal and ulcerated skin. If nodules or plaques are present, the biopsy punch should penetrate the center of the lesion. Eosinophilic ulcer (i.e., feline indolent ulcer, “rodent ulcer”, see Figure 66-2) shows hyperplastic, ulcerated, superficial perivascular to interstitial dermatitis. Fibrosis may also be
(A)
TABLE 66-1: Types of Lesions and Most Common Lesion Locations Associated With Feline Eosinophilic Granuloma Complex Type of Skin Lesion
Lesion location
Eosinophilic ulcer Eosinophilic plaque Linear granuloma
Upper lip Ventral abdomen and flank Caudal aspect of hind legs
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
154
(B) Figure 66-1 Mosquito bite hypersensitivity is one of the underlying causes for the electrocardiogram. Thinly haired areas, such as the dorsum of the nose (A), the pinna (B), and preauricular area (C), are the most common sites of mosquito bites. Photo courtesy Dr. Gary D. Norsworthy.
Eosinophilic Granuloma Complex
(C) Figure 66-1 Continued
(A)
(B)
Figure 66-2 The eosinophilic ulcer (“rodent ulcer”) is located on the upper lips. They are usually between the upper canine teeth and are usually bilateral. This one is so large that it has extended past the canine teeth. Photo courtesy Dr. Gary D. Norsworthy.
• Impression Cytology: Eosinophilic plaques exfoliate easily. Eosinophils often predominate the sample. See Figure 66-5. Eosinophilia via impression is not typical of eosinophilic ulcers or linear granulomas.
(C) Secondary Diagnostics • Complete Blood Count: Peripheral eosinophilia may be seen with eosinophilic plaque (consistent finding) and eosinophilic granuloma (variable).
Figure 66-3 The eosinophilic plaque is usually located on the ventral abdomen (A). (The cat’s head is to the left.) When present other lesions are often located between toes (B) and on the base of the tongue (C). Photo courtesy Dr. Gary D. Norsworthy.
155
SECTION 1: Diseases and Conditions
Figure 66-4 The linear granuloma is located along the caudal aspect of the rear legs. It is usually bilateral. In some cats they are ropey ridges of tissue; other cats have linear ulcerated lesions similar to an eosinophilic plaque. This cat has a combination of the two. Photo courtesy Dr. Gary D. Norsworthy.
Treatment Primary Therapeutics • Primary Treatment: If possible the underlying allergy should be identified and addressed. • Corticosteroids: EGC is extremely responsive to both injectable and oral steroids. • Although not approved for use in cats, cyclosporine has also been useful for treating difficult cases of EGC.
Prognosis The prognosis is good if the allergy is identified and addressed. If an underlying allergy is not identified and addressed then the affected cat may be condemned to long-term systemic steroids or cyclosporine.
156
Figure 66-5 This is an impression cytology sample of an eosinophilic plaque. Eosinophils are the primary cell. Eosinophilia via impression is not typical of eosinophilic ulcers or linear granulomas. Photo courtesy Dr. Gary D. Norsworthy.
Suggested Readings O’Dair H. 1996. An open prospective investigation into aetiology in a group of cats with suspected allergic skin disease. Vet Derm. 7:193–196. Power HT. 1990. Eosinophilic granuloma in a family of pathogen-free cats. Proc Ann Memb Meet Am Acad Vet Derm/Am Col Vet Derm. 6: 45–46. Prost C. 1998. Diagnosis of feline allergic diseases: A study of 90 cats. In KW Kwochka, T Willemse, C Von Tscharner, eds., Advances in Veterinary Dermatology III, pp. 516–518. Boston: ButterworthHeinemann. Song MD. 1994. Diagnosing and treating feline eosinophilic granuloma complex. Vet Med. 89:1141.
CHAPTER 67
Eosinophilic Keratitis Gwen H. Sila and Harriet J. Davidson
Overview Eosinophilic keratitis is a unique inflammatory condition of the feline cornea that is most often unilateral. There are occasional reports of this condition in horses as well, but it has never been reported in the dog. Sometimes the condition is referred to as proliferative keratoconjunctivitis because it can affect the conjunctiva as well as the cornea. The etiology of the condition is unknown although feline herpesvirus (FHV-1) may be associated with the disease. In one report 76% of eosinophilic keratitis samples tested positive for FHV-1. This may seem to be a high rate of detection, but it should be pointed out that a different report found 46% of normal feline eyes positive for FHV-1. This information coupled with the longstanding therapeutic use of steroids for eosinophilic keratitis does not support a cause and effect relationship with FHV-1. When both diseases are present at the same time, treatment may be more complicated, but one study found no significant difference in response or recurrence rates of eosinophilic keratitis in cats that also tested positive for FHV-1. Eosinophilic keratitis is most likely caused by an abnormal allergic response of either type I (immunoglobulin E-[IgE]-mediated) or type IV (T-cell mediated) hypersensitivity. The ocular lesions are not associated with dermal eosinophilic lesions. Eosinophilic keratitis can have a classic appearance but must be confirmed with cytologic analysis.
Figure 67-1 This eosinophilic keratitis lesion began at the limbus on the temporal side and has grown to cover nearly 40% of the cornea. Photo courtesy Dr. Gary D. Norsworthy.
Diagnosis Primary Diagnostics • Appearance: The cornea is the primary site of involvement. The lesions consist of raised, white to pinkish or yellow, granular, or vascular plaques on the corneal surface. See Figure 67-1. Lesions most often begin at the temporal limbus but can start nasally. Without appropriate treatment the plaques slowly progress to involve the central cornea. In most cases this is a nonpainful condition, but some cats do display signs of ocular irritation (i.e., blepharospasm, ocular discharge, or elevated third eyelid). The lesions do not take up stain, although stain may pool in and around their edges and care must be taken not to mistakenly diagnose an ulcer. However, concurrent ulceration is reported in 12 to 28% of cases of the disease. If the conjunctiva is affected it will have a hyperemic, proliferative surface. Less commonly, the conjunctiva may be the only portion of the eye affected. • Cytology: Brush cytology is the best method for collecting a sample of the raised lesions See Chapter 299. A normal corneal cytology sample contains epithelial cells and occasional cellular debris. Eosinophils or mast cells found on a cytologic preparation are the hallmarks used to diagnose the condition. Neither cell type is a normal resident of the feline cornea or conjunctiva. The presence of a single eosinophil is considered abnormal and enough to make a tentative diagnosis of eosinophilic keratitis. However, if peripheral blood is present on the slide then the diagnosis is only supported if eosinophils are present in greater numbers than would normally be seen on a blood smear.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Treatment There is not always a cure for this disease, but it can be controlled with consistent medication and monitoring.
Primary Therapeutics • Steroids: Topical ophthalmic dexamethasone or prednisolone acetate q4 to 12h depending on disease severity is the treatment of choice. If the cat is suspected to be positive for FHV-1, concurrent antiviral therapy may be indicated to minimize viral recrudescence during treatment See Chapter 41. Re-examination should be planned for approximately 2 to 4 weeks after initiating therapy. If there has been marked improvement the frequency of drops should slowly be slowly tapered over 4 to 6 months then stopped. The eye should be monitored for recurrence; if lesions begin to develop, the steroids should be reinstated and slowly weaned to the lowest level capable of controlling the disease which could be as infrequent as every 7 days. If the condition has not improved with initial steroid therapy, cytology should be repeated to reconfirm the diagnosis. The topical steroid should be changed and increased in frequency. The cat should be rechecked in another 2 to 4 weeks. Severe cases or cats that cannot be treated with ophthalmic medications may be treated with a subconjunctival injection of a long-lasting steroid. This has the advantage of being a singular treatment, but it will need to be repeated. Repeated subconjunctival injections may lead to granuloma formation. A subconjunctival injection may be used initially to cause regression of the lesion followed by topical ophthalmic drugs at a lower frequency. Another alternative is prednisone (5–10 mg/cat q24h PO) for 1 to 2 weeks. Oral steroids may be easier to administer, but they have a higher rate of systemic side effects.
157
SECTION 1: Diseases and Conditions
Secondary Therapeutics • Progesterone: The synthetic progesterone, megestrol acetate, is a controversial alternative. Because of its potential for profound efficacy, it is indicated in cats with refractory eosinophilic keratitis or with concurrent active ulceration. The initial dose is 0.5 to 1.0 mg/kg q24h PO for 1 to 2 weeks. This dose is progressively lowered until the cat is maintained at 2.5 to 5.0 mg q7d PO; however, most cats can be maintained on corticosteroids after the disease is controlled with megestrol. Caution must be used because synthetic progesterone has been shown to trigger clinical diabetes in a borderline diabetic and to cause an increase in mammary tumors. • Antiviral Medications: If the feline herpes virus is suspected or confirmed, treatment for the virus should be initiated. See Chapter 41. • Cyclosporine A 1.5%: A recent group had success treating eosinphilic keratitis with topical cyclosporine (diluted in corn oil) every 8 to 12 hours. The majority of cases (88%) showed improvement in
158
lesions by the first recheck. All cases of disease recurrence were associated with cessation of treatment. The cases (11%) that were refractory to treatment with cyclosporine were responsive to a topical steroid. Therefore, cyclosporine may be the preferred therapy in cats with concurrent corneal ulceration as cyclosporine is less likely to delay corneal wound healing.
Suggested Readings Andrew SA. Immune-mediated canine and feline keratitis. 1991. In Vet Clin North Am Small Anim Pract. 38(2):269–290. Pentlarge VW. 1991. Eosinophilic conjunctivitis in five cats. J Am Anim Hosp Assoc. 27:21–28. Speiss AK, Sapienza JS, Mayordomo A. 2009. Treatment of proliferative feline eosinophilic keratitis with topical 1.5% cyclosporine 35 cases. Vet Ophthalmol. 12(2):132–137.
CHAPTER 68
Epilepsy Teija Kaarina Viita-aho
Overview Epilepsy is a disease characterized by recurrent seizures originating from the brain. Epileptic seizures occur typically when the cat is quiet, sleeping, or upon awakening because then the brain′s excitatory threshold is lowest. In cats with epilepsy, seizures can be provoked by external factors such as excitement or flashes of light. There are four ways epileptic seizures can occur. (a) Reactive seizures secondary to metabolic or toxic conditions. Metabolic conditions include hepatic encephalopathy, uremia, hypoglycemia, hyperthyroidism, and hyperparathyroidism. Toxic conditions include lead, organophosphates, ethylene glycol, and pyrethrin/pyrethroid poisoning. (b) Symptomatic seizures caused by intracranial disease such as neoplasia, inflammation or infection, trauma, congenital, degenerative or vascular disease. Symptomatic epilepsy is a common form of epilepsy in cats and intracranial disease is the most common cause of it. (c) Probable symptomatic seizures, which occur due to a suspected symptomatic cause (e.g., previous head trauma or infection), but the actual cause remains unclear. (d) Idiopathic seizures where no identifiable cause can be defined. This is called idiopathic epilepsy. Seizures resulting from idiopathic epilepsy usually begin between 1 and 4 years of age. There are four events in the course of an epileptic seizure. (a) The prodome is the period prior to the seizure. This phase may occur hours to minutes before seizure activity. Cats may have behavior abnormalities, restlessness, or changes in daily behavior pattern such as eating or sleeping. (b) The aura is the beginning of the seizure. Changes in electroencephalography can be seen. (c) The ictus is the actual seizure event. During this phase the cat may exhibit a number of abnormal behavior patterns depending on whether the seizure is partial or generalized. (d) The postictal period follows the ictus. This phase may last minutes to hours and, in some instances, several days. Behavior abnormalities are characteristic. Typically, the animal is tired, disoriented, ataxic, hungry, thirsty, or aggressive. Cats may have focal neurologic examination abnormalities during this period. Seizures occur in three fairly distinct types, although they are much more variable in their presentation than those in the dog. Epileptic seizures can be classified as primary generalized seizures, focal seizures (also known as partial seizures), or focal seizures with secondary generalization. Focal seizures can be simple or complex. In a primary generalized seizure abnormal electrical activity occurs throughout both cerebral hemispheres. The seizure is tonic, clonic, or tonic-clonic, and it usually involves autonomic release (i.e., urination, defecation, salivation). The symptoms are symmetrical, bilateral, and generalized, and the patient is unconscious. Generalized seizures can also occur as an absence attack. Single, generalized seizures often are only 30 to 90 seconds in duration. Generalized tonic-clonic seizures in cats may be violent. Focal seizures are due to abnormal electrical activity arising from an epileptic focus in the brain, and the clinical signs reflect the functions of the area involved. Focal seizures are either simple or complex. In simple focal seizures partial seizure activity can be seen;
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
examples include twitching of the face or whiskers, cramping of one limb, or abnormal rhythmic blinking. The mental status remains normal in simple focal seizures. In a complex focal seizure all the same symptoms as in a simple focal seizure are seen but additionally the mental status is altered, behavioral changes are seen, and usually it also involves autonomic release. Focal seizures with secondary generalization can spread to involve the entire brain. The initial seizure symptom will be localized but then followed by tonic, clonic, or tonic-clonic convulsions. Status epilepticus (SE) is a state of continuous seizure activity lasting at least 5 minutes or when two or more seizures occur without complete recovery between them. To date, a specific etiology of SE is not known. It is reported to occur more commonly in cats with symptomatic or reactive epilepsy than in cats with idiopathic epilepsy. In cats, focal continuous seizures occur more often as a presentation of SE than in dogs. SE is a type of seizure activity that can rapidly have life-threatening consequences and should be considered as an emergency situation. Untreated SE may lead to hyperthermia, hypoxia, acidosis, hypotension, hypoglycemia, hyperkalemia, renal failure, disseminated intravascular coagulation (DIC), and irreversible neurological defects. Differential diagnoses for epilepsy include syncope, narcolepsy, cataplexy, behavior disorders, weakness episodes, vestibular disorders, cramping syndromes, tremors, and other episodic movement disorders. These can usually be ruled out by thorough interview of the owner and careful clinical and neurological examination.
Diagnosis Primary Diagnostics • Exclusion: Idiopathic epilepsy is a diagnosis made through exclusion of all other possible causes of seizures. • Neurological Examination: Idiopathic epilepsy is usually not associated with interictal neurological deficits unless seizures are severe or persistent. However, the neurologic status can be abnormal 24 hours after a seizure so the evaluation is better to perform the next day. Symmetrical neurologic defects are seen in symptomatic and reactive epilepsy. If neurologic defects are asymmetrical (e.g., circling) the clinician should start looking for a structural brain disease. Cats can also be free from any neurological signs in the interictal period. • Minimum Data Base: Evaluation for metabolic and infectious abnormalities include a complete physical examination, complete blood count (CBC), serum biochemical panel, urinalysis, fecal examination, thoracic and abdominal radiographs, tests for the feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV), blood pressure measurement, and electrocardiography. Bile acids testing or other liver function tests should also be performed in case of any suspicion of a liver problem. • Cerebrospinal Fluid (CSF): Evaluation for possible inflammatory/ infectious, hemorrhagic, or neoplastic causes in the central nervous system includes CSF collection and analysis. The typical result of CSF analysis in cats with brain tumor is an increase in protein in the presence of a normal cell count. However, it is possible to have normal results. Tumor cells are rarely seen in CSF. CSF collection should be
159
SECTION 1: Diseases and Conditions
done carefully because increased intracranial pressure may be present in association with a brain tumor and the removal of CSF may cause brain herniation.
•
Secondary Diagnostics • Imaging: Evaluation for a possible structural intracranial abnormality includes either computerized tomography (CT) or magnetic resonance imaging (MRI). • Electroencephalography (EEG): This is used to identify abnormal electrical activity in epileptic patients. It is not a routinely available veterinary diagnostic option. EEG readings are not abnormal in all patients suffering from epilepsy, and a normal EEG does not rule out epilepsy.
•
•
Treatment Primary Therapeutics: Seizures • Any underlying disease causing seizures should be treated appropriately. • Goals of Therapy: The aim of anticonvulsant therapy is to reduce the frequency of seizures as much as possible but to avoid excessive drug-induced side effects. The patients may not be totally seizure free but can have nearly normal life. Animals that have idiopathic epilepsy will most often continue to have at least some seizures even when receiving appropriate anticonvulsant medications. • Phenobarbital: Initial dose is 1.5 to 3.0 mg/kg q12h PO. The serum concentration of phenobarbital varies between cats, and it is therefore necessary to monitor it. The therapeutic serum concentration is 15 to 45 µg/ml (65–150 µmol/l). Drug concentration in serum should be obtained 2 to 3 weeks after initiating therapy or changing dosage. Serum separator tubes should not be used when collecting serum for phenobarbital level determination. Silicone binds phenobarbital which results in falsely low concentration.
Secondary Therapeutics: Seizures • Diazepam: This is an effective anticonvulsant in the acute treatment of epilepsy but is not useful in the long-term treatment as it is reported to cause liver necrosis in cats. It is given 0.5 to 1.0 mg/kg IV as an emergency therapy. If intravascular access is not available, diazepam may be administered intrarectally in an emergency situation. • Gabapentin: This has been used as an anticonvulsant in cats. Initial dose of 5 to 10 mg/kg q24h PO is increased to the same dose every 12 hours after 3 to 5 days of therapy. Excessive sedation is possible, especially in the beginning of the therapy. Therefore, gradually increasing dosages are recommended to avoid this adverse effect. • Levetiracetam: This may be an effective anticonvulsant drug when given as an adjunct to phenobarbital or as a single agent. The dose is 20 mg/kg q8h PO. The dosage should be decreased in patients with impaired renal function; however, it should be relatively safe in cats with liver disease. • Zonisamide: This may be used at 5 to 10 mg/kg q12h PO. However, adverse reactions, such as anorexia, diarrhea, vomiting, somnolence and locomotor ataxia, have been reported. • Pregabalin: This may also be used at 2 to 4 mg/kg q8 to 12h PO.
Therapeutic Notes: Seizures • Anticonvulsant treatment should be started if seizures occur more often than once in 6 weeks, if seizures occur in clusters, if the duration of one seizure is more than 5 minutes, or in case of SE. • There is known to be a kindling phenomenon in epileptic patients. Seizure activity can perpetuate or lead to further seizure activity.
160
• •
Thus, it is better to start anticonvulsant medication sooner than later. Side effects of phenobarbital include sedation, polyuria, polydipsia, and polyphagia. It is important to mention these to the owner. Sedation usually lasts only for 3 to 5 days, and other side effects usually subside within the first weeks of treatment. There is a theoretical concern regarding liver damage. Hepatotoxicosis is a well-recognized complication in dogs; however, it has not been reported in cats. When using phenobarbital hematology and clinical chemistry profiles should be obtained every 6 months. Immune-mediated neutropenia and thrombocytopenia have been described due to phenobarbital so monitoring is suggested. Uncommonly, a mild rise in alanine aminotransferase (ALT) and alkaline phosphatase (AP) occurs in long-term therapy due to enzyme induction. Potassium bromide (KBr) is not recommended for cats because there is only little documentation of its effect in this species and many cats develop irreversible chronic bronchitis when receiving it. Other historically used anticonvulsants such as primidone and phenytoin may be toxic to cats and should be avoided. Treatment of epilepsy is not necessarily long term. Spontaneous remission is possible, and it is, therefore, possible to attempt to wean the patient off therapy in cases when there has been no seizure activity within the preceding year. Weaning should be done with gradual dose reduction over a long period of time (6–8 months). A rapid dose reduction should be avoided because there is an increased risk of seizure relapse and because, in the case of phenobarbital, the drug is addictive.
Primary Therapeutics: Status Epilepticus • Goals: The goal of treatment is to quickly terminate the seizure activity, to determine the cause of the SE, and to treat any associated systemic or intracranial consequences of the seizure activity. Management of SE requires immediate and aggressive treatment. • Priorities: Stop the seizure activity and take care of the airway, breathing, and circulation (ABCs)! • Diazepam: Give 0.5 to 1.0 mg/kg IV. It can be repeated two to three times in 5- to 10-minute intervals. If intravenous access is not available, it can also be given intrarectally. Another benzodiazepine, midazolam, can also be used at a bolus of 0.2 mg/kg IV if diazepam is not available. • Phenobarbital: Give as a bolus at 3 mg/kg IV; it is longer acting than diazepam. Remember that the effect is not immediate but rather can take 15 to 25 minutes, so overdosing needs to be avoided. It can be repeated every 20 to 30 minutes until the seizure ceases. Phenobarbital can also be used as a constant rate infusion (CRI) at 2 to 4 mg/kg per hour.
Secondary Therapeutics: Status Epilepticus • Propofol: If seizure activity continues, use propofol. It is administered initially as a bolus of 1 to 6 mg/kg to effect and can be followed by CRI of 0.1 to 0.6 mg/kg per hour. If CRI of propofol is used, the dose should be tapered by 25% every 6 hours. • Medetomidine or Dexmedetomidine: These can be used IV or IM to stop the seizure activity. Dose for medetomidine is 20 to 40 mcg/kg and for dexmedetomidine 10 to 20 µg/kg. These have been used empirically, and no research has been published to date. • Levetiracetam: This can be given IV as an alternative emergency drug. It is administered in a bolus of 20 mg/kg. The anticonvulsant effect is rapid and is maintained for several hours. In addition, cats do not become sedated and appear to recover from the seizure episode more quickly than with diazepam administration. The patient can then be maintained on levetiracetam or transitioned to phenobarbital.
Epilepsy
Therapeutic Notes: Status Epilepticus • As soon as is feasible place an intravenous catheter and take a blood sample for at least a CBC, electrolytes, glucose, liver, and kidney panel. • To correct and maintain body homeostasis, give intravenous fluids at 10 ml/kg per hour. • Control body temperature, and cool the patient if necessary. • Start maintenance therapy to prevent further seizures. • The patient must be monitored carefully until normal mental status is regained. Parameters such as blood pressure, respiratory rate, heart rate, pO2, peripheral pulse, and body temperature should be monitored, and neurological examinations performed.
Prognosis Prognosis of the epileptic cat primarily depends upon the underlying disorder and whether the patient responds to therapy. Prognosis is better in idiopathic epilepsy compared to reactive or symptomatic epilepsy and cats with reactive epilepsy have reported to have longer
1-year survival rate than those with symptomatic epilepsy. SE has been reported to associate negatively with survival time. About 25% of patients with SE die or are euthanized.
Suggested Readings Bagley RS. 2005. Clinical Evaluation and Management of Animals with Seizures. In RS Bagley, ed., Fundamentals of Veterinary Clinical Neurology, pp. 363–376. Ames, IA: Blackwell Publishing, Iowa. Bailey KS. 2008. Levetiracetam as an adjunct to phenobarbital treatment in cats with suspected idiopathic epilepsy. J Am Vet Med Assoc. 232(6):867–872. Berendt M. 2008. Epilepsy in the dog and cat: Clinical presentation, diagnosis, and therapy. Eur J Compan Anim Pract. 18(1):37–45. Kline KL. 1998. Feline epilepsy. Clin Tech Sm Anim Pract. 13(3):152–158. Schriefl S. 2008. Etiologic classification of seizures, signalment, clinical signs, and outcome in cats with seizure disorders: 91 cases (2000– 2004). J Am Vet Med Assoc. 233(10):1591–1597.
161
CHAPTER 69
Esophageal Disease Andrew Sparkes
Overview Feline esophageal disease is relatively uncommon, but there are many well-characterized conditions. Broadly the causes of esophageal disease can be classified as: • Obstructive: luminal (e.g., foreign body), mural (e.g., neoplasia, stricture), and extra-esophageal (e.g., anterior mediastinal mass or vascular ring anomaly). • Inflammatory: esophagitis. • Motility Disorders: Megaesophagus and esophageal hypomotility. Dysphagia and regurgitation are the usual signs of esophageal disease, but some cats may demonstrate dullness, inappetence, pain, anorexia, and ptyalism. Reliably distinguishing vomiting and regurgitation on the basis of history, and even clinical investigations, can be challenging in some cases. When regurgitation or esophageal disease is suspected, other important clinical and historical features include the cat’s age and whether the disease was acute in onset (e.g., foreign body), progressive (e.g., neoplasia or stricture), or associated with a recent anesthesia or administration of ulcerogenic drugs. Additionally, evidence of other neuromuscular signs, evidence of secondary pneumonia, and inability to swallow fluids are all important aspects of the history and examination. Oral examination may sometimes reveal the presence of oropharyngeal inflammation or ulceration consistent with infection (i.e., feline calicivirus [FCV]) or caustic ingestion; evidence of foreign body ingestion may also occasionally be seen. Careful neck palpation may reveal pain (i.e., foreign body or esophagitis), a dilated esophagus, or a palpable foreign body or mass lesion. Rib spring, a measure of anterior thoracic compressibility, should be assessed to help determine the likelihood of an anterior thoracic mass, and thoracic auscultation and percussion should be performed to detect intrathoracic disease and secondary complications such as inhalation pneumonia.
Diagnosis Primary Diagnostics • Direct Observation: Diagnosis may require hospitalization to observe the cat eating, which may be facilitated by administration of diazepam at 0.1 to 0.2 mg/cat IV or mirtazapine (3.25 mg/cat q2-3d). • Endoscopy: Endoscopy can be of value when mucosal or mass lesions are present including esophagitis, neoplasia foreign bodies, strictures, and perforations. • Radiographs: Plain radiographs can be extremely useful and should be taken in a conscious or lightly sedated cat that is awake enough to maintain esophageal tone. Administration of barium contrast (e.g., barium paste or barium mixed with food) may facilitate identification of lesions or confirm the presence of megaesophagus. However, if esophageal perforation is possible, an iodine-based contrast agent should be used, and if endoscopy is going to be performed one should wait at least 24 hours after a barium swallow. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
162
• Fluoroscopy: Although facilities for fluoroscopy are more limited, this can be extremely valuable and may be crucial in the diagnosis of some disorders, especially with altered motility.
Esophageal Foreign Bodies Overview A variety of foreign bodies may lodge in the esophagus. Linear foreign bodies and bones are probably the most commonly encountered in cats, but toys, fish hooks, hair balls, and others may also be found. The most common sites for foreign body entrapment are the three narrowest areas or where there is a flexure. These are the thoracic inlet, immediately cranial to the heart base, and in the terminal esophagus just cranial to the cardia.
Diagnosis Typically a foreign body will induce partial (or occasionally complete) obstruction and esophagitis with an acute onset of clinical signs, pain, ptyalism, and anorexia. The diagnosis is based on history, clinical, and radiographic findings, and endoscopy.
Treatment Treatment involves endoscopic foreign body removal or surgery. Cats will also need to be managed for esophagitis. The prognosis in most cases is good.
Esophagitis Overview Esophagitis may occur as a primary complaint, or may be a part of many other esophageal disorders. Important causes include: • Anesthesia-Associated Gastroesophageal Reflux: This is one of the most common causes of severe esophagitis in cats. Predisposing factors include drugs that reduce the lower esophageal tone (e.g., atropine or xylazine), increased abdominal or gastric pressure during surgery, food in the stomach at the time of surgery, and positioning so that the head is lower than the abdomen during surgery or recovery. • Drug-Associated Esophagitis: Some cases are associated with severe esophageal strictures. Initial reports incriminated doxycycline, but many drugs may have the potential to induce esophagitis including clindamycin, potassium salts, propranolol, nonsteroidal anti-inflammatories, and ascorbic acid. Studies have shown that the passage of tablets or capsules to the stomach after oral administration is often delayed in the esophagus unless their administration is followed by a bolus of water or food or the tablet or capsule is lubricated. These measures are likely to dramatically reduce the risk of drug-induced esophagitis. • FCV infection. • Foreign body. • Ingestion of caustic chemicals.
Esophageal Disease
• Gastroesophageal Reflux: This is associated with esophagostomy tubes that enter the stomach. • Persistent vomiting. • Hiatal hernia and Gastroesophageal intussusception. • Neoplasia. • Lower esophageal sphincter incompetence. Esophagitis varies tremendously in severity. Mild cases only involve the mucosal surface and, with appropriate therapy, will usually heal without long-term complications. More severe cases involve inflammation extending into the muscular layers and are much more likely to lead to stricture formation. Mild cases may have minimal signs (i.e., mild pain/discomfort, dysphagia, occasional regurgitation, inappetence), whereas in more severe cases there may be marked regurgitation (and possibly blood in the regurgitated food), pain, ptyalism, anorexia, and dysphagia.
be extensive. Typical causes include postanesthetic esophagitis, which typically occurs within 1 to 3 weeks of anesthesia, foreign body trauma, caustic/drug ingestion following esophageal surgery, and rarely, neoplasia. Major clinical features are severe dysphagia and regurgitation, usually soon after feeding. Signs will vary according to the severity of the stricture. Most cases have quite dramatic clinical signs. Initially regurgitation of solid food occurs, but that is followed by regurgitation of semi-liquid food and liquids.
Diagnosis • Contrast Imaging: Diagnosis is usually based on a barium swallow with radiographs, fluoroscopy, and endoscopy. See Figures 69-1 and 69-2.
Diagnosis • Contrast Studies or Fluoroscopy: These may suggest mucosal abnormalities or altered motility. • Endoscopy: Definitive diagnosis requires endoscopy, which will readily demonstrate the presence of esophagitis, its severity, and the extent of the lesions. • Plain Radiographs: These rarely show any abnormalities.
Treatment • Mild/superficial Cases: Food is withheld for 24 to 48 hours and then reintroduced. A soft, low-fat, high-protein diet should ideally be used. A diet of this composition improves the lower esophageal tone and minimizes delays in gastric emptying. Combining this with short-term use of mucosal protectants and antacids may be curative. • Moderate to Severe Cases: More aggressive therapy is needed, possibly for several weeks. If esophageal “rest” is considered beneficial to allow adequate healing, consideration should be given to placing a gastrostomy tube. This can be valuable for 5 to 10 days during the initial healing process, but oral therapy in the form of mucosal protectants should not withheld during this period. • Mucosal Protectants: Sucralfate suspension (100–200 mg/kg q8–12h PO) forms a protective barrier over the ulcerated mucosa. Gastric antacids reduce gastric acidity and help prevent further damage during reflux. Suitable drugs include ranitidine (1–2 mg/kg q8–12h PO), famotidine (0.5 mg/kg q12–24h PO), and omeprazole (0.7 mg/ kg q24h PO). Anti-inflammatory drugs (prednisolone at 1–2 mg/kg q24h for 2–4 weeks) may help limit further inflammation and fibrosis. In the presence of significant and deep inflammatory changes, it may be prudent to provide antibiotic cover during the use of prednisolone. In the presence of severe pain, oral lidocaine gel may also be of value.
Figure 69-1
Appearance of an esophageal stricture on fluoroscopy.
Figure 69-2
Endoscopic appearance of an esophageal stricture.
Prognosis Response to therapy should be monitored with serial endoscopy, which will also allow early treatment of stricture formation if this occurs. In many cases, early aggressive therapy will produce a very good outcome.
Esophageal Stricture Overview Stricture formation (fibrosis and scar tissue) is usually an end result of severe esophageal trauma or esophagitis. The site of the stricture can be extremely variable, and, although some are focal, others can
163
SECTION 1: Diseases and Conditions
Figure 69-3
Balloon dilator for treating esophageal strictures.
(A)
Treatment • Balloon Catheter Dilatation: See Figure 69-3. This produces radial forces to stretch as opposed to the shearing forces induced by using bouginage. Depending on the size of the stricture, a balloon with a diameter of 10- to 20 mm will be required. With severe strictures, larger diameter balloons can be used over time as the stricture dilates. The balloon is passed into the esophagus and, under endoscopic guidance, it is placed so that the stricture is approximately central in the length of the balloon. The balloon is inflated to a pressure of approximately 30 to 50 psi and held at this pressure for 45 to 60 seconds before deflating. Once deflated the esophagus should be reexamined endoscopically. If minimal damage or mucosal tearing have been induced, the procedure can be repeatedly immediately once or twice. Depending on the severity of the stricture, the degree of damage induced during stretching, and the clinical response, repeat balloon dilation can be performed at intervals of 2 to 7 days. In one retrospective study, cats that responded typically required between one and eight dilations to produce a good clinical response. Some cats though may require 20 or more procedures. • Postdilation Supportive Therapy: Sucralfate, antacids, and possibly antibiotics are used. Although of unproven efficacy, prednisolone therapy is also a rational choice. When possible, feeding should be started after 24 hours using soft foods and postural feeding if necessary.
Prognosis Although some severe cases require prolonged therapy, in the majority of cases a good and acceptable clinical response can be achieved. Some cats will have complete resolution of the stricture and the clinical signs. However, in many cases the response will be partial often with some stricture remaining.
(B) Figure 69-4 A, Radiograph appearance of a vascular ring anomaly with a barium plus food swallow. B, The vascular ring is seen at the end of the scissors. Images courtesy of Dr. Gary D. Norsworthy.
Diagnosis • Clinical Signs: The presenting clinical sign is usually severe and sudden-onset regurgitation beginning after weaning. Owners may sometimes recognize proximal (cervical) esophageal dilation as food tends to accumulate proximal to the constriction. There are also rare reports of late-onset clinical signs, presumably as a result of less severe esophageal constriction. • Imaging: Plain radiographs may be suggestive, especially with an appropriate history and dilatation of the esophagus proximal to the heart base. However, contrast studies or fluoroscopy may be needed in some. See Figure 292-32.
Vascular Ring Anomaly Treatment Overview The most common vascular ring anomaly is a persistent right aortic arch. A vascular ring, comprised of the aorta on the right, the pulmonary trunk on the left, the heart base ventrally, and the ligamentum arteriosum between the aorta and the pulmonary artery, encircles the esophagus and prevents its dilation. There has been some suggestion that this may be seen somewhat more frequently in Siamese cats, but it is a rare condition. See Figure 69-4.
164
• Surgery: Resection of the ligamentum arteriosum is usually highly successful if performed early enough. However, delayed surgery may lead to some persistent esophageal dilatation.
Prognosis With early surgical repair the prognosis is good. It is poor if surgical repair is not performed.
Esophageal Disease
Figure 69-5 Radiographic appearance of a hiatal hernia after administration of barium. Some rugal folds are clearly identifiable cranial to the diaphragm.
Hiatal Hernia Overview Hiatal hernia refers to the protrusion of abdominal contents (usually the abdominal esophagus, possibly the cardia, and possibly the proximal stomach) through the esophageal hiatus of the diaphragm. There have been some unconfirmed reports that the condition is more common in Siamese cats. Most cases are considered to be congenital abnormalities, but hiatal hernias can also occur following trauma. See Figure 69-5. The major clinical findings are intermittent regurgitation with distal esophagitis caused by gastroesophageal reflux. This is a rare condition, and many cases are so called “sliding” hiatal hernias meaning the herniation is intermittent instead of permanent.
Diagnosis • Imaging: The diagnosis of hiatal hernia can be difficult. Plain radiographs may be suggestive, and the diagnosis may be confirmed by contrast radiography or endoscopy. See Figure 69-2. Cranial displacement of the lower esophageal sphincter is usually apparent, and there may be some degree of megaesophagus. However, sliding hiatal hernias may be much more difficult to diagnose.
Figure 69-6 Esophageal squamous cell carcinoma. This tumor occurred at the junction of the striated (longitudinal folds) and smooth (herringbone pattern) muscle portions of the esophagus. Photo courtesy of Dr. Gary D. Norsworthy.
Esophageal Neoplasia Primary esophageal neoplasia is uncommon; squamous cell carcinoma is the most common tumor reported. See Figure 69-6. Periesophageal neoplasia (e.g., mediastinal lymphoma) is seen much more commonly. The major clinical signs seen are due to mechanical esophageal obstruction. The prognosis for cases of primary esophageal neoplasia is poor.
Megaesophagus Overview Megaesophagus is a generalized dilatation and lack of motility of the esophagus. Esophageal hypomotility, in the absence of true megaesophagus, may also be seen in some cats. Megaesophagus is an unusual condition, but there are a number of important differential diagnoses including idiopathic congenital cases (most commonly seen in Siamese cats, often with concurrent gastric motility disorders), idiopathic acquired, and cases secondary to polymyopathies, polyneuropathies, junctionopathies, dysautonomia (See Chapter 58), esophageal obstruction, esophagitis, and so on. The major feature is regurgitation, which may occur at a variable time after eating. Although megaesophagus is seen less commonly in cats with myasthenia gravis than in dogs (that have a higher proportion of striated muscle in the esophagus), it is sometimes seen in myasthenic cats. See Chapter 143. As in dogs, “focal” myasthenia occurs when the signs predominantly or exclusively appear to affect the esophagus.
Treatment • Conservative: Approximately 50% of cases are reported to respond to conservative management alone consisting of sucralfate, antacids, small frequent meals, and postural feeding. • Surgery: If signs are refractory, esophagopexy should be considered.
Esophageal Diverticulum Esophageal diverticula are rare congenital or acquired (secondary to other esophageal abnormalities) outpouchings that may lead to clinical signs (e.g., regurgitation) when they are large or severe. Contrast radiography or endoscopy is required for diagnosis, and treatment is usually conservative (i.e., postural feeding, liquid or semi-liquid foods, and so on) or surgical resection in those cases that fail to respond.
Diagnosis • Imaging: Initial diagnosis is by radiography or fluoroscopy. See Figure 69-7. Additional tests should be undertaken, as appropriate, to investigate potential underlying causes, These tests include autonomic function assessment, anti-acetylcholine receptor antibody titers, blood lead levels, electromyogram, muscle and nerve biopsies, and assessment of gastric emptying in Siamese cats, a breed in which a more generalized gastroesophageal motility disorder may occur. Cases of primary idiopathic megaesophagus are assumed to be similar to the canine condition in which the defect appears to be a lack of afferent input to the brain, and thus, effectively a lack of recognition that a food bolus is in the proximal esophagus. However, this has not been carefully studied in cats.
165
SECTION 1: Diseases and Conditions
Treatment • Postural Feeding with Small, Frequent Meals: If postural feeding cannot be achieved, holding the cat up after feeding with its head higher than its body for 5 to 15 minutes may be equally effective. • Food Type: Feeding foods of various consistencies to find which is best tolerated. Although feeding liquid or semi-liquid foods appears logical, some cats tolerate dry food better. This can only be determined by trial and error. However, one should feed high quality, calorie-dense foods. • Pro-Motility Agents: The use of pro-motility agents (i.e., metoclopramide and cisapride) can be tried, but generally the response to these agents in cats with megaesophagus is poor. • Spontaneous Resolution: Occasional spontaneous resolution of cases of idiopathic megaesophagus has been reported. The mechanism of disease and resolution in these cases has not been determined. If there is concomitant esophagitis or inhalation pneumonia, appropriate therapy for these should be instituted.
(A)
(B) Figure 69-7 A, Radiographic appearance of generalized megaesophagus. The arrow points to the ventral esophageal wall. It is visible because of air in the esophagus. B, Radiographic appearance of megaesophagus with a barium plus food swallow.
166
Suggested Readings Adamama-Moraitou KK, Rallis TS, Prassinos NN, et al. 2002. Benign esophageal stricture in the dog and cat: a retrospective study of 20 cases. Can J Vet Res. 66(1):55–59. German AJ, Cannon MJ, Dye C, et al. 2005. Esophageal strictures in cats associated with doxycycline therapy. J Fel Med Surg. 7(1):33–41. Glazer A, Walters P. 2008. Esophagitis and esophageal strictures. Compend Contin Educ Vet. 30(5):281–292. Graham JP, Lipman AH, Newell SM, et al. 2000. Esophageal transit of capsules in clinically normal cats. Am J Vet Res. 61(6):655–657. Han E, Broussard J, Baer KE. 2003. Feline esophagitis secondary to gastroesophageal reflux disease: clinical signs and radiographic, endoscopic, and histopathological findings. J Am Anim Hosp Assoc. 39(2):161–167. Leib MS, Dinnel H, Ward DL, et al. 2001. Endoscopic balloon dilation of benign esophageal strictures in dogs and cats. J Vet Intern Med. 15(6): 547–552. Trumble C. 2005. Esophageal stricture in cats associated with use of the hyclate (hydrochloride) salt of doxycycline. J Fel Med Surg. 7(4): 241–242. Westfall DS, Twedt DC, Steyn PF, et al. 2001. Evaluation of esophageal transit of tablets and capsules in 30 cats. J Vet Intern Med. 15(5): 467–470.
CHAPTER 70
Ethylene Glycol Toxicosis Tatiana Weissova and Gary D. Norsworthy
Overview Ethylene glycol (EG) toxicosis is a life-threatening condition. EG is used primarily as an antifreeze and windshield de-icing agent. It is also used as an ingredient in photographic developing solutions, hydraulic brake fluid, motor oils, inks, wood stains, and some cosmetics. EG toxicosis can also occur after ingestion of plants that contain oxalates. Antifreeze solutions contain approximately 95% EG. EG has a sweet taste, and cats consume it readily. EG itself is not toxic, but its metabolites are toxic. EG is rapidly absorbed after ingestion, although food in stomach may slow absorption. Metabolism occurs primarily in the liver, where is oxidized by alcohol dehydrogenase (ADH) to several metabolites, including glycoaldehyde, glycolid acid, glyoxylic acid, and oxalic acid. Oxalic acid combines with calcium to form calcium oxalate crystals which are deposited in renal tubules and may cause renal epithelial and interstitial damage (necrosis), possible obstructive uropathy, and hypocalcemia, resulting in seizures. EG is primarily eliminated through the kidneys; about 50% of it is excreted unchanged. The toxic dose has not been established. The lethal dose of undiluted antifreeze (95–97% by volume) is 1.4 ml/kg or as little as 8 mL for a 5-kg cat. The clinical signs are dose dependent and are divided in three stages: (a) early: neurologic, (b) intermediate: cardiopulmonary and metabolic (i.e., cardiac and respiratory compromise with severe acidosis and electrolytes disturbances), and (c) late: renal (i.e., oliguric renal failure). Early signs develop in 30 minutes to 12 hours and include nausea, vomiting, salivation, central nervous system (CNS) depression, ataxia, disorientation, seizures, hypothermia, decreased reflexes, coma, and possible death. Intermediate signs may occur within next 12 to 24 hours and include tachypnea, pulmonary edema, tachycardia, hypertension, depression, severe metabolic acidosis; cats do not exhibit polydipsia. Late signs (12–72 hours) include increased depression, anorexia, vomiting, azotemia, abdominal pain, oliguria progressing to anuria, swollen and painful kidneys. EG has a highest fatality rate of all feline poisons. Therefore, early diagnosis and timely and aggressive therapy are essential in reversing this potentially fatal toxicity. Aggressive treatment must begin within 6 hours of ingestion for it to be successful. The differential diagnoses vary by the stage of EG toxicosis. During the acute phase of CNS and gastrointestinal signs, other causes of increased anion gap must be considered. These include ketoacidotic diabetes mellitus, pancreatitis, gastroenteritis, hypocalcemia, hypomagnesemia, hypokalemia, salicylate, ethanol, methanol, and marijuana toxicosis. During the late phase of renal failure, other causes of acute renal failure and metabolic acidosis must be considered. These include acute decompensation of chronic renal failure, glomerulonephritis, nephrotoxic antibiotics, urinary obstruction, overdose of nonsteroidal anti-inflammatory drugs (NSAIDs) or aspirin, hypervitaminosis D, heavy metal intoxication (i.e., lead, mercury, arsenic, cadmium, or zinc) plant ingestion (including Lilium spp., Hemerocallis spp., Oxalis spp., and rhubarb leaves), metaldehyde intoxication, septic shock, and hypovolemia.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Diagnosis Primary Diagnostics • History: Exposure, possible exposure, or evidence of exposure, especially in the fall, when people winterize their cars. Outdoor cats are high risk; indoor-only cats should not be at risk. • Clinical Signs: EG toxicosis should be suspected when vomiting, lethargy, ataxia, hypothermia, or acute renal failure is present. The kidneys may be palpably enlarged and painful. • EG Serum Concentration: This peaks 1 to 6 hours post-ingestion, is not detectable after 72 hours, and may be detected by a test kit that is for rapid identification of EG in whole blood (Ethylene Glycol Test Kit®, PRN Pharmacal Inc., Pensacola, FL). This test kit measures the concentration at >50 mg/dL; cats may be intoxicated with a lethal dose of EG that is below the detectable level. Therefore, positive results in cats are significant, but negative results do not rule out toxicosis. False-positive results can occur due to the presence of propylene glycol in some activated charcoal solutions and injections solutions, such as pentobarbital and diazepam; metaldehyde; other glycols; or formaldehyde. Other alcohols (i.e., ethanol, methanol, or isopropanol) do not interfere. • Hemogram: The packed cell volume is often high due to dehydration. A stress leukogram is common. • Acid-Base Evaluation: Blood pH, plasma bicarbonate concentration, and total CO2 are low by 3 hours post-ingestion and markedly low by 12 hours; the anion gap (>25 mEq/L) and serum osmolality (>20 mOsm/kg) are high within 1 hour post-ingestion and remain elevated for about 18 hours • Biochemistry Profile: The creatinine and blood urea nitrogen are elevated by 12 hours post-ingestion. The creatinine value is often greater than 1325 µmol/L (15 mg/dL). Hyperphosphatemia may occur transiently (3–6 hours post-ingestion) due to phosphate rust inhibitors in the antifreeze. Hyperkalemia occurs if the cat is oliguric or anuric. Hypocalcemia occurs in approximately half of patients. Hyperglycemia occurs in approximately half of patients due to inhibition of glucose metabolism by aldehydes, increased epinephrine and endogenous corticosteroids, and uremia. • Urinalysis: The pH and specific gravity are decreased by 3 hours post-ingestion, but the latter may be above the isosthenuric range. Calcium oxalate crystalluria may be observed as early as 3 hours post-ingestion; the monohydrate form is more often found than the dehydrate form.
Secondary Diagnostics • Imaging: Ultrasound examination typically shows bright kidneys (hyperechoic) as a result of calcium oxalate crystals. See Figure 70-1. Later, the medullary rim sign (Figure 70-2) and halo sign may develop. At this point, the therapy is unlikely to be successful. • Wood′s Lamp: Examination of the oral cavity, face, paws, vomitus, and urine with a Wood′s lamp is done to determine if fluorescence is present because many antifreeze solutions contain sodium fluorescein; a negative test does not eliminate the possibility of EG ingestion. • Kidney Aspiration: This may be considered when other tests are not available. The presence of oxalate crystals is consistent with EG toxicosis, especially if the kidneys are enlarged and painful.
167
SECTION 1: Diseases and Conditions
Figure 70-1 Ethylene glycol toxicosis causes formation of calcium oxalate crystals in the cortex and medulla resulting in these structures (arrow) being very hyperechoic.
• Activated Charcoal: This is controversial because aliphatic alcohols may not be well adsorbed by it. • Fomepizole (4-methylpyrazole, Antizol-Vet®): This is an effective and nonhepatotoxic ADH inhibitor. Initially, give 125 mg/kg IV within 1 to 3 hours post-ingestion; then give 31.25 mg/kg IV at 12, 24 and 36 hours after the initial dose. Note that this dose is much higher than the canine dose; the canine dose is not effective. • Ethanol 20%: Use if fomepizole is not available. It should be given as soon as the diagnosis is made, but it must be within the first 6 hours post-ingestion. To make a 20% solution, remove 105 mL from a 500-mL bag of normal saline and replace 105 mL of 95% grain alcohol (Everclear®). The dose is 5.0 mL/kg q6h intraperitoneally (IP) for five treatments, then q8h IP for four treatments. Alternatively, it can be given IV when diluted in intravenous fluids and given over 6- and 8-hour intervals, respectively. Ethanol treatment has two serious drawbacks; it worsens metabolic acidosis and causes CNS depression. • Sodium Bicarbonate: This is used to correct metabolic acidosis according to plasma bicarbonate and base deficit with monitoring every 4 to 6 hours. If close monitoring is not possible, give 5 mEq/kg per hour. • Fluid Therapy: Aggressive intravenous fluid therapy is needed to correct dehydration, electrolyte imbalances, metabolic acidosis, to increase tissue perfusion, and to promote diuresis.
Secondary Therapeutics • Peritoneal Dialysis: This should be done only by persons experienced with this technique. Referral centers are usually equipped to do so. • Osmotic Diuresis: Give dextrose 20% (20 mL/kg q6–8h IV) or mannitol 20% (1.25–2.5 mL/kg q6–8h IV) to re-establish renal output and oliguria or anuria is present. • Renal Transplantation: If the cat is relatively young and otherwise healthy, it can be a good candidate for this procedure. See Chapter 327.
Prognosis The prognosis is always guarded. If the therapy is initiated more than 6 hours after ingestion, mortality rate in cats is nearly 100%.
Suggested Readings Figure 70-2 The medullary rim sign may develop in ethylene glycol toxicosis. It is a linear area of increased echogenicity occurring in the outer zone of the medulla parallel to the corticomedullary junction.
Treatment Primary Therapeutics • Gastric Emptying: Induction of emesis and gastric lavage are helpful only if performed less than 1 hour post-ingestion and the cat is conscious. Give 3% hydrogen peroxide (5 mL PO of per 2.25 kg [5 lb], not to exceed 15 mL). This dose can be repeated once.
168
Connally HE, Thrall MA, Hamar DW. 2002. Safety and efficacy of high dose fomepizole as therapy for ethylene glycol intoxication in cats [abstract]. J Vet Emerg Crit Care. 12:191. Richardson JA, Gwaltney-Brant SM. 2003. Ethylene glycol toxicosis in dogs and cats. NAVC Clinician′s Brief. 1:13–18. Thrall MA, Connally HE, Grauer GF, et al. 2006. Ethylene glycol. In ME Peterson, PA Talcott, eds., Small Animal Toxicology. pp. 702–726. St. Louis: Elsevier Saunders. Thrall MA, Grauer GF, Connally HE, et al. 2007. Ethylene glycol poisoning. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 454–455. Ames, IA: Blackwell Publishing. Thrall MA, Hamar DW. 2007. Alcohols and glycols. In RC Gupta, ed., Veterinary Toxicology: Basic and Clinical Principles, pp. 608–614. New York: Academic Press/Elsevier.
CHAPTER 71
Exocrine Pancreatic Insufficiency Jörg M. Steiner
Overview Exocrine pancreatic insufficiency (EPI) used to be considered a rare disease in cats. But since 1995, when a new test for exocrine pancreatic function, feline trypsin-like immunoreactivity (fTLI), was introduced, EPI is being diagnosed in cats with considerable frequency. Over a recent 5-year period (2004–2008) a total of 1,342 cats were diagnosed with EPI, based on a severely decreased serum fTLI concentration. Contrary to dogs but similarly to humans, EPI in cats is due to chronic pancreatitis in almost all cases. The exocrine pancreas has an exceptional functional reserve, and it has been estimated that more than 90% of the functional reserve of the exocrine pancreas has to have been lost for clinical signs to ensue. Although there are other sources of digestive enzymes, such as salivary amylase, gastric lipase, or pepsinogen, pancreatic digestive enzymes play a crucial role in the digestion of all dietary components. Lack of pancreatic digestive enzymes leads to malassimilation, in turn leading to clinical signs of EPI, such as weight loss, loose stools, steatorrhea (see Figure 71-1), and greasy soiling of the hair coat. Results from clinical pathology and diagnostic imaging are usually within normal limits, unless the cat has concurrent conditions that lead to abnormalities, such as hyperglycemia in cats with concurrent diabetes mellitus, mild elevations in serum alkaline phosphatase activity, or thickening of bowel loops on abdominal ultrasound in cats with concurrent inflammatory bowel disease.
Diagnosis Primary Diagnostics • Serum Concentration of fTLI: An fTLI ≤8 µg/L (reference range 12– 82 µg/L) is considered diagnostic for EPI in cats. Under physiologic conditions, the exocrine pancreas releases the bulk of digestive enzymes into the pancreatic duct system. However, a small amount of trypsinogen is released into the vascular space. The assay for fTLI measures the amount of trypsinogen that is present in serum. Serum fTLI concentration is highly specific for EPI in cats (specificity 85– 100%). Also, the sensitivity of serum fTLI concentration is believed to be high for EPI. It is recommended that the cat be fasted for at least 6 hours prior to blood collection for test results to be valid. Also, the serum sample must not be lipemic because this can interfere with the radioimmunoassay.
Secondary Diagnostics • Fecal Proteolytic Activity: Until the introduction of the fTLI assay, measurement of fecal proteolytic activity was the diagnostic test of choice for EPI in cats but has since been shown to be inferior to measurement of serum fTLI concentration. This test is based on the measurement of total proteolytic activity in feces using one of several different assay methods. X-ray film digestion, the most popular technique, is highly unreliable and should not be used. Radial enzyme diffusion using a suitable substrate, such as casein, is considered more reliable. However, false-positive results can be observed because proteolytic enzymes are highly unstable in fecal material. False-negative results have also been described. Three stool samples from consecutive days should be evaluated and the fecal samples must be frozen immediately and sent on ice to preserve fecal proteolytic activity. • Serum Cobalamin Concentration: Serum cobalamin concentration is decreased in almost all cats with EPI due to the fact that in cats more than 99% of intrinsic factor is secreted by the exocrine pancreas. Intrinsic factor binds to cobalamin, and the cobalamin/intrinsic factor complexes are absorbed by specific receptors in the ileum. Unfortunately, a subnormal serum cobalamin concentration is not specific for EPI, and cats with chronic gastrointestinal diseases other than EPI commonly have a decreased serum cobalamin concentration.
Treatment Primary Therapeutics
Figure 71-1 Exocrine pancreatic insufficiency (EPI) stools: This large stool sample is from a cat with EPI. Note the typical loose consistency, the light brown color, and the greasy appearance. Also, the stool sample appears to contain a lot of undigested food particles. Photo courtesy of Dr. Kenneth Jones, Jones Animal Hospital, Santa Monica, CA.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Pancreatic Enzyme Supplementation: Powdered products are preferable over enteric-coated capsules or tablets. Initially, one teaspoon of pancreatic enzyme supplement should be given per meal. The enzyme supplement is thoroughly mixed with the food. If the cat is eating dry food the food should be moistened with water then mixed with the enzyme supplement. • Other Enzyme Sources: Cats that refuse to eat the enzyme supplement can be given raw pancreas from pigs, cows, or game. At meal time, 1 to 3 ounces of minced pancreas should be given. Pancreatic tissue can be acquired from a meat packing plant and can be stored frozen for several months without losing its enzymatic activity. See Therapeutic Notes.
169
SECTION 1: Diseases and Conditions
Secondary Therapeutics • Cobalamin: As mentioned previously, most cats with EPI are cobalamin deficient. See Chapter 37. These cats may not respond to pancreatic enzyme supplementation, unless they are also treated with cobalamin supplementation. In cats with cobalamin deficiency, cobalamin (vitamin B12) has to be supplemented parentally. Initially, 100 to 250 µg (depending on the size of the cat) cyanocobalamin are given q7d SC for 6 weeks, followed by 100 to 250 µg per cat q14d SC for 6 weeks. This is followed by one more injection 4 weeks later and re-evaluation of serum cobalamin concentration 4 weeks after that. Reevaluation will help to determine whether cobalamin supplementation needs to be continued. Although in some cats only temporary cobalamin supplementation will be required, other cats will require lifelong therapy.
the activity of gastric lipase, thus potentially leading to no net gain in lipid digestion. If antacids have no beneficial effect, antibiotic therapy can be attempted. In dogs with EPI, small intestinal bacterial overgrowth (SIBO) is a common complication. However, SIBO has not yet been documented in cats. However, cats with EPI that do not respond to therapy should undergo a treatment trial with an antibiotic, such as tylosin or metronidazole. A last resort in attempting to treat cats with unresponsive EPI is to decrease the fat content in the diet of these patients. However, this measure further decreases fat absorption and may lead to deficiencies in essential fatty acids or fat-soluble vitamins. • There is a single report of a cat with EPI that had a vitamin K-responsive coagulopathy. Thus, if bleeding diathesis is observed in a cat with EPI, the coagulation system should be evaluated and the cat be treated with vitamin K supplementation.
Therapeutic Notes • There is a small infectious risk when feeding raw pancreas. Bovine pancreas may lead to the transmission of bovine spongiform encephalitis (BSE), porcine pancreas of Aujeszky disease, and game pancreas can be infested with endoparasites, most significantly Echinococcus multilocularis. A commercial source for BSE-free bovine pancreas is Salzman International Inc., Davenport, IA; phone: 319-324-1028. • If none of the aforementioned sources are successful in administering pancreatic enzymes to the cat, a fish oil suspension can be prepared with pancreatic replacement enzymes that will be consumed eagerly by most cats. After complete remission of clinical signs the dose of pancreatic enzymes should be decreased to the smallest effective dose. This dose may change slightly over time and may also have to be readjusted when a new jar of pancreatic enzymes is started. • Cats that do not respond adequately to enzyme and cobalamin supplementation should be evaluated for potential concurrent conditions. Most commonly, cats with EPI may have concurrent inflammatory bowel disease or diabetes mellitus, but other conditions may also be present. If concurrent conditions cannot be identified, H2 antagonists or proton pump inhibitors can be tried to decrease destruction of orally administered pancreatic lipase in the stomach. Unfortunately, although an increased gastric pH will decrease destruction of exogenous pancreatic lipase, it also decreases
170
Prognosis EPI is considered irreversible. However, there are some anecdotal reports of rare cases of a spontaneous remission in dogs but not in cats. However, cats with EPI that are treated appropriately are expected to have a normal life expectancy and an unaltered quality of life.
Suggested Readings Steiner JM. 2009. Exocrine pancreatic insufficiency. In JR August, ed., Consultations in Feline Internal Medicine, pp. 225–231. St. Louis: Elsevier Saunders. Steiner JM, Williams DA. 2000. Serum feline trypsin-like immunoreactivity in cats with exocrine pancreatic insufficiency. J Vet Intern Med. 14:627–629. Thompson KA, Parnell NK, Hohenhaus AE, et al. 2009. Feline exocrine pancreatic insufficiency: 16 cases (1992–2007). J Fel Med Surg. 11(12): 935–940. Westermarck E, Wiberg M, Steiner JM, et al. 2005. Exocrine pancreatic insufficiency in dogs and cats. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1492–1495. St. Louis: Elsevier Saunders.
CHAPTER 72
Eyelid Diseases and Surgery Gwen H. Sila and Harriet J. Davidson
Overview The feline eyelids or palpebrae consist of four basic layers from deep to superficial: conjunctiva, tarsal plate, muscle, and skin. The conjunctiva covers the sclera then turns back on itself at the conjunctival fornix of both the upper and lower eyelids to cover their inner aspects. The tarsal plate is a band of thickened connective tissue which separates the conjunctiva from the muscle layer and helps maintain the eyelids’ shape. The major muscles of importance in the eyelids are the levator palpebrae superioris muscle, which is responsible for elevating the upper eyelid, and the orbicularis oculi muscle, which surrounds the palpebral fissure causing the eyelids to close when it contracts. These muscles are innervated by cranial nerve (CN) III and CN VII, respectively. In contrast to many other species, cats do not have true upper or lower eyelashes. Most cats do have a row of hairs close to the lid margin that function similarly to true eyelashes. Lining the eyelid margins are the ductal openings to the meibomian glands, which secrete the oily component of the tear film. Smaller Glands of Moll and Glands of Zeis are found in close association with hair follicles along the lid margin. In comparison to dogs, cats are relatively infrequently affected by eyelid disease; however, eyelid conditions can have significant impact on ocular and potentially systemic health.
Figure 72-1 The upper eyelid in this cat has a large defect due to agenesis. Photo courtesy Dr. Gary D. Norsworthy.
Congenital and Inherited Conditions Eyelid Agenesis This condition occurs sporadically and is the most common congenital abnormality of the feline eyelid. In the vast majority of cases the upper, temporal eyelid is affected, but the amount of tissue missing from the eyelid varies (see Figure 72-1). Usually the condition is bilateral. Diagnosis is based on appearance of the lesion. Affected animals will not have a continuous eyelid margin as the lid is followed from medial to lateral. The condition may be associated with congenital intraocular abnormalities as well. Sequelae include exposure keratitis and mechanical irritation from facial hairs, which are able to contact the cornea without an intact eyelid. These conditions can lead to severe scarring, discomfort, and loss of the globe if deep corneal ulceration results. Treatment is usually surgical, and the method employed depends on the size of the defect. Small defects (less than one-fourth of the eyelid margin) may be closed directly by incising the edges of the missing portion of the lid, carefully apposing the eyelid margins, and then suturing the defect. Cryotherapy to destroy the follicles of irritating hairs may be sufficient to reduce discomfort and corneal disease if the defect is small. Three, 60-second freezes with complete thawing between freezes of the offending hair follicles may be effective. Larger defects or defects resulting in exposure-related corneal disease require more advanced procedures for repair.
Entropion Rolling in of the eyelid margin (entropion) is a less common condition in the cat. See Figure 72-2. Many cases of entropion are secondary to
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 72-2 Chronic entropion results in lid hair (not eyelashes) rubbing the cornea causing chronic keratitis. Photo courtesy Dr. Gary D. Norsworthy.
ocular surface irritation, which results in blepharospasm and a subsequent spastic entropion. Ocular irritation and spastic entropion should be ruled out prior to any surgical correction for entropion. Spastic entropion should improve with the instillation of topical anesthetics. If spastic entropion is suspected, a temporary tarsorrhaphy suture can be placed to prevent the lids from rolling in while the underlying ocular irritation is resolving. The eyelid position can then be assessed after the ocular irritation has resolved and corrected if necessary. Primary entropion often manifests early in life, usually by 1 to 2 years
171
SECTION 1: Diseases and Conditions
of age, and is most common in brachycephalic breeds including Persians and in the Maine coon, but it can be seen in any breed. In brachycephalics the entropion often involves the medial lower eyelid. Older cats can also be affected by entropion secondary to loss of orbital fat as part of the aging process. Most entropion in cats can be corrected surgically with a modified Hotz-Celsus procedure. Eyelid position should be assessed while the cat is awake and under topical anesthetic, so any spastic component is minimized, to determine how much tissue should be removed.
Ectopic Cilia This condition has been rarely reported in the cat. Hair(s) can grow from the palpebral conjunctiva along the posterior lid and contact the cornea causing irritation and ulceration. Often corneal ulcers associated with this condition are linear and oriented dorsoventrally. Treatment is surgical excision of the hair follicle and can be followed by cryotherapy.
(A)
Acquired Conditions Blepharitis This condition presents as swelling and hyperemia of the eyelids with variable involvement of the conjunctiva. Depending on the duration, the periocular skin may be alopecic. Excoriations or ulcerations may be present due to self-trauma because the condition can be painful or pruritic.
Drug Reactions Both systemic and topical medications can cause allergic reactions resulting blepharitis. It is common for cats to have severe localized reactions to some common topical ophthalmic medications including neomycin, polymyxin B, bacitracin, gentamicin, and oxytetracycline (Terramycin™). A drug reaction should be considered with any acute swelling of the conjunctiva and eyelids within 24 to 48 hours after starting a new medication. The medication should be discontinued immediately, and, if corneal ulceration is not present, topical corticosteroids may be administered two to four times daily until the swelling resolves. In the case of a systemic drug reaction, systemic anti-inflammatories may be necessary as well.
Dermatophytosis Skin lesions can be variable in appearance but are often present on the head including the periocular skin. The lesions are usually alopecic and are variably pruritic. Diagnosis is based on visualization of fungal hyphae or spores within the hair shaft upon microscopic examination or culture of hairs plucked from suspicious lesions. See Chapter 48.
Demodicosis This is a rare disease in cats with a regional distribution (most commonly seen in Texas), and the etiologic agents are Demodex gatoi and Demodex cati. The former is highly contagious, causes intense pruritus, and is found in the superficial stratum corneum of the skin. The latter is a follicular mite associated with immunosuppressive conditions. Both mites can cause periocular alopecia and inflammation. Diagnosis is via skin scrapings which must be deep in the case of D. cati. See Chapter 201.
Eyelid Neoplasia Eyelid neoplasia is rarely diagnosed in cats. In fact, tumors of the eye and orbit represent only about 2% of all feline neoplasms. Although
172
(B) Figure 72-3 A, Squamous cell carcinoma frequently affects the eyelids. There are two adjacent lesions in this cat. B, A CO2 laser can be used to ablate the tumor. More than one treatment may be needed. Photo courtesy Dr. Gary D. Norsworthy. uncommonly encountered, eyelid tumors in cats may be malignant; they are frequently squamous cell carcinoma. See Figure 72-3. Cytology via fine-needle aspiration or histopathology for tumors removed via wedge resection is always warranted. To ensure the best tumor margins and outcome, it is preferable to have a good idea of the tumor type prior to attempting removal. Only up to one-third of the eyelid can be removed with a wedge resection making it an unforgiving location if additional resections are necessary to obtain more appropriate surgical margins.
Squamous Cell Carcinoma Squamous cell carcinoma (SCC) is the most common eyelid tumor. Cats with nonpigmented and poorly pigmented eyelids are most often affected and solar radiation is thought to play a role in development of SCC. It often presents as a pink lesion, which can be raised or depressed and is often ulcerated. These tumors are typically late to metastasize but can spread to local lymph nodes. Histologic grade (Broder ’s classification grades I to IV) correlates with prognosis. Multiple treatment modalities exist. Wide surgical excision can be curative, but SCC is often invasive, and it may be hard to determine the tumor ’s
Eyelid Diseases and Surgery
extent making resection difficult. Excision may necessitate complicated grafting procedures to replace the defect left from tumor removal. Radiation therapy, cryotherapy, photodynamic therapy, CO2 laser, and hyperthermia have all been shown to be effective treatment methods in some cases. See Chapter 203.
Basal Cell Tumor Basal cell tumors represent 2 to 6% of feline eyelid neoplasms. These tumors are typically round and well circumscribed but can become ulcerated. For this reason, they can be difficult to differentiate from SCC based on appearance. Histologically these tumors may appear malignant, but they typically act in a benign fashion. Surgical excision via a simple wedge resection (see Figure 72-4) or cryotherapy is usually curative. See Chapter 18.
excision is recommended, but it is often difficult due to the degree of tumor invasion. Follow-up radiation therapy for incomplete surgical margins may decrease rate of recurrence. See Chapter 198.
Apocrine Hidrocystoma The etiology of these masses is unknown, and there is debate as to whether these represent cystic or benign neoplastic lesions arising from the glands of Moll. Most cases have been reported in Persians. The masses are usually dark-colored, sometimes reddish, discrete nodules. They often contain clear to red-brown fluid. Treatment options include complete excision, drainage, and treatment with 20% trichloroacetic acid following surgical debridement. In many cases new lesions develop within 8 to 12 months.
Metastatic Neoplasms Mast Cell Tumor A recent retrospective study found mast cell tumors accounted for 25% of feline eyelid neoplasms; previous studies report an incidence between 3 to 12%. Cats with eyelid mast cell tumors were found to be significantly younger than cats with other types of eyelid neoplasia. Mast cell tumors may be raised or ulcerated. They range from well circumscribed to diffuse involvement of surrounding tissues. Significantly increased survival times have been found in cats with single, solitary dermal masses when compared to cats with multiple cutaneous masses and cats with lymph node or visceral (i.e., liver, spleen, intestinal) involvement. Additionally incomplete excision of solitary cutaneous tumors does not seem to impact survival time or recurrence rate of these tumors. For solitary tumors surgical excision or corticosteroid therapy is recommended. See Chapter 135.
Fibrosarcoma These represent between 5 to 9% of feline eyelid neoplasms. Their behavior is similar to elsewhere in the body. They tend to be locally invasive and aggressive but late to metastasize. They are often alopecic and may be ulcerated. The mitotic index correlates with prognosis. Wide surgical
The most common metastatic neoplasms to affect the eyelids include lymphosarcoma (6–12%) and hemangiosarcoma (2.3%).
Surgery of the Eyelids Temporary Tarsorrhaphy • This is a procedure used to hold the eyelids in apposition to prevent them from rolling in and rubbing on the cornea or to act as a protective covering/bandage for the cornea. • Equipment Needed: 4-0 to 6-0 nonabsorbable suture such as P nonabsorbable polypropylene (Prolene™), needle holders, forceps, with or withoutmagnification. • Procedure: A single mattress suture is placed through the eyelid margin (see Figure 72-5) to close it by approximately one-third. When correctly positioned suture should exit and enter the margin of the eyelid by passing very near to a meibomian gland opening. If more closure is desired, additional sutures may be placed. • Complications: Premature suture failure resulting in eyelid opening can occur. The owner should be advised to remove any remaining suture from the eyelid margin to prevent it from rubbing on the cornea. Incorrect positioning of the suture (posterior to the meibomian glands) can allow it to rub against the cornea potentially resulting in deep corneal ulceration.
3
2
1
4
4 1
5
6
2 Figure 72-4 The eyelid margin following wedge resection is depicted. Numbers 1 through 4 depict the bites taken during placement of the figure-8 suture at the eyelid margin. The simple interrupted suture placed more proximally to close the remainder of the incision is labeled 5 and 6.
3 Figure 72-5 The four bites taken during placement of the temporary tarsorrhaphy suture are depicted.
173
SECTION 1: Diseases and Conditions
Modified Hotz-Celsus This procedure is used to correct entropion and causes the eyelid to roll outward by removing skin and muscle from above or below the eyelid. • Equipment Needed: Number 11 or 15 scalpel blade, tenotomy scissors or other small scissors, 4-0 to 6-0 suture, small forceps such as Bishop-Harmon, needle holders. • Procedure: A skin incision is made about 2 mm from the eyelid margin along the affected region. See Figure 72-6. A semilunar incision is then made ventral to and connecting to either end of the first incision so that a wedge of tissue the same width as the amount of eyelid that was rolling inward is defined. It is best to remove less tissue and perform an additional procedure at a later date rather than remove too much tissue and create ectropion. The wedge of tissue is completely undermined with scissors and blunt/sharp dissection to the level of the tarsal plate and removed. The incision is closed with simple interrupted 5-0 to 6-0 sutures. The initial suture should be placed in the center of the incision and subsequent sutures between these (closed by halving) to prevent “dog ears” at the ends of the wound. • Complications: Suture dehiscence due to self-trauma is possible, and cats should be discharged with an E-collar. Over correction of the
3 4
Wedge Resection This procedure is used to remove small eyelid masses up to one-fourth the length of the eyelid. • Equipment Needed: Jaeger lid plate or flat smooth instrument, number 15 scalpel blade, tenotomy scissors or other small scissors, 5-0 to 6-0 suture, needle holders, small forceps such as Bishop-Harmon. • Procedure: The wedge, or triangle, removed should have a height that is twice the base in order to allow appropriate wound closure. The lid plate is placed beneath the mass to be removed, between the lid and globe, the eyelid is stretched slightly over the plate. The scalpel blade is used to incise perpendicular to the lid margin on either side of the mass. The incisions are extended proximal and connected to form a wedge. See Figure 72-3. The palpebral conjunctiva may not be cut using the scalpel blade, and the tenotomy scissors should be used to incise the conjunctiva and complete the mass removal. A figure-8 suture pattern should be used to close the eyelid margin. This suture pattern minimizes tension, aligns the eyelid margins, and directs the suture ends away from the cornea. Simple interrupted sutures should then be placed in the incision, moving from near the eyelid margin to more proximal. The ends of all sutures should be left long and then incorporated into the second throw of the last, most proximal suture to keep them from inadvertently rubbing on the cornea. • Complications: Inappropriately placed sutures could rub against the cornea and cause ulceration. If the eyelid margin is not aligned correctly irritation and ulceration can result. Infectious are rare. Patients may need to be sent home with an E-collar because self-trauma can result in suture breakage or dehiscence. • Depending on the size of the defect in eyelid agenesis referral to a veterinary ophthalmologist may be a good option. Lesions greater than one-fourth of the eyelid margin can require more involved grafting procedures. • Eyelid tumors in cats have the potential to be malignant, so any eyelid mass in a cat should be investigated by either fine-needle aspiration or histopathology. Cats with less pigmented eyelid skin are at an increased risk for development of squamous cell carcinoma, the most common eyelid tumor in this species.
2 1
Figure 72-6 The light blue line along the lower lid depicts the region of entropion. The modified Hotz-Celsus incision with the intervening skin already removed is shown beneath the rolled in lid margin. The simple interrupted sutures are numbered in order of placement in the figure because the wound is closed by repeatedly halving the incision.
174
entropion can result in ectropion. Infectious are rare due to the vascular nature of the eyelids.
Suggested Readings Aquino SM. 2008. Surgery of the eyelids. Top Companion Anim Med. 23(1):10–22. Aquino SM. 2007. Management of eyelid neoplasms in the dog and cat. Clin Tech Small Anim Pract. 22(2):46–54. Martin, CL. 2005. Eyelids. In CL Martin, ed., Ophthalmic Disease in Veterinary Medicine, pp. 145–178. London: Manson Publishing. Williams DL, Kim JY. 2009. Feline entropion: a case series of 50 affected animals (2003–2008). Vet Ophthalmol. 12(4):221–226.
CHAPTER 73
Feline Enteric Coronavirus Infection Amanda L. Lumsden and Gary D. Norsworthy
Overview The feline coronavirus group is a large genus that includes numerous strains, serotypes, and biotypes (enteric or infectious peritonitis viruses). The feline enteric coronavirus (FECV) is a ubiquitous, worldwide intestinal virus that infects domestic and other species of cats. It is tropic for the mature apical epithelium of the intestinal villi. Infection is typically subclinical or manifested by a mild, transient gastroenteritis that usually produces diarrhea. It is not considered a life-threatening infection unless it mutates into the fatal feline infectious peritonitis Virus (FIPV), which it does with variable frequency. (For a discussion of feline infectious peritonitis [FIP], see Chapter 76.) One author concluded that the mutation rate is as high as 20%; however, in few of these does FIP result. FECV is easily transmitted on fomites, including clothing. Therefore, transmission in a multicat environment is problematic even when a queen and her litter are kept in a separate room from other cats in the facility. Primary infection lasts from 7 to 18 months with the highest viral shedding occurring during this time. Following primary infection there are three possible outcomes: (a) recovery, (b) persistent shedding, and (c) recurrent or intermittent shedding. Reinfection is a common occurrence because many infected cats are housed with other infected cats. Reinfection can resemble a primary infection in magnitude and duration. In a laboratory setting and in cattery cats, shedding was not affected by parturition and lactation or by methylprednisolone treatment. However, there is a relationship between feline coronavirus (FCoV) titers and shedding. Cats with titers of 1 : 100 or greater are typically shedding virus. Cats with titers of 1 : 25 or less are not likely to be doing so. Following initial infection or reinfection, kittens shed virus at higher levels than adults. This is significant because FECV-to-FIPV mutation and the onset of FIP are more likely to happen in cats less than one year of age. Feline immunodeficiency virus (FIV)-induced immunosuppression, and presumably other forms of immunosuppression, will cause FECV-infected cats to shed 10 to 100 times more FECV that can subsequently result in an increased likelihood of cats developing FIP. Kittens born to queens infected with FECV are not likely to shed virus until about 9 weeks of age; therefore, virus passage is not likely to be in utero but by postpartum contact with the queen. Control programs of early weaning at less than 6 weeks of age are based on this observation. However, occasionally infection will occur as early as 3 weeks of age.
Diagnosis Primary Diagnostics • Polymerase Chain Reaction (PCR) test: This test allows amplification of FECV. The fecal level of FECV is high; the blood level is low. When used on a blood sample it has low sensitivity and specificity for FECV. Testing a fecal sample results in high sensitivity and specificity. • FCoV Titer: This test detects antibodies to FECV and FIPV. Cats with either virus usually have positive titers; therefore, this test lacks specificity for FECV.
Diagnostic Notes • One should be cautious about interpreting FCoV titers. They may be positive in cats with FECV and FIPV infections and positive or negative in cats with clinical FIP. When clinically normal cats have positive titers, there is no predictive value for the onset of FIP. Although the PCR test is much more specific for FECV infection, predictive value for mutation to the FIPV is still negligible.
Treatment Primary Therapeutics • There is no known treatment to eradicate this virus in cats.
Therapeutic Notes • Most cats infected with FECV will carry the virus lifelong but generally only have one episode of transient diarrhea.
Prognosis The prognosis for the vast majority of cats with an FECV infection is good. Once the transient diarrhea resolves, no further clinical manifestations occur unless reinfection occurs. Subsequent disease only occurs when the virus mutates to the FIPV. However, most of these cats serve as a source of the FECV for other cats. FECV infection is considered self-limiting without constant re-exposure to other infected cats and new cats, especially kittens. Therefore, closed households of adult cats rarely have mutation to the FIPV.
Suggested Readings
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Pedersen NC. 2009. A review of feline infectious virus infection: 1963– 2008. J Fel Med Surg. 11:225–258. Pedersen NC, Allen CE, Lyons LA. 2008. Pathogenesis of feline enteric coronavirus infection. J Fel Med Surg. 10:529–541.
175
CHAPTER 74
Feline Idiopathic Cystitis Tatiana Weissova and Gary D. Norsworthy
Overview Feline lower urinary tract disease (FLUTD) is a group of diseases with many possible causes that include urolithiasis, urethral plugs, neoplasia, bacterial, viral, or fungal infections, neurologic diseases (e.g., reflex dyssynergia, urethral spasm, hypotonic or atonic bladder), anatomic malformations (urachal anomalies), and feline idiopathic cystitis (FIC). It may exist in nonobstructive or obstructive forms. FIC is the most common diagnosis in young cats with FLUTD, occurring in approximately 50 to 60% of cases. The causative agent of FIC is still unknown. Many theories have been proposed including stress, urothelium abnormalities (a defect in the protective glycosaminoglycan [GAG] layer of the urinary bladder or increased bladder wall permeability after distension), neuroendocrine disorders, viral infection (feline calicivirus, feline herpesvirus, feline syncytial-forming virus), ash content of the diet, dry cat foods, and fish-flavored cat foods. The pathophysiology of FIC likely involves complex interactions between several body systems (i.e., nervous, endocrine, and even cardiovascular); therefore, it is not only a “bladder” disease. Part of our confusion regarding this disease is that all nonobstructive forms of lower urinary tract disease cause one or more of a limited list of clinical signs that include periuria (inappropriate urination), pollakiuria, stranguria, dysuria, and hematuria. In addition, most of these may precede the obstructive form of the disease. The obstructive form is life-threatening; cats will likely die if urine flow is not reestablished within 24 to 48 hours. Urethral obstruction in cats with FIC may result from one or more of the following: inflammatory swelling of the urethra, urethral muscular spasm, reflex dyssynergia, intraluminal accumulation of sloughed tissue, inflammatory cells or red blood cells, and formation of matrix-crystalline urethral plugs. See Chapter 220. Obstructive uropathy is rare in female cats. Most cats with FIC are between 2 and 6 years of age; the occurrence is uncommon in cats less than 1 year of age or greater than 10 years of age. Clinical signs may subside within 5 to 7 days without therapy in many cats (60–85%), but the signs may recur within weeks, months, or 1 to 2 years after the initial episode. Recurrent episodes of acute FIC decrease as the cat become older. The risk is higher for spayed or castrated cats, indoor cats, obese cats, cats that are fed only with dry food, and cats that have decreased intake of water. Other risk factors include stress, multicat or multianimal households, and changes in common daily routine. Cats with FIC have a significant increase in tyrosine hydrolase immunoreactivity in the brainstem, and during the initial stress period, norepinephrine, dopamine, and other catecholamines are significantly elevated. There is a small subset of cats in which clinical signs may persist for weeks to months due to chronic idiopathic cystitis; ultrasound will reveal significant bladder wall thickening. See Figure 292-75B. Other cats have frequently recurrent disease. Differential diagnoses are the other causes of FLUTD.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
176
Diagnosis Primary Diagnostics • Specific Diagnostic Tests: FIC is a diagnosis of exclusion; it is diagnosed when all diagnostics fail to confirm the presence of another low urinary tract disease. • History: A typical history includes pain during urination (crying or howling), pollakiuria, licking of the genital area, passage of small amounts of urine, hematuria, and periuria. Obstructed cats exhibit frequent trips to the litter box without urine passage (often described by owners as constipation) and abdominal pain when palpated; as the bladder enlarges and renal function declines depression, anorexia, and vomiting may occur. • Clinical Findings: In cats with the nonobstructive form the bladder may be thickened and sensitive to direct palpation; it may also be normal in thickness and normal to palpation. On presentation the bladder is usually small or empty. In obstructed cats the abdomen is firm and painful to even gentle palpation; these cats are often vocalizing in pain. The bladder is large and firm, and there is a small possibility of rupture and subsequent uroperitoneum. Cats with obstruction are often dehydrated, depressed, and anorectic. • Urine Tests: The urinalysis (UA) may reveal gross or microscopic hematuria and occasionally proteinuria. The sediment is variable; crystalluria may or may not be present. When present crystals are typically struvite but in lesser frequency than 10 to 15 years ago; calcium oxalate crystals are occurring in increasing frequency. Urine culture is typically negative unless secondary bacterial infection occurs. About 20% cats have normal urinalyses.
Secondary Diagnostics • Complete Blood Count (CBC) and Blood Chemistry: These are typically normal in nonobstructive disease. Cat with a urethral obstruction will have changes typical of acute renal failure or obstructive uropathy. These include elevated blood urea nitrogen (BUN), creatinine, phosphorus, and potassium values with metabolic acidosis. • Electrocardiogram (ECG): Abnormalities are due to hyperkalemia. See Chapters 106 and 220. • Imaging: Abdominal radiographs should be made to include the caudal abdomen and penile urethra. High quality radiographs can detect radiopaque calculi as small as 1 mm in diameter, which are often found in the urethra. See Figures 292-77 and 292-79. In cats with recurrent signs the use of contrast radiography, including double contrast cystography and urethrography, may be helpful in detection of small calculi, radiolucent calculi, urachal diverticula, neoplasia, and to determine bladder wall thickness. Ultrasound examination may detect small calculi, radiolucent calculi, bladder masses, and it is more sensitive than radiographs in evaluating bladder wall thickness. • Endoscopy: Uroendoscopy may be helpful in cats with recurrent or persistent clinical signs for evaluating the urethral and bladder mucosal surfaces. Cats with FIC may have submucosal petechial hemorrhages, glomerulations, mural edema, increased vascularity,
Feline Idiopathic Cystitis
debris in the lumen of the bladder, or small calculi. Urachal remnants and small uroliths may be seen. However, the size of the urethra limits the size of the endoscope such that the presence of a working (biopsy) channel and controllable flexion are usually not possible.
Diagnostic Notes • The absence of hematuria or crystalluria does not exclude a diagnosis of FIC. • Mild crystalluria may be a common finding in many healthy cats. • Often cellular debris may be misinterpreted as bacteria because of Brownian motion and similar morphology. Differentiation is made with a urine culture. • House soiling (inappropriate elimination) is the most common behavior problem of cats. In these cats the urinary bladder may be full at the time of presentation; it is almost always empty in cats with nonobstructive FIC. With house soiling there is no hematuria, dysuria, or stranguria; these signs are usually consistent, not intermittent, as in FIC. House soiling is diagnosed when the other medical disorders are ruled out. See Chapter 234. • Nonobstructive FIC is self-limiting, and signs will usually resolve within 5 to 7 days. If dysuria or hematuria continues more than 14 days (with or without therapy) the cat should undergo further diagnostics. Urinalysis, urine culture, abdominal ultrasound, double contrast cystourethrogram, or cystoscopy can be performed to be certain no other lesions are in the lower urinary tract. • The lower urinary tract is relatively resistant to infection because of an ability to produce concentrated acidic urine with high urea content.
Treatment Primary Therapeutics: Nonobstructive Form • Therapeutic approaches are only symptomatic because of the unknown etiology of FIC. This is not a bacterial disease so antibiotic therapy is not necessary unless there is a positive urine culture. • FIC is principally a disease of young cats. Older cats with symptoms of lower urinary tract disease should be evaluated for bacturia, uroliths, and bladder tumors as well as systemic diseases such as renal disease, diabetes mellitus, and hyperthyroidism. • Analgesics: Butorphanol (0.2–0.4 mg/kg q8–12h PO, SC), buprenorphine (0.01–0.02 mg/kg q8–12h PO), or meloxicam (0.05–0.1 mg/kg q24h PO) may be used for acute bladder pain. • Combination: Some authors recommend a combination of buprenorphine (5–20 µg/kg q6–12h PO for 3–5 days) and acepromazine (2.5 mg q8–12h PO of the injectable form or 2.5 mg [one-fourth of a 10-mg tablet] q8–12h PO for 3–5 days). If acepromazine in tablet form is used, it can be given orally, in a chewable treat, or crushed and made into a suspension for oral syringing. • Multimodal Environmental Modification (MEMO): This includes making changes within a cat’s environment to reduce stress, fear, and nervousness. It centers on improvement of interactions between this cat and other household members or pets, sufficient numbers of clean litter boxes in quiet undisturbed places, positive interaction (play) between owners and the cat, the use of canned food or running water fountains to increase fluid intake, and Feliway® (Ceva Animal Health, Phoenix, AZ). MEMO is a promising adjunctive therapy for indoor-housed cats with lower urinary tract signs. • Stress-relieving Drugs: If the aforementioned approach is not successful, add amitriptyline (2.5–5 mg per cat q24 h PO) because it may provide analgesia by inhibition of norepinephrine reuptake. How-
ever, it is only for long-term treatment because it may take several weeks to produce clinical response. It seems to be successful only in therapy of recurrent or chronic FIC; it is not indicated in cats with acute FIC. Other antidepressants as clomipramine, fluoxetine, or buspirone have variable success rate. • Feline Facial Pheromone: Feliway is a synthetic analogue for reduction of anxiety experienced by cats in unfamiliar circumstances. • Canned Food: This should be strongly considered for cats with FIC because cats consuming only dry food usually ingest up to 50% less water than cats fed canned food. Cats should be fed small amounts frequently throughout the day and should have access to clean fresh water. Special diets are recommended for cats with significant struvite or oxalate crystalluria.
Secondary Therapeutics: Nonobstructive Form • Propantheline: This is used to minimize hyperactivity of the bladder detrusor muscle and urge incontinence. It is dosed at 0.25 to 0.5 mg/ kg q12 to 24 h PO. • GAG replacers: Pentosan polysulfate sodium and glucosaminechondroitin sulfate combination products (Cosequin™ and Dasuquin™, Nutramax Laboratories, Edgewood, MD) have been used with clinical success; however, their efficacy in control studies has not been confirmed. According to recent information both GAG replacers appear to be ineffective therapy for acute FIC.
Therapeutics Notes: Nonobstructive Form • Not all cats with FIC will require intense treatment and environmental modifications. • Antispasmodics are no longer recommended because of potential adverse affects. • Corticosteroids do not consistently offer significant antiinflammatory effects for FIC.
Primary Therapeutics: Obstructive form • See Chapter 220 for in-depth details.
Prevention • Urine pH modification may be preventative. Urine acidification may prevent struvite crystalluria, but it is contraindicated in the presence of calcium-oxalate crystals or uroliths. Low carbohydrate-high protein diets produce significant acidification of the urine. Acidifying drugs and acidifying diets are rarely needed together. Do not do so without monitoring urine pH. • Canned Food: The higher water content of canned food is considered beneficial for cats with FIC. • Other Diets: Some diets are designed to induce polyuria and others claim to prevent lower urinary disease by reducing the building blocks of urinary crystals and uroliths. • MEMO: This can be used to minimize stress in the cat’s environment.
Prognosis The prognosis in nonobstructive cats is good even without treatment, but recurrence is common. Obstructed cats with uremia have a guarded prognosis; however, full recovery is likely if urine flow is restored quickly as full renal function generally returns.
177
SECTION 1: Diseases and Conditions
Suggested Readings Chew D, Buffington T. 2009. Managing cats with non obstructive idiopathic interstitial cystitis. Vet Med. 104(12):568–569 Hostutler RA, Chew DJ, DiBartola SP. 2005. Recent concepts in feline lower urinary tract disease. Vet Clin North Am Small An Pract. 35:147–170. Kruger JM, Osborne CA, Lulich JP. 2008. Changing paradigms of feline idiopathic cystitis. Vet Clin North Am Small An Pract. 39:15–40. Osborne CA, Kruger JM, Lulich JP, et al. 2007. Feline idiopathic lower urinary tract disease. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s
178
5-Minute Veterinary Consult, 4th ed., pp. 482–483. Ames, IA: Blackwell Publishing. Westropp JL. 2006. Feline idiopathic cystitis—Demystifying the syndrome. Hill’s Symposium on Advances in Feline Medicine, Symposium proceedings, Brussels, pp. 64–69. Westropp JL. 2008. Feline idiopathic cystitis: Pathophysiology and management. 33rd WSAVA and 14th Fecava World Congress Proceedings, Dublin. Ireland.
CHAPTER 75
Feline Immunodeficiency Virus Infection Sharon Fooshee Grace
Overview The feline immunodeficiency virus (FIV) is a member of the lentivirus subfamily of retroviruses. Six subtypes (A–F) have been well characterized; a possible seventh subtype has been described in New Zealand (U). The most common viral subtypes found in the United States and Canada are subtypes A and B with subtypes C and F being less frequent. Prevalence of FIV in the general population of both owned and feral cats in North America is less than 5%. Although the prevalence of feline leukemia virus infection (FeLV) has declined over the past two decades, that of FIV has remained essentially unchanged. Like other lentiviruses, FIV is species-specific and poses no apparent public health risk. Since it was first isolated in the 1986 from a cattery in northern California, it has remained a focus of research interest. Bite wounds appear to provide the major mode of transmission, although there is evidence that it can be casually transmitted among cats who live peaceably in close proximity over a prolonged period of time. This contrasts with early findings that suggested that casual contact was highly unlikely to result in transmission. Queens that become infected during gestation may transmit the virus in utero or later through colostrum or saliva, though this is infrequent in naturally occurring infections. Older, sexually intact, free-roaming outdoor male cats are at the highest risk of infection because of their fighting behaviors. Kittens are uncommonly infected and, unlike some other infectious diseases, kittens are not more susceptible to FIV than adult cats. The exact number of clinical stages that exist with FIV varies among investigators, but a simple classification scheme includes three phases: an acute phase, an asymptomatic phase of variable duration, and a terminal phase. During the acute phase, signs are usually nonspecific and may last several days to weeks; signs may include fever, depression, gastrointestinal dysfunction (i.e., enteritis, stomatitis), respiratory tract disease, and peripheral lymphadenopathy. In some cats, the acute phase goes undetected. As an asymptomatic carrier, the cat is free of clinical disease. This stage is known to last for many years in some cats. In later stages, signs are reflective of opportunistic infections, neoplasia, neurologic dysfunction, or a general wasting syndrome. Terminal signs include weight loss, persistent diarrhea, gingivitis or stomatitis, chronic respiratory disease, lymphadenopathy, and chronic skin disease. Profound oral or dental disease is a common finding in the late stages of FIV; in some cats, the mucosa is ulcerated and necrotic. Many cats in the terminal stage present with neoplastic disorders, such as lymphoma or various leukemias. Neurologic dysfunction has been seen in a small percentage of infected cats; behavior changes are the most commonly reported. Inflammatory ocular disease and nonspecific renal disease are also seen. A number of different infectious diseases have been reported concurrent with FIV infection, though the true prevalence of many of these diseases is still unclear. One study demonstrated that immunosuppression caused by chronic FIV infection increased the replication rate of enteric coronavirus and thus could select for mutation into virulent coronavirus (feline infectious peritonitis [FIP]).
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Diagnosis Primary Diagnostics • Clinical Signs: Chronic disease states, gingivitis or stomatitis, and seemingly minor infections (especially upper respiratory) that do not respond well to treatment should alert one to the possibility of an FIV infection. • Antibody Tests: Commercially available enzyme-linked immunosorbent assay (ELISA) kits test for the presence of FIV-specific antibody. The Western Blot and immunofluorescent antibody (IFA) antibody tests have traditionally been recommended for confirming positive ELISA tests. However, one study found that these tests were no more sensitive or specific than in-clinic screening with ELISA test kits. None of the available antibody tests (i.e., ELISA, Western Blot, or IFA) can distinguish between FIV vaccination-induced antibody and that which arises through natural infection. • Polymerase Chain Reaction (PCR) Assay: One commercial veterinary laboratory (IDEXX Laboratories, Westbrook, ME) offers a PCR test for FIV. It should only be used as a confirmatory test in cats that test antibody positive. It is reported to have 100% sensitivity and 80% specificity.
Secondary Diagnostics • Complete Blood Count (CBC): Hematologic abnormalities are nonspecific but common. Leukopenia, neutropenia, and lymphopenia are common in the acute stage and will reappear in the terminal stage, along with a nonregenerative anemia. Occasionally, neutrophilia or thrombocytopenia is reported. • Biochemical Profile: Hypergammaglobulinemia is common. Azotemia may be seen although the role of FIV in causing renal disease is not yet clear.
Diagnostic Notes • Test in Development: A discriminant ELISA test has shown great promise for distinguishing vaccination from true infection. This test is not commercially available in the United States at present. It is available in Japan. • Vaccine-induced antibodies have been shown to persist for more than 2 to 3 years in some cats. • The relative difficulty of recovering virus from blood cells and body fluids varies with the stage of infection. Assays for viral antigen have been unreliable for diagnosis of FIV because infection does not result in sufficient circulating antigen for reliable detection by most antigen testing methods. • Most cats become seropositive within 60 days of infection, though a rare case will require 6 months or more. If an antibody test is negative but recent infection is possible, testing should be repeated 60 days after the last possible exposure. Seroconversion may not occur in rapidly progressive infection. Cats in the terminal stage of infection may have undetectable antibody levels. • Although transmissible from queen to kitten, FIV infection in kittens is uncommon. The majority of kittens tested at any age will be negative and can be declared free of the disease.
179
SECTION 1: Diseases and Conditions
• Negative test results in an asymptomatic kitten or cat with low risk of exposure are highly reliable due to the high sensitivity of screening tests and low prevalence of infection in most populations of cats. Because there is always a slight chance that the cat was infected yet had not seroconverted at the time of initial testing, the test could be repeated in 8 to 12 weeks. If the cat remains seronegative, infection is unlikely. • Antibody positive kittens have most likely received colostral antibody from an infected or vaccinated queen and may have a positive ELISA test result for several weeks to months. Because kittens do not often become infected from their mothers or from other cats, a positive ELISA test in a kitten should be interpreted with caution. Positive kittens should be retested after 6 months of age. Uninfected kittens with maternal antibody will revert to seronegative status. Those that are still positive after 6 months are likely infected. It is prudent to isolate these seropositive kittens from other cats until they become test negative. Alternatively, antibody positive kittens can be tested with a PCR test. With the currently available test result, a positive is confirmation of infection and a negative test result is an 80% likelihood of non-infection. • Cats that receive transfused blood from an FIV-vaccinated cat will likely test antibody positive for several weeks to months. • FIV-infected cats often have a profound leukopenia when griseofulvin is administered. Cats with possible prior FIV exposure should be tested for FIV prior to receiving this drug. • Opportunistic infections are associated with the later stages of FIV infection and should be anticipated. Problems that may develop include viral and bacterial respiratory infection, toxoplasmosis, mycobacteriosis, and hemoplasmosis.
Treatment Primary Therapeutics • Supportive: Treatment of FIV is supportive and is directed toward management of related complications. No specific antiviral therapy for FIV is available at present. It is recommended that FIV-positive cats be examined by a veterinarian every 4 to 6 months to facilitate early intervention when problems arise. Special attention should be given to periodontal disease. • Superoxide Dismutase: Peer-reviewed data has shown that a proprietary form of this product (Oxstrin™, Nutramax Laboratories, Edgewood MD) has been shown to cause immune stimulation that is likely to be of value to FIV-infected cats.
Secondary Therapeutics • Stress Avoidance: To prolong the life of FIV-infected cats, stressful situations should be avoided, a good quality diet fed, and appropriate bactericidal antibiotics administered when necessary. Cats with possible parasite exposure should undergo a fecal examination at 6- to 12-month intervals.
180
• Isolation: FIV-infected cats should be isolated from other cats to avoid transmission of the virus and to avoid exposure to secondary pathogens. Clients should be counseled to keep FIV-positive cats indoors. Alternatively, exposed cats should be vaccinated with FIV vaccine. • Neutering: FIV-infected cats should be neutered to reduce the stress of estrus, pregnancy, and lactation and spread of virus to kittens for queens and to reduce fighting and spread of virus by male cats.
Prevention • An inactivated, whole-cell dual subtype vaccine has been introduced. It contains subtype A (Petaluma) and subtype D (Shizuoka) FIV strains. There is good evidence that it offers cross-protection against subtype B, the most common subtype in the United States. The vaccine is licensed for kittens 8 weeks of age or older. The initial vaccination series consists of three injections given at 2- to 3-week intervals. An annual booster is recommended. Cats receiving the vaccine should be microchipped to facilitate their return should they become lost. This can also prevent euthanasia of such cats should they enter a shelter where they would likely be destroyed because of their FIV test (antibody) positive status.
Prognosis The prognosis is variable and dependent upon clinical stage at diagnosis. Up to 50% of cats will remain asymptomatic for 4 to 6 years following infection and approximately 20% will die during this time.
Suggested Reading Addie DD, Dennis JM, Toth S, et al. 2000. Long-term impact on a closed household of pets cats of natural infection with feline coronavirus, feline leukaemia virus and feline immunodeficiency virus. Vet Rec. 146(15):419–424. Levy J, Crawford PC, Kusuhara H, et al. 2008. Differentiation of feline immunodeficiency virus vaccination, infection, or vaccination and infection in cats. J Vet Intern Med. 22(2):333–334. Levy J, Crawdord C, Hartmann K, et al. 2008. 2008 American Association of Feline Practitioners feline retrovirus management guidelines. J Fel Med Surg. 10(3):300–316. Levy JK, Crawford PC, Slater MR. 2004. Effect of vaccination against feline immunodeficiency virus on results of serologic testing in cats. J Am Vet Med Assoc. 225(10)1554–1557. MacDonald K, Levy JK, Tucker SJ, et al. 2004. Effects of passive transfer of immunity on results of diagnostic tests for antibodies against feline immunodeficiency virus in kittens born to vaccinated queens. J Am Vet Med Assoc. 225(10):1554–1557. Pu R, Coleman J, Coisman J, et al. 2005. Dual-subtype FIV vaccine (FelO-Vax® FIV) protection against a heterologous subtype B FIV isolate. J Fel Med Surg. 7(1):65–70.
CHAPTER 76
Feline Infectious Peritonitis Gary D. Norsworthy
Overview Feline infectious peritonitis (FIP) is one of the more common fatal diseases of young cats obtained from shelters and catteries. It is caused by the FIP virus (FIPV), which is the virulent form (biotype) of feline coronavirus (FCoV). The nonvirulent biotype of FCoV is the feline enteric coronavirus (FECV), which is found commonly in healthy cat populations worldwide. See Chapter 73. Although the FIPV can be inoculated into naïve cats using infected tissue extracts or fluids, it is infrequently transmitted horizontally. It is strongly cell and tissue bound so transmission via urine and feces occurs only when a lesion is adjacent to renal collecting ducts or the intestinal wall. The FIPV occurs as two serotypes, type I and type II; type I strains are more likely to cause FIP. The FECV mutates to become the FIPV, and it appears that this mutation primarily involves loss of the 3c gene, which results in a change in cell tropism from apical bowel epithelium to macrophages; however, new information suggests that the 3c gene may not solely be involved in the mutation. The FIPV binds to the surface of macrophages/monocytes then becomes internalized into the cell. The mutation is more likely to occur during the primary illness phase and in kittens because of rapid FECV replication in both and reduced resistance of kittens. Although considered primarily enterocyte bound, the FECV has a brief systemic phase during primary infection, an important event that affects testing. Initially, it was thought that immunity to FECV infection did not result in immunity to FIPV, but the degree of cross-protection that occurs is primarily related to the relatedness of the FECV and FIPV strains involved. If they are extremely close, there is significant protection, and if they are distant, there is no protection. Up to 20% of cats with FECV infections experience virus mutation. However, only a small number of these mutant viruses actually produce clinical disease due to a strong and rapid cellular response. Cats that develop FIP have FIPV that is allowed to replicate at will within macrophages leading to dissemination to cells throughout the body. Effusive FIP is characterized by formation of pyogranulomas around small venules in the various target organs. Noneffusive FIP is characterized by granuloma formation. These inflammatory lesions begin at the organ surface and expand into the parenchyma of the organ. If strong cellular immunity occurs shortly after infection, virus replication is checked and disease does not occur. If humoral immunity occurs without concurrent development of cellular immunity, effusive FIP results. Noneffusive FIP results when strong humoral immunity occurs with weak cellular immunity. It may begin with a transient episode of effusive FIP, progress to typical granuloma formation, and then become effusive again terminally as the immune system collapses. FIP is found where the FECV is found, which is in virtually all shelters, in nearly all catteries with more than six cats, and in 60% or more of multicat households. FECV infection occurs by the fecal-oral route with viral shedding occurring within a week of exposure. Shedding may persist for 18 months or more, be persistent for 4 to 6 months followed by intermittent periods of shedding, or the virus may be cleared within 6 to 8 months. However, reinfection resembling primary exposure often occurs. Virus shedding is roughly proportional to coronavirus antibody
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
titers. Cats with titers of ≥1 : 100 are more likely to shed virus than those with titers ≤1 : 25. The typical FIP fatality is 3 to 16 months of age; FIP is uncommon in cats over 5 years of age. Losses generally occur as isolated events within a given location (cattery or shelter). They are usually sporadic, unpredictable, and infrequent. Every cattery with sporadic FIP is likely to have more deaths if enough kittens are bred over a long enough period of time. The longer kittens are held before adoption, the greater the risk. After about 3 years of FIP losses the disease tends to diminish due to population resistance. Although some breeds seem to be predisposed to FIP, the disease is more likely related to blood lines than to specific breeds. Rarely, FIP losses occur as an epizootic event with many deaths in succession; however, this pattern typically does not last more than 12 months. Epizootics are usually associated with population stresses such as overcrowding, kitten explosions, adverse genetic concentration, or the introduction of a new strain of FECV. There are two forms of FIP, effusive and non-effusive. They are commonly called wet and dry, respectively. Only rarely do both occur simultaneously, and then it is usually during a transition from one form to the other. The wet form is most common and is also called effusive or non-parenchymatous. It involves the visceral serosa and omentum or the pleural surfaces. See Figure 76-1. The dry form is also called non-effusive, granulomatous, or parenchymatous and involves abdominal organs (notably kidneys, liver, mesenteric lymph nodes, and bowel wall; see Figure 76-2) the central nervous system (CNS), and the eyes (see Figure 76-3). This form produces no inflammatory exudation into body cavities. The time from infection to disease of the effusive form is up to 2 weeks under experimental conditions and several weeks longer for the noneffusive form. Incubation time is unknown in natural infections, but there is evidence that subclinical disease may smolder for months or even years before the onset of overt disease as FIP may occur following a long history of vague illness or poor growth. Thus, the early signs of FIP include progressive lethargy, intermittent fever, poor appetite, and weight loss.
Figure 76-1 Effusive abdominal feline infectious peritonitis causes plaque formation on the viscera, adhesions between organs, and fluid accumulation.
181
SECTION 1: Diseases and Conditions
(A)
As the disease become more clinically evident, lethargy and fever may become consistent, and appetite suppression and weight loss may become more progressive. The effusive form manifests itself as either abdominal distension due to ascites or dyspnea due to pleural effusion. Ocular and CNS involvement occur in less than 10% of cats with effusive FIP. The most common ocular presentation is uveitis; many cats experience an iris color change. CNS signs include posterior paresis, incoordination, hyperesthesia, seizures and palsy of the brachial, trigeminal, facial, and sciatic nerves, convulsions, hydrocephalus, dementia, personality changes, nystagmus, head tilt, and circling. Intact males may develop scrotal enlargement due to peritonitis extension. Polyarthritis due to generalized synovitis occurs frequently. The noneffusive form produces CNS or ocular disease in about 60% of affected cats, and signs related to specific organ failure may predominate. Specific stresses of young cats are often correlated with on onset of FIP. These include pregnancy, parturition, spaying, neutering, and declawing. If these occur concurrently with FIPV challenge, they may be enough to tip the balance in favor of the virus at the host’s expense.
Diagnosis Primary Diagnostics
(B) Figure 76-2 Noneffusive feline infectious peritonitis (FIP) produces granulomas on various organs. This 7-month-old kitten has noneffusive FIP with granulomas on the (A) kidneys, spleen, colon, and (B) liver.
• Combination Testing: Because there is not a single, simple consistently diagnostic test, diagnosis is based on an accumulation of factors. The odds of noneffusive FIP are high with the following: • A young cat from a shelter or cattery. • The presence of uveitis or CNS signs. • Elevated serum proteins. • Increased serum globulins and decreased serum albumin resulting in an A-to-G ratio <0.6. • A fever that is not antibiotic responsive. • Leukopenia, especially if accompanied by leukocytosis. • A nonregenerative anemia. • The odds of effusive FIP are high with the following: • A young cat from a shelter or cattery. • The same laboratory findings as mentioned previously. • Yellow-tinged, mucinous, inflammatory ascites or pleural effusion; occasionally it will be green-tinged. Touching a drop on a slide with a needle and pulling away will usually produce a string of fluid. A stained slide will have a purple background color due to the high protein content. See Chapter 288. • Immunohistochemical examination of cells in the fluid will be positive for viral antigens and is confirmatory. • High levels of FIPV RNA will be detected with real time polymerase chain reaction (RT-PCR). • Histopathology: This is considered confirmatory when it reveals pyogranulomas (effusive FIP) or pyogranulomas (noneffusive FIP) in a cat with appropriate clinical, hematological, and serological findings.
Secondary Diagnostics
Figure 76-3 Uveitis is the most common ocular manifestation of noneffusive feline infectious peritonitis.
182
• Aqueous Humor: They presence of increases in proteins and leukocytes is consistent with non-effusive FIP. • Cerebrospinal fluid (CSF): This often shows increases in proteins (>200 mg/dL) and leukocytes (>100 cells/µL, consisting predominantly of neutrophils) when noneffusive FIP is present. • FCoV Antibody Tests (Titers): These can be helpful but not diagnostic because they are produced by both the FECV and FIPV. Although titers >1 : 1600 are usually found in cats with FIP and negative titers are consistent with an FIP rule out, overlap is so great between the two groups that this test offers little definitive diagnostic value in individual cats.
Feline Infectious Peritonitis
Diagnostic Notes • FCoV antibody titers may fall dramatically in the dying cat, especially with effusive disease. • The diagnosis of FIP should never be made on the basis of an FCoV antibody titer alone. • Antibody titers to the 7b protein are no more specific or sensitive than the direct immunofluorescent antibody (IFA) test. • Tests for FIPV RNA based on the lack of the 7b gene (supposedly to identify the FIPV) are not specific enough to be diagnostic. • Tests based on the levels of certain inflammatory proteins or by products (acute phase reactants, such as alpha-1-acid glycoprotein [AGP]) are not specific for FIP.
Treatment Primary Therapeutics • No treatment to date has proved consistently effective in curing FIP.
Secondary Therapeutics • Possible Treatment: A recent report using the investigational drug Polyprenyl Immunostimulant™ showed control for 2 years in two cats with non-effusive that were continuously treated. A third cat had initial response but died a few months after the owners discontinued therapy. There was no response in cats with effusive FIP. The two cats with long-term control cats were dosed at 3 mg/kg two to three times per week PO.
Therapeutic Notes • Claims of successful treatment are usually based on spontaneous remissions or misdiagnoses. • Discredited treatments include tylosin and prednisolone; prednisolone and phenylalanine mustard; prednisolone and cyclophosphamide; various immunosuppressive drugs; various immunostimulating drugs, including interferon; megadoses of vitamins; numerous nutraceuticals; and pentoxyfiline.
• Testing for FCoV in feces by PCR is not significant because of the near impossibility of maintaining an FECV-free facility with strict (and impractical) quarantine measures.
Prevention • An FIP vaccine with significant efficacy has not been developed. • Proper management can significantly reduce FIP incidence. The following must be avoided or minimized: • Overcrowding. • Longer shelter stays. • Other kittenhood diseases, including panleukopenia and viral respiratory disease. • Breeding cats, especially toms, which have produced FIP kittens. • A form of immunity develops over time. Closed populations will have a decrease in FIP over about 3 years. • Strict isolation of queens and their kittens, weaning of kittens at 4 to 6 weeks of age, and continued kitten isolation until 16 weeks of age can prevent FECV infection and thus FIP. However, needed elaborate quarantine measures include separate quarters (i.e., another building), separate litter, food, and water pans, separate air space, and change-in/change-out protective clothing; measures of this nature are usually not feasible. • The most cost effective way to reduce FIP losses are: • Eliminate overcrowding. Have no more than six breeding queens. • Have proportionally more cats 3 years of age or older. • Reduce fecal-oral transmission by managing litter boxes, litter replacement, and microscopic and gross spread of litter and litter dust. • Select breeding stock carefully. Cull toms and queens that have produced FIP kittens. • Produce a minimum number of kittens each year.
Prognosis The prognosis for FIP is grave. Euthanasia is the correct recommendation when the diagnosis is confirmed or reasonably confirmed.
Suggested Readings Cattery Control • FCoV antibody testing should not be employed because it does not answer the four important issues: (a) Is FIP present in any cat? (b) Is subclinical FIP present in any cat? (c) Will any given cat develop FIP in the future? and (d) Which cats are shedding FECV?
Legendre AM, Bartges JW. 2009. Effect of Polyprenyl Immunostimulant on the survival times of three cats with the dry form of feline infectious peritonitis. J Fel Med Surg. 11(8):624–626. Pedersen NC. 2009. A review of feline infectious peritonitis virus infection: 1963–2008. J Fel Med Surg. 11(4):225–258.
183
CHAPTER 77
Feline Leukemia Virus Diseases Fernanda Vieira Amorim da Costa and Gary D. Norsworthy
Overview The feline leukemia virus (FeLV) is a member of the oncornavirus subfamily of retroviruses. It contains a single-stranded RNA that is transcribed by the enzyme reverse transcriptase into DNA. This DNA is a provirus that is integrated into the cat’s cellular genome. The FeLV is divided into four subgroups: FeLV-A, FeLV-B, FeLV-C, and FeLV-T. Only FeLV-A is infectious and transmittable. FeLV-B, FeLV-C, and FeLV-T are not transmitted but can be generated de novo in an FeLV-A infected cat by mutation and recombination. FeLV-B is usually associated with malignancies, notably lymphoma and leukemia, and FeLV-C usually causes nonregenerative anemia. FeLV-T is highly cytolytic for T lymphocytes and causes severe immunosuppression. The worldwide prevalence is about 5% of free-roaming cats. This rate is reasonably constant regardless of geographic location. Overall, the prevalence in non-free-roaming cats has been declining due to purging of infected cats from closed populations and FeLV vaccination. Transmission is most efficient via saliva although transmission also may occur through blood, nasal secretions, feces, and milk. Currently, most cats are infected via social interaction such as sharing food and water dishes, mutual grooming, and common litter boxes. Transmission also occurs through biting, transplacentally, or via licking and nursing of kittens. A latent infection may be reactivated during pregnancy resulting in reproductive failure, fetal resorption, abortion, neonatal death, or birth of infected kittens. Under dry conditions the feline leukemia virus does not survive for more than a few hours outside the host, and its viral envelope is susceptible to disinfectants, soaps, heating, and drying. But FeLV retains infectivity for several days to weeks when it remains moist at room temperature. Iatrogenic transmission can occur via contaminated needles, surgical instruments, and blood transfusions. The outcome of FeLV infection depends on the age and immune status of the cat, virus concentration, virus pathogenicity, and infection pressure. See Figure 77-1. Susceptibility to FeLV infection is highest in young kittens, and as cats mature, they seem to acquire a progressive resistance. However, up to 50% of susceptible adults will become infected when challenged. After initial infection by the oronasal route virus replicates in local lymphoid tissue in the oropharyngeal area. In many immunocompetent cats, viral replication is stopped by an effective cell-mediated immune (CMI) response, and virus is completely eliminated from the body; these are the regressor cats. In regressor cats, infection remains undetected by antigen tests because they have high levels of neutralizing antibodies and no viremia. If the immune response does not intervene adequately, FeLV infection occurs and p27 antigen is detected in free plasma antigen tests after first viremia, which is within 1 to 3 days. After first viremia virus spreads to target organs including thymus, lymph nodes, and spleen. Cats can show signs of fever and lymphadenopathy. If the cat develops an effective immune response, first viremia is terminated within weeks or months resulting in transient viremia. During this period, lasting 3 to 16 weeks, cats are shedding virus and are infectious to other susceptible cats.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
184
After approximately 3 weeks of viremia, bone marrow precursor cells are infected, and virus starts to circulate in the body within granulocytes and platelets. These cats cannot eliminate virus from the body anymore, and direct immunofluorescence assay (IFA) will detect intracellular antigen. Some cats can clear viremia after it occurs, but provirus DNA is already inserted in bone marrow stem cells; this type of infection is called latent. In these cases, there is a partial immune response, and as antibody concentration increases virus production decreases. No virus is actively produced, and cats with latent infection have negative results from tests that detect FeLV antigen (ELISA [enzymelinked immunosorbent assay] and IFA). Cats with latent infection can develop neoplasia or myelodysplasias, and the presence of provirus can be identified through bone marrow polymerase chain reaction (PCR) testing. Latent infections can be reactivated after immunosuppressive therapy, pregnancy, and lactation, and antigen tests will then detect viremia. As time passes, latent infections become more difficult to reactivate, even with high doses of glucocorticoids. At 3 years postviremia, only 8% of cats still harbor latent infections in bone marrow. If the cat fails to clear viremia after the bone marrow is infected, both ELISA antigen and direct IFA tests will have positive results. This usually occurs after 16 weeks of persistent viremia, and these cats will remain persistently viremic and infectious to other cats for life. Persistently viremic cats develop FeLV-associated diseases, and most of them die within 3 years.
Diagnosis Primary Diagnostics • Clinical Signs: These vary widely but often include dyspnea, lethargy, anorexia, weight loss, fever, gingivitis/stomatitis, and nonhealing abscesses. • Physical Examination: Findings often include evidence of pleural effusion, pale mucous membranes, intraocular and dermatological abnormalities, palpable intra-abdominal masses, and organomegaly (i.e., lymph nodes, spleen, liver, kidneys). See images in Chapter 130. • Complete Blood Count (CBC) and Chemistry Profile: Common findings include nonregenerative anemia, leukopenia, thrombocytopenia, azotemia, increased liver enzymes, and increased serum bilirubin. Some FeLV-infected cats have nucleated red blood cells (RBCs) on a blood smear, but this does not represent a regenerative anemia. Instead, these nucleated RBCs represent a nonspecific bone marrow disturbance, erythremic myelosis, or erythroleukemia. A reticulocyte count is required to identify a regenerative response in anemic cats. • FeLV Antigen Tests (ELISA and IFA): The tests vary in incidence of positivity depending on the stage of the infection, the form of the disease, and the specific organs involved. ELISA identifies free FeLV antigen in plasma, and direct IFA detects intracellular antigen within granulocytes and platelets indicating bone marrow involvement.
Secondary Diagnostics • Bone Marrow Aspirate: It may reveal marrow dysplasia even when the peripheral blood smear is normal. A marrow aspirate is an excellent tissue source for FeLV testing, especially using the PCR and IFA tests, because the virus may be sequestered in the bone marrow of some cats that test antigen negative on blood tests.
Feline Leukemia Virus Diseases
Outcomes of FeLV Infections Salivary or Blood Transmission Spread Systemically
Up to 3 wks
Virus Eliminated
Viremia
Regressor
ELISA Positive IFA Negative AB Neg. to Low
ELISA Negative IFA Negative AB High
Viremia not Terminated
Viremia Terminated Transient Viremia
Virus Elimination
Viremia 3–16 wks
Viremia not Terminated Long Term
ELISA Negative IFA Negative AB High
ELISA Positive IFA Positive AB Neg. to Low Viremia Terminated Transient Viremia
Persistent Viremia ELISA Positive IFA Positive AB Neg. to Low
Latent Infection ELISA Negative IFA Negative AB High
Figure 77-1 Possible outcomes of feline leukemia virus infection. Courtesy of and adapted from Prof. Katrin Hartmann and Virbac.
• Pleural Fluid Analysis: In mediastinal lymphomas, this often reveals lymphoblasts in a fluid with high protein content and high total cell count. See Chapters 171 and 288. • Aspiration Cytology: It often reveals lymphoblasts in enlarged organs and unidentified abdominal masses.
Diagnostic Notes • Because the FeLV causes such a wide variety of diseases, any seriously ill cat should be tested for it, even if the cat has tested negative in the past. • The serum ELISA antigen test should be part of feline health panels; a positive test means that the virus is present. However, its presence does not necessarily mean that the infection will be persistent or that it is the cause of the cat’s current illness.
inations should include CBC, biochemistry profile, urinalysis, urine culture, and fecal examination. Cats should be included in a program to control gastrointestinal parasites, ectoparasites, and heartworms. They should be neutered and vaccinated to prevent serious infectious diseases using inactivated vaccines, although production and duration of immunity is not well described under these circumstances. • Chemotherapy: Various drugs are used for treating cats with lymphoma. Commonly used drugs and protocols are found in Chapter 34. • Blood Transfusion: Because many FeLV-related diseases are accompanied by nonregenerative anemia, transfusion of whole blood may be necessary to stabilize the cat for diagnostics or as an adjuvant to other forms of therapy. In addition, passive antibody transfer reduces the level of FeLV antigenemia in some cats. A well-vaccinated blood donor can provide this adjunctive therapy. See Chapter 295.
Secondary Therapeutics Treatment Primary Therapeutics • Isolation: Infected cats should be confined indoors and separated from FeLV negative cats. Good nutrition and husbandry are essential to maintain good health. Raw meat, eggs, and unpasteurized milk should be avoided. Wellness visits should occur semiannually to detect gum and dental diseases, weight loss, lymphadenopathy, eye and skin lesions, and bone marrow disease. Routine laboratory exam-
• Feline Interferon Omega: Give 106 units/kg q24h SC on 5 consecutive days. This protocol appears to have resulted in less clinical illness and a lower mortality rate, but no immunologic parameters were measured to support an anti-FeLV effect rather than an inhibitory effect on secondary infections. • Zidovudine: Give 5 mg/kg q12h PO or SC. Routine CBCs are necessary because nonregenerative anemia is a common side effect, especially if bone marrow suppression is already present. • Immune-Modulating Agents: Several drugs claim to prevent or treat immunosuppression.
185
SECTION 1: Diseases and Conditions
• Acemannan: 2 mg/kg IP q7d for 6 weeks. • Propionibacterium acnes (ImmunoRegulin®, ImmunoVet): 0.25 to 0.50 ml IV twice weekly then q14d for 16 weeks. • Staphylococcus protein A (SPA®, Sigma): For kittens: 7.3 µg/kg IP twice weekly for 8 weeks. • PIND-ORF (Baypamun DC®, Bayer): 1 mL SC twice in first week then once weekly for 6 weeks. • Lymphocyte T-Cell Immunomodulator (Imulan®, ProLabs): 1 ml (1 µg) q7d for 4 weeks then q14d for 2 treatments then q4 to 6w or as necessary. • Feline Oxstrin Optimized (Nutramax Laboratories, Edgewood, MD): 1 capsule q24h PO. The manufacturer claims that it supports a cat’s antioxidant and nutritional systems and provides bioactive superoxide dismutase that is protected from gastric breakdown. These effects have been documented in cats with FIV infections. • Prednisolone: This drug alleviates stomatitis in many cats and can produce appetite stimulation and short-term reduction in the size of lymphomatous masses. However, immunosuppressive doses may be detrimental.
Therapeutic Notes • Successful treatment of FeLV-induced lymphoma and nonregenerative anemia results in remission, but cure is unlikely. The FeLV remains viable within the cat so future relapse is common, and contagion is present.
186
• Lymphoma appears to also be a spontaneous disease in many cats. Because the FeLV is not involved, concerns about treatment outcome need not include FeLV contagion and FeLV-induced relapse. See Chapter 130.
Prognosis Cats that are infected with the FeLV but show no clinical signs may remain asymptomatic for several months to years. They may be healthy, but they are contagious to other cats. Cats with any FeLVrelated disease have a guarded prognosis. Those with proliferative diseases have an average survival of 6 months when aggressive chemotherapy is used, although some survive much longer.
Suggested Readings Hartmann K. 2006. Feline leukemia virus infection. In CE Greene, ed., Infectious Diseases of the Dog and the Cat, 3rd ed., pp. 105–131. St. Louis: Saunders Elsevier. Levy JK, Crawford RC. 2005. Feline leukemia virus. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 653–659. St. Louis: Elsevier Saunders. Lutz H, Addie D, Belák S, et al. 2009. Feline leukaemia: ABCD guidelines on prevention and management. J Fel Med Surg. 11(7):565–574.
CHAPTER 78
Fever Mitchell A. Crystal and Paula B. Levine
Overview Fever is an elevation of body temperature in response to a disease process, drug, or toxin. Fever (or pyrexia) should be differentiated from hyperthermia because causes and therapies differ. Fever describes an elevation in body temperature due to endogenous heat formation secondary to an elevation of the hypothalamic thermoregulatory set point. Hyperthermia describes an elevation in body temperature with the thermoregulatory set point at its normal setting, such as occurs with an external heat source, excessive activity, or increases in metabolic rate (e.g., hyperthyroidism). Fever results from disease processes, drugs, or toxins that either directly or indirectly (via release of pyrogenic substances, which cause cytokine production from leukocytes) elevate the thermoregulatory set point. Fever may play a positive role in how the body manages infectious diseases by potentiating phagocytosis, interferon release, and lymphocyte transformation. Clinical signs of fever in the cat include lethargy, anorexia, and atypical behavior such as hiding or irritability. Other clinical signs of the underlying disease causing the fever may also be present. Disease processes that cause fever include infectious, inflammatory, neoplastic, and immune-mediated diseases. Common drugs that can cause fever in the cat include cephalosporins, griseofulvin, methimazole, penicillins, propylthiouracil, sulfa or trimethoprim/sulfa drugs, tetracyclines, and thiacetarsamide. Of these, tetracyclines are the most likely to cause fever. The term fever of unknown origin (FUO) is often used to describe cats that have been febrile for 1 to 2 weeks, have no obvious or detected cause of fever, and have no abnormalities on routine diagnostic evaluation. This syndrome is common in cats.
Diagnosis Primary Diagnostics • History: Question the owner about the cat’s environment (i.e., indoor or outdoor, exposure to other cats, exposure to fleas, ticks, or wildlife), travel history (to areas endemic for infectious diseases), and drug therapy. Review the vaccination history to confirm appropriate infectious disease protection and to determine if a vaccine reaction from a recent vaccine (within 1 to 2 weeks) could be the cause of the fever. • Physical Examination: Examine closely for wounds and abscesses, internal or external masses, lymphadenopathy, joint effusion, abdominal effusion, organomegaly, abnormal pulmonary auscultation, and pain. A complete ophthalmologic examination (anterior chamber and retina) will sometimes disclose evidence of infectious or neoplastic diseases. • Database (Complete Blood Count [CBC], Chemistry Profile, Urinalysis, Feline Leukemia Virus [FeLV], and Feline Immunodeficiency Virus [FIV] Tests): Abnormalities may suggest neoplastic, inflammatory or infectious diseases, or organ dysfunction. • Total T4: Thyroid testing is indicated in cats over 10 years of age to detect hyperthyroidism as a cause of hyperthermia.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Thoracic Radiography: Abnormalities may suggest neoplastic or infectious diseases. • Abdominal Radiographs or Ultrasound: Abnormalities may suggest neoplastic or infectious diseases.
Secondary Diagnostics • Serologic Testing: Testing for toxoplasmosis, rickettsial diseases, bartonellosis, systemic mycosis, and tularemia should be considered if other testing is non-diagnostic, if exposure (to other animals or insect vectors) is possible, if chorioretinitis or anterior uveitis is present, or if these diseases are endemic in the area. See Chapters 8, 17, 22, 38, 43, 92, and 97. • Blood and Urine Culture and Sensitivity: These may be helpful but are often non-diagnostic and expensive. • Bone Marrow Aspirate Cytology: This test is indicated when cytopenias accompany fever. FeLV polymerase chain reaction (PCR) and indirect fluorescent antibody (IFA) testing can be requested on unstained bone marrow and blood smears to evaluate for latent or sequestered FeLV infection.
Diagnostic Notes • Because the diagnostic quality of radiographs is dependent upon the amount of body fat, abdominal ultrasound is often more helpful than abdominal radiographs in cats with body condition scores of 3/9 or less. Abdominal palpation approaches the usefulness of abdominal radiography in these cases. • FeLV/FIV tests should be repeated 1 to 2 months following an initial positive or negative test in indoor/outdoor cats with FUO. See Chapters 75 and 77. • Temperatures taken via infrared tympanic membrane thermometers are inaccurate because they have poor correlation with temperatures taken via rectal thermometers.
Treatment Primary Therapeutics • Treat the Underlying Disorder: Finding and treating the underlying cause is the key to resolution of the fever. • Fluid Support: Cats with fever are often anorexic and dehydrated. Fluid support should be provided if needed to treat or prevent dehydration. See Chapter 302. • Antibiotics: Because bacterial infections are common causes of fever, a short course of therapy with a bactericidal, broad-spectrum antibiotic is indicated for cats with FUO.
Secondary Therapeutics • Nutritional Support: This may be needed if prolonged anorexia has occurred or is anticipated. See Chapters 253, 255, and 308. • Antipyretics: Use only when fever exceeds 41°C (106°F). Aspirin (10 mg/kg q48h PO), ketoprofen (1 mg/kg q24h PO for up to 5 days), meloxicam (0.2 mg/kg once PO, followed by 0.1 mg/kg q24h PO for
187
SECTION 1: Diseases and Conditions
up to 4 days, then 0.025 mg/kg q48h PO) or dipyrone (25 mg/kg q12–24h IM, SC, or IV) may be given as needed to control high fevers.
Prognosis The prognosis is variable depending on the underlying disorder. With appropriate support, most cats with FUO recover uneventfully.
Therapeutic Notes • Antipyretics will interfere with both the ability to follow the course of the disease, as well as the effectiveness of and response to therapy. Fevers below 41°C (106°F) will not lead to brain or organ damage or dysfunction and may be beneficial (see Overview). • Nonsteroidal anti-inflammatory drugs have prolonged elimination times in cats and should be used with caution to prevent toxicity, especially renal. They are contraindicated with preexisting dehydration. • Emphasize to the owner the importance of not administering acetaminophen.
188
Suggested Readings Lappin MR. 2000. Fever in cats. In Proceedings of the Eighteenth Annual Veterinary Medical Forum, pp. 18–22. Seattle, WA. Miller JB. Hyperthermia and Fever of Unknown Origin. 2005. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 9–13. St. Louis: Elsevier Saunders. Vianna M, Bucheler J. 2007. Fever. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult. Canine and Feline, 4th ed., pp. 502–503. Ames, IA: Blackwell Publishing.
CHAPTER 79
Flea Allergy Dermatitis Christine A. Rees
Overview Flea allergy dermatitis (FAD) or flea hypersensitivity is the most common allergy in cats. The exact pathogenesis is not known, but it is thought to be an immediate (Type 1) or delayed (Type 4) hypersensitivity reaction from the saliva from the flea bite. The allergic symptoms of this allergy can be intermittent or continual depending on the cat’s exposure to fleas. Differential diagnoses include ectoparasites (other than fleas), fungal skin infection, bacterial skin infection, food allergy, and atopy.
Diagnosis Primary Diagnostics • Clinical Signs: Clinical signs for FAD include -recurrent pruritus, miliary dermatitis, eosinophilic plaque and other forms of the eosinophilic granuloma complex (see Chapter 66), excoriations, alopecia, crusting, excessive grooming, and waxing and waning dermatitis. Fleas or flea dirt may be present. The skin lesions for feline FAD are most commonly located on the neck, head, dorsal lumbar area, caudomedial thighs, and ventral abdomen. Some cats will have an unusual presentation consisting of oral eosinophilic granuloma lesions associated with their FAD. See Figures 79-1 and 79-2 and Figures 66-2 and 66-3C.
• Dermatologic History: The dermatologic history, clinical signs, and response to flea control or steroids are important in initially making the diagnosis of flea allergy dermatitis. Because cats groom themselves often, fleas or flea dirt may not always be present on presentation.
Secondary Diagnostics • Testing: In addition to the previously mentioned exclusions, positive intradermal allergy or serologic test results are confirmatory. Because some cats can have a delayed reaction to fleas, the intradermal allergy flea allergy test should be read again at 24 hours.
Diagnostic Notes • Other differential diagnoses need to be ruled out. See Chapters 16, 48, 82, 131, and 201.
Treatment Primary Therapeutics • Eliminate Flea Exposure: Primary therapy must be directed toward eliminating any possible flea exposure. Even an occasional flea bite has the ability to induce clinical symptoms, which may persist for days and possibly even weeks. All in-contact animals that could serve as food sources for fleas must receive strict flea control. Flea allergic
Figure 79-1 The typical “flea allergy pattern” is alopecia and inflammation on the tailhead, as shown on this cat. The lesions are not as obvious on cats with a dark haircoat that have not experienced significant alopecia. Image courtesy Dr. Gary D. Norsworthy. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 79-2 A flea allergy can also affect other parts of the body. This cat had extreme pruritus and self-mutilation of the head and neck. Image courtesy Dr. Gary D. Norsworthy.
189
SECTION 1: Diseases and Conditions
cats should be treated with flea products that contain active ingredients for the immature as well as the mature stages of the flea life cycle. Wild animals (especially possums) and stray animals can also serve as a source for fleas. Crawl spaces where wild or stray animals can live outdoors should be treated and the area closed off. Rigorous flea control measures should be continued on a regular (or yearround) basis. Patients kept in controlled indoor environments are typically easier to manage. See Chapter 80.
Secondary Therapeutics • Anti-pruritics: The only antipruritic medications that consistently work to treat flea allergy dermatitis are corticosteroids. Cats with FAD do not respond to antihistamine therapy. Oral or injectable
190
steroids will work to control pruritus in a FAD cat. The oral steroids that are most consistently used are prednisolone or methylprednisolone. Prednisone does not appear to work well in some cats.
Suggested Readings Bevier DE. 2004. Flea allergy dermatitis, In KL Campbell, ed., Small Animal Dermatology Secrets., pp. 208–213. Philadelphia: Hanley and Belfus. Carlotti DN, Jacobs DE. 2000. Therapy, control and prevention of flea allergy dermatitis in dogs and cats. Vet Derm. 11:83–98. Scott DW, Miller WH, Griffin CE. Flea allergic dermatitis. 2001. In DW Scott, WH Miller, CE Griffin, eds., Small Animal Dermatology, 6th ed., pp. 632–635. Philadelphia: WB Saunders.
CHAPTER 80
Fleas Sharon Fooshee Grace
Overview The cat flea, Ctenocephalides felis felis, is the most common ectoparasite of cats. This blood-sucking parasite spends its entire adult life on the unwilling host, though the majority of the life cycle is completed off the host. After the female flea lays her eggs on the cat, the eggs drop off and hatch into larvae within a few days. The larvae pupate by spinning a cocoon and may remain in this stage for up to 140 days. Emergence occurs when ideal environmental conditions develop. In warm, humid parts of the country, the life cycle may be completed every 2 to 4 weeks. When all the life stages of the flea are considered as a single population, the egg comprises 50% of the total, leaving the larvae at 35%, the pupae at 10%, and the adult flea at only 5%. As such, effective flea control programs usually focus on control of juvenile (pre-emergent) fleas, instead of on the relatively small population of adults.
Diagnosis Primary Diagnostics • Presence of Fleas: In most cases, flea infestation is readily diagnosed by the presence of fleas crawling through the cat’s haircoat. Occasionally, owners may first notice the problem when entering the home after the cat has been removed for some time; fleas seeking a food source will bite the cat and, perhaps, humans. • Flea Dirt: The presence of flea feces (flea dirt) also indicates flea infestation. This may be demonstrated to the owner by combing the dark material out of the pet’s haircoat onto a moistened white paper towel. The red stain of resuspended digested blood can be easily visualized. If the cat is bathed, the water will often have a reddish appearance due to flea dirt contacting water.
Secondary Diagnostics • Complete Blood Count: Heavily parasitized cats (especially kittens) may develop anemia due to blood loss. Flea infestation may also result in peripheral eosinophilia.
Treatment Primary Therapeutics • Insect growth regulators (IGRs): Lufenuron (Program®) inhibits development of immature flea stages only; it is available as a monthly oral or injectable product. Pyriproxifen (Nylar®) is a traditional juvenoid IGR that has extraordinary stability and high efficacy. Pyriproxifen is available as a spray, flea collar, and room fogger. Selamectin (Revolution®) is a monthly topical adulticide which also contains an IGR. • Insecticides: Imidaclopramide (Advantage® and Advantage Multi®), fipronil (Frontline® and Frontline Plus®), and selamectin have made flea control easier and more effective. Imidaclopramide and fipronil target the adult flea population, while selamectin has coverage against adult fleas and development of eggs. Nitenpyram (Capstar®) is a systemic, orally administered adulticide which has an onset of action of 30 minutes or less but a duration of about 24 hours. It has a wide safety margin. Botanical insecticides include pyrethrins and pyrethroids; these have no activity against juvenile stages of the flea. Some botanicals (permethrins) are associated with toxicity (including death) in cats. Cats are also quite sensitive to organophosphate insecticides; these should be used with extreme caution. Chlorpyrifos is particularly toxic and is commonly found in over-the-counter adulticide treatments. See Chapters 155 and 184.
Secondary Therapeutics • Environmental Flea Control: If topical and oral medications do not eliminate the flea population, indoor and outdoor flea control should be implemented; the use of a professional exterminator is recommended. In both settings, a combination of IGRs and adulticides is most effective. Feral cats, neighbor ’s cats, and wildlife can be sources of continued infestation of lawns.
Therapeutic Notes Diagnostic Notes • Flea allergy dermatitis (FAD) and tapeworms are other problems associated with flea infestation. See Chapters 79 and 207. • Skin Lesions: Papulocrusting lesions of miliary dermatitis are often found on the tailhead and around the neck of flea-allergic cats. See Chapter 140.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Ultrasonic flea collars have not been proven to be of value in flea control. • Flea collars, combs, shampoos, sprays, and dips have nominal value as the sole agents in a flea control program because they primarily kill adult fleas (5% of the population). Clients should be counseled as to a reasonable expectation of success if these are the only products used in their flea control program. • Risk of insecticide exposure to the cat (especially cumulative exposure) may occur when the premises are treated. • Because of the flea’s role in the life cycle of Dipylidium caninum, many flea-infested cats will need to be treated for tapeworms. • The role of the flea in transmission of Bartonella spp. to cats and humans is of increasing public health concern, especially when immunocompromised humans may be living in a flea-infested
191
SECTION 1: Diseases and Conditions
environment. Bartonellosis may be a life-threatening disease in such a setting. See Chapter 17.
Prognosis Successful flea control can be achieved safely with careful attention to the products used. Extensive client education is the key to a successful outcome.
192
Suggested Readings Demanuelle TC. 2000. Modern flea eradication: The best of the old and the new. Vet Med. 95(9):701–704. Medleau L, Hnilica KA, Lower K, et al. 2002. Effect of topical application of fipronil in cats with flea allergic dermatitis. J Am Vet Med Assoc. 221(2):254–257.
CHAPTER 81
Flukes: Liver, Biliary, and Pancreatic Gary D. Norsworthy
Overview The cat may be infected with several species of flukes, including Amphimerus pseudofelineus, Opisthorcus tenuicollis, Metorchus conjunctus, and Platynosomum concinnum. The latter, P. concinnum is the most common, with 15 to 85% of outdoor cats in an endemic area being affected. Infections are limited to cats living in semitropical climates (including Hawaii and south Florida in North America) and exposed to two intermediate hosts. P. concinnum is about 2.0 to 3.5 mm and lives in the bile ducts and gall bladder; it is occasionally found in the small intestine and pancreas. The first intermediate host is the land snail. The second intermediate host is most commonly a lizard (thus the term lizard poisoning), but it may be the Bufo toad, skink, or gecko. Adult flukes develop about 1 week after ingestion of the second intermediate host, and ova can be detected in the cat’s feces about 2 to 3 months later. Many infected cats are asymptomatic, and others have nonspecific signs including vomiting, diarrhea, inappetence, and weight loss. Icterus and peripheral eosinophilia are often present. The latter begins three weeks after infection and persists for months. Because these signs are common in many other diseases, the detection of fluke ova does not necessarily mean that flukes are the causative agent.
Figure 81-1 Ova (arrows) of Platynosomum concinnum are seen at 100× and 1000× in a fine-needle biopsy of the liver. This cat was presented icteric. It lived in Texas but had previously lived in south Florida.
Diagnosis Primary Diagnostics • History and Clinical Signs: Icteric cats with eosinophilia and elevated liver enzymes living in appropriate geographic locations should be suspected of flukes; however, there are many causes of icterus. See Chapter 117. Hepatomegaly is common. • Fecal Examination: This is a specific, but not extremely sensitive, test because egg production is limited in number. See Figure 81-1. Ova may occasionally be found on fecal floatation, but the most sensitive methods are formalin-ether sedimentation and sodium acetate. See Chapter 311. Serial testing will increase the diagnostic yield. • Chemistry Profile and Urinalysis: Liver enzymes, especially alanine aminotransferase (ALT) and aspartate transaminase (AST), and bilirubin are elevated, and bilirubin is often found in urine. • Ultrasound: The findings include one or more of the following: (a) dilated gall bladder, bile duct, and hepatic ducts, (i.e. biliary obstruction); (b) gall bladder sediment with flukes that appear as oval hypoechoic structures with an echoic center; (c) mildly thickened gall bladder wall with double-layered appearance; and (d) overall hypoechoic parenchyma with increased prominence of hyperechoic portal areas.
Secondary Diagnostics • Laparotomy: This is indicated when evidence of biliary obstruction is found. It permits liver biopsy and manual expression of the gall bladder to relieve biliary obstruction. If manual expression is not successful, the gall bladder should be explored and the bile duct
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
cannulated and flushed. Sometimes, flukes and ova can be seen in the bile, grossly or microscopically. See Figures 81-2 and 81-3. • Cholecystocentesis: This procedure may reveal fluke eggs. Ultrasound guidance or laparotomy is required. To prevent leakage of bile and bile peritonitis, a 22-gauge needle should be used with one needle stick, and the gall bladder should be emptied during the centesis process. Bacteriological culturing is also recommended. • Feline trypsin-like immunoreactivity (fTLI) and feline pancreatic lipase immunoreactivity (fPLI): Pancreatic flukes have been associated with pancreatitis. See Chapters 159 and 160.
Treatment Primary Therapeutics • Praziquantel: Administer at 20 mg/kg q24h SC for 3 to 5 days. Some authorities recommend retreatment in 12 weeks. Eggs may pass in the stool up to 2 months after treatment. • Supportive Care: Because some affected cats have profound anorexia, forced enteral feeding (with or without a surgically implanted tube) may be needed for several days to supply nutrition and to prevent hepatic lipidosis. See Chapters 253, 255, and 308. Dehydration should be corrected with a balanced electrolyte solution. • Broad-Spectrum Antibiotics: Ascending infections from the duodenum are common and produce cholangitis and cholangiohepatitis. Amoxicillin and metronidazole are indicated for the organisms usually involved. • Antioxidant Therapy: S-adenosylmethionine (Denosyl® or Denamarin®, Nutramax Laboratories, Edgewood, MD) should be dosed at 20 mg/kg PO q24h.
193
SECTION 1: Diseases and Conditions
Figure 81-2
The adult Platynosomum concinnum is about 5 mm long × 2 mm wide.
Secondary Therapeutics • Prednisolone: This drug is indicated if the histopathology reveals significant eosinophilic pericholangitis. Begin at 1.1 mg/kg q12h PO and taper after 1 week. Some cats require long-term treatment for chronic cholangiohepatitis. • Fenbendazole: This drug is thought to be less efficacious than praziquantel. It has been given at 50 mg/kg q12h PO for 5 days. • Ursodeoxycholic Acid: This drug is a choleretic agent that is dosed at 10 to 15 mg/kg q24h PO. It is contraindicated in extrahepatic biliary obstruction, often evidenced by pale-colored stools.
Therapeutic Notes • Pre-emptive treatment may be the best approach for outdoor cats in endemic area. Give praziquantel at 20 mg/kg q3m SC. • Drugs that appear to be nonefficacious include thiabendazole, levamisole, and mebendazole.
Prognosis The prognosis is good as long as appropriate supportive care is given and secondary infections have not produced biliary fibrosis or hepatic
194
Figure 81-3 long.
The adult Amphimerus pseudofelineus measures about 16 to 24 mm
cirrhosis. Limiting access to the intermediate hosts is important in preventing reinfection.
Suggested Readings Pembleton-Corbett JR. 2007. Liver fluke infestation. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Clinical Consult, 4th ed., p. 817. Ames, IA: Blackwell Publishing. Foley RH. 1994. Platynosomum concinnum infection in cats. Compend Contin Educ. 16:1271–1285.
CHAPTER 82
Food Reaction Christine A. Rees
Overview Food reactions or allergies are the second most common allergy in cats. This allergic reaction can occur at any age. Unlike atopic dermatitis, which is usually seasonal, food allergies are a nonseasonal pruritic problem. Cats are different from other species in that the pruritus can be subtle in cats. In many cats, the pruritus is manifested as excessive grooming. Food reactions or allergies do not typically respond to steroids. The types of skin lesions that can be seen include barbed alopecia, complete alopecia, erythema, miliary dermatitis, eosinophilic granuloma complex, excoriations, crusts and scale. See Figures 82-1A and 82-1B. Diarrhea, Malassezia dermatitis, and ceruminous otitis may also be seen in the food allergic cat. See Chapters 66, 131, 140, and 157.
Diagnosis Primary Diagnostics • Dermatologic History: History is extremely important. Diagnosis begins by exclusion of other pruritic diseases, such as other hypersensitivities, parasitic infections, dermatophytosis, neoplastic conditions, and immune-mediated conditions. • Clinical Appearance: The clinical signs for food allergy can be similar to atopy. These signs include recurrent otitis externa, pruritus, military dermatitis, eosinophilic plaque, and other forms of eosinophilic granuloma complex, excessive grooming, and nonseasonal skin problem. • Food Trial: A food elimination diet and food rechallenge is the only way to definitively diagnose food allergies in cats. Options for food elimination diets include hydrolyzed protein diets or a novel protein source diet (i.e., duck and green pea, rabbit and green pea, venison and green pea, and so on). The chosen diet should be fed for 8 to 12 weeks. At the end of the food elimination diet trial period the cat should be rechallenged to the old food to prove or disprove a food allergy. The clinical signs will reappear within 1 to 2 weeks after the cat is rechallenged to the offending food ingredient.
(A)
Secondary Diagnostics
(B)
• Secondary Infections: Secondary infections may be present and must be identified and treated to get a true picture of the underlying baseline allergic symptoms. Tape cytology to evaluate for presence of secondary bacterial or Malassezia spp. is indicated. Dermatophytosis must be ruled out by direct hair examination and dermatophyte test media (DTM®) culture. See Chapters 48 and 131.
Figure 82-1 This cat had a confirmed allergy to fish. The allergy was manifested as otitis externa, (A) facial dermatitis, and (B) perianal dermatitis. It was not responsive to corticosteroids. Photos courtesy of Dr. Vanessa Pimentel de Faria.
Treatment Diagnostic Notes • No skin testing or blood testing accurately diagnoses food allergies in cats.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Primary Therapeutics • Diet Manipulation: After the cat is rechallenged with the old diet the presence of a food allergy is proved. The options are to feed the test food long term or to individually rechallenge the cat to individual food ingredients to determine which food ingredient or ingredients are causing the allergic reaction. After the individual offending food ingredient or ingredients are known, cat food labels should be read carefully so a nonoffending diet is chosen.
195
SECTION 1: Diseases and Conditions
Secondary Therapeutics • Control Secondary Pruritus: Treat secondary causes of pruritus. Secondary infections of the skin or ears need to be treated. In addition, exposure to external parasites such as fleas can cause an increase in pruritus. Therefore, cats should be on year-round flea control. Corticosteroids may be effective in some cases of food allergies. Prednisolone given at anti-inflammatory doses (2.2–4.4 mg/kg q12h PO for 1 week then tapered) is the drug of choice because some cats have difficulty metabolizing prednisone to prednisolone. Genesis Spray® (0.15% triamcinolone) has been used as an extra-label adjunct in some cats. This medication appears to have relatively minimal systemic absorption and may be of benefit in some patients, but it is not completely without potential steroid side effects. Furthermore, the spray contains alcohol, which some cats find objectionable.
Therapeutic Notes • Antihistamines and fatty acid are not effective medications for controlling the pruritus associated with feline food allergies.
196
Prognosis The prognosis is good with avoidance of the offending allergic food ingredient or ingredients.
Suggested Readings Carlotti DN, Remy I, Prost C. 2008. Food allergy in dogs and cats: A review and report of 43 cases. Vet Derm. 1(2):55–62. Graham-Mize CA, Rosser EJ. 2004. Bioavailability and activity of prednisone and prednisolone in the feline patient. Vet Derm. 15(S1):10. Prost C. 1998. Diagnosis of feline allergic diseases: A study of 90 cats. In KW Kwochka, T Willemse, C von Tsharner, eds., Advances in Veterinary Dermatology, pp. 516–521. Boston: Butterworth Heinemann. Reedy LM, Miller WH, Willemse T. 1997. Food hypersensitivity. In LM Reedy, WH Miller, T WIllemse, eds., Allergic Skin Diseases of Dogs and Cats, 2nd ed., pp. 166–149. Philadelphia: WB Saunders.
CHAPTER 83
Giardiasis Mark Robson and Mitchell A. Crystal
Overview Giardia duodenalis (also known as Giardia intestinalis and Giardia lamblia) is a small intestinal and occasionally large intestinal protozoan parasite that causes acute or chronic diarrhea, occasionally malabsorption and, rarely, vomiting. Giardia exists in two forms: (a) the cyst form, which is shed in the feces, can survive for months in wet, cool conditions in the environment, and is infective to other animals and, (b) the trophozoite form that develops in the small intestine from ingested cysts and causes clinical signs. Giardia is acquired via ingestion of infected feces or contaminated food or water. There is no extra-intestinal migration, and transplacental and transmammary infections do not occur. Once ingested, Giardia cysts may be shed in the feces 5 to 16 days later, but clinical signs can occur in less than 5 days. The prevalence of Giardia in cats ranges from 1.4 to 11%, with higher rates seen in immunodeficient cats and in cats living in high housing density; a 31% prevalence rate was found in a recent study of cats at an international cat show. Most infected cats do not show clinical signs, but when they do occur they can include small intestinal diarrhea, occasionally large intestinal diarrhea, steatorrhea, borborygmus, and weight loss. Rarely, an infection is severe and causes dehydration, lethargy, vomiting, and anorexia. Identification of Giardia in a patient with diarrhea does not mean that the infection is causing the clinical signs. Often there is a primary underlying disease, and Giardia is an incidental finding. Physical examination may be normal or reveal evidence of diarrhea, dehydration, and weight loss. Giardia has been classified into assemblages (genotypes), currently A to G, which can be identified by polymerase chain reaction (PCR) analysis. Assemblage F has, to date, only been identified in cats and may be associated with fewer clinical signs due to host adaptation, although a recent study failed to link assemblage with presence or absence of clinical signs in a statistically significant way. Assemblage A (subdivided into clusters I–IV) is regarded as the most likely to have zoonotic potential as it can infect humans, cats, dogs, and many other species. In practical terms any feline Giardia infection should be considered of zoonotic importance, and appropriate handling of feces should be discussed with owners. Immunocompromised individuals should avoid contact with infected animals because it is potentially zoonotic.
Diagnosis Primary Diagnostics • Enzyme-Linked Immunosorbent Assay (ELISA): There is a variety of in-clinic or laboratory ELISA Giardia test kits available, and generally the sensitivity and specificity are quite high. For example the SNAP ® Giardia test kit (IDEXX Laboratories, Inc., Westbrook, ME) has been shown to be 90% sensitive and 99% specific for detection of Giardia on a single fecal sample when compared to direct immunofluorescence testing. The test detects soluble Giardia antigen in feces and can be performed on fresh samples or on samples stored for up to 7 days at refrigerator temperature (2 °–7 °C [36 °–45 °F]).
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 83-1 Trophozoites may be seen in direct fecal or duodenal juice smears as small (15 × 8 mm) face-like appearing organisms that demonstrate a concave ventral surface and sluggish, rolling leaf/tumbling motility.
The presence of soluble antigen is minimally cyclic, thus the high sensitivity on a single sample. • Zinc Sulfate Fecal Flotation: Cysts may be seen on microscopic examination. See Figure 83-1; the test is described in Chapter 311. It identifies about 77% (examination of one fecal sample) to 96% (examination of three fecal samples collected over 3–5 days) of infected cats. Nematode parasites (i.e., hookworms, roundworms, whipworms, and Physaloptera) will also be identified by this method. • Direct Saline Smear: Cysts or trophozoites are sometimes (about 25–40% of the time) seen on microscopic examination.
Secondary Diagnostics • Direct Immunofluorescent Fecal Testing: This is a highly sensitive and specific test performed at various diagnostic laboratories for detection of Giardia cysts in feces. Check with your laboratory regarding submission requirements. • Duodenal Aspiration: This procedure is performed via endoscopy or during exploratory laparotomy. Ten mL of saline are instilled into the duodenum via a polypropylene tube passed through the biopsy channel (at endoscopy) or via needle and syringe (at exploratory laparotomy). At least 3 mL of material is aspirated for ELISA Giardia testing or for immediate centrifugation and microscopic examination of the sample for motile trophozoites. • Histopathology: Organisms may be occasionally be visualized in biopsies of the intestinal mucosa.
Diagnostic Notes • Testing of cats without clinical signs is not logical because there are many healthy cats with Giardia. Possible exceptions are breeding catteries or households with immunodeficient pets or humans, especially when considering the introduction of a new kitten or cat.
197
SECTION 1: Diseases and Conditions
• When shipping to the laboratory for microscopic evaluation, fecal samples should be kept cool to increase trophozoite survival. • Giardia ELISA tests on feces and the zinc sulfate fecal flotation test are more accurate than duodenal aspiration, do not require general anesthesia, and are inexpensive to complete. Therefore, these are recommended prior to duodenal aspiration. • Trophozoites have a concave ventral surface, two nuclei that help give the characteristic “smiling face” and sluggish, rolling leaf/ tumbling motility. Tritrichomonas foetus is the only other pathogenic feline motile protozoan similar in size to Giardia. T. foetus lacks a concave surface, has one nucleus, has a distinct undulating membrane that runs the length of the organism and has rapid, vigorous, forward erratic motility. See Chapter 218. • Giardia cysts are ovoid and approximately 12 µm long and 7 µm wide. • Cats infected with Giardia should be screened for the feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV).
Treatment Primary Therapeutics • Fenbendazole (Panacur®): Administer 25 to 50 mg/kg q24h PO for 3 to 5 days (also effective for hookworms, roundworms, and Ollulanus).
and severity of diarrhea, prevention of weight loss, clearance of intestinal trophozoites, and reduced cyst shedding in kittens) and safe for use in cats. A recent report could not clearly identify therapeutic efficacy of the vaccine in cats already experimentally infected with Giardia. Killed trophozoite vaccines are in development and may prove more effective.
Prognosis The prognosis is good for resolution of clinical signs that are due to Giardia. However, cysts may persist in the environment and lead to reinfection. If this occurs strict attention to household hygiene using drying and quaternary ammonium compounds may be necessary. Cats that have access to the outdoors may become re-infected from sources that are impossible to control. Occasionally, infections are difficult to clear and may need prolonged therapy, sometimes with multiple drugs. Giardia infections associated with underlying immunosuppressive diseases (i.e., FeLV and FIV) may be more difficult to eliminate. Retesting of patients whose clinical signs have resolved is not logical unless there are immunocompromised pets or humans in the household. Treatment of cats that are positive for Giardia (in healthy households) but have no clinical signs can lead to unnecessary drug administration and owner concern.
Secondary Therapeutics • Metronidazole (Flagyl®): Administer 20 to 25 mg/kg q12h PO for 7 days. • Albendazole (Alben®, Valbazen®): Administer 25 mg/kg q12h PO for 5 days (also effective for hookworms and roundworms). Some do not recommend the use of this drug in cats due to possible idiosyncratic bone marrow suppression.
Therapeutic Notes • Infections may be self-limiting and thus may not require therapy. • Resistance is becoming a problem in human medicine and is probably occurring in cats and dogs. No treatment should be regarded as 100% effective. • A Giardia vaccine (GiardiaVax®, Fort Dodge Animal Health, Kansas) has been tested and proven to be effective (i.e., decreased frequency
198
Suggested Readings Barr SC. 2006. Enteric protozoal infections. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 736–750. St Louis: Saunders Elsevier. O’Conner TP, Groat R, Monn M, et al. 2004. Performance of the SNAP® Rapid Assay for Giardia in dogs and cats. Proceedings of the Annual Meeting of the American Association of Veterinary Parasitologists, pp. 80–81. Rishniw M. 2007. Giardia testing. Veterinary Information Network, www.vin.com, Medical FAQs. Tzannes S, Batchelor DJ, Graham PA, et al. 2008. Prevalence of Cryptosporidium, Giardia and Isospora species infections in pet cats with clinical signs of gastrointestinal disease. J Fel Med Surg. 10(1):1–8. Vasilopulos RJ, Rickard LG, Mackin AJ, et al. 2007. Genotypic analysis of Giardia duodenalis in domestic cats. J Vet Intern Med. 21(2):352–355.
CHAPTER 84
Gingivitis-Stomatitis-Pharyngitis Mark Robson and Mitchell A. Crystal
Overview Feline gingivitis-stomatitis-pharyngitis complex (GSPC), also known as lymphocytic-plasmacytic gingivitis-stomatitis-pharyngitis and plasma cell gingivitis-stomatitis-pharyngitis, is a common disease causing inflammation, ulceration, and proliferation of the soft tissues of the mouth. Cats 4 to 17 years of age are affected with a median age of about 7 years. Purebred cats may be overrepresented. The areas of the mouth most commonly affected are the glossopalatine mucosa (palatoglossitis) and buccal mucosa overlying the premolar and molar arches (buccostomatitis; see Figure 84-1). The gingiva, pharynx, hard palate, lips, and tongue are less commonly affected. The lesions are associated with a dense infiltration of lymphocytes and plasma cells into the oral mucosa and submucosa. The etiology of GSPC is unknown but is felt to be multifactorial with an immune-mediated component, possibly representing a hypersensitivity to bacterial plaque antigens or portions of the teeth. This stems from observations that control of oral plaque is important in the management of GSPC. A significant proportion of cases continue to have GSPC after full mouth extraction, indicating that other antigens must be involved in the pathogenesis. Feline calicivirus (FCV) may play a role in the severity of lesions and lack of response to treatment. However, a recent study found no direct correlation between FCV, feline herpesvirus-1 (FHV-1), feline leukemia virus (FeLV), feline immunodeficiency virus (FIV), and Bartonella in cats with chronic GSPC. Bacteroides spp. are commonly cultured from the oral cavity in association with this disease; however, it is unlikely that bacterial infection is the primary cause because antibiotic therapy does not eliminate the disease and immunomodulating therapy is often helpful in improving lesions.
Clinicians all over the world have found this syndrome to be difficult and expensive to manage, with a frustrating lack of consensus about which therapeutic option is most likely to succeed. Owners should be counseled about the difficulty of achieving easy resolution of the signs. Provision of plenty of information from the veterinary literature may help owners to understand the challenges. The fact that most cats resist medications and topical treatments, especially when the mouth is painful, further complicates therapy. Although there is no consensus among workers in the field as to which treatment is best for cats suffering from GSPC, recently there seems to be a move toward the recommendation of careful total extraction of all molar and premolar teeth. Clinical signs of GSPC vary depending on the severity of the lesions. Rarely, cats may demonstrate no clinical signs, and the disease is noted incidentally at the time of physical examination. Clinical abnormalities may include ptyalism, halitosis, pain to extreme pain on opening of the mouth, difficulty prehending food, change in food preference from a dry to a soft diet, anorexia, and weight loss. Physical examination reveals the lesions of GSPC and may show mandibular lymphadenopathy. Differential diagnoses for GSPC include periodontal disease, retroviral infection, calicivirus infection, eosinophilic-granuloma complex, neoplasia, and systemic diseases such as renal failure and disorders leading to protein-calorie malnutrition or a predisposition to infection (e.g., diabetes mellitus). A variant of this disease is Juvenile GSPC. It occurs in young adults and may begin during teething (about 4–6 months of age). The inflammation is generally limited to the buccal and lingual gingiva near the premolar and molar teeth. See Figure 84-2. Maine Coon cats appear to be at risk suggesting a genetic component. It usually responds to antiinflammatory treatment and may resolve completely after a few months.
Diagnosis Primary Diagnostics
Figure 84-1 Severe inflammation is present in the buccal mucosa and the fauces. Ptyalism and pain when opening the mouth were present. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Clinical Examination: The characteristic lesions accompanied by a pain when opening the mouth and ptyalism are nearly diagnostic for GSPC. See Figure 84-1. The characteristic lesions of Juvenile GSPC (see Figure 84-2) are usually not accompanied by pain when opening the mouth and ptyalism. • Database (Complete Blood Count [CBC], Chemistry Profile, and Urinalysis): This is indicated to look for an underlying cause. Hyperproteinemia due to hyperglobulinemia is seen in about half of the cats with GSPC. The presence of azotemia with a low urine specific gravity suggests renal disease as a concurrent or causative condition. • Thorough Dental Examination and Dental Radiographs: Under anesthesia, the oral cavity should be evaluated for periodontal disease, resorptive lesions, and other causes of inflammation. Radiographs allow for identification of alveolar bone loss, tooth resorption, and retained roots. See Chapter 245. • Oral Tissue Biopsy or Histopathology: This reveals a dense infiltration of plasma cells and lymphocytes into the oral mucosa and submucosa, although some lesions appear to be predominantly plasmacytic. Some neutrophils and eosinophils may be present. Histopathology also serves to rule out neoplasia such as squamous cell carcinoma.
199
SECTION 1: Diseases and Conditions
• Corticosteroids: These are beneficial in 70 to 80% of the cases treated, at least temporarily. Begin prednisone or prednisolone at 1 to 2 mg/ kg q12h PO, then gradually taper its use over 4 to 6 months to the lowest effective dose. Indefinite therapy is often required. If oral therapy is difficult, methylprednisolone acetate may be used at 2 to 5 mg/kg IM, SC, or intralesionally every 2 weeks until a significant response is seen, then decreased to every 4 to 8 weeks as needed. Owners should be warned that injectable steroids carry an increased risk of causing corticosteroid-associated congestive heart failure and diabetes mellitus. Some owners will accept almost any level of risk to attempt to control GSPC because of the severe impact of the disease on the cat’s quality of life. • Analgesia: Oral or injectable buprenorphine (0.01–0.03 mg/kg q6– 12 h PO) or a fentanyl patch may be used. Topical treatments may have a better chance of being tolerated soon after a dose of buprenorphine is administered. • Dental Extractions: See below.
Secondary Therapeutics Figure 84-2 Juvenile gingivitis-stomatitis-pharyngitis complex is characterized by mild to moderate inflammation in the lingual and buccal gingiva adjacent to the premolar and molar teeth. Image courtesy Dr. Gary D. Norsworthy. • Retroviral Tests: Retroviral infections can lead to inflammatory oral disease. The proportion of cats with GSPC that test positive for the FIV varies in reports from 25 to 80%. Cats infected with FIV appear to have poorer response to medical therapy. • Calicivirus Testing: Virus isolation or polymerase chain reaction (PCR) testing will identify the presence of this virus. Affected tissue and the tonsils are swabbed with a moistened, sterile culturette (virus isolation) or dry rayon swab (PCR) and submitted. Contact your laboratory for specific sample handling instructions.
Secondary Diagnostics • Anaerobic Bacterial Culture: This is recommended in refractory cases of GSPC; a sample is taken from the gingival sulcus.
Diagnostic Notes • It is important to exclude systemic diseases as a cause or contributing factor in GSPC, though most cats will have idiopathic disease.
Treatment Primary Therapeutics • Dental Therapy: Any retained roots, diseased teeth, or teeth with resorptive lesions should be extracted. Cats with periodontal disease should have their teeth scaled and polished frequently. Ideally owners should brush the teeth regularly once the initial pain and inflammation has been managed, but this is not practical for most cats and owners. High fluoride toothpaste may be of benefit. A 0.12% chlorhexidine gluconate daily flush may slow the re-accumulation of plaque, if tolerated. Topical treatments have the best chance of being achievable and successful in a patient that has had a thorough dental procedure and medical treatment resulting in control of the acute inflammation and pain. • Antibiotics: Logical antibiotic choices include amoxicillin (22 mg/kg q12h PO), amoxicillin/clavulanic acid (22 mg/kg q12h PO), clindamycin (5–11 mg/kg q12h PO, 11–24 mg/kg q24h PO), and metronidazole (12.5 mg/kg q12h PO) for 4 to 6 weeks.
200
• Gold salts (chrysotherapy): This is beneficial in 75% of the patients treated. Aurothioglucose (Solganol®, 1 mg/kg IM) or gold sodium thiomalate (Aurolate®, 1–5 mg IM initial dose, 2–10 mg second dose, then 1 mg/kg thereafter) is administered once weekly for 16 to 20 weeks until a response is seen (typically within 8 weeks). The dose is then reduced to every 14 days for 2 months, then monthly for 8 months. Therapy should be discontinued at that time. Side effects of therapy are uncommon but include thrombocytopenia, pancytopenia, and renal failure. CBC, chemistry profile, and urinalysis should be performed monthly while the cat is on therapy. • Feline Recombinant Interferon Omega: It is given at 1 mega unit/kg SC q48h for five doses. This may be repeated in 30 days. This has been reported to help in refractory cases of GSPC where persistent FCV shedding is occurring. Success with intralesional injections has also been documented. This drug is not approved or manufactured in the United States. It must be imported through the Food and Drug Administration (FDA), and it is expensive. • Other Immunosuppressive Drugs: There are a number of drugs that can be used in combination with corticosteroids or if corticosteroids have proved unsuccessful. Some recommend azathioprine (0.3 mg/kg q48h PO until a response is seen, thereafter every 3 days). Note that many internists (including the writers) do not recommend azathioprine in cats due to an unacceptably high level of side effects. Chlorambucil (2 mg/m2 or 0.1–0.2 mg/kg q24h PO until a response is seen, then q48h PO) or cyclophosphamide (50 mg/m2 4 days on, followed by 3 days off PO) have been recommended in this setting. Neutrophil counts should be monitored weekly for the first month of therapy, then every 4 to 8 weeks while the cat is on therapy. Drug therapy should be stopped or tapered if the neutrophil count drops below 3000/µL. Lomustine (10 mg/cat q30d PO) may be effective. It is given for four to six treatments on monthly intervals then q4 to 8 w thereafter. Leukopenia can be a problem in some cats so a CBC should be done 7 to 14 days after each treatment. Prednisolone can be given concurrently. See Chapter 34 for more information on lomustine side effects. • Teeth Extractions: Traditionally this option has been only considered when other modalities fail, but increasingly the technique has been seen as a first line choice given the typically poor response to medical therapy. Extracting healthy premolar and molar teeth has been effective in resolving or improving clinical signs in up to 80% of cats with GSPC. Extraction is less likely to be of benefit when the cat is a persistent FCV shedder or FIV infected. • Laser Therapy: Removal of proliferative oral tissue by a carbon dioxide laser may be of benefit in some cases where tooth extraction is not desirable. The abnormal tissue is vaporized aggressively
Gingivitis-Stomatitis-Pharyngitis
monthly for two to four treatments. Many cats are asymptomatic for weeks to months without any medical treatment. Those that had become steroid resistant are often steroid responsive following laser therapy. However, long-term success should not be promised. See Chapter 257. • Coenzyme Q10: Giving 30 to 100 mg daily for 4 months has been suggested as an ancillary therapy. There is no conclusive evidence to support or refute its use. • Hypoallergenic or Novel Protein Diets: There are few reports that this may be of benefit. • Canned Food Diets: Anecdotally, some cats that have been on exclusively dry food diets will improve significantly if changed to an exclusively canned food diet.
medical therapy following these procedures (though less aggressive therapy may be needed). • GSPC has frequently been seen in several cats of multiple cat households. The significance of this is not known.
Prognosis Cats with GSPC can achieve total resolution of the syndrome, but owners should be advised that such an outcome is not guaranteed. Many cats will continue to show persistent or relapsing lesions and will need to be managed chronically. The goal of therapy should be the best possible control of clinical signs and patient oral comfort.
Therapeutic Notes • Antibiotic therapy alone has provided only temporary improvement in a low percentage of cats. • Gold salt therapy can be used in combination with glucocorticoids and antibiotics to help achieve a faster response. • Megestrol acetate has proven very beneficial in many cases of GSPC; however, side effects (diabetes mellitus) limit its use. The dose is 1 mg/kg q48h PO until a response is seen, then change to prednisone or prednisolone for maintenance. Megestrol acetate can be reinstituted for short periods when relapse occurs. It should only be used with informed consent and considered a rescue drug to be used short term when other therapies fail or are declined. • Owners should be warned that no therapy is expected to be 100% effective. This is especially important if multiple or complete dental extractions are planned, as many cats still have lesions and require
Suggested Readings August JR. 2008. Feline gingivostomatitis: Etiopathogenesis and management. Proceedings of the 26th Annual Conference of Veterinary Internal Medicine, San Antonio, Texas, pp 19–21. DeBowes LJ. 2009. Feline caudal stomatitis. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIV. pp. 476–478. St. Louis: SaundersElsevier. Quimby JM, Elston T, Hawley J, et al. 2008. Evaluation of the association of Bartonella species, feline herpesvirus 1, feine calicivirus, feline leukemia virus and feline immunodeficiency virus with chronic feline gingivostomatitis. J Fel Med Surg. 10(1):66–72. Southerden P, Gorrel C. 2007. Treatment of a case of refractory feline chronic gingivostomatitis with feline recombinant interferon omega. J Small Anim Pract. 48(2):104–106.
201
CHAPTER 85
Glaucoma Shelby L. Reinstein and Harriet J. Davidson
Overview By definition glaucoma is increased intraocular pressure (IOP) incompatible with normal ocular health. Normal IOP is maintained by a delicate balance between production and drainage of aqueous fluid or humor. Aqueous fluid is produced by the ciliary body and flows cranially through the pupil, circulates throughout the anterior chamber, then exits through the iridocorneal (drainage) angle. Glaucoma results when there is obstruction to the normal drainage pathways. Elevations in IOP result in damage to the retina and optic nerve and eventual blindness. There are three types of glaucoma in the cat: congenital, primary, and secondary. Congenital glaucoma occurs because of developmental malformation of the eyes. It occurs in young kittens and may be unilateral or bilateral. Primary glaucoma is a congenital or genetic malformation of the drainage angle. The drainage angle may be further described as open or closed. This form of glaucoma is rare in the cat. The Siamese, Persian, European shorthair, and Burmese breeds have a reported breed predisposition. In the majority of cats with primary glaucoma, the drainage angle is open. In one study, Burmese cats were reported to have a narrowed or closed drainage angle. Secondary glaucoma is much more common and occurs when another condition blocks flow of aqueous humor through the drainage angle. The most common causes of secondary glaucoma are uveitis (see Chapter 223) and intraocular neoplasia (see Chapter 122). Uveitis results in secondary glaucoma by clogging the drainage angle with inflammatory cells and protein. Intraocular neoplasia is the other leading cause of secondary glaucoma in the cat. Any tumor may lead to secondary glaucoma by inducing inflammation; however, tumors may also shed neoplastic cells, which obstruct the drainage angle. Diffuse iridal melanoma and lymphoma are the two most common tumors to cause glaucoma in the cat. Other causes of secondary glaucoma in the cat include anterior lens luxations, trauma, and hyphema.
•
•
•
•
•
•
conjunctivitis. By using a cotton tip applicator to move the loosely adhered conjunctiva, you can observe if the vessels move with the conjunctiva or are located deeper in the sclera. Corneal Edema: This is a diffuse, hazy, blue appearance to the entire cornea. Elevations in IOP cause the cornea to swell; the increased water content causes the cornea to appear more opaque. Additionally, the corneal fibers are spread apart by the fluid resulting in further decreased transparency. With treatment the cornea may regain normal clarity. Buphthalmos (Enlarged Eye): This occurs with longstanding elevations in IOP leading to stretching of the globe. Globe rupture is rare. However, lagophthalmos, or the inability to close the eyelids, may occur if the globe enlarges beyond a certain size. Exposure keratitis may occur and could lead to further changes to the eye, including superficial corneal vascularization, corneal fibrosis, and corneal ulceration. Corneal Streaks or Haab’s Striae: These are cracks in Descemet’s membrane and are seen as irregular, opaque line in the cornea. Occasionally there will be multiple lines. These cracks are permanent and will not resolve with treatment. This is an uncommon finding in the cat. Deep Corneal Vascularization: The injected scleral vessels may extend across the limbus into the cornea creating a brush border, sometimes called a limbal blush because of its appearance. This is a late stage change and indicates more chronic disease. Optic Nerve Head Changes: Extremely high pressure within the eye causes damage to the nerve head. Optic nerve cupping is difficult to visualize; however, loss of myelin will cause the optic nerve head to appear darker in color. Retinal Degeneration: Elevated IOP damages the retina. The fundic examination will show loss of vessels, and tapetal hyperreflectivity.
Tonometry Diagnosis Primary Diagnostics Clinical Signs and Ophthalmic Examination Findings (See Figure 85-1.) • Pain: This is a subjective sign in the cat. Cats may be quieter than normal, have a decreased appetite, or hide more than usual. All can be easily missed by the owner. • Dilated NonresponsivePupil: The lack of a pupillary light response (PLR) can be a result of acute paralysis of the iris sphincter muscle from elevated IOP or from damage to the retina. A positive consensual PLR (shine the light in the affected eye and observe pupil in normal eye) will help confirm the retina of the affected eye is still working. • Scleral Injection: This indicates inflammation deep in the eye. Blood vessels within the sclera must be differentiated from those in the more superficial conjunctiva, which would indicate only
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
202
• Multiple instruments are available for measuring the IOP in cats. The same instrument should be used each time, as values may differ slightly between instruments. • Normal intraocular pressure is 15 to 25 mm Hg in the cat. • Intraocular pressures greater than 25 mm Hg with consistent clinical signs confirms glaucoma. • Once therapy has been initiated, IOP should be rechecked routinely and maintained at less than 25 mm Hg. See Therapeutic Notes for suggested monitoring intervals. • Trends in IOP should be used to monitor response to medication and help determine the need for surgical treatment. • IOPs less than 15 mm Hg while being treated for glaucoma are not immediately pathologic. Ophthalmic examination to rule out uveitis (see Chapter 223) should be performed. • Treatment of secondary glaucoma should be modulated as the underlying condition resolves. Monitoring IOP during this period is crucial to assess disease resolution.
Secondary Diagnostics • Gonioscopy: This procedure uses a special lens to visualize and evaluate the iridocorneal angle. This procedure should be performed by a veterinary ophthalmologist.
Glaucoma
• Electroretinogram: This test measures the electrical activity of the retina. It may be used to assess the function of the retina prior to extensive medical or surgical procedures in cases where visualizing the retina is difficult (e.g., cataract).
Diagnostic Notes • Do not dilate an eye with glaucoma, suspected glaucoma, previous glaucoma, or primary glaucoma in the opposite eye. Dilation may increase the IOP and cause further damage to the eye. • In cases of secondary glaucoma, treatment should be aimed at both the underlying condition and the glaucoma. As the underlying condition resolves so will the need for antiglaucomatherapy.
Treatment Primary Therapeutics • Emergency Treatment: Many times cats will present with IOP greater than 50 mm Hg. It is critical to lower the IOP to a near normal value prior to beginning maintenance therapy to preserve retinal function. Osmotic diuretics are most commonly used in the emergency setting. These medications reduce IOP by dehydrating the vitreous body in the eye. Therefore, they are most effective if water is withheld for up to 4 hours. The systemic effectiveness of these medications can be monitored using the normal eye as IOP should lower in the normal eye as well. • Intravenous Mannitol: Mannitol should be administered through an intravenous catheter at a dose of 1.0 to 1.5 gm/kg once slowly (over 15–20 minutes). If ineffective in 30 minutes, the dose may be repeated once. • Glycerin (50 or 70% solution): This is given at 1 gm/kg PO. It may be repeated once in 30 minutes. This substance has a foul taste and may be difficult to administer; an orogastric tube is preferable. It has been known to cause vomiting. • Maintenance Therapy: These drugs may be used in various combinations once the IOP has reached a normal level. Consultation or referral to a veterinary ophthalmologist should be considered for long-term management. • Carbonic Anhydrase Inhibitor (CAI): CAIs decrease production of aqueous. They are available in both oral and topical forms. Oral CAIs include methazolamide (Neptazane®; 2.5–10 mg/kg q12h PO), dichlorphenamide (Daranide®; 1–2 mg/kg q8–12h PO), and acetazolamide (Diamox®; 10–25 mg/kg q12h PO). The oral CAIs have several side effects including gastrointestinal disturbance, skin tingling sensation (which may be demonstrated as excessive licking of the extremities), metabolic acidosis (which may be demonstrated with excessive panting), hypokalemia, and malaise. The topical CAIs are easy to administer and do not have the same side effects. They include dorzolamide 2% solution (Trusopt®; 1 drop q6–8h) and brinzolamide 1% suspension (Azopt®; 1 drop every 8–12 hours). • Parasympathomimetics: These topical medications increase aqueous drainage. Parasympathomimetic drugs should be used
Figure 85-1 The progression of glaucoma is seen in these three cases. A, The right eye demonstrates early clinical signs of glaucoma, including slight mydriasis, increased iris vascularization and slight buphthalia. B, The right eye demonstrates increased iris vascularization and a secondary anterior luxation of the lens. C, This cat has changes consistent with chronic glaucoma, including buphthalmos, exposure keratitis, an opaque cornea, and debris accumulated on corneal surface due to a loss of normal blink. Photos courtesy Dr. Gary D. Norsworthy.
(A)
(B)
(C)
203
SECTION 1: Diseases and Conditions
judiciously when severe uveitis is present because they may result in synechia formation. Pilocarpine is a direct acting parasympathomimetic and is administered as either a 1 or 2% solution given q6 to 12h. Demecarium bromide is an indirect acting parasympathomimetic and must be compounded. This drug is administered as either a 0.125 or 0.25% solution given q6 to 12h. • Sympathomimetics: These topical medications are thought to decrease aqueous production. They are not used often on their own, but they are combined with other classes of medications. Available medications include dipivalyl epinephrine (Propine®) administered q6 to 8h and epinephrine (Epitrate®) administered q6 to 8h. • β-Blockers: These topical medications are thought to decrease aqueous production. Timolol maleate (Timoptic® 0.5–4% solution q12h) and levobunolol (Betoptic® q12h) are available for use; however beta blockers alone are not strong enough to control feline glaucoma. A combination of dorzolamide and timolol maleate (Cosopt®) is available and used topically q8h to control IOP. • Corticosteroids: Topical steroids are used to decrease the inflammation surrounding the optic nerve as well as to treat primary uveitis in cases of secondary glaucoma. See Chapter 223. A 1% prednisolone acetate suspension or a 0.1% dexamethasone suspension are used topically q4 to 12h.
Secondary Therapeutics • Surgery for Visual Eyes: The objectives for surgery for visual eyes are to maintain vision while decreasing the frequency of medications. • Drainage Valve Implants: These devices consist of tubing that is implanted into the anterior chamber and a drainage valve that allows aqueous to exit the eye. This procedure is generally performed by a veterinary ophthalmologist. • Destruction of the Ciliary Body: Damaging the ciliary body and thus decreasing production of aqueous can be accomplished using either a diode laser or cryotherapy applied to the outer surface of the sclera. The energy penetrates into the ciliary body and causes necrosis of the tissue. This procedure will cause inflammation in the eye, and medications may be needed to control this as well as the IOP perioperatively. • Surgery for Blind Eyes: Uncontrolled glaucoma is a painful condition and surgical alleviation of a blind, painful eye is often indicated. • Enucleation: This surgical technique is easy to perform and has minimal complications. Removal of the globe will provide immediate pain relief as well as eliminate the need for topical medications. Placement of an orbital prosthesis will enhance cosmesis. • Evisceration with Intrascleral Prosthesis: This procedure enhances the cosmetic appearance of the cat even more by leaving the eyelids open and a globe in the orbit. However, the cornea remains at risk for injury and infection, which may require topical medications.
204
• Chemical Ablation: This procedure causes necrosis of the internal structures of the eye by injecting gentamicin and dexamethasone into the vitreous chamber. The procedure is controversial in cats due to the risk of sarcoma formation from lens trauma.
Therapeutic Notes • Prostaglandin analogs are a relatively new class of topical medications that increase drainage of aqueous humor through the nonconventional, or uveoscleral, outflow pathway. Currently available medications include latanoprost (Xalatan®), bimataprost (Lumigan®), travaprost (Travasal®), or unoprostone (Rescula®). These medications are effective in the dog; however, none of them has been shown to be effective at lowering IOP in normal cats. This is thought to be due to prostaglandin receptor differences between species. • In cases of secondary glaucoma, treatment should be aimed at both the underlying condition and the glaucoma. As the underlying condition resolves, so will the need for antiglaucoma therapy. • When the IOP has been lowered to near normal, the first recheck should be scheduled for 24 hours. Assuming the IOP is nearly normal, rechecks may be reduced to biweekly then monthly intervals. If the IOP begins to trend upward, medical therapy should be increased to regain control. • Owners should be made aware of more subtle signs of glaucoma and should have the IOP measured if any signs are observed.
Prognosis It is crucial to differentiate primary versus secondary glaucoma and acute disease from chronic disease. Although every case of primary glaucoma has a poor long-term prognosis for vision, secondary glaucoma has a good prognosis for vision if the underlying cause is treated. In general, if initial therapy is not approached aggressively, there will be a higher failure rate. Chronic or untreated glaucoma usually results in blindness, pain, and a noncosmetic eye (i.e., buphthalmos, exposure keratitis).
Suggested Readings Blocker T, van der Woerdt A. 2001. The feline glaucomas: 82 cases (1995– 1999). Vet Ophthal. 4(2):81–85. Jacobi S, Dubielzig RR. 2008. Feline primary open angle glaucoma. Vet Ophthal. 11(3):162–165. Rainbow ME, Dziezyc J. 2003. Effects of daily application of 2% dorzolamide on intraocular pressure in normal cats. Vet Ophthal. 6:147–150. Sapienza JS. 2008. Surgical procedures for glaucoma: what the general practitioner needs to know. Top Companion Anim Med. 23(1):38–45.
CHAPTER 86
Glomerulonephritis Gary D. Norsworthy
Secondary Diagnostics for Underlying Disease
Overview Glomerulonephritis is an immune-mediated glomerular disease seen most commonly in young male cats. Although it may occur in some species due to antibodies reacting to antigens within the glomeruli, the only form documented in the cat is due to circulating immune complexes being filtered out by the glomeruli. The clinically significant infectious causes of these antigen-to-antibody complexes are diseases due to the feline leukemia virus (FeLV), the feline infectious peritonitis virus (FIPV), feline immunodeficiency virus (FIV), Anaplasma spp., or Mycoplasma spp. (polyarthritis). Noninfectious causes include chronic pyoderma, neoplasia, gingivitis-stomatitis, dirofilariasis, systemic lupus erythematosis (SLE), pancreatitis, possibly diabetes mellitus, and incompatible insulin (usually of human origin). Most cases begin long before clinical presentation so the etiopathogenesis usually cannot be determined at the time of presentation. This often makes a specific primary diagnosis impossible. Thus, most cases are classified as idiopathic. Affected cats, which are usually young adult males, have two clinical forms of the disease. The first is the nephrotic syndrome. These cats often develop extensive subcutaneous edema and ascites but are otherwise reasonably healthy. They often have mild weight loss and a depressed appetite. The second form is chronic renal failure. These cats have more pronounced weight loss and appetite depression, polyuria, and polydipsia, and they may be vomiting. Cats with either form of glomerulonephritis typically have small, firm kidneys, although the kidneys may enlarge in the early stages of the disease.
Diagnosis Primary Diagnostics • Clinical Signs: Signs of the nephrotic syndrome are typical of the first form of this disease. Signs of chronic renal failure occur in the second form but do not differ from chronic renal failure due to other causes. If polyarthritis is the cause of the disease, multiple joints will be swollen and painful. • Complete Blood Count and Chemistry Profile: The common findings are proteinuria, hypoalbuminemia, hypercholesterolemia, and nonregenerative anemia. Azotemia occurs as the disease causes renal failure. The urine protein-to-creatinine ratio is greater than 2.0, which is consistent with glomerular disease. • Renal Biopsy: This can be the most effective way to differentiate glomerulonephritis from amyloidosis. A diagnostic sample must contain six or more glomeruli so a wedge biopsy or multiple needle biopsies is required. Amyloidosis is a genetically induced disease primarily in Abyssinians. This option should be used with caution as further renal damage will occur.
• Infectious Organism Testing: These cats should be tested for the FeLV, FIV, feline coronavirus (FCoV), and Anaplasma. See Chapter 73 and 76 for interpretation of FCoV titers. • Insulin Antibody Level: This test is to diagnose insulin incompatibility. See www.animalhealth.msu.edu.
Diagnostic Notes • Because glomerulonephritis is often due to an underlying disease, it is important to perform a thorough diagnostic workup.
Treatment Primary Therapeutics: Nephrotic Syndrome Without Azotemia • Underlying Disease: The ultimate diagnostic goal is to identify and cure the underlying disease. However, identifying the disease may be impossible, and, if it is found, a cure may be impossible. • Furosemide: This drug is to reduce edema and ascites. It is dosed at 2 to 4 mg/kg q24h PO. • Corticosteroids: An anti-inflammatory dose of prednisolone (2–4 mg/kg q24h PO) may be tried. Some cats respond well and others not at all. If it is successful, it should be continued until the underlying disease is cured. After 2 to 3 weeks of therapy, a reduced, alternating day schedule should be used for long-term therapy. • Angiotensin-Converting Enzyme Inhibitor: Benazepril (0.5–1.0 mg/ kg q24h PO) or enalapril (0.25–0.5 mg/kg q12–24 h PO) may be effective to reduce urinary protein loss. Monitor serum creatinine levels and discontinue if they are increasing. • Diet: Due to the protein loss occurring, a dietary level of protein should be fed to maintain normal body weight and serum albumin levels. A low-salt diet should be fed to minimize fluid retention. • Hypotensive Agent: Amlodipine (0.625 mg/cat q24h PO initially, then adjusted to response) is indicated if hypertension is present. See Chapter 107.
Primary Therapeutics: Azotemia • Medical: Fluid therapy, potassium supplementation, etc. are indicated. See Chapter 190.
Secondary Therapeutics: Underlying Diseases • See appropriate chapters.
Therapeutic Notes th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Azotemic cats should not receive salt supplementation, furosemide, or corticosteroids.
205
SECTION 1: Diseases and Conditions
Prognosis The prognosis depends on the form of glomerulonephritis, the stage of diagnosis, and the underlying disease. Nonazotemic cats with the nephrotic syndrome diagnosed early can often be managed for months or years, especially if an underlying disease can be cured. Cats in endstage renal failure have a poor prognosis.
206
Suggested Readings Gunn-Moore D, Miller JB. 2006. The cat with weight loss and a good appetite. In J Rand, ed., Problem-Based Feline Medicine, pp. 301–329. Philadelphia: Elsevier Saunders. Pressler BM, Grauer GF. 2007. Glomerulonephrtis. In LP Tilley, FWK Smith Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 548–549. Ames, IA: Blackwell Publishing.
CHAPTER 87
Granulosa Cell Tumor Fernanda Vieira Amorim da Costa and Heloisa Justen Moreira de Souza
Overview Ovarian tumors are rare in dogs and cats, in part due to the high rate of neutering in companion animals. Feline ovarian tumors are defined as epithelial, germ cell, or sex-cord stromal tumors. Granulosa cell tumor is a sex cord stromal tumor considered the most common ovarian tumor in cats. The neoplasm arises from the highly differentiated gonadal stroma of the cortical ovary. More than a half are malignant, and reported metastatic sites include peritoneum, lumbar lymph nodes, omentum, diaphragm, kidney, spleen, liver, and lungs. These tumors often show evidence of hormonally induced changes and are most commonly unilateral. The signalment of hyperestrogenism includes persistent estrus, aggressive behavior, alopecia, and cystic or adenomatous hyperplasia of endometrium. Cats can also show vomiting, weight loss, ascites due to peritoneal implantation, and abdominal distention. Tumor rupture and intra-abdominal bleeding can occur. Affected cats range in age from 6 months to 20 years (median, 7 years), and domestic short hair females are more affected. Differential diagnoses include other rare ovarian tumors, such as luteoma, thecoma, dysgerminoma, teratoma, and epithelial and interstitial cell tumor.
Diagnosis Primary Diagnostics • Histopathology: Definitive diagnosis rests with histopathologic evaluation of resected tissue. Granulosa cell tumors are usually smooth, white to yellow in color, and may be round or irregularly lobulated. Usually they are a combination of solid and cystic structures. The metastatic lesions are described as mushroom-like nodules attached to the diaphragm, peritoneum, and liver. Call-Exner bodies are often seen as rosette formations of degenerative cells undergoing cariorhexis surrounded by active granulosa cells.
Secondary Diagnostics • Physical Examination: Examination reveals a distended abdomen and a large, irregular, spherical palpable mass. Signs of ascites (malignant effusion) or systemic effects of hormone production can be evident. • Abdominal Ultrasonography: Smaller tumors may be identified as ovarian in origin, and the greater the solid proportion, the more likely the neoplasm is to be malignant. Uterine changes were commonly found with sex-cord stromal tumors, including cystic endometrial hyperplasia or pyometra. • Effusion Cytology: Cytologic evaluation of abdominal fluid often is suggestive of malignant effusion. • Vaginal Cytology: Look for evidence of estrogen-induced cornification that can confirm hyperestrogenism.
Diagnostic Notes • An abdominal mass in an intact female with or without signs referable to the reproductive tract should place an ovarian tumor on the list of differentials. Some cats have tumor in ovarian remnants. • Needle Biopsy: Transabdominal needle biopsies of the ovary are not recommended because of the propensity of this tumor to readily implant and grow on peritoneal surfaces. • Staging: Staging of cats with a suspected granulose cell tumor should include a minimum data base, abdominal ultrasound, thoracic radiographs, abdominocentesis, and fluid cytology.
Treatment Primary Therapeutics • Surgery: Treatment of ovarian tumors relies primarily on ovariectomy or ovariohysterectomy and carries, in general, an excellent prognosis if performed prior to metastasis.
Secondary Therapeutics • Chemotherapy: In the cases of peritoneal metastases or malignant ascites, intravenous or intracavitary chemotherapy with carboplatin may prove therapeutic. Doses ranges from 180 to 200 mg/m2 and are diluted to be infused intracavitary. The procedure can be repeated every 3 weeks. • Supportive: Supportive therapy, including analgesia, antiinflammatories, nutritional support, and anti-emetics, should be provided as needed.
Therapeutic Notes • Gentle handling of tissues to minimize tumor spread is warranted. Careful examination of all serosal surfaces, including the omentum and diaphragm, and removal or biopsy of any lesions suspected of metastatic disease is recommended for staging proposes.
Prognosis The prognosis is good when single tumors are completely excised at surgery. With any evidence of metastatic disease, the prognosis must be considered poor.
Suggested Readings Giacóia MR, Maiorka PC, Oliveira CM, et al. 1999. Granulosa cell tumor with metastasis in a tumor. Braz J Vet Res Anim Sci. 36(5):250–252. Klein MK. 2007. Tumor of the female reproductive system. In SJ Withrow, DM Vail, eds., Withrow & MacEwen’s Small Animal Clinical Oncology, pp. 610–618. St. Louis: Saunders Elsevier. Souza HJM, Amorim FV, Jaffé E, et al. 2005. Timoma e tumor de células da granulosa em gata. Acta Scientiae Veterinariae. 33(2):211–217.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
207
CHAPTER 88
Heartworm Disease Jane E. Brunt
Overview Heartworm infection in cats and dogs is caused by the filarial endoparasite, Dirofilaria immitis. Successful infection requires mosquito transmission from an infected canid host and favorable environmental factors. Twenty-two species of mosquitoes have been shown to carry D. immitis in the field, half of which are common. Heartworm disease occurs in cats wherever it exists in dogs and other canids; coyotes represent a significant reservoir for D. immitis. The life cycle of the worm (see Figure 88-1) is similar to that of the dog. In the context of disease pathogenesis, the key difference is that in cats most juvenile worms that enter into the bloodstream die in the pulmonary arteries rather than becoming adults. Additionally, because of the presence of pulmonary interstitial macrophages (PIMs) in cats, the death of the juvenile worms produces a more intense
inflammatory response than dogs. An acute airway vascular and parenchymal inflammatory reaction occurs with the right caudal lung lobe affected most commonly. Signs at that time may include coughing, dyspnea or tachypnea, and vomiting. In the cases in which juvenile worms mature into adult worms, typically only one to three are found and may be male-only infections. This becomes important in the interpretation of diagnostics. Adult worms have been reported to live up to 4 years. Respiratory manifestations of either juvenile or adult worm death have been identified as Heartworm-Associated Respiratory Disease (HARD). Acute death due to thromboembolism of the pulmonary arterial trunk is an uncommon sequelae. Cats die within minutes without prior warning signs. See Figure 88-2. Differential diagnoses include feline asthma or other bronchial disease, acute or chronic gastroenteritis, and pulmonary thromboembolism.
transient patency
(7–8 months post-infection)
Heartworm in heart and pulmonary vessels (1–3 worms)
L3 Adult 14 days or longer (infective 3rd Stage Larva)
Juvenile Worms (in pulmonary artery day 75–90 post-infection)
L4 (4th Stage Larva) Figure 88-1 The heartworm life cycle in the cat courtesy of KNOW Heartworms. Note that the appearance of juvenile worms in the pulmonary occurs about 75 to 90 days after the cat is bitten by an infected mosquito. Once in circulation juvenile worms are carried to the lungs where they die, causing the onset of clinical signs.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
208
Heartworm Disease
Figure 88-2 Acute death may occur when sudden thromboembolism blocks blood flow through the pulmonary arteries. This cat had 15 adult worms, an extremely unusual occurrence. It was stable and on long-term prednisolone when it died suddenly. Photo courtesy Dr. Gary D. Norsworthy and Dr. Lewis Radicke.
Figure 88-3 The primary sites of interstitial inflammation are the caudal pulmonary lung lobes (white arrow) as seen in the lateral view. Photo courtesy Dr. Gary D. Norsworthy.
Diagnosis Primary Diagnostics • Presentation: If a cat presents in distress with pulmonary signs, all tests should be performed in consideration of the patient’s condition. Emergency treatment to restore proper oxygenation should take precedence over diagnostics until the cat is stable. Measurement of pO2 may assist in determining next best steps. • Complete Blood Count (CBC): This should be part of the minimum database. Eosinophilia or basophilia is found inconsistently in cats with heartworms. • Heartworm Serology: Both antigen and antibody tests should be performed and are available as point-of-care in-house diagnostics and through reference labs, the latter being the most sensitive. A positive antigen test indicates the cat is harboring at least one adult female heartworm. A positive antibody test means the cat has successfully been infected with heartworms because all current tests identify antibodies to various proteins from the L3 or L4 stage of worm development. A positive antibody test cannot differentiate between a current active infection and a recent one in which all the worms have died. It has been documented that positive antibody tests are inconsistent in identifying known cases of heartworm infection in cats. Negative antigen or antibody tests do not rule out heartworm infection. Heartworm serologic tests are rule-in tests and not rule-out tests. • Thoracic Radiography: Suggestive findings are prominent right caudal lobar artery with or without interstitial or bronchointerstitial patterns (see Figures 88-3, 88-4, 291-20, and 291-21. Radiographic signs may be minimal, transient, or change over time so serial radiographs may be indicated.
Figure 88-4 Enlargement of one, or in this case both, caudal pulmonary arteries (black arrows) is a sign of heartworm disease in cats. Often the arteries are tortuous or blunted. Photo courtesy Dr. Gary D. Norsworthy.
Treatment Primary Therapeutics
Secondary Diagnostics • Echocardiography: This may be useful in identifying suspected cases of heartworm infection and as an aid in identifying the extent of infection. Because most adult heartworm infections in cats consist of a single or few worms, they may reside in the pulmonary arteries instead of the right ventricle and thus be difficult to image. See Figure 88-5.
Acute Heartworm-Associated Respiratory Disease • Oxygen: Oxygen should be administered via oxygen cage or face mask. If the latter is resisted by the cat, it may be counterproductive. • Stress Reduction: A low stress environment is strongly urged. Freedom from the sights, sounds, or smells of dogs or other arousing circumstances is highly desirable.
209
SECTION 1: Diseases and Conditions
Therapeutic Notes • Adulticide therapy with melarsomine in naturally infected cats has resulted in a high degree of mortality. • Attempts at surgical removal have been reported with varying degrees of success and may result in and unacceptable mortality rate. • Aspirin is not recommended for cats with diagnosed heartworm infection. • Treatment of Wolbachia with tetracyclines is controversial in cats, although a course of doxycycline is not harmful unless the cat has a hypersensitivity to tetracyclines. • If the patient is asymptomatic and found to be infected with heartworm, the clinician may consider treating preemptively with corticosteroids to mitigate the inflammatory process.
Prevention
Figure 88-5 Adult heartworms are seen in the right ventricle and pulmonary outflow tract as two parallel lines. In the right ventricle they can be confused with the chordae tendineae. The latter move with valve opening and closing but remain in static locations unlike heartworms that move randomly. • Corticosteroids: Give dexamethasone (1 mg/kg IV or IM) or prednisolone sodium succinate (50–100 mg/cat IM). • Bronchodilators: Aminophylline (4.0–6.6 mg/kg q12h PO, IM; 2–5 mg/kg q12h slow intravenous infusion), theophylline sustained release (10 mg/kg PO), or terbutaline (0.1 mg/kg SC). Bronchodilators are not routinely used in long-term management.
Subacute or Chronic Heartworm-Associated Respiratory Disease • Corticosteroids: Prednisolone or prednisone (2 mg/kg q24h PO, declining gradually over 2 weeks to 0.5 mg/kg q48h PO). After an additional 2 weeks, treatment may be discontinued, and the effects of treatment are assessed based on the clinical response or thoracic radiography. Treatment may be repeated in cats with recurrent clinical signs, or the patient may be kept on long-term therapy.
Secondary Therapeutics • Emergency Treatment at Home: Dispensing a prefilled syringe of dexamethasone to administer at home (1 mg/kg IM or SC) may be beneficial in the case of an acute episode.
210
Prevention by administration of approved chemoprophylactic agents is considered the key to management of feline heartworm infection and in avoiding the serious outcomes associated with HARD. Currently there are two available topical products (selamectin and imidacloprid with moxidectin) and two available flavored oral products (milbemycin oxime and ivermectin). All are administered once monthly and are effective in eliminating immature larvae prior to reaching the circulatory system.
Prognosis Prognosis of cats presenting with acute HARD is guarded and best assessed based on response to emergency therapy. For cats diagnosed with heartworm infection with absent or mild clinical signs, the clinician and owner should be aware of potential acute episodes and understand what to do in the event of the occurrence of signs.
Suggested Readings American Association of Feline Practitioners and American Heartworm Society Feline Heartworm Awareness Campaign: Know Heartworms. www.knowheartworms.org Browne LE, Carter TD, Levy JK, et al. 2005. Pulmonary arterial disease in cats seropositive for Dirofilaria immitis but lacking adult heartworms in the heart. Am J Vet Res. 66:1544–1549. Nelson, CT. 2008. Dirofilaria immitis in cats: anatomy of a disease. Compendium. 30(7):382–389. Nelson CT, Seward RL, McCall JW, et al. 2007. Guidelines for the diagnosis, treatment and prevention of heartworm (Dirofilaria immitis) infection in cats. American Heartworm Society. http://www. heartwormsociety.org/article_47.html
CHAPTER 89
Heinz Body Hemolytic Anemia and Methemoglobinemia Sharon Fooshee Grace Overview Oxidative agents cause two major types of injury to feline erythrocytes. The first, Heinz body (HB) formation, occurs when feline hemoglobin is denatured and precipitates on the erythrocyte membrane. Feline hemoglobin is an easy target for oxidative injury because it contains more sulfhydryl groups per molecule than most other species. Additionally, the feline spleen is relatively inefficient at removing HB aggregates from the erythrocyte once they form. Consequently, even clinically normal cats have an occasional HB in circulation unlike most other species. Irreversible cellular damage caused by HB formation leads to a primarily extravascular hemolytic anemia when the erythrocyte reaches a critical level of fragility and must be cleared from circulation. In a few situations, HBs may form by means other than oxidative stress on the red blood cells (e.g., propylene glycol), though the exact mechanism remains unknown. The second type of oxidative injury, methemoglobinemia, is reversible; it develops when the ferrous (+2) iron of hemoglobin is oxidized to the ferric (+3) state, rendering hemoglobin incapable of carrying oxygen.
Causes of Heinz Body Formation or Methemoglobinemia • • • • • • • • • • • • • • •
Acetaminophen Benzocaine (topical and local anesthetics) Copper Diabetes mellitus DL-methionine Hyperthyroidism Lymphoma Methylene blue Naphthalene (moth balls) Onions or onion powder Phenazopyridine (urinary analgesic) Propofol (possible cause) Propylene glycol Vitamin K3 Zinc
MR MC
HB
Figure 89-1 Heinz bodies are seen on many of the erythrocytes in this field (HB). The larger erythrocytes, called macrocytes (MC), and the metarubricyte (MR) are indicative of bone marrow response to anemia. Image courtesy Dr. Gary D. Norsworthy.
AR HB
Diagnosis Primary Diagnostics • Clinical Signs and Physical Examination Findings: With Heinz body hemolytic anemia (HBHA), mucous membranes will be pale and perhaps icteric. Weakness, depression, tachycardia, and tachypnea are other significant clinical signs. When methemoglobinemia is present, the membranes will be cyanotic or brownish. • Complete Blood Count and Reticulocyte Count: Heinz bodies may be seen with modified Wright’s stains (see Figure 89-1) and with wet mounts of new methylene blue stain (the stain commonly used to identify reticulocytes, see Figure 89-2). HBs appear as large single inclusions that may bulge from the cell surface. Within a few days of
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 89-2 When stained with new methylene blue, Heinz bodies (HB) are seen as dark foci on the edge of the red blood cells. An aggregate reticulocyte (AR) is seen because the reticulum also uptakes the stain. Image courtesy Dr. Gary D. Norsworthy.
HBHA onset, a regenerative response is reflected with increasing numbers of circulating aggregate reticulocytes.
Secondary Diagnostics • Screening Test: Methemoglobinemia is sometimes difficult to discern in a blood sample because venous blood is normally dark. As a clinical screening test, one drop of patient blood can be placed on a white paper towel or filter paper next to a drop of normal
211
SECTION 1: Diseases and Conditions
“control” blood. If the methemoglobin content is greater than 10%, the patient’s blood is expected to be noticeably browner than the brighter red of the control blood. Some larger diagnostic laboratories are able to assay blood for methemoglobin levels. The Wisconsin Veterinary Diagnostic Laboratory offers methemoglobin analysis and may be contacted at 1-800-771-8387.
Diagnostic Notes • Abnormal forms of hemoglobin (such as methemoglobin) can interfere with accurate reading of pulse oximeters. • The presence of large numbers of HBs in a cat does not necessarily indicate an impending hemolytic crisis because the HBs may be present in a variety of diseases. Because a number of chemical agents may cause oxidant injury to feline erythrocytes, a detailed history is important.
may not be effectively delivered to tissues due to vasoconstriction and reduced cardiac output caused by the drug. • Acetaminophen Toxicosis: See Chapter 1 for appropriate therapy. Acetylcysteine (Mucomyst®) is the mainstay of therapy. • S-Adenosylmethionine (SAMe): SAMe, currently marketed as Denosyl® and Denamarin® by Nutramax Laboratories, demonstrates hepatoprotective and systemic antioxidant properties. SAMe has been shown to increase the cat’s resistance to oxidative stress and appears beneficial in managing oxidative injury, especially by decreasing the formation of HBs. It appears to have significantly less benefit in treating methemoglobinemia. At this time, it should be considered an adjunctive therapy of potentially great value. • Supportive Therapy: This includes intravenous fluids and electrolytes and limited handling of the patient. Monitor fluids carefully; if significant hemodilution or lowering of the hematocrit occurs, blood products should be administered. Oxygen may not be of much benefit in treating methemoglobinemia because the functional hemoglobin will already be saturated.
Treatment Primary Therapeutics
Therapeutic Notes
• Methylene Blue: Severe methemoglobinemia may be cautiously treated with methylene blue. The drug should not be given repeatedly or in high doses because it will cause HB formation. The 1% solution may be given at 1 mg/kg IV one time. Overdosing can result in the skin turning blue. See Figure 89-3.
• All potential causes of ongoing oxidative injury to erythrocytes should be addressed. • Depending on the degree of methemoglobinemia, different levels of therapy may be needed. For mild methemoglobinemia, acetylcysteine therapy and SAMe may be helpful. In more severe cases, additional treatment is indicated (i.e., transfusion with whole blood or hemoglobin solutions, ascorbic acid, and cimetidine). • Generally, supportive care is the only requirement for treating HBHA. With appropriate bone marrow stimulation, reticulocytes will replace damaged erythrocytes within a few days. The kidneys should be protected against hemoglobin-induced injury with fluid therapy. Rarely, a transfusion of whole blood (or Oxyglobin, if available) is needed. • Use caution when administering SAMe preparations other than Denosyl® and Denamarin®, potency-confirmed forms of the drug. SAMe is not currently regulated by the government and thus potency in sources is variable. In addition, SAMe loses efficacy when exposed to moisture; thus, appropriate packaging (blister-pack) is necessary. • Propofol is probably safe to use in cats so long as repeated usage over a short period of time (days) is avoided.
Secondary Therapeutics • Transfusion with Blood or Hemoglobin Solutions: With methemoglobinemia and HBHA, oxygen-carrying capacity of the blood is diminished. Administration of whole blood (See Chapter 295) or Oxyglobin® (5–15 ml/kg IV) may be useful in cats with severe hemolytic anemia and should be considered if the hematocrit falls below 20%. Note that signs of hypoxemia warrant a transfusion, even with a normal hematocrit because the hematocrit is not a true reflection of the oxygen-carrying capacity of the blood. Oxyglobin has the potential to cause volume overload in cats so slow infusion rates of 0.5 to 5 ml/kg per hour are recommended. Although it may increase the amount of oxygen carried by blood, the oxygen
Prognosis Although HBHA is nonreversible, the prognosis for recovery is better than for methemoglobinemia. Methemoglobinemia will result in death if oxygen-carrying potential of the blood drops below a critical level. The cat with methemoglobinemia is less likely to survive without intervention than is the cat with HBHA.
Suggested Readings
Figure 89-3 Methylene blue, found in some urinary antiseptics and sometimes used for treating methemoglobinemia, can cause bluing of the skin. Image courtesy Dr. Gary D. Norsworthy.
212
Center SA, Randolph JF, Warner KL, et al. 2005. The effects of S-adenosylmethionine on clinical pathology and redox potential in the red blood cells, liver, and bile of clinically normal cats. J Vet Intern Med. 19(3):303–314. Christopher MM, White JG, Eaton JW. 1990. Erythrocyte pathology and mechanisms of Heinz body-mediated hemolysis in cats. Vet Pathol. 27(5):299–310. Harvey JW. 1995. Methemoglobinemia and Heinz-body hemolytic anemia. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XII, pp. 443–446. Philadelphia: WB Saunders. Webb CB, Twedt DC, Fettman MJ, Mason G. 2003. S-adenosylmethionine (SAMe) in a feline acetaminophen model of oxidative injury. J Fel Med Surg. 5(2):69–75.
CHAPTER 90
Helicobacter Mark Robson and Mitchell A. Crystal
Overview Helicobacter spp. are gram-negative, microaerophilic, curved to spiralshaped, motile bacteria that inhabit the stomach and, to a lesser degree, the intestine and liver of various animal species. Helicobacter organisms can survive in the acidic environment of the stomach by residing within and below the gastric mucus layer. They also break down urea into ammonia and bicarbonate and thus create a less acidic microenvironment that is more conducive to survival. There is much debate on the pathogenicity of these organisms in both humans and animals. Although the prevalence of Helicobacter is high in cats (57 to 100%), most Helicobacter infections occur in asymptomatic cats. In humans, the severity of gastritis and clinical outcome of infection is due to a combination of host genetic susceptibility, immune response, virulence of bacterium, age at initial time of infection, and environmental factors. This may explain why the clinical outcome of Helicobacter infections is so variable. Helicobacter infections have the potential to cause gastritis (i.e., animals and humans), gastric ulcer disease (i.e., humans, cheetahs, and ferrets), and gastric neoplasia (i.e., humans and ferrets). There are more than 30 different Helicobacter species, each having various unique characteristics (see Table 90-1). Helicobacter heilmannii is the predominant species isolated from domestic cats; however, cats are colonized by a variety of Helicobacter spp., often simultaneously. Helicobacter pylori is of special note because it has been shown to cause significant disease in people (i.e., peptic ulcers and gastric neoplasia), and natural infection was confirmed in a colony of research cats. Experimental infection with H. pylori has been successful in cats; however, H. pylori has never been isolated from stray or domestic cats. Although reports of clinical disease in cats are limited, possible signs include chronic vomiting, weight loss, abdominal pain, anorexia, and diarrhea. The differential diagnoses for Helicobacter gastritis should include those of chronic vomiting (see Chapter 229) and possibly diarrhea (see Chapter 54). Further research is needed to ascertain whether helicobacteriosis is associated with cholangiohepatitis, enterocolitis, and gastric lymphoma of cats. The mode of transmission of Helicobacter is uncertain. Humans usually acquire H. pylori at an early age and have a lifelong infection rather than transmitting the organism from adult to adult. This may also be true for cats and dogs; Helicobacter has been isolated from puppies as young as 6 weeks. In humans, fecal-oral and oral-oral transmission is suspected. Recently, H. pylori was identified in surface water in the United States and Sweden, suggesting the possibility of water-borne infection as an important route of transmission. Helicobacter has been identified in the feces and saliva of infected cats. The prevalence of Helicobacter in cats and dogs living in high population-density housing (e.g., research colonies) commonly reaches 100%, indicating that animal-animal transmission through mutual grooming and environmental contamination is probably occurring. Currently, the zoonotic risk posed by Helicobacter appears to be small. H. heilmannii, the most commonly isolated species in cats, is only found in the mucosa of 0.4 to 4% of people. A recent study found that H. heilmannii type 1 is the dominant subtype in humans, which was not consistent with the subtypes found in cats and dogs. There are numerous
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
TABLE 90-1: Selected Helicobacter Organisms Currently Recognized in Animals Potential Clinical Diseases
Organism (site)
Site
Host
Helicobacter pylori
Stomach
Cat, human
Helicobacter heilmannii (formerly Gastrospirillum spp.)
Stomach
Helicobacter felis
Stomach
Helicobacter cinaedi Helicobacter pametensis Helicobacter colifelis Helicobacter acinonyx Helicobacter bilis
Liver Intestine Stomach
Cat, cheetah, dog, human, non-human primates, pig Cat, dog, human Cat, dog, human Cat
Unknown
Intestine
Cat
Diarrhea
Stomach
Cheetah
Ulcer Disease
Stomach Liver Stomach
Dog
Unknown
Dog, cat
Unknown
Dog
Helicobacter bizzozeronii Helicobacter canis Helicobacter fennelliae Helicobacter salomonis Flexispira rappini Helicobacter mustelae Helicobacter suis
(Humans) Ulcer disease, carcinoma, lymphoma Unknown
Unknown Unknown
Liver Intestine Intestine
Dog, human
Diarrhea, hepatic necrosis Unknown
Stomach
Dog
Unknown
Intestine Stomach
Dog Ferret
Stomach
Pig
Unknown Ulcer Disease, carcinoma Unknown
case reports implicating contact with cats and dogs as the source of H. heilmannii and Helicobacter feli infection in humans; however, few studies have used molecular epidemiology to classify subtypes. If H. pylori infection is demonstrated in domestic cats the zoonotic threat of Helicobacter would increase substantially.
Diagnosis Primary Diagnostics • Gastric Biopsy and Histopathology: Routine histopathologic evaluation of mucosal (endoscopic) or full-thickness (surgical) biopsies can detect spiral-shaped bacteria, although special silver staining (e.g., Warthin-Starry) is needed to see smaller organisms or low density colonization. See Figure 90-1. Biopsies should be collected from multiple areas of the stomach as the distribution of infection can be
213
SECTION 1: Diseases and Conditions
Helicobacter in general has a low culture rate, and H. heilmannii has never been successfully cultured on artificial media. • Serologic assays for immunoglobulin G (IgG) are effective in the diagnosis of H. pylori in humans and Helicobacter mustelae in ferrets, but at this time they are unreliable for use in cats. • Polymerase chain reaction (PCR) testing has been developed for Helicobacter, but this is primarily used for research purposes. PCR may have a higher sensitivity compared with cytology and can be used for species differentiation. • Urea breath testing is accurate for diagnosing Helicobacter, but obtaining needed equipment, handling radioactive materials, and collecting breath samples make it of limited clinical value.
Treatment Primary Therapeutics
Figure 90-1 The spiral shaped Helicobacter organisms are seen in a biopsy specimen of the gastric mucosa. (H & E stain). Image courtesy Dr. Gary D. Norsworthy.
patchy. False-negatives may occur. Histopathology is important to assess the degree of inflammation. • Gastric Brush, Gastric Biopsy Impression Smear, or Gastric Wash Cytology: This is a simple, effective way to screen for the presence of Helicobacter organisms. In-house modified Wright’s quick-stains can be used for the cytology. This method may be more sensitive than histopathology at detecting Helicobacter organisms, although the extent of gastric inflammation cannot be assessed.
Secondary Diagnostics • Rapid Urease Test: This test is performed on gastric biopsies. The commercially available test media (Campylobacter-like organism test, CLOtest®, Kimberly-Clark/Ballard Medical Products, Draper, UT) is an agar that contains urea, sodium azide (a preservative to help prevent positive reactions due to growth of urease-positive contaminates), and phenol red (an indicator that is yellow at a low pH and changes to a red color as the pH increases). The agar assay is left at room temperature and inspected frequently for 24 hours. A positive test result occurs if the media changes from yellow to a deep pink; this often occurs within half an hour of adding the tissue sample. The rapidity of the change in color estimates the number of organisms that are present. False-positives and false-negatives can occur.
Diagnostic Notes • Because gastric spiral bacteria are present in most cats, exclusion of all other diagnoses and confirmation of typical pathologic changes in addition to the presence of the organism are necessary to confirm a diagnosis of Helicobacter gastritis. • Endoscopic Helicobacter-associated lesions may have a wide variety of appearances, including diffuse rugal thickening, mucosal flattening, and superficial pockmarks (suggestive of lymphoid follicle hyperplasia). Overt ulcers have not been seen in cats with Helicobacter. The body and fundus are often more severely affected than the pyloric antrum. Some cats will have a normal endoscopic examination. Typical histopathologic lesions include lymphoid follicle hyperplasia or lymphoplasmacytic gastritis. • Culture is an insensitive and difficult-to-perform procedure for the diagnosis of Helicobacter spp. The organisms require special handling, special media, and a special growing environment (microaerophilic).
214
• Dual or Triple Antibiotic Therapy: Combinations of the following for 2 to 4 weeks: amoxicillin (20 mg/kg q12h PO), azithromycin (5 mg/ kg q24h PO), clarithromycin (7.5–10 mg/kg q12h PO), metronidazole (15 mg/kg, q12h PO), doxycycline (5 mg/kg q12h PO), tetracycline (20 mg/kg q8h PO). • Coating Agents: Bismuth subsalicylate or bismuth subcitrate (10– 15 mg/kg q12h PO [0.6–1.0 ml/kg q12h PO of regular strength Pepto-Bismol]) can be used in addition to the antibiotics. • Antacid Therapy: Use in cats and dogs is questionable because helicobacteriosis rarely causes ulceration, but it may improve antibiotic efficacy. Give one of the following in addition to antibiotic therapy: famotidine (0.5 mg/kg q12h PO), ranitidine (2.5–3.5 mg/kg q12h PO), cimetidine (10 mg/kg q8h PO), or omeprazole (0.5–1 mg/kg q24h PO).
Therapeutic Notes • A treatment trial is warranted in cats that have Helicobacter, have concurrent clinical signs that could be ascribed to Helicobacter infection, and have no other obvious underlying cause. • Failure to respond quickly to treatment suggests there may be another underlying cause for the clinical signs. • Treatment regimes with a single antibiotic have resulted in eradication rates less than 20%. • In recent controlled trials, cats with H. pylori treated with 14 days of clarithromycin (7.5 mg/kg q12h PO), metronidazole (10 mg/kg q12h PO) and amoxicillin (20 mg/kg q12h PO [without an antacid]) were PCR negative, urease negative, and spiral bacteria negative 30 days after therapy.
Prognosis High eradication rates are achieved in people but not animals. Most cats are asymptomatic and do not require therapy. Therapy in cats suspected to have clinical disease has seemed to be successful in limited reports; however, response rates have not been evaluated long term and recurrence of infection has been commonly identified. It is not known whether recurrence represents reinfection or recrudescence.
Suggested Readings Fox JG. 2006. Gastric Helicobacter infections. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 343–354. St. Louis: SaundersElsevier. Leib MS. 2008. Chronic gastritis and vomiting: The role of Helicobacter spp. Proceedings. Atlantic Coast Veterinary Conference, Atlantic City. Leib MS, Duncan RB. 2009. Gastric Helicobacter spp. and chronic vomiting in dogs. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIV. pp. 492–497. St. Louis: Saunders-Elsevier. Simpson KW. 2009. Helicobacter infection in dogs and cats. Proceedings, Western Veterinary Conference, Las Vegas, NV.
CHAPTER 91
Hemangiosarcoma Bradley R. Schmidt
Overview Hemangiosarcoma is an uncommon malignant tumor characterized by rapidly proliferating anaplastic cells derived from blood vessels and lining blood-filled spaces. It generally develops in older cats. The most common site of hemangiosarcoma development is the skin, followed by the mesentery, spleen, liver, mediastinum, nasal cavity, oral cavity, and other sites. When all abdominal forms are grouped together as visceral hemangiosarcoma, cutaneous and visceral forms occur with similar frequency. Within the skin, cutaneous and subcutaneous hemangiosarcoma and cutaneous hemangioma occur with similar frequency. The skin of the head appears to be the most common locations for cats with cutaneous hemangiosarcoma (see Figure 91-1), but in one study the flank and ventral abdominal regions were more common in cats with subcutaneous hemangiosarcoma. See Figure 91-2. Ulceration, bleeding, and subcutaneous hemorrhage are the most common clinical findings in cats with cutaneous hemangiosarcoma, with an increase in size of the mass associated with the hemorrhage being reported by many owners. Studies vary with regard to the metastatic potential of cutaneous hemangiosarcoma; however, metastasis may not be as common as with the visceral forms. Of the visceral forms, hemangiosarcoma of the mesentery may present as a large mass incorporating the intestinal tract or pancreas making the true site of origin difficult to determine. Splenic hemangiosarcoma may be solitary or multiple. See Figure 91-3. Hepatic hemangiosarcoma generally present as a large hepatic mass with smaller nodules in the hepatic parenchyma. See Figure 91-4. Clinical signs associated with visceral hemangiosarcoma include abdominal swelling and dyspnea secondary to hemoabdomen, acute or intermittent weakness
(A)
(B) Figure 91-2 Subcutaneous hemangiosarcomas are usually found in the flank and ventral abdominal regions. A, This one occurred as multiple nodules on the dorsum of the cat. B, Wide surgical excision is often curative. The blood-filled tumor is usually well encapsulated. Photos courtesy Dr. Gary D. Norsworthy.
Figure 91-1 Cutaneous hemangiosarcomas appear as blood-filled masses, usually on the head. Photos courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
and collapse, lethargy, and vocalization. Chylous effusion (ascites) has also been reported. Abdominal, lung, and cardiac metastasis is common for mesenteric and splenic hemangiosarcoma but may be less common for hepatic hemangiosarcoma. Mediastinal hemangiosarcoma has been reported in cats presenting with hemothorax and dyspnea. Metastasis within the thorax is common in these cats. Nasal and oral hemangiosarcomas are rare and differ from the anatomic sites because metastasis has not been reported; however, they are locally aggressive. Differential diagnoses for cutaneous hemangiosarcoma and hemangioma include other soft-tissue sarcomas, mast cell tumors, infections,
215
SECTION 1: Diseases and Conditions
or excisional of cutaneous masses) is preferred to an incisional biopsy because many lesions are associated with continued hemorrhage and excision may be therapeutic as well as diagnostic. When possible, a coagulation profile should be performed prior to tissue biopsies or surgery. Core needle biopsy is discouraged due to sample insufficiency and hemorrhage following the procedure.
Secondary Diagnostics
Figure 91-3 Splenic hemangiosarcoma may be solitary or multiple. Photos courtesy Dr. Gary D. Norsworthy.
• Thoracic Radiographs: Thoracic radiographs should be performed to evaluate for the presence of pulmonary metastasis. • Abdominal Ultrasound: Abdominal ultrasound should be performed to evaluate for metastatic lesions in the liver, spleen, omentum, and other abdominal organs. • Lymph Node Fine-Needle Aspiration and Cytology: A fine needle biopsy should be performed if lymphadenopathy is present; however, lymph node metastasis is less common than organ metastasis. • Echocardiogram or Thoracic Ultrasound: A cardiac evaluation is recommended to evaluate for cardiac metastasis, and a mediastinal ultrasound should be considered if a mass effect is suspected radiographically. Unlike the dog, cardiac metastasis is uncommon in cats. • Advanced Imaging: Prior to removal of a cutaneous hemangiosarcoma, computerized tomography (CT) scan or magnetic resonance imaging (MRI) may be helpful in determining the extent of the disease prior to surgery. • Minimum Date Base: A complete blood count (CBC), serum biochemistry profile, urinalysis, and retroviral serology should be performed to evaluate the overall health of the patient. Anemia is a common finding in many cats secondary to hemorrhage. Other possible abnormalities may include thrombocytopenia, hypoproteinemia, azotemia that may be renal or prerenal in origin, hepatic enzyme elevation, and hyperglobulinemia. Fragmented red blood cells are not frequently reported in the cat in association with this tumor. • Coagulation Profile: A coagulation profile is recommended prior to surgical procedures as well as to evaluate for a primary coagulopathy as a cause for cavitary hemorrhage.
Diagnostic Notes • With the possible exception of the cutaneous forms, hemangiosarcoma should be considered a metastatic neoplasm. Figure 91-4 Hepatic hemangiosarcoma generally present as a large hepatic mass with smaller nodules in the hepatic parenchyma. In the liver they are friable. Photos courtesy Dr. Gary D. Norsworthy.
Treatment Primary Therapeutics
trauma, or coagulopathy with resultant cutaneous hemorrhage. Differential diagnosis for cats with abdominal or mediastinal masses with associated cavitary hemorrhage include other sarcomas, trauma, and coagulopathy.
Diagnosis Primary Diagnostics • Fine Needle Biopsy and Cytology: Fine needle biopsy and cytology may be a screening tool for the diagnosis of neoplasia; however, due to the highly vasculature nature of the tumor, peripheral blood with no evidence of neoplastic cells is commonly seen on cytology. It has been the my experience that marked suppurative or pyogranulomatous inflammation may also be noted. • Tissue Biopsy and Histopathology: Histopathology is recommended for all lesions. When possible, excisional biopsy (e.g., splenectomy
216
• Surgery: This is the mainstay of treatment, when possible, and may be palliative in cases where hemorrhaging is occurring. Due to the large, invasive nature of the tumor, in many cases, local recurrence may be common.
Secondary Therapeutics • Chemotherapy: Intravenous chemotherapy is recommended for visceral and metastatic forms of hemangiosarcoma; however, critical studies evaluating tumor responses have not been performed. Commonly recommended chemotherapy agents include doxorubicin (1 mg/kg or 25 mg/m2 q3w IV), carboplatin (225–240 mg/m2 q3–4w IV), or mitoxantrone (6.0–6.5 mg/m2 q3w IV). The addition of cyclophosphamide to doxorubicin has also been advocated by some. Careful monitoring of the while cell counts is recommended. Carboplatin is excreted by the kidneys; therefore, use with caution in cats with renal compromise.
Hemangiosarcoma
• Pericardectomy: This is an aggressive procedure that may help relieve clinical distress due to pericardial effusion, but this procedure may result in significant hemothorax.
Therapeutic Notes • Supportive Care: Supportive care including intravenous fluids, red blood cell or plasma transfusions, and nutritional support is recommended when indicated. • Radiation Therapy: Radiation therapy may reduce the local tumor burden and reduce hemorrhage; however, its use in the cat has not been reported.
Prognosis The prognosis for most cats with visceral hemangiosarcoma is poor due to the development of widespread metastasis. The prognosis for cats with cutaneous hemangiosarcoma may be more favorable with complete surgical resection because, although reports vary, metastasis may be less common in these cats. Incomplete surgical margins and a high mitotic rate negatively influence survival times. Subcutaneous tumors have a higher local recurrence rate when compared to cutaneous tumors and may be associated with a poorer prognosis. The prognosis for hemangioma and hemangiosarcoma of the conjunctiva also appears to be favorable with resection; however, recurrence is possible. Tumor grade and cutaneous forms may be associated with longer survival times with surgery alone.
The role of chemotherapy in the treatment of feline hemangiosarcoma has not been critically evaluated. Overall, the prognosis for many cases of hemangioma appears to be favorable based on the information available.
Suggested Readings Culp WTN, Drobatz KJ, Glassman MM, et al. 2008. Feline visceral hemangiosarcoma. J Vet Intern Med. 22(1):148–152. Hartley C, Ladlow J, Smith KC. 2007. Cutaneous haemangiosarcoma of the lower eyelid in an elderly white cat. J Fel Med Surg. 9(1):78–81. Johannes CM, Henry CJ, Turnquist SE, et al. 2007. Hemangiosarcoma in cats: 53 cats (1992–2002). J Am Vet Med Assoc. 231(12):1851–1856. Kisseberth WC, Vail DM, Yaissle J, et al. 2008. Phase I clinical evaluation of carboplatin in tumor-bearing cats: a Veterinary Cooperative Oncology Group Study. J Vet Intern Med. 22(1):83–88. Moore AS, Ogilvie GK. 2001. Skin tumors. In AS Moore, GK Ogilvie, eds., Feline Oncology, pp. 398–428. Trenton, NJ: Veterinary Learning Systems. Moore AS, Ogilvie GK. 2001. Splenic, hepatic and pancreatic tumors. In AS Moore, GK Ogilvie, eds., Feline Oncology, pp. 295–310. Trenton, NJ: Veterinary Learning Systems. Pirie CG, Dubielzig RR. 2006. Feline conjunctival hemangioma and hemangiosarcoma: a retrospective evaluation of eight cases (1993– 2004). Vet Ophthalmol. 9(4):227–231. Vail DM, Withrow SJ. 2007. Miscellaneous tumors, section A Hemangiosarcoma. In SJ Withrow, DM Vail, eds., Small Animal Clinical Oncology, 4th ed., pp. 785–795. Philadelphia: Elsevier Saunders.
217
CHAPTER 92
Hemoplasmosis Sharon Fooshee Grace and Gary D. Norsworthy
Overview Hemoplasmosis (formerly hemobartonellosis) is also known as feline infectious anemia. At present, three species of Mycoplasma organisms have been identified: Mycoplasma haemofelis, Candidatus Mycoplasma haemominutum, and the recently named Candidatus Mycoplasma turicensis. (The term Candidatus is used because there is not currently enough information to give them an official scientific name.) Haemoplasma spp. were previously grouped together in the genera Hemobartonella and Eperythrozoon but have now been moved to the genus Mycoplasma. The prefix hemo denotes its affinity for erythrocytes. These species differ in pathogenicity with M. haemofelis recognized as the most pathogenic of the known species. Following Haemoplasma spp. attachment to the surface of red blood cells (RBCs), the immune system targets the parasitized cells. The immune stimulus is likely derived from a combination of parasite adherence exposing previously hidden RBC antigens, parasitic alteration of normal RBC antigens, and in some cases, stimulation of antibody-mediated complement fixation. Erythrocytes targeted for removal are fragile and have a shortened life span compared to normal erythrocytes. They are removed from circulation primarily through phagocytosis in the spleen, liver, lungs, and bone marrow, with lesser contributions by splenic sequestration and intravascular hemolysis of cells. It is believed that there is no breed or sex predilection for this disease; however, males seem to be overrepresented in the affected populations, presumably due to lifestyle differences. The typical presentation caused by the pathogenic M. haemofelis is an overt, acute life-threatening anemia. Candidatus M. haemominutum may not be significantly pathogenic without the presence of a retroviral co-infection and may act as a cofactor in the progression of retroviral, neoplastic, and immune-mediated diseases. Candidatus M. turicensis is a recent discovery, and its significance remains unclear, although current evidence suggests that it most often appears as a co-infection with other species. Clinical signs depend upon the stage of disease, the rapidity with which anemia develops, and the Haemoplasma species involved. Cats acutely infected with M. haemofelis may be presented for rapidly progressive signs of only a few days duration. Physical examination may reveal weakness and dehydration, pale mucous membranes (which are occasionally icteric), normal to increased body temperature, tachypnea, and palpable splenic enlargement. Moribund animals are usually hypothermic. Severely affected cats may die within a few days. In other cases, a more chronic course may be suggested by weight loss and mild anemia in a relatively bright, alert patient. The mode of transmission is not fully understood but is suspected to occur via blood-sucking arthropod vectors such as fleas, although this has not been conclusively proven. The organism is effectively transmitted in transfused blood. Also, queens have been known to pass the infection to newborns kittens, but the mechanism of transmission has not been determined.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
218
Diagnosis Primary Diagnostics • History: A bite wound or similarly stressful event is commonly reported in the history of affected cats. • Complete Blood Count (CBC): The packed cell volume (PCV), RBC count, and hemoglobin are variably decreased (anemia). It is usually classified as a severe anemia with a PCV less than 15%. A marked bone marrow response is evidenced by polychromasia (reticulocytosis), anisocytosis, and Howell-Jolly bodies. M. haemofelis and Candidatus M. haemominutum are present on RBCs and appear as small, blue-staining cocci, rings, or rods on the cell surface. See Figure 92-1. • Reticulocyte Count: Aggregate reticulocytes are substantially increased unless the count is performed immediately after a precipitous fall in the hematocrit or if a bone marrow-suppressing disease is concurrent. It takes 4 to 6 days for the reticulocyte count to increase following RBC destruction. Only aggregate reticulocytes should be counted; punctuate reticulocytes should be ignored. See Figures 9-1 and 9-2. • Some laboratories offer a polymerase chain reaction (PCR) test for M. haemofelis, Candidatus M. haemominutum, and Candidatus M. turicensis, which is more sensitive than observing the organisms on a stained blood smear.
Secondary Diagnostics • Coombs’ Test: This test identifies antibodies or complement on RBCs and is usually positive with hemoplasmosis. However, this test is neither specific nor sensitive for immune-mediated hemolytic anemia. Autoimmune (primary) hemolytic anemia is rare in cats; thus, a positive Coombs’ test in a cat with a regenerative anemia is more likely secondary to hemoplasmosis or another disease, which can alter RBC surface antigens (e.g., feline leukemia virus [FeLV]
Figure 92-1 This photomicrograph shows the organisms on the erythrocytes (arrows) and strong evidence of a regenerative anemia (i.e., nucleated red blood cells, macrocyte, and polychromasia). Both are required for a confirmed diagnosis of hemoplasmosis.
Hemoplasmosis
infection, lymphoma). Some drugs, such as methimazole and propylthiouracil, can also cause positive Coombs’ tests. • Retroviral Testing: All cats with suspected or confirmed hemoplasmosis should be tested for retroviral infection. In the 1980s, it was reported that about half of all cats with clinical hemoplasmosis were FeLV positive; the number is likely considerably lower now that the FeLV is better controlled with testing and vaccination. Although FeLV is known to suppress immunity and predispose cats to a variety of infectious diseases, the reverse may also be true. Experimental studies have shown that hemoplasmosis may predispose cats to FeLV infection. A recent study reported a significant association between FeLV and feline immunodeficiency virus (FIV) and infection with M. haemofelis. • Chemistry Profile: The values are usually normal; occasionally, total bilirubin is elevated due to hemolysis, but this is an inconsistent finding.
Diagnostic Notes • Haemoplasma spp. may detach from the surface of RBCs when blood is stored in ethylenediamine tetraacetic acid (EDTA). Smears should be prepared immediately after blood is drawn. • Precipitated bloodstain may be confused with M. haemofelis and Candidatus M. haemominutum. New methylene blue stain (used to count reticulocytes) should not be used to identify M. haemofelis and Candidatus M. haemominutum because the organisms cannot be distinguished from precipitated ribosomal material. • The presence of M. haemofelis and Candidatus M. haemominutum on RBCs is cyclic. Their presence, coupled with a regenerative anemia, is justification for a diagnosis of hemoplasmosis. Their presence in a nonanemic cat is probably incidental because they are often found in a nonpathogenic state. Their presence alone is not justification for a diagnosis of clinical hemoplasmosis. The absence of M. haemofelis and Candidatus M. haemominutum in a cat with a regenerative anemia is not justification for dismissing this disease as a possibility; subsequent blood samples should be examined. It is probably the most common causes of regenerative anemia in cats. • The presence of M. haemofelis or Candidatus M. haemominutum in a cat with a nonregenerative anemia can be confusing. These organisms result in RBC destruction but not bone marrow suppression. When a nonregenerative anemia exists, a cause of bone marrow disease should be sought; bone marrow aspiration or biopsy is indicated, as well as an FeLV test. However, it should be remembered that a potentially regenerative anemia may be present because it takes the bone marrow a few days to respond following a precipitous drop in the RBC count.
Treatment Primary Therapeutics • Whole Blood Transfusion: Transfusion of typed, cross-matched blood should be employed for cats with PCVs less than 15%. Transfused blood cells are also subject to parasitism. See Chapter 295.
• Doxycycline: Give 5 mg/kg q12h PO or 10 mg/kg q24h PO for 21 to 28 days. Doxycycline tablets should be followed with 5 to 6 mL of water to assure that the tablet reaches the stomach. • Enrofloxacin: This is an effective, alternative therapy to doxycycline. Give 5 mg/kg q24h PO for 21 to 28 days. • Prednisolone: 1 to 2 mg/kg q12h PO may be given to reduce erythrophagocytosis, stimulate the bone marrow, and increase appetite. • Nutritional Support: Following blood transfusion, the cat should be supported nutritionally via orogastric or nasogastric tube feeding until its appetite returns. See Chapter 308. If anorexia persists for more than a few days, consider placing an esophagostomy tube. See Chapter 253.
Therapeutic Notes • The PCV of treated cats should be rechecked every 24 to 48 hours. A steady increase is expected from successful treatment. • Doxycycline induces fever and esophageal stricture in a few cats. • In one study, azithromycin at 15 mg/kg q12h PO for 7 days was not effective in treating this disease. • One cannot rely on antimicrobial therapy to clear the cat of the organism. A carrier state generally exists following clinical recovery from disease, although relapse seldom occurs. • Pradofloxacin has been shown to clear the carrier state, but this drug is not available in the United States, Europe, or Australia.
Prognosis The prognosis of hemoplasmosis is generally good if the anemic crisis can be quickly averted, but some cats die due to severe anemia. The carrier state that often occurs leaves the cat susceptible to recurrence. This cat should not be used as a blood donor, but otherwise it is considered noncontagious to other cats, even in the carrier state.
Suggested Readings Dowers KL, Tasker S, Radecki SV, et al. 2009. Use of pradofloxacin to treat experimentally induced Mycoplasma haemofelis infection in cats. Am J Vet Res. 70(1):105–111. Harvey JW. 2006. Hemotrophic Mycoplasmosis (Hemobartonellosis). In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 252–260. Philadelphia: Saunders Elsevier. Peters IR, Helps CR, Willi B, et al. 2008. The prevalence of three species of feline haemoplasmas in samples submitted to a diagnostic service as determined by three novel real-time duplex PCR assays. Vet Micro. 126(1–3):142–150. Sykes JE, Terry JC, Lindsay LL, et al. 2008. Prevalence of various hemoplasma species among cats in the United States with possible hemoplasmosis. J Am Vet Med Assoc. 232(3):372–379. Willi B, Boretti FS, Tasker S, et al. 2008: From Haemobartonella to hemoplasma: Molecular methods provide new insights. Vet Micro. 125(3–4): 197–209.
219
CHAPTER 93
Hepatic Lipidosis Gary D. Norsworthy
Overview Hepatic lipidosis (HL), also called fatty liver syndrome, is the most common liver disorder of cats. It is a potentially lethal intrahepatic cholestatic disease characterized by an accumulation of triglycerides or neutral lipid within more than 80% of hepatocytes. It is associated with anorexia of 7 or more days and catabolism; obesity is a predisposing factor. However, the pathogenesis of this disease is not well understood and is likely multifactoral. It has been considered a primary, idiopathic disease in many cats, but aggressive history taking and diagnostics almost always reveal a circumstance or another disease that initiates the anorectic state. The most commonly reported primary diseases are cholangiohepatitis, biliary obstruction and inflammation, intrahepatic or extrahepatic neoplasia, inflammatory bowel disease, pancreatitis, and diabetes mellitus. Circumstances causing anorexia include being separated from the owner (e.g., boarding), harassment by another pet in the household, especially a new puppy or a more dominant cat, and diet change. The most common clinical signs are anorexia, weight loss, icterus, and vomiting. Rarely, signs of hepatic encephalopathy are seen.
Diagnosis Primary Diagnostics • History and Clinical Signs: An icteric, obese cat that has been anorectic for at least 1 week should be suspected of having hepatic lipidosis. • Chemistry Profile: The most consistent biochemical finding is a 2- to 5-fold increase in alkaline phosphatase accompanied by a normal or minimally increased γ-glutamyltransferase (GGT or GGTP). Hypoalbuminemia is present in over 60% of cats with HL. • Cytopathology or Histopathology: Confirmation requires a study of hepatic tissue. Cytosolic vacuolation with empty fat vacuoles will be seen in over 80% of hepatocytes. See Chapter 284. Hepatic cells or tissue may be collected by fine-needle aspirate, fine needle biopsy, cone needle biopsy, or wedge biopsy. Ultrasound guided fine-needle aspiration or fine needle biopsy is preferred due to the minimal invasiveness of the procedure and because this disease is easily diagnosed with the samples obtained in these manners. Laparotomy for biopsy is strongly discouraged during the first few days of treatment in cats with severe disease as the intraoperative or postoperative mortality rate is very high.
Secondary Diagnostics • Complete Blood Count (CBC) and Chemistry Profile: Other common biochemical findings include increased serum alanine aminotransferase (ALT), aspartate transaminase (AST), fasting and postprandial bile acids and bilirubin, bilirubinuria, and a mild nonregenerative anemia. • Serum Cobalamin: Low cobalamin (Vitamin B12) is often present with inflammatory bowel diseases and pancreatitis. These contribute to the pathogenesis of HL. Testing prior to treating with Vitamin B12
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
220
will allow one to determine whether short-term (a few days) or longterm (a few weeks) therapy is needed. See Chapter 37 for treatment protocol. • Radiography: Radiographs may reveal hepatomegaly, but this is an inconsistent and non-specific finding. • Ultrasound: Ultrasound may reveal a diffusely hyperechoic liver.
Treatment Primary Therapeutics: Phase I—Stabilization (2–7 days) This is the hospitalization phase. The more critical the patient, the longer it lasts. It is important not to stress the cat with diagnostics, such as a laparotomy, or the cat may not survive. Some cats are so stable that anesthesia for liver biopsy and feeding tube placement can occur on the first day of hospitalization. Others require several days of therapy first. • Fluids: Rehydrate with intravenous (or subcutaneous) fluids using a polyionic crystalloid fluid. It has been recommended to avoid lactatecontaining fluids because lactate metabolism is impaired in severe HL. However, clinical experience shows that lactated Ringer ’s solution, Ringer ’s solution, or normal saline are good choices. Avoid glucose containing fluids. • Potassium: Add 20 to 40 mEq to each liter of fluids, but do not exceed administration of 0.5 mEq/kg per hour if given IV or a concentration of 35 mEq of potassium chloride per liter of fluids if given AQ. Alternatively oral potassium may also be given (2–4 mEq/day). Monitor serum for hyperkalemia or hypokalemia, and adjust potassium administration accordingly. • Vomiting: Vomiting must be controlled for a successful outcome. Uncontrollable vomiting results in a poor prognosis. Options include: (a) Metoclopramide (0.01–0.02 mg/kg per hour by constant rate infusion or 0.2–0.5 mg/kg q8–12 h), (b) ondansetron (0.5–1.0 mg/kg SC, IM q6–12 h), (c) maropitant (Cerenia®, Pfizer; 1 mg/kg q24h SC) Cerenia is approved for dogs but is in widespread use in cats. Feeding small quantities of food frequently is essential initially as cats with HL may have a gastric capacity of only 10% of normal; overfeeding is easily done and causes vomiting. Trickle feeding using a liquid diet (CliniCare, Abbott Laboratories, Abbott Park, IL) through a nasoesophageal tube may be successful for a few days until an esophagostomy or gastrostomy tube can be safely placed. • Nutritional Support: Administer a balanced diet via syringe or orogastric tube beginning with 10 to 15 mL q4 to 8 h and adding 5 to 10 mL to each feeding on each subsequent day until 50 to 65 mL q6 to 8 h is given. The goal is 60 to 90 kcal/kg ideal weight per day. Maximum Calorie™ (The Iams Company, Dayton, OH) is an excellent diet for cats with hepatic lipidosis due to its overall nutrient balance and high protein and caloric density. • Antibiotics: Amoxicillin (10 mg/kg q12h PO) or metronidazole (10–15 mg/kg q12h PO) should be given because suppurative cholangiohepatitis is often a concurrent problem, and these drugs will concentrate in the bile. • S-adenosylmethionine (SAMe): This drug improves hepatocyte function and shortens recovery period. It should be given until the cat’s appetite returns (90 mg q12–24h PO). • Milk Thistle: Silybin is the most biologically active component of an extract from the milk thistle plant known as silymarin. Silymarin/
Hepatic Lipidosis
silybin has been shown to have beneficial effects on liver function. Denamarin™ (Nutramax Laboratories, Edgewood, MD) is a combination of SAMe and silybin. • Vitamin K1: Decreased bile flow and lack of dietary fat caused by anorexia impair intestinal absorption of vitamin K. Give 0.5 to 1.5 mg/kg q12h SC or IM for two doses prior to liver biopsy, then give 0.5 to 1.5 mg/cat SC q24h as needed. • Vitamin B12 (Cobalamin): In addition to being an appetite stimulant, cobalamin administration can stimulate methylation reactions and endogenous SAMe production. If the serum cobalamin level at presentation is normal, give Vitamin B12 (250 µg/cat q24h SC or IM) for 3 to 5 days. If it is subnormal, give it for several weeks at 250 µg/cat q3 to 4 d SC. See Chapter 37 for details. • Other B Vitamins: The liver is an important organ for storage and activation of many water-soluble vitamins. It is recommended that 2 mL of a fortified B-complex solution be added to each liter of fluids administered to the cat with HL. Fluids containing B vitamins should be protected from direct light.
Secondary Therapeutics: Phase I—Stabilization (2–7 days) • It has been speculated that cats recover faster if supplemented with L-carnitine (250–500 mg/cat q24h PO) and arginine (250 mg/cat q24h PO). However, convincing evidence is lacking. • Phosphate: Cats may be hypophosphatemic initially, or it may develop due to the refeeding phenomenon. See Chapter 188. Hypophosphatemia may lead to life-threatening hemolysis and respiratory failure. If serum phosphorus is less than 0.64 mmol/L (2.0 mg/dL), treat with potassium phosphate or sodium phosphate at an initial dose of 0.01 to 0.03 mmol/kg per hour IV. Recheck serum phosphate every 3 to 6 hours and when the cat undergoes refeeding. Discontinue phosphate supplementation when serum phosphorus is greater than 0.64 mmol/L (2.0 mg/dL). Watch for hyperkalemia if potassium phosphate is used.
Primary Therapeutics: Phase II—Long-Term Care (4–8 weeks) • Definition: This phase is from the time the feeding tube is placed until the cat’s appetite returns. • Food: Feed a balanced diet with the same nutritional goals as above. Feed in small quantities three to six times per day if the client’s schedule permits. An indwelling feeding tube, such as an esophagostomy tube or a gastrostomy tube, is needed. See Chapters 253 and 255. • Antibiotics: Continue antibiotics for the balance of 2 weeks. • Liver Support: Continue SAMe and Marin until the appetite returns.
Therapeutic Notes • The goal of nutritional support is 60 to 90 kcal/kg ideal weight and 3 to 4 g/kg ideal weight of protein per day supplied by a balanced feline diet.
• It is essential not to restrict protein as adequate protein is needed to form lipoproteins necessary for transporting triglycerides out of the liver. Hepatic encephalopathy is rare. • Do not substitute DL-carnitine for L-carnitine. The former is potentially toxic to cats. • The end point of treatment is reached when the cat returns to normal eating. Do not remove the feeding tube until the cat has been eating well for 2 to 3 days. The average recovery period is 6 weeks, but some cats may require 3 to 4 months of treatment before the appetite returns. • The author has observed several cats that pulled out their esophagostomy tubes when they were ready to eat. If this occurs, do not replace the tube for 1 to 2 days to see if the cat will eat. • Appetite stimulants such as diazepam, clonazepam, oxazepam, mirtazapine, and cyproheptadine are not indicated and may be hepatotoxic because they may require hepatic biotransformation, and their appetite stimulating effects typically do not produce adequate food intake in the presence of HL. • Also Avoid: The contraindication list includes barbiturates, stanozolol, glucocorticoids, tetracyclines, etomidate, onion powder flavoring, and foods and treats with propylene glycol. • Ursodeoxycholic acid is probably not beneficial for cats with HL and may promote taurine deficiency.
Prognosis The survival rate is high if the aforementioned protocol is aggressively followed, if the underlying disease or factor initiating anorexia is treated successfully or removed, if vomiting can be controlled, and if the owner is persistent. Almost all deaths occur during Phase I. Increased survival occurs if stress can be minimized during that time. This can be achieved if the diagnosis is made by fine-needle aspiration or biopsy, the cat is fed with a syringe or an orogastric tube until it is stable, and anesthesia for feeding tube placement is delayed until the cat is stable. Total bilirubin concentrations usually decline by 50% during the first 7 to 10 days of treatment in cats that survive. Recurrence is possible if prolonged anorexia recurs, but this seldom happens. This disease does not result in chronic liver dysfunction.
Suggested Readings Armstrong PJ, Blanchard G. 2009. Hepatic lipidosis in cats. Vet Clin North Am Small Anim Pract. 39(5):599–616. Center SA. 2005. Feline hepatic lipidosis. Vet Clin North Am Small Anim Pract. 35(1):225–269. Center SA. 2007. Hepatic lipidosis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 598–599. Ames, IA: Blackwell Publishing. Griffin B. Feline hepatic lipidosis. 2000. Treatment and recommendations. Compend Contin Educ. 22:910–922.
221
CHAPTER 94
Hepatitis, Inflammatory Sharon Fooshee Grace
Overview Inflammatory disease represents the second most common category of feline liver diseases after hepatic lipidosis. Lack of consensus among pathologists regarding nomenclature and classification groups for feline inflammatory liver disease has led to a simplified scheme consisting of two distinct histopathologic types: cholangitis/cholangiohepatitis complex (CCH) and lymphocytic portal hepatitis (LPH). Cholangiohepatitis refers to inflammatory disorders targeted toward the bile ducts (cholangitis) and hepatic parenchyma; it is divided into acute (suppurative) and chronic (nonsuppurative) forms. Some reports suggest a predisposition for both forms of CCH in male cats, with young cats more prone to the acute form and middle-aged adults having the chronic form. Many cats with cholangiohepatitis have concurrent inflammatory bowel disease or pancreatitis, collectively known as Triad Disease. See Chapter 216. The acute form of cholangiohepatitis is characterized by neutrophilic infiltration of bile duct lumens and walls and areas around the portal triad with invasion into the parenchyma. Ascension of enteric bacteria from the intestine (most commonly Escherichia coli) or hematogenous spread of bacteria may be the initiating factor in some cases; recent work has also addressed the potential role of Helicobacter. The acute form is characterized by a short course of illness (about 1 week), lethargy, vomiting, fever, icterus, and sometimes abdominal pain. The liver is normal to enlarged. The chronic form of cholangiohepatitis demonstrates mixed infiltrates of neutrophils, lymphocytes, and plasma cells with chronic changes in the bile ducts. This form may terminally progress to cirrhosis. The cause is unknown; some speculate that it is a continuation of the acute form whereas others propose a progressive immune-mediated etiology. Infectious and parasitic causes are responsible in some cases. The duration of illness is usually longer than the acute form (2 or more weeks) and may be long term; icterus and hepatomegaly are often found, though the cat may appear to feel relatively well. Fever is uncommon as compared to the acute form. Ascites is rare in both acute and chronic CCH. Lymphocytic portal hepatitis is an inflammatory disorder that targets the area around the portal triad. It is histopathologically distinct from CCH with portal infiltrates of plasma cells and lymphocytes but not neutrophils. Bile duct proliferation and portal fibrosis are often present. Cholangitis is not present and the hepatic lobules remain intact. An immune-mediated cause is proposed. Anorexia, weight loss, and hepatomegaly are common, although the severity of illness is usually less than that with CCH. Fever is rare.
observation of the sclerae or soft palate. Clinical signs may closely mirror those seen with hepatic lipidosis. • Complete Blood Count, Biochemical Profile, Urinalysis, and Retroviruses: The minimum data base cannot help distinguish CCH from LPH. Acute CCH is typified by neutrophilia (sometimes with a left shift), normal or mildly increased alkaline phosphatase (ALP), moderate to markedly increased alanine aminotransferase (ALT), and moderate to marked increase in total bilirubin. A left shift is uncommon with chronic CCH and liver enzymes are moderately increased; bilirubin is moderately increased. Poikilocytosis is often present with LPH; liver enzymes and bilirubin are only mildly affected. Most cats with CCH or LPH are retrovirus negative. • Abdominal Ultrasound: This is a useful tool for assessing the size and architecture of the liver parenchyma, biliary system, and pancreas. Ultrasound can differentiate focal from diffuse hepatic disease and may detect concurrent pancreatitis. Liver echogenicity is usually normal, although gall bladder and bile duct abnormalities can be observed. Typical findings include distention and partial or complete obstruction of the common bile duct, gall bladder, or intrahepatic bile ducts, along with bile sludging (see Figures 94-1 and 94-2). Ultrasound is the most sensitive and specific tool available for detecting the choleliths. The gall bladder is normally enlarged with anorexia. • Liver Biopsy, Histopathology, and Culture: Biopsy is essential for distinguishing the two main categories of inflammatory diseases. Biopsy will provide details about hepatic architecture and disease severity. A platelet count and coagulation test should be performed prior to biopsy. Percutaneous liver biopsy is acceptable for obtaining tissue so long as there is no ultrasound evidence of biliary obstruction or cholelithiasis; if ultrasound indicates that there is significant potential to rupture the common bile duct or a fragile gall bladder, surgical biopsy via laparotomy would be indicated. Aspiration cytology is not recommended for diagnosis of inflammatory liver disease, although it is a useful tool for detection of hepatic lipidosis and
Diagnosis Primary Diagnostics • Clinical Signs: Clinically CCH and LPH may appear similar with nonspecific signs of fever, anorexia, weight loss, and vomiting. All cats with jaundice or hepatomegaly should be suspected of having inflammatory liver disease. Jaundice is most easily detected with
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
222
Figure 94-1 Increased echogenicity of the gall bladder walls often correlates with chronic cholangitis/cholangiohepatitis complex. Image courtesy Dr. Gary D. Norsworthy.
Hepatitis, Inflammatory
is normal, a T3 suppression test or free T4 by dialysis should be considered. See Chapter 109.
Diagnostic Notes • The minimum data base should include retrovirus testing. Where appropriate, the cat should also be screened for toxoplasmosis (see Chapter 214) and feline infectious peritonitis (see Chapter 76) because these are associated with inflammatory liver disease and pancreatitis. • All cats with suspected liver disease should be evaluated at venipuncture sites after blood collection. Coagulation tests are not routinely predictive of bleeding potential, but a clinical clue may be provided by cutaneous hemorrhage or prolonged bleeding after venipuncture. Clinical bleeding in cats with liver disease is uncommonly due to overt hepatic failure. It more likely results from vitamin K deficiency caused by impaired bile acid efflux into the intestine (necessary for absorption of fat-soluble vitamins), anorexia, and impaired intestinal absorption due to concurrent inflammatory bowel disease. Figure 94-2 The presence of sludged bile in the gall bladder (arrow) often correlates with chronic cholangitis/cholangiohepatitis complex. Image courtesy Dr. Gary D. Norsworthy.
Treatment Primary Therapeutics
lymphoma. Cytology is superior to histopathology in demonstrating bacterial organisms in the liver. Liver biopsy samples should be submitted for aerobic and anaerobic culture.
Secondary Diagnostics • Serum Fasting and Postprandial Bile Acids: Bile acid determination is of no value if the cat is already hyperbilirubinemic, has elevated liver enzymes, or is visibly icteric because bile acid increases only further affirm the presence of liver disease and are not disease specific. • Coagulation Profile: A coagulation profile and platelet count should be performed prior to liver biopsy, although these are usually unnecessary for fine-needle aspiration (FNA) or fine needle biopsy (FNB). In one study, 75% of cats with liver disease had at least one coagulation abnormality. An activated clotting time (ACT) may be performed in-house. Prothrombin time (PT) and activated partial thromboplastin time (APTT) can also be performed in-house or sent to an outside lab. An alternative test with potentially increased sensitivity compared to routine PT and PTT is proteins invoked by vitamin K absence (PIVKA) prothrombin time. Automated platelet counts are highly inaccurate in cats, but a platelet estimate by blood smear evaluation may be performed if there is minimal platelet clumping on the blood smear. • Radiography: Liver size is variable although in most cases of CCH or LPH, the liver is enlarged and extends beyond the costal arch. The caudal edges of the liver may have a rounded appearance. Radiographs are more specific for assessing liver size than ultrasound. Radiographs may also reveal evidence of choleliths or unrelated concurrent disease. • Bile Culture: If surgical exploration of the abdomen and liver biopsy are indicated, a sample of bile should be obtained and submitted for aerobic and anaerobic culture. Bacterial yield is higher from bile than from liver tissue. Alternatively, bile may be aspirated using a 22- or 25-gauge needle using ultrasound guidance. To minimize bile leakage and bile peritonitis, the gall bladder should be emptied of bile by aspiration when the sample is taken. • Total T4: In older cats, hyperthyroidism is a common cause of elevated liver enzymes. A total T4 (TT4) should be submitted if the patient is geriatric. If the thyroid gland is palpably enlarged and TT4
Acute Cholangiohepatitis • Antimicrobial Therapy: Antibiotics are the cornerstone of therapy and should be administered for 8 to 12 weeks or until liver enzymes normalize. Therapy should be based on culture results from bile, liver aspirate, or a biopsy. Preferred drugs are non-hepatotoxic, concentrate in bile, and are effective against aerobic and anaerobic intestinal organisms. Monotherapy with a single broad-spectrum drug or a combination of antibiotics may be employed. Good choices for single agent therapy are ampicillin (10–20 mg/kg q6–8h IV or IM) or amoxicillin/clavulanate (22 mg/kg q12h PO); however, amoxicillin/clavulanate is not a good choice if vomiting is part of the clinical picture. Either of these may be combined with metronidazole (7.5–12.5 mg/ kg q12h PO) to extend the spectrum against anaerobes and coliforms. Combined therapies may include enrofloxacin (2.2 mg/kg q12h PO) and amoxicillin (11 mg/kg q12h PO) or amoxicillin and metronidazole (7.5–12.5 mg/kg q12h PO). All of these are good choices when culture and sensitivity results are not yet available. • Ursodeoxycholic Acid: This bile acid has proven helpful for decreasing immune injury to hepatocytes, promoting synthesis of less toxic bile acids, and improving bile flow. It should not be used as a sole therapy. Additionally, there are no published studies on its use in cats, though it is widely used. It is administered at 10 to 15 mg/kg q24h PO. Note that ursodeoxycholic acid is contraindicated with biliary obstruction. Some specialists recommend taurine supplementation (250–500 mg q24h PO) for cats receiving ursodeoxycholic acid because high bile acid concentrations can increase urinary loss of taurine. • S-adenosylmethionine (SAMe; Denosyl®, Nutramax Laboratories) or SAMe and silybin (Denamarin®, Nutramax Laboratories): These nutraceutical agents have marked anti-inflammatory and antioxidant properties that can be of benefit to cats with all forms of inflammatory liver disease. These medications are best absorbed in the fasted state and should be given one hour before feeding.
Chronic Cholangiohepatitis • Antimicrobial Therapy: Antibiotics should be administered for 4 to 6 weeks. See Acute Cholangiohepatitis therapy for suggested antimicrobials.
223
SECTION 1: Diseases and Conditions
• Glucocorticoids: These should be added to the aforementioned therapies when chronic CCH has been proven by biopsy or if proven acute CCH has lasted more than several months. An immunosuppressive dose of prednisolone is initiated (2.2–4.4 mg/kg q24h PO) then decreased to alternate-day therapy for long-term maintenance. Because this is a chronic disease, continuous use of corticosteroids is needed in many cats. • Ursodeoxycholic Acid: See Acute Cholangiohepatitis. • SAMe or SAMe/silybin: See Acute Cholangiohepatitis.
Lymphocytic Portal Hepatitis • Prednisolone: This should be administered at 2.2 mg/kg q24h PO. Therapy may be tapered over weeks based on improvement in clinical signs and laboratory values. Cats who fail to improve on prednisolone may benefit from low-dose weekly pulse therapy with methotrexate, with consideration given to drug toxicity. • Ursodeoxycholic Acid: See Acute Cholangiohepatitis. • SAMe: See Acute Cholangiohepatitis.
Secondary Therapeutics • Fluids: For all types of inflammatory liver disease, attention should be given to fluid and electrolyte balance. Good hydration status encourages bile flow. Nonlactated, nonglucose fluids should be given. • B-Soluble Vitamins: These may be supplemented at 5 to 10 mg/kg q24h SC or IM. • Nutrition: Cats that continue to eat should be fed a palatable maintenance diet. Cats in need of nutritional support can have a feeding tube placed while under anesthesia for liver biopsy, a procedure which has the additional advantage of enhanced owner compliance because most medications can be administered through the tube (see Chapters 253 and 255). • Vitamin K1: This may be indicated due to malabsorption of fatsoluble vitamins. Injections of 5 mg/cat IM or 0.5 mg/kg per day SC should be given every 1 to 2 days if bleeding occurs and may be beneficial if liver biopsy is anticipated. Three or four consecutive doses are usually adequate. Overdosing vitamin K1 may cause Heinz body hemolytic anemia.
224
Therapeutic Notes • Antibiotics that are best avoided include tetracycline (hepatotoxic), chloramphenicol (causes anorexia), and erythromycin (inappropriate bacterial spectrum). • Metronidazole is dependent on biliary excretion; in some cats, the dose may need to be decreased. The maximum dose is 50 mg total every 24 hours. • Hepatic encephalopathy is uncommon but may be medically managed with oral lactulose, neomycin, and dietary modification. Cats without hepatic encephalopathy should remain on a normal diet. Ptyalism is noteworthy as a sign of hepatic encephalopathy in cats but not dogs. • Cats that fail to respond to prednisolone therapy alone (chronic CCH or LPH) may require immunosuppressive therapy. Chlorambucil may be used in addition to LPH but is myelosuppressive. Low-dose intermittent methotrexate is an alternative drug but it, too, causes myelosuppression. Azathioprine has been associated with significant anorexia.
Prognosis Although prognosis is variable and depends on the severity of disease and response to therapy, the majority of cats with inflammatory liver disease survive greater than 1 year. LPH tends to be more slowly progressive than CCH.
Suggested Readings Center SA. 2009. Diseases of the gallbladder and biliary tree. Vet Clin North Amer. 39(3):543–598. Center SA, Warner K, Corbett J, et al. 2000. Proteins invoked by vitamin K absence and clotting times in clinically ill cats. J Vet Intern Med. 14(3):292–297. Sartor LL, Trepanier LA. 2003. Rational pharmacologic therapy of hepatobiliary disease in dogs and cats. Compend Contin Educ. 25(6):432–446. Weiss DJ, Gagne JM, Armstrong PJ. 2001. Inflammatory liver diseases in cats. Compend Contin Educ. 23(4):364–373.
CHAPTER 95
Herpesvirus Infection Sharon Fooshee Grace
Overview Feline herpesvirus-1 (FHV-1) and feline calicivirus (FCV, see Chapter 28) are responsible for most cases of infectious upper respiratory disease in cats and kittens. These viruses are especially problematic in stressful, population-dense settings, such as shelters, boarding facilities, catteries, and multicat households. All ages of cats are susceptible to FHV-1, although it is particularly virulent for young kittens. Therefore, early conferral of vaccine-induced immunity is important. As protective maternal antibodies begin to decline by 7 to 9 weeks of age, kittens have the opportunity for viral exposure and successful infection before immunizations are started. Additionally, residual maternal immunity may interfere with early vaccination efforts. Most cats that become infected with FHV-1 and recover will remain infected for life because the virus becomes latent in neural tissue, especially the trigeminal ganglia. A lifelong course of relapsing disease interposed with periods of viral quiescence is the hallmark of FHV-1. Shedding may be reactivated during periods of stress, illness, or immunosuppressive therapy. Parturition and lactation may reactivate the virus in latently infected queens with subsequent infection of the kittens. During periods of active viremia, FHV-1 does not stimulate significant immunity in the host because it is an obligate intracellular virus, which travels from cell to cell. The virus is transmitted to naïve cats primarily by direct contact with ocular, nasal, or oral secretions of infected cats. Aerosolization of virus by sneezing does occur but is not an important means of transmission. Respiratory droplets are not spread more than 2 m (approximately 6 feet) in distance and, as a fragile enveloped virus, FVH-1 is short-lived outside the cat. Thus, residual virus in the environment is not a significant source of infection for unprotected cats, except perhaps in the cattery setting. Transplacental transmission has not been demonstrated. Initial viral replication occurs in the mucosa of the upper respiratory tract, conjunctiva, and tonsils. The average incubation period for susceptible cats is 2 to 6 days. Shedding begins early in the infection and typically persists for a period of 1 to 3 weeks before becoming inactive. Two major groups of clinical signs are seen with FHV-1 infection: signs related to acute infection and signs caused by chronic infection. Acute viral replication in respiratory and conjunctival epithelium causes necrosis with neutrophilic infiltration and inflammation; the term rhinotracheitis has been incorrectly used for this disease because the trachea is not involved. The cornea and skin may also be affected. Disorders associated with chronic infection may have an immune-mediated component and are most often associated with ocular disorders; overt respiratory disease is usually not evident. Corneal sequestra, stromal keratitis, eosinophilic keratitis, and anterior uveitis have been linked to FHV-1 infection. When virus is reactivated in a latently infected cat, especially
Figure 95-1 Severe keratoconjunctivitis may be caused by the feline herpesvirus-1 and result in permanent damage to the eyes. Photo courtesy Dr. Richard Malik.
a mature cat, there may be no observed clinical signs. See Figures 41-1 and 95-1. Ocular complications of chronic FHV-1 are discussed in Chapter 41. Nonspecific signs of acute FHV-1 infection include fever, depression, and anorexia. Ulcerative rhinitis results in an initially serous nasal discharge that becomes mucopurulent after secondary bacterial infection is established. The sinuses often become secondarily involved. Acute viral-mediated cytolysis may severely damage the nasal turbinate bones and underlying cartilage, leading to chronic rhinosinusitis or “snuffling.” Conjunctivitis, blepharospasm, photophobia, and ocular discharge are frequently observed, along with geographic or dendritic ulcers if viral replication occurs in the cornea. Oral ulceration may be severe, leading to anorexia, oral pain, and ptyalism. Interstitial pneumonia develops occasionally. Death typically results from anorexia, dehydration, and secondary bacterial infection. Unusual signs caused by FHV-1 include abortion and an eosinophilic ulcerative facial dermatosis, which is being recognized with increasing frequency. The facial dermatosis is usually situated close to the nares or the eyes. See Chapter 226. FHV-1 is not zoonotic; there is no evidence of human infection with FHV-1.
Diagnosis Primary Diagnostics
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• History and Clinical Signs: Although there are several causes of sneezing in cats, sneezing that persists over 48 hours is highly suggestive of a viral upper respiratory infection, especially if the cat is unvaccinated and has any of the aforementioned signs.
225
SECTION 1: Diseases and Conditions
Secondary Diagnostics
Secondary Therapeutics
• Retroviral Testing: The retrovirus status of all cats, healthy or sick, should be known. Retroviral infections can complicate recovery from viral respiratory disease. • Viral Isolation: Veterinary reference laboratories can isolate and identify FHV-1 in cell culture from oropharyngeal or conjunctival swabs. This test is rarely used because it is time consuming, and there is no test standardization between different laboratories. • Polymerase Chain Reaction (PCR) Testing: Molecular methods can detect the presence of FHV-1 DNA in corneal or conjunctival scrapings, corneal sequestra, blood, and tissues. These tests are known to be more sensitive than viral isolation and are considered the preferred method for virus detection. However, because they are so sensitive, they may detect viral DNA, which is not associated with active disease. Also, a recent study indicated that PCR detects viral DNA in modified-live virus vaccines, although it remains unclear whether vaccinal strains are detected in recently vaccinated animals. Therefore, a positive PCR test could potentially indicate low level shedding, viral latency, vaccination, or viral particles that are unrelated to an existing clinical problem. Recent work has also demonstrated considerable variation among testing laboratories, resulting in different test results from the same patient.
• Antiviral Therapy: Historically, systemic antiviral therapy has been associated with minimal efficacy and significant side effects. Recently, famciclovir was introduced as a systemic antiviral drug for human use. It holds promise for cats with either acute or chronic FHV-1-related disease, but further study is needed. Positive ocular responses to famciclovir have included reduced conjunctival inflammation, improved ocular comfort, and detachment of corneal sequestra. Many cats with chronic rhinosinusitis (“snufflers”), which have been refractory to antibiotic therapy, have also shown improvement in early reports. However, antiviral therapy should not replace antibiotics when secondary bacterial infection is present. A number of cats with FHV-1 dermatitis have also shown improvement with famciclovir. The drug is expensive even in generic forms. The potential for teratogenicity of the drug is unknown at this time. Dosage protocols are still under investigation. Most cats seem to tolerate 62.5 mg/cat (approximately 15 mg/kg) q8 to 12h PO. Cases of FHV-1 dermatitis have been treated for 3 to 6 weeks with 62.5 to 125 mg/cat q8-12h PO without adverse effects. • Ophthalmic Antibiotics: These are indicated when conjunctivitis exists. Do not use products containing corticosteroids if a corneal ulcer is present. Cats may be sensitive to ophthalmic tetracycline and neomycin. If conjunctivitis worsens, discontinue products containing these drugs. • Nasal Decongestants: Oxymetazoline hydrochloride (Afrin Pediatric Nasal Drops®) is advocated by some. One drop is placed in one nostril once daily. Most cats object to nasal drops. After-congestion (also called “rebound congestion”) may develop, and efficacy has not been clearly demonstrated. • Interferon: Oral human alpha interferon is no longer available in the United States. It may reduce clinical disease but not viral shedding. It is typically used in conjunction with lysine therapy. Feline omega interferon is a fairly new product and is not available in the United States. However, it may be imported for use in individual cats. The product has not been widely researched for use in viral respiratory disease but has promise. Oral therapy may be provided once daily with 50,000 to 100,000 units per cat; subcutaneous therapy consists of 1 MU/kg q24h or q48h SC. It has also been used topically in the eye after dilution. The current recommendation is to dilute a 10 MU vial of omega interferon in 19 mL 0.9% sodium chloride and use it as an eye drop, placing 2 drops in each eye five times a day for 10 days. It should be used in conjunction with lysine. • Lysine: For several years, lysine (250–500 mg/cat q12h PO) has been thought to have activity against the acute and chronic phases of FHV-1 infection. However, two recent studies failed to demonstrate efficacy of lysine against upper respiratory infections in groups of shelter cats. In one of these studies, lysine therapy was associated with worsening of clinical signs and increased detection of FHV-1 viral DNA in oropharyngeal and conjunctiva mucosal samples. As such, use of lysine for treating FVH-1 must be reconsidered. If it is used, cats receiving protracted courses of therapy should have plasma arginine concentrations monitored because lysine competitively inhibits absorption of arginine in many species.
Diagnostic Notes • Serology that detects virus neutralizing antibodies is not useful for diagnosis of active respiratory viral infections. It cannot distinguish active infection from those of past infection or vaccine-associated antibodies. • Because treatment of FHV-1 and FCV is essentially identical, there are few instances in clinical practice in which differentiation is indicated.
Treatment Primary Therapeutics • Antibiotics: Viral infections can become complicated by bacteria. Although viral infections are usually self-limiting in a few days, bacterial infections can become life-threatening if not treated. Good choices for mild-to-moderate disease are amoxicillin (12.5 mg/kg q12h PO) or amoxicillin-clavulanic acid (15 mg/kg q12h PO). If severe disease occurs, either azithromycin (10 mg/kg q12h PO for 10 days) or clavulanic acid/amoxicillin plus marbofloxacin (3–5 mg/kg q24h PO) is a good choice for outpatients and amoxicillin (12.5 mg/ kg q12h SC) plus enrofloxacin (2.5 mg/kg q12h SC) offers broad spectrum coverage for hospitalized cats. • Hydration: Nasal and ocular secretions thicken when dehydration occurs. To prevent this added discomfort, cats should receive rehydrating and maintenance doses of balanced electrolyte fluids IV or SC. • Nutritional Support: Anorexia is common and is a serious and common complication of upper respiratory infections. Nutritional support using orogastric (OG) or nasoesophageal (NE) tubes should begin as early as possible. Contraindications for OG and NE tubes include dyspnea and severe depression. Cats that are having difficulty breathing due to nasal obstruction will panic when these tubes are passed and feeding could result in death of the cat. If a tube is to be passed, nasal blockage must be cleared prior to feeding. Severe nasal congestion and irritation are contraindications for the use of NE tubes. If tube feeding is needed, the cat may need to be anesthetized for placement of an esophagostomy tube or a gastrostomy tube. See Chapters 253, 255, and 308.
226
Therapeutic Notes • Sneezing cats should be separated from other cats while in the hospital. However, affected cats should not be placed in a kennel or canine ward with barking dogs because this will significantly add to their stress level and negatively impact recovery.
Herpesvirus Infection
Prevention • Subcutaneous Vaccine: FHV-1 vaccine is considered a “core” vaccine for all cats by the American Association of Feline Practitioners (AAFP). Modified-live virus and inactivated or killed virus vaccines for injection are available. In high-risk situations, intranasal (IN) vaccines may be used to provide rapid immunity. Kittens may be unprotected against FHV-1 as early as 5 weeks of age or have interference from maternal immunity until 14 weeks of age. The AAFP advises that kittens may receive their initial FHV-1 vaccination as early as 6 weeks of age and that vaccination should be repeated every 3 to 4 weeks until 16 weeks of age. Herpes vaccination should be boostered at 1 year of age, then once every 3 years thereafter. However, FHV-1 vaccine is approved as “an aid in the control of disease due to feline rhinotracheitis.” This is the lowest level of protection a vaccine can meet and be approved in the United States. Therefore, many practitioners still give it annually. • Intranasal Vaccine: IN vaccination has not been shown to shorten clinical infection or to terminate the carrier state. However, immunity develops more quickly with IN vaccines than with injectable vaccines, so they have merit in situations in which exposure is likely. IN vaccines may also prevent the carrier state. Some cats receiving IN vaccine develop chronic sneezing. • Vaccine Limits: FHV-1 vaccine does not confer sterilizing immunity. As stated previously, it is only able to dampen the severity of clinical signs rather than prevent infection, disease, and virus shedding. It produces a poorer level of immunity than FCV.
Prognosis The prognosis is variable because of the vast array of clinical problems caused by the virus. Most cats recover fully from an acute infection.
Suggested Readings Drazenovich TL, Fascetti AJ, Westermeyer HD, et al. 2009. Effects of dietary lysine supplementation on upper respiratory and ocular disease and detection of infectious organisms in cats within an animal shelter. Am J Vet Res. 70(11):1391–1400. Gaskell RM, Dawson S, Radford A. 2006. Feline respiratory diseases. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 145–154. Philadelphia: Saunders Elsevier. Gaskell RM, Dawson S, Radford A, et al. 2007. Feline herpesvirus. Vet Res. 38(2):337–354. Malik R, Lessels NS, Webb S, et al. 2009. Treatment of feline herpesvirus-1 associated disease. J Fel Med Surg. 11(1):40–48. Rees TM, Lubinski JL. 2008. Oral supplementation with L-lysine did not prevent upper respiratory infection in a shelter population of cats. J Fel Med Surg. 10(5):510–513. Thiry E, Addie D, Belak S, et al. 2009. Feline herpesvirus infection: ABCD guidelines on prevention and management. J Fel Med Surg. 11(7): 547–555.
227
CHAPTER 96
High-Rise Syndrome Mitchell A. Crystal
Overview High-rise syndrome describes the collection of injuries sustained by a cat that falls from a substantial height, usually greater than or equal to two stories (about 4.0 m [12 feet] per story). This syndrome is most common in younger cats living in urban areas. The term high-rise refers to the tall buildings from which these animals have fallen. Greater than 90% of the cats affected by high-rise syndrome will survive. Between 25 and 33% of high-rise cats require life-sustaining treatment, the remainder require nonemergency or no treatment. Cats surviving 24 hours after falling rarely die from causes related to high-rise syndrome. Findings of several retrospective studies of high rise syndrome cats are summarized in Table 96-1. See Figure 96-1 for a summary of Table 96-1. Most studies report a linear increase in injuries sustained from falling from distances up to about six or seven stories. Above this height, the
number of injuries (especially fractures) either levels off or decreases. This is believed to occur because cats falling greater than six or seven stories have reached their terminal velocity of fall (due to body mass and drag, about 100 k/hr [60 mph]), at which point the vestibular apparatus is no longer stimulated. Prior to reaching terminal velocity, continued vestibular stimulation is believed to result in limb rigidity and failure to maximally prepare for a horizontal landing. The latter causes an uneven and smaller area of distribution of the force of impact, which, along with rigid extremities, causes a greater number of injuries. After reaching maximum velocity (greater than six or seven stories), it is believed that cats assume a less rigid, more horizontal posture. These cats are more prepared for landing and have the force of impact evenly distributed throughout the body, preventing an increase, and in some cases causing a decrease, in the number of injuries. See Figure 96-1 for a summary of injuries.
TABLE 96-1: Findings of Retrospective Studies of High-Rise Syndrome Cats Authors Year published Study Location Number of Cases Age
Collard, et al. 2005 Marcy l’Etoile, France 42 (37 cats, 42 falls) Mean 2.66 years
Vnuk, et al. 2004 Zagreb, Croatia 119 (4 years) Mean 1.8 years (2.5 months– 10 years)
Papazoglou, et al. 2001 Thessaloniki, Greece 207 (11 years) 1.2 years (2.4 weeks–20 years)
<1 Year of Age
43.9%
59.6%
74%
4.0 (median, 4; 2–16)
3.7 (2–8)
Whitney, et al. 1987 New York City 132 (5 months) Mean 2.7 years (3 months–16 years) Not listed (64% <3 year) 5.5 (2–32)
96.5% (deaths were in cats falling two to nine stories) 9.2% 2.5% 46.2% 21.0% (humerus 6.7%, radius and ulna 6.7%) 33.6% (tibia 16.8% and femur 11.8%) 38.7% 7.6% 2.5% 13.4% 20.2% 3.4% 1.7% 10.9% NA 8.4% 5.0%
93%
90%
8% 11.7% 50% 32%
3% 2.3% 39.4% 33.3%
68%
28.0%
81.6% 7.7% 8% 6.8% 3.9% NA 0.5% 17% 9% 2% 3%
22.7% 16.7% 17.4% 68% 63% NA NA 24% NA NA 17%
Mean Number Stories Fell Survival
4.42 97.3%
Pelvic Fractures Spinal Fractures Limb Fractures Forelimb Fractures
NA NA 42.9% NA
Hindlimb Fractures
NA
Single Fractures Multiple Fractures Luxations Pulmonary Contusions Pneumothorax Hemothorax Ruptured Diaphragm Shock Cranial Trauma Epistaxis Split Hard Palate
NA NA 11.4% 41.7% 38.9% 2.8% NA 35.1% 11.1% 22.2% 16.7%
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
228
TABLE 96-1 Continued Dental Fractures Mandibular Fractures Retinal Detachments Hematuria Ruptured Bladder Abdominal Wall Hernia Severity of injuries follows a curvilinear pattern from the third to the seventh story. Shock and thoracic lesions were more common in falls from the sixth story. (Information published as abstract.)
19.4% NA 2.8% 19.4% NA NA
NA 3.4% NA NA 0.8% 1.7%
NA 2% NA 2% 0.5% 1%
17% 9% NA 4% 2.3% 2%
Severity of lesions follows a curvilinear pattern from third to seventh story. Higher rates of shock and thoracic trauma in cats falling from sixth story. Mean injury score increases up to the sixth story. Limb fractures maximum at fourth and fifth stories. Split hard palates only seen in falls greater than three stories.
Injuries increased from the second to the third story, then became variable from the third to sixth story, then increased above the seventh story. Fractures decreased in falls above the third story. Thoracic trauma increased in falls above the sixth story. Most Zagreb buildings do not exceed six stories.
As the number of stories increased (from the second to the sixth), the total number of injuries were increased. There were significantly more injuries in cats falling from the sixth story compared to those falling from the second, third, or fourth story. Thessaloniki apartments do not exceed eight stories.
Rate of injury linear up to seven stories, then injury rate did not continue to increase and fracture rate decreased.
NA, not available
Retinal Detachment 3% Cranial Trauma 10% Epistaxis 11% Split Hard Palate 10%
Spinal FX 7%
Pelvic FX 7%
Dental FX 18% Mandibular FX 5%
Forelimb FX 29%
Pulmonary Contusion 32% Pneumothorax 32%
Ruptured Diaphragm 1%
Hematuria 8%
Hindlimb FX 43% Shock 22%
Figure 96-1 The common injuries are listed for cats of the high-rise syndrome. These numbers are averages of the reported incidences in Table 96-1. The total is more than 100% because multiple injuries usually occur.
229
SECTION 1: Diseases and Conditions
Diagnosis
Treatment
Primary Diagnostics
Primary Therapeutics
• History: Most cats involved in a high-rise fall are not observed falling, indicating the need to question the client as to the possibility or opportunity of this occurrence. • Physical Examination: Examine for common injuries associated with high-rise syndrome. • Thoracocentesis (Diagnostic and Therapeutic): Any cat with respiratory distress should undergo this procedure prior to thoracic radiographs to assess for pneumothorax or hemothorax. • Quick Assessment Tests: These include packed cell volume (PCV), total protein, blood glucose, blood urea nitrogen (BUN), urine dipstick, and urine specific gravity. They help to identify cats in shock and cats with blood loss or compromised urinary tracts.
• Thoracocentesis (diagnostic and therapeutic): This procedure should be performed in all high-rise syndrome cats with dyspnea. • Oxygen Therapy: This is indicated for cats with respiratory difficulty. • Fluid Support: Administer if needed for shock or dehydration. Prolonged fluid support may be needed if oral trauma is present.
Secondary Therapeutics • Fracture, Wound, and Other Injury Repair: These should occur after the cat is stable. • Nutritional Support: This may be needed once the cat is stabilized if oral trauma is present. An esophagostomy or gastrostomy tube should be used.
Secondary Diagnostics • Thoracic Radiography: This should be performed once the cat is stable to investigate for thoracic trauma. • Abdominal Radiographs: This should be performed if abdominal trauma or abdominal effusion is suspected. • Abdominocentesis: This should be performed if abdominal trauma or abdominal effusion is suspected. Any fluid collected should be submitted for fluid analysis.
Diagnostic Notes • If the patient is dyspneic or stressed, thoracocentesis, and oxygen administration should be performed prior to any diagnostics. • The PCV requires several hours to decrease and equilibrate after acute blood loss. It should not be used to determine the presence of internal bleeding.
230
Prognosis The prognosis is good to excellent for recovery and long-term survival as long as initial emergency therapy is provided and is successful.
Suggested Readings Collard F, Genevois JP, Decosnes-Junot C, et al. 2005. Feline high-rise syndrome: a retrospective study on 42 cases. J Vet Emerg Crit Care. 6(Supplement 1):S15–S17. Papazoglou LG, Galatos AD, Patsikas MN, et al. 2001. High-rise syndrome in cats: 207 cases (1988–1998). Aust Vet Practit. 31(3):98–102. Vnuk D, Pirkic B, Maticic D, et al. 2004. Feline high-rise syndrome: 119 cases (1998–2001). J Fel Med Surg. 6: 305–312. Whitney WO, Mehlhaff CJ. 1987. High-rise syndrome in cats. J Am Vet Med Assoc. 191(11): 1399–1403.
CHAPTER 97
Histoplasmosis Sharon Fooshee Grace
Overview Cats appear fairly susceptible to infection with the dimorphic fungal organism Histoplasma capsulatum; however, most cats probably develop only a transient, clinically inapparent infection. In North America, the St. Lawrence, Missouri, and Mississippi River valleys and their related tributaries are areas of endemic infection. The organism is commonly associated with topsoil enriched by the nitrogen of bird and bat feces. Most evidence supports a respiratory route of infection with hematogenous and lymphatic routes of dissemination, although primary gastrointestinal infection has been reported. The infectious form (mycelial phase) lives in the environment; once inside the body, the organism converts to the noninfectious yeast phase. Histoplasmosis is essentially a disease of the mononuclear phagocyte system. A competent cellmediated immune response must be present to contain infection. Infection with the feline leukemia and feline immunodeficiency viruses does not appear to predispose cats to histoplasmosis. Humans and other pets are not at risk for the disease from contact with infected cats but may become infected because of similar environmental exposure. Diagnosis can be a challenge because most cats have disseminated disease with a wide variety of vague, nonspecific signs, such as fever, weight loss, depression, and anorexia. Less than half of infected cats demonstrate organ-specific dysfunction. When signs are localizing, the respiratory system is commonly affected, although coughing is uncommon. See Figures 97-1 and Figure 291-40. Tachypnea, dyspnea, and abnormal lung sounds are found in many cases. Hepatosplenomegaly (see Figure 97-2), subcutaneous nodules, soft-tissue swelling, lameness secondary to osteomyelitis (see Figure 97-3), diarrhea, and inflammatory ocular lesions (see Figure 223-1) have been reported. Ocular signs may be more common with disseminated histoplasmosis than with any other feline systemic mycosis, with both the anterior and posterior chambers involved (anterior uveitis and granulomatous chorioretinitis). Intestinal histoplasmosis is much less common in cats than in dogs. Because the clinical signs are often quite vague and non-localizing, the differential diagnoses for feline histoplasmosis are extensive and should include diseases that could cause fever, anemia, respiratory distress, inflammatory ocular disease, bone lesions, or hepatosplenomegaly.
(A)
Diagnosis Primary Diagnostics • Clinical Signs: Clinical signs are described in the Overview. Persistent, antibiotic-resistant fever in a cat living in or having been in an endemic area warrants a consideration of histoplasmosis. • Cytology: Organisms are usually numerous in infected tissues. With modified Wright’s stain, single or multiple small (2–5 µm) round blue yeasts with light halos appear within phagocytic cells. See Figure 289-1. Bone marrow and lymph node aspiration and cytology appear to be high-yield diagnostic procedures. Subcutaneous
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
(B) Figure 97-1 A, B, A fine, diffuse, or linear interstitial pattern in the lungs is common. Images courtesy Dr. Gary D. Norsworthy.
nodules or an enlarged liver should also be aspirated. Organisms may be found on peripheral blood smears (counting 1,000 white blood cells versus the normal 100 on a differential count enhances organism detection) or buffy coat smears. Bronchioalveolar lavage, rectal scraping, or colonic biopsy can also be considered when organ-specific involvement warrants these tests. A lung aspirate may be helpful; careful technique is needed to avoid damage to the lungs and possible death. See Chapter 304.
231
SECTION 1: Diseases and Conditions
Figure 97-2 Hepatosplenomegaly is seen in the abdominal radiographs of this 7-month-old cat with histoplasmosis. Image courtesy Dr. Gary D. Norsworthy.
• Histopathology: The organism is not seen with H & E stain. Special fungal stains (periodic acid-Schiff reaction [PAS], Gridley, Gomori) are needed; therefore, the pathologist should be alerted to the potential need for additional stains. When histoplasmosis is suspected, make an impression smear before putting biopsy tissue in formalin so cytology can be performed.
(A)
Secondary Diagnostics • Radiography: A fine, diffuse, or linear interstitial pattern in the lungs is common (see Figure 97-2); the disease may also appear as a more prominent nodular pattern. Hepatosplenomegaly may be seen (see Figure 97-2). When osteomyelitis is present, the lesions are often osteolytic (see Figure 97-3), although concurrent osteoproduction may be found. • Complete Blood Count, Biochemical Profile, Urinalysis, and Retroviral Tests: Nonregenerative anemia is common. Hypoalbuminemia is a fairly consistent finding. Other evidence of organ involvement may be seen (e.g., increased hepatobiliary parameters, cytopenias, and so on). Even when the minimum data base does not yield a definitive diagnosis, it is helpful in assessing the overall health of the patient for prognostic purposes. • Intradermal Skin Testing and Serology: The former is not a reliable indicator of infection. However, an antigen test is being felinevalidated for use on urine, serum, and bronchoalveolar lavage fluid. (MiraVista Diagnostics, www.miravistalabs.com.)
(B) Figure 97-3 Lytic bone lesions are seen in the distal radius and ulna and in two metacarpals in the (A) anterior-posterior and (B) lateral views. Images courtesy Dr. Gary D. Norsworthy.
Treatment Diagnostic Notes • History of prior living locations and travel should always be obtained for any sick cat. • The organism does not always stain well with H & E stain; as such, cytology using a modified Wright’s stain may be a superior tool over histopathology for organism identification. • Indoor-only cats may contract histoplasmosis. Potting soil is usually cited as the source in such cases, but situations exist in which the cat is not exposed to potting soil and the source of the organism cannot be determined.
232
Primary Therapeutics • Itraconazole: This is the antifungal drug of choice. It is dosed at 5 mg/ kg q12h PO and given with a meal; an acid environment in the stomach enhances absorption of the drug. Most cats take 0.25 capsule (25 mg) twice per day. The capsule may be opened and the contents divided into gelatin capsules or mixed into canned food. An oral solution is available. Duration of therapy will usually extend over several months. It may be combined with amphotericin B in fulminant disease.
Histoplasmosis
Secondary Therapeutics • Nutritional Support: Affected cats are often debilitated and may be anorectic, and appetite may decline over the first 4 to 6 weeks of treatment. Placement of a feeding tube permits the owner to administer proper nutritional support and should be considered at the time of diagnosis.
should be normal prior to its use, and they should be monitored following treatment. See Chapter 43. One to three treatments are given prior to the use of itraconazole or fluconazole. • Many cats will worsen after therapy is initiated, especially after Amphotericin B therapy; this is due to the intense inflammatory response to dying organisms. Special attention should be given to respiratory support during this time if the lungs are heavily involved. Short-term corticosteroid administration may be of benefit.
Therapeutic Notes • Itraconazole solution is more consistently absorbed than capsules. • Although itraconazole is usually well tolerated, serum chemistries should be periodically checked during itraconazole therapy to assess for hepatotoxicity. Consequently, liver enzyme levels should be determined prior to itraconazole administration as they may be elevated due to fungal hepatitis. For cats with clinical evidence of hepatotoxicity (i.e., anorexia or jaundice), the drug should be discontinued, at least temporarily. Asymptomatic cats with increased liver enzymes (alanine aminotransferase [ALT]) do not need cessation of therapy but should be closely monitored clinically and biochemically. • Fluconazole (5 mg/kg q12h PO) and amphotericin B are alternative treatments if the cat does not respond to itraconazole. Fluconazole has superior penetration of the central nervous system and ocular tissues and is considerably less expensive than itraconazole. • A subcutaneous amphotericin B protocol appears to significantly reduce the nephrotoxic potential of the drug and may hasten the fungal kill. It should be considered when the disease is severe because clinical response to itraconazole is not rapid. Renal values
Prognosis The prognosis for infected cats has improved with the introduction of itraconazole, fluconazole, and subcutaneous amphotericin B. Severely debilitated cats with advanced systemic disease still have a guarded prognosis. However, aggressive treatment started prior to severe debilitation often results in a cure including resolution of pulmonary and osseous lesions.
Suggested Readings Bromel C, Sykes JE. 2005. Histoplasmosis in dogs and cats. Clin Tech Sm Anim Pract. 20(4):227–232. Greene CE. Histoplasmosis. 2006. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 378–383. Philadelphia: Saunders Elsevier. Johnson LR, Fry MM, Anez KL, et al. 2004. Histoplasmosis infection in two cats from California. J Am Anim Hosp Assoc. 40(2):165–168.
233
CHAPTER 98
Hookworms Mitchell A. Crystal and Mark C. Walker
Overview Ancylostoma are small intestinal nematode parasites also known as hookworms. Three species of hookworms are found in the cat: Ancylostoma tubaeforme (most common), Ancylostoma braziliense, and Uncinaria stenocephala. A. tubaeforme is a moderately blood-sucking parasite, whereas A. braziliense and U. stenocephala are minimally bloodsucking parasites. Hookworms are acquired via ingestion of infected feces or transport hosts (e.g., rats) and have a 2- to 3-week life cycle without extraintestinal migration. Infection is occasionally acquired via skin penetration; transplacental and transmammary infection does not occur in cats. Clinical signs are more severe in kittens than in adult cats and include diarrhea, dark stools, vomiting, weight loss or failure to gain weight (kittens), and weakness or lethargy due to anemia (kittens). Infection may also be asymptomatic. Physical examination may be normal, reveal evidence of weight loss (kittens) or diarrhea, or demonstrate pallor (kittens). A. braziliense is of zoonotic importance because it is the major cause of cutaneous larval migrans in humans.
Diagnosis
• Hookworm and Heartworm Prevention Combination: Ivermectin (Heartgard for Cats®): Give per label instructions or 0.024 mg/kg q30d; not effective for roundworms at label dose. Imidacloprid and Moxidectin (AdvantageMulti for Cats®): Give per label instruction or 10.0 mg/kg imidacloprid and 1.0 mg/kg moxidectin once by topical application. Milbemycin oxime (Interceptor®): Give per label instruction or 2 mg/kg PO once a month; also effective for roundworms. Selamectin (Revolution®): Apply per label instruction or 6 mg/kg as a spot-on topical once a month; also effective for roundworms, ear mites, and fleas.
Secondary Therapeutics • Fenbendazole (Panacur®): Give 50 mg/kg q24h PO for 3 days; repeat in 2 to 3 weeks (also effective for roundworms, whipworms, Giardia, and Ollulanus tricuspis). • Ivermectin (Ivomec®): Give 200 µg/kg PO; repeat in 2 to 3 weeks (also effective for roundworms). • Emodepside and Praziquantel (Profender®): Topical therapy. Give 3 mg/kg emodepside and 12 mg/kg praziquantel. Treat at 8 and 12 weeks of age then 3 months later.
Primary Diagnostics • Fecal Flotation: Eggs are seen on microscopic examination.
Secondary Diagnostics • Direct Saline Smear: Eggs are sometimes seen on microscopic examination.
Secondary Diagnostics • Packed Cell Volume, Total Protein, and Complete Blood Count: These should be performed in kittens with hookworms to determine if anemia is present.
Therapeutic Notes • Treat kittens routinely or if hookworm infection is suspected, even if fecal floatation is negative. • A second treatment is needed 2 to3 weeks following initial therapy to kill new adults arising from eggs and larva that were initially resistant to therapy.
Prognosis The prognosis is excellent for cure, although hookworms often persist in the environment, and reinfection is common. This may be a problem in outdoor cats. Sodium borate may be applied to the environment at a rate of 5 kg/100 square feet to kill hookworm larvae.
Diagnostic Notes • Clinical signs may develop in kittens before eggs are detected in the feces.
Treatment Primary Therapeutics • Pyrantel Pamoate (Strongid®, Nemex®, generic): Give 20 mg/kg PO; repeat in 2 to 3 weeks (also effective for roundworms). • Praziquantel/Pyrantel Pamoate (Drontal®): For cats 1.8 kg (4 lbs) or less: 6.3 mg/kg PO; for cats greater than 1.8 kg (4 lbs): 5 mg/kg PO; repeat in 2 to 3 weeks. This drug is also effective for roundworms and tapeworms.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
234
Suggested Readings Blagburn BL. 2004. Expert recommendations on feline parasite control. DVM best practices. A supplement to DVM magazine. An update on feline parasites, pp. 20–26. Blagburn BL. 2000. A review of common internal parasites in cats. Vet CE Advisor. A supplement to Vet Med. An update on feline parasites, pp 3–11. Hall EJ, German AJ. 2005. Helminths. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1358–1359. St. Louis: Elsevier Saunders. Reinemeyer CR. 1992. Feline gastrointestinal parasites. In RW Kirk, JD Bonagura, eds., Kirk’s Current Veterinary Therapy XI. Small Animal Practice, pp. 1358–1359. Philadelphia: WB Saunders.
CHAPTER 99
Horner ’s Syndrome Sharon Fooshee Grace
Overview Horner ’s syndrome is a disorder resulting from loss of sympathetic innervation to the eye and adnexa. Sympathetic innervation is responsible for maintenance of smooth muscle tone to the periorbita and eyelids, including the membrana nictitans. It is also important in balancing pupillary dilation (via the iris dilator muscles) against the parasympathetic effect of pupillary constriction (via the iris constrictor muscles). A lesion lying anywhere along the sympathetic pathway may cause Horner ’s syndrome. Preganglionic lesions involve a pathway originating in the hypothalamus and midbrain. This pathway courses down the brainstem and spinal cord to the level of the first few thoracic vertebrae, along the T1 to T3 nerve roots, and up the vagosympathetic trunk to its termination at the cranial cervical ganglion. Postganglionic lesions lie along the path of the cranial cervical ganglion, which courses through the middle ear and terminates in the eye. In the majority of cats, the cause of Horner ’s syndrome is not determined (idiopathic). When an etiology is found, trauma to the pathway is the most common cause. Such injuries include bite wounds to the neck, surgical trauma (i.e., total ear canal ablation, bulla osteotomy), and brachial plexus avulsion. Other causes include otitis media (including iatrogenic injury caused by ear cleaning), nasopharyngeal polyps, and cranial thoracic neoplasia.
Signs of Horner ’s syndrome include miosis, enophthalmos, prolapse of the third eyelid, and ptosis. See Figure 99-1. In some cases, all of the signs will not be present; miosis is the most consistent finding in the absence of other signs. Visual deficits are not a part of Horner ’s syndrome except for the effects of miosis and the prolapsed third eyelid. Evaluation of Horner ’s syndrome begins with a thorough history and complete physical examination, with special attention given to recognition of recent trauma, recent surgery, examination of the ear canal, and evaluation for any additional neurologic deficits that might aid in localizing the lesion.
Diagnosis Primary Diagnostics • Clinical Signs: One or more of the signs of miosis, enophthalmos, prolapse of the third eyelid, and ptosis should raise one’s index of suspicion.
Secondary Diagnostics • Radiographs: Thoracic radiographs may be useful to identify cranial thoracic masses. Bulla radiographs may provide evidence of a softtissue density in the bulla (i.e., middle-ear polyp, otitis media, or neoplasia). • Pharmacologic Testing: Testing with ocular medications may aid in distinguishing preganglionic from postganglionic lesions, though the results sometimes contribute little to identifying a cause or prognosis. Also, results vary according to the time since the insult occurred, the completeness of the lesion, and its distance from the iris. An indirectacting sympathomimetic agent (1% hydroxyamphetamine with 0.25% tropicamide) instilled into each eye results in dilation of the miotic pupil when the lesion is preganglionic. This response occurs because the nerve endings of the postganglionic neuron are intact and able to respond. When the lesion is postganglionic, the miotic pupil dilates incompletely or not at all. To further confirm a postganglionic lesion, a dilute direct-acting sympathomimetic agent (1% phenylephrine [dilute a 10% stock solution 1:10 with saline]) should be administered in each eye. If the lesion is postganglionic, dilation of the pupil will occur within 20 minutes due to denervation hypersensitivity of the iris dilator muscle; no dilation occurs if the lesion is preganglionic.
Figure 99-1 This cat is exhibiting miosis, ptosis, and prolapse of the third eyelid as manifestations of Horner’s syndrome.
Diagnostic Notes
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Anisocoria may be more pronounced in a dark room because the normal pupil is allowed to dilate. • The eye is nonpainful with Horner ’s syndrome. Painful conditions, such as uveitis and corneal injury, may result in miosis and should not be confused with Horner ’s syndrome.
235
SECTION 1: Diseases and Conditions
Treatment Primary Therapeutics • Treat the Underlying Disease: If identified, the underlying disorder should be treated. Depending on the cause and the damage to the neurologic pathway, this may or may not lead to resolution of the Horner ’s syndrome. Primary therapy for Horner ’s syndrome is usually not required.
Secondary Therapeutics • Topical 10% Phenylephrine: This can be used twice daily to resolve clinical signs if needed in severe cases (e.g., visual impairment from severe third eyelid protrusion). This treatment is supportive only and does not help in the resolution of idiopathic Horner ’s syndrome or in the treatment of any underlying disorder. In most instances, the patient does not benefit from this therapy.
236
Prognosis Idiopathic, traumatic, and surgically induced Horner ’s syndrome usually resolves spontaneously within 4 to 6 months. When Horner ’s syndrome occurs secondary to an underlying disorder, the prognosis is dependent on identification of the cause and a positive response to treatment.
Suggested Readings Barnett KC, Crispin SM. 2002. Neuro-ophthalmology. In KC Barnett, SM Crispin, eds., Feline Ophthalmology, pp. 169–183. London: Elsevier. Collins BK. 1994. Disorders of the pupil. In JR August, ed., Consultations in Feline Internal Medicine, 2nd ed., pp. 421–428. Philadelphia: WB Saunders. Collins BK. 2000. Neuro-ophthalmology—Pupils that teach. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 5th ed., p. 661. St. Louis: Elsevier Saunders. Neer TM. 1984. Horner ’s syndrome. Compend Contin Educ Pract Vet. 6(8):740–747.
CHAPTER 100
Hydronephrosis Gary D. Norsworthy
Overview Hydronephrosis develops when an obstruction to urine outflow leads to collection of urine within the renal pelvis or diverticula. The pelvis dilates, resulting in pressure and ischemic atrophy of the renal medulla and cortex. With unilateral hydronephrosis, the obstruction involves a single ureter or kidney. Bilateral disease may result from obstruction in the urethra, urinary bladder, or both ureters. If unilateral disease occurs, the normal kidney may continue to function until the abnormal kidney reaches enormous proportions. With bilateral disease, the cat may develop uremia and die before renomegaly becomes significant. Hydronephrosis may be caused by congenital malformation of the urinary tract; the presence of calculi in the bladder, urethra, or ureter(s); neoplasia; ureteral ligation during ovariohysterectomy; pelvic masses; and, rarely, bilateral ureteral fibrosis. Except for the presence of a ureteral urolith, the etiology is often not determined. Cats with unilateral disease may present for abdominal distention or an abdominal mass may be found incidentally on a routine physical exam, whereas, bilateral disease may lead to overt signs of renal failure. If pyelonephritis develops, lethargy, fever, anorexia, and hematuria occur. Cats with bilateral disease are generally presented for signs of renal failure.
Diagnosis Primary Diagnostics • Physical Examination: Abdominal palpation will reveal mild to marked renal enlargement. • Ultrasound: Ultrasound examination will reveal a dilated, anechoic, fluid-filled kidney with varying amounts of renal parenchymal tissue present. See Figures 100-1, 100-2, and 100-3.
Secondary Diagnostics • Excretory Urogram: This study reveals little or no contrast material in the affected kidney. The cortex will be seen as a thin rim of tissue, and the renal pelvis and ureter will be dilated. If unilateral disease is present, the other kidney will be normal. See Figure 100-4. • Antegrade Pyelogram: Using ultrasound guidance, a 22-gauge needle is passed into the renal pelvis avoiding the renal artery and vein. After aspirating 2 to 10 mL of urine, 1 to 2 mL of an iodinated contrast material or iohexol (240 mg/mL) is injected into the renal pelvis. Lateral and ventral-dorsal radiographs are made immediately. This is especially helpful when renal filtration of intravenous contrast material does not occur, such as in ureteral obstruction.
Diagnostic Notes • Do not give radiographic contrast material IV if the patient is dehydrated.
Figure 100-1 Because there is substantial cortical and medullary tissue present, this is an example of early hydronephrosis.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 100-2 Late hydronephrosis results in destruction of nearly all cortical and medullary tissue and a nonfunctioning kidney.
237
SECTION 1: Diseases and Conditions
Figure 100-3 The kidney from the cat in Figure 100.2 shows that the pelvis has destroyed nearly all of the cortex and medulla.
Treatment Primary Therapeutics • Underlying Disease: When possible, the underlying disease causing the obstruction should be treated and the obstruction relieved. This generally involves surgery. In many cases, this is not possible; however, if treatment occurs quickly, renal function may return to a near-normal state. • Nephrectomy: If renal function is lost and pain or infection is present, the kidney should be removed as long as the other kidney has normal function, which should be determined with an excretory urogram and renal function tests. It is not essential to remove a nonfunctional kidney that is not painful or infected.
Therapeutic Notes • Systemic antibiotic therapy is indicated if bacteria are detected within the urinary tract. • When a ureter is obstructed, it enlarges and the wall will thicken enough to make ureterotomy feasible for a relatively experienced surgeon. See Chapter 275. • If a ureteral obstruction is relieved within 1 week, return of renal function is expected. Irreversible renal damage begins 15 to 45 days after the obstruction; however, some return of renal function may occur with obstruction that has been present for as long as 4 weeks.
238
Figure 100-4 An excretory urogram shows a dilated renal pelvis with renal uroliths in the left kidney and renal uroliths in the right renal pelvis.
• A perinephric pseudocyst may be mistaken for hydronephrosis. However, the former is a fluid-filled sac surrounding a kidney. The two can be differentiated with ultrasound or an excretory urogram.
Prognosis The prognosis for the affected kidney is good if the underlying disease is successfully treated within 2 days. The cat’s prognosis is good in the presence of unilateral disease even if nephrotomy is necessary, assuming the other kidney is functioning normally. Cats with bilateral disease without a treatable underlying disease have a grave prognosis once azotemia occurs.
Suggested Reading Bercovitch MG. 2007. Hydronephrosis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 642–643. Ames, IA: Blackwell Publishing. Cuypers MD, Grooters AM, Williams J, et al. 1997. Renomegaly in dogs and cats. Part II. Diagnostic approach. Compend Contin Educ. 19:1213–1229.
CHAPTER 101
Hyperadrenocorticism Karen M. Lovelace
Overview Albeit a rare endocrine disease of cats, hyperadrenocorticism is a debilitating and life-threatening condition. Also known as Cushing’s disease, hyperadrenocorticism in the feline patient is frequently misdiagnosed as diabetes mellitus (DM) and is often only recognized after a primary diagnosis of DM has been made. DM has been documented in approximately 80% of feline hyperadrenocorticism cases. Cats are sensitive to the diabetogenic effects of steroids, and insulin resistance is, therefore, commonly encountered in cases of feline hyperadrenocorticism. Hyperadrenocorticism should be suspected as a concurrent disease process in any diabetic patient in which regulation is difficult to achieve or where secondary infections are common or recurrent. In addition to the increased likelihood of diabetes mellitus, chronic high levels of cortisol in the cat have been associated with skin fragility, cardiovascular disease, poor wound healing, frequent infections due to decreased immune function, and death. Middle-aged to older cats are more frequently affected, and females are more likely to be affected than males. No breed association has been established. In addition, adrenal tumors in cats may secrete excess amounts of not only cortisol but also sex steroids such as progesterone. Similar to their canine counterparts, roughly 85% of feline cases of hyperadrenocorticism are classified as pituitary-dependent hyperadrenocorticism (PDH), and approximately 15% of cases are classified as functional adrenocortical tumors (FAT). The true incidence of Cushing’s disease in cats is unknown, and success associated with the treatment of documented cases has been poor. Medical management is unrewarding, and success is more likely with surgical intervention. Early recognition and diagnosis of hyperadrenocorticism is, therefore, paramount to a successful outcome.
Diagnosis Primary Diagnostics • Clinical Signs: The most common signs are polyphagia, polydipsia, and polyuria. The onset of polydipsia and polyuria may be delayed until the hyperglycemia and glucosuria, resultant from osmotic diuresis, become clinically evident. Other findings include obesity, lethargy, pendulous abdomen, generalized muscle wasting, alopecia (i.e., truncal or patchy, unkempt coat, fragile skin that is thin and easily torn (see Figure 45-1), and secondary infections. Hepatomegaly and weight loss occur with decreased frequency. • Concurrent Disease: Hyperadrenocorticism should be a differential diagnosis in patients with DM (especially in difficult to regulate diabetics), and in various dermatologic conditions such as frequent infections, wounds that will not heal, and fragile skin syndrome. • Biochemistry Profile: Hyperglycemia is the most consistent finding on blood work; glucosuria is also consistent. Hypercholesterolemia, as well as increases in liver enzymes such as alanine aminotransferase (ALT) and less frequently, alkaline phosphatase (ALP), may also be documented.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Low-Dose Dexamethasone Suppression Test (LDDST): Failure to suppress plasma cortisol concentrations is suggestive of hyperadrenocorticism in cats without nonadrenal illness, most notably concurrent diabetes. Because diabetes is a common concurrent disease for cushinoid cats, it should be noted that many noncushinoid diabetic cats fail to suppress, resulting in a false-positive LDDST. In addition, many normal cats as well as cats with nonadrenal illness (e.g., diabetes) will fail to suppress at a dose of 0.01 mg/kg, the dose commonly used in dogs. Therefore, a dose of 0.1 mg/kg of dexamethasone given IV is recommended. Blood is collected prior to dexamethasone injection and again 4 and 8 hours after injection. • Urine Creatinine-to-Cortisol Ratio: A high urine creatinine-tocortisol ratio is indicative of hyperadrenocorticism, although falsepositives may occur as a result of other disease processes. • Adrenocorticotrophic Hormone (ACTH) Stimulation Test: The ACTH stimulation test evaluates adrenal reserve and is most frequently used to diagnose hypoadrenocorticism. The test has a low sensitivity and a low specificity. Various protocols exist. Cosyntropin, a synthetic form of ACTH, is the diagnostic drug of choice for feline hyperadrenocorticism and is used at a dose of 125 µg/cat IV. Intravenous administration produces greater degree and duration of adrenocortical stimulation when compared to intramuscular administration, so intramuscular administration is not recommended. If an intravenous protocol is used, the postadministration collection times are at 60 and 90 minutes. Alternatively, ACTH gel at 2.2 U/kg given IM may be used. Following this protocol, blood is collected before administration and again at 60 and 120 minutes after drug administration. Two postadministration blood samples are generally recommended because the time to peak effect of cortisol in cats can vary.
Secondary Diagnostics • Discrimination Tests: The following tests are used to differentiate PDH from FAT. See Diagnostic Notes to consider the importance of differentiation in relation to therapy selection and outcome. • Ultrasonography: Unilateral enlargement of an adrenal gland with irregular or rounded shape is consistent with FAT. Adrenal tumors will usually exhibit increased or mixed echogenicity. Symmetrical adrenal glands that are bilaterally normal or enlarged are consistent with PDH. • Measurement of Endogenous ACTH: This test should be performed only after a diagnosis of hyperadrenocorticism has been made, due to the fact that normal cats can have low levels of endogenous plasma ACTH. Normal to increased concentrations of ACTH supports PDH, whereas low to negligible levels supports FAT. • High-Dose Dexamethasone Suppression Test (HDDST): Dexamethasone should be used first at a dose of 0.1 mg/kg (LDDST) then at a dose of 1.0 mg/kg (HDDST). The two tests should be performed on different days. Cortisol concentrations of 41 nmol/L (1.5 µg/dL) or greater and less than 50% of baseline are consistent with PDH. Concentrations between 28 and 41 nmol/L (1.0–1.5 µg/ dL) are considered borderline. Lack of suppression (<28 nmol/L [1.0 µg/dL] at 4 or 8 hours) cannot be used to differentiate PDH from FAT.
239
SECTION 1: Diseases and Conditions
Primary Therapeutics • Adrenalectomy: This is currently the most successful treatment option available and is, therefore, the current treatment of choice. Medical stabilization with the goal of transient resolution of hyperadrenocorticism prior to adrenalectomy has improved surgical outcome in many cases. Adrenalectomy will be unilateral in cats with a single FAT or bilateral in cats with PDH or bilateral FAT. Successful surgical intervention usually results in resolution of disease or significant improvement of clinical signs in 2 to 4 months. In over half of the cases, diabetes is resolved, and in the remaining cases the amount of exogenous insulin administered can be reduced.
•
•
•
Secondary Therapeutics
•
• Medical Therapy: Success with medication has yielded results that are poor to variable at best, and long-term management is frequently ineffective. However, medical therapy may be indicated to stabilize a presurgical candidate, thereby decreasing postsurgical complications owing to infection and poor healing. Metyrapone is the drug of choice; however, this drug is not readily available. Its use has been successful at transient resolution of hyperadrenocorticism in a patient prior to surgery. The dose used is 65 mg/kg q12h PO.
•
Therapeutic Notes • PreSurgical Management: A constant rate infusion (CRI) of hydrocortisone at a dose of 625 µg/kg per hour beginning at induction and continuing for 24 to 48 hours postoperatively is recommended. Intravenous fluid therapy and parenteral antibiotics are also strongly recommended. In cats with concurrent DM, intermediate-acting insulin should be given at one-half dose the morning of surgery. Anticoagulant therapy may be considered to prevent the chance of thromboembolic complications. • PostSurgical Management: After discontinuation of the hydrocortisone CRI, prednisone is given at a dose of 2.5 mg/cat q12h PO. For those patients undergoing bilateral adrenalectomy or for those
240
experiencing hyperkalemia or hyponatremia, mineralocorticoid therapy should be instituted and serum electrolytes should be checked twice daily for several days. PostSurgical Complications: Common complications include sepsis, surgical wound dehiscence, adrenal insufficiency, thromboembolic disease, and pancreatitis. Surgery related death has been reported in up to 40% of cases. Transsphenoidal Hypophysectomy: This procedure has already yielded some success and is currently being investigated as a potential alternative to adrenalectomy for cats with PDH. Ketoconazole and Mitotane: The use of these drugs has been discouraged due to adverse side effects in cats and poor to absent therapeutic response. Trilostane: Currently there is scant data available on the use of this medication in the feline species. Radiation treatment is not currently recommended.
Prognosis The prognosis in cats with hyperadrenocorticism is guarded to grave. The success of medical therapy is poor, and there are significant risks associated with surgery due to the debilitated state of the patient and the common occurrence of postsurgical complications. Early recognition of disease and presurgical medical treatment offers the best chance for a successful outcome.
Suggested Readings Herrtage ME. 2005. Hypoadrenocorticism. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1612–1622. St. Louis: Elsevier Saunders. Reusch CE. 2005. Hyperadrenocorticism. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1592–1610. St. Louis: Elsevier Saunders. Sherding RG. 1994. Endocrine Diseases. In RG Sherding, ed., The Cat: Diseases and Clinical Management, 2nd ed., pp. 1481–1489. New York: Churchill Livingstone.
CHAPTER 102
Hyperaldosteronism Andrew Sparkes
Overview Since first reported in 1983 there have been numerous case reports of primary hyperaldosteronism (HAD; also known as primary aldosteronism or Conn’s Disease), giving evidence that this disease may be more common than was appreciated in the past. The disease is caused by an adrenal gland aldosterone-secreting adenoma or, rarely, a carcinoma. There has also been a recent report of cases associated with adrenal gland hyperplasia, apparently similar to idiopathic hyperaldosteronism in humans. Aldosterone is the principal hormone responsible for control of serum potassium levels and is the major mineralocorticoid produced by the adrenal gland. Physiologically, production and secretion of aldosterone is mainly stimulated by hyponatremia, hyperkalemia, and renal hypotension, acting via the renin angiotensin aldosterone system (RAAS). The primary functions of aldosterone are to increase serum sodium and decrease serum potassium levels and to regulate extracellular fluid volume. Renin is produced by cells of the afferent arterioles in the kidney forming part of the juxtaglomerular apparatus. Increased secretion of renin in response to reduced arteriolar pressure or reduced sodium concentrations leads ultimately to the formation of angiotensin II, which is largely responsible for increasing cardiac output and circulatory volume. In addition, angiotensin II acts upon the cells of the zona glomerulosa of the adrenal cortex to cause increased synthesis and release of aldosterone. Aldosterone then stimulates sodium retention and potassium secretion at the distal renal tubule. Hyperkalemia also directly stimulates the release of aldosterone and thus aldosterone can directly control potassium homeostasis in addition to the sodium level and circulating volume. In addition to potassium, excretion of hydrogen, magnesium, and ammonium ions is also increased under the influence of aldosterone. Most reported cases of hyperaldosteronism have been in older cats, although there are also reports of middle-aged cats (5–6 years of age) being affected. The onset of signs is often insidious although sudden development of more striking signs may prompt first presentation. The two commonly recognized presenting complaints with this disease are generalized muscle weakness due to hypokalemia (hypokalemic polymyopathy; see Figure 33-1), and ocular, or occasionally neurologic, manifestations of hypertension such as hyphema, retinal vascular tortuosity, retinal hemorrhage, and retinal detachment. See Figures 193-1, 193-2, and 193-4. Overt clinical signs of hypokalemia are generally not seen until the serum concentration falls below 3.0 mEq/L (3.0 mmol/L). The neuromuscular and cardiovascular systems are mainly affected by hypokalemia. Signs typically include focal or generalized mild to profound skeletal muscular weakness. See Chapter 143. In hyperaldosteronism, serum potassium levels do not necessarily remain consistently low; marked fluctuations may occur. Serum creatine kinase (CK) values may, therefore, indicate that there is, or has been, intermittent hypokalemia because CK will remain elevated longer than the potassium remains low. Generally, potassium levels must drop to below 2.5 mEq/L (2.5 mmol/L) for significant leakage of CK to occur.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Hyperaldosteronism is often not suspected unless hypokalemia or hypertension is found during routine evaluations. Investigations into the cause of hypokalemia or hypertension are warranted in all cases. In older cats with hypokalemia, assessment of renal function, serum glucose, and thyroid status are important, but if these are normal and other causes of the findings are not obvious, testing for HAD is appropriate. Other changes seen in association with HAD should also trigger an investigation. Metabolic alkalosis may occur due to the increased renal excretion of hydrogen and ammonium ions. Cats are often in generally poor condition with inappetence, weight loss, and reduced grooming. There may be polyuria and polydipsia associated with the hypokalemia. If the hypokalemia is chronic, renal damage (hypokalemic nephropathy) may occur. Although hypokalemic polymyopathy is the most common presenting sign, hypertension is frequently also present, and blood pressure assessment is important in all suspected cases. Presenting clinical signs may relate to systemic hypertension, including sudden impairment of vision (e.g., retinal hemorrhage or detachment) or overt intraocular hemorrhage causing hyphema. An anterior abdominal mass, just cranial to the kidneys, may be palpable. Differential diagnoses include chronic renal failure, hyperthyroidism, myasthenia gravis, and other causes of systemic hypertension. Note that persistent, profound hypokalemia may lead to impaired renal function and thus discerning whether hypokalemia is secondary to chronic renal disease or a cause of the chronic renal disease can be problematic.
Diagnosis Primary Diagnostics • Presumptive Diagnosis: This can be made on the basis of appropriate signs, blood panel findings, and an enlarged adrenal. • Blood Panel: The important initial findings are hypokalemia, markedly elevated creatine kinase (e.g., >10,000 U/L), elevated “muscle enzymes” (e.g., aspartate transaminase [AST] and alanine aminotransferase [ALT]). Both the potassium and CK concentrations are variable. In some cases the changes may be mild or even within normal limits due to the typical waxing and waning nature of the disease. • Aldosterone and Renin Assays: In conjunction with the blood panel findings, an elevated plasma aldosterone concentration (PAC) will confirm the presence of HAD. Even more ideally, the diagnosis of HAD is achieved by demonstrating a high PAC with a concomitant low plasma renin concentration.
Secondary Diagnostics • Imaging: An adrenal mass may be identifiable radiographically (See Figure 102-1), but ultrasound is more sensitive. See Figure 102-2. Additionally, ultrasonography allows an assessment of the surrounding structures and may give information about the local invasiveness of the mass. • Urinary Potassium: Increased urinary potassium loss accompanies the high levels of aldosterone secretion. This can be documented by measuring the renal fractional clearance of potassium, which should normally be less than 15 to 20%, and, in the face of hypokalemia in a normal cat, should be much lower than this. The fractional clearance is usually markedly elevated in cases of HAD.
241
SECTION 1: Diseases and Conditions
ideal, and along with this in primary HAD, PAC is generally well above reference ranges.
Treatment Primary Therapeutics • Surgical Management: Surgical removal of the abnormal adrenal gland is the treatment of choice; the disease is usually unilateral. However, although the tumors are usually adenomas, they are often locally invasive, and there may be invasion of local blood vessels, including the vena cava. In such cases, surgical management may be much more challenging. If adrenalectomy is performed it is often curative although the rare malignant forms have a poorer long-term prognosis.
Secondary Therapeutics Figure 102-1 Lateral abdominal radiograph showing an adrenal mass (arrow) cranial to the kidneys.
• Potassium Supplementation: If hypokalemia is severe, potassiumsupplemented intravenous fluid therapy is important initially. Oral therapy should follow or be the initial treatment. Potassium gluconate is given at a dose of 2 to 4 mmol (mEq)/cat q12h PO as a starting dose and adjusted according to response. • Spironolactone: This drug is a potassium-sparing diuretic that acts as an aldosterone antagonist, thus helping control the effects of the disease. It is dosed at 1 to 2 mg/kg q12h PO.
Therapeutic Notes • If surgical treatment is regarded as impractical or declined by the owner, medical treatment may control clinical signs for variable periods. • Medical management is also indicated to stabilize a patient prior to undertaking adrenalectomy. • Although there are occasional reports of signs being controlled for a considerable period, generally cats become progressively less responsive to medical treatment over time.
Prognosis
Figure 102-2 Ultrasonographic appearance of an adrenal mass in a cat with primary aldosteronism.
Diagnostic Notes • All cats with HAD should have systemic blood pressure measured, whether showing clinical signs or not. • Plasma renin is more difficult to assay because this is a species-specific hormone. Cross-reactivity with human assays does not occur and, unless the function assay plasma renin activity (PRA) is used, a species-specific feline assay is required. • Once HAD is identified, care should be taken to distinguish primary HAD from secondary HAD. Secondary HAD occurs when there is increased physiological production of aldosterone as a result of the activation of the RAAS. Measurement of plasma renin is, therefore,
242
The long-term prognosis for adrenal adenomas is clearly better than for adenocarcinomas, and surgical removal can be completely curative. However, even with successfully removed adenomas, recurrence of disease affecting the contralateral gland has been encountered up to a year or more after the adrenalectomy.
Suggested Readings Ash RA, Harvey AM, Tasker S. 2005. Primary hyperaldosteronism in the cat: a series of 13 cases. J Fel Med Surg. 7(3):173–182. Javadi S, Djajadiningrat-Laanen SC, Kooistra HS, et al. 2005. Primary hyperaldosteronism, a mediator of progressive renal disease in cats. Domest Anim Endocrinol. 28(1):85–104. MacKay AD, Holt PE, Sparkes AH. 1999. Successful surgical treatment of a cat with primary aldosteronism. J Fel Med Surg. 1(2):117–122. Rose SA, Kyles AE, Labelle P, et al. 2007. Adrenalectomy and caval thrombectomy in a cat with primary hyperaldosteronism. J Am Anim Hosp Assoc. 43(4):209–214.
CHAPTER 103
Hypercalcemia Michele Fradin-Fermé
Overview Hypercalcemia is defined as a serum concentration of total calcium over 3 mmol/L (12.0 mg/dL). Clinical signs appear when total calcium (tCa) concentration is over 3.75 mmol/L (15 mg/dL). It is often mild to moderate in severity without clinical signs. Hypercalcemia has several deleterious effects. (a) Vasoconstrictive properties can decrease renal blood flow and glomerular filtration rate leading to renal failure. (b) Mineralization of tissues in all parts of the body, most commonly in the kidneys, cardiovascular system, lungs, and nervous system, known as ectopic calcification, can have adverse effects on the organs affected. Interaction with serum phosphorus is important because mineralization will occur in tissues when the Ca × P product is greater than 70. (c) Electrolyte imbalance results in constipation, muscle weakness, and nervous signs. Regulation of serum calcium concentration is complex and involves the interaction of parathyroid hormone (PTH), calcitonin, and vitamin D. The intestines, kidneys, and bones are the major regulators of calcium balance. Serum calcium exists in three forms: ionized (iCa; 50–60% of serum calcium), protein bound (35%), and complexed calcium (10%). The most common causes of hypercalcemia in cats are acute and chronic renal failure, humoral hypercalcemia of malignancy (HHM), secondary or primary hyperparathyroidism, and idiopathic hypercalcemia. Idiopathic hypercalcemia has been recognized more frequently in cats since 1990, but its etiology remains idiopathic. See Table 103-1 for other less common causes. Common clinical signs include vomiting, weight loss, anorexia and dysuria.
TABLE 103-1: Causes of Hypercalcemia in Cats Common Causes Hyperparathyroidism (secondary and primary) Neoplasia and humoral hypercalcemia of malignancy (lymphosarcoma, lung cancers, multiple myeloma) Chronic or acute renal failure Vitamin D toxicosis (i.e., iatrogenic or rodenticide) Idiopathic Iatrogenic (i.e., excessive calcium containing phosphate binders) Uncommon Causes Spurious lab result Granulomatous disease (i.e., histoplasmosis, blastomycosis, or schistosomiasis) Hypoadrenocorticism Hyperparathyroidism Vitamin A intoxication
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Diagnosis Primary Diagnostics • History: Determine if the cat has a history of renal insufficiency or cancer (especially squamous cell carcinoma or lymphoma). Ask about hunting habits and if the cat is eating an acidifying diet. • Clinical Signs: These are usually mild and non-specific and include anorexia, lethargy, and weight loss. Vomiting, polyuria, and polydipsia are not as common as in dogs, but symptoms related to the urinary system are quite frequent in cases of chronic hypercalcemia. These include dysuria and hematuria associated with calcium-containing uroliths. Severe symptoms include bradycardia, cardiac arrhythmias, muscle twitching and seizures, stupor, and coma secondary to hypercalcemia-induced renal failure. Death may occur if hypercalcemia is over 5 mmol/L (20 mg/dL), as in HHM, or when it develops rapidly, as in rodenticide intoxication. In primary hyperparathyroidism an enlarged parathyroid gland may be palpable. • Minimum Data Base: Complete blood count, serum biochemistry panel, urinalysis, and retroviral tests should be performed. Blood urea nitrogen and creatinine values may be elevated either due to primary or secondary renal failure. A low urine specific gravity will be present in conjunction with renal failure. • Ionized Calcium: iCa concentration should be used to verify the presence of hypercalcemia. In idiopathic hypercalcemia ionized calcium is often increased disproportionately in comparison to tCa. A panel for measuring serum iCa, PTH, and parathyroid hormonerelated protein (PTHrP) is available from Michigan State University. (1-517-353-0621; www.animalhealth.msu.edu) • Parathyroid Hormone Concentration: Primary hyperparathyroidism is characterized by elevated PTH levels above the normal range. However, this is not a consistent finding because some cats will have normal PTH levels. • PTHrP: PTHrP is secreted from some neoplastic cells. This causes hypercalcemia secondary to increased osteoclastic bone resorption and renal tubular reabsorption of calcium. Lymphoma, squamous cell carcinoma, carcinomas of the lung, and multiple myeloma are most likely.
Secondary Diagnostics • Diagnostic Imaging: Look for ectopic calcification (i.e., arterial, gastric, intestinal, renal, and so on), pulmonary masses, bone masses, or uroliths. Approximately one-third of cats with calcium oxalate urolithiasis have hypercalcemia. See Table 103-2 for differential diagnoses.
Diagnostic Notes • In cats there is no valid formula for adjusting serum calcium concentration to albumin levels. • Always confirm an elevated calcium concentration. Lipemia or hemolysis can falsely elevate total serum calcium concentration reported by colorimetric analyzers. • Blood samples have to be collected and handled anaerobically for accurate iCa measurement.
243
SECTION 1: Diseases and Conditions
TABLE 103-2: Differential Diagnosis Etiology
Symptoms
Diagnosis
Idiopathic
Absent to mild
Renal Insufficiency
Polydipsia, polyuria, or constipation
Hyperparathyroidism (Primary, Secondary, and Tertiary)
Slow onset Palpable cervical mass in primary hyperparathyroidism
Humoral hypercalcemia of malignancy
Slow onset Lethargy, anorexia, nausea, fatigue, dehydration, azotemia, and coma Rapid onset
Normal to elevated total calcium Severely elevated ionized serum calcium Low parathyroid hormone Normal phosphorus initially Normal ionized serum calcium Elevated urea and creatinine Elevated phosphorus Elevated parathyroid hormone Elevated parathyroid hormone in primary Normal parathyroid hormone in secondary or tertiary Normal to decreased phosphorus Moderate to elevated total calcium Elevated parathyroid hormone-related protein Normal to decreased phosphorus Severely elevated total calcium Increased serum phosphorus
Vitamin D rodenticide or plants containing calciferol
Treatment Primary Therapeutics • Treatment of the underlying condition should be the primary goal of therapy. • Mild idiopathic hypercalcemia may not justify treatment. • Fluid Therapy: Correct dehydration with subcutaneous or intravenous fluid therapy with normal saline. • Calcium Control: Enhance calcium excretion and prevent calcium resorption from bone. • Diuretics: Furosemide is administrated following rehydration in cases of persistent and severe hypercalcemia not associated with renal failure. It should be dosed at 2 to 4 mg/kg q8 to 12h IV, SC, or PO. Thiazide diuretics cause calcium retention and can worsen hypercalcemia; therefore, they are contraindicated. Diuretic use should not be long term. • Glucocorticoids: They are indicated for cases that do not respond to intravenous fluids and furosemide. They reduce bone resorption, decrease intestinal absorption, and increase renal excretion of calcium. They can significantly reduce calcemia in patients with lymphosarcoma, multiple myeloma, hypervitaminosis D, granulomatous disease, hypoadrenocorticism, idiopathic hypercalcemia, but they should not be initiated until a definitive diagnostic has been made. Increased renal excretion of calcium may cause or aggravate hypercalciuria and increase calcium urolithiasis. Prednisolone is given at 1.0 to 2.2 mg/kg q12h PO, IV, or SC. Alternatively, dexamethasone is given at 0.1 to 0.22 mg/kg q12h IV or SC.
Secondary Therapeutics • Calcitonin: Salmon calcitonin reduces osteoclastic activity and can be effective temporarily in decreasing serum calcium concentration due to hypervitaminosis D. It is dosed at 4 IU/kg q8 to 12h IM or SC. • Diet: nonacidyifying diets and high fiber diets are recommended for idiopathic hypercalcemia. Low carbohydrate-high protein diets used for diabetes management are strongly acidifying and, thus, contraindicated.
Therapeutic Notes • For comparison purposes 1 mmol of calcium = 2 mEq of calcium = 40 mg of calcium.
244
• In the United States: 1 mL of a 10% calcium gluconate solution contains 94 mg of calcium gluconate and 4.5 mg of calcium saccharate. This differs from some other countries. • Hospitalized patients should have their serum calcium level and renal values monitored every 12 to 24 hours during treatment. • Serum calcium and phosphorus levels in growing kittens will be significantly higher than adults. Some laboratory normal phosphorus values are appropriate for kittens but not adults. • Although primary hyperparathyroidism is uncommon, older cats presenting with hypercalcemia, hypophosphatemia, normal renal function, and no evidence of neoplasia should have their PTH level checked, especially if cervical (i.e., thyroid/parathyroid) palpation reveals enlargement. An enlarged parathyroid gland may be interpreted as thyroid enlargement based on palpation. • Phosphate binders and vitamin D, vitamin A, and calcium supplementation may promote hypercalcemia.
Prognosis The prognosis is largely determined by the underlying cause of hypercalcemia and the cat’s response to therapy. Cats with idiopathic hypercalcemia are predisposed to chronic renal disease and, possibly, calcium oxalate urolithiasis.
Suggested Readings Feldman EC. 2003. Disorders of the parathyroid glands. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1508–1535. Philadelphia: WB Saunders. Midikff AM, Chew DJ, Randolph JF, et al. 2000. Idiopathic Hypercalcemia in Cats. J Vet Intern Med. 14(6):619–626. Rosol TJ, Chew DJ, Nagode LA, et al. 2000. Disorders of Calcium: Hypercalcemia and Hypocalcemia. In SP DiBartola, ed., Fluid Therapy in Small Animal Practice, 2nd ed., pp. 108–162. Philadelphia: WB Saunders. Schenk PA, Chew DJ, Behrend EN. 2006. Update on Hypercalcemic Disorder. In JR August, ed., Consultations in Feline Internal Medicine, 5th ed., pp. 157–168. St Louis: Elsevier.
CHAPTER 104
Hypereosinophilic Syndrome Sharon Fooshee Grace
Overview Feline hypereosinophilic syndrome (FHS) is a rare disorder characterized by chronic peripheral eosinophilia and an associated eosinophilic infiltrate in various organs, especially the gastrointestinal tract, spleen, liver, bone marrow, and lymph nodes. The cause is unknown but is possibly due to an excessive reaction to an antigenic stimulus or uncontrolled immune regulation of eosinophil production. The tissue infiltrate eventually leads to dysfunction or failure of the involved organ(s). It is not considered a neoplastic condition because the eosinophils are morphologically mature and normal in appearance. However, the biologic behavior of the disease is similar to neoplasia in that the clinical course is rapidly progressive and response to therapy is poor. Although FHS has been reported in young cats, most cases involve middle-aged to older cats. No breed predisposition is apparent; females may be more frequently affected. Some authors have speculated that eosinophilic enteritis may be a prelude to FHS. Differential diagnoses include other causes of eosinophilia: endo- and ectoparasitism, hypersensitivity disorders, immune-mediated disease, eosinophilic granuloma complex, asthma, and neoplasia (i.e., mast cell tumor, lymphoma, or paraneoplasia). The distinction between FHS and eosinophilic leukemia is not clear. For unknown reasons, cats appear predisposed to a variety of eosinophil-mediated diseases.
Diagnosis Primary Diagnostics • Clinical Signs: In the few cases reported, the most consistent signs were vomiting, diarrhea (sometimes bloody), weight loss, and anorexia. Intractable pruritus is sometimes seen. Seizures and fever are reported but uncommon findings. Cutaneous involvement and polyphagia are reported but rare. Abnormalities on physical examination include thickened bowel loops, mesenteric and peripheral lymphadenopathy, and hepatosplenomegaly. • Complete Blood Count: Persistent, unexplained eosinophilia is a hallmark of FHS. The absolute eosinophil count is frequently in excess of 3,000 eosinophils/µL. The mean count in one report was approximately 42,000 eosinophils/µL. The eosinophils are morphologically normal. • Tissue Biopsy and Histopathology: A variety of soft tissues are infiltrated with eosinophils. In most cases, both the mucosa and submucosa of the small intestine are extensively involved. • Bone Marrow Aspiration and Cytology: Bone marrow examination reveals eosinophilic hyperplasia (making up as many as 40% of the nucleated cells), whereas the other cell lines are present in normal numbers. The erythroid series may be depressed in some cats.
Secondary Diagnostics • Biochemical Profile and Urinalysis: This will help assess general health and determine if organ dysfunction is present.
Diagnostic Notes • Because the cause of FHS remains unknown, diagnosis of the disorder necessitates eliminating other possible causes of peripheral and tissue eosinophilia (see Differential Diagnosis).
Treatment Primary Therapeutics • Steroids: Prednisolone is the primary therapeutic agent for FHS. High doses are required to induce remission (4–6 mg/kg per day for 2–4 weeks). The dose may then be slowly tapered over, if possible, over 4 to 6 months.
Secondary Therapeutics • Chemotherapy: Alkylating agents, such as chlorambucil, azathioprine, and cyclophosphamide, may be considered for refractory cases, but these drugs are often not tolerated well by cats and do not appear to alter the progressive course of the disease. • Hydroxyurea or cyclosporine A: These drugs are optional therapies for refractory cases. Experience with their use in treating FHS is limited.
Therapeutic Notes • Most cases will require long-term treatment.
Prognosis In most cases, relentless progression of the disease leads to a grave prognosis. Death often occurs within a few weeks of diagnosis.
Suggested Readings Huibregtse BA, Turner JL. 1994. Hypereosinophilic syndrome and eosinophilic leukemia. J Amer Anim Hosp. 30(6):591–599. Lilliehook I, Tvedten H. 2003. Investigation of hypereosinophilia and potential treatments. Vet Clin North Amer. 33:1359–1378. Neer TM. 1991. Hypereosinophilic syndrome in cats. Compend Contin Educ. 13(4):549–555.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
245
CHAPTER 105
Hyperesthesia Syndrome Amanda L. Lumsden
Overview Hyperesthesia syndrome is a disorder in cats that results in rippling or rolling of the skin along the spine. It has also been called “ripple back,” “rolling skin disease,” “neurodermatitis,” “neuritis,” “psychomotor epilepsy,” and “pruritic dermatitis of Siamese.” There has been little research on the disorder, and the underlying pathophysiology of the syndrome remains elusive. It appears to be a central nervous system disease causing peripheral neuritis. Males and females are equally affected, and although it can occur at any age, it is more commonly seen in cats 1 to 5 years old. The condition has been more frequently reported in Siamese, Burmese, Persian, and Abyssinian cats but can affect all breeds. As the name ripple back implies, cats present with twitching or rippling or rolling of the skin along the dorsum. It generally begins in the area of the thoracolumbar spine and continues down the skin to the tail. Cats will often run wildly as if attempting to escape the sensation and may vocalize during the time it is occurring. The period of time that the rippling occurs is usually brief (30 seconds to 5 minutes), and the frequency of occurrence varies between individual cats. During the attacks mydriasis is common. A cat may also stare at or attack and bite its tail as well as the flanks. They are often sensitive to being stroked along the area and may display aggressive behavior toward humans when touched along the lumbar spine, especially just prior to, or during, an episode.
Diagnosis Primary Diagnostics • Clinical Signs: See Overview. • Response to Therapy: See Treatment for the drugs used in treating this disorder.
• Other Rule Outs: These include musculoskeletal (i.e., myositis or myopathy), neurological (i.e., epilepsy, brain tumors, or spinal disease), and behavioral (i.e., compulsive disorder or displacement behavior).
Treatment Primary Therapeutics • Phenobarbital: Give 8 to 32 mg q12h PO for 1 to 3 months (or longer). Use the lowest effective dose that does not cause sedation. The recommended initial dose is 16 mg q12h PO.
Secondary Therapeutics • Clomipramine: Give 0.5 to 1 mg/kg q24h PO. • Fluoxetine: Give 0.5 to 2.0 mg/kg q24h PO.
Therapeutic Notes • When using phenobarbital, check liver enzymes every 3 to 6 months; however, liver enzyme elevation is rare in cats. Do not use a serum separator tube because it falsely lowers the level. • If the cat does not respond to phenobarbital or if the side effects (i.e., sedation or polyphagia) are too severe, it should be discontinued and a secondary therapeutic medication should be tried.
Prognosis The prognosis is usually good for controlling the signs of hyperesthesia syndrome, especially if the cat responds to phenobarbital initially.
Suggested Readings Secondary Diagnostics • Primary Rule Outs: These include flea allergy dermatitis (i.e., response to steroids or flea control), food allergy (food trial), and atopy (response to steroids).
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
246
Bagley RS. 2007. The Cat with Tremor or Twitching. In J Rand, ed., Problem-Based Feline Medicine, pp. 862–863. Philadelphia: Elsevier Saunders. Ciribissi, J. 2009. Feline syperesthesia syndrome. Compendium. 31(3):116.
CHAPTER 106
Hyperkalemia Michele Fradin-Fermé
TABLE 106-2: Electrocardiogram Abnormalities Caused by Hyperkalemia
Overview Hyperkalemia is defined as a serum concentration of potassium over 5.5 mmol/L (5.5 mEq/L) with normal values being 4.0 to 5.0 mmol/L (4.0–5.0 mEq/L). Mildly elevated values are without clinical signs; however, it becomes life-threatening when over 7.5 mmol/L (7.5 mEq/L). Potassium is principally an intracellular cation; only approximately 2% of total body potassium is found in the blood. Potassium is eliminated by the kidneys, and elimination is enhanced by aldosterone. Serum changes vary with intake, distribution, or excretion. Hyperkalemia is often associated with oliguric states, most commonly acute renal failure and urethral obstruction, and massive cellular lysis typically following thromboembolism. Hyperkalemia can also be iatrogenic due to an overzealous intravenous infusion of potassium chloride (KCl), usually due to too rapid a rate of infusion, the concentration being too high, or KCl added in the infusion set without sufficient mixing. See Table 106-1 for other causes. Hyperkalemia can have toxic effects on the heart. It enhances and then depresses myocardial excitability leading to bradycardia and arrhythmias, although some cats will show tachycardia. The electrocardiographic abnormalities become more intense as hyperkalemia increases. See Table 106-2. The clinical signs of hyperkalemia are dependent on the etiology and are also related to the toxic effects of the potassium on the heart. Lethargy, weakness, poor perfusion, and death may occur. Clinical signs occur when the potassium concentration exceeds 8 mmol/L (8 mEq/L).
Diagnosis Primary Diagnostics
TABLE 106-1: Etiologies of Hyperkalemia in Cats Decreased excretion
Intravenous infusion of potassium (Note: It is unlikely that hyperkalemia will be induced by oral potassium because vomiting will likely be induced first.)
Acute renal failure Ruptured bladder Urethral tear Hypoadrenocorticism Primary hypoaldosteronism Marked hypovolemia Drugs (spironolactone, angiotensin converting enzyme inhibitors, and nonsteroidal antiinflammatory drugs)
Moderate hyperkalemia (6.0–8.0 mmol/L [6.0–8.0 mEq/L]) Severe hyperkalemia (>8.0 mmol/L [8.0 mEq/L])
Peaked T waves Decreased amplitude of R waves Prolongation of the P-R interval Flattening or absence of P waves Bradycardia Prolongation of the PR and QT intervals Widening of the QRS complex Sinoventricular rhythm No P waves Widening of QRS complex Ventricular fibrillation Ventricular asystole Cardiac arrest
• Clinical Signs: Auscultation is important. Bradycardia and arrhythmias are common; some cats exhibit tachycardia. • Chemistry Profile: The cause of hyperkalemia must be identified. In patients with azotemia, consider anuric or oliguric renal failure (see Chapter 189) or a ruptured or obstructed urinary tract. If the sodiumto-potassium ratio is less than 27, consider hypoadrenocorticism. See Chapter 111. Serum potassium may be increased or decreased with diabetic ketoacidosis. See Chapter 51. • Electrocardiogram (ECG): ECG abnormalities are characteristic of hyperkalemia but vary with the potassium concentration. See Table 106-2 and Figures 106-1, 106-2, and 106-3.
Treatment
• History: Hyperkalemia should be anticipated with ureteral or urethral obstruction and should be expected 3 to 4 days following a thromboembolic event. See Chapters 212, 220, and 221.
Increased intake
Mild hyperkalemia (<6.0 mmol/L [6.0 mEq/L])
Redistribution of potassium Metabolic acidosis Hypertonic solutions Prostaglandin inhibitors β-blockers Succinylcholine Thromboembolism Tumor lysis Pleural effusion
Primary Therapeutics • Underlying Disease: Correction of the underlying cause is essential. Most are urinary in origin. • Fluid Therapy: In cats without life-threatening cardiac abnormalities institute dilutional fluid therapy. Give normal saline (0.9%) IV. Lactated Ringer ’s solution has only 4 mmol/L (4 mEq/L) of potassium so it is acceptable. • Emergency Cardiac Therapy: Initially give 1 g/kg of 50% dextrose IV with 0.25 to 1.0 IU/kg of regular insulin to drive potassium intracellularly and rapidly lower the serum potassium level. • Arrhythmia Control: Give 50 to 100 mg/kg (0.5–1.0 mL/kg) of 10% calcium gluconate over 10 to 15 minutes IV for life-threatening arrhythmias. Monitor the heart rate during administration and discontinue if bradycardia develops. This will not lower serum potassium levels; its cardioprotective effects only last about 30 minutes. • Emergency Lowering of Potassium: Give 1 to 2 mmol/kg (1–2 mEq/ kg) of sodium bicarbonate slowly IV. Give one-half the dose over 20 to 30 minutes and add the remainder to the intravenous fluids. Monitor serum calcium because this may induce hypocalcemia in hyperphosphatemic urinary-obstructed cats.
Therapeutic Notes th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• For Comparison Purposes: 1 mmol of potassium = 1 mEq of potassium = 39.3 mg of potassium.
247
SECTION 1: Diseases and Conditions
Recorded: 27 Nov 2003 06:18
Scale: 10mm/mV, 50mm/s
HR:
bpm
00:00.0
00:03.5
Figure 106-1 This cat was presented with a urethral obstruction. Its serum potassium was 7.6 mmol/L (7.6 mEq/L). Note the peaked T waves, decreased amplitude of the P and R waves, and a prolonged P-R interval. Electrocardiogram courtesy Dr. Gary D. Norsworthy.
Recorded: 30 Nov 2003 06:37
Scale: 10mm/mV, 50mm/s
HR: 128 bpm
00:00.0
00:03.5
Figure 106-2 This cat was in anuric renal failure with a serum potassium of 10.4 mmol/L (10.4 mEq/L). Note the widened QRS complexes, absence of P waves, and bradycardia. Electrocardiogram courtesy Dr. Gary D. Norsworthy.
• For Comparison Purposes: KCl comes as a 15% solution with 20 mmol (20 mEq) in a 10-mL vial. It contains 2 mmol (2 mEq)/mL of potassium = 149 mg/mL of KCl = 4 mOsmol/mL. • When potassium is given IV, the rate of infusion of KCl should be less than 0.5 mmol/kg/h (0.5 mEq/kg per hour).
248
Prognosis The prognosis is related to the serum potassium level. Levels over 8.0 mmol/L (8.0 mEq/L) are life-threatening. If it can be lowered rapidly, the prognosis is good as long as the underlying disease is
Hyperkalemia
Device: BIOLOG VET 007364 Recorded: 01 Oct 2009 16:55 00:00.0
Single Lead ECG
Patient:
Scale: 10mm/mV, 50mm/s
Doctor:
Ref.: HR: 63 bpm
00:03.5
Figure 106-3 This cat had a urethral obstruction and a serum potassium of 11.6 mmol/L (11.6 mEq/L). There are an arrhythmia, widening of the QRS complex, no P waves, and severe bradycardia. These are common in severe hyperkalemia. His abnormalities corrected after relief of the obstruction, intravenous fluids with dextrose, and regular insulin. Electrocardiogram courtesy Dr. Gary D. Norsworthy.
corrected. The prognosis is grave in the case of acute anuric or oliguric renal failure.
Suggested Readings Bell R, Mellor DJ, Ramsey I, et al. 2005. Decreased sodium:potassium ratios in cats: 49 cases. Vet Clin Pathol. 34(2):110–114.
Cowgill L, Francey T. 2005. Acute Uremia. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1731–1751. Philadelphia: WB Saunders. DiBartola SP. 2001. Management of hypokalaemia and hyperkalaemia. Proceedings of AAFP/ESFM Symposium at WSAVA Congress. J Fel Med Surg. 3:181–183.
249
CHAPTER 107
Hypertension, Systemic Beate Egner
Overview Systemic hypertension is not a rare finding in feline patients. It can be considered a sign of a disease but also a disease itself. In cats with cardiac and renal disease hypertension is a severe risk factor and needs to be controlled aggressively. Because many cats develop renal disease at some point in their life and because renal disease is a main cause of hypertension, hypertension is particularly common in the cat older than 8 years of age. A chronic increase in blood pressure (BP) above the normal values is referred to as hypertension. Ideally, the arterial systemic BP of a cat should be 124/84 mm Hg (±15 mm Hg) with normal daily variations during physical activity. This means that BP should be measured at least once a year, averaging three to five consecutive readings, to determine an individual’s normal. In the absence of such a sensitive parameter, the transition to hypertension is likely to occur above a value of 150/95. In the case of elevated results, BP should be measured several times to confirm hypertension versus individual variations. In veterinary medicine we look at different stages of hypertension, according to its risk category for target organ damage (TOD). See Table 107-1. High BP causes arterial wall stress, resulting in potential damage of mainly four organs. (a) The eyes are affected resulting in hypertensive retinopathy, hypertensive choroidopathy, and hypertensive optic neuropathy. The symptoms include mydriasis (unilateral or bilateral), hyphema, sudden blindness, tortuous retinal vessels, retinal hemorrhage, and retinal detachment. See Chapter 193. (b) The kidneys are affected resulting in glomerular sclerosis, tubulonecrosis, and interstitial inflammation and fibrosis (due to proteinuria associated with hypertension and reabsorption of proteins into the interstitium). The symptoms of acute or chronic renal disease are present. See Chapters 189 and 190. (c) The heart is affected in 70% of hypertensive cats. The results are left ventricular hypertrophy resulting in long-term oxygen deprivation to the myocardium leading to cell death and foci for developing arrhythmias. Clinically these cats have heart murmurs, gallop rhythms, tachycardia, elevated R-waves, and dysrhythmia. See Chapter 108. (d) The brain is affected causing hypertensive encephalopathy that manifests as brain edema and bleeding producing increased intracranial pressure. The symptoms are vocalization (likely due to a headache), head pressing (also likely due to a headache), change of behavior (i.e., lethargy, hyperactivity, and so on), aggression (likely due to pain), and seizures. In contrast to human medicine, almost all hypertensive cats are experiencing secondary hypertension; it is due to an underlying disease.
TABLE 107-1: Categories of Hypertension Risk Category I II III IV
Systolic Blood Pressure
Diastolic Blood Pressure
<150 150–159 160–179 >180
<95 95–99 100–119 >120
Diagnosis Primary Diagnostics • Clinical Findings: The most common clinical findings are seizures, stroke-like signs, vocalization, mydriasis, hyphema, retinal vessel tortuosity, retinal hemorrhage, retinal detachment, and sudden blindness. See Figures 193-1, 193-2, 193-4, and 211-2. • BP measurement can be performed using several technologies. Each has pros and cons.
Direct (Intra-Arterial) Measurement Risk of Target Organ Damage Minimal Mild Moderate Severe
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
250
(a) Renal disease can elevate BP dramatically, even up to 300 mm Hg systolic. (b) Hyperthyroidism usually does not cause a BP rise above 180 mm Hg systolic and rarely leads to diastolic hypertension. There may be a mild decrease of the diastolic pressure due to a thyroid hormone induced vasodilation of the resistance arterioles; tachycardia is a common finding. (c) Diabetes mellitus may produce mild elevation of BP without tachycardia. (d) A pheochromocytoma is an extremely rare tumor of the sympathetic nervous system, mainly in the adrenal medulla. Episodic secretion of catecholamines can raise BP to extremely high values followed by normal readings during the nonactive period of this tumor. (e) Primary and secondary hyperaldosteronism can also be a reason for high BP. Primary hyperaldosteronism mainly increases BP due to volume increase (sodium increase and water retention). See Chapter 102. Secondary hyperaldosteronism (renal hyperaldosteronism) is associated with high renin and angiotensin levels. Regardless of which type of hyperaldosteronism is present, fibroses and arterial remodeling occur resulting in impaired arterial compliance, presystolic amplitudes if measured with the HDO, and an increase in peripheral resistance. (f) Other causes of hypertension include obesity, acromegaly, hyperparathyroidism, intracranial lesions (e.g., tumor), hypercalcemia, polycythemia, arteriovenous fistula, and other tachycardia-inducing diseases. Idiopathic hypertension is defined as hypertension secondary to an undiagnosed underlying disease. In some cases, the underlying disease will be diagnosed months to years after the diagnosis of hypertension is made. Hypertension can be isolated systolic hypertension (high systolic only), isolated diastolic hypertension (high diastolic only), or mixed (systolic and diastolic pressures are elevated). Differential diagnoses include pain and the white coat effect (i.e., elevated BP caused by excitement or stress due to the presence of the veterinarian or the clinical environment).
• Considered the gold standard. • Not practical for clinical practice.
Doppler Flow Meter • Considered by some to be the method of choice for clinical practice. • Designed to measure the systolic pressure although sometimes the reading is closer to the mean arterial pressure. • Measurement of diastolic pressure is difficult and often not possible.
Hypertension, Systemic
• It measures the cuff pressure, not the vascular pressure. In theory they should be the same. • The correlation of the cuff pressure with arterial pressure may be affected by the user, soft-tissue compliance, the speed of deflation, cuff size and placement, the pressure itself, and the auditory acuity of the examiner. • Its most reliable readings occur within the range of 70 to 160 mm Hg due to valve limitations. • Doppler units are the least expensive of the available technologies but show the greatest variations compared to direct BP measurements.
• •
•
•
Conventional Oscillometry • It calculates the systolic and diastolic arterial pressures out of the mean pressure. • All types of hypertension are detectable. • It works with an eight-bit processor by analyzing signals according to how much are they matching with an ideal preprogrammed shape of a human pulse wave. • It tends to be less accurate in smaller animals, at high heart rates, and in the presence of vasoconstriction. • Its accuracy is possible only within 70 to 160 mm Hg due to valve limitations and processor capacities. • Artefacts cannot be differentiated from pulse waves on some machines. • It will produce no measurement in severely affected cardiac output situations (arrhythmia) or with poor peripheral perfusion (i.e., shock, drug-induced massive vasoconstriction, and so on). • The readings are limited by high heart rates. • Movement affects the readings.
High Definition Oscillometry (HDO™) • It measures systolic, diastolic, and mean blood pressure; therefore, all types of hypertension can be detected. • It provides graphical analysis of the reading permitting visible control of the results (pulse versus artefact), visible analysis of arterial
•
compliance, visible information on cardiac output, and visible information on rhythm and related problems. See Figure 107-1. It is not limited by a weak pulse, vasoconstriction, or arrhythmia. It works with a 32-bit processor allowing for real-time assessment of the incoming signals and real-time programming of the valves toward linearity over the entire pressure range (5–300 mm Hg). The processor speed further allows scanning of the incoming signal and measures directly the pressure instead of matching it with a preprogrammed curve. It is highly sensitive to pulse signals and to movement of the patient. It will not function with a patient that is uncooperative. Readings are best taken at the base of the tail because this area is least affected by patient movement. Pulse wave analysis requires that the unit be connected to a computer with Windows™.
Secondary Diagnostics • Electrocardiogram (ECG): Abnormalities that may be seen include increased R-wave amplitude (high voltage), wide QRS complexes, deep S-waves, increased duration of P-waves, and arrhythmias. These changes are not specific to hypertension. Interpret them cautiously in the absence of BP measurement. • Echocardiography: Abnormalities that may be seen include left ventricular hypertrophy (predominantly asymmetric with the interventricular septum thicker than the left ventricular free wall), hypercontractility, and functional mitral valve insufficiency. These changes are not specific to hypertension. Interpret them cautiously in the absence of BP measurement. • Thoracic Radiography: Changes include pressure-induced wide aortic arch (mimicking enlarged right atrium), wide and sometimes tortuous thoracic aorta (see Figures 107-2 and 291-20), and parallel (not diverging) caval vein walls. Because the hypertrophy is concentric cardiomegaly it is not always perceptible. • Urinalysis: Urine protein-to-creatinine ratio greater than 0.2. This is indicative for proteinuria associated with chronic renal disease, the most common cause of hypertension.
Figure 107-1 This high definition oscillometry curve shows an arrhythmia in a hypertensive cat with hypertensive hypertrophic cardiomyopathy due to chronic kidney disease. Cardiac output (height of the amplitudes) is clearly affected by the arrhythmia (yellow arrows) and the functional mitral regurgitation (fluctuating height, green circles).
251
SECTION 1: Diseases and Conditions
disease associated with hypertension, in cats above 8 years of age, and in cats presented with unclear symptoms such as anorexia, polydipsia, behavioral change (aggression), weakness, and lethargy. • Ideally, BP measurement should be part of a routine examination at least once a year.
Treatment Primary Therapeutics • Hypotensive Drugs: Administer drugs to lower BP.
Emergency Treatment
(A)
• Urgency: Rapidly reduce pressure values below the high risk level (180/120). This is indicated for acute retinal detachment or unresponsive seizures. • Nitroglycerin Paste: This reduces BP rapidly but is only effective for about 48 hours. Apply 6 mm (1/4 inch) to the concave side of the pinna. If the pinna is cold (due to vasoconstriction), warm it before drug application to increase absorption. Caution: It is also absorbed through human skin readily. • Angiotensin-Converting Enzyme Inhibitor (ACEi): ACEi have an immediate effect on BP (several hours) and a long-term effect (2 weeks). Depending on the substance ACEi lowers systolic BP up to 15 to 20 mm Hg (i.e., enalapril, benazepril, or imidapril) or as much as 40 mm Hg (ramipril). ACEi can be increased in dosage to further optimize effect. They are well tolerated by cats. Enalapril, benazepril, and imidapril are dosed at 0.5 mg/kg q12 to 24 h PO. Ramipril is dosed at 0.25 to 0.375 mg/kg q24h PO. • Amlodipine: This drug is a strong systemic and intrarenal vasodilator with minimal effect on the heart due to a more peripheral than central blockade of calcium channels (ratio 15:1). It protects the heart and the kidney by decreasing systemic BP. It has a faster onset and more effective decrease of BP. Within 24 hours it will decrease BP up to 40 mm Hg or more; its maximum effect is reached within 3 days. The dosage can be increased to further improve outcome. It is well tolerated and dosed at 0.1 to 0.5 mg/kg initially (approximately 0.625 mg/cat PO) then increased to 1.25 mg/cat PO after 3 to 4 days if needed based on BP readings. • For a hypertensive crisis that does not respond to the drugs already discussed, use sodium nitroprusside at a dosage of 1 to 3 (up to 10) µg/kg per minute administered in a constant rate infusion. It has immediate onset with a plasma half-life of only a few minutes. Alternatively, administer hydralazine at 2.5 mg/cat q12h PO. It is effective after 1 to 2 hours and lasts for 12 hours.
(B) Figure 107-2 Aortic tortuosity can be seen in the lateral view (A) and as a knob-like structure (arrow) in the ventral-dorsal view (B). There is a high degree of correlation with this aortic change and systemic hypertension.
• Biochemical Profile and Serology: Evaluate for signs of renal disease (i.e., creatinine, blood urea nitrogen [BUN], potassium, sodium), hyperthyroidism (i.e., total T4, liver enzymes), diabetes mellitus (glucose), pheochromocytoma (catecholamines), and hyperaldosteronism (plasma aldosterone concentration).
Diagnostic Notes • Idiopathic hypertension is diagnosed when a reasonable work-up has ruled out the known causes of hypertension. It is a diagnosis of exclusion. It is highly likely that the underlying disease is in an early stage. • BP measurement should be performed in all cats with any sign of end organ damage, hypertension-related symptoms, history of a
252
Nonemergency Initial Treatment • Reduce pressure values below the moderate risk level (160/100). • Amlodipine: See previous discussion. • ACEi: See previous discussion. Use if hypertension is due to chronic kidney or heart disease because it protects the heart and the kidneys; use it if the renin-angiotensin-aldosterone system (RAAS) is activated for any other reason. ACEi can be the treatment of choice if the BP is not dramatically elevated, no TOD is present, and the desired decrease of BP is within the level of an ACEi’s maximum effectiveness. Also use it with amlodipine if amlodipine alone is not sufficient to achieve the desired BP. Some always use it when amlodipine is given because amlodipine activates the aldosterone.
Maintenance • Maintain the pressure values in the mild risk level (150/95). This may not be achievable or desirable for cats with chronic, severe hypertension.
Hypertension, Systemic
• Amlodipine: See previous discussion. • ACEi: See previous discussion. • Treat the Underlying Process
Hyperaldosteronism • See Chapter 102.
Prognosis Hyperthyroidism • See Chapter 109. • Add a β-blocker for additional short-term hypertension control if needed. Atenolol is cardioselective and dosed at 0.25 to 2.0 mg/kg q12 to 24h PO. • If hyperthyroidism is under control, BP should be controlled as well. If BP rises during treatment occult kidney disease is likely. Check for kidney disease. Treatment has to be adjusted accordingly (see previous discussion).
Renal Disease • See Chapters 189, 190, and 191.
Pheochromocytoma • Surgical removal of the tumor is the only treatment that may be curative.
The earlier hypertension is detected and controlled the better the prognosis, up to normal life expectancy. The later hypertension is detected or the less it is controlled sufficiently the more it will affect life expectancy.
Suggested Readings Carr A, Egner B. 2009. Blood Pressure in Small Animals—Part 2: Hypertension—Target Organ Damage, Heart and Kidney. Euro J Compan Anim Pract. 19(1):13–17. Egner B, Carr A, Brown S. 2007. Essential Facts of Blood Pressure in Dogs and Cats. Babenhausen, Germany: VetVerlag, Buchhandel und Seminar GmbH. Elliot J, Barber PJ, Syme HM, et al. 2001. Feline Hypertension: clinical findings and response to antihypertensive treatment in 30 cases. J Small Anim Prac. 42:122–129. Jepson RE, Elliott J, Brodbelt D, et al. 2007. Effect of control of systolic blood pressure on survival in cats with systemic hypertension. J Vet Intern Med. 21:402–409.
253
CHAPTER 108
Hypertensive Cardiomyopathy Beate Egner
Overview Hypertensive cardiomyopathy, sometimes called hypertensive hypertrophic cardiomyopathy (HHCM), is heart disease secondary to chronically elevated blood pressure. It is not to be confused with hypertrophic cardiomyopathy, a primary, genetically driven disease. See Chapter 110. Approximately 70% of hypertensive cats develop HHCM. Frequently these cats are presented with a sudden onset of a heart murmur or a gallop rhythm. Some of these cats additionally show mydriasis (i.e., unilateral or bilateral, indicative of persistent hypertensive retinopathy). See Chapters 107 and 193. The term thyrotoxic cardiomyopathy is used when the cause for hypertension is hyperthyroidism with resulting left ventricular hypertrophy. Preload and afterload are increased with chronic hypertension. Increased preload results in increased end diastolic diameter and volume. The heart needs to pump increased volume into the circulation against increased resistance (afterload). As a result myocardial contractility increases equal cardiac workload increases. Similar to weight training in a gym, the myocardium undergoes hypertrophy and hyperplasia of the cardiomyocytes. Interestingly this commonly results in asymmetric hypertrophy with the interventricular septum being more affected than the free wall. This asymmetry leads to a vertical shift in the valvular orifice, resulting in a murmur due to functional mitral insufficiency. The primary differential diagnosis is hypertrophic cardiomyopathy.
and parallel caval vein walls (not diverging). However, because it is a concentric hypertrophy with wall thickening directed inward cardiomegaly is not always visible. • Echocardiography: This will show left ventricular hypertrophy, predominantly asymmetric (i.e., thicker interventricular septum compared to left ventricular free wall), hypercontractility (i.e., increased fractional shortening), and a functional mitral valve insufficiency. See Figures 294-10A and 294-10B. • Urinalysis: The urine protein-to-creatinine ratio (UPC) is often greater than 0.2, indicative of proteinuria associated with chronic kidney disease (CKD). • Biochemical Profile: Evaluate for signs of CKD (i.e., creatinine and blood urea nitrogen, potassium, sodium), hyperthyroidism (i.e., total T4 and liver enzymes), and diabetes mellitus (i.e., glucose).
Diagnostic Notes • Blood pressure measurement should be performed on all cats with any sign of heart disease as hypertension may be the cause. If hypertension is present it is a significant risk factor for overall survival. • HDO Graphical Analysis: It adds information regarding how much cardiac output is affected on a beat-by-beat basis.
Treatment Diagnosis Primary Diagnostics • History: These cats typically exhibit one or more of the following: changes in behavior (i.e., ataxia, head pressing, bumping against objects, vocalization, and so on), changes in temperament (i.e., calmer, agitated, or aggressive), seizures, or lethargy. • Clinical Examination: This often reveals injected scleral vessels, bright red mucous membranes, decreased capillary refill time, a cardiac murmur (i.e., point of maximum intensity [PMI] over mitral valve), gallop rhythm, tachycardia, and pulse deficits. • Blood Pressure Measurement: This is the most important examination to evaluate for HHCM. See Chapters 107 and 311. Severe hypertension is defined as the systolic pressure above 180 mm Hg, the diastolic pressure above 120 mm Hg, or both. Using the HDO™ blood pressure machine, also look for high presystolic waves, variable cardiac output, and arrhythmic cardiac output variations. See Figure 107-1.
Secondary Diagnostics • Electrocardiogram: This shows increased R-wave amplitude (high voltage), wide QRS complexes, deep S-waves (bundle branch block [BBB]), occasionally increased duration of P-waves, or occasionally arrhythmias. • Thoracic Radiography: There is often a pressure-induced wide aortic arch (mimicking an enlarged right atrium), a wide thoracic aorta,
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
254
Primary Therapeutics • Underlying Disease: Treat the underlying process. This is the key to resolution of the problem. Especially evaluate the cat for CKD because this is the predominant reason for markedly elevated pressures (especially above 200/120). • Amlodipine: This is a strong systemic and intrarenal vasodilator with almost no effect on the heart. It protects the heart and the kidneys by decreasing systemic blood pressure. It has a faster onset and more effective decrease of blood pressure than other known drugs. Blood pressure will decrease within 24 hours and up to 40 mm Hg or more; within 3 days its maximum effect reached. The dose can be increased to achieve blood pressure of 150/95 mm Hg or less. It is well tolerated by cats. Dose at 0.1 to 0.5 mg/kg. Begin with 0.625 mg/ cat. If the blood pressure is not 150/95 mm Hg or less in 3 to 4 days, increase to 1.25 mg/cat or more every 24, or even every 12, hours.
Secondary Therapeutics • Angiotensin-Converting Enzyme Inhibitors (ACEi): This class of drugs are protective to the heart (i.e., preload and afterload reduction, inactivation of growth factors [remodelling], and decrease of sensitivity to catecholamines) and to the kidney (i.e., stabilizes the mesangial cells in the glomeruli preventing proteinuria, dilates the efferent arteriole of the glomeruli, and blocks the growth factor angiotensin II [AII] and other factors activated by AII [antiproliferative effect]). ACEi lowers intraglomerular and systemic blood pressure. ACEi have an mild immediate effect (several hours) and a stronger long term effect (2 weeks). Depending on the substance ACEi lower systolic blood pressure up to 15 to 20 mm Hg (i.e., enalapril, benazepril, imidapril) or as much as 40 mm Hg (i.e., ramipril).
Hypertensive Cardiomyopathy
ACEi can be increased in dosage to further optimize effect. They are well tolerated by cats. Enalapril, benazepril, and imidapril are dosed at 0.5 mg/kg q12 to 24 h PO. Ramipril is dosed at 0.25 to 0.375 mg/kg q24h PO. • Diuretics: Furosemide or thiazides can aid management of mainly diastolic hypertension. • Aldosterone-antagonists: Besides AII, aldosterone plays a key role in the remodelling process involving the heart and the arteries. The presence of cardiac and arterial remodeling is a negative prognostic factor for survival. If the HDO presystolic amplitudes remain high after initiating treatment with ACEi, activation of the arterial remodeling process is likely and the aldosterone-antagonist spironolactone should be added at a dosage of 2 mg/kg q24h PO.
Therapeutic Notes • If amlodipine is not successful alone, add an ACEi. They are effective together. • For hypertension caused by hyperthyroidism treat for hyperthyroidism (see Chapter 109) and add a β-blocker for additional short-term hypertension treatment. Preferably use atenolol because it is cardioselective at a dosage of 0.25 to 2 mg/kg q12 to 24 h PO. When the cat becomes euthyroid, blood pressure should be controlled as well. If blood pressure rises during treatment, occult kidney disease is likely. Check for kidney disease. See Chapters 190 and 191. Treatment must be adjusted accordingly. • For a Hypertensive Crisis: Use sodium nitroprusside at a dosage of 1 to 3 (up to 10) µg/kg per minute administered in a constant rate infusion. It has an immediate onset with a plasma half-life only a few minutes. Alternatively, give hydralazine (2.5 mg/cat q12h PO). It is effective after 1 to 2 hours and lasts for 12 hours).
Prognosis Chronic activation of the renin-angiotensin-aldosterone system (RAAS) can initiate cardiac and arterial remodeling leading to a poorer prognosis. HHCM is, however, reversible provided blood pressure can be controlled prior to extensive remodeling. HDO analysis can be helpful to rule out such changes. High presystolic amplitudes (PSA) seen prior to treatment should decrease in height after 2 to 3 weeks of treatment with ACEi and possibly an aldosterone antagonist (i.e., transient vasoconstriction or arterial remodelling unlikely). Should the PSA remain high after treatment, arterial remodeling cannot be ruled out.
Suggested Readings Carr A, Egner B. 2009. Blood Pressure in Small Animals—Part 2: Hypertension—Target Organ Damage, Heart and Kidney. Europ J Comp Anim Pract. 19(1):13–17. Diez J, Gonzalez A, Lopez B, et al. 2005. Mechanisms of disease: pathologic structural remodelling is more than adaptive hypertrophy in hypertensive heart disease. Nature Clin Pract Cardiovas Med. 2:209–216. Egner B, Carr A, Brown S. 2007. Essential Facts of Blood Pressure in Dogs and Cats. Babenhausen, Germany: VetVerlag, Buchhandel und Seminar GmbH. Elliot J, Barber PJ, Syme HM, et al. 2001. Feline Hypertension: clinical findings and response to antihypertensive treatment in 30 cases. J Small Anim Prac. 42:122–129. Jepson RE, Elliott J, Brodbelt D, et al. 2007. Effect of control of systolic blood pressure on survival in cats with systemic hypertension. J Vet Intern Med. 21:402–409. Klein I, Ojamaa K. 2001. Thyroid hormone and the cardio-cascular system. N Engl J Med. 344(7):501–509.
255
CHAPTER 109
Hyperthyroidism Gary D. Norsworthy and Mitchell A. Crystal
Overview Hyperthyroidism (HT) is the most common endocrinopathy of cats. It is caused by excess production of thyroxine (T4) resulting in a sustained increase in the metabolic rate. Of cats with HT, 98 to 99% have functional adenomatous hyperplasia (or adenoma), and 1 to 2% have thyroid adenocarcinomas. The pathogenesis of the adenomatous or carcinomatous changes seen in the thyroid glands of hyperthyroid cats is unknown. Several epidemiological studies revealed that cats that eat primarily canned cat foods, cats that use cat litter, and cats in contact with flame retardants commonly used on carpet and upholstery may have an increased risk of developing the disease. However, there is not a published study reporting induction of the disease in an experimental setting. The normal thyroid gland consists of two lobes located adjacent to the fifth or sixth tracheal ring, just caudal to the larynx. Small amounts of ectopic thyroid tissue are also present from the base of the tongue to the base of the heart. A small, pale-colored external parathyroid gland is located in the fascia, usually at the cranial pole of each thyroid lobe. An internal parathyroid gland is located within each thyroid lobe and is not grossly visible. The thyroid gland is not palpable in the normal animal. In HT, bilateral lobe (70%), unilateral lobe (25–30%), or ectopic tissue (3–5%) enlargement may occur. Unilateral or bilateral lobe enlargement is palpable in up to 95% of affected cats depending on the expertise of the veterinarian, the body condition of the cat, and the size and location of the lobes. Enlarged thyroid lobes sometime descend caudally and, thus, may be detected in their normal location or in the caudoventral cervical area. Enlarged thyroid lobes will be non-palpable if they descend through the thoracic inlet. Benign adenomatous hyperplasia and thyroid gland enlargement have been documented without increased thyroid function, thus gland enlargement is not always indicative of HT. The likelihood of progression from a nonfunctional adenoma to a functional adenoma is currently unknown but appears to be likely. HT occurs in cats 4 to 22 years of age (median age 13 years), and 95% of affected cats are over 10 years. There is no breed or sex predilection, although one study reported Himalayan and Siamese cats may have a decreased risk. Common clinical signs include weight loss (88–98%), polyphagia (49–67%), polyuria/polydipsia (PU/PD; 36–45%), vomiting (33–44%), increased activity (31–34%), and diarrhea (15–45%). Occasionally cats will present with lethargy, depression, anorexia, or weakness. This is known as apathetic HT and occurs in 5 to 10% of affected cats. Dyspnea due to congestive heart failure (CHF) is also an uncommon presenting sign (2%), and a small number of cats will present with ventral neck flexion due to hypokalemia (1–3%). Common physical examination findings include emaciation (65–97%), enlarged thyroid lobe(s) (75–95%), tachycardia (42–57%), unkempt hair coat (9–52%), and gallop rhythm (15–17%). Consequences of untreated HT include thyrotoxic cardiomyopathy and hypertension. In addition HT in rare cases leads to dilated cardiomyopathy. Therefore, any older cat with cardiac disease, especially involving ventricular hypertrophy, should be assessed for HT. Up to 87% of hyperthyroid cats are hypertensive. Hypertension is more common as the severity of HT increases. Diagnosis and management of hypertension should be closely considered in hyperthyroid cats.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
256
Hypertension may resolve following successful treatment of HT; however development of hypertension following successful HT therapy has been documented to occur in cats with and without concurrent kidney disease. See Chapters 107 and 108. On occasion, treatment of HT can result in decompensation of preexisting chronic renal disease due to reduction of renal plasma flow and glomerular filtration rate. Although HT has not been demonstrated to directly induce renal pathology, decreased renal size or chronic renal disease are seen in many cats with HT because these conditions are common in older cats. When these cats are treated for HT, deterioration of renal function may occur leading to clinical and biochemical signs of renal failure. Another misleading event is the decrease in creatinine values due to moderate to severe weight loss, a common finding in HT. Following treatment the disease resolves and weight gain occurs resulting in a creatinine value that becomes more representative of renal function. Recent reports indicate that hypocobalaminemia may occur in up to 40% of cats with HT. The mechanism is unknown, but possible explanations include compromised cobalamin uptake due to changes in gastrointestinal transit time or changes in cobalamin requirements or metabolism. It is unknown if serum cobalamin concentrations normalize when a euthyroid state is achieved or if some cats remain cobalamin deficient following successful HT therapy. Assessment, management and monitoring for hypocobalaminemia should be considered in HT cats. See Chapter 37.
Diagnosis Primary Diagnostics • Clinical Signs: The typical hyperthyroid cat is over 10 years of age and experiencing weight loss and polyphagia. PU/PD is also common. Cats showing these signs should be tested for HT. • Cervical Palpation for Thyroid Enlargement: This is a sensitive and specific test for thyroid enlargement when the technique is performed properly. A thyroid lobe that is palpable should be considered abnormal though not necessarily representative of clinical hyperthyroidism. See Table 109-1 and Figure 109-1. • Chemistry Profile: Around 90% of affected cats have an elevation of either alanine aminotransferase (ALT) or alkaline phosphatase (ALP), but this is not thought to represent significant hepatic disease because these values normalize following treatment for HT. Azotemia is present in some cats. • Complete Blood Count (CBC): Half of the affected cats may demonstrate a mildly elevated packed cell volume (PCV). A normal CBC should be confirmed prior to beginning medical management of HT because hematologic side effects may occur with medical therapy. • Urinalysis: Poorly or nonconcentrated urine may be present as a result of HT or concurrent chronic renal failure. • Total T4 (TT4): This value is elevated in 90 to 98% of affected cats. Some cats have normal TT4 levels as a result of either fluctuation of TT4 levels in and out of the normal range or suppression of elevated TT4 levels into the normal range secondary to concurrent nonthyroidal illness. In cases where TT4 is normal and HT is suspected, a repeat TT4 should be performed 1 to 2 weeks later or a triiodothyronine (T3) suppression test should be performed.
Hyperthyroidism
TABLE 109-1: Sensitive Thyroid Palpation Technique A sensitive means of thyroid palpation can be accomplished by palpating for only one thyroid lobe at a time. 1. To palpate the left lobe, the cat’s head is turned to the right about 45 degrees and the chin lifted about 45 degrees. One’s left index finger is placed in the trachea-muscle groove near the larynx. It is passed to the thoracic inlet. Second and third passes are made in the same manner. 2. To palpate the right lobe, the cat’s head is turned 45 degrees to the left while raising the chin 45 degrees. One’s right index finger is placed in the right trachea-muscle groove and passed from larynx to thoracic inlet. Second and third passes are made in a similar manner. 3. If thyroid enlargement is not detected, the left and right sides are palpated again. This is important because one will invariably hold the head in a slightly different position on subsequent attempts. This small change may be enough to permit a positive palpation following a previously negative effort.
• Thoracic Imaging: Radiography or ultrasonography may demonstrate cardiac changes, pleural effusion, or rarely, metastatic or mediastinal disease. The thyroid gland is not visible radiographically but may be seen and sized with ultrasound using a high frequency transducer. • Blood Pressure: Hypertension is present in up to 87% of affected cats. It is more likely in advanced cases of HT. • Electrocardiogram (ECG): Tachycardia, left anterior fascicular bundle branch block, cardiac chamber changes, and arrhythmias may be present. However, many hyperthyroid cats have normal ECGs. • Pertechnetate Thyroid Scanning (99mTc): Nuclear scanning accurately indicates overt and occult HT and can differentiate bilateral and unilateral disease. It can also determine if ectopic thyroid tissue is involved and whether metastasis is present. It cannot differentiate adenomas from adenocarcinomas. Its primary use is for situations in which the diagnosis or the extent of thyroid involvement is in doubt. • Serum Cobalamin Levels: This test should be considered to assess for concurrent hypocobalaminemia that requires management and monitoring.
Diagnostic Notes • Serum T3 levels are of limited usefulness in the diagnosis of feline HT because 25% of affected cats with elevated serum T4 levels have normal serum T3 levels. Few, if any, hyperthyroid cats have normal levels of T4 and elevated levels of T3. • If fT4 is to be measured, the equilibrium dialysis and direct dialysis assay methods are accurate and reliable, whereas radioimmunoassay or analogue methods are not. • The in-house TT4 Snap® test was reported to be inaccurate 36 to 56% of the time in one study; another study found much better accuracy. • The thyroid stimulating hormone (TSH) stimulation test is an inaccurate test and is not useful in the diagnosis of HT.
Treatment Primary Therapeutics Figure 109-1 Sensitive thyroid palpation is performed on one side at a time with the tip of one’s index finger placed in the groove between the trachea and the sternohyoideus muscle. It is important that the chin be lifted 45 degrees and turned 45 degrees away from the side to be palpated. See Table 109-1.
Secondary Diagnostics • T3 Suppression Test: This test is indicated when HT is suspected and T4 levels are normal (2–10% of cases). Results are extremely accurate. The test procedure is described in Chapter 311. • Thyroid Releasing Hormone (TRH) Response Test: This test is indicated when HT is suspected and T4 levels are normal (2–10% of cases). Transient side effects (i.e., salivation, vomiting, tachypnea, and defecation) are common during the testing period. The test procedure is described in Chapter 311. • Free T4 (fT4): This is a sensitive test for HT; however small numbers (6–12%) of false-positive results occur in cats with nonthyroidal illness. This test is indicated with a TT4 when HT is suspected and prior TT4 levels are normal (2–10% of cases). High fT4 levels in association with a high normal TT4 (>40 nmol/L [>3.0 µg/dL]) and clinical signs of HT support HT. High fT4 levels in association with a low normal or low TT4 (<32 nmol/L [<2.5 µg/dL]) supports nonthyroidal illness. We do not recommend this test as a sole or screening test for HT because the potential for false-positive results makes this test difficult to accurately interpret.
Initial Phase • Methimazole, Oral: This drug inhibits the synthesis of thyroid hormone. It is used during the initial phase of treatment to stabilize the cat and reverse the clinical signs, unless radioactive iodine therapy will be performed 7 to 10 days following diagnosis. Side effects (see Therapeutic Notes) are seen in about 18% of cats. A common approach to oral therapy begins with 2.5 mg q12h PO for 7 to 10 days followed by assessment of TT4, CBC, and blood chemistries. If TT4 levels remain elevated and lab values and clinical signs do not reveal significant side effects, the dose is increased to 5.0 mg q12h PO for 7 to 10 days and TT4, CBC, and blood chemistries are again assessed. If the TT4 level is still elevated, the dose is increased to 7.5 mg q12h PO. Gradual dose escalation and lab assessment are followed until the TT4 reaches the normal range; most cats are controlled on 5.0 mg q12h PO. • Methimazole, Transdermal: This drug may be administered transdermally in the inner pinna. Initial studies evaluating blood levels of methimazole following a single transdermal dose demonstrated low to undetectable dermal bioavailability; however, chronic dosing has been demonstrated to be effective, likely due to grooming, development of a drug depot within the skin, and effects of chronic transdermal gel on the stratum corneum. Studies have shown that TT4 decline is faster with oral methimazole; however, euthyroidism can be achieved with the transdermal form. The transdermal form offers a significant reduction in gastrointestinal (i.e., anorexia and vomiting)
257
SECTION 1: Diseases and Conditions
signs. Because transdermal therapy takes longer to achieve effectiveness, recommended dosing is as described previously for oral administration with lab assessments at 2- to 4-week intervals rather than 7- to 10-day intervals. Additional side effects noted include pinnal dermatitis and otitis.
•
Definitive or Long-Term Treatment • Radioactive Iodine (131I): With proper dosing this isotope destroys hyperfunctioning tissue without affecting normal thyroid tissue. It is reported to be effective in more than 95% of cats and is a noninvasive, simple, safe procedure. The only stress involved is the travel to the facility and the 2-day to 2-week post-treatment hospitalization period as dictated by the various state regulations. Cats usually become euthyroid within 1 week of therapy. 131I therapy is only available at approved facilities and is moderately expensive. Cats must be off all antithyroid medications but should continue to receive treatment for any concurrent conditions (e.g., hypertension). Check with the facility performing 131I to confirm how long methimazole therapy should be withheld prior to 131I treatment. Some prefer for the treatment to be performed without the cat having been on antithyroid medication; however, this approach prohibits prediction of posttreatment renal disease. • Surgical Excision (See Chapter 273): Removal of one or both thyroid lobes or hyperfunctioning ectopic tissue is an effective, invasive, moderately difficult, and moderately expensive procedure for the treatment of HT. Because anesthesia is necessary, preoperative stabilization of the hyperthyroid state (medical management with methimazole) and any associated conditions (i.e., cardiomyopathy and hypertension) is required. Some surgeons remove only the affected lobe(s), whereas others prefer to do bilateral thyroidectomy on all hyperthyroid cats. Original and modified intracapsular and extracapsular techniques have been used for many years. A parathyroid transplant technique has been successfully used and is considerably less difficult to perform and has a small chance for development for hypocalcemia. A recent study using 99mTc scanning following bilateral surgery showed that 15 to 20% of operated cats still had hyperfunctional thyroid tissue. • Methimazole: This drug can be continued as long-term therapy. It is an effective, inexpensive to moderately expensive treatment for HT. It inhibits the synthesis of thyroid hormones but does not prevent progression of thyroid enlargement. The serum half-life is short and side effects are frequent. Therefore, serum TT4, CBC, and blood chemistries should be checked every 4 to 6 months. Side effects have occurred up to 6 months after therapy has begun. Anorexia and vomiting are most common (less common with transdermal therapy), but several others are possible.
Secondary Therapeutics • Carbimazole: This drug is metabolized into methimazole and thus its use and monitoring for the initial and definitive/long-term treatment of HT are similar to methimazole. Carbimazole is not available in the United States. Plasma methimazole levels following carbimazole dosing are about one-half that of methimazole, thus dosing is double (initiate with 5 mg q12h PO, adjust if needed). A controlled-release tablet was recently reported to be effective at once daily dosing (Vidalta®, 15 mg q24h PO with food). Transdermal formulations have also been effective in HT management similar to methimazole. • Propylthiouracil (PTU): This drug inhibits the synthesis of thyroid hormones. It is an effective, inexpensive to moderately expensive treatment for HT. Side effects are more frequent (20–25%) and potentially more severe compared with methimazole. Thus, this drug should only be used if 131I, surgery, methimazole, or carbimazole are
258
•
•
•
unavailable or if the cat reacts to methimazole or carbimazole. PTU is initially dosed at 11 mg/kg q12h PO and adjusted to effect as per methimazole. Hypertension Management: Hypertension should be treated, if present, with amlodipine (0.625–1.25 mg/cat q12–24h PO); secondary agents can be added or substituted if amlodipine is ineffective or not tolerated (benazepril 2.5–5 mg/cat q24h PO or atenolol 6.25– 12.5 mg/cat q12-–24h PO.) See Chapter 107. Once HT has been corrected, hypertension therapy should be tapered while reassessing blood pressure. Effective treatment of HT will result in correction of hypertension in many cats, although some cats may require indefinite hypertension management and some normotensive cats may develop hypertension following successful HT treatment as aging results in the onset of renal disease. Therapy for Cardiac Disease: Treatment for cardiac disease should be instituted if indicated. Atenolol (6.25–12.5 mg/cat q12–24h PO), diltiazem (7.25 mg/cat q8h PO or 15–30 mg/cat q12h PO of the sustained release formulation), or propranolol (5 mg/cat q8–12h PO) are most commonly used. Angiotensin-converting enzyme inhibitors and diuretics may also be appropriate, depending on the severity and type of heart changes. Thyrotoxic cardiomyopathy typically resolves with treatment of HT, allowing discontinuation or reduction of cardiac medications. Hypocobalaminemia Management: Cobalamin should be administered and serum cobalamin levels monitored if hypocobalaminemia is identified See Chapter 37. Some cats with hyperthyroidism develop one or more cysts within the thyroid. These may be 6 cm or more longitudinally. Following radiation therapy, they may persist and require thyroidectomy. This can be a tedious surgery because the recurrent laryngeal nerve, vagosympathetic trunk, carotid vein, and jugular vein may become attached to the thyroid lobe. See Figure 109-2.
Therapeutic Notes • Clinical side effects of methimazole, carbimazole, and PTU therapy include anorexia, vomiting, lethargy, facial pruritus or excoriation, icterus, peripheral lymphadenopathy, and bleeding. Pinnal dermatitis and otitis may also occur when agents are administered transdermally. Laboratory abnormalities seen include eosinophilia, neutropenia, lymphocytosis, agranulocytosis, thrombocytopenia, positive antinuclear antibody titer and Coombs’ tests, and increases in liver enzymes. Many side effects from methimazole and carbimazole are mild and resolve following cessation of therapy for a few days; however, rare hepatotoxicity can be fatal. Severe side effects or persistent mild side effects will usually resolve when the drug is discontinued. The side effects of PTU are often more severe. Because frequent side effects are seen with these drugs, CBC and blood chemistries should be monitored along with serum TT4 levels every 4 to 6 months and sooner if mild changes are noted. If severe clinical or laboratory abnormalities occur (especially hepatotoxicity), therapy should be discontinued and 131I therapy or surgery should be recommended. • Compounding pharmacies use a wide variety of transdermal antithyroid preparations with variable effectiveness, shelf life, and safety. It is important to consider these factors when selecting and determining how to monitor therapy. If a compounded form of the drug is not effective, try a different compounding pharmacy. • Because treatment of HT has the potential to reveal pre-existing chronic renal disease, methimazole or carbimazole should be attempted prior to 131I or surgery in animals with possible renal compromise, determined by assessment of blood urea nitrogen (BUN), creatinine, and urine specific gravity. BUN and creatinine determination alone will not identify cats with possible early renal disease. If worsening of renal failure occurs, HT should not be treated or should be treated with methimazole or carbimazole to bring the
Hyperthyroidism
(B) (A)
Figure 109-2 A, Ultrasound of a thyroid cyst reveals the large hypoechoic cyst. B, Surgical removal usually requires careful dissection of vital structures that may become adherent to the thyroid lobe. The vagosympathetic trunk and carotid artery (arrow) were adherent laterally, and the recurrent laryngeal nerve was adherent medially. C, The cystic nature of the lesion is appreciated when it is cut open following surgical removal. Images courtesy Dr. Gary Norsworthy.
T4 into the range of 65 to 75 nmol/L (5–6 µg/dl) or to the lowest achievable level that stops weight loss and does not cause worsening of azotemia. In addition, the cat should be placed on a home maintenance program for renal insufficiency or failure. See Chapters 190 and 191. • Serum calcium should be checked once daily for 3 days following surgery and again 1 week after surgery. Transient, clinical hypoparathyroidism is seen in 5 to 15% of cats undergoing bilateral thyroidectomy with the extracapsular or intracapsular techniques due to damage to the parathyroid glands or their blood supply. Transient, mild hypocalcemia without clinical signs is common but does not warrant therapy. Clinical signs usually occur within 1 to 3 days following surgery but may occur up to 7 days following surgery. Resolution usually occurs in 3 weeks but may take up to 6 months. Uncommonly, hypoparathyroidism may be permanent. Clinical signs of hypocalcemia include tetany, seizures, muscle twitching, or anorexia. Clinical or severe (<1.9 mmol/L [<7.5 mg/dl]) hypocalcemia needs immediate therapy because this is a life-threatening condition. Therapy is discussed in Chapter 113. It should be noted that postthyroidectomy hypocalcemia can usually be avoided by performing bilateral thyroidectomies in two stages, allowing 3 to 4 weeks between removal of each lobe, and by use of the parathyroid transplant technique.
(C)
• HT is reported to recur in 5 to 10% of cats undergoing bilateral thyroidectomy and in 20% of cats undergoing unilateral thyroidectomy using standard intracapsular and extracapsular techniques, although the recurrence rate is less than 10% in all cats undergoing thyroidectomy. Recurrence may occur 8 to 63 months following surgery but usually occurs within 2 years. • Thyroid levels are transiently low (usually 1–3 months) following routine 131I therapy or bilateral thyroidectomy, but persistent hypothyroidism as a result of either is rare. Thyroid supplementation is not indicated following these procedures unless thyroid levels are persistently low 6 months following 131I therapy or surgery or unless significant weight gain or renal compromise is recognized in conjunction with a subnormal TT4 level. However, if thyroid adenocarcinoma is being treated the dose of 131I is two to four times the routine dose and hypothyroidism is expected; supplementation with thyroid replacement hormone should occur. • It is important to weigh the advantages and disadvantages of medical, surgical, and 131I therapy prior to making recommendations to the client. Items to consider include the age of the cat, ability and willingness of the owner to administer medication, how well the cat does away from home (for those 131I facilities that require prolonged hospital stays), the financial ability of the client, the presence or absence of renal failure and other diseases, the willingness of owners
259
SECTION 1: Diseases and Conditions
to travel, and the availability of a facility that offers a surgeon who performs thyroidectomies.
131
I therapy or
Prognosis Most cats with HT have an excellent prognosis for successful treatment. Cats with concurrent renal disease have a less favorable prognosis.
Suggested Readings Feldman EC, Nelson RW. 2004. Feline hyperthyroidism (thyrotoxicosis). In EC Feldman, RW Nelson, eds., Canine and Feline Endocrinology and Reproduction, 3rd ed., pp. 152–218. Philadelphia: WB Saunders.
260
Harvey AM, Hibbert A, Barrett EL, et al. 2009. Scintigraphic findings in 120 hyperthyroid cats. J Fel Med Surg. 11:96–106. Hoffman G, Marks SL, Taboada J, et al. 2003. Transdermal methimazole treatment in cats with hyperthyroidism. J Fel Med Surg. 5(2):77–82. Lurye JC, Behrend EN, Kemppainen RJ. 2002. Evaluation of an in house enzyme-linked immunosorbent assay for quantitative measurement of serum total thyroxine concentration in dogs and cats. J Am Vet Med Assoc. 221(2):243–249. Norsworthy GD. 1995. Feline thyroidectomy: a simplified technique that preserves parathyroid function. Vet Med J. 90(11):1055–1063. Sartor LL, Trepanier LA, Kroll MM, et al. 2004. Efficacy and safety of transdermal methimazole in the treatment of cats with hyperthyroidism. J Vet Intern Med. 18(5):651–655.
CHAPTER 110
Hypertrophic Cardiomyopathy Larry P. Tilley
Overview Hypertrophic cardiomyopathy (HCM) is the most common cardiac disease of the cat and is characterized by unexplained and significant left ventricular hypertrophy. The left ventricle is non-dilated and often hyperdynamic. There is no definable cause contrasting left ventricular hypertrophy that occurs secondary to hyperthyroidism, systemic hypertension, or subaortic stenosis. Although the etiology is currently unknown, myocardial β-myosin heavy chain mutations have been demonstrated in humans with HCM and may be responsible for the disease in cats as well. Other theories include altered myocardial calcium transport, enhanced myocardial sensitivity to catecholamines, and increased production of myocardial trophic factors. Left ventricular hypertrophy results in a stiff, noncompliant chamber, causing diastolic (ventricular filling) dysfunction. See Figure 110-1. This results in elevated left ventricular filling pressures and subsequent left atrial enlargement (dilatation). As the disease progresses, pulmonary venous pressures increase, and pulmonary edema develops. Left atrial enlargement predisposes affected cats to atrial arrhythmias. Stasis of blood within the dilated left atrium may result in thrombus formation and thromboembolic disease. See Chapter 212. Affected cats may also develop fatal ventricular arrhythmias secondary to myocardial ischemia. The mean age of affected cats is 6 years with an age range from 8 months to 16 years. Approximately 75% are male. Reported breed incidences are: domestic shorthair (DSH; 89.1%), Persian (6.5%), domestic
Figure 110-1 Left ventricular wall thickening is the primary lesion of hypertrophic cardiomyopathy. In this cat, the left ventricular chamber (LV) is smaller than the right ventricular chamber (RV) because the thickening of the left ventricular wall is directed inward. IVS, interventricular septum. LVFW, left ventricular free wall. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
longhair (DLH; 2.2%), and Maine coon (inherited as an autosomal dominant trait; 2.2%). A familial association is also found in British and U.S. shorthairs, Ragdolls, and Rex breeds. In one study, 16 of 103 apparently healthy domestic cats were reported to have echocardiographic measurements consistent with a diagnosis of cardiomyopathy. Clinical signs are variable. Many cats have no clinical signs at the time HCM is documented. These cats are most often examined because a murmur, gallop rhythm, or other arrhythmia is detected during routine examination. On the other hand, cases may be first diagnosed only after severe clinical signs, such as fulminant pulmonary edema or systemic thromboembolism, become apparent. Physical examination abnormalities are dependent on the stage of disease. Cats with congestive heart failure will exhibit tachypnea and labored breathing. Those with systemic thromboembolism will have characteristic signs of acute onset paralysis and severe pain. A heart murmur is present in the majority of cats with HCM. Other auscultatory findings may include a gallop rhythm (40%) and other arrhythmia (25%).
Diagnosis Primary Diagnostics • Electrocardiography: Evidence of left atrial enlargement (i.e., P-mitrale or widened P-waves) and left ventricular enlargement (i.e., increased R-wave amplitude or increased QRS duration) are present. Arrhythmias are frequent. Most cats with HCM will have a sinus tachycardia. Atrial and ventricular arrhythmias may be present. Intraventricular conduction deficits, such as left anterior fascicular block (i.e., bundle branch block), are occasionally present. • Radiography: Variable enlargement of the cardiac silhouette is seen. Left atrial enlargement is often most prominent. Early in the course of the disease, the cardiac silhouette may be normal because the left ventricular wall thickening is directed inward. Cats with congestive heart failure may demonstrate enlargement of the pulmonary veins, variable pulmonary edema, and pleural effusion. See Figures 110-2, 294-11, 294-12, and 294-13. • Echocardiography: Left ventricular hypertrophy involving the left ventricular free wall and, usually to a greater degree, the interventricular septum is present. The mean septal thickness of affected cats is reportedly 6.5 mm (normal 3.7 ± 0.7 mm). Values of septal or left ventricular free wall thickness in diastole greater or equal to 6.0 mm can indicate hypertrophy. See Figure 110-3. Refer to Chapter 318 because ultrasound normal values for Maine coon cats are slightly different from other breeds. Left ventricular hypertrophy is diffuse in approximately 67% of cats and regional in 33%. Affected cats tend to have greater hypertrophy of the basilar portion of the left ventricle than the apical portion (57%), whereas others have fairly equal hypertrophy in both regions (43%). In several cats, a localized area of hypertrophy is often found at the proximal interventricular septum, which protrudes into the left ventricular outflow tract. This is often referred to as asymmetric septal hypertrophy (ASH) and is thought to cause a variable degree of obstruction to left ventricular emptying. A stenotic lesion such as this results in compensatory ventricular hypertrophy, which may lead to further obstruction. The diameter of the left ventricle in diastole is typically within normal limits, whereas the left ventricular diameter in systole is often
261
(A)
(B)
Figure 110-2 Radiographs of cats with hypertrophic cardiomyopathy often show pulmonary edema and cardiomegaly (A). Aerophagia was also present. Two views were not possible due to the degree of dyspnea. The cat was given intravenous furosemide; 6 hours later the lateral (B) and dorsal-ventral (C) views show significant reduction in pulmonary edema and aerophagia. The classic “valentine-shaped heart” is seen in the dorsal-ventral view. It was not possible to get a true dorsal-ventral view after several attempts because of the dyspnea and anxiety that was still present. The cat was 6 years old, presented for an annual examination, and had a 2/6 murmur and a normal electrocardiogram tracing. Images courtesy Dr. Gary D. Norsworthy.
(C)
(A)
(B)
Figure 110-3 A, A short-axis view of the left ventricle revealed a thickened interventricular septum (0.89 cm) and left ventricular free wall (0.90 cm). Left ventricular wall thickness greater than 0.6 cm is consistent with hyptertrophic cardiomyopathy. B, The left atrium is severely enlarged. The left atrium-to-aortic valve ratio is 2.6. Images courtesy Dr. Gary D. Norsworthy.
Hypertrophic Cardiomyopathy
decreased, resulting in an increased fractional shortening in some cats; however, most cats with HCM will have a normal fractional shortening (30–60%). Left atrial enlargement is consistently present (mean of 18 mm; normal 11 mm) and, if absent, should cause one to question the diagnosis in cats with slight left ventricular hypertrophy. Other echocardiographic findings may include mitral valve leaflet thickening, occasionally a slight pericardial effusion, and intracardiac thrombi. Systolic anterior motion (SAM) of the mitral valve is observed in approximately 67% of affected cats. See Figures 110-2, 294-11, and 294-13 through 294-16.
Secondary Diagnostics • Doppler Echocardiography: Mild to marked left ventricular outflow obstruction occurs in cats with SAM. Due to the malposition of the anterior leaflet in systole, mitral insufficiency is present in cats with SAM. • Myosin Binding Protein C Assay: Some families of cats have been identified with a high prevalence of the disease, and the disease appears to be inherited as an autosomal dominant trait in Maine coon cats, where in at least one large family a mutation in the gene encoding myosin binding protein C (MyBPC) has been identified. • DNA testing in Maine coon and Ragdoll: See www.catgenes.org.
• Other Cardiac Drugs: Alternatively to diltiazem, a β-blocker such as atenolol (6.25 mg/cat q12–24h PO) may be used. Atenolol is effective for ventricular arrhythmias and possibly for outflow obstruction; it will slow the heart rate so be observant not to induce bradycardia. However, a β-blocker should not be used until the cat is out of heart failure. • Angiotensin-Converting Enzyme (ACE) Inhibitor: Enalapril (0.25– 0.50 mg/kg q24h PO) or benazepril (0.25–0.5 mg/kg q24h PO) may be beneficial. ACE inhibitors may reduce left ventricular hypertrophy in cats with HCM (cardiac remodeling). • Anticoagulation Therapy: Aspirin may reduce the chance of thrombus formation: Give 81-mg tablet q48 to 72h PO. In one study though, no significant difference was found in survival or recurrence rate between cats receiving the traditional dose and cats receiving lowdose aspirin (5 mg q72h PO). Clopidogrel (18.75 mg q24h PO) is also used alone or with aspirin if smoke or a clot is visualized in the left atrium. Recurrence of thrombi occurs at a high rate (43.5%) even with anticoagulation. Cats with left atrial enlargement, especially greater than 20 mm in diameter, are at greatest risk for aortic thromboembolism. See Chapter 212. • Fluid Removal: Thoracocentesis or abdominocentesis may be needed periodically. • Spironolactone: This drug has been used at subdiuretic dose for congestive heart failure, but is reported to cause ulcerative facial dermatitis.
Diagnostic Notes • Because systemic blood pressure is not routinely measured in cats, inevitably cats with hypertensive heart disease are included in descriptions of HCM because both disorders will result in left ventricular hypertrophy. Hypertension can occur with primary HCM but is not common. • Always rule out overt or occult hyperthyroidism as the cause of left ventricular hypertrophy in cats over 6 years of age. • Long-acting injectable steroids have been associated with congestive heart failure in cats with hypertrophic cardiomyopathy that are in a state of pre-congestive heart failure.
Treatment
Therapeutic Notes • There are relative advantages of either diltiazem (calcium channel blocker) or β-blockers (atenolol), and no consensus has been reached on the most effective therapy. Cats with persistent tachycardia may benefit more from a β-blocker than a calcium channel blocker. • Monitor renal function if enalapril is used. • Warfarin may be used in lieu of aspirin or clopidogrel but has a much greater chance of inducing a hemorrhagic crisis and much closer monitoring is required. • The dose of a diuretic and the need for antiarrhythmic agents may change during the course of the disease. Frequent monitoring is recommended.
Primary Therapeutics
Therapeutic Notes
• Reduce Stress: Take all measures to minimize any stress to cats exhibiting respiratory distress (e.g., delay radiographs and catheter placement). • Facilitate Breathing: Thoracocentesis should be performed in all dyspneic cats when pleural effusion is suspected (muffled lung sounds). With the cat sternal, place a 19- to 22-gauge butterfly catheter just into the pleural space (fifth to seventh intercostal space, just cranial to adjacent rib) and aspirate. Use a closed system, and tap both sides of the chest. Give furosemide when pulmonary edema is present. In the crisis setting, give 2 to 4 mg/kg IV (or IM if necessary) initially, then 1 to 2 mg/kg q4 to 6h IV or IM until the edema has resolved. Furosemide is often continued as needed (6.25–12.5 mg q12–24h PO) to control edema formation. Apply 6 mm (1/4 in) of nitroglycerin to a hairless area q4 to 6h or 2.5 mg24h patch until the edema has resolved. Absorption is poor if the skin is cold (vasoconstriction). • Oxygen: Administer via face mask if tolerated; otherwise use an oxygen cage or tent (50% oxygen).
• Treatment of the Asymptomatic Cat with HCM: Currently there is no evidence that any drug alters the natural history of HCM in domestic cats until they are in heart failure. Diltiazem, atenolol, and benazepril are commonly administered to cats with mild to severe HCM that are not in heart failure on an empirical basis. Because there are likely many cats with mild to moderate HCM in the cat population that presumably never progress to a more severe form of the disease, condemning owners to pill their cat twice, or even once, a day for the rest of the cat’s life is questionable, given the lack of data. Many veterinarians feel compelled to treat a patient with a disease, and some owners demand treatment for their cat, even if there is only a theoretical case for using a drug. Consequently, whenever HCM is diagnosed in a cat the veterinarian must explain the situation to each owner and try to let the owner make an informed decision based on their wishes and lifestyle. Because no intervention is known to change the course of the disease, there is no mandate to treat at this stage.
Secondary Therapeutics • Diltiazem: This may improve myocardial relaxation and control arrhythmias. Give 7.5 mg/cat q8h PO or 30 mg/cat of a sustained release preparation q24h PO. Some reports indicate that effective blood levels may not be reached with sustained preparations.
Prognosis The prognosis of affected cats is dependent on the severity of disease. Those with no clinical signs have a median survival of nearly 5 years. Cats presented with evidence of congestive heart failure reportedly have a median survival of 3 months, although this appears to be increased
263
SECTION 1: Diseases and Conditions
with advances in therapeutics. Systemic thromboembolism is a concern and often results in exacerbation of the congestive heart failure state; recurrence is also likely.
Suggested Readings Kienle RD. 2008. Feline cardiomyopathy. In LP Tilley, FWK Smith, Jr., M Oyama, et al., eds., Manual of Canine and Feline Cardiology, 4th ed., pp. 151–175. St. Louis: Elsevier Saunders.
264
Kittleson MD. 2009. Treatment of feline hypertrophic cardiomyopathy (HCM)—lost dreams. In ACVIM Forum Proceedings, pp. 117–119. Montreal: ACVIM. Paige CF, Abbott JA, Elvinger F, et al. 2009. Prevalence of cardiomyopathy in apparently healthy cats. J Am Vet Med Assoc. 234:1398–1403. Rush JE, Freeman LM, Fenollosa NK, et al. 2002. Population and survival characteristics of cats with hypertrophic cardiomyopathy: 260 cases (1990–1999). J Am Vet Med Assoc. 220(2):202–207.
chAPTER 111
Hypoadrenocorticism Karen M. Lovelace
Overview Hypoadrenocorticism is a rare disease in cats. First described in cats in 1983, only a small number of cases have since been reported. In naturally occurring cases, destruction of greater than 90% of the adrenal cortices occurs, and a deficiency of glucocorticoids and mineralocorticoids results. This condition is also known as Addison’s disease, or primary hypoadrenocorticism. Although a cause for feline hypoadrenocorticism is unknown, an immune-mediated etiology is suspected. Secondary hypoadrenocorticism, or a deficiency in the production and secretion of adrenocorticotropic hormone (ACTH), primarily results in glucocorticoid deficiency due to the minor effect of ACTH on mineralocorticoid production. Naturally occurring secondary hypoadrenocorticism has not been documented in cats, but iatrogenic secondary hypoadrenocorticism after administration of glucocorticoids or progesterone hormones has been described.
Diagnosis Primary Diagnostics • History: Lethargy, anorexia, and weight loss are the most common clinical signs. Vomiting, polydipsia, and polyuria occur with less frequency. Unlike dogs, cats with hypoadrenocorticism are not reported to have diarrhea. • Clinical Signs: Clinical findings are non-specific for disease but include hypothermia, weakness, weak pulse, lethargy, prolonged capillary refill time, and dehydration. Less frequent findings include bradycardia, collapse, or pain on abdominal palpation. Signs may be present several days to several months before the cat is presented for evaluation. • Chemistry Profile: The majority of patients with hypoadrenocorticism has Addison’s disease and, therefore, exhibits a classic hyperkalemia, hyponatremia, and hypochloremia due to a deficiency in aldosterone. Hyperkalemia is usually in the range of 5.7 to 7.6 mmol/L (5.7–7.6 mEq/L), which is lower than that of canine patients. Mild hypercalcemia may be present but usually resolves after corticosteroid replacement therapy. Other findings, many of which are secondary to dehydration, may include prerenal azotemia, hyperphosphatemia, and urine specific gravity less than 1.030 (despite dehydration). Mild metabolic acidosis may be found, and anemia, eosinophilia, and lymphocytosis are less common findings. • ACTH Stimulation Test: The ACTH test is a test of adrenal reserve used to rule in or rule out Addison’s disease. The test has a low sensitivity and a low specificity. Various protocols exist. A synthetic ACTH drug, such as cosyntropin (Cortrosyn®), is usually used at a dose of 125 µg/cat IV. ACTH gel, at 2.2 U/kg IM, may also be used, but cosyntropin is preferred because it is better at stimulating the adrenal cortex, and intravenous drug administration is preferred over intramuscular administration, especially if the patient is dehydrated. Blood is usually collected before administration and again at 30 and 60 minutes after drug administration. If ACTH gel is used, postcollection times are 60 and 120 minutes. Two postadministration
blood samples are generally recommended because the time to peak effect of cortisol in cats can vary. Diagnosis of hypoadrenocorticism is made if the basal cortisol concentration is low or negligible and minimal or no increase occurs after ACTH stimulation. Baseline ACTH and poststimulation cortisol values in cats with hypoadrenocorticism range from 2.8 to 22 nmol/L (0.1–0.8 µg/dL) and 2.8 to 35.9 nmol/L (0.1–1.3 µg/dL), respectively.
Secondary Diagnostics • Thoracic Radiographs: Due to dehydration, radiographs of the chest may indicate microcardia or lung hypoperfusion. • Electrocardiogram: A few cases have shown either sinus bradycardia or atrial premature contractions. • Endogenous Plasma ACTH: Endogenous plasma ACTH levels can be assessed to discriminate between Addison’s (primary hypoadrenocorticism) and secondary hypoadrenocorticism. Endogenous plasma concentrations will be significantly elevated in cats with primary disease. Reported ranges in normal cats are less than 0.000276 to 0.00345 nmol/L (10–125 pg/mL), whereas cats with primary disease had concentrations of 0.0138 to 0.0221 nmol/L (500–800 pg/mL).
Diagnostic Notes • Reference ranges for feline patients will differ from those used in canine species and should be established by the individual laboratory. • The majority of cases are a result of direct destruction of the adrenal cortices. Naturally occurring secondary hypoadrenocorticism has not been documented in the cat, but iatrogenic secondary hypoadrenocorticism may occur.
Treatment Primary Therapeutics • Emergency Fluid Therapy (Addisonian Crisis): Administer 0.9% sodium chloride (normal saline) IV at a rate of 40 ml/kg per hour for the first 1 to 4 hours. • Short-Term Fluid Therapy: After dehydration is corrected, the rate should be decreased to 60 ml/kg per day. Fluids may be discontinued once the patient begins to eat and drink and does not vomit. • Glucocorticoid and Mineralocorticoid Therapy: After the ACTH stimulation test is completed glucocorticoid and mineralocorticoid replacement therapy should be initiated. Specific feline dosages have not been formulated; therefore canine doses are used as guidelines. For glucocorticoid replacement, either prednisolone sodium succinate or dexamethasone may be given at doses of 4 to 20 mg/kg IV or 0.1 to 2 mg/kg IV or IM, respectively. Repeated dosages should be reduced as indicated by patient response. For mineralocorticoid replacement, desoxycorticosterone pivalate (DOCP) can be given at 2.2 mg/kg q24h IM.
Secondary Therapeutics th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Long-Term Therapy: Prednisolone (or prednisone) should be given by mouth twice daily at a dose of 0.25 to 1.0 mg/cat for long-term
265
SECTION 1: Diseases and Conditions
glucocorticoid replacement. If daily oral therapy is not possible, once monthly intramuscular injection of 10.0 mg of methylprednisolone acetate may be used as an alternative. However, very infrequently congestive heart failure and diabetes mellitus have been reported after use of methylprednisolone in the cat. For long-term mineralocorticoid replacement, either fludrocortisone acetate (0.05–0.1 mg/cat q12h PO) or DOCP (2.2 mg/kg q25d IM) should be used.
Therapeutic Notes • Response to therapy is slower than the quick response that dogs exhibit, and anorexia, depression, and weakness may persist for 3 to 5 days. • Long-term replacement therapy requires periodic reassessment to ensure optimal dosing schedules.
266
Prognosis With proper therapy and owner compliance to medical management, the long-term prognosis for cats is good.
Suggested Readings Herrtage ME. 2005. Hypoadrenocorticism. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1612–1622. St. Louis: Elsevier Saunders. Sherding, RG. 1994. Endocrine Diseases. In RG Sherding, ed., The Cat: Diseases and Clinical Management, 2nd ed., pp. 1490–1493. New York: Churchill Livingstone.
CHAPTER 112
Hypoalbuminemia Sharon Fooshee Grace
Overview Albumin is an important and unique protein that serves several important functions, the most significant being maintenance of colloid osmotic pressure (COP), or the force that holds macromolecules within the vascular space. Albumin is a negatively charged molecule that escapes glomerular filtration because the glomerular basement membrane is similarly charged and repels it. Also, albumin is slightly larger than the glomerular pores and, thus, is further prevented from entering the glomerular filtrate. The liver synthesizes almost all of the plasma proteins, with more than 50% of its metabolic effort dedicated to albumin production. Fortunately, more than 75 to 80% of liver function must be lost before hypoalbuminemia develops as a consequence of liver failure. The rate of albumin synthesis is dictated primarily by COP. Hypoalbuminemia is a clinically significant condition because it decreases COP and disrupts the balance between intravascular and interstitial fluid compartments, thereby promoting edema. Causes of hypoalbuminemia are generally grouped into four categories (i.e., increased loss, decreased production, movement into the extravascular compartment, and dilution), though multiple mechanisms are often responsible. Consequences of hypoalbuminemia are varied but most significant are loss of fluid and vascular volume into the extravascular compartment; increased risk for thromboembolism; and, decreased transport capacity for various drugs and endogenous compounds.
Differential Diagnoses There are many disease processes that must be considered. See Table 112-1.
TABLE 112-1: Differential Diagnoses for Hypoalbuminemia Increased Loss of Albumin Protein losing nephropathy (PLN) Amyloidosis, glomerulonephritis Protein losing enteropathy (PLE) Inflammatory bowel disease Protein losing dermatopathy (PLD) Severe thermal burns, toxic epidermal necrolysis Hemorrhage Pancreatitis Lymphangiectasia (rare) Decreased Synthesis of Albumin Chronic hepatic insufficiency Portosystemic shunt Inflammation Sepsis, systemic inflammatory response syndrome (SIRS) Chronic protein malnutrition Loss of albumin into the extravascular compartment (“third spacing”) Septic peritonitis Septic shock Effusion into a body cavity Vasculitis Right-sided heart failure (uncommon cause) Dilution Fluid therapy Fluid retention
Diagnosis Primary Diagnostics • History: A thorough dietary history should be assessed (chronic protein malnutrition). A medication history should be obtained (i.e., NSAIDS). The owner should be questioned about color of the cat’s stool (gastrointestinal [GI] bleeding). Chronic vomiting and weight loss may suggest inflammatory bowel disease (IBD). • Physical Examination: Clinical signs of hypoalbuminemia include peripheral edema (see Figure 112-1), ascites, and poor wound healing. Cutaneous lesions sufficient to cause hypoalbuminemia (i.e., a protein-losing dermatopathy [PLD]) would have to be significant. Small, firm kidneys could suggest chronic renal disease (protein-losing nephropathy [PLN]). The intestines should be palpated for evidence of protein-losing enteropathy (PLE; normal to thickened intestines). Stool color should be examined for evidence of melena (GI bleeding). Hypoalbuminemia does not tend to cause pulmonary edema. • Minimum Data Base (Complete Blood Count [CBC], Chemistry Profile, and Urinalysis with Sediment Examination): A minimum
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 112-1 This cat has three edematous feet. The one with the catheter bandage was more swollen than the others due to circulatory impairment. Her serum albumin was 1.7 g/dL (17 g/L). She had underlying biliary carcinoma.
267
SECTION 1: Diseases and Conditions
data base should be completed to assess the cat for evidence of renal disease (i.e., nonregenerative anemia, azotemia, hypercholesterolemia, or proteinuria); chronic hepatic insufficiency (i.e., microcytosis, poikilocytosis, decreased blood urea nitrogen [BUN], and ammonium biurate urine crystals); IBD (i.e., mild nonregenerative anemia, elevated liver enzymes); and sepsis (i.e., leukocytosis or hypoglycemia). • Retroviral Screen: Feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) tests are not confirmatory for a particular disease but are essential for establishing the overall health of the patient.
•
•
Secondary Diagnostics • Abdominal Radiography and Ultrasound: The size (radiographs) and architecture (ultrasound) of the liver and kidneys can be evaluated with diagnostic imaging. Thickened bowel loops and ascites can be detected with ultrasound. • Urine Protein-to-Creatinine (UPC) Ratio: This test can be used to estimate the magnitude and, therefore, significance, of urinary protein loss. UPC is far more accurate than the urine dipstick test, which is qualitative. Normal cats should have little or no protein in the urine when the urine sediment is benign (inactive). If the UPC is greater than 1.0, the clinician should investigate for glomerular disease. • Fasting and 2-Hour Postprandial Serum Bile Acids (SBA): Determination of SBA can assess liver function. The postprandial sample is critical because some animals with severe liver disease may have normal fasting SBA. • Liver Biopsy: If liver disease is suspected, biopsy may be indicated. Fine-needle core biopsy and surgical techniques may be used. Clotting profiles and a platelet count should be determined prior to liver biopsy, regardless of the technique used. • Intestinal Biopsy/Histopathology: Where indicated, an intestinal biopsy (preferably full thickness) should be submitted to evaluate for intestinal diseases. However, low albumin can contribute to poor wound healing and possible dehiscence. It may be prudent to first attempt endoscopic biopsy. • Antithrombin III (ATIII) Level: Patients with PLN may be at increased risk of thromboembolism. ATIII, the most important anticoagulant in the body, is similar in size to albumin and may be lost when glomerular disease is present. This test is not widely available. • Central Venous Pressure (CVP): If possible, monitoring of CVP can prevent overhydration from fluid therapy. Volume expanded patients will have a CVP of 4 to 8 cm H20; overhydrated patients approach or exceed 10 cm H20. If CVP cannot be attained, frequent assessment of body weight, auscultation of the lungs for edema, thoracic radiography, and measurement of packed cell volume and total protein will help gauge adequacy of hydration. Consult a critical care text for details on setting up a CVP catheter. • Thoracic Radiology and Ultrasound: Thoracic radiographs and ultrasound may be indicated if the cat is suspected of having heart failure, although this is an uncommon cause of ascites and thirdspace albumin loss in cats. • Skin Biopsy: Vasculitis is uncommon in cats but should be investigated with a biopsy, including a skin biopsy if indicated.
Diagnostic Notes • Urine dipstick tests for protein have a high frequency of false-positive results. Any urine sample which is dipstick “positive” and has quiescent sediment should be further evaluated. The sulfasalicylic acid (SSA) turbidometric test can be used to confirm albuminuria. • Concurrent evaluation of serum globulins can be helpful in determining the cause of hypoalbuminemia. If both albumin and globulins are
268
•
•
•
decreased, important considerations include hemorrhage, PLD, PLE, and dilution. Dilution typically causes only mild changes in albumin, whereas PLE and PLD result in moderate hypoalbuminemia. If albumin is decreased and globulins are normal to increased, consider PLN, chronic hepatic insufficiency, and down-regulation of albumin production due to inflammation. For more information, see Chapters 6, 86, 120, and 178. If panhypoproteinemia and anemia are present, blood loss should be considered even if the source of the blood loss is not apparent. Melena points to GI hemorrhage. Right-sided heart failure is an uncommon cause of hypoalbuminemia in cats because they rarely develop ascites with heart failure. Effusions attributed to hypoalbuminemia alone will be pure transudates. Development of a transudative effusion is not expected until albumin levels become very low, usually less than 1 to 1.5 g/dL (10–15 g/L). Normal liver enzymes do not eliminate the possibility that liver failure or a portosystemic shunt is present. It is also important to note that cats with liver disease, including cirrhosis, typically do not have small livers. One exception to this is liver disease due to a portosystemic shunt in which microhepatica is present. Measurement of COP in the general practice setting is impractical as it is difficult to justify the significant expense and daily maintenance requirements of a colloid osmometer. Wescor, Inc. (www.wescor. com, Logan, Utah) manufactures an osmometer that is used in some critical care hospitals.
Treatment Primary Therapeutics • Treatment of Primary Disease: The underlying cause of hypoalbuminemia should be identified and managed, when possible.
Secondary Therapeutics • Crystalloids: Loss of intravascular COP may cause hypovolemia because body fluids can easily pass through capillary membranes. Volume depletion may be treated with intravenous fluids in the form of crystalloids or colloids, natural or synthetic. Crystalloids include 0.9% saline and lactated Ringer ’s solution. They will not have a significant impact on COP because they contain small particles that are quickly and easily extravasated with increased vascular permeability. • Colloids—Natural: Colloids contain larger particles than crystalloids and are thus able to maintain COP better than crystalloids. Colloids are available as natural or synthetic products and should be considered when total protein levels fall below 3 to 4 g/dL (30–40 g/L). Colloids offer many benefits but can also cause a reciprocal decrease in albumin synthesis. Also, should colloids leak into the interstitium, edema may worsen. Natural colloids include plasma and albumin. Cats receiving plasma do not need to be blood typed or crossmatched. As a practical matter, plasma is not used for management of hypoalbuminemia caused by chronic diseases because of the volume needed to raise serum albumin and the cost involved. Species-specific serum albumin is not yet available in veterinary medicine. Human albumin solutions have been used on a limited basis in animals; a recent report indicated that 25% human serum albumin significantly increased serum albumin levels in cats above pretransfusion levels. Given the paucity of research and potential antigenicity, their use remains controversial but holds promise for the future. • Colloids—Synthetic: Synthetic volume expanders include dextrans, hemoglobin-based oxygen carriers (e.g., Oxyglobin®), oxypolygelatin and hydroxyethyl starches (e.g., Pentastarch® and Hetastarch®).
Hypoalbuminemia
Side effects include volume overload, coagulopathies, and anaphylaxis. Dextran and the starch solutions cannot support COP on a long-term (weeks to months) basis because of their short half-lives (Pentastarch = 2.5 hours, Hetastarch = 25 hours). However, with Hetastarch, this can be circumvented if it is provided by constant rate infusion or multiple dosing; it is highly effective in maintaining plasma COP. The feline dose for Hetastarch (6% solution) is 5 to 15 ml/kg per day IV given over 15 to 30 minutes. Ideally, it should be given in 5 ml/kg increments.
Therapeutic Notes • Some drugs need dosage adjustments in the hypoalbumenic cat. Highly albumin-bound drugs include penicillins, cephalosporins, tetracyclines, furosemide, diazepam, glipizide, and warfarin. • Cats are easily volume overloaded and should be carefully monitored when receiving crystalloids or colloids.
Suggested Readings Chan DL, Rozanski EA. 2003. Colloid osmotic pressure in health and disease. Compend Contin Educ. 23(10):896–903. Lees GE, Brown SA, Elliott JA, et al. 2005. Assessment and management of proteinuria in dogs and cats: 2004 ACVIM Forum consensus statement (Small Animal). J Vet Intern Med. 19:377-385. Mathews KA, Barry M. 2005. The use of 25% human serum albumin: Outcome and efficacy in raising serum albumin and systemic blood pressure in critically ill dogs and cats. J Vet Emerg Crit Care. 15(2): 110–119. Throop JL, Kerl ME, Cohn LA. 2004. Albumin in health and disease: Protein metabolism and function. Compend Contin Educ. 26(12): 932–939. Throop JL, Kerl ME, Cohn LA. 2004. Albumin in health and disease: Causes and treatment of hypoalbuminemia. Compend Contin Educ. 26(12):940–949.
Prognosis The prognosis depends upon the underlying cause of hypoalbuminemia. In general, the diseases which cause chronic hypoalbuminemia can be difficult to manage.
269
CHAPTER 113
Hypocalcemia Karen M. Lovelace
Overview The majority of causes of hypocalcemia in cats are secondary, and many of these causes are also iatrogenic in nature. Primary causes for hypocalcemia, such as hypoparathyroidism, occur less often. The causes for hypocalcemia are numerous (see Table 113-1). Processes that cause elevations in the levels of serum phosphate can cause hypocalcemia. Hypocalcemia occurs when calcium mobilization and resorption cannot meet the demand due to calcium loss from blood and other extracellular compartments. However, calcium levels are tightly regulated in the body, and levels above or below this narrow range can be life-threatening.
history of eating house plants; or outdoor exposure (ethylene glycol toxicosis). • Clinical Signs: Clinical signs are due to increased excitability of nervous and muscle tissues. Signs may include nervousness, listlessness, generalized weakness, muscle fasciculations, tetany, seizures, intense facial rubbing, prolapsed nictitating membranes, biting or licking of the paws, panting, aggression, cramping or pain in the legs, inappetence, or depression. • Chemistry Profile: Total serum calcium below 2 mmol/L (8.0 mg/ dL), especially in a patient with a normal blood albumin level, is diagnostic for hypocalcemia.
Secondary Diagnostics Diagnosis Primary Diagnostics • History: Relevant history includes a lactating or pregnant queen; recent thyroid surgery; history of chronic renal disease, crystalluria, or urolithiasis; dietary imbalances or supplementations/home prepared diets; pathologic fractures; previous medical therapy (i.e., phosphate-containing enemas, antibiotics, diuretics, and so on);
• Ionized (Free) Calcium: This test is especially helpful in borderline cases. Hypocalcemia is present when the ionized calcium level is <0.87 mmol/L (<3.5 mg/dL). • Electrocardiogram: Patients will exhibit bradycardia and prolonged S-T and Q-T segments. Prolongation of the Q-T interval and bradycardia are the most consistent findings. Patterns may progress to various degrees of heart block and ventricular tachyarrhythmias. • Fundic Examination: Papilledema occurs due to increased intracranial pressure may be present.
Diagnostic Notes TABLE 113-1: Conditions Associated with Hypocalcemia in the Feline Patient Hypoalbuminemia(hypoproteinemia) Chronic Renal Disease Acute Renal Disease Ethylene Glycol Toxicity Puerperal Tetany Iatrogenic Iatrogenic parathyroid damage during thyroidectomy Postoperative phase of thyroidectomy or other surgeries of the neck Calcitonin therapy Furosemide treatment Intravenous bicarbonate infusion Tetracycline administration Transfusion with anti-coagulated blood (i.e., citrate, ethylenediaminetetra-acetic acid) Cancer pharmaceuticals Anticonvulsant therapy Phosphate enemas (Fleet® enema) Urinary tract obstruction Plant toxicity: Lily, philodendron Intestinal malabsorption Lymphangiectasia Primary intestinal disease Nutritional secondary hyperparathyroidism Unbalanced diets Acute tumor lysis syndrome
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
270
• Although clinical signs of hypocalcemia vary, cats will typically show clinical signs of hypocalcemia between 1.62 and 1.87 mmol/L (6.5–7.5 mg/dl) or below. • Equations that are frequently used for dogs to calculate corrected serum calcium are inaccurate in cats. • Patients with low ionized calcium may have high or normal total calcium. A common example is renal failure. This may be due to complex formation with organic or inorganic ions such as phosphate, sulfate, or citrate. • When evaluating total calcium, the clinician should remember that total calcium may be low due to hypoalbuminemia. • Acute (subclinical) pancreatitis in dogs results in calcium complexes with saponification of peripancreatic fat. The incidence of this phenomenon in cats is unknown.
Treatment Primary Therapeutics • Emergency Therapy for Clinical or Severe Hypocalcemia (<1.87 mmol/L [<7.5 mg/dL]): Administer calcium gluconate intravenously slowly to effect over 10 to 30 minutes. The dose is 1 to 1.5 ml/kg, using a 10% (i.e., 100 mg/mL) calcium gluconate solution. During administration, the heart should be ausculted for arrhythmias and bradycardia, and an electrocardiogram (ECG) should be monitored for bradycardia, premature ventricular complexes, and shortening of the Q-T interval. If arrhythmias or ECG abnormalities are detected, the infusion should be briefly discontinued. Response to therapy is usually notable within minutes. The emergency dose is a guideline only; patient response should be used to determine when to stop administering calcium.
Hypocalcemia
• Immediate Maintenance Therapy: After stabilization of tetany, calcium gluconate administration should be repeated every 6 to 8 hours IV. Doses should always be given slowly. The total serum calcium should be checked several times daily, and should be maintained above 2 mmol/L (8.0 mg/dL). Immediate maintenance therapy should be maintained until oral vitamin D therapy takes effect (1–4 days).
Secondary Therapeutics • Long-Term Maintenance Therapy: Calcitriol (active vitamin D3, or 1,25-dihydroxycholecalciferol) is the preferred method of long-term calcium maintenance because it has a rapid onset (1–4 days), as well as rapid resolution of toxicity (less than 2 weeks). If hypercalcemia ensues, it can be easily corrected by discontinuing the drug. The halflife of calcitriol is under 24 hours. The dose for chronic renal failure is 1 to 3 ng/kg per day PO. The dose for hypoparathyroidism is initially 30 ng/kg per day PO for 3 days then 5 to 15 ng/kg per day PO. Doses should be divided twice daily to sustain the priming effects for calcium transport to the gastrointestinal epithelium. • Oral Calcium Supplementation: Because the primary means of therapy for hypocalcemia is the administration of vitamin D and the mechanism by which vitamin D works is through absorption of dietary calcium, it is imperative that dietary calcium exist in sufficient quantities. Although dietary calcium is usually adequate, oral calcium is usually administered early in therapy and discontinued later depending on serum calcium levels. The dose is 0.5 to 1.0 g/day. • Dihydrotachysterol: This drug has a more rapid onset of action than vitamin D2 (ergocalciferol; 1–7 days) and a faster resolution of toxicity (1–3 weeks), but calcitriol is considered the drug of choice. The initial dose is 0.02 to 0.03 mg/kg q24h PO, and the maintenance dose is 0.01 to 0.02 mg/kg q24 to 48h PO. • Vitamin D2 (Ergocalciferol): This method of treatment is not frequently recommended because its onset is slow (5–21 days) and resolution of toxicity is slow (1–18 weeks). The recommended initial therapeutic dose is 4000 to 6000 U/kg q24h PO.
Therapeutic Notes • Use caution in administering calcium-containing fluids to patients with hyperphosphatemia because excess calcium can result in softtissue mineralization, including in the kidneys. • Calcium gluconate is preferred over other calcium salts. Calcium chloride tends to produce gastric irritation in cats. Calcium carbonate produces alkalosis, which may exacerbate hypocalcemia.
• Calcium is irritating to tissues, and even diluted solutions of calcium have been associated with tissue necrosis when given via the subcutaneous route. Although many texts list doses for calcium gluconate given subcutaneously as a diluted solution, calcium should ideally be given IV (slowly) or orally. • Cats are sometimes resistant to vitamin D in the tablet form. Using the liquid form of vitamin D or use of calcitriol will avoid this problem. • Hypocalcemic lactating cats will usually be febrile [40.6°–41°C (105–106°F)] as a result of excessive muscle activity and tetany. The fever usually resolves with resolution of the tetany, and therefore, once calcium therapy is started fever should be monitored instead of treated. • To avoid the risk of hypercalcemia or hypercalciuria, the ideal serum calcium level in patients with a history of hypocalcemia is 2.0 mmol/L (8.0 mg/dL), which is just below the low normal end of the reference range. Many laboratories will report the reference range for normal cats up to 3 mmol/L (12.0 mg/dL). Total serum calcium should be monitored daily until stabilized, then weekly during maintenance therapy until target serum calcium is reached. Monitoring serum calcium quarterly is advised for cats with chronichypoparathyroidism.
Prognosis Iatrogenic causes are often transient, and long-term therapy is not usually needed. In postthyroidectomy cases, hypoparathyroidism is rarely permanent, and recovery of parathyroid function may occur within days to several months. With proper therapy, the prognosis, as well as the chance for a normal life expectancy, is excellent.
Suggested Readings Chew DJ, Nagode LA. 2000. Treatment of Hypoparathyroidism. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIII, pp. 340–345. Philadelphia: WB Saunders. Feldman EC. 2005. Disorders of the Parathyroid Glands. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1529–1535. St. Louis: Elsevier Saunders. Stockham SL, Scott MA. 2002. Erythrocytes. In SL Stockham, MA Scott, eds., Fundamentals of Veterinary Clinical Pathology, pp. 105–135. Ames: Iowa State Press.
271
CHAPTER 114
Hypokalemia Mark Robson and Mitchell A. Crystal
Overview Potassium is the major intracellular cation, and although the vast majority of body potassium is intracellular, the extracellular component is tightly regulated (primarily by aldosterone) due to its influence on the resting cell membrane potential in all tissues, especially nerve, muscle, and kidneys. The most obvious clinical effects of hypokalemia concern muscle and manifest as generalized weakness, ataxia, and ventral neck flexion. An important, but often unrecognized, complication of hypokalemia is nephropathy. This can comprise both functional and morphologic changes. The deleterious effects of hypokalemia on renal function may be reversible with appropriate treatment. Potassium must be considered along with the patient’s acid-base status and the concentration of other ions, such as magnesium and calcium. Acidemia will mask hypokalemia because hydrogen ions are driven into the cell in exchange for potassium. This can lead the clinician to underestimate the degree of total body depletion of potassium as the measured serum potassium concentration (2% of total body potassium) may look normal even in the face of a severe global deficit. In the kidney, acute metabolic acidosis tends to reduce potassium excretion, but chronic acidosis increases it. Many cases of hypokalemia are subclinical until interventions in the veterinary hospital are initiated. Mild hypokalemia due to anorexia or renal disease can rapidly become more severe if potassium-depleted fluids are used. Use of insulin in diabetic patients (especially if combined with inadequately supplemented fluids) can lead to rapid and sometimes fatal hypokalemia. Aggressive use of furosemide in congestive heart failure might also provoke hypokalemia, especially because fluid therapy is usually discouraged at times when a patient is receiving diuretics. Hypokalemia is the most common cause of cervical ventroflexion and generalized muscle weakness in cats. See Chapter 33. A common cause of hypokalemia is excessive urinary loss and is usually concurrent with loss of concentrating ability and azotemia. Renal loss may be combined with reduced food intake and the effects are exacerbated by chronic metabolic acidosis. Decreased dietary intake of potassium may lead to a chronic state of whole body depletion, but it usually will not lead to measurable hypokalemia unless another syndrome or fluid therapy is concurrent. Gastrointestinal (GI) disease may lead to hypokalemia, especially if vomiting causes concurrent loss of potassium and hydrogen ions from gastric secretions. Metabolic alkalosis in this setting drives potassium into cells in exchange for hydrogen ions and serum potassium concentration decreases. Diabetes mellitus, especially when complicated by ketoacidosis, often causes hypokalemia. Factors include chronic metabolic acidosis, decreased food intake, and polyuria, and these can be acutely exacerbated by treatment. Hyperthyroidism has been associated with hypokalemia, but the mechanism is not well understood. It may be due to polyuria, loss of muscle mass, or to direct effects of excessive thyroid hormone. The association between hyperthyroidism, hypokalemia, and ventral neck flexion is well recognized.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
272
Postobstructive diuresis following the relief of urethral obstruction is a well-known cause of acute hypokalemia. Other rare kidney disorders such as distal (Type 1) renal tubular acidosis have been reported to cause hypokalemia in cats. Ingestion of bentonite clay (in cat litter) has been associated with hypokalemia. Other causes such as hypothermia and rattlesnake envenomation have been seen in dogs but not confirmed in cats. An idiopathic hypokalemic nephropathy has been identified in the young Burmese cat (usually less than 1 year of age) that is believed to be a homozygous recessive hereditary condition that resembles hypokalemic periodic paralysis in humans. Mineralocorticoid excess is becoming more commonly recognized as a cause of hyperkalemia in cats. Primary hyperaldosteronism resulting from unilateral or bilateral adrenal neoplasia (Conn’s syndrome in humans) has typically been regarded as rare, but the authors of a recent report describing 13 cats with this syndrome suggest that it may be more common than previously suspected. See Chapter 102. Recently there has been a report describing a syndrome of primary hyperaldosteronism in cats that does not involve an adrenal neoplasm. These cats have adrenal glands that are normal or mildly bilaterally enlarged when imaged ultrasonographically and changes on histopathology in some affected cats were described as micronodular hyperplasia. Consistent findings were elevated or highnormal plasma aldosterone concentration with plasma renin concentration at the low end of the reference range and an aldosterone-to-renin ratio greater than normal. The underlying cause of this syndrome is unknown. Categorizing hypokalemia is complicated by the fact that serum potassium concentration is a poor indicator of total body potassium due to the factors mentioned above. Typically signs of muscle weakness will occur when potassium concentration drops below 3.0 mmol/L (3.0 mEq/L) with worsening signs and creatine kinase elevations when levels drop below 2.5 U/L. Hypokalemia can be classified as chronic or acute and mild, moderate, or severe. Other than the Burmese syndrome noted, there is no breed predilection and most affected cats are middle aged to older, usually around 9 years of age.
Diagnosis Primary Diagnostics • Clinical Signs: Mild to moderate hypokalemia can cause reduced appetite, gradual weight loss, low-grade anemia, poor haircoat, and reduced activity. These are easily confused with aging. Cats may also be polyuric and polydipsic as a result of hypokalemia or underlying chronic renal failure. Clinical signs of the severe form usually appear acutely and include ventral neck flexion and generalized muscle weakness. About 25% of cats will demonstrate a stiff or stilted gait and muscle pain. Rarely, cats with severe hypokalemia may demonstrate dyspnea due to respiratory muscle paralysis. • Data Base (Complete Blood Count [CBC], Chemistry Profile, and Urinalysis): Serum potassium is usually decreased and creatine kinase is often markedly increased (5,000 to 50,000 U/L). Abnormalities associated with chronic renal failure may also be present; these include azotemia, hyperphosphatemia, decreased urine specific gravity, acidosis, and anemia. Other causes of hypokalemia may be identified (i.e., diabetes mellitus or hypomagnesemia).
Hypokalemia
Secondary Diagnostics • Blood Pressure Determination: Check for hypertension. • Ocular Examination: Look for changes referable to hypertension. See Chapter 107 and 193. • Therapeutic Trial: Because serum potassium levels may be normal in mild or moderate hypokalemia it may be impossible to be sure whether low total body potassium is causing clinical signs. A trial of 2 mEq q12h PO of potassium gluconate for 4 to 6 weeks may be warranted, and this can result in obvious improvements in affected cats. • Total T4: This should be checked in cats over 8 years of age to determine if hyperthyroidism is contributing to or causing hypokalemia, clinical signs (i.e., weakness, cervical ventroflexion, weight loss, or polyuria/polydipsia) or renal failure. • Abdominal Ultrasound: This should be performed to evaluate the kidneys and to exclude adrenal neoplasia. • Urinary Fractional Excretion of Potassium: This is usually greater than 6% in affected cats. This is calculated as follows: FEK+ = (urinary K+/plasma K+) × (plasma creatinine/urinary creatinine) × 100. • Iohexol Clearance Renal Function Fest: This test is indicated to identify renal insufficiency or early renal failure, which may cause decreased urine specific gravity without azotemia. See Chapter 311.
Diagnostic Notes • Chronic hypokalemia should not be ruled out based on a low-normal or normal serum potassium level. Only 2% of the body’s potassium is found in the blood, and there may be poor correlation between blood and tissue potassium levels. • Diagnostic tests for other causes for ventral neck flexion and generalized muscle weakness should be performed if indicated by clinical signs or chemistry abnormalities. See Chapter 33. • Other causes of hypokalemia should be considered and evaluated if suggested by clinical signs or history. • Muscle biopsies are generally not needed but, if performed, are normal. • Conditions that falsely elevate potassium (e.g., thrombocytosis or hemolysis) can mask hypokalemia.
Treatment Primary Therapeutics • Oral Potassium Therapy: Potassium gluconate is given at 2 to 4 mEq/ cat q12h PO until serum potassium is within the normal range (severe form) or until clinical response is achieved (mild to moderate form), followed by 1 to 2 mEq/cat PO q12h indefinitely. Oral potassium therapy is more effective than parenteral potassium supplementation and should be used for all but the most severely affected cats. Potassium gluconate as a powder, gel, or tablet (several sources) or elixir (several sources) provides the most available source of potassium. Elixirs tend to be less palatable to cats. Avoid potassium chloride as it is less palatable and may worsen pre-existing acidosis. • Manage Underlying or Concurrent Condition: Provide appropriate therapy for any causative or concurrent diseases identified.
until normalization and stabilization of serum potassium are achieved. Fluids should be given at slow rates and contain a high concentration of potassium (e.g., 160 mmol/L [160 mEq/L] administered at 2.0 mL/kg per hour). Fluids with low potassium concentrations administered at rapid rates may further lower serum potassium and worsen clinical signs, leading to respiratory muscle paralysis. Oral therapy should be started concurrently, if possible.
Therapeutic Notes • Intravenous administration rates of fluids containing high concentrations of potassium should be closely monitored to prevent cardiac arrhythmias; the rate should be <0.5 mEq/kg per hour). • Administration of dextrose, insulin, or bicarbonate will worsen hypokalemia by causing an intracellular shift of potassium. • Because the chronic form of hypokalemia is fairly common in geriatric cats and because those cats may have normal serum potassium values, a therapeutic trial lasting 4 to 6 weeks should be considered for these patients. When given orally, potassium has a wide margin of safety; vomiting is usually induced well before the onset of hyperkalemia. • The concentration of potassium and other electrolytes can change quickly during acute illness and aggressive treatment. Using a single measurement of any electrolyte (especially potassium) to make treatment decisions for 1 to 3 days will often lead to inappropriate treatment decisions. In view of the dynamic nature of serum potassium concentrations in response to therapeutic interventions such as fluids, insulin, and bicarbonate careful consideration must be given to monitoring this electrolyte. Frequency of measurement needs to tailored to the severity of illness, owner budget, and logistics within the practice, and could vary from several times per hour to once or twice daily.
Prognosis The prognosis for the subclinical form is excellent. In the severe form, response to therapy usually begins within 24 hours. Considerable improvement is seen in 2 to 3 days, although complete remission may take several weeks. With appropriate therapy and long-term potassium supplementation, the prognosis for recovery from hypokalemic polymyopathy is excellent, although underlying renal dysfunction, if present, may carry a less favorable prognosis for long-term survival. Treatment failure usually results from administering fluids of low potassium concentration at a rapid rate.
Suggested Readings Ash RA, Harvey AM, Tasker S. 2005. Primary hyperaldosteronism in the cat: a series of 13 cases. J Fel Med Surg. 7(3):173–182. DiBartola SP, de Morais HE. 2005. Disorders of potassium: hypokalemia and hyperkalemia. In SP DiBartola, ed., Fluid, Electrolyte and Acid-Base Disorders in Small Animal Practice, pp. 91–121. St Louis: Saunders Elsevier. Javadi S. 2005. Primary hyperaldosteronism, a mediator of progressive renal disease in cats. Domest Anim Endocrinol. 28(1):85–104.
Secondary Therapeutics • Parenteral Potassium Therapy: For the severe form, intravenous potassium is given at 0.25 to 0.5 mEq/kg per hour in parenteral fluids
273
CHAPTER 115
Hypomagnesemia Michele Fradin-Fermé
Overview Hypomagnesemia is defined as a total serum magnesium (Mg) concentration below 0.8 mmol/L (1.89 mg/dL). In humans, hypomagnesemia is quite common and responsible for tetany crises and increased mortality in hospitalized patients. Unfortunately, the importance of hypomagnesemia is still unclear in the cat. The serum concentration does not accurately reflect the total Mg of the body or the ionized Mg level, which is implicated in cellular metabolism. When serum hypomagnesemia is found the cat is often asymptomatic. Nonetheless, it seems to be a common finding in diabetes, diabetic ketoacidosis, refractory hypokalemia, and the refeeding syndrome. Most of the body’s Mg is located in the skeletal bone mass (53%). The remainder is in soft tissue, and 0.3% is in the serum. Mg is intracellular in muscle, soft tissue, and erythrocytes; it is mainly bound to chelators with only 5 to 10% ionized. In serum, Mg is extracellular with 67% ionized. Mg is involved in more than 300 enzyme systems. Intracellular Mg affects calcium and potassium metabolism. Mg also interferes with calcium balance by acting directly on parathyroid hormone (PTH). Mg is absorbed primarily in the jejunum and ileum and excreted in the nephron segments of the kidney. Mg deficiency most commonly affects the cardiovascular, skeletal, and nervous systems, both central and peripheral.
Diagnosis Primary Diagnostics • History: Hypomagnesemia should be suspected in diabetic, diabetic ketoacidotic, and critically ill patients. Most veterinary critical care diets contain low levels of Mg. • Clinical Signs: Cats may exhibit dysphagia, weakness, dyspnea, arrhythmias, or seizures, or they may be asymptomatic depending on the rate of development of the Mg deficiency. Symptoms can also be induced by concomitant hypocalcemia (i.e., twitching, tremors and seizures) or hypokalemia (weakness). • Serum Mg Level. Abnormal is less than 0.8 mmol/L (1.89 mg/dL). A serum sample is preferred to plasma as many anticoagulants contain Mg or bind Mg. Citrate will bind both Mg and calcium. • Serum Chemistry Profile: A chemistry profile should include calcium, phosphate, and potassium levels because hypomagnesemia can be associated with refractory hypokalemia.
Treatment Primary Therapeutics • Monitoring: Mild, nonclinical hypomagnesemia usually resolves with treatment of the underlying disease process. • Intravenous Mg: Symptomatic cats and cats with refractory hypokalemia should receive Mg supplementation. When rapid replacement is needed the intravenous route is recommended at a dose of 0.4 to 0.5 mmol/kg per day (0.75–1.0 mEq/kg per day), then the dose is reduced to 0.15 to 0.25 mmol/kg per day (0.34–0.5 mEq/kg per day) as the blood level normalizes. Mg is available as a 50% Mg sulfate solution containing 4 mmol (8 mEq) of Mg/g of Mg sulfate and a 50% Mg chloride solution containing 4.6 mmol (9.25 mEq) of Mg/g of Mg chloride. It should be infused in 5% dextrose in water as a constant rate infusion. • Oral Magnesium: For chronic hypomagnesemia oral supplementation is recommended at the dose of 0.5 to 1 mmol/kg per day (1–2 mEq/kg per day).
Therapeutic Notes • For comparison purposes, 1 mmol of Mg = 2 mEq of Mg; 1 mmol of Mg = 24 mg of Mg, and 1 mmol/L of Mg = 2.43 mg/dL of Mg. • A 50% Mg sulfate solution contains 2 mmol of Mg/mL (4 mEq/mL or 50 mg/mL). • Overdosage of Mg can result in respiratory muscle weakness, hypocalcemia, hypotension, and atrioventricular and bundle branch blocks; however, these adverse effects are more commonly associated with bolus therapy. Calcium gluconate given as a bolus of 50 mg/ kg followed by 10 mg/kg per hour as a constant rate infusion is recommended for the treatment of overdoses. • The major side effect of oral supplementation is diarrhea. • Potassium supplementation should be decreased once Mg supplementation has begun to avoid hyperkalemia. • The more commonly used crystalloid solutions (lactated Ringer ’s solution and sodium chloride) are Mg deprived.
Prognosis: The prognosis is primarily determined by one’s ability to correct an underlying disease process (i.e., diabetes mellitus or diabetic ketoacidosis) or underlying electrolyte imbalances.
Suggested Readings
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
274
Dhupa N. 1998. Hypocalcemia and hypomagnesemia. Vet Clin N. Amer Sm An Pract. 28:587–608. Toll J, Erb H, Birnbaum G., et al. 2000. Prevalence and incidence of serum magnesium abnormalities in hospitalized cats. J Vet Inter Med. 16: 217–221.
CHAPTER 116
Hypophosphatemia Stephanie G. Gandy-Moody
Overview Phosphorus is the major extracellular anion in the body. The majority of the body’s phosphate is in the form of inorganic hydroxyapatite in bone, and the remaining is in soft tissues. Just as potassium (the major intracellular cation) concentration can change quickly, one must use caution when assessing a patient’s phosphorus concentration based on serum concentrations. Phosphorus is primarily reabsorbed by the proximal tubule of the kidney. Low phosphorus concentrations are caused by translocation (shifts from the extracellular fluid into cells), increased loss (reduced renal reabsorption), decreased intake (reduced intestinal absorption), or laboratory error. Hypophosphatemia is present when serum phosphorus concentration is less than 1.0 mmol/L (3 mg/dL), although some variances exist between laboratories. When phosphorus concentrations reach severely low levels (0.5 mmol/L [<1.5 mg/dL]) neurological signs, cardiac abnormalities, hemolytic anemia, and myopathy can occur. Several causes of hypophosphatemia exist. See Table 116-1. The most common in the feline patient includes diabetes mellitus, hepatic lipidosis, and overdose of oral phosphate binders.
Diagnosis Primary Diagnostics • Clinical Signs: Muscle weakness, anorexia, seizures, coma, nausea and vomiting, pale mucus membranes (due to hemolysis), and impaired myocardial contractility. • Minimum Data Base: This includes a complete blood count (CBC), serum chemistry, urinalysis, retroviral testing. Information gained
TABLE 116-1: Causes of Hypophosphatemia Increased Renal Loss Primary hyperparathyroidism (rare) Hyperadrenocorticism (rare) Diabetes mellitus (with or without ketoacidosis) Sodium bicarbonate or diuretic administration Decreased Intestinal Absorption Vomiting/Diarrhea Vitamin D deficiency Phosphate binders administration Dietary deficiency Malabsorption Transcellular Shifts Enteral or total parental nutrition (hyperalimentation-refeeding syndrome) Insulin administration Parental glucose administration Respiratory alkalosis
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
from your minimum data base will rule out underlying disease that may predispose to or worsen hypophosphatemia. A blood smear analysis should be included as part of the CBC; it is important for monitoring for hemolysis or Heinz body formation and classifying the anemia.
Treatment Primary Therapeutics • Avoidance: Discontinue any oral phosphate binders if low serum phosphorus concentrations are noted or if patient is demonstrating clinical signs associated with hypophosphatemia. Discontinue diets that are restricted in phosphorus (i.e., renal diets). • Underlying Disease: Correct or anticipate the underlying disease process that is causing hypophosphatemia. These include patients receiving total parenteral nutrition, insulin treatment for diabetic ketoacidosis (DKA), or phosphate binders due to renal failure. • Oral Supplementation, Mild Cases: Oral phosphate supplementation may be instituted in cases of mild hypophosphatemia if the patient is not vomiting. Oral supplementation is much slower in correcting hypophosphatemia and should, therefore, only be used in mild cases. A buffered laxative (i.e., Phospho-Soda®), balanced commercial diets, or low-fat milk may be used. • Intravenous Supplementation, Moderate to Severe Cases: Potassium phosphate (which contains 3 mmol/mL of phosphate and 4.4 mEq/ mL of potassium) and sodium phosphate (which contains 3 mmol/ mL of phosphate and 4 mEq/ml of sodium) are available for intravenous supplementation. The safest way to administer phosphate is by a constant rate infusion, monitoring the serum phosphorus concentration every 6 to 12 hours. To prevent precipitation of calcium phosphate, potassium should only be added to calcium-free fluids (i.e., normal saline). The initial dosage of phosphate is 0.01 to 0.03 mmol/ kg per hour with monitoring every 6 hours and adjustment of the phosphate infusion accordingly. Cats being treated concurrently for DKA with insulin therapy may require higher dosages due to the intracellular shifts of phosphorus because of the insulin administration; a rate of 0.03 to 0.12 mmol/kg per hour for 6 to 24 hours may be needed.
Secondary Therapeutics • Prophylactic Therapy: When treating patients with severe hepatic lipidosis or DKA by supplementing potassium, one can administer 25% of supplemental potassium as potassium phosphate and the rest as potassium chloride. • Blood Transfusion: When hemolysis is severe a transfusion with fresh whole blood is preferred. Stored red blood cells use serum phosphate and may complicate hypophosphatemia.
Therapeutic Notes • Serum phosphorus concentrations should be monitored every 6 to 12 hours during intravenous phosphorus administration. Potential complications of intravenous phosphate administration include hypocalcemia, acute renal failure, and soft-tissue calcification.
275
SECTION 1: Diseases and Conditions
Diuresis should be initiated immediately and phosphate infusion should be discontinued. If hypocalcemia occurs calcium gluconate should be administered. • Use caution when using potassium phosphate for supplementation. Intravenous potassium administration should not exceed 0.5 mEq/ kg per hour.
Prognosis The prognosis is variable depending on the underlying cause and duration of the hypophosphatemia as well as response to therapy.
276
Suggested Readings DiBartola SP, Willard MD. 2006. Disorders of Phosphorus: Hypophosphatemia and Hyperphosphatemia. In SP DiBartola, ed., Fluid Therapy in Small Animal Practice, pp. 195–209. Philadelphia: Elsevier. Nelson RW, Couto CW. 2003. Electrolyte Imbalances. In RW Nelson, CW Couto, eds., Small Animal Internal Medicine, 3rd ed., pp. 842–843. Philadelphia: Mosby.
CHAPTER 117
Icterus Sharon Fooshee Grace
Overview Icterus, also known as jaundice, is a common clinical disorder in cats and occurs when excess bilirubin is deposited in tissues. The normal serum bilirubin value in cats is less than 17 µmol/L (1.0 mg/dL). Clinically apparent tissue icterus generally does not occur until serum levels of bilirubin exceed 35 µmol/L (2 mg/dL), whereas the serum is visually icteric at about 25 to 35 µmol/L (1.5–2.0 mg/dL). Therefore, the total bilirubin exceeds the normal range before serum hyperbilirubinemia and tissue icterus are present, and the former occurs before the latter. Causes of icterus can be broken down into three main categories: prehepatic (hemolytic), hepatic, and post-hepatic. Hemolytic causes of icterus are less common in cats than dogs, in part because immunemediated causes of hemolysis are uncommon for this species. The most common cause for hemolysis in cats is hemoplasmosis (formerly hemobartonellosis). Feline icterus is most often caused by disorders that primarily or secondarily involve the liver resulting in decreased hepatocyte function or intrahepatic cholestasis; hepatic lipidosis or inflammatory liver diseases (i.e., cholangitis/cholangiohepatitis or lymphocytic portal hepatitis) are often responsible. Posthepatic (extrahepatic) causes are associated with obstructive processes involving the common bile duct and known as extrahepatic bile duct obstruction (EHBDO). Disorders that cause posthepatic obstruction are less common in cats than dogs. The distinctions between categories are not always clear cut, and in many cases there is overlap. Clinical findings are referable to the underlying disease but usually include anorexia and lethargy. Tissue icterus is first seen in the mucosa of the soft palate; the skin, especially the pinnae, third eyelids, sclera, and irises are also areas where icterus is clinically evident.
Differential Diagnoses Many diseases need to be considered for icterus in cats. They are listed in Table 117-1.
Diagnosis Primary Diagnostics • History: The history is often vague and only general, nonlocalizing symptoms (e.g., anorexia, lethargy, and vomiting) are present. History of a previously obese cat that has undergone a period of anorexia may suggest hepatic lipidosis. Diabetic cats may demonstrate icterus as a result of pancreatitis or secondary hepatic lipidosis. Owners should be questioned regarding exposure to ticks and drugs or toxins. Cats that have traveled or lived in southern Florida, Hawaii, or Puerto Rico may have liver flukes; those that have traveled or lived in Texas and the Mississippi, Ohio, or Missouri River valleys may have systemic mycoses; and those that have traveled or lived outdoors in the Gulf coast and surrounding states may have Cytauxzoon. • Clinical Signs: Lethargy, weakness, pale or yellow mucous membranes, tachypnea, tachycardia, cardiac murmur, and hepatospleno-
TABLE 117-1: Known Causes of Icterus in the Cat Pre-hepatic Hemoplasmosis (formerly hemobartonellosis) Incompatible blood transfusion Neonatal isoerythrolysis Heinz body associated Zinc, onion, methylene blue, acetaminophen, benzocaine, propylene glycol, copper, vitamin K1 overdose Microangiopathic hemolysis Disseminate intravascular coagulation, vasculitis, hemangiosarcoma Immune-mediated disease Systemic lupus erythematosus; infectious disease (e.g., feline leukemia virus and feline immunodeficiency virus) Sepsis Babesiosis Cytauxzoonosis Hypophosphatemia Most often occurs following insulin therapy; sometimes caused by refeeding syndrome with hepatic lipidosis Hepatic Hepatic lipidosis Cholangitis/cholangiohepatitis complex Hepatic amyloidosis Abyssinian, Oriental Shorthair, Siamese Hepatic necrosis Toxins, drugs, plants (i.e., pine oil, arsenicals, tetracyclines, acetaminophen, griseofulvin, ketoconazole, methimazole, diazepam, glipizide, sago palm, and certain mushrooms); heat stroke Infectious disease Feline leukemia virus, feline immunodeficiency virus, feline infectious peritonitis, panleukopenia, calicivirus, fungal diseases, toxoplasmosis, tularemia, histoplasmosis, and endotoxemia Liver flukes Sepsis Drugs Tetracycline, diazepam, and methimazole Polycystic liver disease Persians and Himalayans Paraneoplastic syndrome Primary or metastatic neoplasia (espeically lymphoma) Post-hepatic Pancreatitis Neoplasi Rupture of bile duct or gall bladder Abscess/granuloma of bile duct Cholelithiasis Inspissated bile Liver flukes
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
277
SECTION 1: Diseases and Conditions
•
•
•
•
megaly may be evident with prehepatic icterus. Most cats with acquired liver disease, either primary or secondary, have hepatomegaly. Abdominal pain is suggestive of an obstructive process, cholecystitis, pancreatitis, or cholangitis/cholangiohepatitis. Neurologic signs and ptyalism may indicate hepatic encephalopathy (although portosystemic shunting is rarely associated with icterus). A complete ophthalmologic examination is essential to aid in identifying multisystemic disease (i.e., lymphoma, feline infectious peritonitis [FIP], systemic mycoses, or toxoplasmosis). Complete Blood Count (CBC): A CBC is the most important test to perform on initial evaluation of the icteric cat. If the hematocrit is within the reference range or close to it (accounting for the effect of dehydration) and the blood smear is normal, hemolysis is not the cause. Anemia must be acute and massive (i.e., hemolysis would have to be severe) to overwhelm a normal liver and cause icterus. If several days have passed since onset of the hemolysis, the blood smear and reticulocyte count may indicate a regenerative response (i.e., macrocytosis and reticulocytosis), though it should be noted that sick cats often do not always mount a strong regenerative response, especially compared to the dog. The smear should also be examined for red blood cell parasites and Heinz bodies. Occasionally, microvascular angiopathy (disseminated intravascular coagulation) will be causative and schistocytes will be evident on the smear. Hepatic causes of icterus can be suggested by poikilocytosis, which is a common finding in cats with liver disease. A nonregenerative anemia may also suggest a hepatic cause. Granulocytopenias or granulocytophilias may be found with systemic mycoses or septicemia. Chemistry Profile: Liver enzymes may be increased with prehepatic, hepatic, and posthepatic causes of icterus. In most cases, enzymes are normal or only marginally increased with prehepatic causes, though hepatocellular hypoxia will increase alanine aminotransferase (ALT). Hypercholesterolemia may be present with persistent EHBDO. Hypoalbuminemia is not typical of primary liver disease unless the liver is functioning at less than 20% capacity. Significant hyperglobulinemia may be present in cats with FIP or other systemic inflammatory conditions. Serum feline pancreatic lipase immunoreactivity (fPLI) is a good test for pancreatitis in the cat. See Chapters 159 and 160. Urinalysis: The presence of bilirubin in feline urine is never normal and warrants immediate investigation. Isosthenuria may result from the medullary washout associated with chronic liver disease. Viral Screen: Icteric cats should be tested for feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV). Feline coronavirus (FCoV) serology is not recommended due to the lack of specificity of currently available tests.
Secondary Diagnostics • Abdominal Radiography and Ultrasound: The size and architecture of the liver and pancreas, the patency of the biliary system, the structure and contents of the gall bladder, and the presence of inspissated bile or choleliths may be evaluated with these diagnostic imaging techniques. Ultrasound is more specific than radiography in evaluating the biliary system. The presence of an enlarged gall bladder is not specific for hepatobiliary causes of icterus because anorexic animals will have an enlarged gall bladder; however, the additional finding of dilated, tortuous bile ducts is significant. • Fine-Needle Aspiration (FNA) or Fine-Needle Biopsy (FNB) of the Liver and Gall Bladder: Aspiration of the liver with a 22-gauge needle (via ultrasound guidance) is a relatively noninvasive means of screening for many liver disorders. See Chapter 301. It is useful for establishing or supporting a diagnosis of hepatic lipidosis, neoplasia, fungal diseases, and so on. FNA or FNB with cytology provide limited information as to liver architecture, hepatic fibrosis, or focal disease, so a surgical biopsy may still be needed. Bile can also be sampled with ultrasound guidance or during laparotomy; it should
278
be submitted for aerobic and anaerobic culture. The recovery of bacteria is higher than FNA or FNB of the liver. Complications are generally infrequent though vagal stimulation can lead to asystole in an occasional patient so atropine should be available. A distended or friable gall bladder may tear or rupture with this procedure. • Liver Biopsy: Clotting profiles and a platelet count should be determined prior to liver biopsy, regardless of whether the procedure involves an ultrasound-guided biopsy or laparotomy. Core needle biopsy and surgical techniques may be used. A wedge biopsy yields the maximum information. • Coagulation Profile: The liver must be severely and diffusely affected to cause coagulopathy. An activated clotting time (ACT) may be performed in-house. Prothrombin time (PT) and activated partial thromboplastin time (APTT) can also be performed in-house if an analyzer is available, or they may be sent to an outside lab. Coagulation tests are not routinely predictive of bleeding potential. Automated platelet counts are highly inaccurate in cats. If the automated count is below normal, a platelet estimate should be performed from a blood smear. A clinical clue may be provided with prolonged bleeding after venipuncture. • Screening for Nonviral Infectious Diseases: Other infectious causes should be considered: toxoplasmosis (Chapter 214), hemoplasmosis (Chapter 92), liver flukes (Chapter 81), and systemic mycosis (Chapters 22, 38, 43, and 97).
Diagnostic Notes • It may be easier to palpate the cat’s liver if the cat’s forequarters are held up, allowing the viscera to fall farther down into the abdominal cavity. In general, cats with liver disease (including cirrhosis) do not have small livers. One exception to this is liver disease due to a portosystemic shunt, where microhepatica is present in close to 50% of cats, though these cats are rarely icteric (Chapter 178). • Abnormal liver enzymes are always considered significant and warrant a diagnostic evaluation. However, normal liver enzymes and absence of icterus do not eliminate the possibility that primary liver disease is present. In a nonicteric animal with suspected liver disease, consider performing bile acids. In an icteric animal, serum bile acids do not provide any diagnostic information because they are dependent on biliary excretory mechanisms. • If significant prolongations are identified during coagulation screening, yet biopsy is necessary, vitamin K1 (see Therapeutics) or feline plasma can be administered, followed by repeat coagulation screening to confirm resolution of the coagulopathy. • Abdominal effusion may be seen with a number of hepatic and posthepatic disorders, including rupture in the biliary tree. If fluid is present, abdominocentesis should be performed promptly. The fluid should be evaluated cytologically and biochemically and culture submitted. Bile peritonitis requires immediate surgical attention.
Treatment Primary Therapeutics • Treat the underlying disease: This is the key to successful management. No therapy is indicated for the icterus itself.
Secondary Therapeutics • Ursodeoxycholic Acid: This is a synthetic bile salt that may benefit some cats with cholestasis. It thins the bile secretions to improve flow and also has a beneficial effect in reducing liver inflammation. It is dosed at 10 to 15 mg/kg q24h PO until cholestasis subsides. Ursodeoxycholic acid should not be used when extrahepatic bile duct obstruction is suspected due to the increased risk of biliary rupture.
Icterus
• S-adenosylmethionine (SAMe; Denosyl® and Denamarin®, Nutramax Laboratories): These nutraceutical agents have marked anti-inflammatory properties that can be of benefit to cats with acute cholangiohepatitis and hepatic lipidosis. They are dosed at 90 mg q24h PO and can be used indefinitely. • Vitamin K1: This vitamin may need to be supplemented in cholestatic disorders because of fat malabsorption. Dosage is 5 mg/kg q12 to 24h SC until coagulation tests are normalized; usually only one to three doses are needed. • Fluids and Electrolytes: Appropriate attention should be given to fluid and electrolyte balance in icteric cats. In particular, fluids supplemented with potassium may be necessary.
Therapeutic Notes • Antibiotics: Generally, tetracyclines should be avoided in cats with liver disease. Metronidazole or penicillins (e.g., amoxicillin) are useful to treat anaerobic bacteria, whereas fluoroquinolones and aminoglycosides are of value for suspected gram-negative bacteria. • Methionine: This drug is contraindicated in the management of cats with liver disease as it may exacerbate hepatic encephalopathy.
Prognosis The prognosis depends on the underlying cause of icterus.
Suggested Readings Armstrong PJ, Weiss DJ, Gagne JM. 1997. Inflammatory liver disease. In JR August, ed., Consultations in Feline Internal Medicine, 3rd ed., pp. 68–78. Philadelphia: WB Saunders. Center SA. 2009. Diseases of the gallbladder and biliary tree. Vet Clin North Amer. 39(3):543–598. Sherding RG. 2000. Feline jaundice. J Fel Med Surg. 2(3):165–169. Taboada J. 2001. Approach to the icteric cat. In JR August, ed., Consultations in Feline Internal Medicine, 4th ed., pp. 87–90. Philadelphia: WB Saunders. Webb CB, Twedt DC, Fettman MJ, et al. 2003. S-adenosylmethionine (SAMe) in a feline acetaminophen model of oxidative injury. J Fel Med Surg. 5(2):69–75.
279
CHAPTER 118
Idiopathic Ulcerative Dermatitis Christine A. Rees
Overview Idiopathic ulcerative dermatitis is a rare feline dermatitis with an unknown cause and pathogenesis. Patients may present at any age, breed, or sex. Most patients have a heavily crusted nonhealing ulcer that has a surrounding border of thickened skin. This lesion may be painful and occurs most commonly on the dorsal midline of the caudal neck or between the scapulae. No systemic signs are usually noted. A peripheral lymphadenopathy is possible. Infections, injections, foreign bodies, and trauma do not appear to play a direct role. I have seen several cases for which ectoparasites or hypersensitivities (such as atopic dermatitis, flea allergy dermatitis or food reaction) appear to be primary inciting or contributory factors. In these intensely pruritic or painful cases, primary differentials should include atopic dermatitis, food reaction, flea allergy dermatitis, injection site sarcoma, and dermatophytosis. In nonpruritic or painful cases, the differential list should also include injection site reaction, trauma, burn, infection (i.e., bacterial or fungal), viral infection, Demodex gatoi, flea allergy, food allergy, atopy, and neoplasia.
Diagnosis Primary Diagnostics • Clinical Appearance: Lesions are typically solitary and arise on the dorsal cervical or interscapular skin. Ulcerations with adherent crusting and often purulent surface debris are present. See Figure 118-1. The lesion often has a thickened border around the ulcerated lesion. The typical history for feline idiopathic ulcerative dermatosis is an ulcerated lesion that slowly enlarges over a period of weeks to months. Some cats will be intensely pruritic or painful. • Histopathology: A skin biopsy is the most useful diagnostic test. The skin biopsy samples should be collected to include ulcerated tissue and normal surrounding tissue. The skin biopsy reveals an ulcerative dermatitis with superficial perivascular to interstitial mixed dermatitis. A linear band of superficial dermal fibrosis extends from the periphery of the ulcer.
Secondary Diagnostics • Other Diagnostic Tests: Dermatophytosis should be ruled out by fungal culture. Skin scrapings should be performed to rule out D. gatoi, Demodex cati, Cheyletiella spp., and Notoedres cati mites, and Felicola subrostratus lice. It is also advisable to check the patient’s retroviral status.
Figure 118-1 This is an example of idiopathic ulcerative dermatitis characterized by a large ulcerating, crusting lesion in the interscapular space. Image courtesy Dr. Gary D. Norsworthy.
food allergy, flea allergy, injection site sarcoma, retroviral infections, dermatophytosis, mites (D. gatoi, D. cati, Cheyletiella spp., N. cati) and lice (F. subrotratus). • Local Therapy: The best wound management treatment regimen is topical silver sulfadiazine and light bandaging (such as tube gauze or a cotton baby T-shirt). The use of SoftPaws® nail coverings on the rear feet may be useful in trying to prevent the cat from scratching of the lesion. Wound management therapy may need to be continued for weeks to months. Relapses are common if contributory factors are not identified. • Systemic Therapy: Injectable or oral steroids may be effective in treating the ulcerated lesion. The two steroids that appear to more consistently work are methylprednisolone and prednisolone. Analgesics may be helpful if the lesion is painful.
Secondary Therapeutics
• Treat Concomitant Disease: Any potential inciting factors need to be addressed and treated. Examples of inciting factors include atopy,
• Surgical Excision: Occasionally patients will respond favorably to surgical excision of the lesion; however, more typically, surgical intervention leaves the patient with a more significant nonhealing wound than prior to surgery. Surgery should be the last therapeutic choice.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
The prognosis for feline ulcerative dermatitis is guarded to poor because lesions are often refractory to medical therapy and many have lesions too large to completely surgically excise. The best hope
Treatment
Prognosis
280
Idiopathic Ulcerative Dermatitis
is to try to identify any possible underlying cause and treat the underlying cause.
Suggested Readings
Scott DW, Miller WH, Griffin CE. 2001. Feline Ulcerative Dermatitis. In DW Scott, WH Miller, CE Griffin, eds., Muller & Kirk’s Small Animal Dermatology, 6th ed., p. 18. Philadelphia: WB Saunders. Spaterna A, Mechelli L, Rueca F, et al. 2003. Feline idiopathic ulcerative dermatosis: Three cases. Vet Res Commun. 27:S795–S798.
Tackle GL, Hnilica KA. 2004. Eight emerging feline dermatoses. Vet Med. 99:456–467.
281
CHAPTER 119
Immune Mediated Hemolytic Anemia Anthony P. Carr
Overview Immune-mediated hemolytic anemia (IMHA) is a disease process whereby red blood cells (RBCs) are marked as foreign and are then destroyed by the patient’s own immune system. This tagging occurs when immunoglobulin G (IgG), immunoglobulin M (IgM), complement, or a combination of these bind to the RBCs. There may be an identifiable trigger present (secondary IMHA), or it may be a primary disease (i.e., idiopathic or primary IMHA, sometimes termed autoimmune hemolytic anemia). Unlike dogs, primary IMHA in cats is relatively rare. Triggers for the development of secondary IMHA include drugs (propylthiouracil), blood transfusions, neoplasia (i.e., lymphoma or multiple myeloma), and infectious diseases (i.e., hemoplasmosis, cytauxzoonosis, Babesia spp., feline infectious peritonitis [FIP], and the feline leukemia virus [FeLV]). There is no convincing evidence that vaccines are involved in cats. With IMHA the anemia is expected to be regenerative in nature. When a regenerative anemia is seen the major differentials are either hemolysis or hemorrhage. In cats, judging whether an anemia is regenerative or not is more complicated because the changes in the RBCs are far more subtle in cats than in dogs. In some cases of IMHA, regeneration might not be present, however. This can be because either there hasn’t been adequate time for a regenerative response to occur (usually around 5 days) or because the immune reaction is directed at RBC precursors limiting the number of immature cells that are released into circulation. Clinical signs in cats with IMHA will depend on a variety of factors. The degree of anemia will have a significant impact; however, the rapidity at which the anemia developed is also a major factor. If the anemia develops rapidly there is less time for the patient to compensate so that signs will be worse than if the anemia developed over a longer period or time. Common signs include lethargy, anorexia, dyspnea, tachypnea, pale mucous membranes, and tachycardia. With severe anemias, cardiac murmurs can develop. With IMHA splenomegaly is common as well. More variable signs include icterus and fever. Differential diagnoses are listed in Table 119-1.
Diagnosis Primary Diagnostics • Complete Blood Count (CBC): The CBC reveals anemia, usually quite severe. The erythrogram can provide valuable information on the cause of the anemia. With hemolysis or hemorrhage regeneration should be evident. Polychromasia is a good indicator of regeneration, though in cats it may not be abundantly present in milder anemias. The presence of increased reticulocytes is the optimal way to differentiate between regenerative and nonregenerative anemias. Heinz bodies can be seen with oxidative injury, though up to 5% Heinz bodies can be seen in normal cats. Low mean corpuscular volume (MCV) suggests iron deficiency anemia that implies chronic blood loss. High MCV can be seen with regeneration but can also be a
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
282
TABLE 119-1: Differential Diagnoses for Anemias in Cats Regenerative anemia Hemorrhage Hemoplasmosis (see Chapter 92) Cytauxzoonosis (see Chapter 47) Idiopathic immune-mediated hemolytic anemia Babesia spp. Severe hypophosphatemia Heinz body anemia (see Chapter 89) Acetaminophen toxicity (see Chapter 1) Increased osmotic fragility (Abyssinian and Somali cats) Nonregenerative anemia Inadequate time for regeneration with hemorrhage or hemolysis Immune-mediated hemolytic anemia with targeting of red blood cell precursors (red cell aplasia) Idiopathic red cell aplasia Iron deficiency Neoplasia with widespread bone marrow involvement Chronic renal disease (see Chapter 190 and 191) Anemia of chronic disease
marker of FeLV infection. Spherocytes are a classic marker for IMHA; however, they are more difficult to identify in cats. Autoagglutination also confirms the presence of IMHA. This can be differentiated from Rouleaux formation by adding two to three drops of saline to a drop of blood and then looking for macro- or microscopic agglutination. Sometimes, it can be observed on a microscope slide. Figure 119-1. Any form of agglutination confirms the diagnosis of IMHA. Other cytopenias may be present as well, especially thrombocytopenia. Concurrent cytopenias are most likely indicative of immune-mediated disease or primary bone marrow disease (i.e., neoplasia, bone marrow suppression by drugs, myelofibrosis, and so on). • Reticulocyte Count: When anemia is present a reticulocyte count will be provided automatically by many reference laboratories, although it would be ideal to know what is counted (aggregate only or aggregate and punctate). Reticulocyte counts can also be determined inhouse by mixing and incubating ethylenediaminetetra-acetic acid (EDTA) anticoagulated blood with an equal amount of new methylene blue stain for 10 to 20 minutes. The percentage of aggregate and punctate reticulocytes is then determined on a blood smear at high power. See Chapter 311. An aggregate percentage greater than 0.5% likely represents normal bone marrow response to mild anemia, whereas, with moderate (2%) or severe anemias (>4%) a greater percentage is expected. In absolute terms more than 40,000/µL aggregate reticulocytes are indicative of regeneration. Punctate reticulocyte counts are usually ignored except when the anemia is mild; then their presence can suggest a regenerative response. • Chemistry Profile: Most values are expected to be normal. Low total protein could be an indicator of hemorrhage as the cause of regeneration. Hyperbilirubinemia is consistent with a hemolytic process (i.e., prehepatic icterus).
Immune Mediated Hemolytic Anemia
excluding other causes of anemia. In some cases, however, a definitive diagnosis of IMHA is not possible, especially in cases that are non-regenerative. Bone marrow findings in these patients are usually either pure red cell aplasia, erythroid hyperplasia, or erythroid maturation arrest. These changes can be idiopathic as well.
Treatment Primary Therapeutics
Figure 119-1 A presumptive diagnosis of auto-agglutination can be made when a drop of anticoagulated blood is allowed to run on a microscope slide. The speckled areas are red blood cell clumps.
• Blood Transfusion: Transfusions are commonly used, though there is no consensus when to give them. Generally with a packed cell volume (PCV) of less than 15%, even if the patient is not symptomatic for the anemia, a transfusion of typed whole blood is indicated. Transfusion is also indicated in anemic patients with a PCV greater than 15% if they are symptomatic for anemia (i.e., dyspnea, tachypnea, or tachycardia) that is generally seen in patients in which the anemia developed rapidly. Instead of whole blood, a hemoglobin based blood substitute (Oxyglobin®) can be used; however, it is expensive and only lasts a few days at best. • Antibiotic Therapy: Given the prevalence of Mycoplasma spp. as a cause of secondary IMHA, it is advisable to administer doxycycline (5 mg/kg q12h PO for 3 weeks) even if the organism is not identified on a blood smear or PCR assay. • Corticosteroids: Prednisolone is administered (1–2 mg/kg q12h PO initially) with primary or secondary IMHA. Tapering is variable depending on the underlying reason for the IMHA. In those patients that do not respond or do not tolerate prednisolone, other medications, such as cyclosporine or cytotoxic drugs, such as chlorambucil, can be considered.
Secondary Therapeutics Secondary Diagnostics • Coombs’ Test: When hemolytic anemia is suspected a Coombs test is indicated if Mycoplasma spp. or Cytauxzoon felis are not seen on initial blood film evaluation. See Chapters 47 and 92. Coombs’ tests can be positive with secondary IMHA as well as in some patients with other diseases even if they are not anemic (e.g., neoplasia and inflammation). False-negatives occur as well although they are unlikely with primary IMHA. • Polymerase Chain Reaction (PCR) testing for Mycoplasma haemofelis, Candidatus Mycoplasma haemominutum, and Candidatus Mycoplasma turicensis is indicated with hemolytic anemias if organisms are not seen on a blood smear. • FeLV Testing: FeLV infection has been shown to be associated with secondary IMHA as well as bone marrow suppression. • Bone Marrow Aspirate/Core Biopsy: In cases in which the anemia is non-regenerative, especially if there are other concurrent cytopenias, bone marrow sampling is vital. This will help to rule out such disorders as myelofibrosis or neoplasia. Typical findings with IMHA would be erythroid hyperplasia, erythroid maturation arrest or pure red cell aplasia. See Chapter 296. • Imaging Studies: Imaging studies are indicated to help rule out neoplasia.
Diagnostic Notes • In cats secondary IMHA predominates with the majority being caused by infections (i.e., Mycoplasma spp., Cytauxzoon felis, and Babesia spp.) and considerable effort towards ruling out Mycoplasma spp. especially is justified. Many times, though, the organisms can be identified on a blood smear. Diagnosis of primary IMHA is by
• If an underlying cause of IMHA is identified it should be treated as indicated.
Therapeutic Notes • Treatment in cats with IMHA focuses on transfusion to minimize clinical signs and appropriate therapy to prevent additional hemolysis. Given the ubiquitous nature of Mycoplasma spp., doxycycline therapy should be administered to patients suspected of having IMHA. • Immune suppression tends to be relatively successful in treating IMHA in cats.
Prognosis The prognosis is good with most cases of IMHA if the anemia can be addressed appropriately with transfusions, if needed, and adequate supportive care is given. Unlike dogs, in cats thrombosis does not appear to be a significant complication of IMHA.
Suggested Readings Cowell RL, Tyler RD, Meinkoth JH. 2006. Diagnosis of anemia. In JR August, Consultations in Feline Internal Medicine, 5th ed., pp. 565–573. St. Louis: Elsevier Saunders. Kohn B, Weingart C, Eckmann V, et al. 2006. Primary immune-mediated hemolytic anemia in 19 cats: diagnosis, therapy and outcome (1998– 2004). J Vet Intern Med. 20:159–166. Weiss DJ. 2007. Bone marrow pathology in dogs and cats with nonregenerative immune-mediated haemolytic anaemia and pure red cell aplasia. J Comp Path. 138:46–53.
283
CHAPTER 120
Inflammatory Bowel Disease Mark Robson and Mitchell A Crystal
Overview Inflammatory bowel disease (IBD) is a term that describes a group of enteropathies. Affected patients have persistent gastrointestinal (GI) signs and histopathological evidence of inflammatory cell infiltration within the GI mucosa. The World Small Animal Veterinary Association (WSAVA) GI Standardization Group defines IBD as: GI clinical signs for greater than 3 weeks duration; incomplete response to dietary modulation and anthelmintics; histologic lesions of mucosal inflammation on biopsy; and evidence of clinical response to immunomodulatory therapies. Although the precise etiopathogenesis is unknown, in both veterinary and human medicine there is increasing evidence that IBD (an uncontrolled inflammatory response) develops as a consequence of loss of mucosal tolerance to nonspecific antigens from the environment, diet, or luminal bacteria. Genetic susceptibility probably plays a large role in determining which individuals develop clinical disease. More specifically, we know that molecular-level alterations characteristic of IBD patients include up-regulation of major histocompatibility complex (MHC) class II molecules and interleukin (IL)-1, IL-8, and IL-12 mRNA. Whether this response is an inherent, primary response due to a genetic anomaly or a secondary response to an inciting antigen is not yet known and may vary between individuals. More recently, studies have revealed marked differences in the mucosal microbiota between healthy cats and dogs and those with IBD. The changes are not predictable or immediately logical by traditional interpretations. Sometimes apparently pathogenic bacteria will diminish in IBD patients, sometimes they increase. A consistent feature seems to be a reduction in the variety of species present in the gut when IBD occurs. Whether this is a cause of IBD or a consequence of IBD remains to be proven. Studies have demonstrated a histological link between the density and composition of the mucosal flora and the severity of intestinal inflammation and mucosal architectural damage. Anecdotally and increasingly in the literature there is support for the existence of a population of apparent IBD cases in which antibiotics are necessary to achieve remission of signs. These factors support the theory that GI bacteria may play a primary role in the etiology of feline IBD in some patients. Feline IBD may present with a variety of clinical signs, the most common being chronic intermittent vomiting, in contrast to the dog in which the most common clinical sign is diarrhea. Other clinical signs include weight loss, anorexia, and, less commonly, intermittent polyphagia and diarrhea. Physical examination is often unremarkable or may demonstrate weight loss and thickened intestinal loops on abdominal palpation. IBD is classified according to both the region of the intestinal tract and the predominant inflammatory cell. Lymphocytic-plasmacytic IBD is the most common in both cats and dogs, and eosinophilic IBD is the second most common. Other less common forms of IBD include granulomatous, suppurative (neutrophilic), and histiocytic gastroenteritis, or colitis. IBD is most commonly seen in middle-aged to older cats, and there is no reported breed or sex predilection. Many GI diseases clinically resemble IBD, and because the GI mucosa responds to many insults with an inflammatory response, histological evidence of inflammatory infiltrates alone does not always constitute a diagnosis of IBD. Differential diagnoses to consider include parasites
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
284
and other infectious agents (i.e., nematodes, Giardia, Tritrichomonas, Cryptosporidium, heartworm, Helicobacter, feline leukemia virus [FeLV] infection, feline immunodeficiency virus [FIV] infection, salmonellosis, campylobacteriosis, or feline infectious peritonitis [FIP]), neoplasia (i.e., alimentary lymphoma or adenocarcinoma), endocrinopathies (i.e., hyperthyroidism or diabetes mellitus), metabolic diseases (i.e., chronic renal failure, hepatic disease, or chronic pancreatitis), and exocrine pancreatic insufficiency (EPI). For this reason a detailed history and step-bystep diagnostic sequence is essential to establish a confident diagnosis of IBD.
Diagnosis Primary Diagnostics • Data Base (Complete Blood Count [CBC], Chemistry Profile, and Urinalysis): Baseline data is often unremarkable; however, mild increases in liver enzymes, serum globulins, or eosinophils may be noted. The data base will help exclude diabetes mellitus (i.e., hyperglycemia, glucosuria, and low urine specific gravity), liver disease (i.e., hyperbilirubinemia, decreased blood urea nitrogen, increased liver enzymes, and bilirubinuria) and renal disease (i.e., elevated creatinine with decreased urine specific gravity). Alterations suggestive of hyperthyroidism (i.e., increased liver enzymes, a mild increase in packed cell volume [PCV], and low urine specific gravity) and lymphoma (i.e., circulating lymphoblasts [rare], anemia, or other cytopenias) may be present. Protein-losing enteropathy from a variety of causes is an uncommon finding in cats with diarrhea (i.e., hypoalbuminemia or hypoglobulinemia). • Total T4 (TT4): Ruling out hyperthyroidism is indicated in all cats over 8 years with signs of chronic GI disease. • Infectious Disease Testing: A variety of fecal examinations and tests are appropriate to rule out infectious disease, especially in cases in which diarrhea is a consistent clinical sign. Culture and sensitivity for Salmonella and Campylobacter should be done on all cats with diarrhea. Samples are best submitted in special media to prevent overgrowth of endogenous species (check with laboratory prior to submission). A positive culture or stain without evidence of other disease processes can support an infectious diagnosis. Fecal evaluation for Cryptosporidium should also be done on all cats with diarrhea. A zinc sulfate flotation should be performed to evaluate for nematodes and Giardia. Further fecal testing for Giardia (i.e., SNAP Giardia® test, direct saline smear, or submission of feces for Giardia direct immunofluorescence testing) and Tritrichomonas (Tritrichomonas foetus culture, direct saline smear, submission of feces for T. foetus polymerase chain reaction [PCR]) should be considered. See the relevant chapters on these infectious agents for more detail. All of these except Campylobacter are included on a chronic diarrhea PCR profile (IDEXX Laboratories, Westbrook, MA). • Folate and Cobalamin: Serum folate and cobalamin concentrations can provide further information prior to biopsy. Low serum folate is consistent with proximal small intestinal malabsorption. Low serum cobalamin is a common finding in cats with chronic GI disease, especially in those with low body condition scores (BCS) and can be suggestive of ileal malabsorption due to infiltrative disease or pancreatic insufficiency.
Inflammatory Bowel Disease
• Abdominal Ultrasound: The presence of intestinal wall thickening and enlarged or hyperechoic abdominal lymph nodes is a common finding in patients with IBD. However, many cats with IBD have no visible ultrasonographic changes because the disease is often microscopic and can cause clinical signs before any visible or palpable changes occur in the gut or associated nodes. If nodes are enlarged, then ultrasound allows aspiration, which is a helpful modality to rule out other abdominal diseases. • Intestinal Biopsy: Histological assessment is essential for establishing a definitive diagnosis of IBD. Biopsies may be collected via endoscopy, laparoscopy, or exploratory laparotomy. The former technique is less invasive and risky than surgery but does not allow the collection of full-thickness biopsies and biopsy is limited to the areas that can be reached with an endoscope; however, at best this is still a portion of the duodenum. Laparotomy has greater morbidity and mortality but does allow full-thickness biopsies to be taken at sites that are chosen after visualizing the entire GI tract. As discussed, many cats with IBD have no palpable changes to their gut, so biopsies should always be taken. Stomach, duodenum, and jejunum would represent the minimum areas of interest, with the ileum and colon being sampled depending on clinical signs. In many cases it will be appropriate to biopsy the pancreas and liver, even if there is no obvious pathology, an approach known as “abdominal harvest.” Histopathological changes characteristic of IBD include inflammatory cell infiltration, villous atrophy or fusion, cryptal separation with edema, mucosal fibrosis or necrosis; epithelial flattening and dilated lacteals. Alternatively, histopathology may provide a definitive diagnosis of alimentary lymphoma, Cryptosporidium, Giardia or Helicobacter gastritis. • FeLV/FIV Test: These tests are not confirmatory for GI disease but may determine the presence of secondary diseases.
Secondary Diagnostics • Feline-Specific Trypsin-Like Immunoreactivity [fTLI] and FelineSpecific Pancreatic Lipase Immunoreactivity [fPLI]): EPI is rare in cats; however, fTLI should be tested in every polyphagic, cachexic cat with diarrhea that is not diabetic or hyperthyroid. A fasted serum sample can be submitted for both fTLI (to screen for EPI) and fPLI (to screen for pancreatitis). See Chapters 71 and 160. • Heartworm: Heartworm testing is indicated in cats with chronic vomiting living in endemic areas when other common causes have been excluded. See Chapter 88.
Diagnostic Notes • When possible, all differential diagnoses must be excluded prior to making a diagnosis of IBD. Many clinicians will try dietary change, anthelminthics, and perhaps antibiotics before recommending more invasive tests such as endoscopy or surgery. This is not an inappropriate approach, as along as the owner is kept informed and an objective set of criteria is used to assess response. More aggressive drugs, such as steroids, will affect the diagnostic process and should only be used “blind” when the owner has resolutely declined further diagnostics and has been made aware of the effects of steroids on tissue if biopsies are eventually taken. • Many cases of IBD have mild to moderate elevations in liver enzymes. This is believed to be a result of periportal inflammation or hepatic injury due to inflammatory efflux from the GI tract or concurrent pancreatitis. Theoretically mucosal permeability is increased with inflammation leading to easier translocation of bacteria to the liver. See Chapter 94. • The clinician should be alert to the possibility that a patient being evaluated for possible IBD could also be suffering from some combination of hepatitis, cholangiohepatitis, and pancreatitis as well as GI disease. See Chapter 216.
• The differentiation of alimentary lymphoma from severe lymphocytic IBD can be difficult, even with full-thickness biopsies. Consultation with your pathologist, collaboration between pathologists, and clonality testing (e.g., immunohistochemistry, PCR for Antigen Receptor Rearrangements [PARR], flow cytometry) may assist with this differentiation. See Chapters 34 and 130. • The WSAVA GI Standardization group has issued a detailed set of criteria describing the number, type, and distribution of inflammatory cells that support a diagnosis of IBD. Furthermore the associated structural changes that are expected (i.e., villous atrophy, mucosal ulceration, and so on) are also defined. All pathologists should be working to these guidelines now. The standards also apply to the size, number, and quality of endoscopic and surgical GI biopsies. • Contrast GI radiographs are rarely helpful and never diagnostic in the diagnosis of chronic GI diseases.
Treatment Primary Therapeutics • Goals of Therapy: They are to minimize antigenic stimulation to the GI environment and to modulate the local gut immune response. • Dietary Modulation: Diet is a critical part of therapy in all forms of IBD. If an elimination diet is desired, it should be highly digestible, easily assimilated, and reduced fat. It should consist of a novel protein source and be milk free, wheat free, and corn free. An alternative to elimination diets are commercial hydrolyzed diets such as Hill’s z/d Ultra Allergen Free or Royal Canin Feline Hypoallergenic diet. All cats with colonic IBD can benefit from supplementing a highly digestible fiber source such as psyllium (Metamucil®) at 1.7 to 3.4 g (1/2 to 1 teaspoon) PO with food q12 to 24h or canned pumpkin at 1 to 2 teaspoons PO with food q12 to 24h. Up to 50% of cats with idiopathic GI signs will respond well to elimination diets, and cats with lymphocytic-plasmacytic IBD may achieve clinical remission with diet alone. • Immunomodulatory Therapy: Prednisolone or prednisone is the drug of choice (in combination with dietary modulation) for all types of IBD except lymphocytic-plasmacytic colitis. Some believe that lymphocytic-plasmacytic colitis can be successfully treated with dietary changes alone. One suggested prednisolone or prednisone regime is: Begin at 1 mg/kg q12h PO for 4 weeks and taper the dosage as follows: 1.5 mg/kg q24h PO for 4 weeks, 1.0 mg/kg q24h PO for 4 weeks, 0.75 mg/kg q24h PO for 4 weeks, 0.5 mg/kg q24h PO for 4 weeks, 0.5 mg/kg q48h PO for 4 weeks. Thereafter discontinue therapy if clinical remission is achieved. If clinical signs recur during the taper, maintain the cat on the lowest effective dose for 4 to 6 months and attempt to taper at that time. Other clinicians prefer to keep the dose the same but gradually increase the interdose interval. There is no proof that any single approach is superior. • Other Immunosuppressive Therapy: Budesonide is an orally administered glucocorticoid, with more local and less systemic absorption, approved for the use in humans with Crohn’s Disease and has been effective in some cats with IBD (0.5–1.0 mg/cat q24h PO). Anecdotally there have been concerns regarding cases of intestinal perforation with the use of budesonide. Chlorambucil is an alkylating agent that is less potent than cyclophosphamide and effective (with prednisone) for GI small cell lymphoma and in many cats with IBD (2.0 mg/cat q48–72h PO or 20 mg/m2 q14d PO). Cyclosporine is an immunomodulatory agent that inhibits T cell function, specifically IL-2 production and has been effective in IBD dogs that are refractory to glucocorticoids. Anecdotally it is effective in cats with refractory IBD (5 mg/kg q12–24h PO).
Secondary Therapeutics • Goals: The use of secondary therapeutics is based on the hypothesis that alterations in commensal microbial communities may perpetuate
285
SECTION 1: Diseases and Conditions
•
•
•
•
intestinal inflammation in predisposed animals. Therefore, altering the balance of microbial populations through probiotics, micronutrition, nutraceuticals, or antibiotics may be of therapeutic benefit. Probiotics and Prebiotics: Probiotics are non-pathogenic, live microorganisms (bacteria and yeasts) that theoretically improve microbial “balance” in the intestinal tract. Prebiotics are nondigestible food ingredients (usually short chain carbohydrates like beet pulp or psyllium) that promote the growth of specific bacteria in the gut. Cobalamin (vitamin B12): Low serum cobalamin can be treated with cobalamin injections (250 µg q7d SC for a 6-week trial). Successful treatment can lead to weight gain, increased appetite, and reduced vomiting episodes. Cobalamin supplementation can be continued long term at a decreased dose (250 µg q14–28d SC) if needed as part of IBD management. Serum cobalamin levels can be assessed to help guide therapy. See Chapter 37. Omega-3 Polyunsaturated Fatty Acids (PUFAs): These compounds have an anti-inflammatory effect on the GI tract, specifically to reduce the production of the potent pro-inflammatory leukotriene molecules. Some PUFAs (e.g., eicosapentanoic acid) can prevent cytokine-induced intestinal permeability defects. PUFAs are available over the counter (e.g., fish oil supplements) and should be added as a single agent with an increasing dose titration because they are unpalatable and can cause diarrhea. There is no objective proof that this therapy is beneficial. Metronidazole: Metronidazole is an antimicrobial with excellent anaerobic and good antiprotozoal spectrum, and there is positive anecdotal evidence for its use in combination with glucocorticoids for IBD in cats. Metronidazole has also been hypothesized to have direct immunomodulatory effects on the GI mucosa; however, this is yet to be demonstrated at therapeutic dosages. The dose is 10 to 20 mg/kg q12h PO for 2 to 3 weeks. Single-agent therapy with metronidazole may be effective in mild cases of IBD.
Therapeutic Notes • Immunomodulatory agents should be used for 4 to 6 months and tapered by 25 to 50% for an additional 2 to 4 months. Neutrophil numbers should be monitored weekly for the first month of therapy and every 2 to 4 weeks thereafter while the cat is on drugs, such as chlorambucil, that can impact bone marrow function. Therapy should be stopped or tapered if the neutrophil count drops below 3000/µL.
286
• In situations in which biopsy is not possible, it may be necessary to adopt a “treat for the treatable” approach. If clinical signs are severe and euthanasia is being considered, a multimodal approach that would assist severe IBD or alimentary lymphoma (e.g., hydrolyzed diet, prednisolone, antibiotics, and chlorambucil) might be appropriate. • Most cats with responsive IBD show signs of clinical improvement within a week of beginning therapy, but true resolution may take months or years. Some cats are never able to return to their previous diet. Many cats will show improvement over time but with many “bad days” and even “bad weeks” in which the owner may feel that deterioration has occurred. In many instances the clinician and owner must learn to tolerate these periods because rapid changes in therapy are rarely helpful and can confuse the owner.
Prognosis With appropriate dietary and pharmaceutical therapy, lymphocyticplasmacytic IBD is often controllable. Lymphocytic-plasmacytic colitis is often manageable with dietary therapy alone. Concurrent hepatic or pancreatic involvement often affords a less favorable prognosis. Eosinophilic IBD and the other less common forms are more difficult to predict.
Suggested Readings Day MJ. 2008. Histological standards for the diagnosis of gastrointestinal inflammation in endoscopic biopsy samples from the dog and cat: a report from the World Small Animal Veterinary Association Gastrointestinal Standardization Group. J. Compar Path. 138:S1–S43. German AJ. 2009. Inflammatory bowel disease. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIV, pp. 501–506. Philadelphia: WB Saunders. Simpson KW. 2009. Host floral interactions in the gastrointestinal tract. In Proceedings of the ACVIM Forum, pp. 437–439, Montreal: ACVIM. Suchodolski JS. 2009. The intestinal microbiome in dogs and cats. In Proceedings of the ACVIM Forum, pp 408–410, Montreal, Canada. Trepanier L. 2009. Idiopathic inflammatory bowel disease in cats: rational treatment selection. J Fel Med Surg. 11:32–38.
CHAPTER 121
Inflammatory Polyps and Masses Gary D. Norsworthy
Overview Respiratory polyps are masses composed of inflammatory cells that contain or are covered with respiratory epithelium. Nasopharyngeal polyps occur in the oral cavity, nasal cavity, nasopharynx, Eustachian tube, and tympanic bulla. They often arise in the tympanic bulla, extend down the Eustachian tube, and enter the nasopharynx. They can arise in the nose and extend into the nasopharynx or out the nasal opening. Inflammatory polyps can arise in the middle ear and extend through the tympanic membrane (TM) into the external ear canal. Respiratory polyps are composed of granulation tissue, which may be quite dense and mature or looser and more vascular. They usually have insignificant numbers of eosinophils. They occur most commonly in young cats; the mean age of diagnosis is 1.5 years. Consequently, they are considered by some to be a congenital disease. However, they have also been found in older cats and may be the consequence of chronic inflammation. The primary clinical signs include noisy breathing, dyspnea, nasal discharge, sneezing, and coughing. They may also cause otorrhea, with secondary bacterial otitis externa, and vestibular signs, such as head tilt. In the oral cavity and pharynx, inflammatory masses typically arise from the gingiva or tongue or in the perilaryngeal area. Drooling and dysphagia are the common clinical signs. They are also composed of inflammatory cells but not neoplastic cells; they resemble respiratory polyps in many structural and functional ways but they do not contain respiratory epithelium. It is believed that their origin is different from respiratory polyps. They are included in this chapter because of several diagnostic and therapeutic features that they share with respiratory polyps.
(A)
Diagnostics Primary Diagnostics • Clinical Signs: The clinical signs are determined by the location of the polyp. Noisy breathing, dyspnea, nasal discharge, and sneezing occur if a polyp is in the nasal cavity or nasopharynx. See Figures 121-1 and 121-2. If located in the external ear canal, otic discharge (often purulent) and head shaking or ear scratching occur. See Figure 121-3. If located perilaryngeally, inspiratory dyspnea occurs. See Figure 121-4. If located in the oral cavity, drooling, halitosis, and dysphagia are common; pain may occur if the cat bites the polyp. See Figures 121-5. • Physical Examination: In some cases, the soft palate will be visibly displaced ventrally suggesting the presence of a mass in the nasopharynx. In some cases, nasopharyngeal masses can be visualized if the soft palate is retracted rostrally while the cat is anesthetized. Those that occur in the external ear canal may be visualized with an otoscope after the fluid is removed from the ear canal. They usually occur on or near the tympanic membrane so a deep otoscopic examination is necessary. Because many are accompanied by otitis externa, they may not be seen until the infection is controlled or unless an otic
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
(B) Figure 121-1 A, This lateral radiograph of the skull shows a soft-tissue mass in the nasopharynx that is so large that it nearly occludes the openings to the larynx and esophagus (solid arrows). The tympanic bullae are thickened suggesting that the mass originated in the middle ear (open arrow). B, This is the inflammatory polyp that was removed.
endoscopic instrument with flushing capabilities is used. Oral polyps may be seen during an oral examination; in some cases anesthesia or sedation are required. • Imaging: A high quality radiograph using a lateral, extended neck view of the skull may demonstrate nasopharyngeal polyps. The bullae may be thickened if otitis media is present. See Figure 121-1A. Computerized tomography (CT) and magnetic resonance imaging (MRI) images are superior and are recommended when available. See Figures 293-12 and 293-13. • Histopathology: This test is confirmatory. Biopsy material may be recovered from the oral cavity, nasal cavity, nasopharynx, middle ear, or external ear canal.
287
SECTION 1: Diseases and Conditions
(A) Figure 121-4 Inflammatory polyps are seen attached to the arytenoid cartilages resulting in near airway obstruction and laryngeal paralysis. An endotracheal tube is seen passing through the larynx into the trachea.
(B) Figure 121-2 A, This inflammatory mass is seen being removed from the caudal nasal cavity and nasopharynx through an incision through the soft palate. A small portion of the same mass was seen protruding from the right nasal opening. B, Traction on the mass resulted in removal of a surprisingly large mass from the nasal cavity.
Figure 121-5
An inflammatory mass is seen ventral to the tongue.
• Endoscopy: This will also permit visualization if the mass has entered the nasopharynx, if appropriate instrumentation is available.
Treatment Primary Therapeutics
Figure 121-3 An inflammatory polyp can be seen deep in the horizontal ear canal. A suction catheter is seen at the top of the image.
288
• Oral Surgery: Oral masses should be biopsied and removed either with excision or laser ablation. Initially, a nasopharyngeal mass should be approached orally with rostral retraction of the soft palate. Its point of attachment in the middle ear may be avulsed with steady traction. Failure to remove all of the mass, a common problem, will often result in regrowth. If it cannot be removed in this manner, the nasopharynx can be approached via an incision through the midline of the soft palate. See Figure 121-2A and Chapter 262. Masses adjacent to teeth are less likely to recur if those teeth are extracted followed by the use of anti-inflammatory drugs. • Bulla Osteotomy: Because these masses typically originate from the middle ear, bulla osteotomy increases one’s chances of removing the base of the mass, thus preventing regrowth. In addition, it permits drainage and curettage of the bulla. See Chapters 248 and 274.
Inflammatory Polyps and Masses
• Anti-Inflammatory Drugs: Inflammatory masses are often difficult to impossible to remove surgically due to their location; if they are removed, they frequently recur. They often respond to prednisolone (2.2 mg/kg q12h PO for 2 weeks then tapered), cyclosporine (4–7 mg/ kg PO for 4 weeks then tapered), lomustine (10 mg/cat q28d PO for 3–6 treatments) or (last choice) megestrol (5 mg/cat q12h PO for 5 days then q24h for 5–10 days. After resolution, long-term treatment, usually with prednisolone, is often required.
Secondary Therapeutics • Antibiotics: Appropriate antibiotics should be used for concurrent bacterial otitis external or media.
Therapeutic Notes • Horner ’s syndrome and facial paralysis are possible complications following bulla osteotomy. Most cases resolve spontaneously in 1 to 3 weeks.
• Inflammatory polyps usually do not respond well to antiinflammatory therapy.
Prognosis The prognosis is good if all of the polyp or mass can be removed. However, because of the typical locations, this is not always possible so recurrence is problematic. Inflammatory masses that respond well to anti-inflammatory therapy have a good prognosis.
Suggested Readings Little CJL. Nasopharyngeal polyps. 1997. In JR August, ed., Consultations in Feline Internal Medicine, 3rd ed., pp. 310–316. Philadelphia: WB Saunders Co. Prueter JC. 2007. Nasal and nasopharyngeal polyps. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., p. 951. Ames, IA: Blackwell Publishing.
289
CHAPTER 122
Intraocular Tumors Karen R. Brantman and Harriet J. Davidson
Overview Although intraocular masses are generally uncommon in the cat, both neoplastic and nonneoplastic tumors can occur. An iris cyst (otherwise referred to as a ciliary or uveal cyst) is a pigmented, translucent, nonneoplastic proliferation of ciliary tissue. Cysts are round and smooth, attaching most commonly to the posterior iris. Pigmentation may be intense, making them difficult to distinguish from a solid mass. Nonetheless, light from a bright transilluminator held close to the eye should penetrate it. A single, simple cyst requires no therapy. Intervention is considered only when the cyst obstructs the pupil, hinders vision, disrupts aqueous flow, obstructs the irido-corneal angle, or touches the corneal endothelium. Cyst removal is accomplished via needle aspiration or laser ablation. An iris nevus or freckle is an excessive accumulation of melanin within the iris and is considered non-neoplastic. The freckle itself and surrounding iris should be smooth, non-vascular, and regular in appearance. If large areas of iris pigmentation or multifocal nevi are present, the condition is referred to as iris melanosis. Freckles and melanoses should be monitored closely throughout the cat’s life for progression. When pigmentation becomes extensive, uneven, or affects iris and pupil appearance and function, neoplastic iris melanoma development must be considered. Finally, uveitis alone may have clinical symptoms resembling proliferation of the iris to such an extent that it appears mass-like. As a result, careful examination for other indicators of uveitis, such as aqueous flare and low intraocular pressure, is imperative. The most common forms of neoplasia are melanoma, sarcoma, and adenocarcinoma. Intraocular melanoma is most often recognized as hyperpigmentation that begins on the iris surface; occasionally neoplastic cells will be amelanotic and have a white appearance. The tumor will eventually become raised, irregular, and spread across the iris. Melanomas are usually circumferential and arise from the anterior iris surface. Less commonly, they can arise from the posterior iris or choroid. See Figure 122-1. Melanomas are often malignant and metastasis is likely. However, metastatic lesions may be detected years after the initial diagnosis. The most common sites of metastasis are the lungs and liver. Because pigmentary changes in the iris can progress over long periods of time, deciding when to enucleate can be difficult. Decreased survival time has been correlated with extension of the tumor outside of the iris and the development of secondary complications. Therefore, enucleation is recommended when cells infiltrate the drainage angle, sclera, or limbus, if glaucoma develops, or if there is a change in pupillary shape. Limbal or epibulbar melanomas are slow growing masses that begin on the outside of the globe. They can enlarge to a significant degree and invade the eye. These tumors are usually benign, with occasional reports of malignancy in the cat. They are not typically metastatic. Close monitoring is usually all that is needed. Surgical excision and laser ablation are both accepted methods for tumor removal. Ocular sarcoma can develop secondary to ocular trauma or chronic inflammation. However, the sarcoma may not develop for many years following the initial insult. Tumors usually arise from the posterior iris or choroid and may be difficult to detect on initial examination. Sarcoma
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
290
Figure 122-1 The black smooth mass (arrow) attached to the anterior surface of the iris is a melanoma. Photo courtesy Dr. Gary D. Norsworthy. has a myriad of clinical presentations, including uveitis, intraocular hemorrhage, or corneal edema. These are aggressive tumors and their biologic behavior is reminiscent of injection-site sarcomas. Tumors infiltrate the choroid, retina, and posterior segment, and metastasis may occur. In most cases, the lens is ruptured. Cats with a history of ocular trauma or chronic uveitis should be monitored closely for evidence of tumor formation. Enucleation of the globe with exenteration of the orbit is recommended. Adenoma or adenocarcinoma of the iris or ciliary body is uncommon in the cat. Tumors appear as solid, nonpigmented masses viewed within or behind the pupil. These tumors are slow growing, and the likelihood of metastasis is low. By the time a mass can be seen clinically, it has usually been present for many months. Secondary disease, such as glaucoma, may develop. Removal of the mass and surrounding ciliary body is recommended; or if the mass infiltrates the sclera, enucleation of the globe is indicated. Lymphoma is the most common metastatic neoplasm of the eye, although ocular metastasis of primary lung tumors, squamous cell carcinoma, and even injection-site sarcoma has been reported. Lymphoma has a wide spectrum of clinical presentations ranging from mild anterior uveitis to proliferative iridal masses to lesions of the fundus. The mass itself may be white to pink in color with a smooth but lobulated appearance. Ocular lesions may assist in staging the lymphoma and generally regress with systemic medical therapy. Secondary uveitis and glaucoma are typically treated with topical anti-inflammatories and antihypertensive agents, respectively.
Diagnosis Primary Diagnostics • Ophthalmic Examination: Visualization of the mass is the primary method of diagnosis. A complete ophthalmic examination is necessary to ensure that uveitis or glaucoma has not resulted from the
Intraocular Tumors
tumor. See Chapter 299. Slit-lamp biomicroscopic examination is necessary to confirm the extent of the disease. • Ocular Ultrasound: On occasion, the eye may be filled with blood or severe inflammatory products that preclude thorough examination of the iris or posterior structures. In these cases, a 10-MHz ultrasound transducer may be used to determine if a mass is present within the eye. Ultrasound can also be used to assess the overall size and shape of the iris as well as detect concurrent retinal, vitreal, or lenticular disease.
Secondary Diagnostics • Fine-Needle Aspiration: This is an invasive diagnostic test, but it can be helpful when determining the type of mass present within the eye or used to remove uveal cysts. The cat should be under general anesthesia to prevent movement of the eye during the procedure. A small needle (about 27 gauge) is inserted into the anterior chamber by advancing it through the limbus. To obtain cells for cytology, the mass itself may be aspirated, the iris surface vacuumed, or a sample of the aqueous (≤0.1 mL) removed. Delicate forceps may be used to stabilize the eye and hold the puncture wound closed in the initial stages of self-sealing. Cytology samples will require cytospin prior to examination to achieve adequate cell numbers within the slide sample. Complications with this procedure can be severe and include intraocular hemorrhage, lens rupture, and uveitis. • Minimum Data Base (MDB): A MDB consisting of a complete blood count and serum chemistry may aid in determination of metastatic disease. Retrovirus tests should be included. • Radiographs or Ultrasound: Thoracic radiographs or abdominal ultrasound should be considered to evaluate the cat for evidence of metastatic disease or to aid in the staging of neoplasia. • Gonioscopy: A goniolens is a prism that allows the observer to view the drainage angle and periphery of the iris. This procedure allows observation of the iridial corneal angle to determine if there has been invasion by the tumor. The lens is placed on the ocular surface along with a special gel. This procedure is difficult to master and is generally performed by an ophthalmologist.
Treatment Primary Therapeutics • Anti-Inflammatories: Many cases of neoplasia will be accompanied by uveitis, which should be treated with topical ophthalmic 0.1% dexamethasone or 1% prednisolone q4 to 12 h if no corneal ulceration
is present. The use of topical steroids is a temporary form of therapy to be used only until a more permanent form of treatment can be carried out. Atropine is not recommended because of the space occupying nature of the mass and the possibility of inducing glaucoma. • Antihypertensive Agents: Obstruction of the drainage angle or uveitis as a result of the tumor may cause secondary glaucoma. See Chapter 85. • Enucleation and Exenteration: Due to the potential for malignancy of intraocular tumors in the cat, this is a reasonable option even in the visual eye. Exenteration is indicated for infiltrative tumors. Histopathology of the globe is strongly recommended for definitive diagnosis, prognosis, and to determine the likelihood of metastasis.
Secondary Therapeutics • Laser Ablation: Diode laser ablation is an option for some forms of intraocular neoplasia or masses, particularly iris melanoma, limbal melanoma, or uveal cysts. This form of therapy causes destruction of the tumor. Ablation of iridial masses will occasionally cause distortion of the iris resulting in pupillary abnormalities. Rarely does it cause severe uveitis. Laser ablation is not possible for large masses or those involving the posterior structures. Early referral to an ophthalmologist is critical for effective treatment of neoplasia using laser ablation. • Surgical Resection: In some cases, the mass may be surgically removed. Epibulbar masses may be resected. Gonioscopy should be performed prior to surgery to determine if there has been intraocular invasion. The iris may be sectioned, and the entire mass removed. This procedure is delicate and can result in severe intraocular inflammation. • Systemic Medical Therapy: In cases of lymphoma, the clinical lesions may regress with chemotherapy. See Chapter 34. The eye should be treated with topical steroids to prevent or control uveitis, provided this does not interfere with the systemic therapy.
Suggested Readings Dubielzig RR, Hawkins KL, Toy KA, et al. 1994. Morphologic features of feline ocular sarcomas in 10 cats: light microscopy, ultrastructure and immunohistochemistry. Vet Comp Ophth. 4:7–12. Hakanson N, Shively JN, Reed RE, et al. 1990. Intraocular spindle cell sarcoma following ocular trauma in a cat: case report and literature review. J Am An Hosp Assoc. 26:63–66. Williams LW, Gelatt KN, Gwin RM. 1981. Ophthalmic neoplasms in the cat. J Am An Hosp Assoc. 17:999–1008.
291
CHAPTER 123
Ischemic Encephalopathy Sharon Fooshee Grace
Overview Feline ischemic encephalopathy (FIE) is a neurologic disorder that develops secondary to disrupted blood flow in a major vessel (usually the middle cerebral artery) of the central nervous system. For many years, the cause was unknown, but recent work has suggested that at least some cases of FIE are likely caused by aberrant migration of a Cuterebra larva. See Chapter 46. Migration of a larva through the cribriform plate and into the brain may provoke vasospasm of cerebral vessels leading to ischemia or infarction. The disorder is not known to exist in parts of the world without Cuterebra. No breed or sex predilection is reported. The disorder usually involves adult cats and is more common in the summer months in the eastern/northeastern United States. The summer months coincide with the migratory phase of Cuterebra larvae. Several reports have suggested that Cuterebra have the potential to erode the cribriform plate and gain access to the central nervous system. This explains respiratory signs preceding neurologic signs. In some studies, about 50% of cats with FIE due to cuterebriasis have a history of a recent upper respiratory tract infection. It has also been speculated that the larva may elaborate toxins which cause cerebral vasospasm and infarction. Neurologic signs are peracute in onset, non-progressive, and often lateralizing. Seizures are commonly reported. Other findings include circling (toward the side of the lesion), motor deficits, blindness, and behavior changes, such as aggression or depression. When blindness occurs, it is usually in the contralateral visual field, and pupillary light reflexes are normal (cortical blindness); rarely, lesions affect the optic chiasm or brain stem and cause dilated, unresponsive pupils. Other than the neurologic disturbance(s), the physical examination is usually unremarkable. Primary differential diagnoses include head trauma, neoplasia, infectious encephalitis, granulomatous meningoencephalitis, thromboembolism (especially with cardiac disease), hypertension-induced hemorrhage, and aberrant heartworm migration.
Diagnosis
• Diagnostic Imaging: Survey radiographs (i.e., thorax and skull) are usually normal. Specialized brain imaging techniques, such as computerized tomography (CT) or magnetic resonance imaging (MRI), may reveal areas of cerebral infarction. • Heartworm Testing: Serologic testing for heartworms should be considered because aberrant heartworm larval migration may cause CNS signs, such as seizures. See Chapter 88. • Testing for Infectious Diseases: When cats have CNS disease, infectious causes should be considered: toxoplasmosis, feline infectious peritonitis, and systemic fungal diseases, especially cryptococcosis. See Chapters 43, 76, and 214.
Diagnostic Notes • The main differential diagnosis of trauma should be ruled out with the history and physical examination. Vestibular disease also can mimic FIE, although FIE does not typically affect the brainstem or cranial nerves. • Lack of peripheral eosinophilia does not rule out a diagnosis of FIE caused by Cuterebra migration.
Treatment Primary Therapeutics • Medical Treatment for CNS Cuterebriasis: Ivermectin is effective against Cuterebra at 0.1 mg/kg SC and is well tolerated up to 0.3 mg/ kg SC. One protocol uses diphenhydramine (4 mg/kg IM), followed in 1 to 2 hours with ivermectin (0.3 mg/kg SC) and dexamethasone (0.1 mg/kg IV). Another protocol suggests ivermectin (0.3 mg/kg SC) on alternate days for three treatments, to include glucocorticoids. Unfortunately, there is no proven treatment protocol for CNS involvement. A broad-spectrum antibiotic should be considered as adjunctive therapy. • Anticonvulsant: Diazepam is given at 0.5 to 1.0 mg/kg IV. Alternatively, phenobarbital may be used at 2 to 3 mg/kg q12h IV, IM, or PO.
Primary Diagnostics • Peracute onset of cerebral dysfunction, especially during the summer months in cats with access to the outdoors, is an important finding. Upper respiratory signs (i.e., nasal discharge or persistent sneezing) may have preceded neurologic signs by a week or two if a Cuterebra larva was in the nasal cavity prior to entering the central nervous system (CNS).
Secondary Diagnostics • Cerebrospinal fluid (CSF) analysis: CSF may be normal or show a mild increase in protein and mononuclear cells or eosinophils. See Chapter 298.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
292
Therapeutic Notes • Supportive Care: Additional therapy, such as oxygen, fluid and electrolyte therapy, and nutritional support, should be provided as needed. • Sedation: Ketamine should be avoided because it may increase intracranial pressure. The impact of acepromazine on the seizure threshold is controversial so it would be reasonable to avoid this drug.
Prognosis The prognosis is often favorable, although signs such as seizures or behavior changes may persist. In some cats, signs can diminish or disappear with time and improvement may be seen over a period of a week or two. In some cats, aggressive behavior requires euthanasia.
Ischemic Encephalopathy
Suggested Readings Glass EN, Cornetta AM, deLahunta A, et al. 1998. Clinical and clinicopathologic features in 11 cats with Cuterebra larvae myiasis of the central nervous system. J Vet Intern Med. 12(5):365–368. Thomas WB. 2000. Vascular disorders. In JR August, ed., Consultations in Feline Internal Medicine, 4th ed. pp. 405–412. Philadelphia: Saunders Elsevier.
Williams KJ, Summers BA, DeLahunta A. 1998. Cerebrospinal cuterebriasis in cats and its association with feline ischemic encephalopathy. Vet Path. 35(5):333–343.
293
CHAPTER 124
Keratitis and Conjunctivitis Shelby L. Reinstein and Harriet J. Davidson
Overview The conjunctiva is the mucous membrane lining of the eyelids and the globe. The palpebral conjunctiva lines the inner surface of the eyelids, including the third eyelid. The conjunctiva reflects onto the surface of the globe, forming the conjunctival fornix, and continues as the bulbar conjunctiva on the surface of the globe. The conjunctiva is contiguous with the corneal epithelium and transitions into this clear tissue at the limbus. The conjunctiva is made of loose connective tissue with the surface being a noncornified, stratified squamous epithelium. There are numerous goblet cells, predominately within the conjunctival fornix, that produce mucin to form the inner layer of the tear film. The conjunctiva is a highly vascularized tissue. Cats have a relatively low load of normal surface pathogens. Commonly isolated organisms include Staphylococcus epidermidis and Mycoplasma. Normal conjunctival cytology consists of epithelial cells, which may contain melanin granules depending on coat color, mucin strands, and occasional free bacteria. Some white blood cells can be seen, but basophils and eosinophils are always abnormal. The cornea is a clear structure that allows light to pass in through the pupil to the retina. The cornea has layers, each of which serves a specific function. The corneal epithelium is the outer layer of the cornea and is composed of nonkeratinized squamous cells. The majority of the cornea is composed of the stroma, which is primarily type I collagen and keratocytes (fibrocytes). The cornea is approximately 75 to 85% water. Descemet’s membrane is the basement membrane of the endothelial cells. The endothelium is the innermost, single cell layer of the cornea and is primarily responsible for maintaining the water balance within the corneal stroma. When this water balance is disturbed, the cornea will become edematous and take on a cloudy appearance. Innervation of the cornea is via the ophthalmic branch of the trigeminal nerve. The nerves enter at the limbus within the stroma and travel centrally to end just underneath the epithelium. Brachychepalic cats have been shown to have diminished corneal sensitivity as compared to short-haired cats. Conjunctivitis is considered the most common feline ocular condition. The condition may be chronic, making identification of the initial cause difficult. Considering all the possible etiologies is important in developing both a diagnostic and treatment plan.
•
•
•
•
kittens can lead to ulceration of the conjunctiva, which may become adherent to itself or the cornea (symblepharon). Recurrent conjunctivitis is a result of recrudescence of the virus, and may be induced by stressful events in some cats. See Chapter 95. Chlamydophila felis: This organism was previously known as Chlamydia psittaci. It is an obligate intracellular organism that infects conjunctival epithelial cells, causing mainly conjunctivitis. The infection is spread through airborne inhalation, direct contact, and fomites. Chronic infections can occur if left untreated, and asymptomatic carrier states are known to exist. Although rare, transmission of C. felis from cats to humans has been reported. Washing hands after handling an affected cat is wise. See Chapter 35. Mycoplasma felis: Also an obligate intracellular organism, this bacterium is considered a second invader to primary pathogens such as FHV-1, or C. felis. Calicivirus: This virus causes a milder form of conjunctivitis when compared to FHV-1. Calici virus infects the respiratory tract and can also cause oral ulcerations and polyarthritis. See Chapter 28. Other organisms: Recently Bartonella spp. has been suspected of causing low-grade chronic conjunctivitis. Fungal or parasitic organisms are possible considerations but are extremely rare. See Figure 124-1 and Chapter 17.
Noninfectious Causes of Conjunctivitis and Keratitis • Eosinophilic Conjunctivitis and Keratitis: Eosinophilic inflammation of the conjunctiva may occur in conjunction with eosinophilic keratitis (Chapter 67) or primarily. The cause of this condition is unknown. • Corneal Sequestrum: This condition is seen relative commonly in cats, especially in Persians and Himalayans. Corneal sequestra usually result from chronic irritation, such as chronic corneal ulcers, FHV-1 keratitis, or entropion and trichiasis. Sequestra appear as brown to black distinct areas of corneal degeneration, which can occupy more than 50% of the cornea. See Chapter 95.
Infectious Causes of Conjunctivitis and Keratitis • Feline herpesvirus-1 (FHV-1): This organism is extremely common among the cat population, with greater than 80% of cats potentially having latent infections. As a result, it is a leading cause of conjunctivitis in cats of all ages. The virus is transmitted by inhalation or direct contact, and kittens are often infected by the queen early in life. FHV-1 infects epithelial cells of the conjunctiva, respiratory tract, and occasionally the cornea and causes necrosis of these cells. Initial clinical signs may be seen as conjunctivitis alone or in association with upper respiratory signs. The clinical disease will typically last 10 to 14 days. However, more severe cases in neonatal
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
294
Figure 124-1 Histoplasmosis is a rare cause of conjunctivitis. This was a 14-month-old cat with multiple manifestations of the disease. Image courtesy Dr. Gary D. Norsworthy.
Keratitis and Conjunctivitis
• Immune-Mediated Disease: External antigens such as pollen may cause a type I hypersensitivity. This is most commonly bilateral and may be accompanied by upper airway disease. Food allergy may have conjunctivitis as a portion of the clinical presentation of the disease. Autoimmune diseases may have a concurrent conjunctivitis but do not cause conjunctivitis as the only clinical symptom. Autoimmune disease may cause unilateral or bilateral keratitis. • Irritants: Chemicals sprayed at or rubbed onto the cat’s face may be irritative to both the conjunctiva and cornea. Insect bites surrounding the eyes may result in conjunctivitis but rarely a keratitis. • Keratoconjunctivitis Sicca: Dry eye is uncommon in the cat. It has been reported as a disease without predisposing factors and as a sequela to FHV-1 infection in young cats. • Abnormal Hair: Chronic inflammation from distichia, trichiasis, or ectopic cilia are not common conditions in the cat but have been identified. See Chapter 72 • Conformation: Entropion is also uncommon in the cat but may develop following ocular trauma, chronic conjunctivitis resulting in contraction of the conjunctiva, or loss of orbital fat. Nasal folds and lagophthalmos with exposure keratitis are seen in certain brachycephalic breeds.
• Organism Identification: A bacterial culture swab can be taken from the conjunctival sac. The results must be carefully interpreted because of normal bacterial flora. Chlamydophila and Mycoplasma require special media for transport as these are obligate intracellular organisms. Chlamydophila, Mycoplasma, and FHV-1 can be tested using polymerase chain reaction (PCR) techniques. See Chapter 95 testing recommendations and limitations. A Dacron swab is rubbed across the conjunctiva or cornea. No topical anesthetic is required, but it may be used.
Diagnostic Notes • Corneal ulcers, uveitis, or glaucoma may have a clinical presentation that includes conjunctivitis. • Additional diagnostics, such as a conjunctival biopsy, can be used when traditional diagnostics are unyielding. • Herpetic keratitis creates a characteristic dendritic ulcer. See Figure 41-1.
Treatment Primary Therapeutics
Diagnosis Infectious Causes of Conjunctivitis and Keratitis Primary Diagnostics • History: It is crucial to take a complete history, including duration or recurrence of clinical signs. FHV-1 infections are frequently recurrent. Chlamydophila and Mycoplasma tend to be chronic for several weeks but are ultimately self limiting and not usually recurrent. Accompanying signs of sneezing or upper respiratory disease suggest viral or systemic disease. • Clinical Signs: The conjunctiva is easily inflamed due to numerous causes. The clinical appearance of inflammation is similar regardless of the cause. Commonly, an ocular discharge is present in cases of conjunctivitis. A serous discharge is due to increased tear production and frequently related to superficial irritation of the conjunctiva or cornea. A mucoid discharge is a result of stimulation to the goblet cells, and a purulent discharge often indicates a bacterial infection. Cytology of the discharge can be used to distinguish simple mucous from purulent material, which contains numerous bacteria and neutrophils. The conjunctiva may appear swollen or edematous, which is referred to as chemosis. There may be hyperemia from engorgement of vessels or even free blood accumulated within the conjunctival tissues. The cornea responds to irritation early with superficial vascularization. With time the cornea may develop pigmentation or white deposits (i.e., lipid, calcium, or cholesterol). • Ophthalmic Examination: Although difficult in cats, a Schirmer tear test is necessary to rule out keratoconjunctivitis sicca. Fluorescein staining of the cornea is indicated to rule out the presence of an ulcer (Chapter 41), and intraocular pressure measurement will help to rule out concurrent uveitis or glaucoma. See Chapters 85 and 223. A fundic examination is used to assist in diagnosis of systemic diseases. See Chapter 299.
Secondary Diagnostics • Cytology: Routine structures found on conjunctival cytology include epithelial cells, melanin granules (both free and intracellular), mucin strands or plugs, and occasional free bacteria. Scrapings from the conjunctiva or cytology of ocular discharge may help to identify obvious ocular infection or unique inflammation such as eosinophilic conjunctivitis. Corneal cytology is generally used in cases of ulcers; however, it can also be diagnostic for eosinophilic disease. See Chapter 67.
• Initial treatment should be aimed at Chlamydia and Mycoplasma spp. • Primary choices are topical ophthalmic tetracycline or erythromycin q6h until resolution of clinical signs. • Cats that are difficult to treat with eye medications or are in large populations may be treated with oral azithromycin (10 mg/kg q24h PO). If cytology or culture results confirm an overwhelming bacterial component, a broad-spectrum topical ophthalmic antibiotic may be used q6h until resolution of clinical signs. • Antiviral medications should be used in cases of suspected or confirmed FHV-1. See Chapter 41. FHV-1 should be suspected when conjunctivitis has no other confirmed cause and lasts longer than 4 weeks or is recurrent.
Secondary Therapeutics Noninfectious Causes of Conjunctivitis and Keratitis • Eosinophilic conjunctivitis and keratitis respond well to topical antiinflammatory medications. Topical ophthalmic steroids, such as 0.1% dexamethasone or 1% prednisolone acetate, may be used q6 to 12 h until resolution of all clinical signs. • Corneal sequestra are best treated by surgical excision. See Figure 124-2. The defect may or may not require a graft, depending upon the depth. • Other noninfective forms of conjunctivitis and keratitis (i.e., allergies, irritation, or chronic keratitis) are treated with various topical ophthalmic medications. The frequency of dosing should slowly be decreased with improvement of clinical signs. Topical Ophthalmic Medications • Topical steroids should be applied q4 to 12 h; preferred drugs include 0.1% dexamethasone or 1% prednisolone acetate or phosphate. Topical steroids should never be used when a corneal ulcer is present. • Topical ophthalmic 0.2 to 2.0% cyclosporine or 0.02 to 0.03% tacrolimus ointments or solutions used q12h are helpful in decreasing vascularization and pigmentation caused by chronic inflammation. • Topical ophthalmic nonsteroidal anti-inflammatory medications, such as diclofenac and flurbiprofen, can be used in addition to other medications, including topical steroids. These medications are applied q8 to 12 h.
295
SECTION 1: Diseases and Conditions
Figure 124-2 The black area in this cornea is a corneal sequestrum. Surgical removal is necessary. Image courtesy Dr. Gary D. Norsworthy.
Figure 124-3 Neonatal conjunctivitis causes swelling behind the eyelids. After gently teasing them open, purulent material will be allowed to escape. Image courtesy Dr. Gary D. Norsworthy.
• Keratitis caused by keratoconjunctivitis sicca (KCS) should be treated with topical ophthalmic 0.2 to 2% cyclosporine or 0.2 to 0.3% tacrolimus ointments or solutions q12h to stimulate tear production. Additionally, long lasting artificial tear solutions should be applied q4 to 12 h and especially prior to sleeping. Therapy for KCS is lifelong. • Antihistamines: Either systemic or topical ophthalmic antihistamine medications may be used q4 to 12 h in place of or in conjunction with ophthalmic steroids to treat allergy.
be treated with a broad-spectrum antibiotic and frequent cleaning of the conjunctiva. FHV-1 is also a common cause, and antiviral therapy should be initiated in the neonate if improvement in clinical signs does not occur in approximately 1 week. Infection with FHV-1 may result in symblepharon. Although it would appear that breaking down the conjunctival attachments would solve the problem, this frequently results in a more aggressive readherence during healing. Symblepharon can be tolerated if the eyes are comfortable and visual. However, if the eyes are not comfortable or the owner wishes to pursue further therapy, referral to an ophthalmologist should be considered. Owners should be made aware that kittens with neonatal conjunctivitis are at risk for chronic herpetic conjunctivitis or keratitis.
Therapeutic Notes • Although feline keratitis and conjunctivitis have not been shown to be zoonotic, they can be considered contagious. Owners and professionals should wash their hands immediately following handling of an infected cat. • Neonatal conjunctivitis may present with the eyelids still fused together (ankyloblepharon). See Figure 124-3. The eyelids should be moistened and gently opened. After samples for culture and cytology are collected, the conjunctival sac should be washed thoroughly. This form of conjunctivitis may be bacterial and should
296
Suggested Readings Ketring KL, Zuckerman EE, Hardy WD. 2004. Bartonella: a new etiological agent of feline ocular disease. J Am An Hosp Assoc. 40:6–12. Martin CL. 2005. Cornea and sclera. In CL Martin, ed., Ophthalmic Diseases in Veterinary Medicine, pp. 241–297. London: Manson Publishing.
CHAPTER 125
Kidneys, Abnormal Size Gary D. Norsworthy
Overview The size of the feline kidney can be determined by palpation or various imaging modalities, including radiographs and ultrasound. Longitudinally it should be approximately 3.5 times the length of the body of the second lumbar vertebra on a ventrodorsal radiograph or 38 to 42 mm when measured with ultrasound. A significant change in size signals a pathologic state. The differentials for abnormally large kidneys (renomegaly) include: • Polycystic renal disease (Chapter 174) • Feline infectious peritonitis (FIP; Chapter 76) • Neoplasia, especially lymphoma but also carcinoma, sarcoma, cystadenocarcinoma, and nephroblastoma (Chapter 130) • Hydronephrosis usually secondary to ureteral or bladder trigone obstruction or ectopic ureters (Chapter 100) • Perinephric pseudocyst (Chapter 167) • Ethylene glycol toxicosis causing tubular swelling and infiltration of calcium oxalate crystals (Chapter 70) • Compensatory hyperplasia, unilateral (The other kidney is smaller than normal, also known as the “big kidney-little kidney” syndrome.) See Figure 125-1. • Renal abscess • Renal hematoma
The differentials for small kidneys include: • Congenital renal hypoplasia • Chronic renal disease or renal failure (Chapter 190) • Other chronic nephropathies
Diagnosis Primary Diagnostics • Physical Examination: The findings of renomegaly include (a) an abnormally large abdomen, (b) one or two palpable abdominal masses, and (c) abdominal pain. Physical examination findings when the kidneys are small include (a) small kidney(s) on palpation and (b) inability to palpate one or both kidneys. • Radiographs: Radiographs can reveal renal size, surface contour, and the presence of uroliths. An excretory urogram can reveal information regarding structure and function. See Figure 292-58. • Ultrasound: Ultrasonography permits visualization of renal architecture and precise measurements. It can be diagnostic for hydronephrosis, perinephric pseudocyst, and polycystic kidney disease. See Figures 292-61 through 292-64 and 292-66. • Biopsy: Fine-needle aspiration, fine-needle biopsy, or core needle biopsy can be diagnostic in some renal diseases including neoplasia and FIP (core needle biopsy).
Treatment Primary Therapeutics • Renal Failure Therapy: This is the state that causes clinical signs and must be treated aggressively. See Chapters 190 and 191. • Underlying Disease: Sometimes this is possible for hydronephrosis, pyelonephritis, glomerulonephritis, benign tumors, and perinephric pseudocysts. See Chapters 86, 100, 167, and 181. • Nephrectomy: This can be curative for unilateral hydronephrosis and unilateral tumors. It is important to establish functionality of the contralateral kidney with an excretory urogram prior to surgery.
Prognosis Prognosis will depend on the underlying disease; however, most cats in severe renal failure with either very large or very small kidneys have a poor prognosis. Figure 125-1 The right kidney in this geriatric cat measures 40.5 mm longitudinally (normal = 38–42 mm). The left kidney measures 28 mm. The left kidney suffered a severe disease many months to years prior. The right kidney underwent compensatory hypertrophy as a result. Diagnosis of the original disease of the left kidney is highly unlikely at this stage of disease.
Suggested Readings Cuypers MD, Grooters AM, Williams J. 1997. Renomegaly in dogs and cats. Part 1. Differential diagnosis. Compend Contin Educ Pract Vet. 19:1019–1033. Forrester D. 2007. Renomegaly. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 1192–1193. Ames: Blackwell Publishing.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
297
CHAPTER 126
Laryngeal Disease Andrew Sparkes
Overview Laryngeal disease is relatively uncommon in cats. The presenting signs associated with laryngeal disease are usually: (a) inspiratory dyspnea, which is often profound and may be accompanied by stertorous breathing, and placing a stethoscope over the larynx and auscultating at this site may help to localize the abnormality to the larynx; (b) dyspnea that is not relieved by mouth-breathing (e.g., by occluding the nostrils during clinical examination); (c) dysphonia or complete loss of voice, often with an inability to purr; (d) gagging, retching, or coughing; and (e) palpable laryngeal abnormalities or clinical signs that may worsen on gentle manipulation of the larynx. Because of the small size of the feline larynx, it is not uncommon for cats with laryngeal disease to have profound dyspnea, and careful handling to avoid severe distress may be required. A variety of types of laryngeal disease have been reported in cats including anatomical abnormalities, edema, and laryngeal cysts, but the major causes disease reported in the literature are laryngeal paralysis, laryngeal inflammation, and laryngeal neoplasia.
Laryngeal Neoplasia
Figure 126-1 A lateral cervical radiograph shows laryngeal narrowing (arrow) with resulting dilated pharynx during inspiration. Image courtesy Dr. Gary D. Norsworthy.
Overview Laryngeal tumors are rare in cats. The two tumors most frequently reported are lymphoma and carcinoma (i.e., squamous cell carcinoma and adenocarcinoma). The clinical presentation of laryngeal tumors is of progressive inspiratory dyspnea and dysphonia. Clinical signs are often quite rapidly progressive although they may appear to have an acute onset. Secondary laryngeal paralysis may occur in some. Laryngeal neoplasia is seen predominantly in older cats.
Diagnosis Primary Diagnostics • Clinical signs: Inspiratory dyspnea and dyspnea not relieved by mouth breathing should put laryngeal neoplasia on the differential list. • Palpation: Careful laryngeal palpation may reveal asymmetry or the presence of a mass lesion. • Imaging: Cervical radiography will often demonstrate a soft-tissue density in the region of the larynx. See Figure 126-1. Laryngeal ultrasonography is generally more helpful when this is available and can also be performed in a conscious cat. See Figure 126-2. • Laryngoscopy: An asymmetrical mass is usually visible on direct visualization under anesthesia; however, care must be taken because the airway will already be narrowed and anesthesia can sometimes induce severe respiratory compromise. See Figures 126-3 and 126-4. Although the diagnosis of a laryngeal mass lesion is usually straightforward, it is important that neoplasia is differentiated from laryngeal inflammation and also that the type of neoplasia is determined.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
298
Figure 126-2
Laryngeal sonogram of a laryngeal cyst.
• Cytology: A tissue study is required for a definitive diagnosis. Fineneedle aspiration cytology is perhaps the easiest diagnostic tool; it can be performed under ultrasound guidance when this is available or through the mouth under direct visualisation. Cytology may allow a specific diagnosis (especially in the case of lymphoma), but samples may be non-diagnostic, especially if peritumor inflammation is present. • Histopathology: Biopsy for histopathology is a more certain way of obtaining a diagnosis. A mass lesion can be biopsied under direct visualisation using cup biopsy forceps or endoscopic biopsy forceps.
Laryngeal Disease
(A) Figure 126-3 Direct laryngoscopy is valuable for assessment of laryngeal function (paralysis) and for visualisation of mass lesions. This view is using a laryngoscope made for intubation.
A video otoscope with a working channel is another way to obtain a biopsy sample. However, often the larynx, the overlying mucosa, and the mass itself can be firm so obtaining good diagnostic biopsies can be challenging. If good biopsies are not readily achieved, surgical biopsies may be an alternative to achieving a diagnosis. Short-acting glucocorticoids may be a valuable addition to the preanesthetic regime to try to lessen the impact of laryngeal edema associated with the trauma of biopsy.
Diagnostic Notes • In some circumstances the mass may make tracheal intubation extremely difficult. If so, initial intubation using a canine urinary catheter as a stylet can be valuable in establishing an airway and facilitating the delivery of oxygen. • In severe cases, and especially if laryngeal biopsy or surgery has been attempted, a tracheostomy tube may be required to allow recovery from anesthesia and during the initial postbiopsy management period. Although temporary tracheostomy tubes can be useful in cats, complications are common, and a permanent tracheostomy tube is rarely practical or successful. • If taking small biopsy samples, making an impression smear with the sample prior to putting it in formalin can offer a more rapid cytologic preliminary diagnosis. However, it is important to keep cytology samples away from formalin. Even slight exposure to formalin fumes can affect staining quality of a cytology smear. Reusing the same needle to transfer samples can destroy the quality of the cytology prep. See Chapter 279.
Treatment Primary Therapeutics • Debulking: Following surgical biopsy or fine needle aspiration, a CO2 laser can be used to debulk the lesion prior to chemotherapy. A special laser tip can be inserted through a video otoscope for access and visualization during the procedure. This is indicated when airway obstruction is life-threatening. See Figure 126-5.
(B) Figure 126-4 A, The mass on the left side of the epiglottis (arrow) was a lymphoma. B, The mass (arrow) adjacent to the endotracheal tube was a squamous cell carcinoma. Neoplasia usually presents as a unilateral or asymmetrical mass. These images are made using a video otoscope (MedRx, Largo, FL). Images courtesy of Dr. Gary D. Norsworthy.
• Chemotherapy: Laryngeal lymphoma may respond very well to conventional chemotherapy. See Chapter 34. Laryngeal carcinoma does not respond to chemotherapy. • Radiation: Because of the radiosensitive nature of lymphoma, radiotherapy is another potential option, although the larynx is a potentially difficult site because the radiation therapy itself can induce some inflammation and edema. Radiotherapy for laryngeal carcinoma in cats has not been reported, but it is likely to be much less efficacious than for lymphoma.
Prognosis The prognosis for laryngeal carcinoma is grave as these cannot be effectively treated, although glucocorticoids may be palliative and reduce peritumoral edema. Laryngeal lymphoma may respond well to chemotherapy. Some cats have rapid improvement with prolonged survival times.
299
SECTION 1: Diseases and Conditions
Figure 126-5 A CO2 laser (Aesculight LLC, Woodinville, WA) can be used to debulk a neoplastic or inflammatory mass following surgical biopsy or fine-needle aspiration. The laser tip is passed through the working channel of a video otoscope. Photo courtesy of Dr. Gary D. Norsworthy.
Laryngeal Inflammation Overview Laryngeal inflammation is a well-described, though poorly understood, phenomenon in cats. Some cats present with mild signs of laryngeal inflammation (e.g., dysphonia alone or dysphonia accompanied by mild dyspnea), and in many cases the inflammation resolves spontaneously within days to weeks. Some such cases can be associated with a respiratory viral infection; other accompanying signs may be present. Other cases remain idiopathic. Trauma may be a factor in some of the idiopathic cases. More profound signs of laryngeal disease are associated with more severe inflammation and the development of inflammatory mass lesions. Histologically, neutrophilic, lymphoplasmacytic (or lymphoid hyperplasia), and granulomatous inflammatory changes have all been described. Laryngeal inflammation, and in particular, granulomatous inflammation, is an important differential diagnosis for laryngeal neoplasia because they can look grossly identical and can have identical presenting signs. The underlying cause of the inflammation in many cases remains undetermined. Cases of neutrophilic inflammation are often assumed to be primarily bacterial in origin, but in many cases, a specific etiological cause remains obscure. When granulomatous inflammation is observed it is prudent to look for unusual infectious agents (e.g., mycobacteria, fungi, and so on) and for the possibility of a foreign body.
Diagnosis Primary Diagnostics • Investigation and diagnosis of inflammatory laryngeal disease is the same as described for neoplastic disease. Inflammatory lesions may sometimes be bilaterally symmetrical. See Figure 126-6. Diagnosis of inflammation and characterization of the type of inflammation requires biopsy evaluation. It should also be remembered that most neoplastic lesions will be surrounded by inflammatory tissue, and it is important that truly representative biopsies are obtained wherever possible.
300
Figure 126-6 Laryngeal inflammation (versus neoplasia) is more likely to be bilaterally symmetrical. The inflammation in this cat has nearly closed the airway; the laryngeal opening is a narrow slit. Photo courtesy of Dr. Gary D. Norsworthy.
Treatment Primary Therapeutics • Anti-Inflammatory Drugs: Unless a specific etiological cause can be identified, treatment of laryngeal inflammation is empirical, usually employing a combination of antibiotic and glucocorticoids. If there is no evidence of any infectious etiology (e.g., lymphoid hyperplasia), the use of glucocorticoids or other anti-inflammatory agents alone may be indicated.
Secondary Therapeutics • Surgery: Occasionally, inflammatory polyps have been reported to affect the larynx. When possible, these should be removed surgically.
Therapeutic Notes • Some cases will resolve spontaneously without the need for therapy. In others, treatment may have to be prolonged.
Prognosis The prognosis for cats with laryngeal inflammation is variable. Although the majority appear to resolve (spontaneously or with appropriate therapy), some are recalcitrant to therapy and progressive resulting in death or requiring euthanasia. This is more likely in cats with granulomatous inflammation.
Laryngeal Paralysis Overview Laryngeal paralysis is not as common in the cat as the dog, but it is an important cause of laryngeal disease in this species. As with other laryngeal disease, dyspnea, stridor, and dysphonia are the most common signs. Laryngeal paralysis may be either unilateral or bilateral. Many cases are idiopathic, but underlying causes include iatrogenic damage (e.g., during thyroidectomy), trauma, cervical masses (e.g., thyroid
Laryngeal Disease
carcinomas), and mediastinal or pulmonary masses. Some cases of laryngeal paralysis may be part of a more generalized neuromuscular disease, and because of the length of the recurrent laryngeal nerve, this can sometimes be the first manifestation of such disease. The majority of cases remain idiopathic, but a search for underlying disease is appropriate when laryngeal paralysis is identified. No breed predisposition has been reported, and the disease has been seen in a wide range of ages although most affected individuals are middle-aged to geriatric cats. Complications of laryngeal paralysis include inhalation pneumonia, which is more common with bilateral than unilateral disease.
Diagnosis Primary Diagnostics • Visualization: Definitive diagnosis requires direct visualisation of the larynx under a light plane of anesthesia. One or both arytenoid cartilages will be seen lacking appropriate movement during inspiration. • Ultrasound: Conscious echolaryngography is a valuable technique. Frequently this will reveal lack of or abnormal laryngeal movement. It greatest advantage is lack of anesthesia.
Treatment Primary Therapeutics • Unilateral: Most cases of unilateral paralysis can be managed conservatively (i.e., weight loss if indicated, avoidance of stress, excitement, or strenuous exercise), and if there is any secondary laryngeal inflammation or edema, this can be managed with glucocorticoids. • Bilateral: When bilateral disease is present and signs are significant, surgery is indicated. Unilateral arytenoid lateralization is the most
commonly performed surgical technique. The risks of inhalation pneumonia appear considerably higher if bilateral surgery is performed, and unless there are no other options, unilateral surgery should be performed. When severe signs persist, consideration may need to be given to a second surgery on the contralateral side.
Prognosis The prognosis for cats with laryngeal paralysis is reasonably good. So long as there is no significant underlying disease process, most cats with unilateral disease can be managed. Even in cats with bilateral disease, from the limited reports published, many are able to cope well after unilateral “tie-back” surgery. However, owners should be warned about potential complications and especially the risks of inhalation pneumonia.
Suggested Readings Hardie RJ, Gunby J, Bjorling DE. 2009. Arytenoid lateralization for treatment of laryngeal paralysis in 10 cats. Vet Surg. 38(4):445–451. Jakubiak MJ, Siedlecki CT, Zenger E, et al. 2005. Laryngeal, laryngotracheal, and tracheal masses in cats: 27 cases (1998–2003). J Am Anim Hosp Assoc. 41(5):310–316. Rudorf H, Barr F. 2002. Echolaryngography in cats. Vet Radiol Ultrasound. 43(4):353–357. Schachter S, Norris CR. 2000. Laryngeal paralysis in cats: 16 cases (1990– 1999). J Am Vet Med Assoc. 216(7):1100–1103. Stepnik MW, Mehl ML, Hardie EM, et al. 2009. Outcome of permanent tracheostomy for treatment of upper airway obstruction in cats: 21 cases (1990–2007). J Am Vet Med Assoc. 234(5):638–643. Tasker S, Foster DJ, Corcoran BM, et al. 1999. Obstructive inflammatory laryngeal disease in three cats. J Fel Med Surg. 1(1):53–59. Taylor SS, Harvey AM, Barr FJ, et al. 2009. Laryngeal disease in cats: a retrospective study of 35 cases. J Fel Med Surg. 11:116–121.
301
CHAPTER 127
Leprosy Syndromes Sharon Fooshee Grace
Overview Mycobacteria are nonmotile, nonspore-forming, gram–positive, acidfast, aerobic bacilli. Noted for wide variations in host affinity and pathogenicity, they are phagocytized by macrophages and grow intracellularly. Cats are susceptible to a number of different mycobacterial infections and several mycobacterial syndromes have been identified in cats, including infection with slow growing mycobacteria (which may or may not produce tubercles); infection caused by rapidly growing mycobacteria (previously called “opportunistic” or “atypical” mycobacteria), and feline leprosy syndrome. Cats with mycobacteriosis are usually presented for care because of nodular skin lesions or thickening of the subcutaneous tissues; there may be associated ulceration or draining tracts. Historically, feline leprosy has been attributed to infection with Mycobacterium lepraemurium, the causative agent of rat leprosy. More recently, it has been demonstrated that a number of different organisms may be responsible for feline leprosy, and the disorder is now termed feline leprosy syndrome. M. lepraemurium infection causes a nodular-to-ulcerative granulomatous skin disease of cats. Mice and guinea pigs are also susceptible to this organism. It is thought to be transmitted to cats through fighting with or ingesting infected rodents. The disease is most prevalent in areas with a large rat population. Although it is geographically widespread, it is reported more in certain geographic locations: the northwestern United States, Canada, Western Europe, New Zealand, Britain, and parts of Australia. Most cases occur in immunocompetent young adult cats. Males may be overrepresented. There is no known breed predisposition. Following introduction into the cat, initial growth of the organism is slow and is thought to follow a latency period of several months. Once established, later growth is aggressive, and widespread lesions may develop. Multiple freely movable nonpainful nodules form in the dermis and subcutaneous tissue, especially around the head, on the extremities, and sometimes the trunk (see Figure 127-1). They are usually soft and fleshy and sometimes ulcerate when they grow large. Initial lesions tend to be concentrated in one area but satellite lesions can develop. Regional lymphadenopathy may be noted. A novel mycobacterial species has recently been described in Australasia. The organism is thought to reside in soil or stagnant water. It causes nodular disease but is clinically and epidemiologically distinct from M. lepraemurium. The lesions are slow growing over months to years and do not tend to become ulcerated. This form strikes older cats that may have an underlying disease causing debilitation of the immune system. As such, it is considered a marker for immunodeficiency because the unnamed organism is considered a saprophyte of relatively low virulence.
Figure 127-1 Mycobacterium lepraemurium infection on the digit of a young cat. The lesion is just beginning to show ulceration. Image courtesy of Dr. Richard Malik.
with a modified Wright’s (Romanowsky-type) quick stain, the presence of macrophages and giant cells containing phagocytized unstained bacilli is highly suggestive of mycobacterial disease. Such a finding should prompt a request for additional stains from a diagnostic laboratory. • Modified Acid-Fast Stain: M. lepraemurium is acid-fast. An acid-fast stain may be performed in-house or requested from a diagnostic laboratory. Organisms are not as acid fast as M. tuberculosis, so less aggressive decolorization is used in the procedure or organisms may be missed. • Histopathology: Organisms do not stain with routine H & E stain but do stain well with Ziehl-Neelsen technique and its modifications. They may be scant in number but are most numerous in areas of necrosis. The unnamed mycobacterial species recently identified in Australia does stain weakly with hematoxylin; it also stains with Ziehl-Neelsen and with Gram.
Secondary Diagnostics
Primary Diagnostics
• Polymerase Chain Reaction (PCR) Testing: Molecular tools are currently being developed to assist practitioners in identification of feline mycobacterial diseases. At present, these specialized diagnostics are limited in availability.
• Cytology: Cytology is a useful tool in the initial evaluation of cats with draining tracts and nodules. When aspirated material is stained
Diagnostic Notes
Diagnosis
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
302
• Culture is not typically rewarding. The organism is fastidious, slow growing, and the culture must be held for 3 months before being called negative. It can be grown only with great difficulty and so far, in only two specialized laboratories.
Leprosy Syndromes
Treatment Primary Therapeutics • Surgery: Surgical excision of tissue infected by M. lepraemurium, as well as the new unnamed species, is the treatment of choice if lesions are caught early and are localized in distribution. Early intervention offers the best chance for cure. Aggressive resection is required; this may later necessitate reconstructive surgery to address tissue deficits. Medical therapy should be initiated several days before the initial surgery. Once lesions have spread, or if multiple lesions are evident at the outset, then medical therapy is the appropriate treatment. • Antimycobacterial Therapy, M. lepraemurium: Clofazimine has the best reported success rate. It may be administered at 25 to 50 mg/cat q24 to 48 PO for ≥12 weeks or 8 to 10 mg/kg q24 PO for ≥12 weeks. Success is likely improved if polymodal therapy with two or more drugs is instituted. Other drugs which may be combined with clofazimine include rifampin (10-15 mg/kg q24h PO for ≥12 weeks) clarithromycin (62.5 mg/cat q12h PO for ≥12 weeks). Clofazimine and rifampicin have the potential to cause reduced appetite and liver disease and are tricky to use in combination. A combination of clofazimine and clarithromycin is preferred by some. Clofazimine is associated with photosensitivity, so cats should be kept indoors during therapy. • Antimycobacterial Therapy, New Unnamed Species: The recently identified mycobacterial species in Australia is reportedly sensitive to traditional antimycobacterial therapy.
Therapeutic Notes • Clofazimine may cause reddish-orange skin and adipose tissue discoloration.
• Both clofazimine and rifampin can cause reversible hepatotoxicity. Baseline bloodwork should be obtained prior to institution of therapy and liver enzymes should be periodically monitored. • Medical therapy should be continued for at least 2 months beyond resolution of all skin lesions.
Prognosis Outcome is dependent on the extent of disease at the time of diagnosis, response to surgical and medical therapy, and the presence of concurrent disease.
Public Health Issues Feline leprosy has never been reported in human patients as a result of contact with cats, so the zoonotic threat is low to non-existent. The organisms involved are likely of limited virulence to humans, even immunosuppressed humans.
Suggested Readings Hughes MS, James G, Taylor MJ, et al. 2004. PCR studies of feline leprosy. J Fel Med Surg. 6(4):235–243. Malik R, Hughes MS, Martin P et al. 2006. Feline leprosy syndromes. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 477–480. Philadelphia: Saunders Elsevier. Malik R, Hughes MS, James G, et al. 2002. Feline leprosy: Two different clinical syndromes. J Fel Med Surg. 4(1):43–59. Malik R, O’Brien D, Fyfe J. 2009. Infections of cats attributable to slow growing or “non-culturable” mycobacteria. Microbiology Australia. 30(2):92–94.
303
CHAPTER 128
Linear Foreign Body Gary D. Norsworthy
Overview A linear foreign body is a gastrointestinal (GI) foreign body that is linear in shape. It may lodge in the GI tract due to its diameter or composition, or it may lodge because it exceeds the length of a peristaltic wave (i.e. about 30 cm [12 in]). Most linear foreign bodies are string, sewing thread, ribbon, Easter basket grass, or Christmas tree tinsel. Materials of this type often lacerate the intestinal wall, resulting in bacterial peritonitis. Clinical signs include anorexia, retching, vomiting, lethargy, and fever. Rapid weight loss will occur if the foreign body is present for several days.
Diagnosis Primary Diagnostics • Clinical Signs: Cats with repeated vomiting or retching for several days should be suspected of ingesting a linear foreign body. Abdominal pain occurs in many cats, especially if bowel perforation and peritonitis occur. • Oral Examination: Some linear foreign bodies, especially sewing thread, are wrapped around the base of the tongue. See Figure 128-1. They may be visualized by lifting the tongue by pressing in the intermandibular space with one’s finger. • Imaging: Thin linear foreign bodies (e.g., string) often cause loops of small bowel to become bunched or accordion pleated. See Figure 128-2. Thick linear foreign bodies (e.g., shoe lace) cause obstruction without the typical accordion pleating. See Figure 128-3. These may be suspected on survey radiographs or ultrasound, but they are much more easily detected by using positive contrast material.
(A)
(B) Figure 128-2 A, A thin linear foreign body (string) produces tight plications in the small bowel as seen on a barium series. B, The intraoperative view shows the plications. Figure 128-1 Careful inspection under the tongue may reveal the loop of a linear foreign body. Both ends were swallowed and passed into the small bowel.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
304
Linear Foreign Body
Figure 128-5 Two enterotomy incisions were all that were needed to remove this linear foreign body. The string was tied through the side ports in the catheter, and the catheter and the string were extracted from the distal enterotomy site. Care should be taken not to spill barium into the peritoneal cavity because it is irritating; bile peritonitis results. Figure 128-3 A thick linear foreign body (heavy shoe lace) fills the small bowel so the classic plications are not seen on a barium series. However, a technique can be used in many cats that requires only two enterotomy incisions. See Figure 128-5. A 12 French rubber catheter is inserted into the bowel through the initial enterotomy incision, which is made near the distal end of the foreign body. It is threaded retrograde through the bowel to the proximal end of the foreign body. A second enterotomy incision is made over the end of the catheter exposing it and the foreign body. The foreign body is tied to the catheter using the side ports, and the catheter is withdrawn from the bowel in the distal direction. Aggressive treatment of bacterial peritonitis should be part of the surgical procedure. • Peritonitis: Because many of these cats have bowel perforation, antibiotics should be given before and after surgery. Aggressive peritoneal flushing should occur prior to abdominal closure. See Chapter 168.
Therapeutic Notes
Figure 128-4 Bowel perforation occurs when the linear foreign body cuts through the bowel wall (arrow). Peritonitis results.
• Symptomatic treatment for vomiting will only prolong and worsen this condition. • Some cats have a propensity for playing with sewing thread, string, and ribbons. These items should be removed from their environment to prevent future ingestion.
Prognosis Diagnostic Notes • If bowel perforation is suspected, barium is contraindicated; an iodine-based contrast material or iohexol should be used. See Figure 128-4.
Treatment Primary Therapeutics • Surgery: Surgery is required to remove a linear foreign body. Surgery may require a gastrotomy and multiple enterotomies.
The prognosis is good if surgery is performed before bacterial peritonitis occurs. The prognosis is guarded if bacterial peritonitis is present.
Suggested Readings Sherding RG. Diseases of the intestines. 1994. In RG Sherding, ed., The Cat: Diseases and Clinical Management, 2nd ed., pp. 1211–1285. Philadelphia: Churchill Livingstone. Zoran DL. 2006. The cat with signs of chronic vomiting. In J Rand, ed., Problem-Based Feline Medicine, pp. 662–696. Philadelphia: Elsevier Saunders.
305
CHAPTER 129
Lung Parasites Gary D. Norsworthy
Overview Lungworms are helminths that live in the alveoli, bronchioles, bronchi, and trachea of cats. Many affected cats are asymptomatic, whereas others develop a dry cough. This is one of the few causes of chronic coughing of cats and should be considered if the geographic area is endemic for feline lungworms or the cat has traveled to an endemic area. There are two lungworms found in cats: Eucoleus aerophila, sometimes called Capillaria aerophila (North America) and Aelurostrongylus abstrusus (worldwide distribution). E. aerophila has a direct life cycle and may be transmitted through earthworms and rodents. Cats are infected by ingestion of the embryonated ova or one of the paratenic hosts. Adult worms live within the epithelium of the trachea, bronchi, and bronchioles and produce ova about 40 days after infection. The ova are coughed up, swallowed, and passed in the feces. They become embryonated in 1 to 2 months but can survive in the environment for over a year. The cat becomes infected with A. abstrusus when it eats the intermediate hosts (i.e., snails or slugs) or paratenic hosts (i.e., birds, rodents, amphibians, or reptiles). The adults, about 0.8 mm long, live in the alveoli and are capable of producing ova about 25 days after ingestion. The ova hatch and become L1 larvae, which migrate up the bronchi and trachea into the pharynx. They are swallowed and passed in the feces, where they can survive for several months. An intense immune response, causing focal interstitial pneumonia, is responsible for eventual elimination of the worms from the lungs of most cats. Paragonimus kellicotti is the lung fluke of cats (and dogs) that live in the southern, Midwestern, and Great Lakes regions of the United States. The adult is about 1 cm long. See Figure 129-1. Intermediate hosts, the freshwater snail and the crayfish, are the source of infection. The fluke migrates from the small bowel to the lungs, where it lives within a bulla or cyst
within the pulmonary parenchyma. Coughing dislodges the eggs; they are coughed up and swallowed. Feces laden with fluke eggs are ingested by the intermediate hosts. The most common clinical sign, coughing, is due to the inflammatory reaction that occurs in the lungs. Rupture of one of the cysts can be fatal due to rapid-onset pneumothorax. The juvenile adults and adults of Dirofilaria immitis (heartworms) primarily reside in the pulmonary arteries and are carried into the pulmonary parenchyma when they die. This form of “lungworm” is discussed in Chapter 88.
Diagnosis Primary Diagnostics • Clinical Signs: Many cats with lungworms or lung flukes are asymptomatic. Others have a nonproductive cough, which can be elicited by tracheal palpation or dyspnea due to secondary bacterial pneumonia. • Thoracic Radiographs: Many cats with lungworms have normal thoracic radiographs. Others have peribronchial infiltrates, bronchial thickening, or a diffuse interstitial pattern. Cystic or bullous lesions in one or more lung lobes are characteristic of Paragonimus kellicotti infections, although some cats will have nodular lesions due to pulmonary granulomas. • Sedimentation (Baermann) Fecal Examination: Lungworm larvae (see Figure 129-2) may be found in the sediment, sometimes in large numbers. Fluke ova (see Figures 129-3 and 129-4) may be found in the same manner; however, shedding may be intermittent so multiple fecal examinations may be needed. • Transtracheal Wash, Bronchial Wash, or Bronchoalveolar Lavage: Lungworm larvae and fluke ova may be recovered; however, these techniques are less sensitive than the Baermann fecal examination. • Complete Blood Count (CBC): Absolute and relative eosinophilia may occur in cats with lungworms.
Treatment Primary Therapeutics • Fenbendazole: Give 50 mg/kg q24h PO for 5 days for capillariasis, for 21 days for aelurostrongylosis, and for 14 days for paragonamiasis. However, praziquantel (25 mg/kg PO q8h for 3 days) is the drug of choice for paragonamiasis. Treatment should be extended if subsequent fecal examinations remain positive for larvae or ova; however, spontaneous remission can occur with both species of lungworms.
Figure 129-1
This is an adult Paragonimus kellicotti. It is about 1 cm long.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
306
Figure 129-2 The larvae of Aelurostrongylus abstrusus can be recovered in a fecal sample using a sedimentation technique. They are approximately 360 to 390 µm long.
Lung Parasites
Figure 129-3 The eggs of Capillaria aerophila (60–80 µm long) can be found in a fecal sample using a sedimentation technique.
Secondary Therapeutics • Ivermectin for Lungworms: Give 400 µg/kg q14d PO for two to four treatments or 200 µg/kg SC once. This is not considered as effective as fenbendazole. Observe for 6 hours for side effects. • Thoracentesis or Thoracostomy Tube: One of these may be necessary for pneumothorax due to paragonimiasis. See Chapter 272.
Prognosis Feline lungworm infections may be self-limiting but also respond well to the listed anthelminthics. The prognosis is generally good. With fenbendazole therapy, the prognosis for paragonamiasis is considered good as long as uncontrollable pneumothorax does not occur.
Figure 129-4 The eggs of Paragonimus kellicotti can be recovered in a fecal sedimentation. Their size is approximately 70 to 100 µm in length by 39 to 55 µm in width.
Suggested Readings Lacorcia L, Gasser RB, Anderson GA, et al. 2009. Comparison of bronchoalveolar lavage fluid examination and other diagnostic techniques with the Baermann technique for detection of naturally occurring Aelurostrongylus abstrusus infection in cats. J Am Vet Med Assoc. 235(1):43–49. Little SA, Brown SA. 2007. Capillariasis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 202. Ames, IA: Blackwell Publishing. Nelson OL, Sellon RK. 2005. Pulmonary Parenchymal Disease. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1239–1266. St. Louis: Elsevier Saunders.
307
CHAPTER 130
Lymphoma Bradley R Schmidt and Mitchell A. Crystal
Overview Lymphoma (also known as malignant lymphoma or lymphosarcoma) is the most common neoplasia in the cat, accounting for one-third of all feline neoplasms and 90% of all feline hematopoietic neoplasms. It arises from lymphoid tissue and may involve any organ or tissue. In the past, infection with the feline leukemia virus (FeLV) was a common cause for the development of lymphoma in the cat, although current reports demonstrate only 25% of cats with lymphoma test positive for FeLV based on antigen testing (a dramatic decrease from the 60–70% rate reported prior to availability of the FeLV vaccination). Alimentary, cutaneous, and nasal lymphoma are usually negative for FeLV antigen; renal and multicentric lymphomas test negative for FeLV in over half of the cases; and mediastinal and central nervous system (CNS) lymphoma typically test positive for FeLV. Other forms of lymphoma may be positive or negative for FeLV. Cats with feline immunodeficiency virus (FIV) infection are also at increased risk of developing lymphoma. Household environmental tobacco smoke exposure increases the relative risk of lymphoma development in cats compared to those living in nonsmoking households. The overall median age for cats with lymphoma is 8 to 10 years, with cats that are positive for FeLV (usually with the mediastinal, spinal, or multicentric form) having a younger age of onset (median age 3 years) compared to cats who are negative for FeLV (median age 10–12 years; generally the alimentary form). There is no sex or breed predilection, although some reports demonstrate a slightly higher incidence in male cats. The most common anatomic form of lymphoma is alimentary, followed by mediastinal and multicentric (i.e., hepatosplenomegaly and generalized lymphadenopathy) sites. Extralymphoid tissue sites are less common and include renal, bone marrow, CNS (usually spinal leading to posterior paresis), cutaneous, nasal, ocular, bone, and pulmonary locations. Peripheral lymphadenopathy alone is rare and is more likely to be due to hyperplasia than lymphoma. Renal lymphoma has a 40 to 50% chance of later involving the CNS. Clinical signs and differential diagnoses are variable, depending on the organ/tissues involved.
Diagnosis Primary Diagnostics • Physical Examination: This may be normal or only demonstrate nonspecific findings (e.g., evidence of weight loss). Thickened intestinal loops, palpable intestinal masses, (see Figure 130-1) or mesenteric lymphadenopathy may be present in alimentary lymphoma. Unilateral or bilateral renomegaly (see Figure 130-2) may be present with renal lymphoma. Hepatosplenomegaly, hepatic (see Figure 1303) or splenic masses, or other abdominal masses may be present with multicentric lymphoma. Dyspnea may be present with mediastinal lymphoma (see Figure 130-4). Other signs referable to tissue involvement may be present (nasal discharge [see Figure 130-5], neurologic deficits, ocular changes [see Figure 130-6], skin lesions, and so on). • Complete Blood Count (CBC): Circulating lymphoblasts are uncommonly found. Some cats may demonstrate cytopenias due to bone marrow involvement or anemia of chronic disease. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
308
• FeLV/FIV test: About 25% of cats are positive for FeLV antigen. See Chapter 77. • Fine-Needle Aspiration and Cytology or Biopsy and Histopathology: This is necessary to cytologically or histopathologically confirm lymphoma involving these tissues. The common tissues for sampling are liver, spleen, mediastinal mass, kidney, and lymph node. Organomegaly is the indication. • Intestinal Biopsy: Intestinal biopsy by endoscopy, exploratory laparotomy, or ultrasound guidance is necessary to confirm a diagnosis of alimentary lymphoma.
Secondary Diagnostics • Advanced Diagnostics: Tests such as polymerase chain reaction (PCR) and flow cytometry performed on simple aspirates may be performed at various universities and laboratories that may aid in the diagnosis and phenotyping feline lymphoma. • Chemistry Profile and Urinalysis: Abnormalities may be found in renal (i.e., azotemia and decreased urine specific gravity) and multicentric (i.e., liver enzyme elevation) lymphoma. Hypercalcemia is a rare finding; when present, it is more common with the mediastinal form. Hyperglobulinemia, specifically monoclonal gammopathy, is uncommon. • Abdominal imaging: Radiographic or ultrasonographic abnormalities may be found in renal, multicentric, and alimentary lymphoma. • Thoracic Imaging: A mediastinal mass with or without pleural effusion is present in mediastinal lymphoma and may be seen with radiographs or ultrasound. • Cytology: The presence of lymphoblasts in effusive fluids may aid in the diagnosis of lymphoma. See Chapters 171 and 288. • Bone Marrow Aspirate and Cytology: This is necessary to confirm a diagnosis of bone marrow lymphoma and document bone marrow involvement with other forms of lymphoma. It also is helpful in confirming a diagnosis of spinal lymphoma; spinal lymphoma usually has bone marrow involvement and is more easily diagnosed with a bone marrow aspirate than with a cerebrospinal fluid (CSF) tap. See Chapter 296. • CSF Tap and Cytology: This can confirm CNS lymphoma but is less definitive than bone marrow aspiration; only 30 to 50% will demonstrate lymphoblasts in the CSF. See Chapter 298. • Skin Biopsies and Histopathology: These are needed to confirm a diagnosis of cutaneous lymphoma.
Diagnostic Notes • A subset of feline lymphoma, especially in the gastrointestinal tract, is classified as small cell lymphoma or lymphocytic lymphoma. This variant can be difficult to differentiate from inflammatory bowel disease histologically and is more indolent than large cell lymphoma. Some advocate full-thickness intestinal biopsies to obtain a more definitive diagnosis; however, this may be not be possible depending on the patients clinical status. • A negative FeLV test or lack of CBC changes does not exclude lymphoma. • A positive FeLV test (without cytologic or histologic evidence of lymphoma in involved tissue) does not confirm or indicate a
(A)
(B)
(C) (D) Figure 130-1 Lymphoma in the small bowel may be seen at various stages. A, It may cause segments of the bowel to become diffusely thickened. The abnormal segment (top) is compared to the normal small bowel (below). B, The more common presentation is discrete masses in the small bowel. This was diagnosed when the masses were small. Note that one had already been removed at the anastamosis site. C, Large masses are generally palpable. D, When seen on ultrasound, the bowel wall is thickened and loses its layering. Images courtesy of Dr. Gary D. Norsworthy.
Figure 130-2 Renal lymphoma may be unilateral or bilateral. It was asymmetrically bilateral in this cat and caused widespread destruction to the kidneys and renal failure. Image courtesy of Dr. Gary D. Norsworthy.
Figure 130-3 Lymphoma of the liver is usually diffuse; however, in this cat a discrete mass was found. The cat also had severe hepatic lipidosis; the gross appearance of the liver is typical for hepatic lipidosis. Image courtesy of Dr. Gary D. Norsworthy.
309
SECTION 1: Diseases and Conditions
Figure 130-4 Mediastinal lymphoma occurs as a mass cranial to the heart (arrow). The light colored mass (M) is the lymphoma. The dark red tissue dorsal to it is the left caudal lung lobe (L). The diaphragm (D) marks the caudal boundary of the thorax. The left thoracic wall is reflected cranially. Image courtesy of Dr. Gary D. Norsworthy.
Figure 130-6 The cat has lymphoma in the left eye; note that the right eye appears normal. It also had a lymphomatous mass in the small bowel. Image courtesy of Dr. Gary D. Norsworthy.
appear to be shorter than that seen with combination chemotherapy. See Chapter 34. • Chlorambucil and Prednisone: This is recommended for small cell/ lymphocytic lymphoma of the intestinal tract or of other organs and may be associated with survival times of 1 year or more with limited expense and toxicities. See Chapter 34.
Secondary Therapeutics • Radiation Therapy: This may be indicated in some cases, including possibly nasal lymphoma and mediastinal lymphoma; however, it is not clear if the addition of radiation therapy is superior to chemotherapy alone. • Supportive Care: Fluids, nutritional supplementation, feeding tubes, or other supportive measures may be needed depending on the location and severity of the lymphoma and the cat’s tolerance for chemotherapy.
Therapeutic Notes
Figure 130-5 Nasal lymphoma causes chronic sneezing with purulent, often bloodtinged nasal discharge. This radiograph shows it in the left rostral aspect of the nasal cavity of a 4-year-old cat; it is usually unilateral. Image courtesy of Dr. Gary D. Norsworthy.
diagnosis of lymphoma. It only indicates the presence of the FeLV which may or may not be clinically active.
Treatment Primary Therapeutics • Combination Chemotherapy: This is recommended for forms other than alimentary lymphocytic lymphoma. See Chapter 34. • Single Agent Chemotherapy: This may be less expensive and associated with less toxicity; however, the disease free interval times
310
• Chemotherapy is generally well tolerated. Most cats experience selflimiting side effects (i.e., anorexia, lethargy) at some point in the protocol. Serious side effects are infrequent and include vomiting, diarrhea, protracted anorexia (especially associated with vincristine in some cats), and sepsis (due to neutropenia). For more information on recognizing and managing chemotherapy reactions, see Chapter 34. • Prednisone: Given alone this drug may achieve remission in many cats; however, response rates and survival times are less than those achieved with combination chemotherapy. Prolonged use of prednisone alone (weeks) may induce multidrug resistance and negatively affect expected response rates to chemotherapy. If the owner wishes to treat with prednisone alone, it must be understood that other chemotherapy options will likely no longer exist. • Cats that test positive for FeLV antigen will remain positive after successful chemotherapy and are contagious to other cats.
Prognosis Overall response rates to initial chemotherapy (complete response) generally range from 50 to 80%, with the duration of initial response ranging
Lymphoma
TABLE 130-1: Factors That Improve the Response and Prognosis in Cats with Lymphoma Factor
Comments
Reference
Negative feline leukemia virus (FeLV) test
Median first remission duration and survival time of 146 and 170 days for cats negative for FeLV versus 27 and 37 days for cats positive for FeLV. Median first remission duration and survival time of 211 and 253 days for cats achieving CR versus 22 and 48 days for cats not achieving CR. Complete response for stage 1 = 93%, stage 2 = 83%, stage 3 = 48%, stage 4 = 42% and stage 5 = 58%; Median survival times for stages 1 and 2 = 7.6 months, stage 3 = 2.6 months, stage 3 and 4 = 2.6 months.
Vail DM, Moore AS, Ogilvie GK, et al., 1998
Median first remission duration and survival time of 230 and 282 days for substage a versus 90 and 102 days for substage b. Median first remission duration and survival time of 273 and 225 days when doxorubicin included versus 90 and 102 days without doxorubicin. Median first remission duration and survival time 615 and 510 days for lymphocytic form (50 cats, 69% CR) versus 435 and 81 days for lymphoblastic form (17 cats, 18% CR); only 2 cats with lymphoblastic form achieved CR
Vail DM, Moore AS, Ogilvie GK, et al., 1998
Complete response (CR) to chemotherapy
Early clinical stage (stage 1 = single tumor or lymph node; stage 2 = single tumor with regional lymph node involvement or two tumors on same side of diaphragm without lymph node involvement or two lymph nodes on the same side of the diaphragm or resectable gastrointestinal tumor with or without associated lymph node involvement; stage 3 = two tumors or ≥ two lymph nodes on opposite sides of the diaphragm or nonresectable intra-abdominal disease or spinal disease; stage 4 = stages 1–3 with liver or spleen involvement; stage 5 = stages 1–4 with central nervous system or bone marrow involvement) Clinical substage a (substage a = no significant clinical illness, substage b = significant clinical illness) Doxorubicin inclusion in treatment protocol
Lymphocytic form of alimentary lymphoma
Vail DM, Moore AS, Ogilvie GK, et al., 1998
Mooney SC, Hayes AA, MacEwen EG, et al., 1987
Vail DM, Moore AS, Ogilvie GK, et al., 1998 Richter K, 2001
TABLE 130-2: Affect of Anatomic Site on Prognosis in Cats with Lymphoma Anatomic Site
Comments
Reference
Alimentary Mediastinal
See Table 130-1. Approximate survival times of 2–3 months; most are positive for feline leukemia virus (FeLV). Median first remission duration and survival time of 112 and 143 days. Median survival times of 3–6 months; worse prognosis if BUN >150 mg/dL or if FeLV positive; progresses to CNS involvement in 40–50% of cases. Response rates <50% in two studies of 13 cats; survival times were usually less that 5 months; many cats also underwent surgery (2) or radiation (3); 2 cats lived 13 months. Median first remission duration and survival time 380 and 456 days. Only small amounts of available information exist for most other sites; one study 49 cats with ocular lymphoma (most treated via enucleation with or without prednisone) reported an average survival of 14 months but survival times were markedly variable.
Richter K, 2001 Vail DM, 2007
Multicentric Renal Spinal
Nasal Other
from 4 to 9 months. Second-time response rates (rescue) and duration of response are much reduced. About 30 to 35% of cats with lymphoma undergoing chemotherapy have prolonged response rates and survival times (>1 year). Prognostic factors affecting response and survival times are listed in Table 130-1. The affect of anatomic site on prognosis is listed in Table 130-2. Information on the prognosis of different chemotherapy protocols can be found in Chapter 34.
Vail DM, Moore AS, Ogilvie GK, et al., 1998 Vail DM 2007 Vail DM, 2007
Vail DM, Moore AS, Ogilvie GK et al., 1998 Moore AS, Ogilvie GK, 2001
Suggested Readings Bauer N, Moritz A. 2005. Flow cytometric analysis of effusions in dogs and cats with the automated haematology analyser ADVIA 120. Vet Rec. 156(21):674–678. Bertone ER, Snyder LA, Moore AS. 2002. Environmental tobacco smoke and risk of malignant lymphoma in pet cats. Am J Epid. 156:268–273.
311
SECTION 1: Diseases and Conditions
Moore AS, Ogilvie GK. 2001. Lymphoma. In AS Moore, GK Ogilvie, eds., Feline Oncology: A Comprehensive Guide to Compassionate Care, pp. 191– 219 and 423–428. Philadelphia: Veterinary Learning Systems. Moore PF, Woo JC, Vernau W, et al. 2005. Characterization of feline T cell receptor gamma (TCRG) variable region genes for the diagnosis of feline intestinal T cell lymphoma. Vet Immunol Immunopathol. 106(3–4):167–178. Vail DM. 2007. Feline Lymphoma and Leukemia. In SJ Withrow, DM Vail, eds., Small Animal Clinical Oncology, 4th ed., pp. 733–756. Philadelphia: Elsevier Saunders.
312
Vail DM, Moore AS, Ogilvie GK, et al. 1998. Feline lymphoma (145 cases): proliferation indices, cluster of differentiation 3 immunoreactivity, and their association with prognosis in 90 cats. J Vet Intern Med. 12:349–354. Werner JA, Woo JC, Vernau W, et al. 2005. Characterization of feline immunoglobulin heavy chain variable region genes for the molecular diagnosis of B-cell neoplasia. Vet Pathol. 42(5):596–607.
CHAPTER 131
Malassezia Dermatitis Christine A. Rees
Overview Malassezia dermatitis is a dermatologic condition in which a normal floral organism, Malassezia pachydermatis, is present in the skin in abnormal numbers. The end result of this yeast overgrowth is inflammation of the skin with pruritus. Anatomical abnormalities (i.e., skin folds) can predispose cats to developing this type of dermatitis. In addition, abnormalities in keratinization (i.e., seborrhea) or allergies can predispose cats to developing Malassezia dermatitis. Neoplasia has also been associated with the development of Malassezia dermatitis in the cat. Examples of neoplastic conditions associated with the development of a yeast skin infection include thymoma and paraneoplastic alopecia (i.e., commonly associated with a pancreatic tumor). Some examples of Malassezia dermatitis in cats include facial fold dermatitis (Persians) and nail bed or fold dermatitis (Sphinx). Differential diagnoses for Malassezia dermatitis include allergies (i.e., flea allergy, atopy, or food allergy), endocrinopathies (i.e., hyperthyroidism or hyperadrenocorticism), metabolic disease (i.e., diabetes mellitus), retroviral infection, dermatophytosis, and mite infestations.
• Cytology: Tape strip or skin scrape cytology is used to confirm the presence of yeast organism. I use Durotak Adhesive Slides® (Delasco Dermatologic Lab and Supply, Inc, Council Bluffs, IA) for suspected Malassezia cases. For cases of yeast otitis, ear swab cytology samples are diagnostic. Malassezia organisms appear as round to oval or budding deep blue staining organisms. See Chapter 157.
Secondary Diagnostics • Any underlying cause or complicating factors for the cat developing Malassezia dermatitis needs to be identified and addressed. Diagnostic tests that might be useful are blood tests (i.e., retroviral tests, complete blood count [CBC], serum chemistry, and total T4), skin scrapings (for mites), food trial, intradermal allergy testing, and fungal cultures.
Treatment Primary Therapeutics
Diagnosis Primary Diagnostics • Clinical Appearance: Typical dermatologic lesions for Malassezia dermatitis include seborrhea olesosa, alopecia, erythema, chin acne, ceruminous otitis externa, or exfoliative dermatitis with or without pruritus. See Figure 131-1.
• Treat Underlying Disorders: Every effort should be made to treat underlying conditions that may mitigate fungal infection. Chronic infections, relapses, or poor response to treatment should raise the suspicion of underlying pathology. • Systemic Antifungal Medication: Systemic antifungals are indicated for generalized infections. Itraconazole is the treatment of choice, at a dose of 5 mg/kg q12h PO for 30 days. Alternatively, “pulse dosing” may be an effective therapy. Pulse doing involves administering the recommended dose of itraconazole daily for 7 days, then administering no medication for 7 days followed by administering medication for 7 days. This cycle can be repeated as needed.
Secondary Therapeutics • Medicated Shampoos: Topical 2% ketoconazole, 2% miconazole, or 2 to 4% chlorhexadine administered at least once weekly is a good adjunctive therapy. These products are recommended to hasten the therapeutic response.
Prognosis The prognosis depends on identification and management of any preexisting underlying disease. However, secondary Malassezia infections typically respond very well to therapy and therefore carry a good prognosis.
Suggested Readings Figure 131-1 Malassezia dermatitis may occur on the skin rostral to the pinna associated with Malassezia otitis externa. Image courtesy of Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Matousek JL, Campbell KL. Malassezia dermatitis. 2002. Compendium. 24:224–232. Mauldin EA, Morris DO, Goldschmidt MH. 2002. Retrospective study: the presence of Malassezia in feline skin biopsies. A clinicopathological study. Vet Dermatol. 13:14. Takle GL, Hnilica KA. 2004. Eight emerging feline dermatoses. Vet Med. 99:456–468.
313
CHAPTER 132
Mammary Gland Neoplasia Bradley R. Schmidt and Mitchell A. Crystal
Overview Mammary gland neoplasia is the third most common neoplasia in the cat, accounting for 17% of all neoplasms in the female cat. Mammary tumors are rare in male cats. Mammary gland neoplasia occurs at an average age of 10 to 12 years (12.8 years in male cats) but has a reported age range of 9 months to 23 years. Siamese cats and domestic short haired cats may be at an increased risk of developing mammary gland neoplasia, and Siamese cats may acquire tumors at a slightly younger age. Reports have shown that some mammary tumors contain progesterone receptors, and that some cats have developed mammary neoplasia following prior progestin administration. As in the dog, early ovariohysterectomy has a sparing effect on the incidence of malignant (but not benign) mammary neoplasia. Cats spayed prior to 6 months of age are 91% less likely to develop mammary carcinoma. Feline mammary tumors are malignant 80 to 93% of the time in contrast to 41 to 53% of the time in dogs. The most common tumor type is the adenocarcinoma (i.e., tubular, papillary, or solid), which presents as singular or multiple nodules or as a diffuse swelling. Multiple gland involvement is common, and tumors are often ulcerated. See Figure 132-1. In addition, they may incite a marked inflammatory response or produce secretions that resemble that during lactation. Lymphatic and vascular invasion is common and metastasis is frequent; 80% of cats demonstrate metastasis by the time of euthanasia or death. Metastasis often involves regional lymph nodes, lungs (see Figure 132-2), pleura, or liver. Many cats present for dyspnea secondary to metastases-induced pleural effusion. Generally, regional lymph node metastasis typically occurs in the inguinal lymph nodes for tumors involving the caudal four mammae (glands 3 and 4 on the left and right) and in the axillary lymph nodes for tumors involving the cranial four mammae (glands 1 and 2 on the left and right).
Figure 132-2 Pulmonary metastasis usually appears as a diffuse interstitial pattern without discrete nodules. It can be confused for fungal pneumonia. Image courtesy Dr. Gary D. Norsworthy.
Benign mammary gland adenoma is uncommon and typically presents as a small, single, firm nodule. This is a differential diagnosis for malignant mammary neoplasia. Other differential diagnoses include malignant and benign skin tumors, mastitis, and fibroepithelial hyperplasia. Fibroepithelial hyperplasia may occur in cats up to 2 years of age after estrus or during pregnancy or in cats treated with progestins and can present as one or more massive mammary gland enlargement with erythema and ulceration. Fibroepithelial hyperplasia may represent neoplasia or severe mastitis. See Chapter 133.
Diagnosis Primary Diagnostics • Palpation: This is the test that usually finds the mass. Because 80 to 93% of mammary gland tumors are malignant, a mammary mass in a cat must be taken seriously and approached aggressively. Owners who wish to monitor growth over time need to be told that metastasis may occur while the palpable mass is still small. • Surgical Excision and Histopathology: This is the procedure of choice for diagnosis and treatment. Because so many mammary gland tumors are malignant, excisional biopsy rather than an incisional biopsy is generally preferred unless fibroepithelial hyperplasia is suspected. A fine-needle biopsy may be performed to help distinguish between malignant and nonmalignant lesions, but interpret with caution. Figure 132-1 This cat has a solitary mammary adenocarcinoma. As many of these tumors are, this one was ulcerated at the time of presentation. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
314
Secondary Diagnostics • Lymph Node Cytology: This may reveal evidence of regional metastasis. Lymph node cytology, preferably using the fine-needle biopsy technique (Chapter 301) should be performed whenever lymphadenopathy is identified in combination with mammary tumors.
Mammary Gland Neoplasia
• Thoracic Radiographs: These may reveal evidence of metastasis to the lungs, pleura, or intrathoracic lymph nodes. See Figure 132-2. Thoracic radiographs should be performed prior to anesthesia and surgery in all cats with mammary tumors. Three views are recommended (left and right laterals and a ventral-dorsal view). • Abdominal Ultrasound: This should be performed to evaluate for evidence of metastasis and lymph node enlargement. • Pleurocentesis and Cytology: This is indicated if pleural effusion is present. Cytologic evaluation of fluid collected may reveal evidence of metastasis although some cats with intrathoracic neoplasia will have effusion void of neoplastic cells. • Fine-Needle Aspiration and Cytology: This may suggest whether a tumor is malignant or benign, but histopathology is more accurate.
Diagnostic Notes • Mammary tumor fine-needle biopsy and cytology alone should not be used to determine a definitive diagnosis unless fibroepithelial hyperplasia or a nonmalignant lesion is a major consideration because a geographical miss during aspiration of a tumor may delay a diagnosis of malignancy and rapid surgical intervention. • Pulmonary metastases may be more diffuse or interstitial and less likely to form discrete nodules as compared to the dog. • Pleural metastasis and effusion are more common in feline mammary neoplasia than in canine mammary neoplasia.
Treatment Primary Therapeutics • Surgical Excision: This is the treatment of choice for mammary gland neoplasia. As local recurrence is common with conservative surgery, the current recommendations include unilateral radical mastectomy for mammary tumors confined to one side. See Figure 132-3. Bilateral radical mastectomy (i.e., simultaneous bilateral radical mastectomy or unilateral radical mastectomy staged 2 to 3 weeks apart) is indicated if there is disease in both left and right mammary chains. The inguinal lymph nodes should always be removed at the time of surgery, whereas the axillary lymph nodes should only be removed if they are palpably enlarged or cytologically test positive for neoplasia. It is unclear if concurrent ovariohysterectomy is associated with a reduced recurrence rate, but it is advocated by some. Ovariohysterectomy or discontinuing progestins generally results in regression of fibroepithelial mass lesions. See Chapter 261.
Secondary Therapeutics • Chemotherapy: Doxorubicin (25 mg/m2 IV, slowly over 15 minutes, on day 0) used alone or followed by cyclophosphamide (50 mg/m2 PO on days 3,4,5, and 6) can be used once every 3 weeks for up to eight treatments in cats with metastatic or nonresectable disease. This protocol has been suggested to significantly increase survival time. Complete or partial responses can be seen in 50% of cats. Doselimiting side effects include profound anorexia, moderate myelosuppression, and cumulative renal injury. Mitoxantrone (6.5 mg/m2 q21d IV) or carboplatin (220 to 260 mg/m2 q21–28 d IV) in place of doxorubicin in the aforementioned protocol may lower side effects. Other studies have not substantiated these beneficial effects. • Pleurocentesis and Intracavitary Chemotherapy: Evacuation of pleural fluid followed by intracavitary mitoxantrone or carboplatin at dosages listed previously may be helpful in treating malignant effusions. See Chapter 29. • Supportive Care: This should include nutritional support, analgesics, and antibiotics if the lesions are ulcerated for cats with mammary neoplasia or fibroepithelial hyperplasia.
Figure 132-3 Aggressive mastectomy is the first-line treatment. Four glands on one side have been removed even though there was only one tumor present. Image courtesy Dr. Gary D. Norsworthy.
Therapeutic Notes • Radiation, immune therapy, and endocrine therapy have not been shown to improve survival times in cats with mammary gland neoplasia. • Recurrent local tumors can be managed effectively with repeated surgeries until metastasis occurs. • Controlled studies evaluating mastectomy with or without chemotherapy and chemotherapy with or without mastectomy have not been published.
Prognosis The overall average time from detection of malignant mammary gland neoplasia to death is 1 year. Significant factors affecting survival include the size (most important), extent of surgery, and histologic grade of the tumor. Female cats with tumors that are greater than 3 cm (1 1/8 inch) in diameter have a median survival time of 4 to 12 months; it is less than 2 months in male cats. Female cats with tumors that are 2 to 3 cm (3/4-1 1/8 inch) in diameter have a median survival time of 2 years; it is 5 months in male cats. Female cats with tumors that are less than 2 cm (<3/4 inch) in diameter have a median survival time of over 3 years; it is 14 months in male cats. Tumors with a high histologic grade (i.e., poor cellular differentiation and high mitotic index) have a worse prognosis than those of low histologic grade. About 10% of cats with a high-grade histologic tumor type will survive 1 year compared with 50% of cats with a low-grade histologic tumor type. Lymphatic invasion is a significant negative prognostic factor; cats with lymphatic invasion had a median survival of 6.5 to 7 months, compared to 18 (female cats) to 29 (male cats) months when lymphatic invasion was absent. Unfortunately, most cats present with aggressive tumors at the initial presentation. With regard to the extent of surgery in the treatment of feline mammary tumors, a recent study reported survival times of 917 days when bilateral mastectomies were performed, 428 days when regional mastectomies were performed, and 348 days when unilateral mastectomies were performed. As mentioned previously, the additional of chemotherapy may improve survival times, but additional studies are needed. The prognosis with cats with fibroepithelial hyperplasia is generally favorable when ovariohysterectomy is performed.
Suggested Readings Couto CG, Hammer AS. Oncology. 1994. In RG Sherding, ed., The Cat: Diseases and Clinical Management, 2nd ed., pp. 755–818. New York: Churchill Livingstone.
315
SECTION 1: Diseases and Conditions
Moore AS, Ogilvie GK. 2001. Mammary tumors. In AS Moore, GK Ogilvie, eds., Feline Oncology, pp. 355–367. Trenton: Veterinary Learning Systems. Skorupski KA, Overley B, Shofer FS, et al. 2005. Clinical characteristics of mammary carcinoma in male cats. J Vet Intern Med. 19:52–55.
316
Vail DM, Withrow SJ. 2007. Tumors of the mammary gland. In DM Vail, SJ Withrow, eds., Small Animal Clinical Oncology, 4th ed., pp. 619–636. Philadelphia: Elsevier Saunders.
CHAPTER 133
Mammary Hyperplasia Gary D. Norsworthy
Diagnostic Notes
Overview Mammary hyperplasia, also known as fibroadenomatous mammary hyperplasia, is a disorder characterized by rapid and dramatic enlargement of multiple mammary glands. In most cats, it affects all mammary glands and involves both epithelial and mesenchymal tissue. It typically occurs in young, cycling females and is related to high progesterone levels in pregnancy. It may occur during false pregnancy about 40 to 50 days after induced ovulation. It also has been associated with exogenous progestin administration in neutered male and female cats, growth hormone, or prolactin. It is considered a benign condition, but it must be differentiated from mammary neoplasia. Milk production may occur, although most affected cats are not lactating.
• Serum progesterone concentrations are increased in about one-third of affected cats, so this is not a sensitive diagnostic tool. It is often normal by the time of diagnosis.
Treatment Primary Therapeutics • Progesterone Withdrawal: If the source of progesterone can be withdrawn, the condition will usually correct itself in several weeks. Unspayed females should be spayed. • Spontaneous Remission: Cats not receiving progesterone compounds usually have remission within a few weeks.
Diagnosis Secondary Therapeutics Primary Diagnostics • Clinical Findings: Rapid growth of multiple mammary glands is typical. See Figure 133-1. This may occur in cycling female cats and in cats of both genders receiving progesterone compounds. • Cytology of Mammary Secretion: The fluid expressed from a mammary gland should be aseptic, non-inflammatory, and void of cells with characteristics of neoplasia.
Secondary Diagnostics • Biopsy and Histopathology: These may be used for differentiating this condition from mammary neoplasia. They are indicated for mammary glands that contain discrete masses.
• Analgesics: Pain-relieving medication can make the cat more comfortable. • Mastectomy: This surgical procedure should be considered if the abnormal tissue outgrows its blood supply so sloughing occurs or if progesterone withdrawal does not produce a cure. • Prolactin Inhibitor: Bromocriptine mesylate (0.25 mg/cat q24h PO for 5–7 days) may be used for this purpose. It is not labeled for feline use and may cause nausea, anorexia, or vomiting. • Progesterone Receptor Blocker: Aglepristone (15 mg/kg SC on 2 consecutive days or 20 mg/kg q7d SC) may be used for this purpose. It is not approved for cats. It is likely to cause abortion in pregnant cats. • Testosterone Therapy: Testosterone cypionate or enanthate (2 mg/ kg IM once) may be used to suppress mammary hyperplasia.
Therapeutics Notes • Caution should be used in handling the mammary tissue to prevent mammary or venous cutaneous thrombosis or pulmonary arterial thrombosis. • If an ovariohysterectomy is preformed, a flank incision may be preferable.
Prognosis The prognosis for mammary hyperplasia is good. Spontaneous remission occurs in some cats, and progesterone withdrawal cures most others.
Suggested Readings
Figure 133-1 glands.
This cat has severe mammary hyperplasia affecting all eight mammary
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Grundy SA, Davidson AP. 2006. Feline Reproduction. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1696–1707. St. Louis: Elsevier Saunders. Loretti AP, Ilha MRS, Ordas J, de las Mulas JM. 2005. Clinical, pathological and immunohistochemical study of feline mammary fibroepithelial hyperplasia following a single injection of depot medroxyprogesterone acetate. J Fel Med Surg. 7(1):43–52. Root-Kustritz MV. 2007. Mammary Gland Hyperplasia—Cats. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, Canine and Feline, 4th ed., pp. 852–853. Ames, IA: Blackwell Publishing.
317
CHAPTER 134
Manx Syndrome Vanessa Pimentel de Faria
Overview Manx is a breed with a naturally occurring mutation of the spine. Manx cats that are homozygous for the mutation die before birth, and stillborn kittens show gross abnormalities of the central nervous system. If there is no overt problem with a Manx syndrome kitten at birth, the difficulties will show up in the first few weeks or months of life. The syndrome is often characterized by severe bowel or bladder dysfunction or by extreme difficulty walking. Heterozygous Manx are affected to an equal or lesser degree. The most visible effect is taillessness, which is a dominate trait. That characteristic varies from having no coccygeal vertebrae (“rumpy”), several coccygeal vertebrae fused in an upright position (“rumpyraiser”), several coccygeal vertebrae, but deformed (“stumpy”), and finally a complete or nearly complete tail (“tailed” or “longy”). The rumpy form seems to have more spinal cord abnormalities in addition to absent or rudimentary caudal vertebrae. It is hypothesized that the problems associated with the taillessness condition may be related to a disturbance of central nervous system development during early embryonic life. The variable expression of Manx taillessness is a salient and consistent feature of the Manx syndrome. In addition, it is associated with sacral or caudal vertebral deformities (dysgenesis or agenesis) that may be associated with spina bifida or malformations of the terminal spinal cord or cauda equina. The spinal cord may terminate prematurely with absence of certain spinal nerves from the sacral cord segments, which supply innervation to the colon, bladder, hindlimbs, and perineal regions. In addition, the pelvis may be malformed and fused, and the anal opening may be narrow, causing constipation. However, some tailless cats have a normal sacrum, spinal cord, and cauda equina. Spina bifida is the most commonly reported vertebral malformation in Manx cats, and urine and fecal incontinence are often the earliest presenting signs. In some cases, spina bifida (see Figure 134-1) is associated with meningocele (see Figure 134-2), a condition in which the dura mater communicates with the skin surface, resulting in loss of cerebrospinal fluid.
Figure 134-1 This Manx kitten died at birth exhibiting spina bifida. Photo courtesy of Dr. Gary D. Norsworthy.
Diagnosis Primary Diagnostics • Clinical Signs: Clinical signs depend on the degree of spinal cord and cauda equina malformation and include lower limb paralysis or paresis, megacolon, atonic bladder, absent anal and urinary bladder sphincter tone, absent anal reflex, urinary and fecal incontinence, and reduced cutaneous sensation in the perineal region. The principal gait problem consists of a plantigrade posture when walking or standing. Cats exhibiting this stance are commonly described as having a characteristic rabbity or hopping gait. • Physical Examination: A complete neurologic examination with special emphasis on caudal spinal cord function should be performed to identify neurologic causes of colonic dysfunction. It is particularly important to test for a perineal reflex. See Chapter 307. • Radiographs: Radiographs of the spinal cord should be performed to confirm that a malformation exists. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
318
Figure 134-2 A meningocele is a communication of the spinal canal through the skin allowing spinal fluid to exit. Positive contrast was injected into the meningocele to demonstrate the fistulous tract. Photo courtesy of Dr. Richard Malik.
Secondary Diagnostics • Advanced Imaging: A myelogram, computerized tomography (CT) study, or magnetic resonance imaging (MRI) study can be performed to diagnose a malformation causing spinal cord compression. These tests may also uncover a meningocele or attachment of the spinal cord to subcutaneous tissues in the lumbosacral region.
Manx Syndrome
Diagnostic Notes • Advanced imaging is especially important in older animals, in which malformations may show up as incidental findings accompanying other spinal cord disorders.
Treatment Primary Therapeutics • Medical Therapy: Anti-inflammatory drugs may be beneficial in cases where congenital abnormalities (such as luxations) have led to repeated injuries. However, medical therapy is generally unrewarding, especially in spina bifida. • General Care: Manual bladder expression is necessary when urinary incontinence is presented. Moreover, when fecal incontinence is presented, fecal softening medications such as docusate sodium (DSS) and lactulose, are warranted, unless diarrhea or soft stool is present. If so, consider frequent small meals of low-residue diets to decrease the amount and frequency of defecation. Recurrent urinary tract infections, megacolon, and chronic constipation are common sequelae.
patients with spina bifida or meningocele, the meningocele must be resected in addition to repairing the bony defect. Meningocele is usually surgically correctable in cats with minimal neurologic deficits. If agenesis of the terminal spinal cord is present, surgery is fruitless.
Prognosis The degree of spinal deformity does not always correspond with the degree of neurologic impairment. Clinical findings are the most important factors to consider in determining prognosis. However, the longer the signs are present, the worse the prognosis. Prognosis for severely affected cats is poor, and no treatment is available.
Suggested Readings Fenner WR. Diseases of the brain, spinal cord, and peripheral nerves 1994. In RG Sherding, ed., The Cat: Diseases and Clinical Management, 2nd ed., pp. 1507–1568. Philadelphia: WB Saunders. LeCouteur Ra, Grandy JL. 2005. Diseases of the spinal cord. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 842–887. St. Louis: Elsevier Saunders.
Secondary Therapeutics • Surgery: Surgical decompression and stabilization are indicated in cases in which imaging reveals spinal cord compression. For
319
CHAPTER 135
Mast Cell Tumors Bradley R. Schmidt and Mitchell A. Crystal
Overview Mast cell tumors (MCT) are the second most common feline skin tumor and fourth most common tumor in the cat. There are two forms: a mastocytic form that histologically resembles normal mast cells and a histiocytic form that histologically has features of histiocytic mast cells. The median age of cats with the mastocytic form is 10 years. The median age for the histiocytic form is 2.4 years. Siamese cats appear to be overrepresented in both variants of the disease. MCT are generally cutaneous; however, the visceral form can be present in up to 50% of all affected cats, in contrast to dogs. The etiology is not known, but due to the high incidence of mast cell tumors in Siamese as compared to other breeds, a genetic predisposition is suspected. As in dogs, mast cell granules contain vasoactive substances, such as heparin and histamine, and degranulation may result in systemic signs, most commonly in cats with disseminated disease. Cutaneous MCT occur more commonly on the head and neck, may be pruritic or non-pruritic, and present as a solitary mass, multiple lesions, or as a diffuse form. Up to 20% of cases involve multiple lesions, and approximately 50% of these are of the diffuse form. See Figure 135-1. The presence of diffuse disease (greater than five tumors) may be indicative of systemic involvement, with the exception of some Siamese cats, which may experience spontaneous regression, even years after the initial diagnosis. (See the histiocytic form which will be discussed). The histologic grading system used in the canine is not valid in the cat, though mastocytic MCT occur in either a compact or diffuse histologic form. The compact form occurs in 50 to 90% of the cases and has a more benign behavior, while the diffuse form appears more anaplastic and has a more
malignant behavior. Overall, the metastatic rate for the compact form varies from 0 to 22%, with most metastatic reports being associated with the diffuse form. Therefore, most MCT are benign, especially when five or fewer lesions are present. The histiocytic form seen in 6-week-old to 4-year-old Siamese cats appear as multiple, firm, pinkish, hairless papules on the head and pinnae that usually regress spontaneously over 4 to 24 months. Histologic confirmation of histiocytic MCT can be challenging as mast cells may compromise only 20% of the cells present, with the remaining cells comprised of histiocytes; this may lead to an erroneous diagnosis of granulomatous disease. Clinical signs in cats with cutaneous MCT without metastasis are limited to the presence of the tumor. Differential diagnoses for cutaneous MCT include squamous cell carcinoma, melanoma, basal cell tumor, fibrosarcoma, cutaneous hemangioma or hemangiosarcoma, eosinophilic granuloma complex, panniculitis, poorly healing wounds, hair follicle tumors, and sebaceous gland tumors. Visceral MCT occur most commonly in the spleen (see Figure 135-2) and less commonly in the intestine (see Figure 135-3). Fifteen percent of cats with splenic disease have MCT as a cause, and MCT is the third most common intestinal tumor after lymphoma and adenocarcinoma. Visceral MCT are much more likely to metastasize than the cutaneous form, with metastasis occurring in up to 90% of the cases. Common metastatic sites in cats with splenic MCT include the liver, abdominal lymph nodes, bone marrow, lung, and intestinal tract. Eosinophilic-rich pleural effusion or ascites may be seen. Peripheral blood mastocytosis is more commonly seen in cats with the splenic form when compared to the intestinal form. Common presenting signs as a result of mast cell degranulation or large tumor burdens include lethargy, anorexia, vomiting, anaphylactoid reactions, coagulation disorders, dyspnea, and weight loss. Splenomegaly, hepatomegaly, pallor, effusion, or an abdominal mass may be found on physical examination. Differential diagnoses for systemic MCT include lymphoma, neoplasia of abdominal organs or structures, or hypereosinophilic syndrome.
Figure 135-1 This Siamese has the diffuse cutaneous form. Over 40 lesions on the head and neck were present. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
320
Figure 135-2 Severe organ enlargement is characteristic for mast cell disease of the spleen. This is the most common site of visceral mast cell tumors. Image courtesy Dr. Gary D. Norsworthy.
Mast Cell Tumors
Diagnostic Notes • The histologic appearance of cutaneous MCT (mastocytic or histiocytic) may help predict metastatic potential. The grading scale used in the dog does not apply to feline MCT. • A complete systemic evaluation (CBC, buffy coat preparation, bone marrow aspiration, and abdominal or thoracic imaging) will define the extent of the disease and assist in selection of the most appropriate therapeutic approach. This should be performed in all cases of visceral MCT and in cases of cutaneous MCT associated with clinical signs or in cases that have multiple cutaneous tumors. • When performing fine-needle biopsies of splenic lesions, pretreatment with antihistamines may be indicated to reduce the effects of degranulation. • Mast cell granules occasionally do not stain well with quickstaining methods. Leaving the slide in the fixative (first dip jar in quick Wright’s-type stains) for several minutes may help improve mast cell granule staining. See Chapter 287. Figure 135-3 The small bowel is the second most likely site of visceral mast cell tumors. In this cat, two lesions were found in the small bowel at surgery. The gross appearance of the mesentery is typical of metastasis. Image courtesy Dr. Gary D. Norsworthy.
Diagnosis Primary Diagnostics • Fine-Needle Biopsy and Cytology: This simple test may be performed on cutaneous and visceral (i.e., spleen, liver, lymph nodes, or intestine) lesions. Effusions are often diagnostic. Occasionally large numbers of eosinophils may be seen on cytology of effusions, and abdominal masses and may erroneously lead to the diagnosis of eosinophilic diseases. The histiocytic form is more difficult to diagnose with fine-needle biopsy. See Chapter 287. • Surgical Removal or Biopsy and Histopathology: This is usually definitive and generally is required to diagnose the histiocytic form. • Complete Blood Count (CBC): Anemia may be present from splenic sequestration, gastrointestinal hemorrhage, bone marrow involvement, or chronic disease. Anemia is seen in one-third of the cats with visceral MCT. Basophilia is sometimes seen. Mastocythemia may be present, especially in cats with the splenic form.
Secondary Diagnostics • Buffy Coat Preparation: This may reveal mastocytemia in cats with metastatic disease. A negative result does not exclude metastatic disease. • Bone Marrow Aspiration: This may reveal infiltration with malignant mast cells and is indicated in cats with the visceral form of the disease. • Abdominal Imaging: Radiographs and ultrasound may reveal hepatomegaly with or without nodules, splenomegaly with or without nodules, abdominal lymphadenopathy, abdominal effusion, or intestinal masses. • Thoracic Imaging: MCT rarely metastasize to intrathoracic locations, although pleural effusions and a cranial mediastinal form of MCT have been reported. • Coagulation Profile: Abnormalities have been reported in a significant number of cats with splenic MCT. These abnormalities are rarely clinically significant.
Treatment Primary Therapeutics • Surgical Excision: Complete removal is curative in most cases of cutaneous MCT. Wide surgical margins should be attempted, although margins are not as critical as in the canine because most demonstrate a benign behavior. Wide margins are indicated for the diffuse mastocytic form. • Splenectomy: This should be performed in cats with splenic MCT (with or without effusions or involvement of other organs); doing so will significantly prolong survival time. Pretreatment with antihistamines, serotonin inhibitors, and corticosteroids is recommended prior to surgery. • Intestinal MCT require removal of 5 to 10 cm of bowel on either side of the lesion. Microscopic extension usually exceeds visible gross disease.
Secondary Therapeutics • Cryotherapy, Laser Ablation, and Electrosurgery for Cutaneous Lesions: These may be used to remove lesions on the skin and may result in local control due to the benign behavior of most tumors. These modalities increase the risk of massive histamine release so cats so treated should be pretreated with antihistamines. • Chemotherapy: There is limited data on the efficacy of chemotherapy as an adjunctive treatment or in the treatment of disseminated MCT. Lomustine (median remission dose of 56 mg/ m2) is reported to have a 50% response rate, with a median disease free interval of 168 days. Vinblastine combined with prednisone has also been advocated by some. • Corticosteroids: They may reduce the effects of degranulation; however, the anticancer activity of prednisone or prednisolone or topical triamcinolone is not known and may be limited. • Others: The antihistamine famotidine (0.5 mg/kg q12–24 h PO) and the serotonin inhibitor cyproheptadine (2 mg/cat q12h PO) may help control systemic effects in cats with disseminated or extensive disease and may be considered preoperatively as well.
Therapeutic Notes • Radiation Therapy: Information is limited as most are treated with conservative surgery. Radiation therapy of solitary cutaneous MCT has had response rates of up to 60%. A recent study
321
SECTION 1: Diseases and Conditions
evaluating strontium 90 irradiation of cutaneous mast cell tumors reported a 98% response rate for a median survival time of 1075 days.
Prognosis Most cutaneous MCT are cured with complete surgical excision; local recurrence rates are reported at less than 36% (typically occurring within 6 months), and metastatic rates are reported at less than 22%. Cats undergoing splenectomy for splenic MCT have a median survival time of 12 to 19 months, with anorexia, weight loss, and the male gender carrying a less favorable prognosis; positive buffy coat smears and bone marrow aspirates (which occur in up to 50% of cats with splenic MCT) does not affect survival. Cats with splenic MCT survive less than 6 months without splenectomy. Nonsplenic, visceral, and metastatic mast cell tumors carry a poor prognosis; cats with intestinal MCT usually have survival times of less than four months.
Suggested Readings Moore AS, Ogilvie GK. 2001. Skin tumors. In AS Moore, GK Ogilvie, eds., Feline Oncology, pp. 398–428. Trenton: Veterinary Learning Systems.
322
Moore AS, Ogilvie GK. 2001. Tumors of the alimentary tract. In AS Moore, GK Ogilvie, eds., Feline Oncology, pp. 271–294. Trenton: Veterinary Learning Systems. Moore AS, Ogilvie GK. 2001. Splenic, hepatic and pancreatic Tumors. In AS Moore, GK Ogilvie, eds., Feline Oncology, pp. 295–310. Trenton: Veterinary Learning Systems. Rassnick KM, Williams LE, Kristal O, et al. 2008. Lomustine for treatment of mast cell tumors in cats: 38 cases (1999–2005). J Am Vet Med Assoc. 232(8):1200–1205. Scott DW, Miller WH, Griffin CE. 2001. Mast cell tumors. In DW Scott, WH Miller, CE Griffin, eds., Miller & Kirk’s Small Animal Dermatology, 6th ed., pp. 1320–1330. Philadelphia: WB Saunders. Turrel JM, Farrellu J, Page RL, et al. 2006. Evaluation of strontium 90 irradiation in treatment of cutaneous mast cell tumors in cats: 35 cases (1992–2002). J Am Vet Med Assoc. 228(6):898–901. Vail DM, Withrow SJ. 2007. Tumors of the Skin and Subcutaneous Tissues. In DM Vail, SJ Withrow, eds., Small Animal Clinical Oncology, 4th ed., pp. 416–424. Philadelphia: Elsevier Saunders.
CHAPTER 136
Megacolon Mitchell A. Crystal
Overview Idiopathic megacolon is an acquired condition of colonic dilation and decreased motility that usually is associated with constipation or obstipation due to a generalized dysfunction of colonic smooth muscle. Cats of a wide age range are affected (1–15 years of age), with an average age of 5 to 6 years of age. There is no breed or sex predilection, although one source suggests males are predisposed. Obese, less-active cats may be at an increased risk. Clinical signs of megacolon include chronic constipation or obstipation with poor responses to treatment with laxatives and enemas. Cats may also demonstrate anorexia, lethargy, and vomiting. Rarely, diarrhea is noted secondary to straining and mucosal irritation, and owners may erroneously present these cats for diarrhea. Clinical signs may be present for weeks to years. Physical examination reveals a distended colon, usually with no other abnormal findings, although dehydration is often present. The differential diagnosis for idiopathic megacolon should include causes of acquired colonic distention and constipation such as extraluminal constriction (i.e., pelvic fractures or neoplasia), intraluminal constriction (i.e., foreign bodies, impacted ingesta, neoplasia, or polyps), pseudocoprostasis (matting of hair and debris in the perineal area obstructing passage of feces), colonic or rectal stricture, atresia ani, perineal hernia, dyschezia causing reluctance to defecate (such as that due to inflammatory disease or wound of the rectoanal area), lumbosacral disease (i.e., trauma, stenosis, or deformities like those of the Manx cat), hypokalemia, dehydration, drug therapy (i.e., antacids, anticholinergics, antihistamines, barium sulfate, diuretics, narcotic analgesics, sucralfate, phosphate binders, or vincristine), and dysautonomia. Environmental stress or changes (unavailability of, dirty, or unwillingness to use litter box) as well as an inability to posture and use the litter box (e.g., due to hindlimb fractures, lumbosacral disease, hip or stifle arthritis, or luxating patella) may also lead to decreased bowel movements and subsequent constipation and colonic distention. See Chapter 40. Straining due to lower urinary tract disease, including urethral obstruction, must be differentiated from constipation, obstipation, or megacolon because some clients may mistakenly present these cats for constipation problems or vice versa.
Diagnosis Primary Diagnostics • History: The client should be questioned about any changes in the environment, the household, diet, whether the cat’s defecation seems painful, stool is segmented and hard, and if any current drug therapy is in use. • Neurologic Examination: A complete neurologic examination should be performed with close attention paid to the perineal area. See Chapter 307. Signs of lumbosacral disease, such as poor anal tone, easily expressible bladder, hindlimb weakness, or pain on lifting the tail or palpating the caudal spinal area, may be evident. If these signs are found, imaging (lumbosacral spinal radiographs with or without an epidurogram [see Figure 136-1]), computerized tomography (CT), or magnetic resonance imaging (MRI) should be The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 136-1 Lumbosacral disease is present in this cat that developed chronic constipation. Instability at L7 to S1 caused pain that made defecation painful. After the instability resolved with new bone formation, constipation was perpetuated by the size of the spondylitic lesion. Image courtesy Dr. Gary D. Norsworthy.
performed. Signs of diffuse autonomic dysfunction (e.g., megaesophagus or regurgitation, urinary incontinence, mydriasis, prolapsed nictitans, bradycardia, or decreased lacrimation) indicating the need for further evaluation of the autonomic nervous system may be seen in the rare event of dysautonomia. See Chapter 58. • Chemistry Profile and Urinalysis: These may reveal abnormalities in serum potassium, hydration status, or renal function. • Abdominal or Pelvic Radiographs: These are indicated to confirm diffuse colonic distention (i.e., colonic diameter greater than twice the length the body of L7; see Figures 136-2 and 136-3), look for masses and foreign bodies, search for evidence of stricture (i.e., colonic fecal distention in the cranial but not the caudal portion of colon), evaluate the pelvis for fractures (see Figure 136-4), and examine the lumbosacral area for obvious abnormalities. • Rectal Examination: This is best performed under anesthesia in conjunction with initial therapy (i.e., enema administration or manual colonic evacuation). The rectoanal area should be evaluated for rectal strictures, masses, wounds, and perineal hernias.
Secondary Diagnostics • Abdominal Ultrasound: This is indicated if radiographs or physical and rectal examination reveals the possibility of a mass, intestinal thickening, or foreign body. • Colonoscopy with Biopsy and Histopathology: This is indicated if the cat has a history of painful defecation or if radiography or rectal examination reveals the possibility of a colonic mass, stricture, or foreign body. Colonic evacuation and preparation with oral cathartic solutions (polyethylene-glycol solutions [GoLytely, Colyte, NuLytely] at 30 mL/kg PO via orogastric or nasogastric tube 18 to 24 and 8 to 12 hours prior to colonoscopy) are needed prior to performing colonoscopy.
323
(A)
(B)
(C)
Figure 136-2 (A) A diagnosis of megacolon is appropriate when the colonic diameter is greater than two times the length of the body of L7, as in this cat. The stool is extremely hard and dry and it has the radiographic density of bone. (B,C) This is an example of how distended the colon can become if not treated. Cats like this are usually critical. Image courtesy Dr. Alana Jenkins. Image courtesy Dr. Gary D. Norsworthy.
Figure 136-3 This 10-kg (22-lb) obese cat’s colon met the criteria of megacolon. The cat’s colon was extremely large, flaccid, and distended. He had an excellent response to subtotal colectomy. Image courtesy Dr. Gary D. Norsworthy.
324
Figure 136-4 Pelvic stenosis due to an old-healed pelvic fracture can cause chronic constipation leading to megacolon. Image courtesy Dr. Gary D. Norsworthy.
Megacolon
Secondary Therapeutics • Lactulose: This is an osmotic stool softener that may help in managing megacolon when used in combination with cisapride. The dose is 0.5 to 1.0 mL/kg q8 to 12 h PO. Some cats find the taste objectionable. • Subtotal Colectomy: This is an effective therapy for megacolon and should be recommended if medical management has failed on more than two or three attempts. See Chapter 249. When performed on cats with a pelvic stricture, the prognosis is not as good; continued medical management may be needed. When performed on cats with a prior history of fecal incontinence, notably Manx cats, severe fecal incontinence may return during the postoperative diarrheic period.
Therapeutic Notes
Figure 136-5 A large, hard stool-filled colon may compress the urethra at the entrance to the pelvic canal resulting in urethral obstruction. Image courtesy Dr. Gary D. Norsworthy.
Diagnostic Notes • Barium enemas may be helpful in identifying colonic strictures or masses but are usually less helpful than colonoscopy. • Abdominal radiographs may also reveal a firm, distended bladder due to urethral obstruction caused by pressure of the colon on the urethra. See Figure 136-5. • Other differential diagnoses for colonic distention or constipation must be excluded prior to making a diagnosis of idiopathic megacolon. See Chapter 40.
Treatment Primary Therapeutics • Treat Underlying Causes: The idiopathic form of this disease has no definable underlying cause, but many cases are secondary to another disease. • Enema Administration and Manual Colonic Evacuation: This is indicated as the initial step in the medical management of megacolon. This is best performed following prior subcutaneous or intravenous fluid administration and with the cat under anesthesia. The enema should utilize 15 to 20 mL/kg of warm water without soap or other additives (to minimize mucosal irritation and damage). The volume delivered should be expelled then repeated several times to completely empty the colon. Manual evacuation via abdominal palpation and rectal digital manipulation should be performed in conjunction with enema administration for maximal colonic evacuation. A small amount of water-soluble lubrication will help in removing feces. • Cisapride: This is a prokinetic motility enhancer that has proven effective in stimulating contraction of megacolonic smooth muscle and is the drug of choice in combination with stool softeners in the medical management of megacolon. The dose is 2.5 to 5 mg/cat q8h PO; it can be increased to 10 mg q8h PO. • Diet: Easily digestible, low-bulk diets are indicated in cats with megacolon. Supplementation with small amounts of fiber (e.g., psyllium [Vetasyl®, Metamucil®] at 1/2–1 teaspoons or about 1.7–3.4 g PO with food q12–24 h or canned pumpkin at 1–2 teaspoons PO with food q12–24 h) may help soften the stool and stimulate defecation; however, diets moderate to high in fiber often create excessive fecal bulk and complicate or worsen colonic distention.
• Assuring proper hydration by administering intravenous fluids at one-and-a-half times the maintenance dose (70–80 mL/kg per day) for 12 to 24 hours prior to anesthesia and enema will contribute to a safer anesthetic protocol and facilitate a more complete, faster, and easier colonic evacuation. Potassium should be supplemented within fluids if indicated. • Having the owner give fluids subcutaneously (150 mL two to three times per week) may aid in keeping the stool soft. • A large number of stool softeners, available commercially, can be used in combination with cisapride to attempt to medically manage megacolon. Stool softeners, laxatives, and diet change, in combination or alone (without cisapride), are rarely effective in the long-term management of idiopathic megacolon. • Medical management will be unsuccessful if colonic evacuation is not performed prior to initiating therapy. Performing post colonic evacuation abdominal radiography may be helpful in confirming complete evacuation. • Phosphate-containing enemas (e.g., Fleet® enemas) should never be used in the cat due to the potential for significant and possibly fatal hypocalcemia. • To reduce the risk of peritoneal contamination from fecal spillage into the surgery site, cats should not undergo colonic evacuation or enema administration within 12 hours prior to subtotal colectomy.
Prognosis Megacolon can often be controlled with long-term therapy with cisapride, stool softeners, and diet, although a large number of cats will require subtotal colectomy to prevent frequent recurrences of constipation or obstipation. Cats that respond to medical management may still have infrequent episodes of constipation or obstipation that require enema therapy. Significant postoperative complications occur in only 2% of cats that undergo subtotal colectomy and may include stricture at the surgical site, loss of vascularity to the bowel, and anastamosis dehiscence or peritonitis. See Chapter 249.
Suggested Readings Jergens AE. 2007. Megacolon. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 872–873. Ames, IA: Blackwell Publishing. Washabau RJ. 2005. The colon: dietary and medical management of colonic disease. In Proceedings of the 23rd Annual Veterinary Medical Forum, pp. 496–499. Washabau RJ. 2005. The colon: obstruction and hypomotility disorders. In Proceedings of the 23rd Annual Veterinary Medical Forum, pp. 493–495. Washabau RJ, Holt D. 2000. Feline constipation and idiopathic megacolon. In JD Bonagura, ed., Current Veterinary Therapy XIII: Small Animal Practice, pp. 648–652. Philadelphia: WB Saunders.
325
CHAPTER 137
Meningioma Sharon Fooshee Grace
Overview Meningioma, the most common primary brain tumor of cats, arises from connective tissue elements of the meninges. Intracranial meningiomas are more common than intraspinal ones, and the tumor is most often found in the meningeal covering of the cerebral hemispheres. Growth is by expansion or excavation of nearby brain tissue rather than by infiltration of tissue, thus explaining the typical slow onset of clinical signs. In cats, the tumor is typically benign, and its cause is unknown. Multiple tumors are present in about 15 to 20% of cases. There is no known breed disposition; old cats are more frequently affected than young cats. Males have a slightly greater incidence of meningioma than females. Neither the feline leukemia virus nor the feline immunodeficiency virus appears related to development of feline meningioma. Signs of neurologic disturbance may be acute or chronic in onset but are typically slowly progressive in nature. A change in behavior or mentation is commonly noted, including aggression, depression, or stupor. Physical examination is suggestive of a focal cerebral lesion. If circling occurs, it is toward the side of the lesion, although visual, postural, and proprioceptive deficits are contralateral to the tumor. Occasionally, the fifth and seventh cranial nerves demonstrate \ial deficits. Seizures, though not a consistent feature of this tumor, are usually generalized when they occur. Many cats have clinically silent meningiomas, and diagnosis is incidental.
Diagnosis
Figure 137-1 A meningioma (M) is present in this cat. Note the compression on the brain causing marked distortion. Surgical excision of the tumor was successful.
recommended when meningioma is strongly suspected. See Chapter 298. • Electroencephalogram (EEG): The EEG will not establish a definitive diagnosis of meningioma but occasionally can be useful in localizing a cerebral lesion.
Primary Diagnostics
Diagnostic Notes
• Minimum Data Base: Cats with signs of brain dysfunction should have a complete blood count, serum chemistry panel, urinalysis and, if warranted, a total T4. Because most affected cats are geriatric, blood tests may reveal concurrent problems and are recommended prior to anesthesia for special procedures. • Radiography: Radiographic changes are uncommonly seen; however, occasionally a calcified meningioma may be seen. Hyperostosis or erosion of the adjacent calvarium may be recognized. Chest radiographs are indicated to evaluate for metastatic, cardiac, or systemic illness. • Magnetic Resonance Imaging (MRI) and Computerized Tomography (CT) Scans: These advanced diagnostic imaging techniques are helpful in detecting the presence of an intracranial mass. See Figure 137-1.
• Other types of primary brain tumors and tumors that metastasize to the brain are usually more rapidly progressive than meningiomas.
Treatment Primary Therapeutics • Surgical Excision: Surgical excision of all visible tumor gives a good prognosis. This tumor grows so slowly that even if microscopic tumor remains, most cats will do well for a long period after surgery. One retrospective study suggested that adjunctive radiation therapy is only indicated when surgery does not remove all visible tumor cells or there is recurrence of the tumor. Tumor recurrence has been estimated at 20 to 25%.
Secondary Diagnostics
Secondary Therapeutics
• Cerebrospinal Fluid (CSF) Analysis: This rarely establishes the diagnosis of meningioma. Nonspecific findings of increased CSF protein and normal cell counts (albuminocytologic dissociation) may be reported. Occasionally, cell counts are increased. Cytology is usually normal. Collection of CSF may lead to herniation when intracranial pressure (ICP) is increased; therefore, this procedure is generally not
• Corticosteroids: Tumor-related cerebral edema may be temporarily managed with glucocorticoids. • Anticonvulsant therapy: Phenobarbital (2–4 mg/kg q12h PO) is the anticonvulsant of choice for cats with meningioma. Side effects of anticonvulsant therapy may appear similar to tumor-related signs.
Therapeutic Notes th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
326
• Only those experienced with cranial surgery should attempt to remove this tumor.
Meningioma
• Preoperative CT or MRI is recommended to identify the correct location for craniotomy. • The anesthetic protocol should strive to minimize increases in ICP. Ketamine should be avoided for this reason. Propofol (or an ultrashort-acting barbiturate) is preferred for induction because of the effect on ICP. Mildly hyperventilating the patient is also beneficial because it causes vasoconstriction and a decrease in ICP. • Brain herniation is a risk during the immediate postoperative period; the patient should be monitored carefully for signs of this complication.
Prognosis The prognosis is improved significantly when surgical intervention succeeds in localizing and excising the tumor. Up to 70% of cats have longterm control of their signs. Prognosis is guarded when the tumor cannot be removed or at least debulked.
Suggested Readings Adamo PF, Forrest L, Dubielzig R. 2004. Canine and feline meningiomas: Diagnosis, treatment, and prognosis. Compend Contin Educ Pract Vet. 26(12):951–966. Forterre F, Tomek A, Konar M, et al. 2006. Multiple meningiomas: Clinical, radiological, surgical, and pathological findings with outcome in four cats. J Fel Med Surg. 9(1):36–43. Gallagher JG, Berg J, Knowles KE, et al. 1993. Prognosis after surgical excision of cerebral meningiomas in cats: 17 cases (1986–1992). J Am Vet Med Assoc. 203(10):1437–1440. Troxel MT, Vite CH, Van Winkle TJ, et al. 2003. Feline intracranial neoplasia: Retrospective review of 160 cases (1985–2001). J Vet Intern Med. 17(6):850–859.
327
CHAPTER 138
Mesothelioma Fernanda Vieira Amorim da Costa
Overview Mesothelioma is a rare, usually malignant, tumor arising from the mesodermal cells lining the abdominal or thoracic cavities. Primary mesotheliomas have been reported in cats in the pleural surfaces, peritoneum, or pericardium, as well as throughout the abdomen with lung and mediastinal lymph node metastasis. It has a poor prognosis. Mesotheliomas are considered malignant due to their ability to seed the body cavity through fluid accumulation, resulting in multiple tumor growths. Distant metastasis is rare but may occur in the lungs, liver, kidneys, spleen, diaphragm, and mesenteric lymph nodes. To date no predisposing causes have been identified, but chronic inflammation and irritation may lead to neoplastic transformation of mesothelial cells. There have been too few cases in cats to link the development of mesothelioma with exposure to asbestos as has been done in dogs and humans. Clinical signs associated with mesothelioma depend on the body cavity implicated. The tumor occurs as a diffuse nodular mass or multifocal masses covering the surfaces of the body cavity involved. See Figure 138-1. The proliferation of malignant mesothelial cells results in fluid accumulation (i.e., pleural effusion or ascites), probably due to obstructed lymphatic drainage or secondary to inflammation induced by the tumor. Dyspnea is common due to pleural effusion or ascites. Abdominal distention may be acute or recurrent. Cardiac tamponade and coughing can occur if pericardium is affected. Other signs include pallor, anorexia, lethargy, emaciation, muscle wasting, and intermittent vomiting. Disseminated intravascular coagulation and thromboembolism can occur.
There is no gender predilection and affected cats range from 1 to 17 years age (median age 5 years). Siamese and domestic short hair cats are overrepresented. Three main histological types of mesotheliomas are described: epithelioid, fibrosarcomatous (or fibrous), and biphasic (or mixed) types. Histologically, differential diagnosis includes carcinoma, adenocarcinoma, and sarcoma.
Diagnosis Primary Diagnostics • Histopathology: Diagnosis requires adequate tissue sampling preferably through thoracotomy or laparotomy. Thoracoscopy and laparoscopy provide a less invasive way to evaluate these cases.
Secondary Diagnostics • Effusion Evaluation: Cytologic evaluation of fluid may be inconclusive because differentiating physiologic reactive mesothelial cells from neoplastic mesothelial cells is difficult. Usually, there are clusters of large pleomorphic round, oval, or polygonal mesothelial cells displaying anisocytosis, anisokaryosis with variably coarse and clumped chromatin, binucleate cells and mitoses, and an increased nuclear-to-cytoplasmic ratio. Nucleoli are prominent and large. Fluid usually is a modified transudate. See Chapter 288. • Radiography: Fluid can obscure details of abdominal and thoracic cavities. There may be pleural or peritoneal effusion, enlarged cardiac silhouette, generalized pulmonary interstitial pattern, and displacement of abdominal viscera if masses are large. • Ultrasonography: This modality may reveal masses on the organs, irregularly thickened pleural lining, particularly of the mediastinum, mesentery, and omentum, but only the surfaces of the viscera are affected. • Computerized tomography (CT): Scan of the thorax and abdomen can be performed to determine the presence of pleural and peritoneal thickening or masses. Abdominocentesis or thoracocentesis prior to performing CT scan may aid in the interpretation.
Diagnostic Notes • Ultrasound-guided biopsy may be difficult or impossible due to small size of the neoplastic tissues.
Treatment Primary Therapeutics Figure 138-1 An abdominal mesothelioma (arrow) 12 cm (8.5 in) in diameter is attached to the stomach, pancreas, and spleen. The intestine is plicated and cyanotic due to vascular compromise.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
328
• Chemotherapy: Palliative intracavitary carboplatin therapy remains the treatment of choice because excision of all of the neoplastic tissue is virtually impossible. The recommended dose is 180 to 200 mg/m2; it is diluted to a total volume of 15 to 30 mL to be infused intracavitarily. In cases of pleural effusion, the dose should be divided and administered equally into the right and left hemithoraces. After the procedure is complete, the patient should be gently rolled to aid in the diffusion of the chemotherapy. Mild
Mesothelioma
sedation may be indicated. The procedure should be repeated every 3 weeks. Although minimal systemic effect is expected, the patient should be monitored for leukopenia and renal toxicity. If large masses or metastasis are found, intravenous chemotherapy with doxorubicin, carboplatin, or mitoxantrone should be preferred.
Prognosis The prognosis of cats with mesothelioma is grave because there is no proven effective treatment for this disease.
Suggested Readings Secondary Therapeutics • Fluid Drainage: Although palliative, fluid removal may alleviate potentially life-threatening clinical signs and discomfort. • Anti-Inflammatories: Administration of oral piroxicam (0.3 mg/kg q48h PO) combined with palliative intracavitary carboplatin may improve survival. • Pericardectomy: This may palliate mesothelioma patients that present with cardiac tamponade.
Therapeutic Notes • No satisfactory treatment exists for mesothelioma. Radical excision may benefit some cats, but usually the tumors are too invasive at the time of diagnosis. • Chemotherapy is the treatment of choice for mesothelioma. Unfortunately, penetration of chemotherapy is only to a small depth (2–3 mm; 1/8 inch) so large masses will not be affected significantly. • Steroids may be used to improve clinical signs.
Garret LD. Mesothelioma. 2007. In SJ Withrow, DM Vail, eds., Withrow & MacEwen’s Small Animal Clinical Oncology, pp. 804–808. St. Louis: Saunders Elsevier. Moore AS, Ogilvie GK. 2001. Thymoma, mesothelioma and histiocytosis. In AS Moore, GK Ogilvie, eds., Feline Oncology: A Comprehensive Guide to Compassionate Care, pp. 389–397. Trenton, NJ: Veterinary Learning Systems. Sparkes A, Murphy S, McConnell F, et al. 2005. Palliative intracavitary carboplatin therapy in a cat with suspected pleural mesothelioma. J Fel Med Surg. 7(5):313–316. Spugnini EP, Crispi S, Scarabello A, et al. 2008. Piroxicam and intracavitary platinum-based chemotherapy for the treatment of advanced mesothelioma in pets: preliminary observations. J Exp Clin Cancer Res. 27:6.
329
CHAPTER 139
Metaldehyde Toxicosis Tatiana Weissova
Overview Metaldehyde is a neurotoxicant. Although cats are quite susceptible to this agent, only few toxicoses have occurred in cats. Metaldehyde, a tetramer of acetaldehyde, is used as a molluscacide worldwide and is the active ingredient in many commercial snail and slug baits. These are in the form of granules, powder, pellets, or a liquid. Bran and molasses are sometimes added to the bait to make it more attractive to snails and slugs, but these additives also attract dogs and cats. The concentration of metaldehyde in baits sold for domestic use is generally between 1.5% and 5.0% (United States), 1.5% to 2.0% (Australia), and up to 50% (Europe). Some baits may also contain other toxicants such as carbaryl or arsenic. In some countries (but not United States), it is also used as a solid fuel for camping stoves and lamps or small heaters. Metaldehyde is highly toxic by inhalation, moderately toxic by ingestion, and slightly toxic by dermal absorption. The major form of exposure is ingestion of molluscacides. The oral LD50 is 207 mg/kg body weight for cats. Metaldehyde and its metabolites are readily absorbed from gastrointestinal tract. They can also be absorbed from the lungs and skin. The exact mechanism of action is unknown, but gastric acidity promotes its hydrolysis to acetaldehyde. The metabolites get trapped in enterohepatic circulation, can cross the blood-brain barrier, and are excreted in urine and feces. Central nervous system (CNS) signs of metaldehyde toxicosis may be due to decreased brain concentrations of γ-aminobutyric acid (GABA), norepinephrine, and serotonin (5-hydroxytryptamine, [5-HT]) and increased monoamine oxidase (MAO) activity. Decreased GABA concentrations can lead to seizures and can increase mortality. Another contributing factor to morbidity and mortality is hyperthermia. When body temperature exceeds 42.2°C (108°F) all organ systems begin to experience cellular necrosis within minutes. Metaldehyde also affects electrolyte and acid-base balances, causing metabolic acidosis associated with CNS depression and hyperpnea. Clinical signs may develop within a few minutes or up to 3 hours after ingestion. Typical signs include anxiety, tachycardia, nystagmus (more likely than in dogs), mydriasis, hyperpnea, panting, hypersalivation, and ataxia. Vomiting, diarrhea, dehydration, tremors, hyperesthesia, continuous seizures, metabolic acidosis, rigidity, opisthotonos, and severe hyperthermia may be seen. External stimuli may initiate further seizure activity. Death from respiratory failure can occur within a few hours of exposure. These characteristic signs (seizures and hyperthermia) have led to the term “shake and bake syndrome.” Differential diagnoses may include other intoxications, such as strychnine, Compound 1080 (sodium monofluoroacetate), bromethalin, chlorinated hydrocarbons, organophosphates, zinc phosphide, methylxantines, lead, tremorgenic mycotoxins, illicit drugs (such as amphetamines), and nontoxic conditions (e.g., neoplasia, trauma, infection, and metabolic disorders).
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
330
Diagnosis Primary Diagnostics • History: The risk factors are exposure, possible exposure, or evidence of exposure and living in area with high prevalence of snails and slugs (coastal and low-lying areas). • Clinical Signs: Early signs are anxiety, panting, hypersalivation or vomiting, ataxia, tachycardia, nystagmus, stiff-legged gait. These are followed by muscle tremors, convulsions, spasms, opisthotonus, diarrhea, severe hyperthermia, acidosis, disseminated intravascular coagulopathy, respiratory failure, cyanosis, narcosis, and death. • Chemical Verification: Positive chemical analysis for metaldehyde in stomach contents, vomitus, plasma, urine, or liver with appropriate clinical signs is diagnostic. Samples must be kept frozen for analysis. Stomach contents may have a “chemical” odor (as formaldehyde).
Secondary Diagnostics • Complete Blood Count, Biochemistry, Urinalysis: Results from these tests are not specific or diagnostic; however, metabolic acidosis may be detected.
Diagnostic Notes • Possible complications include liver or renal dysfunction (several days after recovery from the initial signs), aspiration pneumonia, temporary blindness, and memory loss may occur.
Treatment Primary Therapeutics • No antidote exists for metaldehyde toxicosis. • Vomition: Induction of emesis should only occur if the patient is asymptomatic. It must be performed less than 30 minutes postingestion, and the cat must have no medical conditions precluding emesis. Never induce vomiting in a convulsing animal. Give 3% hydrogen peroxide at 1 to 5 mL PO per 2.25 kg (5 lb) PO, not to exceed 15 mL. The dose can be repeated once. In cases of large ingestions, consider anesthetizing the patient and performing gastric lavage. Use a cuffed endotracheal tube to prevent aspiration. • Activated Charcoal: 1 to 4 g/kg PO is recommended. Administration is best with an orogastric tube. Dose may be repeated at half original dose every 6 to 8 hours. • Colonic Evacuation: Warm water enemas can help to remove metaldehyde from the lower gastrointestinal tract. • Control Seizures: (a) Give methocarbamol at 44.4 mg/kg slowly IV; give the first half of the calculated dose rapidly, but do not exceed an administration rate greater 2 mL/min. Wait until the cat relaxes, then administer to effect. Administration may be repeated as needed, but do not exceed a maximum daily dose of 330 mg/kg per day. (b) Diazepam (1–5 mg/kg IV to effect) or other anticonvulsants may be used on an as needed basis. Do not use depressants if animal is already depressed. • Correct Hyperthermia: Do not use aggressive cooling measures, such as ice water baths, because they may lead to hypothermia.
Metaldehyde Toxicosis
• Fluid Therapy: Correct dehydration, electrolyte imbalances, acidosis, and urine pH with lactated Ringer′s solution or Normosol-R (Abbott) and sodium bicarbonate. • Oxygen: Oxygen administration and ventilatory support should be used if necessary.
Therapeutic Notes • Use barbiturates for seizure control cautiously because they can compete with enzymes that degrade acetaldehyde leading to cardiac arrest.
Prognosis
therapy and survives the first 24 hours after exposure, the prognosis is good. Delayed or nonaggressive treatment may result in death within hours of exposure.
Suggested Readings Dolder LK. 2003. Toxicology brief: Metaldehyde toxicosis. Vet Med. 103(3):213–215. Gupta RC. 2007. Metaldehyde. In RC Gupta, ed., Veterinary Toxicology: Basic and Clinical Principles, pp. 518–521. New York: Elsevier. Plumlee KH. 2007. Metaldehyde poisoning. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 892–893. Ames, IA: Blackwell Publishing.
Prognosis depends mostly on the amount ingested, time to initiation of treatment, and quality of care. If the cat receives prompt aggressive
331
CHAPTER 140
Miliary Dermatitis Christine A. Rees
Overview Miliary dermatitis is a specific dermatologic reaction pattern having multiple etiologies. See Table 140-1. It is not a primary diagnosis, but the clinical presentation is basically the same in each case.
Diagnosis Primary Diagnostics • Clinical Appearance: Miliary dermatitis in cats consists of multifocal to diffuse small papular eruptions, which can exude serum and form a serous crust; they do not contain pus. These lesions can be generalized but tend to be located more dorsally. See Figure 140-1. Pruritus is variable. When pruritus is present excoriations or excessive grooming may occur. In severe cases, a peripheral lymphadenopathy is present.
Secondary Diagnostics • Identify Underlying Disease: A definitive diagnosis is based on the characteristic clinical presentation and history coupled with a workup to define the specific etiologic agent. Always start with a presumptive diagnosis of flea allergy dermatitis (FAD) and recommend strict flea control measures because about 80% of cats with miliary dermatitis are affected by FAD. Specific testing should be performed for dermatophytosis (Chapter 48) and cutaneous parasites (Chapter 201). Food reaction (Chapter 82) and intestinal parasites (Chapters 98, 195, and 207) should also be ruled out.
Diagnostic Notes • Skin biopsy for histopathology can help diagnose military dermatitis, but it is usually not useful for identifying the underlying cause.
TABLE 140-1: Primary Diseases Associated with Miliary Dermatitis Adverse food reaction Atopic dermatitis Dermatophytosis Flea allergy dermatitis (about 80% of cases) Folliculitis (bacterial or yeast) Intestinal parasitism Lice (Felicola subrotratus) Mites (i.e., Cheyletiella, Otodectes, and Notoedres, Trombicula autumnalis) Idiopathic miliary dermatitis
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
332
Figure 140-1 Miliary dermatitis in cats consists of multifocal to diffuse small papular eruptions. They usually exude serum and form a serous crust. They are not easily seen until the hair is shaved; however, they are easily detected by palpation.
Therapeutics Primary Therapeutics • Specific Treatment: Specific treatment for the underlying cause is the key to successful management.
Secondary Therapeutics • Anti-inflammatories: Many of the underlying causes of miliary dermatitis respond, at least temporarily, to corticosteroids. Prednisolone can be given at 1.1 to 2.2 mg/kg q12 to 24 h PO or a long-acting steroid injection can be used.
Prognosis The prognosis is dependent on identification and treatment of the underlying cause.
Suggested Readings Noxon JO. 1995. Diagnostic procedures in feline dermatology. Vet Clin North Am Small Anim Pract. 25:779–799.
CHAPTER 141
Mitral Valve Dysplasia Larry P. Tilley
Overview Mitral valve dysplasia (MVD) is one of the common congenital cardiac anomalies of the cat. A wide spectrum of lesions has been observed including abnormal papillary muscle structure and dysplasia of chordae tendineae and mitral valve leaflets. MVD may be seen in conjunction with other congenital abnormalities such as ventricular septal defects. The typical lesion is one of valvular incompetence that results in mitral regurgitation of blood into the left atrium. Mitral value insufficiency may be a component of hypertrophic cardiomyopathy due to distortion of the valve leaflets as the left ventricular walls thicken. Physical examination typically reveals a prominent (grade IV to VI) holosystolic regurgitant murmur over the mitral valve area. The cardiac impulse may also be displaced due to significant cardiomegaly in association with ventricular volume overload. Cats may be presented for evaluation of a murmur heard during routine examination or may have developed signs of left-sided congestive heart failure (i.e., tachypnea or dyspnea). Weight loss may occur. Most affected cats exhibit a degree of fatigue during exertion.
Diagnosis
Treatment Primary Therapeutics: Congestive Heart Failure • Stress: Take all measures to minimize any stress to cats exhibiting respiratory distress (e.g., delay radiographs and catheter placement). • Facilitate Breathing: Thoracocentesis should be performed when pleural effusion (i.e., muffled lung sounds) is suspected. Care must be taken to minimize stress during this procedure or the net result will be negative. • Furosemide: This diuretic should be administered when pulmonary edema is present. In the crisis setting, give 2 to 4 mg/kg IV initially, and then give 1 to 2 mg/kg q4 to 6h IV or IM until the edema has resolved. Furosemide is often continued as needed (6.25–12.5 mg q12–24h PO) to control edema formation. • Nitroglycerin: Six mm (1/4 in) of nitroglycerin paste should be applied to a hairless area q4 to 6h until the edema has resolved. If the skin is cold, vasoconstriction will be present so absorption is poor. Warm an area of skin prior to applying nitroglycerin paste. • Oxygen: Administer by face mask, if tolerated, or by oxygen cage or tent (50% oxygen).
Primary Diagnostics
Secondary Therapeutics
• Radiography: Prominent left atrial enlargement occurs with variable left ventricular enlargement. There may be enlargement of the pulmonary veins, venous congestions, and pulmonary edema. Pleural effusion is uncommon. • Echocardiography: Left atrial enlargement can be present. Dysplasia of the mitral valve leaflets (i.e., shortened, malformed leaflets) and chordae tendineae are evident. There is variable left ventricular enlargement. Contractility is usually within normal limits or slightly increased. • Electrocardiography: Evidence of left ventricular enlargement (i.e., tall and wide R waves) and left atrial enlargement (i.e., widened P waves) may be seen. Atrial arrhythmias (i.e., atrial premature complexes) may also occur.
• Angiotensin Converting Enzyme Inhibitors (ACEi): Enalapril (0.25–0.50 mg/kg q24h PO) or benazepril (0.25–0.50 mg/kg q24h PO). • Thoracocentesis or abdominocentesis may be needed periodically.
Secondary Diagnostics • Doppler Echocardiography: This will demonstrate significant mitral regurgitation. The extent of the regurgitant jet, rather than the velocity, correlates well with severity.
Diagnostic Notes • Many cats present with signs of heart failure within the first 2 years of life, although it is not unusual for cats to survive for years without clinical signs when the lesion is mild.
Therapeutic Notes • Monitor renal function. • Surgical correction of the defect is associated with high morbidity and cost.
Prognosis The prognosis for cats with MVD depends on the severity of the valvular incompetence and degree of ventricular volume overloading. Cats with mild lesions usually remain asymptomatic and have a good prognosis. Cats with significant lesions and evidence of moderate-to-severe volume overload early in life have a guarded-to-poor prognosis and usually develop congestive heart failure.
Suggested Readings Strickland K. 2008. Congenital Heart Disease. In LP Tilley, FWK Smith, Jr., M. Oyama, eds., Manual of Canine and Feline Cardiology, 4th ed., pp. 236–238. St. Louis: Elsevier.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
333
CHAPTER 142
Murmurs Larry P. Tilley and Francis W. K. Smith, Jr.
TABLE 142-1: Comparison of Canine and Feline Areas of Cardiac Auscultation
Overview Murmurs are defined as vibrations caused by disturbed blood flow associated with high flow through normal or abnormal valves or with structures vibrating in the blood flow. A murmur can include flow disturbances associated with outflow obstruction or forward flow through stenosed valves or into a dilated great vessel. Murmurs can also indicate flow disturbances associated with regurgitant flow through an incompetent valve, septal defect, or patent ductus arteriosus. In one study, heart murmurs were detected in 21% of asymptomatic domestic cats ages 1 to 9 years. In a recent study, color Doppler identified a new cause of variable parasternal systolic murmurs in cats. This new entity is termed dynamic right ventricular obstruction (DRVO) is a physiologic cause of systolic murmurs.
Dog
Cat
1. Mitral Area
L5 ICS at CCJ
2. Aortic Area
L4 ICS above the CCJ L2-4 ICS at left sternal border
L5-6 ICS, 1/4 VD distance from sternum L2-3 ICS just dorsal to pulmonic area L2-3 ICS, one-third to one-half VD distance from sternum R4-5 ICS, one-fourth VD distance from sternum
3. Pulmonic Area
4. Tricuspid Area
R3-5 ICS near CCJ
ICS, intercostal space; CCJ, costochondral junction; VD, ventrodorsal.
Diagnosis Differential Diagnosis • Other abnormal heart sounds (e.g., split sounds, ejections sounds, gallop rhythms, and clicks) • Normal and abnormal lung sounds and pleural rubs • Purring and growling • Anemia-induced murmur (usually pale mucous membranes are present)
Primary Diagnostics • Stethoscope: A pediatric or neonatal size (3/4 inch bell or 1/2 inch, respectively) chest piece is recommended for examining cats. Auscultation should include the parasternal area on both sides of the chest because these are the areas of greatest intensity and the only location soft murmurs may be heard. • Grading of Murmurs: Grade I, barely audible; Grade II, soft, but easily ausculted; Grade III, intermediate loudness (most hemodynamically important murmurs are at least grade III); Grade IV, loud, with palpable thrill; Grade V, very loud and audible with stethoscope barely touching the chest, with palpable thrill; and Grade VI, very loud and audible without the stethoscope touching the chest, with palpable thrill. • Configuration of Murmur: Plateau murmurs have uniform loudness and are typical of regurgitant murmurs such as mitral and tricuspid insufficiency and ventricular septal defect. Crescendo-decrescendo murmurs get louder and then softer and are typical of ejection murmurs such as pulmonic and aortic stenosis and atrial septal defect. Decrescendo murmurs start loud and then get softer and are typical of diastolic murmurs such as aortic or pulmonic insufficiency. • Location of Murmur: Mitral area, left fifth to sixth intercostal space one-quarter the ventrodorsal distance from sternum; aortic area, left second to third intercostal space just above the pulmonic area; pulmonic area, left second to third intercostal space one-third to one-half the ventrodorsal distance from sternum; tricuspid area:
right fourth to fifth intercostal space one-quarter the ventrodorsal distance from sternum. In general, murmurs in cats are best heard near the sternum. See Table 142-1. • Echocardiography: This is recommended when a cardiac cause is suspected and the nature of the defect is unknown.
Secondary Diagnostics • Thoracic Radiographs: These are useful for evaluating heart size and pulmonary vasculature in hopes of determining the cause and significance of the murmur. • Blood Pressure: This is recommended when renal disease or thyroid disease is present. • Complete Blood Count (CBC): Anemia is found in cats with anemic murmurs. Polycythemia is present in cats with right-to-left shunting congenital defects. Leukocytosis is expected with a left shift in cats with endocarditis.
Diagnostic Notes • The causes of systolic murmurs include DRVO, mitral and tricuspid valve endocardiosis, cardiomyopathy, anemia, valve dysplasia, septal defects, pulmonic stenosis, aortic stenosis, hyperthyroidism, systemic hypertension, and heartworm disease. The causes of continuous murmurs include patent ductus arteriosus. The causes of diastolic murmurs include mitral and tricuspid valve stenosis and aortic and pulmonic valve endocarditis.
Treatment Primary Therapeutics • Most cats are treated as outpatients unless heart failure is evident. Treatment decisions are based on the cause of the murmur and associated clinical signs. No treatment is indicated for a murmur alone.
Secondary Therapeutics th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
334
• Drugs and Fluids: Their use depends on the cause of the murmur and associated clinical signs.
Murmurs
• Heart Failure Treatment: If the murmur is associated with structural heart disease, signs of congestive heart failure (e.g., dyspnea) may develop. Treatment for heart failure can include diuretics, angiotensin-converting enzyme inhibitors, and cage rest.
Therapeutic Notes • Murmurs present since birth or murmurs diagnosed in kittens less than 3 months of age are generally associated with congenital defects or physiologic flow murmurs. • Acquired murmurs in geriatric cats are usually associated with cardiomyopathy, hyperthyroidism, or hypertension.
Suggested Readings Cote E, Manning AM, Emerson D, et al. 2004. Assessment of the prevalence of heart murmurs in overly healthy cats. J Am Vet Med Assoc. 225:384–389. Rishniw MJ, Thomas WP. 2002. Dynamic right ventricular outflow obstruction: A new cause of systolic murmurs in cats. J Vet Intern Med. 16:547–551. Smith FWK, Jr., Keene BW, Tilley LP. 2006. Rapid interpretation of heart and lung sounds: a guide to cardiac and respiratory auscultation in dogs and cats. St. Louis: Elsevier Saunders.
Prognosis The prognosis is variable depending upon the cause of the murmur.
335
CHAPTER 143
Myasthenia Gravis Paula Schuerer and Sharon Fooshee Grace
Overview Myasthenia gravis (MG) is a neuromuscular disease of cats, dogs, and humans that may be acquired or congenital in origin. It is characterized by localized or generalized weakness of skeletal muscle. The acquired form is an immune-mediated disease directed against nicotinic postsynaptic acetylcholine (ACh) receptors of skeletal muscle. The congenital form results from a lack of ACh receptors. Both forms are less common in cats than in dogs; only a few cases of congenital MG have been reported. Spontaneous remission of acquired MG is a common occurrence in dogs, but the incidence of remission is unknown in cats. The underlying cause for MG is unknown, although mediastinal masses (primarily thymoma) have been associated with development of acquired MG in a number of cats. It is speculated that thymus cells may develop ACh receptor-like surface antigens, which trigger an immune response, ultimately leading to development of MG. Administration of methimazole has been associated with reversible MG in several hyperthyroid cats. MG has one of three clinical presentations, depending upon muscles affected: generalized, focal, or acute fulminating. Generalized MG is the most common form in cats. Clinical findings may include gait abnormalities (i.e., stiff, choppy movement) and appendicular weakness that becomes more pronounced after exertion. Cervical ventroflexion was seen in about 20% of cats in one report. Additionally, muscles commonly involved with focal MG may be affected with generalized disease as demonstrated by depressed or fatigable menace or palpebral reflexes, dropped jaw, dysphagia, and megaesophagus. A period of rest permits the cat to resume normal activity, only to be followed by recurrence of weakness with further exertion. Megaesophagus is less common in cats with MG than in dogs, perhaps because of the lesser amount of esophageal striated muscle cats have (proximal 2/3 striated) relative to dogs (100% striated). Cats with focal MG display weakness in muscles of the face, pharynx, larynx, or esophagus, resulting in dysphagia, dysphonia, ptyalism, esophageal weakness, vomiting or regurgitation, megaesophagus, or inability to blink. Secondary aspiration pneumonia may result from megaesophagus or dysphagia. Appendicular weakness is not a feature of the focal form. All cats with the congenital form have had generalized signs. Acute fulminating MG presents with a rapid onset of both appendicular weakness and oropharyngeal disorders. This form can also be associated with respiratory distress secondary to diaphragmatic involvement. An increased relative risk for acquired MG has been demonstrated in Abyssinian and Somali cats compared to domestic shorthair cats. A bimodal age distribution is reported with the acquired form, with young adults aged 2 to 3 years and older cats aged 9 to 10 years comprising the majority of cases. Cats with the congenital form of MG usually show signs by a few weeks to a few months of age; there is no known breed or sex predisposition. Important differential diagnoses for MG should include disorders associated with muscle weakness, such as hypoglycemia, hyperthyroidism, organophosphate toxicity, thiamine deficiency, hypokalemia, and other neuromuscular disorders.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
336
Diagnosis • Clinical Findings: Presence of generalized muscle weakness, facial muscle weakness, mydriasis, photophobia, protrusion of nictitating membranes, xerostomia, exercise intolerance, dysphagia, dysphonia, megaesophagus, or aspiration pneumonia or presence of a cranial mediastinal mass would be consistent with feline MG. See Figure 143-1. • Serology: The gold standard test for diagnosis of MG is demonstration of serum auto-antibodies against muscle ACh-receptors. This is a species specific test. An antibody titer greater than 0.3 nM/L is diagnostic. The test should be performed prior to starting therapy and may be sent to the Comparative Neuromuscular Laboratory, University of California-San Diego (web site: http://vetneuromuscular.ucsd.edu/). The magnitude of antibody concentration and disease severity are not linearly correlated. Cats with congenital MG are negative for these specific antibodies. • Radiographs: All cats with suspected MG should have a thoracic radiograph examined for evidence of a cranial mediastinal mass (thymoma). Megaesophagus and aspiration pneumonia may also be evident.
Secondary Diagnostics • Screening Test: A short-acting anticholinesterase (AntiChE) agent (i.e., edrophonium chloride, Tensilon®) which demonstrates reversal or inhibition of postexertional weakness can be used to obtain a presumptive diagnosis. This test is not indicated for cats with localized MG. The dose is 0.25 to 0.50 mg/cat IV. A positive response is short-lived, often lasting less than 5 minutes. Atropine should be available in the event of a cholinergic crisis. There is a less predictable response to edrophonium challenge in cats than in dogs and falsenegative results have been reported. Also, subjective improvement may be seen with other neuromuscular disorders.
Figure 143-1 An anterior mediastinal mass, usually due to thymoma as seen in this cat, is often associated with MG. Image courtesy Dr. Gary D. Norsworthy.
Myasthenia Gravis
• Electrodiagnostics: Repetitive nerve stimulation is used to demonstrate a decremental response to repetitive nerve stimulation. Variable results are known to occur with this test. Single-fiber electromyography is another test that has been described in cats with MG. It is technically challenging but is more sensitive than nerve stimulation. • Muscle Biopsy: Congenital MG is diagnosed with muscle biopsy and demonstration of decreased ACh-receptors. Consult the lab cited previously for additional information.
Diagnostic Notes • Suspect cats that are seronegative should be retested in 1 to 2 months to check for seroconversion. • Hyperthyroid cats treated with methimazole may demonstrate weakness following initiation of treatment. The drug should be discontinued and, if there is resolution of weakness, alternative therapies for managing the hyperthyroidism should be considered.
Secondary Therapeutics • Aspiration Pneumonia: Treatment of aspiration pneumonia, if present, is essential. If the cat is stable a tracheal wash or bronchoalveolar lavage can be performed to culture for bacteria and to obtain an antibiotic sensitivity. Death from secondary aspiration pneumonia is common and needs to be aggressively addressed. • Nutritional Support: The presence of megaesophagus requires feeding in an upright position to allow gravity to assist the movement of food into the stomach. The usage of H2 blockers and motility modifying medication may aid in the treatment of esophageal irritation and gastric emptying. A feeding tube may be placed for temporary support. • Myasthenic Crisis and Cats with Megaesophagus: Cats in crisis and those at risk for aspiration may be treated with neostigmine methyl sulfate (Prostigmin®) at a dose of 0.125–0.25 mg/per cat q6–8h SC or IM. Overdosage may result in nicotinic (muscle weakness) or muscarinic signs (i.e., salivation, lacrimation, defecation, urination, or bradycardia).
Treatment Primary Therapeutics • Removal of Underlying Cause: Although evidence of benefit is still lacking, it is reasonable to consider treatment or removal of neoplastic disease, such as thymoma, which may be associated with MG. Because anesthesia poses significant risk, the disease should be controlled prior to surgery, when possible. The procedure should be performed by an experienced surgeon. • AntiChE Drug Therapy: AntiChE therapy is the cornerstone of maintenance MG treatment in other species, and cats also tend to show a good response, though therapy must be tailored to each animal. Pyridostigmine bromide (Mestinon®) is given at 0.1 to 0.25 mg/kg q8 to 12h PO; ideally, a lower dose is initiated and then titrated to effect. The syrup formulation or a compounded liquid is preferred for cats because of the small dose needed. Overdosage of pyridostigmine may lead to onset of cholinergic signs so the dose should be reduced if these signs are seen; atropine should be available. To aid in absorption, pyridostigmine should be administered prior to feeding. • Immunosuppressive Therapy: Because cats tend to respond better to immunosuppression than dogs, glucocorticoids are often given alone or in combination with antiChE drugs. Steroid-induced exacerbation of muscle weakness (typical of dogs with MG) is not seen in most cats. The usage of therapy must be delayed if aspiration pneumonia is present. The prednisolone dose must be tailored to the patient but a starting range of 1 to 4 mg/kg q24h PO has been reported. Therapy should be decreased as possible. If signs of weakness develop, steroid therapy should be discontinued.
Therapeutic Notes • It is important to avoid drugs that may potentially interfere with neuromuscular transmission. These include (but are not limited to) aminoglycosides, tetracyclines, clindamycin, ciprofloxacin, calcium channel blockers, pyrantel pamoate, propofol, and phenothiazines. • Response to cyclosporine therapy has been anecdotally reported. • Cats are sensitive to antiChE drugs; care should be exercised with administration of all such medications.
Prognosis Some cases will have spontaneous remission and thus not require lifelong treatment. The presence of aspiration pneumonia complicates the treatment and downgrades the prognosis. In cases not involving aspiration pneumonia, the prognosis is generally good. The fulminant form of MG has a grave prognosis.
Suggested Readings Dickinson P, LeCouteur R. 2004. Feline neuromuscular disorders. Vet Clin North Amer. 34(6):1307–1359. Ducote J, Dewey C, Coates J. 1999. Clinical forms of acquired myasthenia gravis in cats. Compend Contin Educ Pract Vet. 21(5):440–447. Shelton G. 2002. Myasthenia gravis and disorders of neuromuscular transmission. Vet Clin North Amer. 21(1):189–206. St. John L. 2002. Pyridostigmine: pharm profile. Compend Contin Educ Pract Vet. 24(2):92–94.
337
CHAPTER 144
Mycobacterial Diseases, Rapidly Growing Sharon Fooshee Grace Overview Mycobacteria are nonmotile, nonspore-forming, acid-fast, aerobic bacilli. Ubiquitous in nature, they are noted for wide variations in host affinity and pathogenicity. They are phagocytized by macrophages, evoking a granulomatous or pyogranulomatous host response. They grow intracellularly, a situation that makes it difficult to resolve infection with some forms of mycobacteria. In recent years, molecular diagnostics have allowed for improved precision in characterization of various mycobacterial species; this new technology may improve therapeutic outcomes in the future. Cats are susceptible to infection by a number of mycobacterial organisms and several mycobacterial categories have been identified in the species, including infection with slow growing mycobacteria (which may or may not produce tubercles); infection caused by rapidly growing mycobacteria (previously called “opportunistic” or “atypical” mycobacteria), and feline leprosy syndrome. Cats with mycobacteriosis are usually presented for care because of nodular skin lesions that may have ulcers or draining tracts. Rapidly growing mycobacteria (RGM) include the following groups: Mycobacteria fortuitum, the Mycobacteria chelonae and Mycobacteria abscessus group, the Mycobacteria smegmatis group, and a variety of other species. The M. fortuitum group has been reported as the most common mycobacterial species of North American cats, whereas M. smegmatis is most commonly reported in Australian cases. The RGM are not noted for having significant virulence for humans or animals and, once introduced into a host, are typically contained by the immune system. They may spread locally but do not usually disseminate via the blood or lymphatics unless the host is severely debilitated. Risk of transmission to humans is small. Three different clinical syndromes have been described in cats (and dogs): (a) mycobacterial panniculitis; (b) pyogranulomatous pneumonia; and (c) disseminated disease. The latter two syndromes are uncommon in cats and will not be addressed here. The panniculus is the subcutaneous deposit of adipose tissue on the caudal ventral abdomen and inguinal area of cats; it is especially prominent in obese cats. Opportunistic infection of the panniculus by RGM is infrequently seen though it is not rare. It most often results from a penetrating injury of the skin, especially when contaminated by soil. Inoculation of mycobacteria through a scratch or by claws during a catfight are considered common scenarios for establishment of infection. Feline RGM organisms have a predilection for adipose tissue and the panniculus provides a favorable environment for their growth. In two reports, feline RGM infection was said to be more common in young-tomiddle aged female cats, although this was not supported in another study. The female sex predisposition is thought related to the tendency of female cats to become obese. RGM infection is not associated with concurrent immunosuppressive disease in reported cases. At some point after infection is successfully established, a nodular lesion develops at the site of initial injury; alopecia and ulceration eventually develop over this primary nodule. Punctate fistulous tracts with a serous to seromucoid discharge are observed in and around the nodule, distinguishing this disorder from the typical cat bite
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
338
abscess, which has a purulent fetid exudate. Near the fistulae, purplish pinpoint lesions or depressions develop, representing thinning dermis overlying accumulations of pus. Lesions increase in size and depth and spread beyond the area of the panniculus to adjacent dermal and subcutaneous tissues; muscle tissue may also become involved. In many cases, the lesions remain regionalized but expand to the limbs, flanks, and abdomen. Affected cats do not appear systemically ill. Owners may report that the lesions have been present for months (or longer). Important differential diagnoses for RGM infection of the panniculus include but are not limited to vitamin E deficiency (pansteatitis), foreign body, actinomycosis, nocardiosis, sporotrichosis, systemic mycoses, leprosy syndrome, mycetoma from Microsporum canis, L-form bacterial infection, and neoplasia.
Diagnosis Primary Diagnostics • Physical Examination: Cats infected with RGM often do not show signs of systemic illness. However, low-grade fever, weight loss, localized pain, and lethargy may be seen, in addition to the cutaneous draining tracts. See Figure 57-1A. • Sample Collection: Samples of pus obtained by fine-needle aspiration of a closed, nondraining subcutaneous pocket of fluid are especially helpful. If necessary, the cat should be sedated or anesthetized to facilitate aspiration of pus. Ultrasound may be helpful in locating appropriate sites for sampling. The skin should be disinfected with 70% ethanol prior to sample collection to avoid sample contamination by other organisms. The fluid sample may be submitted for cytology and culture, and in many cases, will obviate the need for histopathology. Exudate from draining lesions does not provide a desirable sample because of growth of secondary invaders. • Cytology: Smears of exudate may be stained with Romanowskytype “quick stains.” Granulomatous to pyogranulomatous inflammation is evident. The bacilli may be difficult to find and may appear as intracellular “ghosts” because they stain poorly or not at all. See Figures 282-3 and 282-4. • Culture: Fluid or deep tissue biopsies may be submitted for culture. It is important to contact the diagnostic lab prior to sample collection to assure that samples are appropriately collected and maintained for submission. Commercially prepared mycobacterial culture bottles are available at many labs. Alternatively, a syringe with fluid may be submitted after capping the needle with a sterile cover. • Gram Stain: Smears of exudative material will stain gram-positive. • Acid-Fast Stain: Smears of exudative material show acid-fastness. This does not distinguish RGM from other mycobacterial diseases.
Secondary Diagnostics • Histopathology: Histopathology may not be needed if an acceptable subcutaneous fluid sample can be collected for cytology and culture. If tissue is submitted, clinical suspicion of mycobacterial disease should be indicated to the pathologist. Submit a deep-tissue biopsy. • Retroviral Testing: The retrovirus status of cats with draining tracts and nodules must be known. Feline leukemia virus and feline immunodeficiency virus testing is always indicated.
Mycobacterial Diseases, Rapidly Growing
• Complete Blood Count, Biochemical Profile, and Urinalysis: No pathognomonic findings are associated with RGM infection. Changes are typically those of chronic inflammation, such as a mild nonregenerative anemia, inflammatory leukogram, and hyperglobulinemia. Occasionally, a cat is found with the hypercalcemia of granulomatous disease. • Mycobacterial Susceptibility Testing: Antimicrobial susceptibility testing is available at the National Jewish Medical and Research Center in Denver, CO. The health professionals phone number is 1-800-222-5864 and the web link is http://www.njc.org/patientinfo/progs/med/mycobacteria/index.aspx. • Molecular diagnostics: Determination of specific variants of mycobacteria is available through some diagnostic laboratories. State and commercial diagnostic laboratories can provide information about current availability of these tests.
clarithromycin. Many cats will show improvement after a few weeks of therapy, but it is reasonable to consider that most patients will need 3 to 6 months of therapy, or at least 1 month beyond resolution of clinical signs. • Surgical Excision: Surgically excising the affected area can hasten recovery, but it should be seen as an adjunct to antimicrobial therapy. Antibiotics should be started prior to any surgical procedure to maximize the chance for healing of the surgical incision by primary intention. Failure to do so inevitably results in failure and catastrophic wound dehiscence.
Secondary Therapeutics • Medical Approach Only: Some cats respond well enough to antimicrobial therapy alone that surgical excision of infected tissue is not needed.
Diagnostic Notes • When cats with chronic, nonhealing, nodular or draining lesions fail to respond to antimicrobial therapy, it should raise one’s index of suspicion for RGM infection.
Treatment
Therapeutic Notes • Do not give immunosuppressive therapy to cats with RGM infections. • Some have advocated prophylactic therapy with doxycycline for penetrating wounds, especially of the panniculus. Such therapy may prevent successful infection with RGM.
Primary Therapeutics • Antimicrobial Therapy: Long-term therapy with one or more antimicrobials offers the best chance for a cure. In severe cases, this will still be insufficient to effect resolution of the disease. Susceptibility testing is critical for selection of the most appropriate drugs for therapy (see “Secondary Diagnostics”). It is important to note that the same organism appears to behave differently depending on geographic location; thus, the need for culture and sensitivity cannot be overemphasized. Fluoroquinolones have good tissue penetration and will accumulate intracellularly. Enrofloxacin has been recommended at 5 mg/kg q24h PO for a duration of 12 to 52 weeks. Clarithromycin has shown success in treating these infections and is the drug of choice for empiric therapy in the United States, pending lab results. Clarithromycin may be used at 62.5 mg/cat q12 to 24h PO for 12 to 52 weeks. Doxycycline is a more affordable drug but may be associated with occasional esophageal stricture unless owners are vigilant about providing food or a bolus of water after each administration. Doxycycline is recommended at 5 to 10 mg/kg q12h PO for 12 to 52 weeks. Some dermatologists routinely combine enrofloxacin and doxycycline and these drugs, alone or combined, are considered firstline therapy in Australia. Doxycycline should not be combined with
Prognosis Prognosis varies from guarded to good, depending on successful identification of the organism, selection of the appropriate drug, adequate duration of therapy, and removal of devitalized tissue, where indicated. The risk of RGM being transmitted from cats to humans is considered small so this concern should not prevent therapy from being provided.
Suggested Readings Horne K, Kunkle G. 2009. Clinical outcome of cutaneous rapidly growing mycobacterial infections in cats in the Southeastern United States. J Fel Med Surg. 11(8):627–632. Malik R, Martin P, Wigney D, et al. 2006. Infections caused by rapidly growing mycobacteria. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 482–488. Philadelphia: Saunders Elsevier. Manning TO, Rossmeisl JH, Lanz OI. 2004. Feline atypical mycobacterial panniculitis: Treatment, monitoring, and prognosis. I 99(8):7054–712. Rossmeisl JH, Manning TO. 2004. The clinical signs and diagnosis of feline atypical mycobacterial panniculitis. Vet Med. 99(8):694–704.
339
CHAPTER 145
Myiasis Elizabeth Macdonald
Overview Myiasis in cats is caused by infestation of fly larvae (maggots). This condition occurs when an untreated wound or an unsanitary damp area attracts adult flies. Heavily matted hair, especially in the perineal region, can predispose cats to infestation. Urine, feces, and vaginal discharge can accumulate in these areas and harbor a scent that attracts insects. Subsequent secondary bacterial pyoderma can work to further promote fly strike. Geriatric long-haired cats are overrepresented as debilitation can lead to a lack of grooming followed by hair matting that retains urine and fecal material. Markedly obese cats are similarly affected due to their inability to groom the perineal area. Often times, cats in this condition suffer from neglect, usually based on ignorance rather than malice on the part of the owner. An understanding of the fly life cycle can aid a veterinarian suspecting abuse or neglect to determine the duration of the problem. Once flies become attracted to an area, they lay hundreds of eggs that hatch within 24 hours into first instar larvae. These larvae immediately begin to migrate into the tissue and feed on surrounding liquefied material or fluid. They then molt into second instar larvae after 24 hours and begin to swarm together and migrate further. After another 24 hours they molt into third instar larvae, their final larval stage. At this point the larvae grow, develop, and feed for approximately 48 hours before they leave the feeding source to pupate. Larval infection can cause extensive tissue damage creating an environment that predisposes the cat to secondary infection and, in severe cases, septic shock. In addition, ammonia toxicity has been reported in animals with heavy larval burdens. Larvae release ammonia in their secretory and excretory products, and absorption of these products into the bloodstream can cause symptoms of ammonia toxicity in the host.
(A)
Diagnosis Primary Diagnostics • Physical Examination: Diagnosis can be made by gross visualization of larvae in a wound. See Figure 145-1A. Because the larvae can migrate and burrow, the skin and subcutaneous tissue should be explored thoroughly for fistulas and tracts. Anesthesia should be used in stable patients with extensive lesions.
(B) Figure 145-1 A, Copious numbers of fly larvae are seen in an open wound in the perineal region. B, After 5 days of treatment the wound is still sloughing. However, there are no fly larvae present, and healing is progressing well. The cat made a full recovery.
Secondary Diagnostics • Minimum Data Base: Cats suffering from myiasis should be fully evaluated for concurrent and underlying disease. A minimum data base consisting of retroviral testing, complete blood count, serum chemistries, and urinalysis is warranted.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
340
Treatment Primary Therapeutics • Stabilization: Patient stabilization is the first step in treatment. Because infested cats are often severely depressed, debilitated, and potentially septic, antibiotics, intravenous fluids, and pain management should be initiated. • Wound Care: Wounds should be attended to with great care and attention. Hair surrounding lesions should be clipped; manual removal of larvae is preferred. Vigorous flushing with a dilute
Myiasis
antiseptic solution will remove many superficial and more deeply located larvae. If using hemostats or forceps to remove larvae, caution should be taken not to break the larvae because protein released can cause anaphylaxis. Topical pyrethrin sprays can be applied to aid in removal of larvae but should be used judiciously.
Secondary Therapeutics • Nitenpyram (Capstar®): This drug has been reported to be effective at killing fly larvae when given orally. It can also be dissolved in water and given rectally in anesthetized or severely debilitated animals. The dose for nitenpyram in cats is 1 tab (11.4 mg) per 0.9 to 11.4 kg (2–25 lbs). • Ivermectin: This drug may be effective at killing fly larvae and is usually dosed at 200 µg/kg SC once.
wound care for the skin and subcutaneous tissue to heal. See Figure 145-1B. Owners should be counseled regarding the time, care, and costs associated with treating extensive wounds.
Prognosis The prognosis depends on the extent of the wounds, if underlying disease is present, and the presence of sepsis.
Suggested Readings Anderson G, Huitson NR. 2004. Myiasis in pet animals in British Columbia: The potential of forensic entomology for determining duration of possible neglect. Can Vet J. 45:993–998. Schnur HJ, Zivotofsky D, Wilamowski A. 2009. Myiasis in domestic animals in Israel. Vet Parasit. 161:352–355.
Therapeutic Notes • Because of the extent of the wounds created by larval infection, it can often require surgical intervention followed by several weeks of
341
CHAPTER 146
Nasal Discharge Gary D. Norsworthy
Overview A nasal discharge that is present for over 30 days is deemed to be chronic. There are at least eight types of diseases that may be responsible, so a systematic diagnostic approach is important. The nature of the discharge is not indicative of the etiology; the presence of blood in the discharge does not correlate as strongly with neoplasia in the cat as it does in the dog. Affected cats usually have periodic episodes of severe sneezing. Most cats are not systemically affected with the exception of cats with fungal infections or neoplasia.
Diagnosis Differential Diagnoses Many disease processes need to be considered for the cat with a chronic nasal discharge. See Table 146-1.
the pharynx. It is important that a cuffed endotracheal tube be in place. • Polymerase Chain Reaction (PCR) Testing: PCR tests are available for several of the likely pathogens including Chlamydophila, calicivirus, herpesvirus, Bordetella, and Mycoplasma. Samples collected from the nasal cavity or deep in the oropharynx can be submitted. Conjunctival samples are also frequently requested. Contact your laboratory for submission and shipping requirement. • Endoscopy: A 2-mm rhinoscope can permit visualization of some aspects of the cranial aspect of the nasal cavity. See Figure 146-3. Endoscopy can also be used to view the nasopharynx. The Olympus ENF™ scope is suited for this because it has a small diameter insertion tube with a small flexion radius and a viewing angle of up to 160 degrees. It is passed through the oral cavity and retroflexed into the nasopharynx. • Rhinotomy: The nasal cavity can be explored surgically via an incision through the nasal bones. This procedure permits recovery of ample material for histopathology and the opportunity to remove foreign bodies and polyps. See Chapter 269.
Primary Diagnostics • Age of Onset: Cats with an age of onset of 6 years or less are more likely to have viral or bacterial infections or nasopharyngeal polyps. Cats with an age of onset of over 10 years are more likely to have neoplasia. The other diseases are not age-related. • Radiographs: Lateral, Open-mouth (see Figure 146-1), and rostrocaudal (skyline; see Figures 146-2A and 146-2B) views should be taken to localize the infection. It is important to know whether or not the frontal sinuses are involved. See Figures 147-1,2,3. • Culture and Cytology: After the site of the lesion is identified by radiographs, a 20- or 22-gauge disposable needle is drilled through the hard palate into the lesion. See Chapter 305. If this is not feasible or successful, a 3.5 French catheter is passed 1 to 2 cm (3/8 to 3/4 inch) into the nasal cavity and 10 mL of saline is flushed through the nasal cavity. The material is caught on a 2 × 2-inch gauze square in
Secondary Diagnostics • Traumatic Nasal Flush: This procedure is used to recover material for histopathology. The catheter should not be advanced past the medial canthus of the eye to prevent damaging the brain. • Viral Isolation: This procedure is useful if it can be performed properly. Contact your laboratory for specific instructions. In general, virus isolation is significantly slower and less sensitive than PCR testing. • Fungal Serology: False-negatives are common, but high or increasing titers are indicative of fungal exposure (though not necessarily disease). Generally, titers for cryptococcosis are more reliable than those for other fungi.
TABLE 146-1: Known Causes of Chronic Nasal Discharge Viral Infections Feline herpesvirus Feline calicivirus Bacterial Infections Pseudomonas Proteus Staphylococcus Chlamydia Bartonella Fungal Infections Cryptococcus Sporothrix Histoplasma
Neoplasia Adenocarcinoma Lymphoma Fibrosarcoma Others Parasites Cuterebra Inflammatory Polyps Foreign Body Food Allergy Atopy Dental Disease
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
342
Figure 146-1 For the open-mouth view of the nasal cavity the cat is positioned in dorsal recumbency with the mandible pulled to a 90-degree angle from the hard palate. The hard palate is positioned parallel to the X-ray cassette or table top. Gauze strips are used for positioning. The arrow simulates the direction of the X-ray beam.
Nasal Discharge
(A) Figure 146-3 This radiograph shows the depth to which a 1.9-mm arthroscope can be passed into the nasal cavity.
Treatment Primary Therapeutics
(B) Figure 146-2 For the rostrocaudal view of the frontal sinuses, the cat is placed in dorsal recumbency with the nose pointed into the X-ray beam (arrow). The red dot marks the center of the X-ray beam. A, This view is looking from the side. B, This view is an obliqued look at the positioning. The red dot marks the center of the X-ray beam.
• Antibiotics: Antibiotics may offer temporary relief from most conditions because most are complicated with secondary bacterial infections. Fluoroquinolones are often effective because of their effectiveness against Pseudomonas aeruginosa. Azithromycin (10 mg/ kg q24h PO) is also effective in many cats. Others also may be effective on a short-term basis. Preferably, antibiotic selection should be based on culture and sensitivity testing. • Hydration: Fluid therapy, even when dehydration is not present, is helpful in thinning nasal secretions and making the cat more comfortable.
Therapeutic Notes
Diagnostic Notes • One should distinguish between unilateral and bilateral disease. Infectious diseases tend to be bilateral. Neoplasia and nasopharyngeal polyps tend to be unilateral. • Radiographs should be taken prior to nasal aspiration, nasal flush, and other invasive procedures because these will change the radiographic findings. • Radiographs are not sufficient to differentiate neoplasia from inflammatory polyps or infections. However, neoplasia often results in unilateral, bone-destructive lesions and deviation of or destruction of the nasal median septum. • Neoplasia often causes a distortion of the nasal planum or the entire nasal area due to bone destruction. • Inflammatory polyps may cause pressure necrosis of the nasal bone, resulting in draining tracts near the eye. • Food allergy (food reaction) is not a common cause of chronic rhinitis. However, a food trial will be rewarding in some cats. This should be performed if increased eosinophils are recovered from the nasal cavity by aspiration or surgical biopsy.
• Because there are so many differential diagnoses, it is imperative that a thorough workup be performed so that proper therapy may be instituted.
Prognosis The prognosis depends on the specific diagnosis. Many infections are treatable medically or surgically. Most tumors are adenocarcinoma or lymphoma. The former has a poor prognosis, and the latter has a good prognosis with chemotherapy. See Chapter 34. Inflammatory polyps in the nose are difficult to remove completely, so they often recur. If a foreign body is removed, foreign body-induced nasal discharge is curable. Atopy and food reactions are often manageable.
Suggested Readings Cooke K. Sneezing and nasal discharge. 2006. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 207–210. St. Louis: Elsevier Saunders. Lamb CR, Richbell S, Mantis P. 2003. Radiographic Findings in Cats with Nasal Discharge. J Fel Med Surg. 5(4):227–232.
343
CHAPTER 147
Nasal and Frontal Sinus Infection Gary D. Norsworthy
Overview Infections are common in the nasal cavity (rhinitis) and frontal sinuses (sinusitis) of cats. These two structures communicate through an ostium so infections that originate in the nasal cavity frequently ascend into the frontal sinuses resulting in rhinosinusitis. Primary sinusitis is rare. There are three common categories of infection: bacterial, viral, and fungal. All three are likely to be chronic and produce a nasal discharge. Several theories are related to the pathophysiology of these disorders. Some authorities feel that most disorders are idiopathic and due to a self-perpetuating, chronic inflammatory disease much like inflammatory bowel disease occurs in the gastrointestinal tract. Others feel that most begin as a chronic infection with the feline herpesvirus (FHV-1) or the feline calicivirus (FCV). The latter theory states that a chronic viral infection predisposes the cat to secondary bacterial or even fungal infections because the viruses cause permanent damage to the turbinates. The bacteria most commonly cultured include Pseudomonas aeruginosa, Proteus mirabilis, and Staphylococcus aureus. The role of Bartonella in chronic rhinitis is controversial. Many cats with rhinitis, sinusitis, and rhinosinusitis test antibody positive for the bacterium, but so do many asymptomatic cats. See Chapter 17. Most fungal infections are due to Cryptococcus neoformans, but histoplasmosis may also affect the nasal cavities. Underlying immunosuppression due to the feline leukemia virus (FeLV) or the feline immunodeficiency virus (FIV) has not been found to be a factor. The typical clinical signs are recurrent episodes of sneezing and a chronic purulent nasal discharge. Cats with fungal infections may progress to systemic signs of weight loss, inappetence, fever, and lethargy.
Figure 147-1 The right side of the nasal cavity has increased density (arrow), typical of infection or tumor. However, the unilateral nature of this cat’s disease increases the likelihood of neoplasia. This is an open-mouth ventral-dorsal view of the skull. See Chapter 146 for positioning.
Diagnosis Primary Diagnostics • Radiographs: Lateral, open-mouth, and rostral-caudal views should be taken to localize the infection. It is important to know whether the frontal sinuses are involved. Infectious, instead of neoplastic, diseases are more likely to produce bilateral lesions. See Figures 146-1, 146-2, and 147-1 through 147-3. • Culture and Cytology: After radiographs identify the site of the lesion, a transpalatine nasal aspiration is performed. If the site is chosen properly, a diagnostic quality sample may be obtained. See Chapter 146. If this is not feasible or successful, a 3.5 French catheter is passed 1 to 2 cm (3/8 to 3/4 inch) into the nasal cavity. Marks should be placed so it can be determined how far the catheter is passed. Flush 5 to 10 mL of saline through the nasal cavity. The material is caught on a 2 × 2 gauze square in the pharynx. It is important that a cuffed endotracheal tube be in place. See Chapter 305. • Polymerase Chain Reaction (PCR) Testing: PCR tests are available for the likely pathogens including Chlamydophila, FCV, FHV-1, Bordetella bronchiseptica, and Mycoplasma felis. Samples collected from the nasal cavity or deep in the oropharynx can be submitted. Conjunctival samples are also frequently requested. Contact your laboratory for submission requirement. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
344
• Histopathology: Material is recovered via a rhinotomy incision through the nasal bones. This approach should be considered if the previous ones do not recover a diagnostic sample. See Chapter 269.
Secondary Diagnostics • Traumatic Nasal Flush: This procedure is used to recover material for histopathology. The catheter should not be advanced past the medial canthus of the eye to prevent damaging the brain. • Fungal Serology: False-negatives are common, but high or increasing titers are meaningful. The Cryptococcus test detect antigen so it is more accurate than for other systemic fungal infections, which typically detect antibody titers.
Diagnostic Notes • The presence of blood in the nasal discharge does not strongly correlate with neoplasia as it does in the dog. • It is unusual for a primary bacterial infection to cause chronic rhinitis or rhinosinusitis. An underlying viral (or fungal) infection should be suspected even if it is not cultured, especially if the onset of rhinitis is in a young cat or follows an upper respiratory infection.
Nasal and Frontal Sinus Infection
(A)
Figure 147-2 The right frontal sinus has increased density (arrow), typical of infection or tumor. The right frontal sinus is normal. This is a rostral-caudal view of the skull. See Chapter 146 for positioning.
Treatment Primary Therapeutics • Antibiotics: The choice of antibiotic should be made based on culture and sensitivity. If this is not feasible, antibiotics should be chosen that are likely to be effective against P. aeruginosa. The most practical is as fluoroquinolone. Azithromycin (10 mg/kg PO q24h) is also a good empirical choice. • L-lysine: Some evidence suggests that this drug may be useful in treating acutely and cats latently infected with FHV-1 at a dose of 250 to 500 mg/cat PO q12h. Several palatable veterinary brands are available. • Antifungal Drugs: Several, including itraconazole, amphotericin B, and fluconazole, have been used for treating fungal rhinitis and rhinosinusitis. Treatment should continue 1 month past apparent resolution of the disease, which will often being a total of 6 months or more. However, some cats relapse even after aggressive and prolonged therapy.
(B)
Secondary Therapeutics • Nebulization: Many cats will respond to nebulization using the formula and procedure in Table 147-1.
Figure 147-3 A, The frontal sinuses (arrow) are superimposed and seen filled with an air density because they are normal. This is a lateral view of the skull. B, The frontal sinuses are superimposed. The increased density is typical of unilateral frontal sinus disease. This is a lateral view of the skull. C, The frontal sinuses are and appear to have bone density. This is typical of bilateral frontal sinus disease. This is a lateral view of the skull. See Chapter 146 for positioning.
(C)
345
SECTION 1: Diseases and Conditions
TABLE 147-1: Nebulization Therapy for Cats with Chronic Rhinitis* Nebulization Solution 1 mL gentamicin (100 mg/mL solution) 2 mL dexamethasone (4 mg/mL solution) 2 mL albuterol inhalation solution (0.083%) (only used for cats with concurrent lower respiratory disease) 2 mL acetylcysteine (20% or 200 mg/mL) 2 mL chromolyn (optional) (10 mg/mL) 90 mL saline solution (0.9%) The solution must be kept in the refrigerator and protected from light. Equipment Nebulizing unit Tubing and fluid chamber Hard plastic pet carrier (preferably airline style) Nebulizing solution Ice packs Towel Cotton balls Saran Wrap®
Nebulizer Setup Connect the tubing to the nebulizer unit. One end connects to the nebulizer and the other end connects to the fluid chamber at the bottom of the unit. Get the nebulizing solution from the refrigerator and fill the chamber with the proper amount. Place the “T” connection on top of the chamber, wet a cotton ball and stick it in one end of the T connection. Make a hole in the Saran Wrapped cage door only large enough for the other end of the T connection to fit through snugly. Place the cat in the carrier, shut the door, and turn on the nebulizer unit. Procedure Check the clock and nebulize the cat for 20 minutes. There should be a foggy mist coming out of the tubing inside the cage. When the nebulization session is finished, remove the cat from the carrier. Any leftover nebulizing solution can be poured back in the bottle for later use. The nebulizing solution must be stored in a refrigerator.
Carrier Setup Take the wire door off of the carrier, AND then wrap the door completely in Saran Wrap. Put the door back on the carrier and drape a towel over the other ventilation holes on the sides. Place another towel on the inside for the cat to lie on and get several ice packs from the freezer. Place them on the inside against the sides of the carrier with enough room for your cat to lie down. * Courtesy Charla L. Jones, DVM, DACVIM (Cardiology), Austin, Texas.
• Frontal Sinus Obliteration: If infection is present in the frontal sinuses, medical therapy will not be effective. The purpose of this procedure is to remove the frontal sinuses as a site of infection. See Chapter 254.
usually required. The prognosis for cats with fungal infections is variable. Some recover completely after several months of treatment, whereas others succumb to their infections if the infections become systemic.
Therapeutic Notes • Cats with viral and bacterial infections that are controlled may have periodic relapses requiring the use of antibiotics. • Cats with viral and bacterial infections usually do not have systemic signs. If they are not treated, they can be expected to live many years with their nasal discharge.
Prognosis The prognosis is guarded for cats with chronic viral and bacterial infections. Aggressive, long-term chronic or intermittent treatment is
346
Suggested Readings Cape L. 1992. Feline idiopathic chronic rhinosinusitis: a retrospective study of 30 cases. J Am Anim Hosp Assoc. 28:149–155. Gaskell RM, Dawson S. Other Feline Viral Diseases. 2005. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 5th ed., pp. 667–671. St. Louis: Elsevier Saunders. Miller CJ. 2007. Rhinitis and Sinusitis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 1210–1211. Ames, IA: Blackwell Publishing.
CHAPTER 148
Nasal Myiasis Sarah M. Webb
Overview The nasal bot fly (Oestrus ovis), is an insect, the larvae of which occur primarily in the nasal cavity of sheep and goats. In sheep, the adult fly deposits first instar larvae around the nostrils, from where they crawl into the nasal passages. First instar larvae persist for 2 weeks to 9 months before migrating to the frontal sinuses. Finally, fully grown third instar larvae leave the host and drop to the ground, where pupation occurs before hatching into adult flies. Hooks and spines on the larvae cause severe irritation and inflammation of the host mucosa with a marked hypersensitivity reaction. This myiasis occurs worldwide and has been identified on several occasions as an unusual parasite causing nasal myiasis in several other species. For example, O. ovis has been reported to cause severe nasopharyngeal irritation in humans. In affected individuals, there is an acute onset of discomfort and a “foreign body sensation” with extreme irritation of the throat, itching, and coughing followed by nasal, aural, and ocular symptoms. Similar findings have been reported sporadically in the dog, with sneezing as the most prominent clinical sign. Affected cats present with a typical history of roaming with access to outdoors areas populated by sheep. The onset of clinical signs is characteristically severe and sudden with dyspnea, moist coughing, and frequent and vigorous sneezing. Severe upper respiratory tract irritation and inflammation result in marked edema of the mucosa of the nasal turbinates. This can result in near complete occlusion of air flow through the nasal passages. Physical distress is obvious, although once the cat learns to open mouth breathe, its dyspnea improves. Coughing may subside after a few days. Other clinical signs may include vomiting and depression with a poor appetite. Nasal discharge is not an obvious feature of disease in the cat. The differential diagnosis includes acute feline viral upper respiratory disease, neoplasia, nasal polyps, and foreign bodies causing upper airway obstruction. Of these, usually only foreign bodies have a sufficiently abrupt onset to really fit in with the clinical picture.
Figure 148-1 Oestrus ovis: First instar larva viewed on anterior rhinoscopy of the nasal turbinates of a cat.
Diagnosis Primary Diagnostics • Endoscopy: Examination of the pharynx, nasopharynx, and nasal cavity using both anterior rhinoscopy (using a rigid arthroscope) and inspection of the nasopharynx and choanae with a retroflexed flexible endoscope (posterior rhinoscopy). First instar larvae of O. ovis can be seen as small white objects moving across edematous and moderately inflamed nasal mucosa, in association with small amounts of mucoid discharge. See Figure 148-1. • Larval Collection: The larvae should be collected and identified following a vigorous antegrade nasal flush using 5 to 10 mL aliquots of 0.9% sodium chloride or Hartmann’s solution. Gauze swabs are packed into the pharynx to collect the washings which contain the larvae. Larvae can be immediately examined microscopically with further laboratory identification as required See Figure 148-2.
Figure 148-2 Oestrus ovis: First instar larva recovered following saline irrigation of the nasal cavity of a cat.
Secondary Diagnostics • Minimum Data Base: Preliminary diagnostics including hematology and biochemistry profiles and radiographs of both the thorax and the nasal cavity are unlikely to be helpful.
Treatment Primary Therapeutics
th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Physical Removal: Initial treatment consists of a therapeutic flush using 0.9% sodium chloride. Saline irrigation of the nasal cavity
347
SECTION 1: Diseases and Conditions
is continued until washings are negative. This affords significant immediate relief of the acute clinical signs.
Secondary Therapeutics • Medical Therapy: An alternative or adjunctive treatment is ivermectin (0.2–0.3 mg/kg SC or PO) repeated two to three times every 48 hours. Owners should be warned this treatment is off label. • Other Options: Alternative treatments also likely to be effective include selamectin (administered topically per label directions) and oral nitenpyram (1 tab per 0.9–11.4 kg [2–25 lbs] q24h PO).
Therapeutic Notes • Clinical symptoms can take up to 2 weeks to resolve as the mucosal hypersensitivity reaction subsides. Thus, complete recovery is comparatively slow. • It may be prudent to use a broad-spectrum antibiotic such as amoxicillin clavulanate or doxycycline monohydrate to treat likely secondary bacterial infection associated with the infestation and death of the larvae. • Empiric treatment of cats with characteristic signs in an area populated by sheep may be prudent prior to anesthesia and rhinoscopy. The agent nitenpyram is ideally suited for such a trial, based on its safety, likely efficacy, and low cost. • The comparative efficacy of the various treatment options are not supported by much evidence based medicine. In humans, nasal irrigation with large volumes of saline as a sole treatment provided effective removal of the larvae with rapid relief of clinical signs. Ivermectin is widely used as an effective treatment of nasal myiasis in sheep (0.2 mg/kg SC) and has also been successfully used for the treatment of nasal myiasis due to O. ovis in humans as well as for
348
other parasites in the cat. However, occasionally cats can develop neurotoxicosis from administration of this drug at high doses. Selamectin has potential as it is a macrocylic lactone and is efficacious in treating a number of parasites in cats. Critically, it may also be useful as a prophylactic medication or as a therapeutic trial in cases where this diagnosis is suspected. Recent data concerning treatment of “fly strike” in cats likewise suggests nitenpyram is safe, fast and effective at killing insect larvae.
Prognosis With appropriate early treatment, the prognosis is excellent although there is no data for cats infected for longer periods prior to recognition of disease.
Suggested Readings De Souza CP, Verocai GG, Ramadinha RHR. 2009. Myiais caused by the New World screwworm fly Cochliomyia hominivorax.(Diptera: Calliphoridae) in cats from Brazil: report of 5 cases. J Fel Med Surg. 11(12):978–982. Fisher MA, Shanks DJ. 2008. A review of the off-label use of selamectin (Stronghold/Revolution) in dogs and cats. Acta Vet Scand. 25:50:46. Heath AC, Johnston C. 2001. Nasal myiasis in a dog due to Oestrus ovis (Diptera: Oestridae). N Z Vet J. 49(4):164. Macdonald PJ, Chan C, Dickson J, et al. 1999. Ophthalmomyiasis and nasal myiasis in New Zealand: a case series. N Z Med J. 112:445–447. Masoodi M, Hosseini K. 2003 The respiratory and allergic manifestations of human myiasis caused by larvae of the sheep bot fly (Oestrus ovis): a report of 33 pharyngeal cases from southern Iran. Ann Tropic Med Parasitol. 97(1):75–81.
CHAPTER 149
Nasopharyngeal Disease Arnold Plotnick
Overview Nasopharyngeal disease is a significant cause of upper respiratory signs in the cat. The nasopharynx lies dorsal to the soft palate, with the choanae marking the rostral border and the larynx marking the caudal border. A variety of disorders can affect the feline nasopharynx, including neoplasia, inflammatory polyps, nasopharyngeal stenosis, and infectious diseases. Although cats may present with nasopharyngeal disease alone, many have concurrent nasal cavity disease. Clinical signs in cats with nasopharyngeal disease include nasal discharge, sneezing, stertor, phonation change, open-mouth breathing, gagging, epistaxis, and ear discharge. Except for otic discharge these clinical signs may also be seen in cats with nasal disease only. The differential diagnosis list for cats with the clinical signs described previously is extensive, and includes infectious causes of rhinitis (i.e., bacterial, viral, or fungal), noninfectious causes (i.e., lymphoplasmacytic or allergic), foreign bodies in the nasal cavity, periodontal disease, oronasal fistulae, cleft palate, and pharyngitis. See Chapter 147. Because there is much overlap in clinical signs, it is recommended that all cats presenting for nasal disease undergo an oral and nasopharyngeal examination, especially in cats with stertorous breathing or a change in phonation because these signs are more prominent when there is nasopharyngeal involvement. Lymphoma and inflammatory polyps are the most common disorders of the feline nasopharynx.
Diagnosis Primary Diagnostics • History and Physical Examination: Lymphoma and other neoplasms are primarily seen in older animals (mean age 10.7 years) whereas inflammatory polyps are generally seen in younger cats (mean age 3 years). Cats with nasal disease alone are more likely to exhibit nasal discharge and sneezing compared to cats with nasopharyngeal disease; however, a higher percentage of cats with nasopharyngeal disease alone display stertor, weight loss and change in phonation. Unilateral or bilateral waxy otic discharge or an otic mass may also be present in cats with nasopharyngeal disease. • Oral Examination: Although a more thorough examination can be achieved with the cat under anesthesia, oral examination on an awake cat may reveal information regarding periodontal disease, large oronasal fistulae, cleft palate, and soft palate masses. Ventral deviation of the soft palate is common when a nasopharyngeal mass is present. • Nasopharyngeal Palpation: Digital palpation of the soft palate can be done in some cats without sedation. The majority of soft palate masses are digitally palpable in cats. If a mass is palpated, a biopsy specimen should be obtained. • Otoscopic Examination: The presence of an otic mass in the ear canal of a cat with signs of nasopharyngeal disease is suggestive of an inflammatory polyp or neoplasm that has extended from the nasopharynx through the tympanic bulla and into the external ear canal.
• Skull Radiographs: If no mass is palpated but nasopharyngeal disease is suspected based on clinical signs, radiographs may allow for visualization of medium or large-sized masses in the nasopharynx, especially because the palatine bone prevents palpation of masses in the hard palate region. See Figures 149-1A, 149-1B, and 149-2A. Unilateral or bilateral soft-tissue opacity within the tympanic bulla and sclerosis of the osseous bulla may be seen in cats with nasopharyngeal polyps that originate in the tympanic bulla or extend into it. See Chapter 158. • Fungal Serology: Positive results may be supportive of exposure or infection with fungal agents as a cause of nasopharyngeal disease; however, titers alone are rarely diagnostic and usually require fungal culture or cytology. • Bacterial Culture: They are rarely useful because cats have a wide range of normal commensal bacterial flora. Pure culture of an atypical or unexpected organism, however, suggests that the organism is a primary pathogen.
Secondary Diagnostics • Complete Blood Count (CBC): An important part of any preanesthetic workup of procedures requiring anesthesia (skull radiographs, computerized tomography [CT] scan, rhinoscopy, and so on) are required. The CBC may provide information suggestive of an etiology, for example, eosinophila in cases of allergic or parasitic disorders. • Chemistry Profile and Urinalysis: These tests rarely provide an etiology, but they are important components of any preanesthetic profile, should anesthesia be necessary • Oral Examination under Anesthesia: To fully evaluate the nasopharyngeal area for masses and other abnormalities, general anesthesia is required. Use of a dental mirror or a Snook ovariectomy hook helps facilitate visualization of the area above the soft palate. • Dental Probing and Cytology: Diagnosis of smaller, less obvious oronasal fistulae may require meticulous probing of the teeth under anesthesia. Fine-needle aspiration of space-occupying lesions may be performed as part of the oral examination. • Nasopharyngoscopy: Endoscopic evaluation of the nasopharynx should be considered in cats with signs of nasopharyngeal disease that do not respond to empirical therapy. A 1- to 2-mm diameter rhinoscope that retroflexes 160 to 180 degrees is necessary for proper examination. • CT Scan: A CT scan is useful in evaluating the feline nasopharynx. Both the nasal cavity as well as the more caudally located nasopharyngeal region should be imaged for proper evaluation. Masses dorsal to the hard palate, as well as the soft palate, are readily seen on CT scans. • Biopsy: Tissue biopsy should be performed if a mass is palpated on oral examination. Blind biopsy without evaluation of the nasopharynx is discouraged as this could lead to an inaccurate or missed diagnosis.
Treatment Primary Therapeutics
th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Inflammatory polyps may be removed with gentle traction through the external acoustic meatus or from the nasopharyngeal cavity. A surgical
349
SECTION 1: Diseases and Conditions
(A)
(A)
(B) (B)
(C) Figure 149-1 A, A mass can be seen in the nasopharynx on a high quality radiograph of the lateral view of the skull. B, The mass is highlighted with arrows. C, The mass, a lymphoma, was removed through a midline incision through the soft palate. Chemotherapy followed surgery. Images courtesy Dr. Gary D. Norsworthy.
350
Figure 149-2 A, The mass in the caudal aspect of the nasopharynx (arrows) of this cat is easier to see on radiographs because there is less bony superimposition. B, The mass, a mucocoele, is seen during surgical removal. The forceps at the bottom of the picture has everted the soft palate to give access to the mass. The cat’s tongue is at the top of the picture. Images courtesy Dr. Gary D. Norsworthy.
approach through the soft palate permits removal of masses in the nasopharynx. See Figure 149-1C. A total ear canal ablation (Chapter 274) or bulla osteotomy (Chapter 248) is necessary in most cases with otic involvement. Neoplasia is treated with surgery, chemotherapy, or radiation, depending on the type of cancer present. Infectious causes of nasopharyngeal disease are treated with appropriate antimicrobials. Cleft palate and oronasal fistulae (Chapter 265) are treated surgically. Periodontal disease is treated via professional dental prophylaxis. Presumed allergic or inflammatory causes of nasopharyngeal disease may benefit from corticosteroid therapy. Foreign bodies, such as a blade of grass (see Figure 149-3), may be removed with forceps after visualization (i.e., either direct, through the use of a dental mirror, or via rhinoscopy). Nasopharyngeal stenosis may be treated surgically or alternatively by balloon dilatation plus or minus stenting.
Nasopharyngeal Disease
Prognosis The prognosis depends on the cause of the nasopharyngeal disorder. Inflammatory polyps have an excellent prognosis if the entire polyp can be removed. The prognosis for cleft palate and oronasal fistulae is good with surgical correction; it is guarded without it. Surgical correction of nasopharyngeal stenosis has a fair prognosis, with recurrence of the stenosis a common occurrence; the prognosis for balloon dilatation and stent placement, however, is good. Most cases of nasopharyngeal neoplasia have a poor prognosis, except for lymphoma, for which the prognosis is fair to good. Infectious disorders of the nasopharynx have a variable prognosis, depending on the causative agent and the immune status of the patient. Fungal rhinitis has a fair to good prognosis; however, successful treatment may require months of continuous antimicrobial therapy. Viral infections of the nasal cavity and nasopharynx tend to be chronic and persistent in cats regardless of therapy; however, the prognosis for most cats is good.
(A)
Suggested Readings Allen HS, Broussard J, Noone K. 1999. Nasopharyngeal diseases in cats: a retrospective study of 53 cases (1991–1998). J Am Anim Hosp Assoc. 35:457–461. Demko JL, Cohn LA. 2007. Chronic nasal discharge in cats: 75 cases (1993–2004). J Am Vet Med Assoc. 230:1032–1037. Henderson SM, Bradley K, Day MJ, et al. 2004. Investigation of nasal disease in the cat—a retrospective study of 77 cases. J Fel Med Surg. 6:245–257. Hunt GB, Perkins MC, Foster SF, et al. 2002. Nasopharyngeal disorders of dogs and cats: a review and retrospective study. Compend Contin Educ Pract Vet. 24(3):184–199.
(B) Figure 149-3 This cat was presented for gagging for about one week. Nasal radiographs were normal; however, an endoscope retroflexed into the nasopharynx revealed a linear green object. A. A blade of pampus grass is seen being removed through an incision in the soft palate. B. The 7 cm long blade of grass is seen following removal. Images courtesy Dr. Gary D. Norsworthy.
351
CHAPTER 150
Neonatal Isoerythrolysis Sharon Fooshee Grace
Overview Neonatal isoerythrolysis (NI) is an immune-mediated blood disorder of newborn kittens. NI occurs in kittens with blood type A (or rarely, type AB) that are born to queens with blood type B. Colostral transfer of antibodies causes intravascular and extravascular hemolysis within the first few days of life. NI is more likely to occur in purebred cats than in domestic shorthair cats. Some cases of “fading kitten syndrome” (death within the first 2 weeks of life) may be attributed to NI, although the true incidence remains unknown. Other causes of fading kitten syndrome include complications from difficult birth (anoxia), hypothermia, congenital defects and hereditary disorders, infectious causes, and queen-related problems. Cats have one well-defined blood group system with three possible types: A, B, and, rarely, AB. Other feline blood groups are thought to exist, such as the newly discovered Mik group, but have yet to be fully characterized. Inheritance of blood type occurs in a simple dominant fashion via two alleles at the same gene locus. Type A is completely dominant over type B. Cats expressing blood type A may be genotypically homozygous (A/A) or heterozygous (A/B). Cats expressing blood group B are always homozygous (B/B) because type B is recessive to type A. Queens of blood type B possess high levels of naturally occurring alloantibodies to blood type A. These antibodies form spontaneously and are present regardless of previous transfusion. After parturition, these antibodies are secreted into the colostrum and later absorbed through the intestine of the suckling kitten. Type A and type AB kittens from matings between a type B queen and a type A or AB tom are at risk. At present, it is unknown whether the newly discovered Mik antigen and alloantibodies against it may lead to NI. Worldwide, blood type A is consistently the most common blood type. Domestic shorthair cats are typically type A, as are Siamese and their related breeds (i.e., Oriental Shorthair and Tonkinese). The proportion of blood type B can vary considerably depending on breed and specific geographic location. Note that the antigens in the feline AB blood group are not serologically related to the ABO blood group antigens found in humans.
Diagnosis Primary Diagnostics • Clinical Findings: Some kittens may die within a few hours and without any evidence of illness. Others may nurse for a day or two and then “fade” for no apparent reason or demonstrate reddish-brown urine (hemoglobinuria), icterus, tachypnea, and pallor due to anemia. Affected kittens may stop nursing, separate themselves from the litter, and appear weak. Necrosis and eventual sloughing of the tail tip, chromoproteinuric nephropathy (hemoglobinuria), and disseminated intravascular coagulation have been observed. • Complete Blood Count: Severe anemia may be found.
Secondary Diagnostics • Coombs’ Test: A positive Coombs’ test may be reported in some kittens, although this test is not needed for the diagnosis of NI.
Diagnostic Notes • Currently available in-house blood typing kits are affordable and user-friendly (RapidVetH® feline blood type determination kit, DMS Laboratories; Flemington, NJ, phone 1-800-567-4367). • All blood donor cats, blood recipients, and potential breeding cats should be blood typed. The testing card may be mounted in the patient record for future reference. • Newborn kittens can be blood typed with umbilical blood. • Significant variations in the severity of NI may occur within the same litter. This is presumably due to differences in colostral antibody uptake. • Testing for the new Mik antigen is available in the Hematology and Transfusion Lab at the University of Pennsylvania (phone 1- 215-73-6376).
Treatment Primary Therapeutics • Separation of Affected Kittens from Queen: Kittens showing signs of NI (pigmenturia is a key sign) should be removed from the queen as soon as problems are observed but can be returned to her in 24 to 48 hours. After the first day of life, intestinal permeability to antibodies is greatly diminished. • Kitten Support: During the period of separation, affected kittens may receive milk or colostrum from a type A queen to provide passive immunity. Even in later stages of lactation, protective antibodies will still be present in another queen’s milk and will benefit a newborn kitten. It is important to allow newborn kittens the chance to absorb antibodies while the gut is still permeable and they are still able to do so. • Supportive Care: Assessment and management for common concurring conditions, such as hypothermia, hypoglycemia, nutritional compromise, and fluid and electrolyte disturbances, may be necessary.
Secondary Therapeutics • Transfusion: Severely affected kittens may require blood transfusion or blood products (Oxyglobin®, if available). Washed type B blood may be most suitable during the first 1 to 2 days of life because the kitten has circulating anti-A antibodies from colostrum. After that, washed type A blood is preferred. Intraosseous administration of blood is recommended in most cases due to small size of the patient.
Therapeutic Notes The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
352
• Kittens that survive may be returned to their mother after 24 hours. They are no longer at risk for NI once the gut becomes impermeable to colostral antibodies.
Neonatal Isoerythrolysis
Prevention • NI can be prevented in two ways: (a) blood type both the queen and tom, allowing only type B queens and toms to mate; or, (b) remove type A and type AB kittens born to type B queens for the first 24 hours of life and support them with a type A foster queen or, less ideally, milk replacer.
Suggested Readings Knottenbelt CM. 2002. The feline AB blood group system and its importance in transfusion medicine. J Fel Med Surg. 4(2):69–76. Weinstein NM, Blais MC, Harris K, et al. 2007. A newly recognized blood group in domestic shorthair cats: The Mik red cell antigen. J Vet Intern Med. 21(2):287–292.
Prognosis Treatment of NI is often unsuccessful, resulting in significant death losses in kittens. It is a totally preventable condition if blood testing is performed prior to breeding of cats, especially purebred cats.
353
CHAPTER 151
Neurogenic Bladder Sharon Fooshee Grace
Overview Micturition is the physiological process of storage and complete voiding of urine. Normal function of the lower urinary tract (LUT) is dependent on a reciprocal relationship between the detrusor muscle of the bladder wall and the urethral sphincter muscles. Higher centers in the brain and brainstem organize the micturition reflex and oversee voluntary control of voiding. Disorders of micturition can be broadly classified as neurogenic or non-neurogenic in origin. Nonneurogenic causes are associated with obstruction, infection, hormonal imbalances (uncommon in cats), or anatomical abnormalities. Neurogenic causes occur with infectious, traumatic, neoplastic, and other types of lesions involving the higher brain centers, spinal cord, peripheral nerves, urinary tract muscles, or urinary tract neuroreceptors. Neurogenic disorders of the LUT can result in inappropriate voiding, inadequate storage of urine, incomplete voiding, or absence of voiding. Depending on the location of the lesion responsible for the disorder, neurogenic disorders may be classified as upper motor neuron (UMN) or lower motor neuron (LMN) in origin. An UMN bladder results from a lesion above the level of the sacral spinal cord segments. Voluntary control of urination is partially or completely lost. In time, urination may occur through sacral reflexes but without coordination from higher centers, such that reflex dyssynergia results and urination is interrupted, uncoordinated, and incomplete. The bladder is large and difficult to manually express if sphincter hypertonia is present, although occasionally sphincter tone is normal or decreased. Residual urine is retained to excess and urinary tract infections are common. A LMN bladder involves a lesion of the sacral spinal cord or bilateral lesions of the sacral nerve roots. Sphincter tone is decreased, and the bladder is distended, atonic, and easily expressed. Urine may constantly dribble from overflow. Bladder wall reflexes can initiate some detrusor activity, but because it is not coordinated with sphincter relaxation, detrusor-sphincter dyssynergia results.
Diagnosis Primary Diagnostics • History: The history should include information relative to the cat’s environment (indoor versus outdoor); onset and progression of signs; presence of behavioral changes; whether the cat attempts to urinate and has normal posture during urination; volume urinated and continuity of the urine stream; awareness of urination; ability to defecate normally; and, any known history of trauma. • Physical Examination: A complete physical examination should be performed. A neurologic examination is indicated to assess mental status, motor function (including that of the tail), perineal and anal sensation and tone, and sacral reflexes. Urination should be observed and residual volume measured, if possible. Most cats should have less than 2 mL of residual urine after normal voiding.
• Diagnostic Imaging: Radiographs may demonstrate a pelvic mass, urolith, or spinal abnormality. Ultrasound or a contrast study of the bladder and urethra may demonstrate a mass or obstructive lesion.
Secondary Diagnostics • Complete Blood Count, Biochemistry Profile, and Urinalysis: Overall health of the cat can be more completely evaluated if routine bloodwork is performed. Urinalysis and urine culture are an important part of the initial evaluation. • Serologic Testing: Feline infectious peritonitis (FIP) and toxoplasmosis may cause spinal cord lesions. Coronavirus screening will not diagnose FIP but can demonstrate coronavirus exposure. See Chapters 76 and 214. • Retroviral testing: Feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) testing should be considered. FeLV has been associated with urinary incontinence.
Treatment Primary Therapeutics • See Table 151-1. • To Increase Urethral Smooth Muscle Contractility: Internal sphincter tone may be increased with an alpha-adrenergic agonist, such as phenylpropanolamine (1.5–2.2 mg/kg q8–12h PO). Its efficacy is questioned, and it is contraindicated with hypertension, glaucoma, and heart disease. Ephedrine is an alternative therapy; it has been recommended at 2 to 4 mg per cat q8 to 12h PO. • To Decrease Detrusor Contractility: Cholinergic antagonists promote bladder relaxation and inhibit detrusor contractions. Propantheline is recommended at 5.0 to 7.5 mg per cat q24 to 72h PO. Side effects include dry mucous membranes, constipation, increased intraocular pressure, and urine retention. Oxybutynin is another anticholinergic drug that may be used; the dose is 0.5 to 1.25 mg per cat q12h PO. FeLV-associated incontinence is thought to respond to oxybutynin or other anticholinergic agents. • To Decrease Sphincter Hypertonicity: Unless urodynamic studies can determine whether the internal or external sphincter is causative, both sphincters should be pharmacologically managed. The internal sphincter can be managed with alpha-adrenergic antagonists, such as phenoxybenzamine (2.5–7.5 mg/cat q12–24h PO). The drug has a slow onset of action (several days) and may cause hypotension and tachycardia. Striated muscle of the external sphincter can be relaxed with diazepam (2–5 mg per cat q8–24h PO). Idiosyncratic hepatic necrosis occasionally occurs and is a risk with the oral form of diazepam. • To Improve Bladder Tone: Bladder atony can be improved with cholinergic drugs, but it is contraindicated if there is any obstruction of outflow; bladder rupture may occur in this situation. Bethanechol (1.25–7.5 mg per cat q8–12h PO) frequently has associated side effects, such as salivation, diarrhea, and abdominal pain due to smooth muscle cramping.
Secondary Therapeutics th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
354
• Manual Bladder Emptying: A distended bladder that cannot be emptied must be expressed or drained several times daily to prevent
Neurogenic Bladder
TABLE 151-1: Drug Dosages and Indications Indication
Drug
Drug Class
To increase urethral smooth muscle contractility (urethral incompetence) To increase urethral smooth muscle contractility (urethral incompetence) To decrease bladder contractility (bladder overactivity) To decrease bladder contractility (bladder overactivity) To decrease sphincter hypertonicity (urethrospasm or functional obstruction of smooth muscle) To decrease sphincter hypertonicity (urethrospasm or functional obstruction of striated muscle) To improve bladder tone (bladder atony)
Phenylpropanolamine
Alpha-agonist
Ephedrine
Alpha-agonist
Propantheline
Frequency
Route
q8–12h
PO
2–4 mg per cat
q8–12h
PO
Anticholinergic
5–7.5 mg per cat
q24–72h
PO
Oxybutynin
Anticholinergic
0.5–1.25 mg per cat
q12h
PO
Phenoxybenzamine
Alpha-antagonist
q12h
PO
Diazepam
Muscle relaxant
2–5 mg per cat
q8–24h
PO
Bethanechol
Cholinergic
1.25–7.5 mg per cat
q8–12h
PO
damage to the bladder wall. If manual expression is difficult, intermittent catheterization or placement of an indwelling catheter (attached to a closed drainage system) should be considered. An indwelling catheter carries more risk of infection than intermittent catheterization.
Dose Range 1.5–2.2 mg/kg
1.25–5 mg per cat
Prognosis Prognosis is dependent on identification, reversibility, client motivation, and appropriate management of the underlying case.
Suggested Readings Therapeutic Notes • Urinary tract infections are common in cats with neurologic dysfunction of the bladder. These must be aggressively managed to offer the best chance for resolution or improvement of the condition.
Lane IF. 2003. A diagnostic approach to micturition disorders. Vet Med. 98(1):49–57. O’Brien D. 1988. Neurogenic disorders of micturition. In Common Neurologic Problems. Vet Clin North Am, Small An Pract. 18(3):529–544.
355
CHAPTER 152
Nocardiosis Sharon Fooshee Grace
Overview Nocardiosis is a suppurative to pyogranulomatous condition caused by members of the family Nocardiaceae. The Nocardia genus now contains in excess of 30 named species. Nocardia asteroides is the most common isolate in cats in the United States; Nocardia nova, the most common isolate in Australia, has also been reported in several cats in California. It is an opportunistic organism that is ubiquitous in the environment, occurring in soil, water, and on plants. Infection usually results from direct inoculation into the skin by a penetrating injury (including fight wounds) or inhalation of aerosols containing the organism. Cats may carry the organism on their skin or claws. A recent report of 17 cases found that older male cats were over-represented. Clinical forms of disease vary with the site of infection, but the two most common syndromes in cats are cutaneous or subcutaneous disease and pyothorax or pneumonia. Peritonitis and disseminated disease are less often seen. With cutaneous or subcutaneous disease, early signs may resemble a nodule and, in time, develop into nonhealing chronic abscesses, draining tracts, and necrotic ulcers. See Figure 152-1. Appearance of the discharge resembles “tomato soup.” Lesions spread to adjacent tissues in a circumferential direction, possibly by lymphatics. Respiratory infection may involve the lung itself or only the pleural space; pleural infection leads to empyema (pyothorax) and accumulation of a reddish-brown exudate. Dyspnea, weight loss, and fever ensue. Cats with disseminated nocardiosis will present with nonspecific signs of systemic illness. Disseminated disease is especially problematic for patients with an impaired cell-mediated immune response. Important differential diagnoses for nocardiosis include but are not limited to actinomycosis (Chapter 4), mycobacteriosis (Chapter 144), leprosy (Chapter 127), plague (Chapter 169), sporotrichosis (Chapter 202), dermatophyte kerion, dermatophilosis, and panniculitis.
Regarding zoonosis, no cases of human nocardiosis have resulted from direct contact with an infected cat, although there are a few reports of cutaneous disease developing from a scratch or bite by a healthy cat or dog.
Diagnosis Primary Diagnostics • Cytology and Gram Staining: Cytology demonstrates degenerate neutrophils, macrophages, lymphocytes, and plasma cells, along with the organisms, which are branching, beaded, and filamentous. Bacterial macrocolonies sometimes (but not always) appear as “sulfur granules” in exudative material. On Gram stain, the organisms are gram-positive. See Figure 282-1 • Culture and Sensitivity: The importance of culture and sensitivity cannot be overemphasized. Wound exudate or effusive fluid may be submitted. Even when Nocardia is strongly suspected, it is important to determine the species involved because susceptibility patterns vary greatly. The lab should be notified of a suspected “unusual” pathogen (e.g., Nocardia, Actinomyces, or Mycobacterium) for all nonhealing wounds and atypical effusions. If anaerobes are suspected, special transport tubes or culturettes are required but can usually be supplied by the diagnostic laboratory. • Acid-Fast Staining: A small amount of exudate can be smeared onto a microscope slide and submitted for acid-fast staining. Nocardia is a partially or weakly acid-fast organism.
Secondary Diagnostics • Radiographs: Diffuse pulmonary nodules and intrapulmonary or extrapulmonary masses may be seen. Parenchymal infiltrates are bronchointerstitial or alveolar. Pleural effusion is often noted. • Biopsy and Histopathology: Histologic study of tissue reveals a suppurative to pyogranulomatous reaction. Organisms may not be visible with routine H & E stains. • Polymerase Chain Reaction (PCR) Testing: PCR identification and drug susceptibility testing for Nocardia can be performed at the University of Texas Health Center at Tyler, Department of Microbiology Research Mycobacteria/Nocardia Lab, phone (1)-903-8777685, and by some veterinary commercial laboratories.
Diagnostic Notes
Figure 152-1 Multiple draining tracts are seen on the right thoracic wall caudal to the axilla, the site of a fight wound abscess about 3 months prior. Cytology and culture confirmed nocardiosis. Image courtesy Dr. Gary D. Norsworthy.
• Draining tracts may have a thickened or “ropey” feel in the subcutaneous tissues. • The laboratory should be alerted to the potential for Nocardia as a suspect organism. It is a slow-growing organism and may be read out as negative if adequate time is not allowed for growth.
Treatment Primary Therapeutics
th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
356
• Surgical Debridement and Drainage: Where possible, focal lesions should be surgically debrided and adequate drainage established.
Nocardiosis
Because wound dehiscence is a common problem, open wound management with delayed primary closure is often the most suitable option. Pyothorax should be surgically drained.
Secondary Therapeutics • Antibiotic Therapy: While awaiting culture results, treatment may be instituted with a trimethoprim-sulfonamide (TMS) combination. It is dosed at 15 to 30 mg/kg q12h PO. Because not all Nocardia isolates are sensitive to sulfonamides, other drugs may need to be combined with or substituted for sulfonamides. Trimethoprim-sulfa combined with penicillin G benzathine (100,000 u/kg q24h IM for 10 days) results in drug synergism. Doxycycline is a reasonable second choice dosed at 10 mg/kg q24h or 5 mg/kg q12h PO. Therapy should be continued for 4 weeks past clinical cure (at least 3–6 months of continuous therapy); shorter courses of therapy often result in relapse of disease. • Debridement and Lavage of Thoracic Cavity: Pyothorax should be addressed with a thoracic drainage system and saline lavage twice daily. This therapy should be continued until the thoracic fluid is clear and no organisms are found on cytologic examination of the fluid.
bone marrow suppression (i.e., anemia and neutropenia). The bitter taste of some formulations can cause partial to complete anorexia, salivation, and vomiting. • Folate Supplementation: Folate may be administered if long-term sulfa therapy is indicated. Cats are sensitive to TMS and its use may lead to folate deficiency. Folate is dosed at 1 mg/day.
Prognosis Prognosis is generally guarded, especially with systemic disease, but cure has been achieved in many cats with draining tracts as long as prolonged aggressive treatment occurs.
Suggested Readings Edwards DF. 2006. Nocardiosis. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 456–461. Philadelphia: Saunders Elsevier. Malik R, Krockenberger MB, O’Brien CR, et al. 2006. Nocardia infections in cats: A retrospective multi-institutional study of 17 cases. Aus Vet J. 84(7):235–245. Thomovsky E, Kerl ME. 2008. Actinomycosis and nocardiosis. Compend Contin Educ. 10(3):4–10.
Therapeutic Notes • Cats often do not tolerate long-term TMS therapy, especially at high doses. Common adverse effects are anorexia and reversible
357
CHAPTER 153
Obesity Mark Robson, Mitchell A. Crystal, and Debra L. Zoran
Overview Obesity occurs when energy intake (food volume or caloric intake) exceeds energy expenditure (decreased activity or metabolic rate). Obesity is defined by having a body weight greater than 15 to 20% over ideal, with the excess weight in adipose tissue. A number of causative factors are implicated in feline obesity including, overeating (usually owing to free choice feeding or overfeeding), sexual status (neutered cats are more likely to be overweight than intact cats), breed and genetic predisposition (mixed breed cats are more likely to be overweight than pure breed cats), inactivity (confined, indoor cats are more likely to be overweight than active or outdoor cats), and endocrine disturbances or conditions that may alter appetite and metabolic homeostasis. A number of recent papers suggest that of all these factors gonadectomy may be the most important single issue due to the changes in caloric needs and metabolism that occur. Thus, after gonadectomy, a reduction in calorie intake by approximately 30% is needed to meet their new calorie requirements and prevent obesity. Current estimates suggest that 35% of cats in Western society are obese. Given that neutering is essential to the prevention of overpopulation in indoor/outdoor cats and in management of indoor housecats, the amount and type of diet fed is a vital factor. Cats are obligate carnivores that have evolved eating prey and have no requirement for carbohydrates. Therefore, cats are adapted for higher utilization of protein and lower utilization of carbohydrates. As a result of these evolutionary adaptations, cats preferentially use protein as an energy source and store the excess energy from the diet in the form of carbohydrates as fat. Outdoor or highly active cats, or cats with high innate basal metabolism can consume diets with increased carbohydrates and not gain weight, but the key is energy utilization must be high. Obese cats fed low fat, high fiber (usually insoluble) weight-loss diets may experience weight loss; however, unless protein levels are higher than typical diets, this will be at the expense of lean body mass. Preservation of lean muscle mass is not only essential to overall health but is one of the key determinants of basal metabolism, including normal glucose and lipid metabolism. Loss of muscle mass (sarcopenia) leads to increased morbidity and during weight loss can result in metabolic changes that make successful weight loss extremely difficult. Because carbohydrates are necessary for the production of commercial dry diets, all dry diets will contain at least 15 to 20% carbohydrate. Conversely, canned foods are quite variable in their carbohydrate content, but some canned foods contain extremely low concentrations of carbohydrates (less than 6% on a dry matter basis). Dry cat foods, per se, are not detrimental to cats when fed appropriately. However, most owners preferentially feed dry foods because they can be supplied ad libidum (Latin for “at one’s pleasure”), a significant convenience for the owner. Unfortunately, this practice invariably results in excessive calorie intake, and in neutered, indoor cats, makes them especially prone to development of obesity. The physiology of adipose tissue is extremely complex, and this is illustrated by the fact that adipose tissue is not only a passive storage and insulation reservoir but a critical endocrine organ that produces a
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
358
multitude of adipokines. Adipokines are hormones and proteins, including leptin, resistin, and adiponectin that have roles in appetite and satiety, inflammatory response, insulin sensitivity, and metabolism. Leptin was the first adipokine identified in 1994, and since that time over 50 adipokines have been described, all of which are intricately involved in normal metabolic homeostasis as well as the pathophysiology of obesity. We now know that adipocytes in obese animals secrete pro-inflammatory cytokines (i.e., tumor necrosis factor-α and interleukins) and proteins implicated in metabolic homeostasis, neoplastic processes, and altered blood pressure. Therefore, it must be assumed that obesity is not only a phenomenon of carrying excess body weight, but it is a complex, chronic metabolic condition involving altered appetite and energy expenditure that develops into a chronic, low-grade, proinflammatory syndrome that may predispose to a myriad of other disease states. From a clinicians perspective, severe obesity (body condition score [BCS] 9/9 or >35% fat mass) can be extremely difficult to reverse simply because of the numerous metabolic and hormonal changes which make successful weight loss and weight maintanence extremely difficult. Obesity in cats can increase the risk of, exacerbate, or cause a plethora of medical conditions, and as in humans and dogs, obesity is associated with reduced longevity. Obese cats are twice as likely to die in middle age (6–12 years) compared to nonobese cats. Obese cats are susceptible to increased risk or severity of syndromes such as cardiovascular disease, hypertension, type II diabetes mellitus, nonallergic skin conditions, osteoarthritis, neoplasia, lower urinary tract diseases (i.e., urolithiasis and urinary tract infection) and pickwickian syndrome (dyspnea due to thoracic compression). Obesity will further create an increased risk for anesthesia and surgery, decrease reproductive performance (including more cases of dystocia), predispose to hepatic lipidosis, and create heat intolerance. Feline and canine obesity continues to increase worldwide, and although it should be given the same serious consideration as other chronic diseases, obesity continues to be considered an inconvenient problem of diet. And although owner education and compliance are essential to achieve weight loss successfully, it is also important for veterinarians and their staff to recognize their important role in nutrition counseling (e.g., no free-choice feeding, increased protein and lower carbohydrate diets), weight management in young animals after gonadectomy, and early intervention in cats that have gained weight to prevent overt obesity and its clinical consequences.
Diagnosis Primary Diagnostics • History: The owner should be questioned thoroughly about the cat’s diet (i.e., type, amount, frequency, and supplements); method of feeding (free-choice versus scheduled); treats; water intake; activity level; and other relevant medical history. • Physical Examination: Subjective findings from visual examination and palpation are used to generate a BCS. Diagnosis of obesity includes inability to feel the ribs and excessive intra-abdominal or inguinal fat depots. BCS and weight should be recorded in the medical record to generate data that can be followed over time. See Table 153-1.
Obesity
TABLE 153-1: Body Condition Scores (1–9 Scale) Body Condition Score 1
Examination Findings Ribs visible on shorthaired cats; no palpable fat; severe abdominal tuck; lumbar vertebrae and wings of ilia easily palpated. Ribs easily visible on shorthaired cats; lumbar vertebrae obvious with minimal muscle mass; pronounced abdominal tuck; no palpable fat. Ribs easily palpable with minimal fat covering; lumbar vertebrae obvious; obvious waist behind ribs; minimal abdominal fat. Ribs palpable with minimal fat covering; noticeable waist behind ribs; slight abdominal tuck; abdominal fat pad absent. IDEAL: Well-proportioned; observe waist behind ribs; ribs palpable with slight fat covering; abdominal fat pad minimal. Ribs palpable with slight excess fat covering; waist and abdominal fat pad distinguishable but not obvious; abdominal tuck absent. Ribs not easily palpated with moderate fat covering; waist poorly discernable; obvious rounding of abdomen; moderate abdominal fat pad. Ribs not palpable with excess fat covering; waist absent; obvious rounding of abdomen with prominent abdominal fat pad; fat deposits present over lumbar area. Ribs not palpable under heavy fat cover; heavy fat deposits over lumbar area, face and limbs; distention of abdomen with no waist; extensive abdominal fat deposits.
2
3
4
5
6
7
8
9
•
• •
Courtesy Nestle Purina PetCare, St. Louis, MO.
(canned food or low-fat foods). Owners will require repeated counseling that free-choice feeding is not appropriate and that carefully measured meals need to be fed at specific times. Caloric requirement has been traditionally calculated using the formula: KCal (in) = (proper body weight in kg × 30) + 70. However, this will likely overestimate the calories needed by obese cats. It may be simpler to understand that a cat in ideal body condition and weighing 4.5 to 5 kg (10–11 lbs) should eat approximately 180 to 200 kcal per day, and an obese cat will require significantly less than that. Obese cats may require a reduction of up to 60% of the calculated optimum-weight maintenance kilocalories until an optimum body weight is reached. Because of this extreme reduction in caloric intake, it is essential that the diet contain high quality ingredients and enough protein to prevent protein malnutrition. In addition, cats should be fed their recommended caloric intake in two to three divided meals, and it is imperative that free-choice feeding should be discontinued. Diet Composition: Feeding a diet with moderate to high good quality protein, low carbohydrate, and low fat levels is ideal to both promote lean tissue mass and restrict caloric intake. Most recent papers assess the desired protein content in food in terms of percentage of metabolizable energy (ME) and recommend that 45% protein ME is the minimum required to optimize fat loss and preserve muscle mass. Feeding low quality protein will not only promote loss of muscle mass, reduce energy metabolism, and increase the risk of deficiencies of amino acids, antioxidants (glutathione) and important regulators of cell function that come from protein (e.g., nitric oxide), but it can also cause diarrhea and fecal odor due to poor digestibility and changes in the intestinal flora. Supplements: Avoid treats and snacks outside of the dietary schedule. Exercise: Increase activity by increasing play, placing food in a location that increases activity, or acquiring another pet. One effective exercise tool for cats is a laser pointer. For many indoor cats increasing energy expenditure is challenging and often practically impossible, and it is in these cases that caloric restriction is paramount for successful weight loss. Client Education: The owner must be informed of the health risks of obesity. These risks should be gently discussed so as to create awareness but not fear; fear will lead to avoidance of the situation and the veterinarian. An attempt should be made to identify the factors in the household that are leading to obesity so that specific goals of reducing these factors can be set. The client should play a major role in setting these goals.
Secondary Diagnostics
•
• Abdominal Radiographs: In cases of marked abdominal distention, abdominal radiographs may be needed to differentiate obesity from organomegaly, ascites, or intra-abdominal neoplasia. See Figures 292-1, 292-3, and 292-3. • Minimum Data Base: Blood and urine testing may be appropriate to assess the cat’s health status with regard to the secondary effects of obesity, such as diabetes mellitus. • Blood Pressure: Determination of blood pressure may be appropriate in older or very obese cats.
Secondary Therapeutics
Diagnostic Notes • Hypothyroidism is extremely rare in the cat. This disease should not be diagnosed unless more common diseases have been ruled out, severe T4 depression is confirmed, and other obvious signs of hypothyroidism are present (truncal alopecia, bradycardia, low body temperature, hypercholesterolemia on a fasted serum chemistry profile, low-grade nonregenerative anemia). Euthyroid sick syndrome (subnormal T4 due to significant nonthyroidal disease) is common in cats but should not be confused with true hypothyroidism.
Treatment Primary Therapeutics • Diet: Calorie control is essential, irrespective of diet choice. This can be accomplished by using foods that are less calorie dense
• L-Carnitine: Daily supplementation of L-carnitine (250 mg q24h PO) incorporated into a weight loss program may help increase lipid metabolism and reduce the time required to achieve safe weight loss. Vitamin A and retinoic acid supplementation have been suggested to improved weight loss but are not recommended as they can be dangerous if you are not measuring tissue levels for toxicity.
Therapeutic Notes • An effective way to facilitate weight loss is via regular monitoring of success (body weight and BCS), coupled with positive reinforcement to the client. Establishing an in-hospital “weigh-in” program that is directed by technical/nursing staff, by whom the client does not feel threatened or embarrassed, has proven to be a highly successful means of achieving sustainable weight loss as well as a being a great marketing and client-relations tool. • While rapid weight loss (>3% body weight loss per week) is not recommended because of the risk of hepatic lipidosis, studies
359
SECTION 1: Diseases and Conditions
demonstrate that as long as protein needs are met (e.g., diets with very high protein levels), energy requirements as low as 45% of the calculated goal can be used. However, if high fiber weight management diets are being used, the protein concentrations must exceed 45% ME to assure adequate protein intake. • Varying opinions exist as to what type of diet is best to achieve weight loss (i.e., canned versus dry, level of protein required, and fiber effect). Nevertheless, the key to loss of fat is calorie reduction. The most successful weight loss diets achieve calorie reduction while maintaining sufficient quantity and quality of protein to protect essential needs and functions. Feeding strictly controlled portions of food is essential, especially in neutered cats.
Prevention The key elements for preventing obesity in neutered cats include strict control of dietary intake (quality and quantity) following neutering and careful recording of BCS and weight for their lifetime.
Prognosis The prognosis for obesity is good if a weight reduction program is selected and followed.
Suggested Readings German AJ. 2006. The growing problem of obesity in dogs and cats. J Nutr. 136:1940S–1946S.
360
Hoenig M, Ferguson DC. 2002. Effects of neutering on hormonal concentrations and energy requirements in male and female cats. Am J Vet Res. 63:634–639. Laflamme DP, Hannah SS. 2005. Increased dietary protein promotes fat loss and reduces loss of lean body mass during weight loss in cats. Int J App Res Vet Med. 3(2):67–72. Nguyen P, Leray V, Dumon H, et al. 2004. High protein intake affects lean body mass but not energy expenditure in non-obese neutered cats. J Nutr. 134:2084S–2068S. Radin MJ, Sharkey LC, Holycross BJ. 2009. Adipokines: a review of biological and analytical principles and an update in dogs, cats, and horses. Vet Clin Path. 38(2):136–156. Roudebush P, Schoenherr WD, Delaney SJ. 2008. An evidence based review of the use of therapeutic foods, owner education, exercise and drugs for the management of obese and overweight pets. J Am Vet Med Assoc. 233(5):717–722. Vasconcellos RS, Borges NC, Goncalves NV, et al. 2009. Protein intake during weight loss influences the energy required for weight loss and maintenance in cats. J Nutr. 139:855–860. Villeverde C, Ramsey JJ, Green AS, et al. 2008. Energy restriction results in a mass adjusted decrease in energy expenditure in cats that is maintained after weight regain. J Nutr. 138:856–860. Zoran DL. 2002. Timely topics in nutrition. The carnivore connection to nutrition in cats. J Am Vet Med Assoc. 221(11):1559–1567.
CHAPTER 154
Oral Neoplasia Bradley R. Schmidt and Mitchell A. Crystal
Overview Oral neoplasia comprises 3% of all feline tumors. Of these, 60 to 80% are squamous cell carcinomas (SCC) and 10 to 20% are fibrosarcomas (FSA). Other oral tumors including odontogenic tumors (i.e., inductive fibroameloblastoma, calcifying epithelial odontogenic tumor, and epulides), melanoma, lymphoma, and so on comprise less than 3% of all oral tumors. Breed, coat color, or gender has not been associated with oral tumor formation. Results of one study suggests the use of flea collars, feeding a predominantly canned diet, feeding canned tuna fish, and possibly exposure to household tobacco smoke are associated with an increased risk of oral SCC development. Feline oral tumors may arise from any region of the mouth (i.e., mandible, maxilla, palate, and so on), but SCC appears to most commonly involves the sublingual site. See Figure 154-1. Tumors are more common in older cats (i.e., average of 10–12 years for SCC and FSA), with the exception for cats with inductive fibroameloblastoma in which cats are generally young (18 months or younger,) and there is no definitive breed or sex predilection. Oral tumors tend to be locally invasive and often invade the underlying bone and extend to involve the nasal passages, periorbital space, and pharynx. Metastasis to the regional lymph nodes may occur in up to 30% of cats with SCC, but distant metastasis is rare. Regional or distant metastasis is rare in cats with FSA. The odontogenic tumors are benign and do not metastasize. See Figure 154-2. Oral melanoma in the cat has been reported to be highly metastatic. The few reports of cats with oral lymphoma suggest that it should be considered as a systemic disease in most cases. Cats with oral neoplasia commonly present for halitosis, oral hemorrhage, presence of an oral mass, facial deformity, exophthalmos, pytalism, weight loss, dysphagia, or anorexia. See Figure 154-3. Physical examination may not always reveal an oral mass. Loose teeth without
Figure 154-2 Odontogenic tumors typically are benign and do not metastasize. This cat had multiple epulides that recurred after CO2 laser removal but did not recur when the adjacent teeth were extracted. Image courtesy of Dr. Gary D. Norsworthy.
Figure 154-3 The presenting signs for an oral tumor often include halitosis, ptyalism, and oral hemorrhage as with this cat that had a fibrosarcoma involving the maxilla and hard palate. Image courtesy of Dr. Gary D. Norsworthy. Figure 154-1 Oral squamous cell carcinoma most commonly occurs on the ventral surface of the tongue. Image courtesy of Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
significant dental or gingival changes should alert one to the possibility of an oral tumor (see Figure 154-4), and, although metastasis is uncommon, regional lymphadenopathy is sometimes noted. Differential diagnoses for oral neoplasia include eosinophilic granuloma complex, feline lymphoplasmacytic gingivitis, periodontal disease,
361
SECTION 1: Diseases and Conditions
Diagnostic Notes • Educating the client regarding oral examinations and the importance of regular veterinary visits is important for early detection of oral tumors. • Detection of loose teeth during oral examination or dental procedures should prompt strong consideration for radiographs, CT or MRI, and biopsy. • Blood tests may reveal an anemia of chronic disease, paraneoplastic leukocytosis, and other medical conditions that may concurrently be present in older cats. • Feline retroviruses have not been shown to be a risk factor for the development of feline oral tumors but are important in assessing the overall health of the patient. A retrovirus infection will degrade the prognosis.
Treatment Figure 154-4 Loose teeth without significant dental disease may occur due to alveolar invasion of a tumor. This cat’s tumor was a squamous cell carcinoma. Image courtesy of Dr. Gary D. Norsworthy.
tooth root abscessation, ondoclastic resorptive lesions, nasopharyngeal polyps, and tonsillitis.
Diagnosis Primary Diagnostics • Physical Examination: Look closely for a mass, loose teeth, mandibular or maxillary swelling, retrobulbar swelling, nasal congestion, and regional lymph node enlargement. An odor typical of tissue necrosis is sometimes present. • Skull and Dental Radiographs, Computerized Topography (CT), and Magnetic Resonance Imaging (MRI): These should be performed under general anesthesia to determine if lytic and proliferative bony changes are present and to define the extent of the lesion for treatment planning. CT and MRI are generally more sensitive than radiographs to determine the extent of the lesion and may reveal regional lymph node enlargement as well. • Incisional Biopsy and Histopathology: This is the most definitive means of diagnosis. Due to secondary infections and inflammation associated with these tumors, large samples should be collected to optimize the likelihood of an accurate diagnosis. Fine-needle aspirations of the oral mass may result in false-negative results due to secondary inflammation and infections.
Secondary Diagnostics • Lymph Node Fine-Needle Biopsy and Cytology: Fine-needle biopsy should be performed even if the regional lymph nodes are not enlarged; this may be best performed while under anesthesia. Excisional lymph node biopsy may be indicated as well. • Three-View Thoracic Radiographs: Although pulmonary metastasis is not common, radiographs should still be performed to evaluate for metastasis and possibly other concomitant cardiopulmonary conditions. • Abdominal Ultrasound: This should be performed for oral round cell tumors such as lymphoma or if there are other suspected medical conditions present concurrently. • Minimum Data Base: Complete blood count, serum chemistry profile, urinalysis, and retrovirus tests should be performed to evaluate the overall health of the patient.
362
Primary Therapeutics • Surgery: Aggressive surgical excision is indicated when possible for local control but may be difficult due to limited tissue access and the advanced state of the tumor in most cats. Surgical success is greatest for smaller, rostrally located mandibular and maxillary tumors and odontogenic tumors. Lesions adjacent to the maxilla or mandible typically require partial or total maxillectomy or mandibulectomy. Odontogenic tumors are generally cured with surgery. Oral lymphoma generally does not require aggressive surgery because local tumor control may be obtained with chemotherapy or radiation therapy and in most cases the disease is systemic. Radical surgery for oral melanoma likely will not be curative due to the high metastatic rate associated with these tumors. • Radiation Therapy: Radiation therapy may be curative in cats with odontogenic tumors and may be palliative in cats with oral lymphoma and melanoma. For SCC and FSA, response rates when treating gross disease with definitive radiation therapy with or without chemotherapy is variable, but the survival times are generally less than 6 months due to local tumor progression and can be associated with significant morbidity. Therefore, most radiation therapy schedules are designed for palliation only. In carefully select cases radiation therapy may be used to improve control rates in cats with incompletely resected oral tumors.
Secondary Therapeutics • Chemotherapy: This is indicated in the uncommon event of oral lymphoma but is generally ineffective in the treatment of the other oral malignant tumors. The use of chemotherapy as a radiation sensitizer or in combination with radiation therapy has not dramatically improved survival times and can be associated with additional morbidity. Studies have varied regarding the over expression of COX-1 and COX-2 in cats with oral SCC as well as responses utilizing COX inhibitors. There is a report with prolonged survival in cats using a nonsteroidal anti-inflammatory drug.
Therapeutic Notes • Cats generally do not tolerate removal of greater than 50% of the mandible or maxilla and generally suffer from short-term morbidity (i.e., dysphagia, inappetance, inability to groom, pytalism, mandibular drift, and so on); therefore, careful case selection and appropriate imaging prior to surgery is advised. • Enteral nutrition via gastrostomy or esophagostomy feeding tubes may be temporarily needed following surgery. • In a survey of 28 owners with cats undergoing various mandibulectomy procedures, 21 (75%) were pleased with the
Oral Neoplasia
outcome and 7 (25%) regretted the surgery. Most cats had difficulty eating for the first 2 to 4 months post-surgery. Following that period, cats ate canned food well but had difficulty with dry food.
Prognosis Overall, most cats with oral SCC or FSA die due to local progression, generally within 6 months. Smaller, rostrally located tumors treated with aggressive surgery may be associated with longer survival times; therefore, early detection with frequent oral examinations is imperative. SCC is generally associated with a shorter survival time as compared to FSA and other malignant tumors. The combination of surgery with radiation therapy in the treatment of SCC and FSA may result in longer survival times in select patients. With the exceptions of oral melanoma and lymphoma, metastasis is not common. Most cats with odontogenic tumors treated with surgery or radiation therapy are cured.
Suggested Readings Bertone ER, Snyder LA, Moore, AS. 2003. Environmental and lifestyle risk Factors for oral squamous cell carcinoma in domestic cats. J Vet Intern Med. 17(4):557–562. Hayes AM, Adams VJ, Scase TJ, et al. 2007. Survival of 54 cats with oral squamous cell carcinoma in United Kingdom general practice. J Small Anim Pract. J48(7):394–399. Liptak M, Withrow SJ. 2007. Cancer of the gastrointestinal tract. Oral tumors. In SJ Withrow, DM Vail, eds., Small Animal Clinical Oncology, 4th ed., pp. 455–475. Philadelphia: Elsevier Saunders. Moore AS, Ogilvie GK. 2001. Tumors of the alimentary tract. Malignant oral tumors. In AS Moore, GK Ogilvie, eds., Feline Oncology, pp. 271– 277. Trenton: Veterinary Learning Systems. Moore AS, Ogilvie GK. 2001. Tumors of the alimentary tract. Benign oral tumors. In AS Moore, GK Ogilvie, eds., Feline Oncology, pp. 277–281. Trenton: Veterinary Learning Systems. Northrup NC, Selting KA, Rassnick KM, et al. 2006. Outcomes of cats with oral tumors treated with mandibulectomy: 42 cases. J Am Anim Hosp Assoc. 42(5):350–360.
363
CHAPTER 155
Organophosphate and Carbamate Toxicosis Gary D. Norsworthy Overview Cats are commonly exposed to organophosphates (OP) and carbamates found in topical, systemic, and environmental pest control products. Common OPs include fenthion, malathion, parathion, runnel, cythioate, coumaphos, chlorpyrifos, diazinon, dichlorovos, tetrachlorvinphos, phosmet, famphur, fenthion, and propetamphos. Common carbamates include fenoxycarb, methomyl, bendiocarb, aldicarb, carbaryl, carbofuran, and propoxur. All of these products affect the nervous system by inhibiting acetylcholinesterase (AChE) at the neuromuscular junction, resulting in excess AChE and prolonged depolarization of the postsynaptic membrane; effector organs are stimulated. Spontaneous reactivation of AChE is slow in young cats and almost nonexistent in older cats; it occurs more easily in carbamate toxicosis (reversible AChE inhibitors) than OP toxicosis (mostly irreversible AChE inhibitors). Most OP insecticides covalently bind AChE within 24 hours of exposure. Following exposure OPs are stored in fat and released slowly into circulation. Therefore, lean cats will have more rapid OP levels in circulation and experience more severe clinical signs. Clinical signs occur from parasympathetic stimulation and, to some degree, sympathetic stimulation. There is a progression of signs that begins with restlessness and progresses to hyperexcitability or hypoexcitability. Muscarinic (i.e., salivation, lacrimation, bronchial secretion, vomiting, or diarrhea), nicotinic (i.e., muscle tremors or respiratory paralysis), and mixed (e.g., central nervous system depression, seizures, miosis, or hyperactivity) signs occur. Cyanosis and generalized tetany signal that advanced toxicosis is present and shortly precede seizures, respiratory failure, and death. Two notable exceptions are fenthion and chlorpyrifos toxicosis. The former may be tolerated by the cat for several weeks before toxicosis begins; prolonged anorexia may be the predominant clinical sign. The latter also may cause onset of clinical signs after several days of exposure and may cause anorexia, ataxia, posterior paralysis, and cervical ventroflexion. Both may require several weeks of antidotal therapy and nutritional support. OP-impregnated flea collars have been associated with two syndromes. Spinal disease can occur, resulting in posterior ataxia, which progresses cranially. It generally occurs 10 to 14 days after application of the collar. Typically, clinical signs resolve after the collar is removed. Flea collars may cause a local dermatitis if the collar is applied too tightly and gets wet, if more than one collar is applied, or if the cat develops contact hypersensitivity to components of the collar. Collar removal usually results in healing, but some cats need aggressive treatment with oral and locally applied corticosteroids. Chlorpyrifos toxicosis usually occurs several days after exposure, resulting in posterior ataxia, paralysis, or cervical ventroflexion. Tremors and fasciculations are common. Anorexia of several weeks’ duration may also occur.
Diagnosis Primary Diagnostics • History: Recent application of a topical or systemic OP or carbamate should raise the index of suspicion. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
364
• Clinical Signs: Salivation, muscle twitching, vomiting, diarrhea, miosis, bradycardia, abdominal pain, and frequent urination are the common early signs. Cyanosis, generalized tetany, respiratory distress, coma, and death may follow. Prolonged anorexia without other cause and local irritation to the skin near the collar are also possible. • Atropine Test Dose: Give atropine (0.02 mg/kg IV). Onset of tachycardia and mydriasis suggests lack of AChE exposure so OP and carbamate toxicosis are unlikely.
Secondary Diagnostics • AChE level: When reduced to less than 25% of normal, OP and carbamate toxicity is considered likely. The best tissues for analysis include whole blood, serum, plasma, brain (include samples of cerebellum, cerebrum, and brain stem), liver, body fat, stomach and intestinal contents, and skin and subcutaneous tissue. • Tissue Toxins: Tissue levels of OPs and carbamates can be confirmatory.
Diagnostic Notes • Tissue samples for toxin analysis must be taken and frozen quickly because tissue levels of the toxins decrease rapidly. • Carbamate reactivation can occur during sample transport and testing resulting in false-negative test results.
Treatment Primary Therapeutics • Respiratory Support: A patent airway should be secured and oxygen support administered if needed. • Seizure Control: If seizures occur, administer diazepam (0.5–0.1 mg/ kg IV to effect), phenobarbital (5–20 mg/kg IV to effect) or pentobarbital (10–30 mg/kg IV). • Atropine: This drug should be given initially IV at 0.2 to 0.5 mg/ kg for bradycardia, excessive bronchiolar constriction, and mucus hypersecretion. It will not abolish the nicotinic signs of muscle tremors and respiratory paralysis. About 25% of the dose is given IV, and the remainder is given IM. It should be repeated as needed and discontinued if tachycardia, hyperthermia, aggressiveness, or delirium occurs. Atropine is ineffective for nicotinic signs so it will not stop muscle tremors or weakness. • Pralidoxime Chloride (2-PAM): This drug is an AChE reactivator meaning it frees the enzyme and restores normal function. It is dosed at 10 to 20 mg/kg q8 to 12h IM or SC. It is most effective when administered within the first several hours after exposure (i.e., before “aging” occurs). It relieves nicotinic signs (e.g., tremors or respiratory paralysis). It should be given as long as it produces clinical response and discontinued after three doses of non-response. Overdosage may cause tachycardia and cardiac arrhythmias. It is indicated for OP toxicosis only; it is not beneficial for carbamate toxicosis. Reconstituted bottles may be used for 2 weeks if wrapped in foil and refrigerated.
Secondary Therapeutics • Bathing: If dermal exposure has occurred, the cat should be bathed in a mild detergent soap to remove any remaining toxin. If this is not done, the cat may ingest more toxin by grooming.
Organophosphate and Carbamate Toxicosis
• Activated Charcoal and Cathartic: Activated charcoal is given at the rate of 2.0 g/kg (10 mL/kg of the 10% oral suspension) PO (via orogastric tube). Sodium sulfate is given at 1 g/kg. These drugs are combined in some antidotal products (Actidose with Sorbitol, Paddock Laboratories). It should not be given if the cat is seizuring or comatose. • Gastric Lavage/Through-and-Through Enema: These may be used to remove remaining toxins from the gastrointestinal tract. Note that gastric lavage should not be done if the cat is unconscious because of the potential for aspiration. Use of anesthesia and a cuffed endotracheal tube are essential. • Diphenhydramine: This drug may be helpful in controlling muscle fasciculations and delayed neuropathy. It is dosed at 2 to 4 mg/kg q8h IM for 2 days then 2 to 4 mg/kg q8h PO for 21 days as needed. However, its use and dose are controversial. If it is used, the cat should be monitored for progressive central nervous system depression.
Therapeutic Notes • Chlorpyrifos toxicosis often requires several weeks of therapy with 2-PAM. Relapse is common and often requires reinstitution of 2-PAM therapy. Because of the prolonged anorexia that may occur, nutritional support in the form of an implanted feeding tube may be needed. • Although control of seizures is imperative, it is important that central nervous system depression not be induced except for that purpose.
• Phenothiazine tranquilizers, including acepromazine, may potentiate OP toxicosis. • Complete recovery is dependent on resynthesis of sufficient quantities of AChE, which may take 4 to 6 weeks.
Prognosis The prognosis for OP and carbamate toxicoses is good if diagnosed and treated quickly. However, the clinician should note that treatment might require intensive care for several days and continued treatment for several weeks. Long-term effects are not likely.
Suggested Readings Dorman DC, Dye JA. 2006. Chemical toxicities. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 256–261. St. Louis: Elsevier Saunders. Ducote JM, Dewey CW. 2001. Acquired myasthenia gravis and other disorders of the neuromuscular junction. In JR August, ed., Consultations in Feline Internal Medicine, 4th ed., pp. 374–380. Philadelphia: WB Saunders Co. Hansen SR, Curry-Galvin EA. 2007. Organophosphate and carbamate toxicity. In LP Tilley, FWK Smith, Jr., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 998–999. Ames, IA: Blackwell Publishing.
365
CHAPTER 156
Osteoarthritis Andrew Sparkes
Overview The various manifestations of degenerative joint disease (DJD) have become increasingly recognized in cats over recent years; now it seems clear that this has been a considerably underrecognized and undertreated problem in the past. The terms DJD and osteoarthritis (OA) are often used interchangeably, although OA is actually one form of DJD characterised by cartilage deterioration of diarthrodial synovial joints. Radiographic evaluation of axial synovial joints is more difficult, and thus many studies of feline DJD and OA have focussed mainly or exclusively on the disease affecting appendicular joints. Based on retrospective radiographic studies, feline DJD appears to be a prevalent disease (up to 20% of cats), although there is less information available on the pathogenesis and clinical manifestations of this of disease. Posttraumatic OA has been clearly identified in a number of cats, and hip dysplasia has also been identified as a significant cause of feline coxofemoral OA with notable breed predispositions including the Maine Coon and to a lesser extent Persian and Siamese cats. However, despite these recognized causes of feline OA, studies to date suggest that most feline cases are idiopathic and studies of underlying pathophysiological changes have not been reported. However, it is recognized that in many cats with OA, changes are bilateral, and the most frequently reported joints affected are the shoulders, elbows, hips, and stifles. See Figure 156-1. In addition to diarthrodial DJD, previous studies have also documented a high prevalence of vertebral spondylosis in older cats. One study demonstrated that 80% of cats over the age of 12 years had radiographic evidence of spondylosis, although the clinical significance of this remains uncertain. See Figures 40-1 and 156-2. It has been suggested that overt signs of DJD in cats may be less obvious than in other species, and indeed are often quite subtle. Studies suggest that overt lameness may be observed in well under 50% of affected cats. This may partly relate to the fact that cats are not exercised in the same way as dogs so recognizing lameness may be more difficult, may be partly because the disease is often insidious in onset and bilateral, and may also relate to the fact that many cats appear to mask or hide signs of disease well. In one prospective study, the most commonly identified signs of feline OA were so-called lifestyle changes with a reduced willingness to jump, a reduction in the height of the jump, and also the presence of a stiff gait. These signs were reported in around two-third to three-fourths of affected cats. Owners may also recognize joint stiffness manifested as a stilted or shuffling gait. Other signs commonly noted include a reduction in overall activity, difficulty negotiating high-sided litter trays, reduced grooming, and difficulties climbing up and down stairs may be the most common signs. Some of these signs are subtle, and developing an index of suspicion through appropriate questioning is important. Equally, some changes apparently associated with OA may also be changes that can occur for other reasons (e.g., behavioral changes), so careful assessment is needed.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
366
Diagnosis Primary Diagnostics • Clinical Signs: A diagnosis of DJD may be suspected on the basis of presenting clinical signs listed previously. • Physical Examination: One should look for pain on joint manipulation, joint swelling, altered range of movement, and crepitus when moving the joints. However, feline orthopedic examinations are notoriously difficult, and distinguishing a painful response from a cat that simply resents having its limbs manipulated can be difficult. • Radiography: Radiography may reveal osteophytes, subchondral sclerosis, bone or soft-tissue swelling, and intra- or extra-articular mineralization of soft tissues. However, it would appear that as in other species, the severity of radiographic changes of DJD do not necessarily correlate to the clinical manifestations of the disease. See Figure 156-1.
Secondary Diagnostics • Joint Fluid Analysis: Analysis including fluid cytology may be helpful in distinguishing DJD from inflammatory arthropathies. • Therapeutic Trial: When doubt exists about the diagnosis or whether the presence of DJD is the cause of clinical signs, trial therapy may be appropriate.
Treatment Primary Therapeutics • Manage Obesity: There is evidence of a relationship between joint disease and obesity. Obtaining and maintaining optimal body weight should be an important treatment goal. See Chapter 153. • Environmental Modification: Make changes at home so the cat has to do less jumping (up or down). Chairs, stools, ramps, or other objects can be placed strategically to help a cat maneuver into a favored position (e.g., on a windowsill) where it finds difficulty in jumping. High-sided litter trays should be avoided. • Meloxicam: This is a nonsteroidal anti-inflammatory drug (NSAID). In the United Kingdom, meloxicam has recently been granted a license for long-term use in cats for the treatment of musculoskeletal pain. It is only approved as a one-time injection in the United States. The licensed U.K. dose is an initial dose of 0.1 mg/kg PO followed by 0.05 mg/kg q24h PO. However, studies have suggested that in some cats much lower doses (e.g., 0.05 mg/cat q24–48h PO) may still be effective, thus enabling dose-titration when adverse effects are seen or where precautions may be needed. • Other Medications: Other drugs and nutraceuticals may potentially be of benefit in managing feline DJD, either as alternatives or alongside NSAID therapy. Chondroprotectants such as glucosamine and chondroitin are available for cats (Cosequin and Dasuquin, Nutramax Laboratories, Edgewood, MD). Other analgesic therapy, including opioids, may be of benefit. Dietary manipulation with an enhanced n-3 fatty acid intake or supplementation with green-lipped mussel may be beneficial in the management of osteoarthritis. In one feline study the use of an experimental diet rich in n-3 fatty acids and with increased levels of methionine and manganese was shown to improve biomarkers associated with joint disease in older cats.
Osteoarthritis
(A)
(B)
(C)
(D) Figure 156-1 The joints most affected by osteoarthritis are the shoulders (A), elbows (B), hips(C), and stifles (D). In some cases, the disease is bilateral as seen in images B and C. Synovial osteochondromatosis is sometimes seen in older cats accompanying osteoarthritis, but a causal link has not yet been established. More subtle lesions than those shown in images A, B, C, and D occur early in the disease, such as those images E and F. The lesion in this elbow is not as obvious in a true lateral (E) as in an oblique lateral (arrow) view (F). Images courtesy of Dr. Gary D. Norsworthy.
Secondary Therapeutics • Rehabilitation Therapy: Hydrotherapy and physiotherapy are tolerated by some cats and may be of value. See Chapter 268. Therapy lasers also produce relief of clinical signs to some cats. See Chapter 312.
Therapeutic Notes • Owners should spend a greater amount of time grooming the cat because this becomes difficult for many arthritic cats.
• While appropriate NSAID use in many cats should carry a low risk of significant adverse effects, caution is warranted with their use in certain situations, including cats receiving diuretic therapy, angiotensin-converting enzyme inhibitors, or corticosteroids and cats with pre-existing dehydration, gastrointestinal disease, congestive heart failure, liver disease, and renal insufficiency. Some conditions or concomitant therapy may make NSAID therapy absolutely contraindicated (e.g., corticosteroid therapy or advanced renal disease) because of the significant risk of seeing adverse effects. • It is prudent to inform owners to be observant for significant clinical signs in cats receiving NSAIDs. Development of anorexia,
367
SECTION 1: Diseases and Conditions
(E)
(F)
Figure 156-1 Continued
It is sensible to advise owners to administer NSAIDs after the cat has eaten and to stop therapy if the cat stops eating. Dehydration is common in cats that stop eating; the resultant hypovolemia could predispose to adverse renal effects.
Prognosis OA is not a curable disease; however, many cats respond well to multimodal therapy and remain comfortable for many years.
Suggested Readings
Figure 156-2 Vertebral spondylosis is common in older cats, many of which have constipation problems. Although pain has not been documented, the correlation with constipation is strongly suggestive of pain. This cat had a few months of constipation followed by remission of signs. This radiograph shows maturing of the bony bridging that would be expected when vertebral stabilization and abatement of pain occur. Images courtesy of Dr. Gary D. Norsworthy.
gastrointestinal disturbances, such as vomiting or diarrhea, or increased thirst or urination is justification for temporary or permanent cessation of therapy. • Encouraging owners to feed canned foods rather than dry foods to cats receiving NSAID therapy to maximize water intake is prudent.
368
Clarke SP, Bennett D. 2006. Feline osteoarthritis: A prospective study of 28 cases. J Small Anim Pract. 47(8):4394–445. Clarke SP, Mellor D, Clements DN, et al. 2005. Prevalence of radiographic signs of degenerative joint disease in a hospital population of cats. Vet Rec. 157(25):7934–799. Gunew MN, Menrath VH, Marshall RD. 2008. Long-term safety, efficacy and palatability of oral meloxicam at 0.01-0.03 mg/kg for treatment of osteoarthritic pain in cats. J Fel Med Surg. 10(3):235–241. Hardie EM, Roe SC, Martin FR. 2002. Radiographic evidence of degenerative joint disease in geriatric cats: 100 cases (1994–1997). J Am Vet Med Assoc. 220(5):628–632. Lascelles BD, Hansen BD, Roe S, et al. 2007. Evaluation of client-specific outcome measures and activity monitoring to measure pain relief in cats with osteoarthritis. J Vet Intern Med. 21(3):410–416.
CHAPTER 157
Otitis Externa Gary D. Norsworthy
Overview The external ear consists of the auricle, commonly known as the pinna, that acts to collect sound and the external acoustic meatus, commonly known as the external ear canal (EEC), which is a sound-conducting tube that begins at the base of the pinna and terminates at the tympanic membrane (TM). The pinna consists of the 0.5 mm (1/32 inch) thick auricular cartilage covered by skin on each side. Numerous auricular muscles attach to the auricular cartilage for movement of the pinna. The EEC is L-shaped with a horizontal component and a vertical component. Most diseases of the EEC involve the horizontal portion. Otitis externa refers to any inflammatory disease of the pinna or the EEC. Some underlying conditions are not intrinsically inflammatory but may incite an inflammatory response. Lesions that obstruct the EEC impair hearing, trap fluids, and prevent proper movement of air thus creating a warm, dark, moist environment that is ideal for bacterial or fungal growth. Diseases of the pinna include lacerations or abscesses (usually from fighting; Chapter 21), tumors, and aural hematoma. Aural tumors are usually squamous cell carcinoma (Chapter 203), mast cell tumor (Chapter 135), or ceruminous gland adenoma (Chapter 32). Diseases of the EEC include infections by bacteria or yeast, ear mites (See Chapter 62), waxy debris, wax plugs, masses, allergy (Chapters 16 and 82), contact irritants, inflammatory polyps (See Chapter 121), and tumors. The most common tumors of the EEC are ceruminous gland adenomas and squamous cell carcinoma (Chapter 203).
Aural Hematoma Overview An aural hematoma occurs due to excessive shaking of the head. During violent shaking the two layers of skin slide in opposite directions against the auricular cartilage shearing blood vessels. The resultant bleeding is almost always on the rostral (concave) surface of the pinna; an aural hematoma results.
Diagnosis Primary Diagnostics • Physical Examination: An aural hematoma is a soft, nonpainful, odorless, fluid-filled (blood or serum) swelling on the concave surface of the pinna. See Figure 157-1. It may be small (<1 cm [3/8 inch] in diameter) or it may encompass the entire concave surface of the pinna.
Secondary Diagnostics • Aspiration: Aspiration of the swelling with a 22-gauge needle will yield an odorless, serosanguinous fluid. Cytology of the fluid reveals red blood cells with minimal inflammatory cells and no bacteria.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 157-1 An aural hematoma is a nonpainful, fluid-filled mass on the concave side of the pinna. This one is so large that it nearly covers this side of the pinna.
Treatment Primary Therapeutics • Aspiration: Small hematomas may heal if the fluid is removed by aspiration. However, reformation is a problem and is more likely as the size of the hematoma increases. • Surgery: There are several surgical procedures for repair of an aural hematoma. A 1-cm (3/8 inch) incision is made in the skin at the dorsal and ventral aspects of the hematoma. The fluid is removed through the incisions. A drain tube (comprised of a piece of split intravenous tubing) is placed through the body of the hematoma and exits both ends. It is sutured in place on both ends. A mattress suture pattern is used to close the dead space. Sutures are placed through the skin, cartilage, and skin every 1 cm (3/8 inch). Dissolvable sutures are placed so they do not have to be removed. The drain tube is left in place 5 to 7 days. The entry and exit holes are allowed to granulate closed. See Figure 157-2.
Prognosis The prognosis is good as long as the hematoma is drained and the dead space closed. If left untreated, the hematoma will eventually resolve; however, the cartilage will become misshapen resulting in a “cauliflower ear.” See Figure 157-3.
Bacterial and Fungal Otitis Overview Infections in the EEC are usually due to bacteria or yeast. The most common pathogens include Staphylococcus intermedius, Proteus mirabilis, Pseudomonas aeruginosa, Pasturella multocida, and the yeast Malassezia
369
SECTION 1: Diseases and Conditions
Figure 157-2 The surgical repair of an aural hematoma consists of two drain holes: a drain tube (in this case a longitudinally split portion of intravenous tubing) and a series of mattress sutures using dissolvable suture material and placed in the same plane as the long axis of the pinna to minimize interruption of blood flow to the pinna. This is the same cat as in Figure 157-1 but taken 1 week after surgery.
Figure 157-4 Chronic otitis externa can result in stenosis and even closure of the external ear canal.
equipment in relation to the TM. This reduces the likelihood of rupturing the TM.
Diagnosis Primary Diagnostics • Clinical Signs: A discharge from the external ear canal is highly suspicious for otitis externa. The discharge is often fetid. Dark exudates are usually associated with Malassezia, and yellow exudates are usually associated with small rod infections. Scratching caudal to the pinna (see Figure 62-1) and head shaking are common. • Otoscopic Examination: This should be performed to identify ear mites, the degree of debris buildup, foreign bodies, tumorous masses, and whether or not the TM is intact. This may require sedation in some cats. • Cytology: A modified Wright’s stained smear can be used to classify the infection as cocci (Staphylococcus spp., Streptococcus spp., see Figure 157-5), small rods (i.e., usually P. mirabilis, P. aeruginosa, or P. multocida, see Figure 157-6), large rods (usually E. coli), or yeast (M. pachydermatis, see Figure 157-7). This information is important in selecting appropriate medication. Figure 157-3 If an aural hematoma is not treated with either aspiration or surgery, the cartilage will become misshapen as it heals leaving a “cauliflower ear.”
pachydermatis. Streptococcus spp., Corynebacterium spp., and Escherichia coli are less commonly found. Clinical signs include head shaking, ear scratching, and an otic discharge. Severe, untreated infections, especially if accompanied by severe facial dermatitis, can lead to stenosis of the external ear canal. See Figure 157-4. Ruptured TM is another sequel to severe otitis externa. Primary otitis externa is not common in cats. Generally it occurs because the environment of the ear canal has been altered to favor bacterial or fungal growth. This is especially true when the primary pathogen is a rod-shaped bacterium. Therefore, affected ear canals should be examined carefully for an underlying cause. This may not be possible at the time of the initial presentation. Treatment with the appropriate antimicrobial for 1 to 2 weeks may allow proper visualization with an otoscope. Alternatively, general anesthesia with ear canal flushing may be used. The use of a video otoscope is advantageous because flushing and fluid aspiration can be performed while visualizing the location of the
370
Secondary Diagnostics • Bacterial Culture: The bacterial morphology and likely species of the organism usually can be determined by cytology; however, culture and sensitivity testing can be very helpful in determining the appropriate antibiotic. Because M. pachydermatis usually does not grow on aerobic cultures, culturing should not be performed without cytology. • Viral Testing: The feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) may predispose the cat to bacterial otitis. If a bacterial infection is present without ear mites or a mass or if the cat does not respond to initial therapy, these tests should be performed.
Diagnostic Notes • It is important to perform cytology on both ear canals because many cats have different organisms in the two ears. • Primary ear infections are uncommon in cats, so an underlying disease should be sought.
Otitis Externa
Figure 157-5 Cocci are identified in this cytology prep from a cat with a Staphylococcus spp. infection. 1000× magnification.
Figure 157-7 Malassezia pachydermatis are seen in this cytology prep. 1000× magnification.
products are usually effective in dissolving the debris and permitting the cat to shake it out of the ear canal. Excessive force in flushing should be avoided because a fragile TM may rupture. Although it will usually heal, it will produce vestibular signs and may create otitis media. • When the EEC becomes stenotic due to chronic otitis externa surgery may be indicated. See Figure 157-4. Total ear canal ablation and lateral ear resection are usually performed. See Chapter 274.
Therapeutic Notes • The use of cotton-tipped swabs for ear cleaning by owners is contraindicated because they tend to push debris deeper into the ear canal. If owners feel compelled to clean the external ear, alcoholsoaked cotton balls are effective and safe and effective in removing superficial wax and waxy debris.
Prognosis Figure 157-6 Small rods, identified as Pseudomonas aeruginosa, are seen in this cytology prep. 1000× magnification.
Treatment Primary Therapeutics • Antibiotics: Topical antibiotics are indicated when bacterial infections are present. Their choice should be based on culture and sensitivity or cytology. The additional use of systemic antibiotics should be considered in severe or resistant infections. • Antifungals: Topical antifungals (clotrimazole or miconazole) are indicated when fungal infections are present. Resistant infections can be treated with fluconazole (50 mg q12–24h PO) or itraconazole (5 mg/kg q12h PO).
The prognosis is good with proper diagnostics and appropriate therapy, including removal of an ear canal mass, unless the FeLV, FIV, or a EEC mass is present. These viruses warrant a guarded prognosis, and surgery is required to remove a mass, which may be malignant.
Waxy Debris and Wax Plugs Overview Ceruminous glands line the EEC and produce cerumen, commonly known as ear wax. Some cats produce excessive ear wax, especially when inflammation is present in the EEC. Geriatric cats frequently have an increase in wax production. If dust or other environmental material enters the ear canal it may be trapped within the wax and held within the EEC. Concretions of wax, commonly called “wax plugs” or “wax balls” may occur and are usually located adjacent to the TM. Clinical signs are those of other forms of otitis externa and include head shaking and ear scratching.
Secondary Therapeutics
Diagnosis
• Insecticide: This is indicated when ear mites are present. See Chapter 62. • Ear Flushing: Some clinicians are aggressive in flushing the ears of sedated cats. However, wax solvents or solvent-containing antibiotic
Primary Diagnostics • Otoscopic Examination: Waxy debris often fills the ear canal making visualization difficult or impossible. Wax plugs are often found in
371
SECTION 1: Diseases and Conditions
Ear Ticks Overview The spinous ear tick, Otobius megnini, may crawl into the horizontal ear canal. If it stays long enough, it may lay eggs that may hatch producing many small ticks in the EEC. Head shaking and ear scratching result.
Diagnosis Primary Diagnostics • Otoscopic Examination: One or many ticks can be observed. The heat of the otoscope may cause movement of the legs making identification easier. Figure 157-8 A wax plug is seen through a video otoscope (MedRx, Inc., Largo, FL) in the horizontal ear canal. It was so large that it occluded this portion of the external ear canal.
Treatment Primary Therapeutics • Manual Extraction: Ticks may be removed using an otoscope and alligator forceps or a video otoscope and biopsy forceps. Anesthesia is required.
otherwise clean ear canals. They may be seen with an otoscope and often appear to fill the horizontal ear canal. See Figure 157-8. • Cytology: A stained cytology prep, reveals amorphous, waxy debris without cells or microorganisms.
Secondary Therapeutics
Diagnostic Notes
• Cerumenolytics: When anesthesia is contraindicated, a cerumenolytic may kill the ticks by suffocation. Mineral oil can be used for the same purpose.
• Bacterial cultures have no growth unless a secondary bacterial infection is present.
Prognosis Treatment
The prognosis is excellent when the tick is removed.
Primary Therapeutics • Cerumenolytics: A nonirritating drug in this class should be used once or twice daily for 1 week. The ear should be rechecked about 3 to 4 days post-treatment to see if the waxy debris or the wax plug is gone. Some wax plugs may not dissolve without 2 to 3 weeks of treatment.
Secondary Therapeutics • Manual Removal: If a wax plug does not dissolve after 2 to 3 weeks of treatment or if the cat is resistent to treatment, alligator forceps via an otoscope or biopsy forceps via a video otoscope can be used with the cat under anesthesia.
Ceruminous Gland Adenoma Overview Any mass that occurs in the EEC can create an environment that favors bacterial or fungal growth. Excessive wax production often occurs as well. Any of these can produce clinical signs of head shaking and ear scratching. The most common masses are ceruminous gland adenoma, squamous cell carcinoma (See Chapter 203), and inflammatory polyps (see Chapter 121). Ceruminous gland tumors are usually benign (adenoma) and are classified by some as ceruminous gland hyperplasia. They appear as characteristic black masses on the concave surface of the pinna or within the EEC. They enlarge over time, and 30 or more may occur on one ear.
Therapeutic Notes • Many cats with waxy debris or wax plugs will have recurrences. Some cats need to be treated with a cerumenolytic for one week every 1 to 3 months as clinical signs return.
Prognosis With proper treatment the prognosis is excellent.
372
Diagnosis Primary Diagnostics • Clinical Appearance: One to 50 black masses on the concave surface of the pinna or within the EEC are diagnostic. Because they enlarge over time, masses of varying sizes are usually present. See Figure 157-9.
Otitis Externa
Figure 157-9 Multiple dark masses are seen on this pinna. There were identified as ceruminous gland adenomas.
Figure 157-10 A CO2 laser (Aesculight, Woodinville, WA) can be used to vaporize ceruminous gland adenomas. One treatment is sufficient; however, others will occur over time.
Secondary Diagnostics
Secondary Therapeutics
• Aspiration: Aspiration of a red to black-colored fluid adds to the diagnosis. • Histopathology: If needed, biopsy and histopathology are confirmatory.
• Surgical Excision: This is a difficult way to manage the disease unless only a few are present. Access to those in the EEC is difficult so a total ear canal ablation may be needed. See Chapter 274.
Suggested Readings Treatment Primary Therapeutics • Laser Obliteration: A CO2 laser can vaporize the lesions very efficiently. See Figure 157-10. When combined with a video otoscope, masses in the EEC can be treated as well.
Radlinsky AG, Mason DE. Diseases of the Ear. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 5th ed., pp. 1168–1186. St. Louis: Elsevier Saunders. Werner AH, Otitis Externa and Media. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 952–953. Ames, IA: Blackwell Publishing.
373
CHAPTER 158
Otitis Media and Interna Sharon Fooshee Grace
Overview Otitis media and otitis interna are defined as inflammation of the middle and inner ear, respectively. Middle ear structures include the tympanic membrane and air-filled tympanic cavity, the tympanic nerve (a branch of the facial nerve), the opening to the Eustachian tube, and three auditory ossicles (i.e., the malleus, stapes, and incus). Several nerves pass through the middle ear, but only two are clinically relevant, the facial nerve and the sympathetic trunk. Inner ear structures include the cochlea, vestibule, and semicircular canals; these are housed within a membranous labyrinth contained within a bony labyrinth. Otitis media may be difficult to diagnose because it may be clinically silent or overshadowed by concurrent otitis externa. Otitis media may be a primary or secondary disease and may also occur iatrogenically. In many cases, it develops secondary to extension of otitis externa through a ruptured tympanic membrane or by extension up the Eustachian tube following upper respiratory infection. Other possible causes include polyps, tumors, trauma, and bacterial infection. Many cases of otitis interna have an associated otitis media; thus, the middle ear may serve as the most common route of infection for the inner ear. Signs of otitis media include shaking the head or pawing at the ear and, occasionally, a head tilt (caused by pain, not vestibular in origin). When the facial nerve is involved, drooling, paralysis of the lip or ear, diminished or absent palpebral reflexes, and widened palpebral fissures may be seen. Sympathetic nerve involvement may produce Horner ’s syndrome: enophthalmos, protrusion of the membrana nictitans, ptosis, and miosis (see Chapter 99). Signs of otitis interna are usually more straightforward than those of otitis media. They include head tilt toward the affected side or wide head excursions if both sides are affected equally; asymmetric ataxia, typically with leaning, stumbling, falling, or rolling toward the affected side, or truncal ataxia if both sides are affected equally; and spontaneous horizontal or rotary nystagmus with the fast phase away from the affected side. Nausea and vomiting may occur due to disturbance of vestibular connections to the emetic center in the brain stem.
Figure 158-1 An open-mouth anterior-posterior view of the skull shows the tympanic bullae. The left one (arrow) is thickened, evidencing otitis media.
Diagnosis Primary Diagnostics • Clinical Signs: Otitis media or interna should be suspected in cats with shaking of the head, a head tilt, or signs of facial nerve abnormalities. • Physical Examination: Patency of the tympanic membrane should be assessed when examining the external ear canal. Bulging or rupture of the membrane and changes in opacity or color indicate middle ear pathology. If upper respiratory stridor is present, the oral and nasopharygeal cavity should be examined with the cat under anesthesia for evidence of inflammation or polyps protruding from the Eustachian tube. Neurologic evaluation should be performed to look for deficits associated with otitis media and interna.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
374
Figure 158-2 A lateral view of the same cat in Figure 158-1 shows the tympanic bullae (arrow), but they are superimposed making evaluation difficult.
• Imaging: Bulla radiographs taken with the cat under anesthesia may reveal radiographic changes of otitis media, including the presence of a fluid density in the tympanic bulla or thickening of the bulla. See Figures 158-1, 158-2, and 158-3. Radiographic changes may not always be apparent, even when otitis media is present.
Otitis Media and Interna
(A)
Figure 158-4 A computerized tomography scan shows the normal air-filled tympanic bulla in contrast to the abnormal fluid-filled, thick-walled tympanic bulla (arrow).
helpful for draining the fluid, obtaining samples for cytology and culture and sensitivity, and for flushing the middle ear.
Diagnostic Notes • Unilateral otitis media is more suggestive of neoplasia, polyps, or a foreign body.
Treatment Primary Therapeutics • Antibiotics: Systemic antimicrobials should be administered for 3 to 6 weeks. When possible, the antibiotic should be selected based on culture and sensitivity; however, success without bulla osteotomy is not assured. • Bulla Osteotomy: This surgical procedure permits drainage of the bulla. If there is radiographic or otoscopic evidence of fluid or a soft-tissue density in the tympanic bullae, a bulla osteotomy is recommended. See Chapter 248.
(B) Figure 158-3 A, Lateral oblique view isolates the normal tympanic bulla (white arrow) of the cat in Figure 158-1. B, An opposite lateral oblique isolates the thickened tympanic bulla (black arrow). Where available, computerized tomography (CT) or magnetic resonance imaging (MRI) scans are useful. See Figure 158-4. Rarely does otitis interna produce radiographic signs.
Secondary Diagnostics • Myringotomy: If the tympanic membrane is bulging but intact, an exudate may be present in the middle ear. Myringotomy may be
Secondary Therapeutics • Treat Concurrent Otitis Externa: If otitis externa is also present, it should be appropriately managed (see Chapter 157). Patency of the tympanum should be considered before placing medication into the external canal. • Middle Ear Flush: A 20-gauge, 4-cm (1.5 in) or longer needle is usually used for myringotomy. Once the eardrum has been punctured, the middle ear may be gently flushed with warm sterile saline. A reference text should be consulted for details because this procedure poses risk for delicate structures within the middle and inner ear. • Anti-emetics: These may be used to control nausea associated with vestibular signs.
375
SECTION 1: Diseases and Conditions
Therapeutic Notes • The only safe solution for flushing the middle ear is sterile saline. All disinfectants should be avoided. • Known ototoxic agents should not be placed into the ear canal when the eardrum is ruptured. These include aminoglycosides, iodinated compounds, alcohol, and chlorhexidine.
for trauma-induced otitis varies with the severity of the injuries. Nasopharyngeal polyps have a good-to-fair prognosis with surgical removal. See Chapters 149 and 262. Neoplastic disease usually carries a poor prognosis. Neurologic recovery following successful management of infection, trauma, or nasopharyngeal polyps may be partial or total and usually occurs within 2 to 6 weeks.
Suggested Readings Prognosis Prognosis is dependent on the underlying cause. Infections generally have a good prognosis for response to medical management if the underlying cause(s) of the infection can be resolved. The prognosis
376
Cook LB. 2004. Neurologic evaluation of the ear. Vet Clin North Am. 34(2):425–435. Gotthelf LN. 2004. Diagnosis and treatment of otitis media in dogs and cats. Vet Clin North Am. 34(2):469–487.
CHAPTER 159
Pancreatitis, Acute Jörg M. Steiner
Overview Formerly, exocrine pancreatic disorders have been considered to occur infrequently in cats. However, several recent studies have shown that exocrine pancreatic disorders occur in cats almost as frequently as they do in dogs. Pancreatitis is the most common exocrine pancreatic disorder in cats. In a recent study of 115 pancreata evaluated during necropsy from cats that had died or had been euthanized for a wide variety of reasons, there were no lesions in only 38 pancreata (33%), but histopathological evidence of pancreatitis was present in 77 pancreata (67%). These data would suggest that feline pancreatitis is far more common than previously believed. However, it also raises the question whether any evidence of pancreatic inflammatory infiltration is clinically significant. This question remains to be answered in future studies. Acute pancreatitis represents approximately 33% of all cases of feline pancreatitis in several studies. Although acute and chronic pancreatitis are definitions that are based on histopathological rather than clinical findings, patients diagnosed with acute pancreatitis more commonly have severe disease and patients diagnosed with chronic pancreatitis more commonly have mild disease. Pancreatitis in cats is idiopathic in most cases. However, there are several risk factors that have been implicated in causing pancreatitis in cats. Some of these risk factors are trauma (i.e., usually blunt trauma from vehicular accidents or falling from great heights but also surgical trauma), infections (most importantly Toxoplasma gondii, and the hepatic fluke Amphimerus pseudofelineus, and potentially feline infectious peritonitis and others), hypotension, hypertriglyceridemia, and pharmacological substances (most importantly organophosphates such as fenthion but many others may also potentially cause pancreatitis). Ultimately, all of these causes appear to lead to pancreatitis through a common pathophysiological pathway, including premature activation of trypsinogen, activation of other zymogens, autodigestion of the pancreas, release of inflammatory cytokines, and systemic complications, leading to multiorgan failure and death in severe cases. Cats with pancreatitis commonly show only nonspecific clinical signs. In a recent compilation of 159 feline pancreatitis cases anorexia (87%) and lethargy (81%) were reported most frequently, followed by dehydration (54%), weight loss (47%), hypothermia (46%), vomiting (46%), icterus (37%), fever (25%), abdominal pain (19%), and diarrhea (12%). In comparison to humans and dogs with pancreatitis the frequency of these clinical signs are surprising. For example, approximately 75% of human pancreatitis patients are reported to have fever, whereas 46% of cats were reported to have hypothermia. However, this difference is likely not specifically related to pancreatitis but related to the finding that cats with any number of severe systemic diseases commonly present with hypothermia. Vomiting was only reported in 46% of cats with pancreatitis. However, although most cats do not have an immediate history of vomiting, some have a past history of vomiting, often several weeks prior to presentation. Thus, it is important for the veterinary clinician to ask about the past clinical history of the patient on presentation. Abdominal pain, another key clinical sign, especially in humans with pancreatitis, was only reported for less than 20% of cats with pancreatitis. However, this was probably a gross underestimation of the incidence
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
of abdominal pain accompanying pancreatitis as many cats with pancreatitis show a marked improvement in their overall clinical appearance when treated with analgesics, even if they have previously been assessed as not having abdominal pain. Findings on clinical pathology are also quite nonspecific in cats with pancreatitis. Changes in serum hepatic enzyme activities and elevations in serum bilirubin concentration are most common and probably reflect hepatic lipidosis that is recognized as a common complication of severe pancreatitis in cats. Hyperglycemia is also common in cats with pancreatitis, reflecting destruction of islet cells. Hyperglycemia is usually transient in cases of acute pancreatitis, but it can also lead to diabetes mellitus and may require exogenous insulin therapy. Azotemia is often present in more severe cases and can either be a reflection of dehydration or even evidence for renal failure in more severe cases. Finally, hypocalcemia can be secondary to hypoalbuminemia or can be due to formation of calcium soaps (see Figure 159-1A) with fatty acids that have been released by lipolysis of peripancreatic fat. Serum amylase and lipase activities, which have both been used for the diagnosis of pancreatitis in humans and dogs for several decades, are of no clinical value in cats with suspected pancreatitis.
Diagnosis Primary Diagnostics • Serum Feline Pancreatic Lipase Immunoreactivity (fPLI) Concentration: fPLI is a specific marker for exocrine pancreatic function and is now analyzed by a commercially available ELISA, Spec fPL®. The reference range for Spec fPL® is ≤3.5 µg/L, and the cut-off value for a diagnosis of feline pancreatitis has been determined to be 5.4 µg/L. In a group of cats with experimentally induced pancreatitis, both serum feline trypsin-like immunoreactivity (fTLI) and fPLI concentrations increased initially, but serum fPLI concentration stayed elevated much longer than did serum fTLI concentration, showing that serum fPLI concentration is much more sensitive than serum fTLI concentration. Another study in cats with spontaneous pancreatitis showed serum fPLI concentration to be both more sensitive and more specific for diagnosing pancreatitis than serum fTLI concentration or abdominal ultrasonography. • Abdominal Ultrasound: Abdominal ultrasound is an important diagnostic tool for the diagnosis of feline pancreatitis. Unfortunately, while being highly specific when stringent criteria are being used (up to 100% depending on the study), abdominal ultrasound has only 11 to 35% sensitivity for pancreatitis in cats. The success of abdominal ultrasound is highly operator dependent. Peritoneal effusion (ascites) can be localized or generalized but is not specific for pancreatitis and can also be seen with a variety of other diseases. Similarly, enlargement of the pancreas, indicating pancreatic edema, can also be seen in patients with portal hypertension or in cats with hypoalbuminemia. A decrease in echogenicity indicates pancreatic necrosis, whereas an increase in echogenicity indicates pancreatic fibrosis, which is, however, only infrequently observed and only in cases of chronic pancreatitis. Even though abdominal ultrasound is not sensitive for a diagnosis of pancreatitis in cats, it is still one of the best diagnostic tools available and should be undertaken in all cats suspected of having this disease. It should be noted that the technological advances in diagnostic ultrasonography have led to an increased
377
SECTION 1: Diseases and Conditions
sensitivity of abdominal ultrasound over the last decade and insignificant lesions, such as nodular hyperplasia, may be falsely taken as evidence of pancreatitis, leading to a decreased specificity of this diagnostic modality. Thus, caution is advised not to overinterpret ultrasonographic findings. • Pancreatic Cytology: The pancreas can be ultrasonographically localized in most feline patients with pancreatitis, and fine-needle aspiration of the pancreas can be safely performed by an experienced operator. The presence of pancreatic acinar cells and inflammatory cells in the same cytological preparation confirms a diagnosis of pancreatitis. However, a lack of inflammatory cells does not help to rule out a diagnosis of feline pancreatitis.
Secondary Diagnostics
(A)
(B)
• Serum fTLI Concentration: Like serum fPLI concentration, serum fTLI concentration is also a specific indicator of pancreatic function. However, over the last few years some evidence has been provided that fTLI is less specific for exocrine pancreatic function than is fPLI concentration, and it has been reported that some cats with inflammatory bowel disease may have mildly increased serum fTLI concentrations. Also, serum fTLI concentration is rather insensitive for feline pancreatitis (sensitivity 30–60%, depending on the study). The low sensitivity of this assay is probably due to a relatively fast turnover of trypsinogen and trypsin in the serum. • Abdominal Radiographs: Abdominal radiographs can show decreased contrast in the cranial abdomen, dilated and gas-filled small intestinal loops, and transposition of abdominal organs (i.e., duodenum laterally and dorsally, the stomach to the left, and the transverse colon caudally). However, these findings are rather soft and non-specific for pancreatitis. • Abdominal Exploratory: Abdominal exploratory and biopsy of the pancreas is another diagnostic modality for feline pancreatitis. See Figure 159-1. Diagnosis of feline pancreatitis by biopsy is definitive. However, because of the high degree of localization of pancreatic inflammation, exclusion of pancreatitis based on pancreatic biopsy is difficult to impossible, even when several biopsy specimens have been collected from different sites of the pancreas. Also, although pancreatic biopsy overall is relatively safe, many patients with acute pancreatitis, especially severe forms, are poor anesthetic risks, and thus, may be harmed by this procedure.
Treatment Primary Therapeutics
(C) Figure 159-1 Acute pancreatitis may produce several gross appearances including (A) saponification of the peripancreatic fat (arrows), (B) pancreatic hyperemia (arrows), and (C) focal hemorrhage of the pancreas (arrows). Note the abdominal effusion present in images B and C. Photos courtesy of Dr. Gary D. Norsworthy.
378
• Aggressive Fluid Therapy: As in humans and dogs with pancreatitis, aggressive fluid therapy and supportive care are the mainstay of therapy for cats with severe pancreatitis. Also, monitoring for electrolyte and acid-base status is important. Cats should be carefully monitored for systemic complications, and intervention should be aggressive if such complications are suspected. • Nutritional Management: Cats that do not vomit and are not anorectic should be fed frequent small amounts of a low-fat diet. Cats that vomit incessantly despite the use of antiemetic drugs should be held nothing by mouth for 3 to 4 days, after which water should be reintroduced slowly, followed by small amounts of an easily digestible and low-fat diet. However, especially if these cats have a history of anorexia before presentation, alternative routes of alimentation must be considered. Total parenteral nutrition, partial parenteral nutrition, and jejunostomy tube feeding have been described as preferred routes of alimentation. However, they may not be practical in many cases. Depending on the degree of vomition, nasogastric, esophagostomy, or gastrotomy tubes are viable alternatives. Cats that do not vomit but are anorectic should be fed
Pancreatitis, Acute
using a nasogastric, esophagostomy, or gastrotomy tube using a trickle feeding protocol (15–10 mL of food q1–2h). See Chapters 253, 255, and 256. • Anti-emetics: Cats with pancreatitis that vomit can be treated with anti-emetics. Although metoclopramide and other dopamine antagonists do not appear to have a strong antiemetic effect, both HT3 antagonists (i.e., dolasetron or ondansetron) and NK1 inhibitors (maropitant) appear to work well in cats. Dolasetron is effective at a dose of 0.3 to 0.6 mg/kg q12h IV, SC, or PO. Ondansetron can be used at 0.5 to 1.0 mg/kg q12h PO, IM, or SC. Finally, maropitant has not been licensed for use in cats as of yet, but is generally recommended to be used at 50% of the canine dose or 0.5 to 1.0 mg/kg SC q 24h. However, some clinicians have suggested using maropitant at the same dose as is used in dogs. • Pain Management: Analgesia should be provided regardless of whether the clinician considers that abdominal pain is present or not. The overall clinical appearance of many cats with pancreatitis will improve significantly even if they are not considered to have abdominal pain before the application of analgesic medication.
debridement and peritoneal lavage have not been studied in cats and are highly controversial in human patients with pancreatitis. Thus, it would be prudent to be conservative in considering surgical intervention in cats with pancreatitis.
Prognosis The prognosis for cats with acute pancreatitis is dependent on the severity of the disorder and the presence of pancreatic and systemic complications. Pancreatic complications include acute fluid accumulations, infected necroses, pancreatic abscesses, and pancreatic pseudocysts. Septic necrosis has never been reported in a cat, but both pancreatic abscesses and pseudocysts have been reported in a few cases. However, all but one pancreatic abscesses reported in cats to date have been sterile. Another factor that is of great importance for the prognosis of cats with acute pancreatitis is the presence of hepatic lipidosis. Because many of these patients can be anorectic for prolonged periods of time, nutritional support has to be aggressive to prevent hepatic lipidosis.
Therapeutic Notes • No other therapeutic strategies have been shown to be beneficial in cats with acute pancreatitis. Antibiotics are of questionable use in humans with acute pancreatitis, even though infectious complications are common in human pancreatitis patients. In contrast, infectious complications are rarely, if ever, encountered in cats with this disease. Protease inhibitors, antisecretory agents, and anti-inflammatory agents have not shown any consistent beneficial effects in patients with acute pancreatitis. Dopamine has shown efficacy in cats with experimental pancreatitis, but only if administered within 12 hours of induction of the disease. Thus, a beneficial effect would appear unrealistic in spontaneous pancreatitis in cats. However, the use of dopamine would appear beneficial in a cat with pancreatitis undergoing anesthesia. Some studies have shown a beneficial effect of selenium in humans and dogs with pancreatitis; however, these effects were not reproducible by other investigators. Surgical
Suggested Readings DeCock HEV, Forman MA, Farver TB, et al. 2007. Prevalence and histopathologic characteristics of pancreatitis in cats. Vet Pathol. 44:39–49. Forman MA, Marks SL, De Cock HEV, et al. 2004. Evaluation of serum feline pancreatic lipase immunoreactivity and helical computed tomography versus conventional testing for the diagnosis of feline pancreatitis. J Vet Intern Med. 18:807–815. Steiner JM. Exocrine pancreas. 2008. In JM Steiner, ed., Small Animal Gastroenterology, pp. 283–306. Hannover: Schlütersche Verlagsgesellschaft mbH. Steiner JM, Williams DA. Feline exocrine pancreatic disease. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1489–1492. St. Louis: Elsevier Saunders. Washabau RJ. 2006. Acute necrotizing pancreatitis. In JR August, Consultations in Feline Internal Medicine, pp. 109–119. St. Louis: Elsevier Saunders.
379
CHAPTER 160
Pancreatitis, Chronic Jörg M. Steiner
Overview Pancreatitis is an inflammatory disease of the pancreas that occurs almost as commonly in cats as it does in dogs. Approximately twothirds of all pancreatitis cases in cats are chronic. The distinction between acute and chronic pancreatitis is not a clinical one but is based solely on histopathology. While acute pancreatitis is not associated with permanent histopathological changes, chronic pancreatitis is associated with pancreatic fibrosis or atrophy. See Figure 160-1. Although both acute and chronic pancreatitis can be mild or severe, most cases of chronic pancreatitis in cats are mild. Also, most cases of feline pancreatitis are idiopathic, and this holds also true for cases of chronic pancreatitis. Blunt trauma and pharmaceutical agents, such as organophosphates, usually cause more acute pancreatitis. Infectious causes, such as Toxoplasma gondii and Amphimerus pseudofelineus, may cause chronic pancreatitis. It is striking that many cases of feline chronic pancreatitis are associated with other conditions, most importantly inflammatory bowel disease (IBD) or cholangitis. Some authors have termed the concurrent presence of pancreatitis, IBD, and cholangitis triad disease or “triaditis.” See Chapter 216. Although this term is only somewhat helpful, these findings lead to a clinically appealing hypothesis that pancreatic and hepatic inflammation occur secondarily to intestinal inflammation, and that treatment of IBD may also ameliorate chronic pancreatitis. Clinical signs of even the severe forms of acute pancreatitis are nonspecific. This is even more likely in cats with chronic pancreatitis because chronic pancreatitis usually is less severe. In fact, it is believed that many cats with chronic pancreatitis are subclinical. Cats that do show clinical signs often only exhibit lethargy, anorexia, and weight loss. As mentioned previously, many cats with chronic pancreatitis also have
concurrent IBD and, thus, also show loose stools or diarrhea. If IBD involves the stomach, chronic vomiting may also be reported by the owner. Clinical pathology findings are most often non-specific and are limited to changes due to concurrent conditions. Elevations in liver enzyme activities maybe an indication of concurrent cholangitis, and an isolated elevation of alkaline phosphatase activity is commonly present in cats with concurrent IBD. Serum amylase and lipase activities are not clinically useful for the diagnosis of chronic pancreatitis in cats.
Diagnosis Primary Diagnostics • Serum Feline Pancreatic Lipase Immunoreactivity (fPLI) Concentration: Pancreatic lipase is a specific marker for exocrine pancreatic function in cats and can be quantitatively assessed by a commercially available ELISA, Spec fPL®. The reference range for Spec fPL is ≤3.5 µg/L and the cut-off value for a diagnosis of feline pancreatitis has been determined to be 5.4 µg/L. In a group of cats with experimentally induced pancreatitis, both serum fTLI and fPLI concentrations increased initially, but serum fPLI concentration stayed elevated much longer than did serum fTLI concentration, showing that serum fPLI concentration is much more sensitive for pancreatitis than serum fTLI concentration. Another study in cats with spontaneous pancreatitis showed serum fPLI concentration to be both more sensitive and more specific for diagnosing pancreatitis than serum fTLI concentration or abdominal ultrasonography. These studies would suggest that serum fPLI concentration is useful in diagnosing mild chronic cases of feline pancreatitis. • Abdominal Ultrasound: Abdominal ultrasound is specific for the diagnosis of pancreatitis if stringent criteria are applied. However, abdominal ultrasound is not sensitive for feline pancreatitis, and this is especially true for chronic pancreatitis, which often is mild. A specific ultrasonographic finding that is associated with chronic pancreatitis is a hyperechoic pancreas, indicating pancreatic fibrosis. Unfortunately, a hyperechoic pancreas is not a common finding during ultrasonographic evaluation of the pancreas. Also, one should note that the presence of pancreatic fibrosis merely indicates previous pancreatic damage and may or may not be associated with current pancreatic inflammation. Also, advances in technology have led to ultrasonographic equipment that is extremely sensitive. Previously undetectable lesions, mainly nodular hyperplasia, that may mimic lesions associated with pancreatic inflammation, can now be imaged and may be falsely interpreted as evidence of feline pancreatitis.
Secondary Diagnostics Figure 160-1 Fibrosis and atrophy are seen in this pancreas in a cat with a 2-year history of chronic pancreatitis and diabetes mellitus. Photo courtesy of Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
380
• Serum Cobalamin and Folate Concentrations: Many cats with chronic pancreatitis have concurrent chronic small intestinal disease. Thus, serum cobalamin and folate concentrations should be included in a minimum data base in cats with suspected chronic pancreatitis. • Serum Feline Trypsin-Like Immunoreactivity (fTLI) Concentration: Serum fTLI is less specific for exocrine pancreatic function than fPLI concentration and is also not sensitive for feline pancreatitis.
Pancreatitis, Chronic
However, serum fTLI concentration is the diagnostic test of choice for diagnosing exocrine pancreatic insufficiency (EPI). Because clinical signs of both chronic pancreatitis and EPI are vague in cats, it is useful to evaluate both parameters in cats with clinical signs of chronic gastrointestinal disease.
Therapeutic Notes • As in humans, the treatment of chronic pancreatitis in cats is extremely frustrating and can be unrewarding. The primary goal is the treatment of the cause. However, the cause of pancreatic inflammation remains unknown in almost all cases. As a first step the patient should be evaluated for any possible risk factors of pancreatitis. • Dietary History: Many older cats have renal insufficiency or failure and are being managed with a renal diet. Also, other cats may be obese or have diabetes mellitus and may be managed with a lowcarbohydrate diet. Renal diets and low-carbohydrate diets are high in fat, and cats with chronic pancreatitis should be switched to a diet that is lower in fat. A Spec fPL concentration should be evaluated before the diet is changed and again 2 to 3 weeks afterwards. Clinical improvement or a significant decrease in serum Spec fPL concentration should be considered as evidence in support of continuing on the lower-fat diet. However, if there is no subjective or objective measure of improvement the veterinarian may decide to return the cat to its original diet. • Pharmacologic History: Although only few medications have been shown to cause pancreatitis in cats, many medications have been shown to act as possible causes of pancreatitis in humans. Therefore, a careful pharmacological history is important in cats with pancreatitis. The first question that should be evaluated is whether any currently administered medication is still required (e.g., the cat may have a bacterial upper airway disease that requires continued therapy with an antibiotic). If a current need for a medication is established the clinician should seek alternative medications that achieve the same therapeutic goal (e.g., choosing a different antibiotic in a patient that does require continued antibacterial therapy). • Measurement of Fasting Serum Triglyceride Concentration: Although not conclusively proven in cats, hypertriglyceridemia is believed to be a potential cause of pancreatitis in dogs and humans. An 18-hour fasting sample should be evaluated in cats with chronic pancreatitis to rule out hypertriglyceridemia. • Measurement of Serum Calcium Concentration: Hypercalcemia can cause pancreatitis in cats, and serum calcium concentration should be evaluated in cats with chronic pancreatitis. • The next goal is to identify any concurrent conditions in cats with chronic pancreatitis. Conditions that should be considered are IDB, cholangitis, exocrine pancreatic insufficiency, and diabetes mellitus. Thus, at a minimum a full serum chemistry profile and measurement of serum fTLI, cobalamin, and folate concentrations should be performed. Any concurrent condition should be appropriately managed and the pancreatitis be monitored by repeated measurement of serum Spec fPL concentration. • Recently, autoimmune pancreatitis has been described as an important cause of acute and chronic pancreatitis in humans. These patients
all respond favorably to corticosteroid administration. Anecdotally, several cats with chronic pancreatitis have also responded to treatment with prednisolone. However, further studies are required before the use of prednisolone can be recommended for routine treatment of cats with chronic pancreatitis. If a cat with chronic pancreatitis is to be treated with corticosteroids, a Spec fPL concentration should be evaluated before starting the cat on prednisolone and again 2 to 3 weeks after initiating therapy. Clinical improvement or a significant decrease in serum Spec fPL concentration should be considered as evidence in support of continuing prednisolone therapy. However, if there is no subjective or objective measure of improvement prednisolone therapy should be discontinued. • Cats with chronic pancreatitis may be anorectic, and antiemetic therapy may be useful in treating such anorexia. Dolasetron, an HT3 antagonist, is effective at doses of 0.3 to 0.6 mg/kg q12h IV, SC, or PO. Maropitant has not yet been licensed for use in cats but is generally recommended at doses of 0.5 to 1.0 mg/kg SC q 24h. In many cats antiemetic therapy can be discontinued after 5 to 7 days. Alternatively, an appetite stimulant, such as mirtazapine (3.75 mg per cat q72h PO) can be administered. • If a feline patient with pancreatitis is considered to be painful analgesic therapy should be instituted. Oral butorphanol (0.5–1.0 mg/kg q6–8h PO) can be used for mild pain. Tramadol has not been thoroughly studied for use in cats, but anecdotal reports are encouraging. Cats with severe pain should be treated with a fentanyl patch. The dose is one-half of a 25-µg/hr patch; this is achieved by exposing only 50% of the membrane to the patient’s skin. However, due to legal concerns fentanyl patches are not routinely used by most clinicians.
Prognosis As in humans with chronic pancreatitis, in many cats chronic pancreatitis is a slowly progressive disease and ultimately will lead to EPI and diabetes mellitus. However, many cats die of natural causes before either one of these sequelae develop. Also, either one of these conditions may develop first, or they may both develop at the same time.
Suggested Readings DeCock HEV, Forman MA, Farver TB, et al. 2007. Prevalence and histopathologic characteristics of pancreatitis in cats. Vet Pathol. 44:39–49. Steiner JM. 2008. Exocrine pancreas. In JM Steiner, ed., Small Animal Gastroenterology, pp. 283–306. Hannover: SchlüterscheVerlagsgesellschaft mbH. Steiner JM, Williams DA. Feline exocrine pancreatic disease. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine 6th ed., pp. 1489–1492. St. Louis: Elsevier Saunders. Weiss DJ, Gagne JM, Armstrong PJ. 1996. Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis, and nephritis in cats. J Am Vet Med Assoc. 209:1114–1116. Williams DA, Steiner JM, Ruaux CG, et al. 2003. Increases in serum pancreatic lipase immunoreactivity (PLI) are greater and of longer duration than those of trypsin-like immunoreactivity (TLI) in cats with experimental pancreatitis [abstract]. J Vet Intern Med. 17:445–446.
381
CHAPTER 161
Panleukopenia (Feline Parvovirus Infection) Sharon Fooshee Grace Overview Feline panleukopenia is an acute viral enteritis caused by the nonenveloped feline parvovirus (FPV). It is sometimes referred to as feline infectious enteritis or feline distemper. It is thought that canine parvovirus type 2 (CPV-2) developed from a mutation of FPV. Variants of the original CPV-2 have the ability to infect cats and cause clinical disease. When CPV-2 infections first occurred in dogs, FPV vaccine was used in dogs; it offered reasonably good protection at the time. FPV is highly contagious and has an affinity for the rapidly dividing cells of lymphoid tissue, bone marrow, and intestine. Infection of lymphoid tissues and lymphocyte depletion cause functional immunosuppression. Immunity is further undermined by myeloid suppression in the marrow. Viral replication in intestinal crypt cells is responsible for the hallmark finding of enteritis. Development of bacteremia (and sometimes fatal septicemia) is facilitated by destruction of the intestinal barrier in a young animal with a debilitated immune system. Intrauterine infection may occur but fecal-oral transmission is more common. Virus is usually transmitted through direct contact between infected and susceptible cats or through exposure to virus in the environment. Large quantities of the virus are shed into feces and urine during the acute phase of illness, and shedding may continue for a few weeks after recovery. A carrier state of the virus has not been identified. Panleukopenia has the potential to cause significant disease in unprotected cats of all ages, although it poses the greatest risk for unvaccinated kittens less than 12 to 16 weeks of age. Mortality in young cats may reach 50 to 90%. Maternal immunity is protective in most kittens until 6 to 8 weeks of age. FPV is rarely seen in older kittens and adult cats; infection is likely to be subclinical in nature. Clinical signs appear following an incubation period of 2 to 9 days. Patients present with fever, peracute or acute onset vomiting unrelated to eating, prostration, and life-threatening dehydration. Some kittens are reported to hang their head over the edge of the water bowl but not drink. Liquid diarrhea may not occur until later in the course of disease; it may contain blood and sloughed tissue. The abdomen may be painful upon palpation, with either flaccid or thickened, ropey intestines. Excess fluid and gas are often present in the bowel. Prenatal infection of kittens may occur at any point during gestation, but the queen usually remains clinically unaffected. Early in utero infection may result in abortion, stillbirth, or fetal mummification. Infection in late pregnancy or the perinatal period typically results in nonprogressive cerebellar dysfunction: ataxia and hypermetria with a wide-based stance, intention tremors, and truncal sway. Clinical signs of FPV infection may be consistent with poisoning, toxoplasmosis, panleukopenia-like syndrome of the feline leukemia virus (FeLV), and other infectious causes of enteritis. Toxoplasmosis usually has an associated respiratory component and rarely causes profound leukopenia. The panleukopenia-like syndrome of FeLV can be distinguished by a positive FeLV antigen test, a chronic course of illness, or small intestinal histopathology. Primary bacterial enteritis (i.e., Escherichia coli or Salmonella spp.) and enteric corona virus may present with clinical signs of FPV and leukopenia.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
382
Panleukopenia is less common than in the past due to routine vaccination, although it remains a significant problem for unvaccinated cats living in stressful, crowded conditions such as shelters, boarding facilities, and in animal hoarding situations.
Diagnosis Primary Diagnostics • Clinical Signs: Unvaccinated kittens and young cats presented with fever, severe dehydration, vomiting, foul diarrhea, and signs of endotoxic shock should be suspected of having FPV. All of these signs need not be present to suspect panleukopenia. Temperature becomes subnormal prior to death. Kittens with cerebellar disease have likely suffered in utero or perinatal infection. • Complete Blood Count (CBC): Panleukopenia is a consistent finding on the CBC. A nadir of 100 to 200 white blood cells/µL may occur within a few days of infection. Thrombocytopenia may be seen in some cats. A rebound in the leukocyte count may be noted during recovery from infection. • Canine Fecal Parvovirus Antigen Testing: Several in-house kits marketed for detection of canine fecal parvovirus antigen are currently available. Even though not licensed for use in cats, several studies have demonstrated their utility for detection of FPV in feces. Sensitivity and specificity are comparable to traditional gold standard reference methods. Both inactivated (killed) and modified-live virus (MLV) vaccines given SC have the potential to produce a falsepositive test for about 2 weeks. Intranasal vaccines have not been associated with positive fecal tests.
Secondary Diagnostics • Chemistry Profile and Electrolytes: These tests will not diagnose panleukopenia but will aid in identifying secondary problems that require monitoring and management (e.g., hypoglycemia, hypokalemia, hypoproteinemia, and so on). • Fecal Examination: Stool should be examined for the presence of parasitic ova because parasites may be a concurrent problem that could complicate the clinical course of panleukopenia. • Retroviral Testing: Cats of any age suspected of having FPV should be tested for FeLV and feline immunodeficiency virus. • Polymerase Chain Reaction (PCR) Testing: Specialized laboratories offer PCR testing of whole blood or feces. Whole blood can be used when the disease is suspected but a fecal sample cannot be obtained.
Diagnostic Notes • Severe leukopenia is associated with a poor prognosis due to increased risk of bacteremia and endotoxemia. • A history of recent vaccination in a young kitten does not eliminate the possibility of panleukopenia because maternal antibodies may interfere with early vaccination efforts. • Electron microscopy of the stool is available to detect the virus, but it is rarely necessary because the history, clinical signs, and profound leukopenia are suggestive of the disease. If additional pathogens are suspected, contact a diagnostic laboratory for assistance in sample submission.
Panleukopenia (Feline Parvovirus Infection)
• Antibody testing for FPV is of no value as it is impossible to distinguish between infection- and vaccination-induced antibodies.
Treatment
wear gloves, gowns, and shoe covers. A 1:32 bleach solution should be used as a footbath and general hospital disinfectant. Parvovirus is a hearty virus that is not easily destroyed and can persist in the environment for months. • Weighing patients two to four times daily can help assure that hydration needs are being met.
Primary Therapeutics • Fluid Therapy: Intravenous crystalloid fluid therapy should be directed at supplying maintenance needs and correcting ongoing losses due to vomiting and diarrhea. A balanced electrolyte solution such as lactated Ringer ’s solution with 2.5 to 5% dextrose added is acceptable in most situations. Potassium supplementation is usually needed. Subcutaneous fluids would be acceptable in only the mildest cases. See Chapter 302. • Antibiotics: Intravenous, broad-spectrum antimicrobial therapy (e.g., ampicillin, cephalosporins, ticarcillin, or ticarcillin/clavulanate) should be employed due to leukopenia and the high risk of systemic bacterial infections. Ticarcillin/clavulanate or aminoglycosides may be used if gram-negative sepsis is considered likely, although aminoglycosides should be used with caution because their potential for nephrotoxicity in a dehydrated patient increases the risk of drug-induced renal failure. Fluoroquinolone antibiotics may also be considered for gram-negative infections. • Parenteral Treatment: Oral antibiotics should be avoided initially because of vomiting. Water may be offered if vomiting is not persistent. If water is withdrawn, attempt to reintroduce it in small amounts beginning 12 to 24 hours after the last episode. Feeding should be continued as long as possible and restarted as soon as possible. Although not demonstrated in cats, more rapid clinical improvement has been seen in dogs with parvovirus if they are provided enteral nutrition. • Anti-emetics: Newer anti-emetics include maropitant (Cerenia®; 1 mg/kg q24h SC) and ondansetron (0.5–1.0 mg/kg q8–12h by slow intravenous push). Metoclopramide may be administered by continuous infusion at 1 to 2 mg/kg q24h or intermittently at 0.25 mg/ kg q6 to 8 h SC, IV, or IM. Phenothiazines should be avoided because of hypotension.
Secondary Therapeutics • Monitoring Body Temperature: Fever may be present initially. As the disease progresses, some kittens will become hypothermic due to fluid loss and endotoxemia. It is important to monitor body temperature frequently. • Intestinal Protectants and Motility Modifiers and Anti-Diarrheals: These medications are not routinely necessary, and their use provides variable clinical results. • Intravenous Colloid Therapy: If the cat is severely hypoproteinemic, colloid fluid therapy or a plasma transfusion may be needed. See Chapter 112. • Feline Recombinant Interferon-Omega: This has shown benefit in dogs with parvoviral enteritis, but it has not yet been evaluated in cats and is not currently available in the United States. • Passive Antibodies: In a disease outbreak, susceptible cats can be passively protected with serum from cats with a high FPV titer. The recommended dose is 2 mL/kitten given intraperitoneally or SC. This is recommended only for susceptible cats with a known exposure. Products containing highly concentrated immunoglobulins against common feline viruses are available in some areas of Europe.
Therapeutic Notes • Care should be taken to avoid contaminating the hospital with parvovirus. Affected cats should be isolated, and caregivers should
Prevention • Panleukopenia virus vaccine is typically administered in combination with feline herpesvirus-1 (FHV-1) and feline calicivirus (FCV). Kittens should receive FPV/FHV-1/FCV vaccine at 3- to 4-week intervals from 6 to 16 weeks of age. Recent work has shown the maternal immunity may persist and interfere with vaccination until this time. Kittens facing high infection pressure (such as in a shelter) and those born to queens, which have been well-vaccinated (such as in a cattery), should receive a final vaccine at 16 to 20 weeks of age. Regardless of the age of first vaccination, all kittens and cats should initially receive at least two doses of vaccine with an interval of 3 to 4 weeks between them. After the first series of vaccinations is completed, a booster should be given in one year with subsequent immunizations following every 3 years. • Except in high-risk situations, there is no benefit in vaccinating more often than every 3 to 4 weeks. • MLV vaccines should not be used kittens less than 4 weeks of age because of incomplete cerebellar development. • Pregnant queens entering a shelter face serious risk of exposure to FPV. If FPV is not problematic in the shelter and killed vaccines are available, this product should be given. If FPV is present or only MLV vaccines are available, the American Association of Feline Practitioners’ Feline Vaccine Advisory Panel recommends using this product because benefits outweigh the risks to the queen and fetuses. • In the face of an outbreak, MLV vaccines are preferred over inactivated. In such a setting, kittens may receive the first vaccine at 4 weeks of age with boosters every 2 to 4 weeks. • FPV vaccinations provide protection against CPV-2 variants.
Prognosis A recent study reported that negative prognostic indicators at the time of presentation include a leukocyte count <1000 cells/µl, thrombocytopenia, hypoalbuminemia, and hypokalemia. Some of these are related to the complications imposed by gram-negative septicemia. With early intervention and appropriate supportive care, at least half of kittens and cats are expected to survive and be protected by lifelong immunity to FPV.
Suggested Readings Green CE, Addie DD. 2006. Feline parvovirus infections. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 78–88. Philadelphia: Saunders Elsevier. Kruse D, Unterer S, Horbacher K. 2009. Prognostic factors in cats with feline panleucopenia. ACVIM Proceedings, Abstract #107. Neuerer FF, Horlacher K, Truyen U, et al. 2008. Comparison of different in-house test systems to detect parvovirus in faeces of cats. J Fel Med Surg. 10(3):247–251. Patterson EV, Reese MJ, Tucker SJ, et al. 2007. Effect of vaccination on parvovirus antigen testing in kittens. J Am Vet Med Assoc. 230(3): 359–363. Richards JR, Elston TH, et al. 2006. The American Association of Feline Practitioners Feline Vaccine Advisory Panel Report. J Am Vet Med Assoc. 229(9):1405–1441. Truyen U, Addie D, Belak S, et al. 2009. Feline panleukopenia: ABCD guidelines on prevention and management. J Fel Med Surg. 11(7): 538–546.
383
CHAPTER 162
Panniculitis Mark Robson and Mitchell A. Crystal
Overview Panniculitis is the inflammation and necrosis of subcutaneous or intraabdominal fat. It can be a primary disease (idiopathic/sterile nodular panniculitis) or can be secondary to physical or chemical trauma (including post-vaccination), foreign bodies, infection (i.e., bacteria, atypical Mycobacterium, fungi, or Pythium), pancreatic disease (pancreatitis or pancreatic neoplasia), hypovitaminosis E (fish-based diets without adequate levels of vitamin E to prevent polyunsaturated fatty acid oxidation), and immune-mediated disease. There is no breed, age, or sex predilection. Clinical signs of subcutaneous panniculitis include deep, firm to fluctuant nodule formation (in groups or solitary) that rupture and drain an oily, yellow-brown to bloody fluid. See Figure 162-1. These lesions are usually painful, and many cats also have fever, anorexia, lethargy, and regional lymphadenopathy. Clinical signs of intra-abdominal panniculitis include pain (generalized or abdominal), fever, lethargy, anorexia, and weight loss. Abdominal distension (due to effusion or mesenteric/omental tissue inflammation and enlargement) or an intra-abdominal mass may also be present. There is a paucity of peer-reviewed literature concerning this syndrome, and cases present a therapeutic dilemma for the clinician. Many cases will not be associated with an infective agent and immunomodulatory therapy may be appropriate. However, many cases have an infectious cause (especially Mycobacterium spp.) and the consequences of immunosuppression in these cats could be catastrophic. Therefore, cats with panniculitis should be thoroughly evaluated for an underlying cause even though idiopathic disease is probably most common. Differential diagnoses for cutaneous panniculitis include neoplasia
(especially squamous cell carcinoma, basal cell tumors, and mast cell tumors), eosinophilic granuloma complex, poorly healing wounds, abscess, deep pyoderma, foreign bodies, and immune-mediated skin disease. Differential diagnoses for intra-abdominal panniculitis include neoplasia (especially pancreatic or gastrointestinal neoplasia or lymphoma) and intra-abdominal inflammatory disease (e.g., feline infectious peritonitis, tularemia, or pancreatitis).
Diagnosis Primary Diagnostics • History and Physical Examination: Inquire about the cat’s environment (i.e., indoor/outdoor, history of fighting, wounds, or hunting of wildlife), diet, and flea and tick exposure. Examine for deep, draining, painful wounds. Fundic examination may demonstrate changes suggestive of infectious disease or lymphoma. • Surgical Removal or Biopsy for Histopathology and Culture: This will usually confirm the presence of panniculitis, but there will often be doubt about the precise cause. Discuss with the laboratory which special stains may be indicated, but infective agents are often not revealed by histopathology alone, and samples should be submitted for aerobic, anaerobic, and fungal culture and sensitivity. Atypical Mycobacterium and Nocardia cultures should be considered. Check with your microbiology lab for instructions prior to collection and submission because special media and handling is required. • Abdominal Imaging with or without Tissue Sample Collection: Radiographs and ultrasound should be performed in cases of intraabdominal or systemic disease to evaluate for differential diagnoses and causes of panniculitis. Ultrasound-guided aspiration or biopsy of lymph nodes or abnormal tissue can be performed for culture, cytology, and histopathology.
Secondary Diagnostics • Complete Database (Complete Blood Count [CBC], Chemistry Profile, and Urinalysis): These are usually normal but should be completed in cats with systemic illness or intra-abdominal disease to evaluate for other diseases and assist in selecting supportive care. • Retrovirus Testing: These tests are appropriate. • Serology for Pythium or Tularemia: This can be considered for cats with systemic or intra-abdominal disease if other diagnostics have been completed and are non-diagnostic, if other diagnostics support one of these conditions, or if there is no response to initial therapy. • Polymerase Chain Reaction (PCR) Tests: A PCR test is available for Mycobacterium.
Diagnostic Notes Figure 162-1 The subcutaneous-origin draining tracts created panniculitis and were caused by an atypical Mycobacterium infection. Photo courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
384
• Cutaneous samples should be collected by deep incision or excision as punch biopsies do not provide a deep enough sample to confirm the diagnosis. • Histopathology lesions include septal, lobar, or diffuse infiltration of neutrophils, histiocytes, plasma cells, lymphocytes, eosinophils, and multinucleated giant cells with associated necrosis, fibrosis, or vasculitis.
Panniculitis
Treatment Primary Therapeutics • Treat Underlying Cause: This is indicated in cases other than idiopathic sterile nodular panniculitis. • Surgical Excision: Complete removal can be curative for focal, multifocal, or focally diffuse cutaneous disease. Careful consideration of the extent of surgery is needed. Draining tracts and sinuses often extend much further than initially suspected so planned surgical margins may not be sufficient. Be flexible as surgery progresses. Relapse is often seen if the resection is incomplete or if the underlying cause of panniculitis has not been correctly identified. Consultation with or referral to a specialist surgeon may be appropriate. • Vitamin E: This is the treatment of choice in hypovitaminosis E and may help with other forms of panniculitis (200–400 IU q12h PO). • Antibiotics: Antibiotic therapy will be necessary if a causative or secondary bacterial infection is proven. The choice of antibiotic, dose rate, and duration of therapy will be highly variable and must be tailored to sensitivity results and to the nature of the lesion. Deep lesions or those with indistinct margins may take weeks or months of treatment, and the antibiotic course should extend well past the time of apparent resolution of lesions because relapse is common. • Antifungal therapy will be necessary if a fungal etiology is established, and drug choice, dose rate, and duration of therapy will need to be carefully tailored to the individual case. • Systemic Corticosteroids: If infectious causes are conclusively ruled out prednisone or prednisolone (2.2–4.4 mg/kg q24h PO) may be indicated. Treatment should continue until complete regression of lesions is achieved (often 3–8 weeks), then slowly taper therapy over several weeks. Some cats require prolonged or indefinite alternate day therapy. Owners should be informed of the risks of corticosteroid therapy, including the development of diabetes mellitus, decreased muscle mass, and induction of congestive heart failure for cats with subclinical heart disease or a history of heart disease. Using vitamin E and possibly fatty acid supplementation in conjunction with corticosteroids should be considered.
Secondary Therapeutics • Immunomodulator Therapy: If an infectious cause is conclusively ruled out and if corticosteroids alone do not appear to be resolving lesions that are immune mediated or idiopathic then additional drugs can be considered. Azathioprine (0.3 mg/kg q48h PO) is recommended by some, but among internists is a controversial choice for cats. Many clinicians (including the authors) consider the risks of myelosuppression with azathioprine in cats to be too high and do not recommend the drug. Alternatives are chlorambucil (2 mg/ m2 or 0.1–0.2 mg/kg q48h PO), or cyclophosphamide (50 mg/m2 PO 4 days on, then 3 days off). Drugs should be used until regression is achieved then tapered by 25 to 50% for an additional 3 to 4 months. Neutrophil counts should be monitored weekly for the first month of therapy, then every 3 to 4 weeks while the cat is on therapy. Drug therapy should be stopped or tapered if the neutrophil count
drops below 3,000/µL. Cyclosporine is a cell-mediated immunity modulator that may also be considered. The modified form of cyclosporine (Neoral®, Atopica®) has better bioavailability and is dosed at 5 mg/kg q12h PO. Therapeutic trough blood levels should be measured two to three times during the first month, then less frequently; the dose is adjusted to maintain a whole-blood cyclosporine trough level of 250 to 500 ng/mL. • Hyperbaric Oxygen: The use of hyperbaric oxygen therapy has been advocated by some authors and could be considered, but it remains unproven at this time. • Pentoxifylline: The use of the drug pentoxifylline (100 mg/cat q12h PO) has been recommended by some, presumably because of its theoretical effect of improving circulation and its use in other idiopathic cutaneous syndromes. There is no published data to support or refute this recommendation. • Omega-3 Fatty Acids: Although unproven, it might be logical to include omega-3 fatty acid supplementation (5–10 mg/kg q24h PO based on ecosapentanoic acid content) in any treatment regime for their purported membrane-stabilization effects.
Therapeutic Notes • Infectious diseases should be excluded prior to initiating immunomodulatory drugs. • It should be noted that no systematic trials of any immunomodulatory drugs have been published for immune mediated or idiopathic panniculitis, and any recommendations are based on anecdotal evidence only.
Prognosis The prognosis for cats with panniculitis is highly variable. If an underlying cause is identified and resolved then the prognosis is good, but resolution of the inflammation and disappearance of nodules may take weeks to months. If the lesions are idiopathic or immune mediated but can be surgically resolved, the outcome is often good. Extensive subcutaneous lesions and those in the abdomen can be difficult to resolve, and careful communication with the owner about their expectations is advised. Medical treatment for infectious disease or sterile disease may take many months to affect a cure. Cost considerations and owner fatigue with long-term medication may result in euthanasia of cats that could be cured with persistence.
Suggested Readings Adamama-Moraitou KK, Prassinos NN, Galatos AD, et al. 2008. Isolated abdominal fat tissue inflammation and necrosis in a cat. J Fel Med Surg. 10(2):192–197. Fabbrini F, Anfray P, Viacava P, et al. 2005. Feline cutaneous and visceral necrotizing panniculitis and steatitis associated with a pancreatic tumour. Vet Dermatol. 6:413–419. Malik R, Krockenberger MB, O’Brien CR, et al. 2006. Nocardia infections in cats: a retrospective multi-institutional study of 17 cases. Aust Vet J. 84(7):235–245.
385
CHAPTER 163
Paraneoplastic Syndromes Mark Robson
Overview Paraneoplastic syndromes (PNS) are manifestations of malignancy and result from indirect effects of tumors via the release of hormones, cytokines, and growth factors. The effects of a PNS on the patient may be more significant than the direct effects of the primary tumor. Therefore, prompt identification of PNS may improve the outcome for the patient because some PNS (such as hypercalcemia) can cause life-threatening damage to vital organs (e.g., the kidneys) and because a PNS may be the first detectable sign of cancer. Early diagnosis may improve chances for cure or control of the underlying malignancy. To be consistent with a diagnosis of PNS the clinical signs must develop subsequent to the appearance of the neoplasm and must parallel the growth or activity of the tumor. There are few reports specifically relating to PNS in cats in the veterinary literature. Most discussions are anecdotal and concern cancer associated anorexia-cachexia syndrome (CACS), paraneoplastic fever, humoral hypercalcemia of malignancy (HHM), hematological changes, and several cutaneous syndromes. Anemia is commonly mentioned and can be due to anemia of chronic disease (ACD), coagulation disorders, blood loss or immune-mediated hemolytic anemia. Paraneoplastic cutaneous disorders include alopecia associated with pancreatic carcinoma; bile duct carcinoma and thymoma; skin fragility syndrome associated with hyperadrenocorticism; exfoliative dermatoses associated with feline thymoma; pruritus associated with squamous cell carcinoma; and draining nodules of the digits associated with bronchoalveolar adenocarcinoma. See Chapters 45, 55, 101, and 213. Pain might be considered a PNS; for instance, many patients with HHM seem to show bone pain as a result of osteoclast activity.
• Alopecia: Hair loss can occur over 1 to 2 months or be much more rapid in onset. Various treatments may have been tried without success, and the patient is likely to be older than 10 years. Hair loss often begins ventrally and progresses to the extremities. Hair epilates easily from the edges of the alopecic areas, and the skin may have a shiny appearance as the stratum corneum is lost. See Figure 163-1. • Skin Fragility Syndrome: This is a well-described PNS associated with hyperadrenocorticism. The skin is fragile and can tear spontaneously or with very little external trauma. See Chapter 101 and Figure 45-1. The majority of cases of feline hyperadrenocorticism are caused by pituitary adenomas. See Chapter 45. • Pruritus: Severe pruritus which is poorly responsive to standard treatments can be associated with squamous cell carcinoma. Skin can become severely ulcerated and show secondary bacterial infection. • Draining Digital Nodules: These can be a PNS secondary to bronchoalveolar and other carcinomas. These cats are older with a variable history of weight loss, lethargy and antibiotic unresponsive draining nodules on the digits. See Figure 55-1A. Thoracic radiographs are indicated to identify neoplastic lung disease. See Figure 55-1C and Chapter 55. Other organs may be the site of primary or metastatic neoplasia. See Figure 163-2.
Diagnosis
Primary Diagnostics • Clinical Signs: Clinical signs will vary widely depending on the location of the primary malignancy and its associated PNS. • CACS: Clinical signs frequently include reduced appetite, nausea, and weight loss, which can be severe and rapid. • Pyrexia: Fever is caused by the production of various cytokines by the tumor, including interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF). • HHM: The best recognized cancers causing HHM in the cat are lymphoma and various carcinomas. Neoplastic tissue secretes a number of active compounds including parathyroid hormonerelated protein (PTHrP) and Vitamin D derivatives resulting in hypercalcemia due to increased osteoclast activity in bone and increased renal tubular reabsorption of calcium. Clinical signs often include lethargy, weight loss, anorexia, polyuria/polydipsia, and vomiting. See Chapter 103.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
386
Figure 163-1 Paraneoplastic alopecia is seen on the ventral abdomen. Image courtesy Dr. Gary D. Norsworthy.
Paraneoplastic Syndromes
Treatment Primary Therapeutics • Goals: Therapy should be directed at important clinical signs (e.g., anorexia, vomiting, and so on) as well as the primary tumor and should be matched to the acuteness and severity of the PNS. For instance hypercalcemia represents a severe threat to kidney function and should be addressed immediately. In contrast, alopecia, although cosmetically important to the owner, does not require urgent action in and of itself. Resolution of the underlying neoplasm using surgery, chemotherapy, and radiation should be attempted if appropriate. • Nutritional Support: This is frequently required. Placement of a feeding tube (i.e., nasoesophageal, esophageal, gastric, or jejunal) is often the only practical means of feeding the patient if they are not voluntarily eating. Assisted feeding (with or without pharmacologic appetite stimulants) can sometimes work, but careful attention to actual intake of calories is essential. Patients should not be stressed by force-feeding. Figure 163-2 The primary tumor of the cat in Figure 163-1 was a cholangiocarcinoma. Image courtesy Dr. Gary D. Norsworthy.
• Complete Blood Count (CBC), Serum Chemistries, Urinalysis, and Retroviral Tests: A mild normocytic, normochromic, nonregenerative anemia (typical of ACD) is the most common abnormality on the CBC. Other blood values are often normal. Hypercalcemia (total or ionized) is seen with HHM. Hyperglycemia and glucosuria may be noted with hyperadrenocorticism and its secondary diabetes mellitus. Hypoglycemia is rarely seen as a PNS, most likely as a result of insulinoma, which is very uncommon in cats. • Imaging: Thoracic and abdominal radiographs should be obtained and thoroughly evaluated. The thorax should be examined carefully for signs of metastasis or primary lung tumors. See Figure 55-1C. Ultrasound is indicated to evaluate liver, pancreas, and adrenal gland for abnormalities. • Dermatologic Assessment: If skin lesions are noted a full dermatologic work-up should be performed, including fungal culture, skin scraping cytology, tape preparation, and skin biopsy. Skin biopsies are often diagnostic for skin related PNS.
Secondary Diagnostics • Advanced Imaging: Computerized tomography (CT) or magnetic resonance imaging (MRI) should be considered if a PNS is suspected and other imaging modalities have not revealed the cause. • Exploratory Laparotomy: This may be indicated if the source of the disease is not found and the patient’s condition continues to worsen. Rapid diagnosis is essential in many cases due to the debilitating effects of the tumor itself and the associated PNS.
Prognosis The prognosis is highly variable because, by definition, a PNS occurs secondary to the presence of a neoplasm. If the primary tumor is of a type and location that is amenable to surgical resection, the prognosis can be good. A positive and enthusiastic attitude from the clinician can help owners to choose appropriate therapeutic options. Sometimes an encouraging improvement in quality of life can ensue if a PNS is aggressively managed, even if the primary neoplasm cannot be eliminated. In some instances owners will be heartened by the improvement in their cat and will allow treatments to be directed at the neoplasm that they may not have previously considered while the cat was suffering pain, anorexia, nausea and so on. If treatment of the underlying tumor is successful the PNS will usually disappear.
Suggested Readings Gaschen FP, Teske E. 2005. Paraneoplastic Syndrome. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 789–795. Philadelphia: WB Saunders. Marconato L, Albanese F, Viacava P, et al. 2007. Paraneoplastic alopecia associated with hepatocellular carcinoma in a cat. Vet Dermatol. 18(4):267–271. Matousek JL, Campbell KL, Lichtensteiger CA. 2001. Paraneoplastic alopecia. In JR August, Consultations in Feline Internal Medicine, 4th ed., pp. 196–201. Philadelphia: WB Saunders. Vail DM. 2009. Paraneoplastic hypercalcemia. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIV., pp. 343–347. St Louis: SaundersElsevier. Zitz JC, Birchard SJ, Couto GC, et al. 2005. Results of excision of thymoma in cats and dogs: 20 cases (1984–2005). J Am Vet Med Assoc. 232(8): 1186–1192.
387
CHAPTER 164
Patent Ductus Arteriosus Larry P. Tilley
Overview Patent ductus arteriosus (PDA) is not as common in the feline as in the canine; however, it is important because it is one of the few cardiovascular anomalies that may be corrected surgically. In the fetus, the ductus arteriosus allows shunting (right-to-left) of blood away from the pulmonary vascular bed through the pulmonary artery to the descending aorta. Following birth, the ductus arteriosus normally constricts and eventually closes in response to increases in local partial pressure of oxygen and inhibition of prostaglandins. If the ductus remains patent, a left-toright shunt occurs, which eventually causes severe left ventricular volume overload and left-sided heart failure. Changes in the pulmonary vascular resistance may cause reversal of the shunt, which results in right-sided heart failure. The magnitude of left-to-right shunting is dependent on the luminal diameter and resistance within the ductus and on the pulmonary vascular resistance. The clinical features of PDA depend on the direction and degree of the shunting. A left-to-right shunt typically causes a continuous left basilar cardiac murmur, bounding femoral pulses, and left atrial and ventricular enlargement suggested by a caudally displaced cardiac impulse. In right-to-left shunts, a murmur usually is not present, the femoral pulses are not bounding, and signs of right-sided (i.e., ascites and jugular pulses or distention) or biventricular heart failure (i.e., pleural effusion) predominate.
Diagnosis Primary Diagnostics • Auscultation: A continuous-type machinery murmur is a hallmark of left-to-right shunting PDA. The murmur is loudest in mid to late systole and gradually decreases in intensity through diastole. In some cases, this characteristic murmur is restricted to the cranial left-heart base and may be missed if auscultation is limited to the apex. The systolic component of the murmur is usually quite prominent at the cardiac apex. In cases with a right-to-left shunting PDA, there is no murmur associated with the shunt; in these cases blood flows through the shunt rather than jets through it. See Figure 164-1. • Echocardiography: Color flow Doppler reveals left atrial and ventricular dilatation; enlargement of the pulmonary artery and ascending aorta; normal systolic function in most cases (decreased function in cases with cardiomyopathy of overload); continuous turbulent flow in the distal main pulmonary artery; and mitral, and sometimes aortic, regurgitation (secondary to aortic root dilation), as demonstrated by spectral or color-flow Doppler. Cats are more prone to secondary right ventricular hypertrophy.
Figure 164-1 Phonocardiogram. A continuous-type machinery murmur is a hallmark of left-to-right shunting patent ductus arteriosus. The murmur is loudest in mid- to late systole and gradually decreases in intensity through diastole. This characteristic murmur is sometimes restricted to the cranial left-heart base. S1, First sound; S2, Second sound.
Secondary Diagnostics • Electrocardiography: Increased R-wave amplitude suggestive of left ventricular enlargement; wide P wave suggestive of left atrial enlargement; right-axis shift in cases with reversed shunting; premature atrial complexes; and ventricular arrhythmias may be present. • Thoracic Radiography: Left atrial and ventricular enlargement; pulmonary artery and aortic dilation; pulmonary vascular overcirculation; evidence of congestive heart failure (i.e., pulmonary venous congestion or mixed interstitial-alveolar pattern consistent with pulmonary edema) are usually seen. See Figure 164-2.
Diagnostic Notes • Reverse PDA probably occurs less frequently in the cat than in the dog. • Cardiac catheterization is rarely required for the diagnosis. • PDA may occur in the presence of other congenital cardiac defects.
Treatment Primary Therapeutics • Surgical ligation of the PDA is the treatment of choice.
Secondary Therapeutics
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
388
• Preoperative stabilization of patients in congestive heart failure is essential and usually requires diuretic therapy (i.e., furosemide, 1–4 mg/kg q6–24h IV, IM, or PO depending on the severity of the clinical signs), oxygen, and cage rest.
Patent Ductus Arteriosus
(B)
(A) Figure 164-2 A, B, The radiographic changes typical of a patent ductus arteriosus that are seen in these radiographs include left atrial and ventricular enlargement; pulmonary vascular overcirculation; evidence of congestive heart failure (i.e., pulmonary venous congestion and mixed interstitial-alveolar pattern consistent with pulmonary edema).
Therapeutic Notes • Surgical intervention is recommended as soon as possible in most cases. • Never correct right-to-left PDA surgically. • Small shunts are less likely than large shunts to cause significant volume overloading of the left ventricle and potentially may not require surgical intervention. However, the size of the ductus may only be determined accurately by cardiac catheterization and angiocardiography.
with most of the complications occurring in the perioperative period. Cats with evidence of myocardial dysfunction may have irreversible pathology and, therefore, a more guarded prognosis.
Suggested Readings Liska W, Tilley LP. 1979. Patent ductus arteriosus. Vet Clin North Am Small Anim Pract. 9:195–206. Strickland K. 2008. Congenital heart disease. In LP Tilley, FWK Smith, Jr., M. Oyama, et al., eds., Manual of Canine and Feline Cardiology, 4th ed., pp. 218–223. St. Louis: Elsevier.
Prognosis In general, a good prognosis is given to patients that undergo surgical ligation of the ductus. A 5 to 10% complication rate is commonly quoted,
389
CHAPTER 165
Pectus Excavatum Sharon Fooshee Grace
Overview Pectus excavatum (PE), or “funnel chest,” is a congenital deformity of the sternum and costochondral cartilages that creates a dorsal-to-ventral narrowing of portions of the thoracic cavity. The cause (or causes) remains unknown, although genetics may be involved because multiple animals in a single litter may be affected. A breed or sex predisposition has not been identified. Affected animals are often asymptomatic; others will have abnormalities of both the cardiovascular and respiratory systems soon after birth. Abnormal position of the heart in the thorax may lead to a heart murmur and impaired venous return and makes auscultation, electrocardiography, and echocardiography difficult. Dyspnea is the most common clinical sign; hyperpnea, exercise intolerance, and recurrent respiratory infections have been reported. Many affected cats are asymptomatic.
Diagnosis Primary Diagnostics • Physical Examination: The sternal defect is usually palpable (see Figure 165-1). • Radiography: Lateral radiographs demonstrate decreased thoracic volume and elevation of the sternum with varying degrees of severity. See Figures 165-2 and 165-3A. The cardiac position is usually abnormal, with the heart shifted to the left of midline on a ventrodorsal or dorsoventral view. See Figure 165-3B.
Figure 165-1 A palpable concave defect of the caudal sternum is present in this cat with pectus excavatum. Photo courtesy of Dr. Gary D. Norsworthy.
Diagnostic Notes • A cardiac murmur in a cat with PE may be due to malposition of the heart and not heart disease. • Size of the heart is difficult to assess radiographically. True cardiomegaly cannot always be distinguished from malposition of the heart. • Radiographs should be evaluated for concurrent abnormalities. • The electrocardiogram will be difficult to interpret due to abnormal cardiac position in the chest.
Treatment Primary Therapeutics • Medical Management: Young animals without significant deformity (i.e., the chest is simply flattened) may occasionally develop nearnormal confirmation without surgery. Owners should be taught to perform gentle medial-to-lateral compression of the thorax to
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
390
Figure 165-2 This lateral radiograph of a cat with pectus excavatum shows relatively mild dorsal deviation of the mid-sternum with mild displacement of the cardiac silhouette. Image courtesy of Dr. Gary D. Norsworthy.
Pectus Excavatum
facilitate the process of normalizing contour of the chest. Cats with mild sternal deviation (see Figure 165-2) may be clinically normal without any treatment. • Surgical Management: Application of an external splint to the ventral thorax is the most common technique used in correction of PE. The splint is padded and shaped into the contour of the ventral thorax. Several sutures are placed around the sternum and secured to the splint. Periodic tightening of the sutures moves the sternum into a more normal position. This technique offers the advantage of minimal internal intervention, but it is less effective on cats with closed growth plates. Cats that are symptomatic will usually improve after external splinting. Older cats may have a less compliant thorax and require more aggressive techniques (e.g., sternotomy with splinting).
Secondary Therapeutics (A)
• Antibiotics: Some animals with PE are prone to recurring respiratory infections. These should be addressed with appropriate antimicrobial therapy.
Therapeutic Notes • Owners should be advised not to breed animals that have PE or that have produced litters with PE. Animals with PE should be neutered.
Prognosis The prognosis is good for animals without significant underlying disease and severe clinical signs. Older animals have a less favorable response to surgery (e.g., continued or worsening respiratory distress).
Suggested Readings Boudrieau RJ, Fossum TW, Hartsfield SM, et al. 1990. Pectus excavatum in dogs and cats. Compend Contin Educ. 12(3):341–355. Fossum TW. Pectus excavatum. 2007. In TW Fossum, ed., Small Animal Surgery, 3rd ed., pp. 889–894. St. Louis: Mosby. Fossum TW, Boudrieau RJ, Hobson HP. 1989. Pectus excavatum in eight dogs and six cats. J Am Anim Hosp Assoc. 25(5):595–605.
(B) Figure 165-3 A, This lateral radiograph shows severe deviation of the caudal sternum and costal cartilages with resulting displacement of the cardiac silhouette. B, The ventraldorsal view of a different cat with severe pectus excavatum shows significant left deviation of the cardiac silhouette. Images courtesy of Drs. Merrilee Holland and Judy Hudson.
391
CHAPTER 166
Pemphigus Foliaceous Christine A. Rees
Overview Pemphigus foliaceous (PF) is an uncommon autoimmune skin disease in cats that results in the formation of autoantibodies against adhesion molecules on keratinocytes. This autoantibody formation results in loss of cohesion in the epidermis resulting in the presence of acantholytic cells.
The primary skin lesions with pemphigus are pustules. Pustules are fragile and result in excessive crusting. Other dermatologic skin lesions include alopecia, scales, epidermal collarets, and erosions. The skin lesions are variably pruritic, and they may wax and wane. The most common locations for PF lesions include around the eyes, nose, ears (see Figure 166-1), planum nasale (see Figure 166-2), and footpads. Unusual skin lesion locations for PF in cats are the mouth (see Figure 166-3), nail
(A) Figure 166-2 The nasal planum is a less common location for pemphigus foliaceous. Note the other lesion dorsal to the left eye, a more common location. Photo courtesy Dr. Richard Malik.
(B) Figure 166-1 This cat has pemphigus foliaceus in the common locations: near the eyes and on the face (A) and on the pinna (B). Areas of crusty dermatitis and alopecia are typical. Photos courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
392
Figure 166-3 Another uncommon location for pemphigus foliaceous is the oral cavity. This cat had lesions on the tip and base of the tongue and on the underside of the tongue. Photo courtesy Dr. Gary D. Norsworthy.
Pemphigus Foliaceous
Figure 166-4 The nail beds and pads of the feet are another uncommon location for pemphigus foliaceous. Photo courtesy Dr. Gary D. Norsworthy.
(A)
beds (see Figure 166-4), and nipples. Systemic signs that can be seen with feline PF are lymphadenopathy, fever, anorexia, and depression.
Diagnosis Primary Diagnostics • Cytology: The best cytology samples for PF are to rupture a pustule with a 25-gauge needle and put the contents of the pustule on a slide. If no pustule is present, samples should be collected from underneath the crusts. Cytology samples are stained with Diff Quik™ and viewed microscopically. Degenerated neutrophils and acantholytic cells are most commonly seen on PF cytology. • Biopsy: Dermatohistopathology for PF shows subcorneal pustules containing neutrophils and acantholytic cells with varying numbers of eosinophils.
(B) Figure 166-5 The cat in Figure 166-1 was treated with cyclosporine (Atopica™). Note the good response at 2 weeks (A) and 4 weeks (B). Photos courtesy Dr. Gary D. Norsworthy.
Treatment Primary Therapeutics • Corticosteroids: Immunosuppressive doses of corticosteroids are the mainstay treatment to control autoimmune skin disease. The three steroids most commonly used to treat feline PF are prednisolone (induction: 2.0–2.5 mg/kg q12–24h PO; maintenance: 2.5–5.0 mg/kg q2–7d PO), triamcinolone (induction: 0.2–1.0 mg/kg q12–24h PO; maintenance: 0.5–1.0 mg/kg q2–7d PO), and dexamethasone (induction: 0.1–0.2 mg/kg q12–24h PO; maintenance: 0.05–0.1 mg/kg q48– 72h PO). Development of diabetes and infections of the skin and urinary tract secondary to the resulting immunosuppression is possible.
PO. Chlorambucil has also been used as an adjunctive immunosuppressive therapy in cats (induction dose: 0.1–0.2 mg/kg q24h PO; maintenance: 0.1–0.2 mg/kg q48h PO). While taking chlorambucil, complete blood counts (CBC) and chemistry profiles are required to monitor the onset of significant side effects (i.e., bone marrow suppression). See Figures 166-5A and 166-5B.
Prognosis The prognosis for feline PF is fair to good. Some cats may remain in remission as the immunosuppressive therapy is tapered. However, the majority of the cats require lifelong immunosuppressive therapy.
Secondary Therapeutics • Additional Immunosuppressive Drugs: Several other immunosuppressive drugs have been used to treat feline PF including cyclosporine and chlorambucil. The latter is traditionally used in conjunction with steroids. Cyclosporine is not approved for use in cats but has been used by many veterinarians. The immunosuppressive dose for cyclosporine is 5 mg/kg q24h PO then tapered to 5 mg/kg q2 to 3d
Suggested Readings Preziosi DE, Goldschmidt MH, Greek JS, et al. 2003. Feline pemphigus foliaceous: a retrospective analysis of 57 cases. Vet Derm. 14:313–321. Rosenkrantz WS. 2004. Pemphigus: current therapy. Vet Derm. 15: 90–98.
393
CHAPTER 167
Perinephric Pseudocysts Fernanda Vieira Amorim da Costa
Overview Perinephric pseudocysts (PNP) are formed by the accumulation of serous fluid in fibrous sacs surrounding one or both kidneys. They have been reported sporadically as a cause of apparent renomegaly and abdominal distention in the cat. Because the cyst wall is not lined with epithelium, the term pseudocyst is used. The PNP wall is thought to be derived from the renal capsule. Usually the cysts are attached to the hilus or the poles of the kidney. Fluid may accumulate in a subcapsular or extracapsular location, but the most common form reported in the cat is the accumulation of fluid between the renal capsule and renal parenchyma. Fluid usually has low protein content, low specific gravity, and low cell count. The pathogenesis of the perinephric fluid accumulation is not completely understood. Underlying renal parenchymal disease may be a factor because chronic renal disease is often present in association with pseudocysts, and progressive renal parenchymal contraction that impairs venous or lymphatic drainage could result in transudation. Typically fluid is a transudate of serum, although uriniferous pseudocysts have been reported. Uriniferous pseudocysts may occur from extravasation of urine between the kidney and renal capsule because of accidental or surgical trauma or an obstruction. Perirenal pseudocyst formation occurs primarily in older cats (the majority are over 8 years of age) and more often in males. There is no breed predisposition, although Persians, Siameses, domestic shorthair breeds, and domestic long-hair breeds are more represented than others. Even though Persians have PNP, it is a different clinical entity from polycystic kidney disease (PKD). PKD is an inherited autosomal dominant disease in which cats develop multiple, epithelial lined intrarenal cysts derived from proximal and distal tubular epithelium in renal cortical and medullary parenchyma. Affected cats usually are presented for nonpainful abdominal distension over weeks to months, although in many of them signs referable to renal dysfunction, such as polydipsia, polyuria, anorexia, weight loss, and vomiting, are evident. About 90% have at least mild chronic renal disease at the time of diagnosis. The differential diagnoses include renal neoplasia, abscess, hematoma, hydronephrosis, PKD, granulomatous interstitial nephritis due to feline infectious peritonitis (FIP), and pyelonephritis.
Diagnosis Primary Diagnostics • Abdominal Ultrasonography: This provides definitive diagnosis and is used to quickly and noninvasively exclude other causes of renomegaly such as polycystic kidneys, hydronephrosis, and renal neo-
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
394
(A)
(B) Figure 167-1 A, Ultrasonographic appearance of the right kidney of a cat with perinephric pseudocyst showing presence of anechoic fluid between the renal capsule and parenchyma, renal parenchymal atrophy, and lack of a corticomedullary junction. B, Ultrasound image of subcapsular perirenal pseudocyst in the left kidney showing perirenal accumulation of fluid and renomegaly. Images courtesy Dr. Gary D. Norsworthy.
plasia. The presence of anechoic fluid between the renal capsule and parenchyma is diagnostic for PNP. See Figure 167-1. Alterations in renal size, margination, echogenicity, and demarcation between cortex and medulla may be observed.
Perinephric Pseudocysts
Secondary Diagnostics • Physical Examination: Physical examination reveals a distended abdomen with one or two large palpable masses. This is not a pathognomonic for this disease. • Abdominal Radiographs: These usually show a large mass with softtissue radiopacity in the area normally occupied by the kidneys.
Diagnostic Notes • Fine-Needle Aspiration or Biopsy: Differentiation between abscess, hematoma, lymphoma, and PNP can usually be accomplished by obtaining a fine-needle aspirate or biopsy of the lesion. • A biopsy is associated with complications such as hemorrhage and deterioration of renal function but should be considered if there is evidence of renal neoplasia or a clinical suspicion that reversible renal disease may be present. • There is a high prevalence of urinary tract infection associated with PNP so a urine culture should be submitted when the diagnosis is made. • Unilaterally affected cats have lower median serum creatinine concentration than bilaterally affected cats.
Figure 167-3 Suture line breakdown, dehiscence, and evisceration are potential postoperative complications due to inherent poor wound healing as seen in this radiograph.
Treatment Primary Therapeutics • Capsulectomy: Resecting the cyst wall is the most common treatment, although it probably does not stop transudate production but may allow the transudate to be absorbed by the much larger surface of the peritoneal cavity. See Figure 167-2. If the cyst wall is insufficiently removed, a new pseudocyst may form, necessitating dissection to the renal hilus. Because of the continued fluid production from the cyst remnants after capsulectomy, ascites, and dehiscence may occur. See Figure 167-3.
Secondary Therapeutics • Drainage: Because of continual fluid production, needle drainage provides only temporary relief to the patient, lasting from days to months; it should be repeated as needed. This method may be preferable for cats with moderate to severe chronic renal failure depending upon the rapidity with which the PNP refills and the signs that the cat suffers as a result.
Figure 167-4 Intraoperative view of omentalization of the kidney following resection of the cyst wall. Photo courtesy Dr. Gary D. Norsworthy.
• Omentalization: Using the omentum to enhance physiologic draining of the fluid has been reported and may be useful in minimizing abdominal distention. The intrinsic ability of the omentum provides ongoing physiological drainage of continued secretions, eliminates dead space, and provides a source of neovascularization. See Figure 167-4.
Therapeutic Notes
Figure 167-2 Intraoperative view of the incised cyst wall exposing the kidney. Photo courtesy Dr. Gary D. Norsworthy.
• Renal biopsy of the contralateral kidney is useful for identify underlying parenchymal disease, but complications such as hemorrhage and deterioration of renal function must be considered. • Many cats with PNPs have concurrent chronic renal failure, and this should be addressed while managing the PNP. See Chapters 190 and 191.
395
SECTION 1: Diseases and Conditions
Prognosis Prognosis is related to the severity of renal dysfunction at the time the PNP is diagnosed and the ability of the cat to survive abdominal surgery. The length of postoperative survival is inversely correlated with serum creatinine concentration at the time of surgery. Cats with worse azotemia and few signs attributable to renal failure (i.e., anorexia, vomiting, weight loss, or anemia) carry a more guarded prognosis. But PNP still results in a better prognosis than almost any other intra-abdominal mass in an aged cat.
396
Suggested Readings Beck JA, Bellenger CR, Lamb WA, et al. 2000. Perirenal pseudocysts in 26 cats. Aust Vet J. 78(3):166–171. McCord K, Steyn PF, Lunn KF. 2008. Unilateral improvement in glomerular filtration rate after permanent drainage of a perinephric pseudocyst in a cat. J Fel Med Surg. 10(3):280–283. Ochoa VB, DiBartola SP, Chew DJ, et al. 1999. Perinephric pseudocysts in the cat: a retrospective study and review of the literature. J Vet Intern Med. 13(1):47–55.
CHAPTER 168
Peritonitis, Septic Sharon Fooshee Grace
Overview Septic peritonitis is a rapidly progressive life-threatening condition in small animals. Organ dysfunction is not usually limited to the peritoneal cavity alone, making this an exceedingly complex condition to manage. Early identification of the problem, resolution of the underlying cause, and aggressive management are critical to optimize the likelihood of a successful outcome. Septic peritonitis is less common in cats than dogs, and it has been demonstrated that cats with sepsis can present a clinical picture different from that of dogs. This is an important consideration because sepsis may be a concurrent problem with septic peritonitis. Thus, decisions about septic peritonitis in cats must be based on somewhat different information that than used to assess dogs. Septic peritonitis most commonly occurs after the peritoneum is contaminated by leakage of gastrointestinal (GI) contents. The list of possible underlying causes includes GI penetration by a foreign body (especially linear foreign bodies); rupture of the GI tract by blunt trauma; complication from a recent abdominal surgery; perforation of a gastric or intestinal ulcer (see Figure 168-1); bowel perforation by a tumor; rupture of a hepatic, pancreatic, or splenic abscess; rupture of the gall bladder or biliary tree; or a ruptured uterus (see Figures 168-2 and 182-4). Both aerobic and anaerobic bacteria are usually involved; the most common organisms isolated from cats with septic peritonitis are Escherichia coli, Enterococcus spp., and Clostridium spp. Polymicrobial infections, common with GI perforation, portend a worse prognosis. Nonspecific signs include fever, dehydration, and depression. The body temperature may become subnormal with the onset of septic shock. Mucous membranes are pale, and the capillary refill time is slow. Hyperemic mucous membranes did not appear to be a feature of sepsis in cats in one study. The pulse is often weak because of hypotension and hypovolemia. Abdominal palpation may reveal abdominal pain or
Figure 168-2 Pyometra can result in a friable uterus, which may rupture either spontaneously or during surgery. Photo courtesy Dr. Gary D. Norsworthy.
Figure 168-3 Fibrinous adhesions are visible on the spleen and other viscera of this cat with septic peritonitis. Photo courtesy Dr. Gary D. Norsworthy.
Figure 168-1 Perforation of a small bowel ulcer will cause a polymicrobial peritonitis due to gastrointestinal bacteria. Photo courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
distention, a foreign body, the presence of fluid, intussusception or plicated intestines, an abdominal mass, or an enlarged uterus. Release of bacterial toxins, vasoactive substances, and cellular proteases into the abdomen contribute to the systemic nature of this condition, leading to hypovolemia, acidosis, electrolyte disturbances, systemic inflammatory response syndrome, and septic shock. If GI contents are leaked into the peritoneum, chemical constituents of chyme (i.e., bile salts and pancreatic secretions) contribute to peritoneal inflammation and pain. If the cat survives for several days, fibrinous adhesions of organs often develop (see Figure 168-3).
397
SECTION 1: Diseases and Conditions
Diagnosis Primary Diagnostics • History: Anorexia, lethargy, vomiting, or diarrhea may be reported. The onset of illness is usually recent. • Physical Examination: The cat should be thoroughly examined for evidence of an external wound. Particular caution is indicated if a foreign body is suspected. Cats with septic peritonitis do not always have abdominal pain. In one study, only 62% of cats had demonstrable pain. Fluid accumulation may cause abdominal distention. Cats with sepsis may have a heart rate inappropriately low for their hemodynamic status (i.e., bradycardia with hypotension); the reason for this is unclear. • Complete Blood Count, Biochemical Profile, and Urinalysis: Several abnormalities in these tests are common, although not pathognomonic. The leukocyte count may be increased or decreased. A left shift with toxic changes in neutrophils is present is most cases. Hemoconcentration may be present and will contribute to azotemia. Hypoalbuminemia results from sepsis and the loss of large amounts of fluid into the abdominal cavity. Hyperkalemia occurs from transcellular shifts caused by to acidosis and decreased renal excretion. Blood glucose may be increased or decreased. Total bilirubin may be elevated. • Radiography: Abdominal radiographs may demonstrate a foreign body or intestinal plication. Fluid in the abdomen causes loss of serosal detail. Pneumoperitoneum suggests penetration of the bowel. Ileus is often present. If GI rupture is suspected, contrast studies using barium are contraindicated; however, iohexol or iodinated agents approved for intravenous use can be safely put in the GI tract. • Ultrasound: As a noninvasive procedure, ultrasound is particularly useful. It may detect a GI mass, abdominal abscess, pyelonephritis, pyometra, pancreatitis, or foreign body. • Diagnostic Peritoneal Lavage (DPL): For the initial attempt to collect fluid for cytology and culture, a needle or an 18-gauge plastic intravenous catheter may be used. The abdomen should be clipped and surgically prepped and the urinary bladder emptied. If fluid is not readily obtained with gentle suction, probing with the needle should not be attempted. The procedure should be repeated on another quadrant of the abdomen. If fluid is still not obtained, DPL should be considered because it achieves a diagnosis in most cases. Lavage with a multiholed catheter (such as a dialysis catheter) gives superior results to needle abdominocentesis and can detect small volumes of abdominal fluid. If a dialysis catheter is not available, a flexible Teflon vascular catheter with fenestrations cut into the sides is an acceptable alternative. The cat is placed in lateral recumbency, and the catheter is inserted into the abdominal cavity caudal to the umbilicus. The stylet should be withdrawn slightly as the catheter is advanced to prevent laceration of viscera. Warm normal saline, 20 mL/kg of body weight, is infused by gravity into the catheter as the cat is gently rolled from side to side for distribution of the fluid. Fluid should be allowed to flow back into the catheter by gravity. The fluid may appear benign yet still be diagnostic, so it must be evaluated regardless of gross appearance. Part of the fluid should be placed into a sterile container for culture. Microscopic examination of the sediment can be performed after the fluid is spun down in a blood tube containing ethylenediamine tetra-acetic acid (EDTA) anticoagulant. The supernatant should be poured off and the sediment resuspended by gently tapping the tube. A drop of fluid should be placed on a microscope slide, dried, and stained with a Romanowsky-type “quick stain.” Presence of bacteria, both free and intracellular, supports the diagnosis; toxic neutrophils may also be seen in the sediment. Diagnostic peritoneal lavage is not a therapeutic procedure and does not obviate the need for surgical exploration of the abdomen.
398
Diagnostic Notes • If a penetrating wound into the abdomen is found, surgical exploration is always indicated. This situation cannot be managed by flushing or probing the wound. • Because approximately 40% of cats with septic peritonitis in one study had no evidence of abdominal pain, absence of this sign cannot be used to rule out this condition. • Occasionally, the underlying cause for septic peritonitis cannot be identified.
Treatment Primary Therapeutics • Fluid Therapy: Patients with septic peritonitis are hypovolemic and hypotensive. They require aggressive fluid support to maintain adequate cardiac output and tissue perfusion. Most cats will have severe fluid deficits that need replacing, in addition to maintenance fluid requirements. A balanced electrolyte solution such as lactated Ringer ’s solution is a reasonable first choice. If the cat is severely hypotensive, fluid may be given at 45 to 66 mL/kg for 1 hour. Fluid therapy is expected to worsen pre-existing hypokalemia, so the need for potassium supplementation should be anticipated. See Chapters 114 and 302. • Antibiotic Therapy: Empirical therapy should be initiated while culture results are pending. Intravenous bactericidal antibiotics that achieve therapeutic levels in peritoneal fluid should be selected; these should have a broad-spectrum of activity and be effective against anaerobic GI flora. Suggested combinations include ampicillin (22 mg/kg q8h IV) or cefazolin (20 mg/kg q8h IV) or clindamycin (5–11 mg/kg q8–12h IV) or metronidazole (10 mg/kg q8–12h IV) and gentamicin (4.4 mg/kg q12h IV) or amikacin (10 mg/kg q8h IV) or enrofloxacin (5 mg/kg q12h IV). Aminoglycosides should not be used until hypovolemia has been corrected. • Surgery: Septic peritonitis is a surgically managed disease, but it should be postponed, when possible and only briefly, until the patient is stabilized. A ventral midline celiotomy incision should be made from the xiphoid to the pubis. Upon entry into the abdomen, the first priority is to search for perforation in the gastrointestinal tract, the most likely source of the infection. Perforation closure or anastamosis are needed. • Peritoneal Lavage of Abdominal Cavity: Copious amounts of warm normal saline should be used to flush out foreign material, devitalized tissue, and blood clots. Fluid should be suctioned until aspirated fluid is clear. Cold or room temperature fluid should not be used because this will contribute to hypothermia. Antiseptics (e.g., iodine or chlorhexidine) should not be added to the lavage fluid. There is no advantage to adding antibiotics to the lavage fluid because no greater concentration of drug is achieved than that given IV, and some antibiotics will contribute to peritoneal inflammation. If indicated, the abdomen should be closed routinely. • Abdominal Drainage: In some cases, all foreign material cannot be removed by peritoneal lavage. In this setting, open peritoneal drainage is preferred to placement of abdominal drains by most surgeons. After the final lavage, the rectus abdominus muscle is loosely apposed in its entire length with a polypropylene suture in a simple continuous pattern. A gap of 1 cm is left between the edges of the fascia. The subcutaneous tissue and skin are left open and then covered with a nonadherent gauze as the contact layer to prevent adherence of viscera to the bandage. Several additional layers of sterile dressings are applied for absorption of ongoing drainage. A sterile diaper or absorbent pad should be secured with tape or a stockinette. An Elizabethan collar may be indicated. The bandage should be changed several times daily for the first few
Peritonitis, Septic
days under light sedation. The drainage may increase for a few days before it begins to diminish in volume, at which time bandage changes may be needed no more than once daily. Surgical closure can be considered when the drainage is dramatically decreased in volume, the fluid contains no cytologic evidence of bacteria, and the cat’s condition has improved. The average period of open drainage is a few days.
Secondary Therapeutics • Nutritional Support: In most cases, nutritional support is indicated to offset the catabolic state and anorexia. A gastrostomy tube can be placed during the exploratory laparotomy or an esophagostomy tube can be placed after the abdomen is closed if the bowel is functional.
Therapeutic Notes • Acid-Base Derangements: Acid-base disturbances usually normalize or improve once fluid therapy is instituted.
Prognosis Prognosis is dependent on early recognition of peritonitis, management of systemic complications, and resolution of the underlying cause. Polymicrobial infections have been associated with an increased mortality rate.
Suggested Readings Brady CA, Otto CM, Van Winkle TJ, et al. 2000. Severe sepsis in cats: 29 cases (1986–1998). J Am Vet Med Assoc. 217(4):531–535. Costello MF, Drobatz KJ, Aronson LR, et al. 2004. Underlying cause, pathophysiologic abnormalities, and response to treatment in cats with septic peritonitis: 51 cases (1990–2001). J Am Vet Med Assoc. 225(6):897–902. Culp WTN, Zeldis TE, Reese MS, et al. 2009. Primary bacterial peritonitis in dogs and cats: 24 cases (1990–2006). J Am Vet Med Assoc. 234(7): 906–913.
399
CHAPTER 169
Plague (Yersiniosis) Sharon Fooshee Grace
Overview Plague, or yersiniosis, is an infamous zoonotic disease because of its highly contagious nature and associated lethality for humans and animals. The disease is caused by the facultative anaerobic gram-negative bipolar staining (Wrights-type stains) coccobacillus, Yersinia pestis. This organism has received significant attention in recent years because of its potential use as an agent of bioterrorism. Bacteremic rodents (i.e., prairie dogs, squirrels, mice, and rats) and their fleas serve as reservoirs for the organism. The most common route of transmission to humans is via bites from infected rodent fleas. The cat flea, Ctenocephalides felis, is a poor vector of the bacterium. Cats are perhaps the most susceptible of all domestic species to infection by Y. pestis. Although cats may become infected by flea bites, they also contract plague through ingestion of infected rodents or rabbits (via organism inoculation into oral mucous membranes) or very rarely, by inhalation of infected respiratory secretions. The incubation period is 3 to 4 days. Most feline cases in the United States are recognized in the summer and occur in the western states (i.e., New Mexico, California, Colorado, and Arizona). Plague is recognized on every continent except Australia. Three clinical forms of disease are recognized in cats (and humans): bubonic, septicemic, and pneumonic. These forms sometimes compose a continuum and, if untreated, the bubonic form may progress to the septicemic form and, eventually, the pneumonic form. Septicemic plague may occur without development of buboes (i.e., enlarged, suppurative lymph nodes). The pneumonic form is not common in cats but can develop from hematogenous or lymphatic spread of the organism. Respiratory secretions from cats with the pneumonic form can pose a serious risk for humans. The pneumonic form has a rapid incubation period and is almost 100% fatal if untreated; most fatalities are due to a delay in appropriate antimicrobial therapy. Cats suspected of being infected with Y. pestis should be held in hospital isolation and all personnel in contact with the cat should wear protective clothing (i.e., high density surgical masks, gloves, gowns, eye protection, and shoe covers) when handling the cat. Standard precautions may be adopted after 72 hours of therapy and evidence of clinical improvement. For all suspected cases, local and state public health officials should be notified prior to any sample submission and exposed people, including the owner, should consult with their physician immediately. An excellent resource, which includes a training module and video, may be found on the Center for Disease Control web site at (http://www.bt.cdc.gov/agent/plague/).
Diagnosis Primary Diagnostics • Clinical Signs: The bubonic form is most common in cats. It is characterized by very high fever and enlarged lymph nodes (usually in the area of inoculation) that eventually abscess and drain thick white
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
400
pus. The mandibular, cervical, and retropharyngeal nodes are most often involved, particularly after oral inoculation. The septicemic form results in fever, shock (i.e., tachycardia, weak pulses, brick-red mucous membranes, and prolonged capillary refill time), disseminated intravascular coagulation (DIC), and potentially multiorgan failure. In addition to shock and DIC, cats with the pneumonic form may present with cough, dyspnea, sneezing, nasal discharge, and severe acute respiratory distress syndrome. • Cytology: Cytological inspection and Gram stain of exudates or aspirates of lymph nodes or infected tissues should be performed. Samples from cats living in endemic areas should be examined with caution, especially if the lymph nodes of the head and neck are primarily involved. A monomorphic population of bipolar, “safety pin” appearing rods can be detected with routine in-office modified Wright’s stain or Giemsa stain. Gram stain will be negative. Due to significant edema that may surround enlarged lymph nodes, care must be taken to be sure the lymph node itself is aspirated. • Specific Tests: A number of tests can be performed for definitive diagnosis: culture of exudate or tonsillar swabs; rising (four-fold increase) antibody titers over a 10- to 14-day period; polymerase chain reaction (PCR) test of fresh or formalized tissue; and, direct immunofluorescent testing of microscope slides of air-dried exudates (multiple unstained slides should be submitted for evaluation). Check with your laboratory or public health official for where and how to submit samples.
Secondary Diagnostics • Thoracic Radiographs: Any cat suspected of having pneumonic plague should have thoracic radiographs examined immediately. Reported pulmonary lesions include diffuse interstitial pneumonia with coalescing areas of lung that represent pulmonary necrosis. Hilar lymphadenopathy and pleural effusion may be seen.
Diagnostic Notes • Samples submitted to diagnostic laboratories should be chilled and placed on ice (but not frozen), double-wrapped, and clearly marked as “suspected plague” to minimize risk to laboratory personnel. Veterinarians should never try to culture the specimen because of health hazards. • Culture material may be submitted in a red-top serum tube (nonglass tubes are preferred), in a capped sterile syringe, or with specialized transport media. Samples should be collected prior to institution of antibiotic therapy; thus, a high index of suspicion is necessary in endemic areas. • Cytology of uncomplicated cat bite abscesses reveals a mixture of various organisms, whereas buboes caused by plague are typically monomorphic in nature. • Obtaining a recent travel history is key to establishing a presumptive diagnosis in nonedemic areas. Cats with plague that do not have a history of travel to endemic areas could indicate a bioterrorist event; local and state public health officials and the CDC should be advised.
Plague (Yersiniosis)
Treatment Primary Therapeutics • Treatment should begin prior to results of confirmatory tests and should continue for several weeks beyond apparent resolution of signs. Twenty-one days of therapy is considered the minimum. If treatment has been initiated prior to sample recovery, samples should still be submitted. • Antibiotics: Aminoglycosides are considered the most effective; gentamicin is the drug of choice for cats (2–4 mg/kg q12–24h IM or SC). Cats are believed to be non-infectious after 72 hours; therefore, with signs of clinical improvement, route of administration may be changed from parenteral to oral. The Centers for Disease Control and Prevention has a published doxycycline dose of 5 mg/kg PO q12h. Fluoroquinolones have shown effectiveness in mice but have not yet been assessed in other species; however, they would be a reasonable alternative to doxycycline and are recommended by some public health agencies. No medication should be given by the oral route until the cat shows signs of clinical improvement because the organism is present in saliva for the first few days. • Buboes should be drained and flushed with chlorhexidine solution. Material collected should be double-bagged and burned. Consult a diagnostic laboratory or health official if additional information is needed for handling infected material.
Secondary Therapeutics • The patient, environment, and other exposed animals should be treated for fleas if they are noticed on the cat or in the nearby premises.
Therapeutic Notes • The zoonotic risk of this disease should always be considered and discussed with all hospital personnel before any therapy is initiated. Cats should be hospitalized in strict isolation and not sent home until significant clinical improvement is evident (at least 72 hours). • In endemic areas, abscesses should be evaluated by cytology before surgical drainage is established so that appropriate safety measures may be taken for all personnel. • Routine disinfectants are sufficient to kill Y. pestis organisms that contaminate the hospital environment. Owners should be advised to disinfect the home environment. • Control of rodents should be emphasized in areas endemic for plague. Cats should not be allowed to roam and hunt freely. Flea control programs are essential for cats and dogs at risk of rodent exposure.
Prognosis In both cats and humans, all forms of plague warrant a grave prognosis unless treatment is initiated within 24 hours of exposure. The most favorable prognosis belongs to cats that develop the bubonic form without progression to septicemia. Cats that have been previously infected are not protected from reinfection, septicemia, or death.
Suggested Readings Davis RG. 2004. The ABCs of bioterrorism for veterinarians, focusing on category A agents. J Am Vet Med Assoc. 224(7):1084–1104. Macy D. 2006. Plague. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 439–445. Philadelphia: Saunders Elsevier. Orloski KA, Lathrop SL. 2003. Plague: A veterinary perspective. J Am Vet Med Assoc. 222(4):444–448.
401
CHAPTER 170
Plant Toxicities Karen M. Lovelace
Overview
Diagnosis
Poisonous plants are a significant source of morbidity and mortality in cats, second only to pesticide poisonings. In cases of suspected plant ingestion, identification of the inciting agent can be difficult and frustrating for the veterinarian. Usually the event is not witnessed, and the name of the plant is unknown. To complicate matters, several common names often exist for any given plant, and common names may vary geographically. Few antidotes or specific treatments exist, so most patients are treated with supportive care and symptomatic therapy. Nevertheless, an accurate physical or genus and species identification will help direct treatment and improve chances for success as well as aid in serving clients with a prognosis. The chances of successful treatment are increased when treatment is performed early and aggressively. Due to the large number of plant species in existence, the clinician should focus on four key principles: (a) Whether or not identification is achieved, the clinician should have a generic treatment plan for suspected toxic plant exposures, such as that outlined in this chapter. (b) Veterinarians should also be aware of the resources available to them for identifying plants and making therapeutic choices. Several good resources are listed in this chapter. (c) It is also important for the clinician to have a basic knowledge of those plants that are most dangerous to and most commonly encountered by their target species. This chapter highlights some of the most toxic and the most common plant poisonings in cats. (d) Finally, the clinician should be able to educate clients on how to make their environments safer for their pets and how to prevent future exposures.
Primary Diagnostics • Signalment: While no specific signalment exists, at least half of plant poisoning cases occur in cats age 1 year or younger. • History: In addition to attempts at plant identification, questions including quantity consumed, parts of the plant consumed (i.e., leaves, fruit, flowers, stems, berries, nuts, and so on), and time since the ingestion should be asked of any potential witness. • Clinical Signs: Although clinical signs are dependent on the type of plant ingested, the majority of plants will induce vomiting. However, virtually any system can be affected depending on the plant involved. • Examination of Stomach Contents: Stomach contents should be saved for confirmation of exposure and to aid in specific plant identification.
Diagnostic Notes Resources for Plant Identification • See Tables 170-1 and 170-2 and Figures 170-1 through 170-25. • National Animal Poison Control Center: The National Animal Poison Control Center (NAPCC) is a 24-hour emergency service with phones manned by licensed veterinarians and toxicologists. There is a $50.00 consultation fee for each call. From anywhere in the United States, call 1-888-426-4435.
TABLE 170-1: Plants Toxic to Cats African Violet Almond, Bitter Almond (Pits of) Aloe Amaryllis Andromeda japonica Apple (seeds and leaves) Apricot (Pits and leaves) Arrowgrass Arrowhead Vine, African Evergreen, Goosefoot, Nephthytis Asparagus Fern, Plumosa Fern, Emerald Feather, Emerald Fern Autumn Crocus, Meadow Saffron Avacado Weeping Fig, Mistletoe Fig, Creeping Fig, Rubber Plant Baby’s Breath, Covent Garden Baneberry, Doll’s Eyes Bayonet
Colchicum autumnale, Crocus sativus Persea americana Azalea spp.
Beargrass Beech Bird of Paradise Black-eyed Susan Black Locust Bleeding Heart, Dutchman’s Breeches, Staggerweed, Squirrel Corn Bloodroot Bluebonnet (not Texas Bluebonnet), Lupine Boxwood, Box, Common Box Buckeye, Horse Chestnut Buddist Pine Buttercup, Meadow Buttercup, Lesser Spearwort, Crowfoot Candelabra Cactus, False Cactus Caladium, Elephants Ears
Gypsophilia paniculata Actaea spp. Yucca spp.
Calla Lily Carnation, Rainbow Pink, Divine Flower, Clove Pink
Saintpaulia ionantha Prunus dulcis var amara) Any Aloe spp. Amaryllis spp. Pieris japonica Malus spp. Prunus armeniaca Triglochin spp. Syngonium spp. Asparagus spp.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
402
Nolina spp. Fagus spp. Caesalpinia spp. Rudbeckia hirta Robinia pseudoacacia Dicentra spp. Sanguinaria spp. Lupinus spp. Buxus sempervirens Aesculus spp. Podocarpus macrophylla Ranunculus spp. Myrtillocactus cochal Caladium spp., Alocasia spp. Zantedeschia spp. Dianthus spp.
TABLE 170-1 Continued Castor Bean Plant Ceriman, Swiss Cheese Plant, Fruit-salad Plant, Hurricane Plant, Cut-leaf or Split-leaf Philodendron, Mexican Breadfruit Cherry, Groundcherry Cherry Laurel Chinese Evergreen Chinaberry Tree Christmas Rose, Black Hellebore Chrysanthemum, Marguerite, Ox-eye Daisy Cineria, Groundsel, Dusty Miller, Butterweed, Wax Vine, Cape Ivy, German Ivy, Parlor Ivy, Natal Ivy, Water Ivy Virgin’s Bower, Old Man’s Beard, Traveler’s Joy Coriaria Cornflower Cornstalk Plant, Corn Plant Creeping Charlie Croton Cordatum Corydalis, Golden or Bulbous Crown of Thorns Cuban Laurel Cycad Palm Cyclamen Daffodil, Trumpet Narcissus, Jonquil, Tazette, Pheasant’s Eye Daphne Day Lily Death Camas Devil’s Ivy, Goldon, Satin, or Silver Pothos, Hunter’s Robe, Ivy Arum Dracaena, Dragon Tree, Madagascar Dragon Tree, Ribbon Plant, Corn/Stalk Plant, Florida Beauty, Janet Craig, Warneckei, RedMargined, or Striped Dracaena Dumb Cane, Charming Dieffenbachia Eggplant Elderberry, Elder, Danewort, Dwarf Elder, Red Berried Elder Eucalyptus, Blue Gum, Cider Gum, Australian Fever Tree, Silver Dollar Euonymus, Japanese Euonymus, Spindle, Burning Bush Ferns Fiddle-leaf fig Flamingo Plant Flax Four O’Clock Foxglove, Long Purples, Dead Men’s Fingers Geranium Gladiolas Glory Lily Heavenly Bamboo Hellebore, False or White Hemlock, Water Hemlock, Poison Hemlock Henbane Holly, English Holly, Yaupon, Possumhaw Honeysuckle Hyacinth, Dutch or Garden Hydrangea, Hills of Snow, Hortensia, French Hydrangea
Ricinus communis Monstera deliciosa
Physalis spp. Prunus laurocerasus Aglaonema spp. Melia azedarach Helleborus spp. Chrysanthemum spp., hybrids Senecio spp.
Clematis spp. Caesalpinia spp. Centaurea spp. Dracaena frangrans Pilea nummulariifolia Croton tiglium Philodendron oxycardium Corydalis spp. Euphorbia milii Ficus spp. Cycas spp. Cyclamen spp. Narcissus spp. Daphne spp. Hemerocallis spp. Zigadenus spp. Epiprennum aureum Dracaena spp.
Dieffenbachia spp. Solanum melongena Sambucus ebulus
Indian Rubber Plant Iris Ivy, Branching Ivy, English, Nepal, Irish, Atlantic, or Persian Ivy Jack in the Pulpit Japanese Show Lily, (also Asiatic Show Lilies) Java Beans, Lima Beans (Uncooked) Jessamine, Chinese Inkberry Jerusalem Cherry, Winter Cherry, Christmas Cherry, Natal Cherry, Ornamental Pepper Jimson Weed, Moonflower, Thorn apple Kalanchoe Velvet Elephant Ears, Devil’s Backbone, Tree Philodendron, PalmBeach-bells, Lavender-scallops, Feltbush Lantana, Yellow Sage, Bunchberry, Shrub Verbena Larkspur Laurel: Mountain, Dwarf, or Black Lily, including Asian Lilies
Easter Lily Peace Lily, White Anthurium, Snowflower, Mauna Loa, Spathe Flower Lily of the Valley Stargazer Lily Tiger Lily Wood Lily Locoweed Marigolds Marijuana Mescal, Mescal Button or Bean, Peyote Mistletoe Mock Orange Monkshood Moonseed Mother-in Law’s Tongue, Snake Plant Morning Glory, Pearly Gates, Bindweed Mushrooms
Eucalyptus spp. Euonymus spp. Sprengeri fern, Nephrolepis spp. Ficus lyrata Anthurium spp. Hesperolinon spp. Mirabilis spp. Digitalis purpurea Pelargonium spp. Gladiola spp. Gloriosa spp. Nandina domestica Veratrum spp. Conium maculatum Hyoscyamus niger Ilex spp. Lonicera spp. Hyacinthus orientalis Hydrangea macrophylla
Nephthysis, Green-Gold Nephthysis Nightshade: Black, Deadly, or Bittersweet, Wild, or Woody Nutmeg Oleander Onion, Garlic Peach (pits and leaves) Peony Periwinkle Philodendron, Emerald Duke, Red Emerald, Majesty Plant, Panda Plant, Parlor Ivy, Red Princess, Sweetheart Plant, Saddleleaf Philodendron, Variegated Philodendron Pimpernel Plum Poinciana Poinsettia, Christmas Star Poison Ivy, Poison Oak, Poison Sumac Pokeweed, Pokeberry, Poke Salad
Ficus elastica Iris spp. Any Hedera spp. Arisaema triphyllum Lilium speciosum Senna obtusifolia Cestrum spp. Solanum pseudocapsicum Datura stramonium Kalanchoe spp. and Bryophyllum spp. Lantana camara Delphinium spp. Kalmia spp., Leucothoe spp. Any Convallaria spp., any Spathiphyllum spp., any Lilium spp. Lilium longiflorum Spathiphyllum spp. Convalleria majalis Lilium orientalis Lilium lancifolium Lilium philadelphicum Oxytropis and Astragalus spp. Tagetes spp. Cannabis sativa Lophophora williamsii, Sophora spp. Phoradendron flavescens Philadelphus spp. Aconitum spp. Menispermum spp. Sansevieria trifasciata Ipomoea spp. Amanita spp., orellanine, and monomethylhydrazine spp. Syndonium podophyllum Solanum nigrum, Atropa belladonna,.and Solanum dulcamara Myristica fragrans Nerium oleander Allium spp. Prunus serotina Paeonia spp. Vinca spp. Philodendron spp.
Anagallis spp. Prunus spp. Delonix and Peltophorum spp. Euphorbia pulcherrima Toxicodendron spp. Phytolacca americana
403
TABLE 170-1 Continued Poppy Papaver spp., California Poppy Potato Primrose, Poison Primrose, German Primrose Privet, Wax-Leaf Ligustrum Rhododendron, Azaleas Rhubarb, Garden Rhubarb, Pie Plant, Wine Plant, Water Plant Rosary Pea, Prayer Bean, Jequerity, Precatory Bean Rubber Plant (American or Baby), Pepper Face Sago Palm, Leatherleaf Palm, Japanese Fern Palm Schefflera, Umbrella Tree, Starleaf, Rubber Tree Scotch Broom Skunk Cabbage Snowdrop Snow on the Mountain, Ghost Weed Star of Bethlehem, Summer Snowflake, Nap-at-noon, Dove’s Dung
Eschscholzia californica Solanum tuberosum Primula spp. Ligustrum spp. Rhododendron spp. Rheum rhabarbarum
Sweet pea Tansy Ragwort Taro Vine, Marble Queen Tobacco Tomato Plant (nonripe fruit is non-toxic)
Abrus precatorius
Tulip Tung Tree, Tung Oil Tree Virginia Creeper
Peperomia obtusifolia Cycas spp. or Macrozamia spp. Schefflera spp. or Brassaia spp. Cytisus scoparius Lysichiton spp. Galanthus nivalis Euphorbia marginata Ornithogalum spp.
Water Hemlock, Cowbane Weeping Fig, Java Willow, Benjamin Tree, Small-leaved Rubber Plant Wisteria, Chinese Kidney Bean Yellow Oleander Yesterday, Today, and Tomorrow Yews Yucca
Lathyrus spp. Senecio jacobae Scindapsus aureus Nicotiana spp. Lycopersicon lycopersicum Tulipa spp. Aleurites spp. Parthenocissus quinquefolia Cicuta spp. Ficus benjamina Wisteria sinensis Thevetia peruviana Brunfelsia australis Taxus spp. Yucca gloriosa
Note: Underlined item, Commonly Encountered Toxic House Plants; Bolded item, Highly Toxic. Disclaimer: This listing represents some of the most commonly encountered toxic house and yard or garden plants as well as those that are considered to be most dangerous. This list is not intended to be an all inclusive list of toxic plants. Common or dangerous plants may vary by region.
TABLE 170-2: Plants Highly Toxic to Cats For all plants listed, general therapy should include symptomatic and supportive treatment as described in the text, regardless of specific treatment or antidote. Plant Name, Family, or Species
Toxic Principle
Toxic Part of Plant
Clinical Signs
Specific Treatment and Prognosis
Kalanchoe spp. (Devil’s backbone, Mexican hat plant)
Cardiac Glycoside.
All parts, especially flowers.
Vomiting, diarrhea, ataxia, trembling, sudden death.
Oleander
Cardiac Glycoside.
All parts, especially dry or dead leaves.
Vomiting, diarrhea (with or without blood), arrhythmias.
Foxglove
Cardiac Glycoside.
All parts, especially flowers, fruit, and young leaves.
Gastrointestinal signs, then bradycardia and any type of arrhythmia.
Lily of the Valley
Cardenolide: Cardiotoxin.
All parts, especially the roots.
Vomiting and ptyalism, then bradycardia and any type of arrhythmia. Seizures or sudden death may occur.
Antidote: Digibind Fab® at a dose of 1.7 mL Fab per mg digoxin ingested given slowly. Give as a bolus if cardiac arrest is expected. The patient should improve in 30 minutes and recover in 4 hours. Monitor potassium levels and an electrocardiogram rhythm. Prognosis is good, unless hyperkalemia or uncontrollable arrhythmias develop. Antidote: Digibind Fab® at a dose of 1.7 mL Fab per mg digoxin ingested given slowly. Give as a bolus if cardiac arrest is expected. The patient should improve in 30 minutes and recover in 4 hours. Monitor potassium levels and an electrocardiogram rhythm. Prognosis is good, unless hyperkalemia or uncontrollable arrhythmias develop. Antidote: Digibind Fab® at a dose of 1.7 mL Fab per mg digoxin ingested given slowly. Give as a bolus if cardiac arrest is expected. The patient should improve in 30 minutes and recover in 4 hours. Monitor potassium levels and an electrocardiogram rhythm. Prognosis is good, unless hyperkalemia or uncontrollable arrhythmias develop. No known antidote. Monitor potassium levels and cardiac rhythm. Prognosis is good unless hyperkalemia or uncontrollable arrhythmias develop.
404
TABLE 170-2 Continued Plant Name, Family, or Species
Toxic Principle
Toxic Part of Plant
Clinical Signs
Specific Treatment and Prognosis
Taxus genus (Yews)
Taxine: Negative Inotrope/ Chronotrope.
All parts are toxic.
Sudden death, vomiting, or CNS signs.
Prunus genus (Apples, Apricots, Cherries, Peaches, Plums)
Cyanide.
Seeds, although low levels in Cherry laurel leaves and fruit.
Local irritation, anxiety, dizziness, vomiting, dyspnea, and darker mucous membranes. Sudden death may occur due to cardiac or respiratory arrest.
Family Solanaceae (Nightshade)
Inhibit Cholinesterase.
All parts, especially berries and unripe fruit.
Family Ranunculaceae (Buttercup)
Protoanemonina. Unknown: Strong mucosal irritant, which may also cause hypocalcemia. Oxalate crystals and other unidentified enzymes.
Fresh leaves and stems.
Lilies
Unknown: Acute Renal Failure.
All parts, even pollen.
Castor Bean
Ricin: Cell death (blocked protein synthesis).
All parts, especially the beans.
Cycad Palms
Cycasin: Hepatic Failure.
All parts, especially the seeds.
Autumn Crocuses
Colchicine: Alkaloid (prevents cell division).
All parts, especially flower, corm, and seeds.
Vomiting, diarrhea, mydriasis, ataxia, weakness, drowsiness. Vomiting, diarrhea (with or without blood), intense gastrointestinal irritation and abdominal pain. Oral irritation and severe burning, ptyalism, with possible dysphagia and airway compromise; Ocular irritation, renal disease, and central nervous system signs (excitement, tetany, seizures) are possible. Vomiting, depression, lethargy, and anorexia followed by renal failure within 72 hours. Signs are delayed up to 3 days; Gastrointestinal signs, circulatory collapse, cyanosis, convulsions, ataxia, weakness, and renal failure are possible. Severe and rapid vomiting, diarrhea, with possible ataxia, coma, or seizures. Eventual lethal hepatic necrosis. Initially abdominal pain, dysphagia, vomiting, diarrhea, paralysis, convulsions, and eventual multiple organ failure.
No known antidote. Treat with Dobutamine at 0.5–1.0 µg/kg per minute intravenous infusion and atropine 0.02–0.04 mg/kg IV as necessary for heart rate and contractility. Prognosis is guarded if clinical signs are present. No specific antidote. If the poisoning is severe or if a cyanide containing plant is confirmed, 3% sodium nitrite 16 mg/kg IV, followed by 1.65 mL of 25% sodium thiosulfate. Repeat as necessary at one-half the dose in 30 minutes. Sodium nitrite can be fatal if cyanide is not present. Prognosis is good if the cat is still alive 3 hours after consumption, especially if treatment is given early. No specific antidote. Treat with atropine 0.1– 0.5 mg/kg (one-fourth IV and three-fourth IM) and 2-PAM 10–20 mg/kg slowly IV. Prognosis is good if treatment is early and aggressive. No known antidote. Prognosis is good, unless bloody diarrhea or severe abdominal pain is present.
Family Araceae (Peace Lily, Ivy, Philodendron, Dieffenbachia, and Dumbcane).
All parts, but crystals are usually concentrated in the stalks, and sometimes in the leaves.
No known antidote. Prognosis is good if treatment is early and aggressive.
No known antidote. Prognosis is guarded if the cat is oliguric or anuric or if treatment is not initiated within 24 hours. Refer to Chapter 189. Renal function may return within weeks; chronic renal failure may develop as a consequence. No known antidote. If circulatory collapse is imminent, infusion of dobutamine at 5–15 µg/kg/ minute may be warranted. Prognosis is good if treatment is early and aggressive but guarded if clinical signs develop.
No known antidote. Prognosis is poor if liver signs are present.
No known antidote. Prognosis is guarded.
405
TABLE 170-2 Continued Plant Name, Family, or Species
Toxic Principle
Toxic Part of Plant
Clinical Signs
Specific Treatment and Prognosis
Yesterday, Today, and Tomorrow
Brunfelsamidine: Neurotoxin.
All parts are toxic.
Rhododendron, Azalea, Laurel
Grayanotoxins: Na Channel Blockers.
All parts are toxic.
Rapid onset of gagging, sneezing, vomiting, or nystagmus. Tremors progress to rigid seizures and death. Protracted vomiting with significant risk of aspiration. Arrhythmias, seizures, ataxia, weakness, and depression may occur.
No known antidote. For seizure control, diazepam may be warranted at 0.5 mg/kg IV repeated once if necessary, then with pentobarbital at 5–20 mg/ kg IV to effect. Prognosis is guarded. Duration of clinical signs may be days, and recovery may take several weeks. No known antidote. Monitor electrocardiogram and keep the cat’s head elevated above the stomach. Diazepam used as above may be warranted for central nervous signs. The prognosis is good unless seizures are present or aspiration pneumonia results.
Figure 170-1
Azaela (Rhododendron spp.); highly toxic.
Figure 170-3
Catalina Nightshade (Solanum wallacei); highly toxic.
Figure 170-2
Easter Lily (Lilium longiflorum); highly toxic.
Figure 170-4
Cycad Palm (Cycas spp.); highly toxic.
406
Figure 170-5 Stargazer Lily (Lilium orientalis); highly toxic. Figure 170-8
Texas Mountain Laurel (Kalmia spp.); highly toxic.
Figure 170-6 Foxglove (Digitalis purpurea); highly toxic.
Figure 170-9
Oleander (Nerium oleander); highly toxic.
Figure 170-7 Kalanchoe (Kalanchoe spp.); highly toxic.
Figure 170-10 Asparagus Fern (Asparagus spp.); commonly encountered by cats.
407
Figure 170-11
Ceriman (Monstera deliciosa); commonly encountered by cats.
Figure 170-14 Dumbcane (Dieffenbachia spp.); commonly encountered by cats.
Figure 170-12
Chinese Evergreen (Aglaonema spp.); commonly encountered by cats.
Figure 170-15 Dumbcane (Dieffenbachia spp.); commonly encountered by cats.
Figure 170-13 by cats.
Devil’s Ivy or Pothos (Epiprennum aureum); commonly encountered
408
Figure 170-16 English Ivy (Hedera helix); commonly encountered by cats.
Figure 170-17 Euonymus (Euonymus spp.); commonly encountered by cats.
Figure 170-20 by cats.
Figure 170-18 Holly (Ilex spp.); commonly encountered by cats.
Figure 170-21 Hydrangea (Hydrangea macrophylla); commonly encountered by cats.
Figure 170-19
Janet Craig Dracaena (Dracaena spp.); commonly encountered by cats.
Figure 170-22
Red170-Margined Dracaena (Dracaena spp.); commonly encountered
Nephthysis (Syndonium podophyllum); commonly encountered by cats.
409
SECTION 1: Diseases and Conditions
• University Toxicology Departments: Contacting one of the veterinary toxicology departments may be a less expensive, albeit slower, means of acquiring information than contacting the NAPCC. • Reference Books: Numerous toxicology texts exist to guide the practitioner. A detailed list of toxic plants and their various names, clinical signs, prognoses, treatments, toxic agents, toxic plant parts, and lethal doses can be found in Small Animal Toxicology by Peterson and Talcott. See Suggested Readings. • In some areas, local veterinary medical associations have compiled databases on geographically common or important plant poisonings. Reporting your own cases may help to establish or improve already existing local databases.
Treatment Peace Lily (Convalleria majalis); commonly encountered by cats.
Primary Therapeutics
Figure 170-24
Philodendron (Philodendron spp.); commonly encountered by cats.
• Oral Rinse: The oral cavity should carefully be rinsed, especially when irritating plants are ingested. Rinsing should be repeated after the patient vomits. • Decontamination (Emesis): If ingestion of the plant is within 4 hours and the cat is asymptomatic, or if the ingested plant is known to cause systemic effects, emesis should be induced unless contraindicated (see Therapeutic Notes). For clients at home, emesis can be induced with ipecac syrup (2–6 ml/cat PO). Hydrogen peroxide is highly irritating to tissues and can result in orogastric mucosal ulceration. Under veterinary supervision, xylazine can be used (0.4–0.5 mg/kg IV), then reversed with yohimbine (0.1 mg/ kg IV) after vomiting has occurred. Apomorphine is not recommended for use in cats. • Decontamination (Activated Charcoal): Give 2–5 g/kg after induced emesis is completed. Prepared liquid mixtures of activated charcoal should be given according to the manufacturer ’s directions. For dry weight activated charcoal, each gram should be mixed with 5 mL of water. Administration should be repeated every 3 to 6 hours thereafter. A minimum of several doses is recommended. In animals without signs of respiratory compromise, orogastric tube administration is recommended for fast and reliable administration of activated charcoal. (See Chapter 308). • Laxatives: Laxatives should be given no sooner than 30 minutes after administration of activated charcoal. Osmotic cathartics, such as polyethylene glycol electrolyte solution (GoLYTELY®; 25 ml/kg PO) or lactulose (0.22 ml/kg PO), are generally effective. • Fluid Therapy: If systemic signs develop, administer fluids IV. Fluids should be administered as necessary during cathartic therapy. Lactated Ringer ’s solution (LRS) should be avoided in cases of cardiac toxicity, hepatic failure, or acute renal failure. Balanced electrolyte solutions, such as LRS, are the fluid of choice for toxicities primarily involving the gastrointestinal system. • Arrhythmias: An electrocardiograph (ECG) should be performed to monitor for arrhythmias; treat as appropriate. Lidocaine can be given (1 mg/kg IV) as a bolus and repeated as needed for severe ventricular arrhythmias. Cats tend to be more sensitive to the central nervous system (CNS) effects of lidocaine; therefore, caution is advised.
Figure 170-25
Philodendron (Philodendron spp.); commonly encountered by cats.
Figure 170-23
Secondary Therapeutics • Internet: Information is available at no cost through the American Society for the Prevention of Cruelty to Animals (ASPCA) web site: www.aspca.org/apcc. This web page contains useful pictures of toxic and nontoxic plants, as well as general management principles for plant exposures. Other plant databases such as www.plants.usda.gov are useful for finding pictures of various plants.
410
• Enemas: An enema given 6 to 12 hours after ingestion may help clear remaining plant matter from the gastrointestinal tract and prevent further absorption. • Antiemetic Therapy: Maropitant (Cerenia; 1 mg/kg q24h SC), dolasetron mesylate (0.3–0.6 mg/kg q12h PO, SC, or IV), or metoclopramide (0.2–0.5 mg/kg q6–8h SC) can be used to control vomiting.
Plant Toxicities
• Antidiarrheal Therapy: Commercially prepared probiotic preparations containing Enterococcus faecium are available for the symptomatic treatment of diarrhea in cats. Formulations specifically designed for cats include nutritional supplements that can be added to food (FortiFlora; one sachet q24h PO), or oral gels/pastes, which are administered every 8 to 12 hours as needed by mouth. Some preparations include adsorbing and firming agents such as kaolin and pectin. Alternatively, loperamide (Imodium; 0.08–0.16 mg/kg q12h PO) or diphenoxylate with atropine (0.05–0.1 mg/kg q12h PO) can be given to control more retractable cases of diarrhea. • Control Gastrointestinal Irritation: Sucralfate (0.25 g q8–12h PO) can be used as a gastrointestinal protectant, but it should be given at least 30 minutes prior to administration of an H2 receptor antagonists such as ranitidine (2.5 mg/kg q12h IV), famotidine (0.5–1.0 mg/kg q12– 24h PO, SC, or IV), or cimetidine (10 mg/kg q6–8h PO, IV, or IM). • Chemistry Panel Monitoring: Monitor electrolytes, kidney values, and liver enzymes as indicated.
Therapeutic Notes • Emetics are contraindicated if the cat is having seizures or is in a coma or a state of stupor. Emetics are also contraindicated if there is a reasonable chance of aspiration. If seizures are anticipated, phenothiazine tranquilizers are contraindicated. Emesis should not be induced after ingestion of plants causing mechanical irritation or trauma. Emesis with ipecac is contraindicated if a cardiac toxin is suspected. • Emetics will remove no more than 50% of the plant matter from the gastrointestinal tract. Therefore, emetics should always be followed by the use of activated charcoal and laxative therapy. • Laxatives or enemas are contraindicated in patients with diarrhea, and the use of mineral oil as a laxative is contraindicated in dyspneic patients or when vomiting cannot be controlled. • Digoxin immune Fab (Digibind) is commercially available for use in cardiac glycoside toxicity. Although expensive, use should be considered in cases of imminent cardiac arrest, hyperkalemia, or arrhythmias nonresponsive to other medical therapies. The dose is 1.7 mL Fab per mg of digoxin ingested. Give slowly over 30 minutes unless cardiac arrest is expected. The patient should improve after 30 minutes and recover within four hours. • Bismuth subsalicylate as an anti-diarrheal should be used with caution in cats due to salicylate toxicity.
• Loperamide and metoclopramide may decrease gastrointestinal transit time, thereby slowing the excretion of plant matter. • Phosphate enemas (Fleet) are contraindicated in cats.
Prevention • Clients should be directed to databases of nontoxic, cat friendly plants. Such databases exist on various web pages, such as those listed previously, or in various text books. • Efforts to alleviate boredom, increase physical activity or play time, increase supervision, and reduce confinement may reduce a cat’s temptation to eat plant material. • All plants, such as in hanging baskets, should be housed well out of reach of cats. • Safe alternatives may be provided by planting “cat grass” or catnip, which the cat is allowed to eat. Many kits are commercially available, and pregrown and dried sources are available as well. However, any plant that resembles grass may be considered acceptable to eat by the cat, and ingestion of grass may cause gastritis and vomiting in some patients. Catnip is mildly toxic, but large amounts must be consumed to cause vomiting or diarrhea. • Misting plants with water then applying a light dusting of cayenne pepper may inhibit a cat from chewing on plants.
Prognosis Prognosis depends on the type, amount, and part of the plant ingested as well as time from ingestion to initiation of therapy. Early and aggressive therapy offers the best chances for a successful recovery.
Suggested Readings Barr, AC. 2001. Household and Garden Plants. In ME Peterson, PA Talcott, eds., Small Animal Toxicology, pp. 263–320. Philadelphia: WB Saunders. Dunayer, E. 2005. The 10 Most Toxic Plants. NAVC Clinician’s Brief. 3(3):11–14. Hovda, L. 2005. Plant Toxicities. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 250–253. St. Louis: Elsevier Saunders. Smith, G. 2004. Kalanchoe Species Poisonings in Pets. Vet Med. 11: 933–936.
411
CHAPTER 171
Pleural Effusion Gary D. Norsworthy
Overview Fluid flow through the pleural space is a continuous process. Its source is the high-pressure parietal circulation. As pleural fluid forms, it is removed via the low-pressure visceral circulation so that constant movement occurs. An abnormal collection of fluid in the pleural space constitutes pleural effusion. Although the pleural cavity is a negligible space in the healthy cat, the presence of fluid causes pulmonary compression, enlarging the pleural space so that 200 mL or more of fluid may be present. There are five mechanisms responsible for the formation of pleural effusion: Increased venous or capillary hydrostatic pressure; decreased capillary oncotic pressure due to hypoalbuminemia; increased capillary membrane permeability; lymphatic obstruction; or spillage and hemorrhage. (Hemothorax is disputably included as a form of effusion.)
Cats of any age, breed, or sex may be affected. Many cats are reported to have an acute onset of dyspnea or tachypnea. However, most causes of pleural effusion are not peracute. The cat’s ability to conceal disease until the crisis stage is reached prevents many owners from detecting disease in the early stage. Many cats with pleural effusion will have a history of lethargy and anorexia of one to several days duration. Some will also have weight loss. Physical examination may reveal tachypnea, orthopnea, cyanosis, fever, and dehydration. The notable sign in advanced disease is dyspnea; however, diseases of slower onset may cause systemic changes (i.e., lethargy or anorexia) that may cause the owner to seek veterinary care. Some of these cats will only experience tachypnea that may not be perceptible to the owner. The cat’s respiratory pattern should be observed carefully while it is on the examination table, preferably with no one touching the cat.
TABLE 171-1: Interpretation of Pleural Fluid Analysis T
MT
NSE
SE
CE
HE
Yellow or pink
Yellow or pink
Red
Clear to cloudy
Opaque
Opaque
Protein
<1.5
2.5–5.0
2.5–6.0
3.0
Fibrin Triglycer-ide Bacteria Nucleated cells/mL
Absent Absent Absent <1,000
Absent Absent Absent 1,000–7,000 (LSA: up to 100,000)
Present Absent Present 5,000–300,000
Variable Present Absent 1,000–20,000
Present Absent Absent Like peripheral blood
Cytology
Mesothelial cells
Erythrocytes; some macrophages engulfing erythrocytes
Hypoalbuminemia, early CHF
Degenerate PMN; some macrophages and neoplastic cells Pyothorax
Small lymphocytes; some macrophages; PMN
Diseases
Macrophages; Mesothelial cells; nondegenerate PMN; neoplastic cells Chronic CHF; neoplasia; diaphragmatic hernia; pancreatitis
Clear to cloudy; fibrin 3.0–6.0 (FIP: 3.5–8.5 Present Absent Absent 5,000–20,000 (LSA: up to 100,000) Nondegenerate PMN; macrophages
Yellow or pink or brown Clear to opaque; flocculent 3.0–7.0
Milky
Turbidity
Colorless to pale yellow Clear
Chylothorax (obstructed or ruptured thoracic duct; HW; neoplasia; CHF; lung lobe torsion; trauma)
Hemothorax (trauma; coagulopathies; lung lobe torsion; neoplasia)
Color
FIP; neoplasia; diaphragmatic hernia; lung lobe torsion
CE, chylous effusion; CHF, congestive heart failure; FIP, feline infectious peritonitis; HE, hemorrhagic effusion; HW, heartworms; LSA, lymphosarcoma; MT, modified transudate; NSE, nonseptic exudate; PMN, polymorphonuclear leukocytes or neutrophils; SE, septic exudate; T, transudate . Adapted from Sherding RG. 1994. Diseases of the pleural cavity. In RG Sherding, ed., The Cat: Diseases and Clinical Management, 2nd ed., pp. 1053–1091. New York: Churchill Livingstone.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
412
Pleural Effusion
Diagnosis
• Thoracentesis may be necessary before diagnostics can be undertaken, even if only 50-100 ml of fluid are removed.
Primary Diagnostics • Thoracic Radiographs: For most cats the least stressful radiographic view is the dorsoventral (DV); it may be the only view that is practical in some cases. In some cats, the lateral view is less stressful than the DV view. The ventrodorsal (VD) view should not be employed because it will increase respiratory distress. Pleural effusion causes one or more of the following: fluid-filled interlobar fissure lines, separation of lung borders from the thoracic wall, loss or blurring of the cardiac and diaphragmatic borders, widening of the mediastinum, and blunting of the lung margins at the costophrenic angles. Rounding of the caudal lung borders is a radiographic characteristic of fibrosing pleuritis, a sequel to chylothorax, pyothorax, or feline infectious peritonitis (FIP). See Figures 291-8 through 291-11. • Fluid Analysis: Initial tests should include gross observation of color and turbidity, protein determination, specific gravity, cell count, and cytologic examination. This permits the fluid to be categorized as a transudate, modified transudate, nonseptic exudate, septic exudate, chylous, hemorrhagic, or neoplastic effusion. See Table 171-1 for categorizing and interpreting the fluid analysis. See Chapter 288 for cytology of effusions.
Treatment Primary Therapeutics • Oxygen Administration: Oxygen may relieve dyspnea and cyanosis. However, it should be administered in a nonstressful manner. Many cats will fight a face mask so the beneficial effects of oxygen are negated. An oxygen cage is most desirable. An oxygen tent, made from a clear plastic bag, can be effective. • Cage Confinement: This can be life-saving even if oxygen administration is not possible. Do not hurry. Allow the cat time to recover from the stress produced by getting to the hospital and being examined. • Thoracentesis: Removal of large amounts of fluid can be life-saving because it can greatly improve ventilatory capacity. Sedation, if needed, is best administered via face mask or chamber using isoflurane or sevoflurane. Fluid should be saved for analysis. See Figure 272-6B.
Secondary Diagnostics
Secondary Therapeutics
• Lactate Dehydrogenase (LDH) Concentration in the Fluid: If it is <200 IU/L, consider transudate; if >200 IU/L, consider exudate. • pH of the Fluid: If it is <6.9, consider pyothorax. • Glucose Concentration of Fluid: It should be equal to that of the serum. If lower than serum, consider pyothorax or malignancy. • pH of Effusion 7.0 or greater and Glucose Lower than Blood Glucose: When these are both present consider malignancy. • Triglyceride and Cholesterol: A pseudochylous fluid has a cholesterol value higher than serum cholesterol and a fluid triglyceride lower than serum triglyceride. Pseudochylous fluids are rare in cats. • Anaerobic and Aerobic Culture: They should be performed if organisms are seen cytologically or in the presence of inflammatory exudates in which organisms cannot be identified cytologically. • Complete Blood Count (CBC), Chemistry Profile, Urinalysis, Thyroid Panel, and Feline Retroviral Screen: These tests are to determine the presence of systemic diseases that are known to cause pleural effusion. The viral screen should include tests for feline leukemia virus antigen, feline immunodeficiency virus antibody, and coronavirus antibody. • Thoracic Ultrasonography: Image resolution is greatly improved if the study is performed while fluid is still present in the chest; however, it is contraindicated if the positioning required increases dyspnea. Ultrasound allows visualization of small masses and fibrinous adhesions present in the effusion that are not visualized radiographically. It also permits cardiac evaluation, an important aspect of diagnosis for many cases of pleural effusion. • Electrocardiogram: This will help identify cardiac disease as a possible cause of pleural effusion.
• Specific Therapy: This is only possible after a diagnosis has been made. Refer to the chapters concerning these diseases for recommendations on specific therapy. • Thoracostomy Tube: Certain conditions producing pleural effusion are treatable and curable; however, the course of therapy may require daily or twice-daily chest drainage for up to 2 weeks. A thoracostomy tube permits drainage with minimal stress and discomfort to the patient. See Chapter 272.
Diagnostic Notes • Pleural effusion causes dyspnea; sometimes it is severe enough to be life-threatening. It is imperative that diagnostics not be so aggressive that respiratory failure results.
Therapeutic Notes • Pleural effusion is not a disease. It is a symptom of a serious underlying disease that should be diagnosed before involved therapy begins, especially because many of the diseases are not treatable. However, addressing life-threatening respiratory compromise must occur prior to diagnostics.
Prognosis The prognosis depends on the success of relieving the dyspneic crisis and determining a specific underlying cause for the effusion. Although the presence of pleural effusion requires aggressive diagnostics and therapy, the outcome for many cats is good if the cause of the effusion is treatable.
Suggested Readings Nelson OL. 2005. Pleural Effusion. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 5th ed., pp. 204–207 St. Louis: Elsevier Saunders, 2005. Smith FWK. 2007. Pleural Effusion. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s Five Minute Veterinary Consult, 4th ed., pp. 1020–1021. Ames, IA: Blackwell Publishing.
413
CHAPTER 172
Pneumothorax Gary D. Norsworthy
Overview Pneumothorax is an accumulation of air in the pleural space. There are three classifications of pneumothorax: (a) open, in which there is a defect in the chest wall; (b) closed, in which there is an opening in the lungs, bronchi, trachea, or esophagus; and (c) tension, in which a tear or flaplike defect in the pleura permits air to enter the pleural space during inspiration but not to exit during expiration. Pneumothorax occurs spontaneously, due to trauma, or iatrogenically, usually as a complication to lung aspiration. Spontaneous pneumothorax may be idiopathic, but it is most commonly associated with lung disease that causes necrosis of the visceral pleura, permitting air leakage. Clinical signs are acute onset dyspnea, tachypnea (due to anoxia), and cyanosis (due to decreased venous return). Many affected cats are anxious or panicked. Frothy blood may exit the nose and mouth. If the trachea or esophagus is lacerated, cervical subcutaneous emphysema may occur.
Diagnosis Primary Diagnostics • Physical Examination: External signs of trauma may be present. The clinical signs include acute onset dyspnea with shallow, rapid respiration; cyanosis may be present. • Auscultation: Lung sounds are decreased dorsally; heart sounds are usually muffled. • Thoracentesis: This is confirmatory and can be employed prior to radiography if asthma, diaphragmatic hernia, and bleeding disorders are unlikely. A needle is inserted in the dorsal two-thirds of the thorax in the seventh to ninth intercostal spaces; it is inserted just deeply enough to enter the pleural space. Aspiration of free air is confirmatory. • Radiography: On the recumbent lateral view, the heart appears elevated off the sternum due to lateral displacement that occurs when the cat is placed in lateral recumbency. See Figure 291-12. These findings are not present in standing lateral views. Other findings include an identifiable, air-filled pleural space, partial lung collapse, lung margins that are retracted from the thoracic wall, and subcutaneous emphysema (see Figure 291-13.).
Secondary Diagnostics • Bronchoscopy: This may be used to identify tears in the trachea or main stem bronchi.
Diagnostic Notes • Dyspneic cats should be handled carefully because increased stress may be fatal. Extreme care should be taken when doing the physical examination, radiographs, and thoracentesis. It may be necessary to place the cat in an oxygen cage for several minutes prior to diagnostics and between diagnostic procedures. For most cats the least
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
414
stressful radiographic view is the dorsoventral (DV); it may be the only view that is practical in some cases. However, the recumbent lateral view is needed to confirm pneumothorax. In some cats, this view is less stressful than the DV view. The ventrodorsal (VD) view should not be employed because it will increase respiratory distress.
Treatment Primary Therapeutics • Oxygen Therapy: An oxygen-enriched tent or cage can be beneficial and should be used immediately, especially if concurrent pulmonary trauma is present. Face masks are often resisted by dyspneic cats so an oxygen cage is usually the best option. • Thoracentesis: The least amount of sedation possible should be employed. If sedation is needed, the use of isoflurane or sevoflurane by face mask or chamber is generally safe. Aspirate both sides of the chest, and remove as much air as possible. A needle or catheter is inserted in the dorsal two-thirds of the thorax in the seventh to ninth intercostal spaces; it is inserted just deeply enough to enter the pleural space. • Analgesics can be helpful for cats with fractured ribs or severe soft-tissue injuries.
Secondary Therapeutics • Thoracostomy Tube: This permits continuous or intermittent chest drainage without further stress to the cat. Generally, one tube will drain both sides of the chest; however, some cases require bilateral tube placement. A thoracostomy tube is recommended if more than two thoracenteses are needed within 24 hours. If tension pneumothorax is present, pleural aspiration should be used prior to tube placement to relieve pressure within the pleural space. The chest should be aspirated one to two times per day until less than 10 mL of air are removed in 12 hours. • Thoracotomy: Cats that do not respond to 2 to 5 days of needle or catheter thoracentesis, have more than two episodes that recur after proper treatment, have tension pneumothorax, or appear to have pulmonary leakage are candidates for surgery. Lacerations, neoplastic lesions, and pulmonary blebs should be sought.
Therapeutic Notes • Minor lacerations of the visceral pleura or the lung may heal within 48 hours. Therefore, a thoracostomy tube is generally not placed on the first day of treatment unless there are signs of tension pneumothorax or repeated thoracentesis is needed. • Repeated thoracentesis over several days may be used in place of thoracostomy tube placement. However, the former is a painful procedure that may be too stressful for many cats that are fragile patients. The use of a chest drain is recommended for patients that fit the aforementioned criteria. • Heimlich valves are generally not recommended in cats because of their small body size; they are usually unable to produce enough intrathoracic pressure to activate the flutter valve.
Pneumothorax
• Surgical intervention is seldom needed in cats with traumatic pneumothorax. However, nonsurgical management of spontaneous pneumothorax is often not successful. • Re-expansion pulmonary edema has been reported in cats. If dyspnea increases after lung reinflation, radiograph the chest. If pulmonary edema is present, begin furosemide.
Prognosis Traumatic pneumothorax generally has a good prognosis if the source of the air leak is located and successfully controlled or if the leak spontaneously closes. The prognosis for spontaneous pneumothorax is primarily determined by the underlying cause.
Suggested Readings Cooper ES, Syring RD, King LG. 2003. Pneumothorax in cats with a clinical diagnosis of feline asthma: 5 cases (1990–2000). J Vet Emer Crit Care. 13:95–101. Hopper K. 2007. Pneumothorax. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 1092–1093. Ames, IA: Blackwell Publishing. Mertens MM, Fossum TW, MacDonald KA. 2005. Pleural and Extrapleural Diseases. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1272–1283. St. Louis: Elsevier Saunders.
415
CHAPTER 173
Pododermatitis: Lymphoplasmacytic Richard Malik and Gary D. Norsworthy
Overview Lymphoplasmacytic pododermatitis, also called feline plasma cell pododermatitis and “Mushy Pad Disease,” is a poorly understood condition that primarily affects the carpal/tarsal and metacarpal/metatarsal pads. Rarely, a similar pathologic process can involve the nasal planum. The affected pads feel soft and mushy, and their surfaces may appear wrinkled and flaky. See Figure 173-1. In more severe cases, the pads will ulcerate, bleed, and become painful. A single pad may
be involved in some cats; other cats have all pads affected. The cats are often presented for lameness or bleeding. Occasionally, diffuse swelling of the dorsum of the nose will accompany the pad lesions. See Figure 173-2. Some clinicians report increased cases in the fall of the year. The etiology remains unknown although in one study 50% of affected cats were infected with the feline immunodeficiency virus (FIV). The main differentials are pemphigus foliaceous and infestation with Anatrichosoma spp. When the nasal planum only is affected, differentials include infectious agents, such as Cryptococcus, and other fungal and unusual bacterial infections.
Diagnosis Primary Diagnostics • Clinical Presentation: The clinical appearance is generally sufficient for a presumptive diagnosis. • Histopathology: Confirmation can be made with histopathology. There is marked infiltration with lymphocytes and plasma cells. A fine-needle aspirate shows similar changes but is less definitive. Importantly, infectious agents of disease are not evident in needle aspirates or histological sections.
Diagnostic Notes Figure 173-1 The affected pads feel soft and mushy, and their surfaces may appear wrinkled and flaky.
• Special stains have not identified an etiologic agent. Polymerase chain reaction (PCR) studies have so far failed to reveal an infectious etiology. It will be interesting if more sensitive techniques such as fluorescent in situ hybridization (FISH) will help visualize an infectious agent. • Diagnosis of this disease justifies an FIV test, even though a positive result does not prove cause and effect.
Treatment Primary Therapeutics • Immunosuppressive Therapy: The histologic pattern has caused some to treat with immunosuppressive doses of prednisolone, gold salts, and chlorambucil. • Doxycycline: One of the authors has had consistent success with doxycycline (5 mg/kg q12h PO for several weeks), based on a treatment protocol published in the Veterinary Record (Bennenay S, & Muller R, see “Suggested Readings”). This supports an infectious cause as at least part of the disease process. Figure 173-2 In a few cats, diffuse swelling of the dorsum of the nose accompanies pododermatitis.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
416
Secondary Therapeutics • Surgery: Surgical removal of the affected tissue with suturing and either immunosuppressive drugs or antibiotics has been successful in some cats. The role of surgery in the recovery process is not clear.
Pododermatitis: Lymphoplasmacytic
Prognosis Overall, the prognosis is good although it may take several weeks for healing to occur. Recurrence is possible.
Suggested Readings
Medleau L, Kaswan R, Lorenz MD, et al. 1982. Ulcerative pododermatitis in a cat: immunofluorescent findings and response to chrysotherapy. J Am Anim Hosp Assoc. 18(3):449–451. Taylor JE, Schmeitzel LP. 1990. Plasma cell pododermatitis with chronic footpad hemorrhage in two cats. J Am Vet Med Assoc. 173(3): 375–377.
Bennenay S, Muller R. 2003. Prospective study of the treatment of feline plasmacytic pododermatitis with doxycycline. Vet Rec. 152:564–566.
417
CHAPTER 174
Polycystic Kidney Disease Gary D. Norsworthy
Overview Polycystic kidney disease (PKD) causes multiple fluid-filled cysts 1 mm (1/16 inch) to greater than 1 cm (3/8 inch) in diameter to form within the renal parenchyma. See Figure 174-1. The cysts originate from both the proximal and distal tubules and occur in the renal cortex and medulla. They increase in size and number over time. This is a genetic disease most commonly involving Persian (including Himalayans) and other long-haired breeds or long-haired cross-bred cats in general. In the Persian, it is inherited as an autosomal-dominant disease and is present in about 40% of the breed. It is often diagnosed in kittens 6 to 8 weeks of age but may also develop later. The disease may be unilateral or bilateral, and concurrent hepatic cysts may be present. Severely affected kittens may die of renal failure by 8 weeks of age; however, the disease is usually subclinical until the cat is several years old. Typically, affected cats develop chronic renal failure about 7 years of age. Clinical signs include polydipsia, polyuria, weight loss, inappetence, and lethargy. Bacterial infection of the cysts has been reported. This is a serious complication that mandates antibacterial therapy. Because the cysts do not communicate with the tubules or pelvis, most cats have sterile urine. Kidneys that are unusually painful and accompanied by fever are likely to be infected.
• Abdominal Palpation: This will reveal renomegaly involving one or both kidneys, which can be quite severe in some cats. • Ultrasound: This is the most sensitive and specific, noninvasive test available. It reveals multiple, fluid-filled cysts throughout the kidney. See Figure 174-2. The liver should also be imaged. In one study, ultrasound had a sensitivity of 75% and a specificity of 100% when performed at 16 weeks of age. The sensitivity increased to 91% at 36 weeks of age. If cystic infection is suspected, aspiration of one or
Diagnosis Primary Diagnostics • Signalment: risk.
Persian, Himalayan, and other long-haired cats are at
(A)
Figure 174-1 A pair of kidneys with polycystic kidney disease is shown. Although significantly different in size, both kidneys have multiple cysts.
(B) The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
418
Figure 174-2 A, Some cats have many small to moderate-sized cysts in their kidneys. B, Other cats have small to large cysts. These kidneys are from the same cat. This is a progressive disease so the size of the cysts with change over time.
Polycystic Kidney Disease
Secondary Therapeutics • Antibiotics: Bacterial infection of cysts is a complicating factor in some cats. • Nephrectomy: This could be considered when unilateral disease is present and when renal failure is not present. An excretory urogram should be performed first to document function in the other kidney. However, nephrectomy is not recommended in a Persian cat, Persian-crossed cats, or long-haired cats in general due to the genetic nature of the disease and the potential for late onset disease. It is rarely a unilateral disease. Nephrectomy is also indicated when infection in the cysts of one kidney are resistant to antibiotic therapy.
Therapeutic Notes
Figure 174-3 Renomegaly with irregular margins are seen on radiographs in cats with polycystic kidney disease. The urolith in the kidney is incidental. more of the renal cysts using ultrasound guidance can provide a sample suitable for culture.
• Fluid contained within renal cysts tends to be acidic in nature. Some commonly used bacterial antibiotics are acidic and do not penetrate the cysts well (e.g., cephalosporins and penicillins). Alkaline, lipid-soluble antibiotics (e.g., fluoroquinolones, trimethoprin-sulfonamide combinations, and clindamycin) can better penetrate the epithelial barrier of the cysts and become trapped after ionization. • Affected cats should not be bred.
Secondary Diagnostics • Plain Radiographs: Enlarged, irregular kidneys can be visualized, but this finding is not specific for PKD. See Figure 174-3. • Excretory Urogram: The cysts may be seen as multiple radiolucent areas within the renal parenchyma.
Diagnostic Notes • Litter mates and parents of affected cats should have periodic sonograms because there may be many months or years of asymptomatic disease present. Early detection permits early therapy to support renal function and recommendations against breeding of affected individuals.
Treatment Primary Therapeutics • Treatment for Chronic Renal Failure: Overt signs of renal failure are usually apparent and an aggressive approach should be taken to stabilize and maintain an affected cat. See Chapter 190.
Prognosis The prognosis depends on the degree of renal failure, the cat’s response to initial treatment for renal failure, and the owner ’s willingness to continue aggressive management for renal failure.
Suggested Readings Beck C, Lavelle RB. 2001. Feline polycystic kidney disease in Persian and other cats: a prospective study using ultrasonography. Aust Vet J. 79(3):181–184. DiBartola SP. Familial renal disease in dogs and cats. 2005. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1819–1824. St. Louis: Elsevier Saunders. Lulich JP, Osborne CA. 2007. Polycystic kidney disease. In LP Tilley, FWK Smith, eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 1104–1105. Ames, IA: Blackwell Publishing.
419
CHAPTER 175
Polydactylism Sharon Fooshee Grace
Overview Polydactylism, the condition of having extra digits, is common in domestic cats; it has also occasionally been observed in exotic cat species. It is unknown why this condition appears more commonly in cats as compared to other mammalian species. Polydactylism is characterized as a dysostosis, or a morphological abnormality affecting development of bones or parts of bones. The harmless form of this anomaly does not appear associated with other skeletal abnormalities. However, the less common form of polydactylism is associated with serious deformities, such as radial agenesis or hypoplasia (the so-called “twisty cat”). Normally, cats have 5 digits (including the medial digit, or dewclaw) on the front feet and 4 digits on the hind feet. The dewclaw is shorter and more proximal than the more lateral digits. With polydactylism, there are one or more additional digits on the front feet, hind feet, or both. Rarely, only the hind feet are affected. In most cases, the extra digits are present on the medial aspect of the paw. Oftentimes, the extra digit does not contain a full complement of bones. The presence of extra digits on the medial aspect of the limb is called preaxial polydactyly; when present on the lateral aspect of the limb, it is called postaxial polydactyly. Several cats have been reported to have upwards of 25 total digits. This condition likely arose as a genetic mutation and is passed down as an autosomal dominant trait with variable expression (numbers of toes). Cats with polydactylism sometimes have a similarly affected parent that shares the identical numbers and locations of extra toes. Polydactyl cats have been called “mitten cats,” “thumb cats,” and “Hemingway cats.” The latter term refers to the polydactyl cats owned by the writer Ernest Hemingway. He had a remarkable affection for these animals and many polydactyl cats still reside at Hemingway’s former home near Key West, Florida. “Slippers,” a polydactyl cat owned by President Theodore Roosevelt, was once a resident of the White House. These cats also are known for their affectionate personalities. There are well-known geographic pockets of polydactyl cats. Large numbers of polydactyl cats inhabit the northeastern United States and parts of Great Britain. It is speculated that the genetic trait was brought into the United States from England by shipboard cats. Others have argued that polydactyl cats originated in the United States. There is no known sex predisposition and the trait is equally expressed in male and female cats. Several breeds have been historically overrepresented with this condition. Unfortunately, even though the extra digits rarely cause the cat a disadvantage, their presence disqualifies purebred cats from the largest cat registry in North America. Some less wellknown registries do accept the trait. The Pixiebob is a lovely polydactyl cat promoted by such a registry. Historically, Maine Coon cats have had a large proportion of polydactyl cats, but this trait has been bred out of cats destined for the largest feline registry. Other registries will accept polydactyl Maine Coons.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
420
Figure 175-1 Seven digits can be visualized in the forelimb of this cat with polydactyly.
Diagnosis Primary Diagnostics • Physical Examination: Physical examination is the only diagnostic tool needed to identify the trait.
Secondary Diagnostics • Diagnostic Imaging: In some cases, radiographs of the affected paw will reveal digits not discernible by physical examination alone. See Figure 175-1.
Treatment Primary Therapeutics • Normally, no special care is needed for cats with extra digits. However, in some cases, it is difficult for cats to remove the claw sheath of the extra digits by scratching or grooming. The claw may grow into the footpad and can be prone to infection. Owners should be taught to clip the nails or present the cat for nail trims should this situation exist.
Polydactylism
Secondary Therapeutics • If an extra digit is prone to catching on rough surfaces or becoming ingrown or infected, it should be amputated.
Prevention Although the trait of polydactylism rarely causes problems for affected cats, it should be understood that breeding affected cats may result in offspring with extra digits. Affected cats may also have kittens with a normal complement of digits.
Prognosis This condition only rarely affects the quality of life for affected cats.
Suggested Readings Towle HAM, Breur GJ. 2004. Dysostoses of the canine and feline appendicular skeleton. J Am Vet Med Assoc. 225(11):1685–1691. http://www.messybeast.com/poly-cats.html. This site is an excellent resource on the topic of feline polydactylism.
421
CHAPTER 176
Polyphagic Weight Loss Mitchell A. Crystal and Paula B. Levine
Overview Polyphagic weight loss describes the condition of progressive decrease in body weight in the presence of an increased appetite. The two most common diseases that result in this condition are hyperthyroidism and diabetes mellitus. Hyperthyroidism leads to polyphagic weight loss by causing an increase in metabolic rate and a decrease in intestinal transit time. Hyperthyroidism can also cause loss of nutrients as a result of intermittent vomiting and diarrhea. Diabetes mellitus leads to polyphagic weight loss as a result of decreased utilization of glucose, loss of glucose through the urine, and decreased detection of circulating calories by the satiety center in the brain. Less common conditions that can cause polyphagic weight loss include exocrine pancreatic insufficiency (EPI), which usually results from chronic interstitial pancreatitis; intestinal lymphangiectasia; and feeding a poor quality diet. These disorders result in maldigestion (EPI), malabsorption (lymphangiectasia), and malnutrition (poor quality diet). Inflammatory bowel disease (IBD), alimentary lymphoma, and some neoplastic diseases are common disorders that present for weight loss, usually in association with normal or decreased appetite but may occasionally present with polyphagic weight loss. These disorders result in maldigestion or malabsorption (e.g., IBD and alimentary lymphoma) or increased metabolism (neoplasia). Portosystemic shunts and protein-losing nephropathies are also rare causes of polyphagic weight loss. In kittens, and rarely in adult cats, intestinal parasitism can lead to polyphagic weight loss via decreased intestinal absorption. Because hyperthyroidism and diabetes mellitus most commonly cause this condition, cats with polyphagic weight loss are usually older than 7 years of age and often present with polyuria/polydipsia. Cats with polyphagic weight loss due to intestinal diseases or EPI often demonstrate diarrhea with or without vomiting. Cats fed a poor quality diet may present only for polyphagic weight loss or may have other diseases from malnutrition. Cats with portosystemic shunts typically have associated behavior changes, ptyalism, or gastrointestinal signs. Cats with protein-losing nephropathies may present only for polyphagic weight loss, but this condition typically progresses to include clinical signs of renal tubular failure.
Diagnosis Differential Diagnoses • • • • • • • • • •
Hyperthyroidism. See Chapter 109. Diabetes mellitus. See Chapter 52. Exocrine pancreatic insufficiency. See Chapter 71. Intestinal lymphangiectasia. Inflammatory bowel disease. See Chapter 120. Alimentary lymphoma. See Chapter 130. Intestinal parasitism. See Chapters 83, 98, 195 and 218. Poor quality diet. Portosystemic shunt. See Chapter 178. Protein losing nephropathy. See Chapters 6 and 86.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
422
Primary Diagnostics • Physical Examination and Cervical Palpation for Thyroid Enlargement. See Chapter 109 for technique. • Chemistry Profile: Approximately 90% of hyperthyroid cats have an elevation of either alanine amino transferase (ALT) or alkaline phosphatase (ALP). Elevations of liver parameters may also be present in the rare case of portosystemic shunt. Hyperglycemia will be present in cats with diabetes mellitus. Hypoalbuminemia and hypoglobulinemia (panhypoproteinemia) may be present in cats with diseases causing intestinal malabsorption. Hypoalbuminemia with or without increased renal parameters may be present in the rare case of protein-losing nephropathy. • Urinalysis: Poorly concentrated or nonconcentrated urine may be seen with hyperthyroidism, diabetes mellitus, portosystemic shunt, or protein losing-nephropathy. Glucosuria, and possibly ketonuria, will be present in cats with diabetes mellitus. Proteinuria is seen with protein-losing nephropathy. • Fecal Examination: A fecal flotation should be performed to evaluate for intestinal parasites. Consider additional testing for Giardia and Tritrichomonas if diarrhea is present. See Chapters 83 and 218. • Total T4 (TT4): This test is indicated in all cats over 10 years of age with polyphagic weight loss. The serum TT4 is elevated in 90 to 98% of hyperthyroid cats. Some cats have normal TT4 levels as a result of either fluctuation of TT4 levels in and out of the normal range (mild cases) or suppression of elevated TT4 levels into the normal range secondary to concurrent nonthyroidal illness. If hyperthyroidism is suspected despite a normal TT4, then repeat TT4 testing is recommended at a later date along with T3 suppression testing (see Chapter 311), TRH response testing (see Chapter 311), or assessment of free T4 (fT4) by equilibrium dialysis. fT4 by equilibrium dialysis has a higher sensitivity as a diagnostic test compared to TT4, but specificity is lower in sick euthyroid cats leading to some false-positive results. See Chapter 109.
Secondary Diagnostics • Complete Blood Count (CBC): A CBC may demonstrate a mildly elevated packed cell volume (PCV) in cases of hyperthyroidism and may rarely reveal abnormalities in leukocytes in cases of eosinophilic gastroenteritis and lymphoma. Microcytosis may be present with portosystemic shunt. • T3 Suppression Test or TRH Response Test: One of these tests (we prefer T3 suppression test) should be performed if hyperthyroidism is suspected (i.e., palpable thyroid, clinical signs, and liver enzyme elevations) and the TT4 and fT4 are normal. See Chapters 109 and 311. • Retroviral Tests: Retrovirus infection may predispose cats to some causes of intestinal malabsorption. • Feline-Specific Trypsin-Like Immunoreactivity (fTLI): This test is diagnostic for EPI and should be performed after hyperthyroidism and diabetes mellitus have been ruled out. A 12-hour fasting serum sample is submitted. Decreased pancreatic function leads to decreased leakage of trypsinogen into the vascular space, resulting in a subnormal value of fTLI. • Bile Acids: Serum bile acids (fasting and 2-hour post-prandial) should be performed after hyperthyroidism, diabetes mellitus, and EPI have been ruled out to investigate for portosystemic shunt.
Polyphagic Weight Loss
• Urine Protein: Urine Creatinine Ratio: This test should be performed on a cystocentesis sample if proteinuria is present on urinalysis and after the most common causes of polyphagic weight loss have been ruled out to investigate for protein-losing nephropathy. • Thoracic Radiographs: Thoracic radiography may reveal metastatic disease in the case of polyphagic weight loss due to neoplasia and could be informative about cardiac disease related to hyperthyroidism. • Abdominal Radiographs or Ultrasound: Abdominal imaging may reveal an abdominal mass, organ enlargement, or organ architecture change in the case of polyphagic weight loss due to neoplasia. Renal changes may be seen in some cases of protein-losing nephropathy. Microhepatica is seen in some cases of portosystemic shunt. • Intestinal Biopsy and Histopathology: This procedure should be performed after hyperthyroidism, diabetes mellitus, and EPI have been ruled out to investigate for primary intestinal diseases. Biopsies may be collected via endoscopy or exploratory laparotomy. In the case of focal intestinal thickening greater than 2 cm (3/4 inch), ultrasound-guided aspiration for cytology evaluation can be diagnostic.
be used to help regain weight. They are also strongly acidifying to the urine and should not be used when a low urine pH is undesirable (i.e., renal failure, metabolic acidosis, hypercalcemia, or calcium oxalate urolithiasis).
Prognosis The prognosis varies depending on the underlying disorder causing the polyphagic weight loss. With appropriate therapy, hyperthyroidism, intestinal parasitism, and feeding a poor quality diet carry an excellent prognosis for cure. With lifelong appropriate therapy, hyperthyroidism, diabetes mellitus, and EPI carry a good prognosis for controlling the disease, although occasional clinical problems may arise. Lymphocyticplasmacytic IBD is often controllable with intermittent therapy or dietary changes. Other forms of IBD and intestinal lymphangiectasia do not usually respond to therapy. The prognosis with alimentary lymphoma and portosystemic shunt vary. The prognosis for other types of neoplasia will vary depending on the tumor type. Cats with protein-losing nephropathy carry a poor prognosis because they typically progress to chronic renal failure.
Diagnostic Notes • Cats with alimentary lymphoma are usually feline leukemia virus (FeLV) antigen negative. • Some cats with portosystemic shunt will not have microhepatica.
Treatment Primary Therapeutics • Treat the Underlying Disease: See related chapters listed in Differential Diagnoses. • Provide Optimum Nutrition: Diet change will correct poor quality diet-induced polyphagic weight loss and will help in managing polyphagic weight loss from other conditions. Diets with low carbohydrate levels are typically very high in protein and calories and may
Suggested Readings Hawkins EC. 1991. Diagnostic approach to polyphagia and weight loss. In JR August, ed., Consultations in Feline Internal Medicine, 3rd ed., pp. 237–242. Philadelphia: WB Saunders. Houpt KA. 2007. Polyphagia. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult: Canine and Feline, 4th ed., pp. 1108–1109. Ames, IA: Blackwell Publishing. Peterson ME, Melian C, Nichols R. 2001. Measurement of serum concentrations of free thyroxine, total thyroxine, and total triiodothyronine in cats with hyperthyroidism and cats with nonthyroidal disease. J Am Vet Med Assoc. 218(4):529–536. Streeter EM. 2007. Weight Loss and Cachexia. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult: Canine and Feline, 4th ed., pp. 1438–1439. Ames, IA: Blackwell Publishing.
423
CHAPTER 177
Polyuria and Polydipsia Mark Robson and Mitchell A. Crystal
Overview Polyuria (PU) and polydipsia (PD) are defined as excessive urination (greater than 40 mL/kg per day) and excessive fluid intake (greater than 45–50 mL/kg per day), respectively. PU and PD are clinical signs that result from alterations in or failure of the normal homeostatic mechanisms that control urine production and thirst. Such alterations can include osmotic diuresis (secondary to osmotically active compounds), altered tubular sensitivity to vasopressin, reduced renal tubular function, and medullary interstitial hypotonicity. These clinical abnormalities describe primary PU with compensatory PD, the majority of which could be classified as secondary nephrogenic diabetes insipidus. Primary psychogenic PD can occur in rare cases despite normal pituitary and renal function, nonetheless differentiating primary PD and primary PU is often not clinically possible or of urgency. Secondary PD can occur due to pyrexia, pain, and hyperthyroidism. PU/PD is therefore a common complaint that may result from a variety of disease processes and should be differentiated from pollakiuria and dysuria, which commonly result from lower urinary tract diseases. The differential diagnosis for PU/PD in the cat is outlined in Table 177-1.
Diagnosis Primary Diagnostics • History and Physical Examination: Determine diet, medical history, drugs, and (in the intact queen) the last estrus cycle. Confirm that the cat has PU/PD and not pollakiuria or dysuria. This may require measurement of water intake over several 24 hour periods if time permits. If the cat uses a litter box the owner may appreciate increased urine production. The use of clumping litter can aid quantification. Inquire and evaluate for signs attributable to diseases in Table 177-1. • Database (Complete Blood Count [CBC], Chemistry Profile, and Urinalysis): Evaluate for diabetes mellitus and hyperadrenocorticism (i.e., hyperglycemia, glucosuria, low urine specific gravity, and ketonuria), liver disease (i.e., hyperbilirubinemia, decreased blood urea nitrogen [BUN], increased liver enzymes, and bilirubinuria), portosystemic shunt (i.e., increased liver enzymes; decreased cholesterol, mean corpuscular volume [MCV], albumin, BUN and urine specific gravity; and evidence of ammonium biurate crystals), renal disease (i.e., elevated BUN and creatinine with a decreased urine specific gravity and hyperphosphatemia), hyperthyroidism (i.e., increased liver enzymes, mild increase in packed cell volume, and low urine specific gravity) and electrolyte derangements (i.e., hypokalemia and hypercalcemia). Urine specific gravity aids confirmation of PU/PD; urine specific gravity less than 1.025 supports PU/PD. • Total T4: This test is indicated in all cats over 8 years of age who display PU/PD to rule out hyperthyroidism, even if there are no obvious physical changes. • Abdominal Ultrasound: Abdominal ultrasound is pertinent in identifying or ruling out diseases such as pyometra, renal disease (including structural renal anomalies), liver disease, and adrenal disease, and to support findings from previous diagnostics. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
424
TABLE 177-1: Differential Diagnosis List for Polyuria and Polydipsia Common Causes Chronic renal disease Diabetes mellitus Hyperthyroidism Pyometra Less Common Causes Acromegaly (presents for insulin-resistant diabetes mellitus) Acute renal failure Certain diets (Hill’s s/d, Purina’s UR, Royal Canin’s SO) Chronic pyelonephritis Diabetes insipidus Drug therapy (e.g., diuretics) Hyperadrenocorticism (usually presents for insulin-resistant diabetes mellitus and dramatic dermatologic signs) Hypercalcemia Hypokalemia Liver disease Portosystemic shunt Psychogenic polydipsia
See Also Chapters 190, 191 Chapters 51, 52 Chapter 109 Chapter 182 Chapter 3 Chapter 189
Chapter 181 Chapter 49 Chapter 101
Chapter 103 Chapter 114 Chapters 93, 94 Chapter 178
• Urine Culture and Sensitivity: This is almost always indicated even if urinalysis and ultrasound do not clearly suggest pyelonephritis or cystitis. It is not uncommon for urine sediment to be quiet and growth to occur on a culture. Many urinary infections in cats are without obvious hematuria, dysuria or pollakiuria, and the consequences of missing bacterial infection can be severe.
Secondary Diagnostics • Thoracic Radiographs: These are indicated if hypercalcemia is the cause of PU/PD to rule in/out primary (e.g., mediastinal lymphoma) or metastatic neoplasia. • Iohexol Clearance: This is a test of glomerular filtration rate (i.e., renal function) and is indicated for detecting early renal disease (i.e., renal insufficiency or loss of renal concentrating ability without azotemia) if other causes of PU/PD have been excluded. See Chapter 311. • Bile Acid Panel: This is a test of hepatic function, vascular flow, and cholestasis and is indicated after common causes of PU/PD have been excluded and clinical signs and previous diagnostics are suggestive of portosystemic shunt. • Pituitary/Adrenal Screening Tests: Dexamethasone suppression, adrenocorticotropic hormone stimulation, or urinary cortisol:creatinine ratio testing is indicated when signs are consistent with hyperadrenocorticism or in cases of insulin-resistant diabetes mellitus. • Water Deprivation Test: This test is indicated after common causes of PU/PD have been excluded to evaluate for causes of primary PD (diabetes insipidus and psychogenic polydipsia). This test is not without risks and should be done with great care (see Diagnostic Notes).
Polyuria and Polydipsia
Diagnostic Notes • There is currently no test for confirming acromegaly aside from demonstrating a pituitary mass with magnetic resonance imaging (MRI) or computerized tomography (CT). However, Insulin-like Growth Factor-1 and serum growth hormone level can be very helpful and are simple blood tests. The sensitivity and specificity are increased if both tests are performed. • Insulin-like Growth Factor-1: Performed by Michigan State University, 1-517-353-0621, download submission form from: www.animalhealth.msu.edu. Sensitivity is 84%; Specificity is 92%. Normal range: 12 to 92 mmol/L; >200 mmol/L is strongly suggestive of acromegaly. • Serum growth hormone level: Performed at University of Minnesota, Veterinary Diagnostic Laboratory, 1-800-605-8787; www.vdl.umn.edu/ourservices/endocrinology/home.html. As of publication, this test is only performed once per month. • Water deprivation testing is contraindicated in cats with renal insufficiency due to the risk of precipitating decompensation and overt renal failure. Because renal disease is common and diabetes insipidus and psychogenic polydipsia are uncommon in cats, iohexol clearance testing should always be considered prior to water deprivation testing.
Treatment Primary Therapeutics • Treat Underlying Disease: This is essential in obtaining a cure. See related chapters listed in Table 177-1.
• Provide Water: Adequate quantities of and access to water should be available at all times. Because almost all cases of PU/PD arise from obligate polyuria and compensatory polydipsia water must be readily available to prevent dehydration and associated medical complications. Be sure the owner knows not to withhold water “to treat the symptoms.”
Secondary Therapeutics • Fluid Therapy: Fluids are indicated in cats with PU/PD, if dehydration is present or imminent.
Prognosis The prognosis varies depending on the underlying cause of PU/PD.
Suggested Readings Feldman EC. 2005. Polyuria and polydipsia. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 102–105. Philadelphia: WB Saunders. Lunn KF. 2009. Managing the patient with polyuria and polydipsia. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIV, pp. 844–850. Philadelphia: WB Saunders. Polzin DJ. Polyuria and polydipsia. 2004. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 3rd ed., pp. 1052–1053. Philadelphia: Lippincott Williams & Wilkins.
425
CHAPTER 178
Portosystemic Shunt Mark Robson and Mitchell A. Crystal
Overview A portosystemic shunt (PSS) consists of one or more anomalous vessels between the portal and systemic venous systems that allow gastrointestinal blood to be diverted directly into the systemic circulation, therefore bypassing hepatic detoxification and limiting hepatocellular perfusion. In all species, PSS may be extrahepatic or intrahepatic, singular or multiple, and congenital or acquired. Congenital, extrahepatic portoazygous shunts are reported most commonly. Feline splenocaval and splenoazygous shunts are similar to those in dogs; however, they may originate directly from the portal vein adjacent to the junction of the splenic and portal veins. There are two congenital shunts that are specific to the cat. One originates caudal to the portal bifurcation, runs cranially between liver lobes, adjacent to the esophagus, and enters the caudal vena cava (CVC) between the liver and the diaphragm (often via the hepatic vein). The second originates from the cranial mesenteric vein and courses caudally near the colon to the aortic trifurcation, then diverts 180 degrees to run cranially on the left side of the CVC and terminates in the left renal vein or the CVC adjacent to the left renal vein. The incidence of feline PSS is about 1 in 4,000 and can occur in a significant variety of anatomic locations, suggesting that PSS in the cat may be due to isolated embryological errors rather than genetically programmed mutations. Acquired multiple extrahepatic PSS may occur secondary to prolonged portal hypertension, as in chronic hepatic disease or following shunt ligation surgery in cats with hepatic vascular atresia, or following acute single shunt ligation. PSS are most commonly seen in mixed-breed cats, although Himalayan and Persian cats are overrepresented in some reports. Male cats develop PSS slightly more frequently than females, and in some reports, up to 25% of affected male cats are also affected by cryptorchidism. Most cats with PSS demonstrate clinical signs within 1 year of age (often by 6–8 weeks of age), although some cats have been as old as 10 years. Many cats with PSS are reported to have copper-colored irises that lack green or yellow pigments. Hepatic encephalopathy (HE), ptyalism, and unthriftiness are the most consistently reported clinical signs. Signs of HE include seizures (seen more commonly in cats than dogs both preand post-operatively), ataxia, depression, head pressing and tremors. The etiology of HE is not known and is most likely multifactorial including increased blood ammonia concentration, alterations in monoamine and amino acid neurotransmitter concentration or function, or increased cerebral concentration of benzodiazepine-like substances. Other clinical signs include intermittent or permanent amaurotic (central) blindness, aggression, vocalization, mydriasis, anorexia, recurrent vomiting, diarrhea, and prolonged recovery from anesthesia. Because of reduced urea production, increased ammonia excretion and possible ammonium biurate calculi, some cats present for polyuria, polydipsia, pollakiuria, stranguria, and other clinical signs of urinary tract dysfunction. Signs may wax and wane and worsening of clinical signs postprandially is common but is not a consistent finding. Differential diagnoses for PSS include neurologic diseases (i.e., feline infectious peritonitis, illness related to feline leukemia virus and feline immunodeficiency virus, toxoplasmosis, hydrocephalus, neoplasia, vascular accident, or other causes of HE), toxicity, other hepatic diseases,
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
426
metabolic diseases (i.e., hypocalcemia and hypoglycemia), gastrointestinal diseases, and lower urinary tract diseases.
Diagnosis Primary Diagnostics • Data Base (Complete Blood Count, Chemistry Profile, and Urinalysis): Cats with PSS often demonstrate a mild to moderate increase in alanine aminotransferase (ALT) or alkaline phosphatase (ALP), hypocholesterolemia, and erythrocyte microcytosis, hypochromia, and poikilocytosis. Less common changes include hypoalbuminemia, hypoglobulinemia, decreased blood urea nitrogen, mild-to-moderate decrease in urine specific gravity, and ammonium biurate crystalluria. Hyperbilirubinemia is not a feature of PSS, and some cats will have a normal data base. • Bile Acids: Elevated serum bile acid (fasting and 2-hour postprandial) is supportive of PSS. Most fasting samples and all postprandial samples will be elevated. Postprandial samples are typically >100 mmol/L, but the degree of elevation does not correlate with the severity of clinical signs or type of shunt. • Abdominal Ultrasound: This may identify the anomalous shunting vessel, the presence of renal or cystic ammonium biurate calculi, microhepatica, and renomegaly.
Secondary Diagnostics • Ammonia Level: Serum ammonia levels taken while fasted and following an oral ammonium chloride challenge can be used to support a diagnosis of PSS. This test requires special sample handling and may create or exacerbate HE, so it is often only practical in a university hospital or referral center setting. • Abdominal Radiographs: Survey abdominal radiographs may show microhepatica with a more vertically orientated gastric axis and renomegaly. If present, urate calculi (typically radiolucent) may or may not be seen. • Scintigraphy: Rectal nuclear scintigraphy is a noninvasive method to help confirm PSS; however, it does not indicate the type or location of the shunt. Technetium pertechnetate is administered per rectum and, in cats with shunting of portal blood, a greater percentage rapidly passes to the right atrium. • Portography: Surgical mesenteric portography can be performed to help locate the shunt if it is not visible on abdominal ultrasound or exploration. If a PSS is identified, portography is usually combined with surgical ligation of the shunt at the time of exploration to avoid repeated anesthesia and surgery. See Figure 292-14.
Diagnostic Notes • Although serum bile acids and ammonia testing are consistently abnormal, the other hematology and biochemical lab parameters can be within normal limits in greater than 40% of cases. • Left gastric-caval and porto-caval are the most frequent shunt locations. Less common locations include porto-azygous, gastrosplenic-azygous, gastroduodenal-caval, mesenteric-caval, porto-phrenicoabdominal, porto-renal, and colonic-caval.
Portosystemic Shunt
• Liver biopsies should be collected at the time of surgery to allow histologic assessment of hepatobiliary pathology. • The renomegaly that occurs in PSS patients does not have a confirmed cause. • Microvascular dysplasia (MVD), an uncommon canine and rare feline disorder in which there are many microscopic intrahepatic communications between the portal and hepatic circulatory systems (resulting in bypassing of the hepatocytes), can occur in addition to a PSS. It may take a skilled pathologist with experience in hepatic pathology to differentiate the changes that are caused by a PSS from the specific diagnostic features of MVD.
following cohorts of cats whose owners decline surgical management. These cats are usually lost to follow-up.
Secondary Therapeutics • Calculi Removal: Palpation of the urinary bladder should always be a part of the laparotomy and if indicated, calculi should be removed via cystotomy. Because bladder palpation is not sensitive for finding small uroliths, bladder ultrasound prior to surgery is advised.
Therapeutic Notes Treatment Primary Therapeutics • Surgery: Surgical ligation is recommended in most patients to improve long-term outcome. Techniques include acute ligation with suture; gradual occlusion with ameroid constrictors, cellophane or hydraulic occluders, or embolization with coils. Correction via an ameroid constrictor or cellophane is the treatment of choice for single, extrahepatic shunts. The ameroid constrictor device slowly occludes the shunt over days to weeks allowing for hepatic vascular compensation and decreasing postoperative morbidity and mortality. A recent long-term study of surgical outcome reported that 75% of cats had good-to-excellent long-term outcome following ligation with an ameroid constrictor with no medical treatment. Cellophane banding is an alternative technique that provides gradual occlusion by foreign body reaction. A 1- to 2-cm (3/8- to 3/4-in) wide strip of cellophane is passed around the anomalous vessel and fibrosis of the shunt results in occlusion within 6 to 8 weeks. Cats have a limited inflammatory response compared with dogs; therefore, this technique is not the first choice for some surgeons. If acute surgical ligation is performed, portal pressures should be monitored and if pressures rise to greater than 20 cm of water or increase by more than 10 cm of water, the shunt should only be partially ligated so that these criteria are not exceeded. Surgical correction of multiple and intrahepatic shunts is usually unsuccessful. • There are continuous developments in the field of interventional radiology, and intrahepatic shunts may be able to be managed by one of various embolization techniques. A specialist should be consulted if the owner is highly motivated. • Medical Management: Medical therapy is largely based on managing blood ammonia levels and PSS-induced HE and is used as an alternative to or in combination with surgical management. Because ammonia is produced by enteric bacterial degradation of urea, amino acids, and amines/purines, the most profound benefit is seen when protein digestion is limited by decreasing dietary protein, decreasing transit time of ingesta, or reducing the population of urea-producing bacteria. Specific management usually involves: (a) fluid therapy and correction of blood glucose, (b) restriction of dietary protein by feeding low quantity high quality protein, (c) lactulose administration (2.5–5.0 mL q8–12h PO), (d) antibiotic therapy including one or more of metronidazole (12.5 mg/kg q12h PO), amoxicillin (20 mg/kg q12h PO), and neomycin (20 mg/kg q8h PO). Lactulose or dilute iodine retention enemas may also be given in those cases with persistent HE (e.g., following two to three warm water enemas to evacuate the colon, administer a 30% lactulose/70% warm water solution at 20 mL/kg per rectum and leave in for 20–30 minutes). In most cases medical management without surgery is only temporarily successful in controlling clinical signs; however, there are few long-term studies
• Careful selection of preanesthetic and anesthetic agents is pertinent, most notably avoiding the benzodiazepine (BZ) class of drugs. The concentration of endogenous BZ receptor ligands is significantly increased in animals with PSS; thus, administration of exogenous BZs may risk inducing a state of marked central nervous system depression. It has furthermore been hypothesized that postligation withdrawal of endogenous BZ may result in or contribute to postligation seizures. • Postoperative hypothermia and hypoglycemia are commonly reported and can be prevented by using warm water or warm air blankets intra- and post-operatively and by paying close attention to blood glucose concentrations.
Prognosis Cats that undergo partial PSS ligation (see criteria discussed previously) typically experience continued problems that can sometimes be addressed by medical management or attempting a second surgical ligation. “Postligation seizure syndrome” including incoordination and blindness has been reported in up to 25% of cats and to date remains of undefined etiology. Seizures should be treated with standard medical seizure control and fluid therapy, dietary protein restriction, oral lactulose, antibiotic therapy, and possibly enemas. In many cases indefinite and varied combinations of medical management is required to control clinical signs. To date, no defined prognostic factors are described in the literature to predict success in cats undergoing surgical correction of PSS. Long-term success is less likely than in dogs, but cats undergoing surgical ligation have a better positive long-term outcome than with medical management alone.
Suggested Readings Hunt G. 2009. Portosystemic Shunts in Cats: How Do They Differ? Proceedings of the BSAVA Annual Conference. Available at www.vin. com/Members/Proceedings/Proceedings.plx?CID=BSAVA2009&PI D=PR32344&O=VIN. Lipscomb G, Jones HJ, Brockman DJ. 2007. Complications and long-term outcomes of the ligation of congenital portosystemic shunts in 49 cats. Vet Rec. 160:645–470. Szatmari V, and Rothuizen J. 2007. Ultrasonographic identification and characterization of congenital portosystemic shunts and portal hypertensive disorders in dogs and cats. WSAVA Standards for Clinical and Histological Diagnosis of Canine and Feline Liver Disease; pp. 15–39. Tobias KM. Portosystemic shunts. 2009. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIV, pp. 581–586. Philadelphia: WB Saunders. Tobias KM. 2003. Portosystemic shunts and other hepatic vascular anomalies. In D Slatter, ed., Textbook of Small Animal Surgery, 3rd ed., pp. 727–752. Philadelphia: Elsevier-Saunders.
427
CHAPTER 179
Pulmonary Fibrosis Sharon Fooshee Grace
Overview Idiopathic pulmonary fibrosis (IPF) is a recently described chronic progressive interstitial lung disease of cats. Only a limited number of cases have been described in the literature. Nevertheless, recognition of this disorder in cats is highly significant in that it mimics the clinical course and pathologic findings of human IPF more closely than in any other animal model studied to date. The exact cause of IPF in cats remains undetermined, though a genetic basis is speculated. It represents a unique disorder in which the pulmonary interstitium is progressively replaced with foci of fibroblasts and myofibroblasts; interstitial smooth muscle and alveolar epithelium undergo metaplasia; and type II pneumocytes become hyperplastic. It does not have a significant inflammatory component. Infectious causes of interstitial lung disease (e.g., toxoplasmosis and histoplasmosis) are common and have been well described in cats. Other less common causes include toxic, chemotherapeutic (nitrosourea), and environmental agents (e.g., paraquat and asbestos). IPF is diagnosed when all known causes of interstitial lung disease have been eliminated. No apparent breed or sex predisposition has been noted. Most affected cats have been middle-aged or geriatric. Owners are often unaware of the disease because middle-aged and older cats are normally sedentary and can limit exertion even further when respiratory difficulty is present. Most cats do not demonstrate distress until pulmonary gas exchange is severely compromised; thus, recognition of respiratory abnormalities is typically a recent historical finding. Tachypnea, inspiratory dyspnea, and cough are reported with IPF. In some cases, respiratory distress is mixed (inspiratory and expiratory), though lack of a predominantly expiratory component distinguishes IPF from asthma and bronchitis.
(A)
Diagnosis Primary Diagnostics • Physical Examination: Tachypnea, inspiratory (or mixed inspiratory and expiratory) distress, and cough have been reported. Crackles and wheezes are common on lung auscultation. • Thoracic Radiography: Parenchymal disease varies in type, location, and severity with IPF. Abnormalities in cases studied to date have been described as “pronounced” to “severe.” Interstitial, alveolar, and bronchiolar patterns (alone or in combination) are present with a patchy or diffuse distribution. See Figures 179-1 and 179-2. • Lung Biopsy and Histopathology: Definitive diagnosis of IPF requires lung biopsy. Fibrous changes in the lung cannot be reliably detected with cytology, regardless of how the sample is obtained (i.e., aspiration or airway washings).
(B) Secondary Diagnostics • Minimum Data Base: Complete blood count, biochemical profile, fecal flotation, and urinalysis are typically normal unless a concurrent problem is present. However, because most cats affected with
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
428
Figure 179-1 A, B, A mixture of interstitial, alveolar, and bronchiolar patterns are present in this cat. Note the patchy distribution of lesions. Images courtesy Dr. Gary D. Norsworthy.
IPF are older and will require additional diagnostics, a minimum data base can be beneficial in assessing overall health of the cat and determining anesthetic risk. A fecal examination should be performed in all coughing cats that have been in an endemic area to look
Pulmonary Fibrosis
for larvae or eggs of lung flukes. See Chapter 129. Retrovirus screens are typically negative. • Cytology: Cytology obtained via lung aspirate or airway washing may be beneficial in ruling out infectious, parasitic, or neoplastic processes. See Diagnostic Notes for risks. • Heartworm Serology: Heartworm disease is a more common cause of feline cough than IPF and should be investigated in endemic areas. Heartworm disease may cause chronic lung disease with similar radiographic findings. See Chapter 88.
Diagnostic Notes
(A)
• A number of cats with confirmed IPF died during or after airway lavage. Lack of normal airway compliance and the attendant complications (e.g., hypoxemia) renders airway lavage a potentially fatal procedure for cats with IPF. • Concurrent pulmonary neoplasia has been found in a number of cats studied. A well-described association between IPF and pulmonary carcinoma exists in humans and animals.
Treatment Primary Therapeutics • Corticosteroids: Immune-suppressive doses of glucocorticoids may be administered but improvement seldom occurs. • Bronchodilators: Bronchodilator therapy may be included in the treatment plan, but most affected cats have not shown a response to these drugs.
Therapeutic Notes • Cytotoxic Therapy: Cyclophosphamide was utilized in one reported case, and the cat survived for at least 4 years. The cat received concurrent corticosteroids.
Prognosis Because of the progressive nature of IPF, the prognosis is grave. Most cats survive only days to months following diagnosis.
(B) Figure 179-2 A, B, The findings are basically the same as 179-1 but with less of a patchy pattern. Both cats had a history of coughing for months to years. Images courtesy Dr. Gary D. Norsworthy.
Suggested Readings Cohn LA, Norris CR, Hawkins EC, et al. 2004. Identification and characterization of an idiopathic pulmonary fibrosis-like condition in cats. J Vet Intern Med. 18:632–641. Secrest SA, Bailey MQ, Williams KJ, et al. 2008. Imaging diagnosis: Feline idiopathic pulmonary fibrosis. Vet Radiol Ultrasound. 49(1):47–50. Williams K, Malarkey D, Cohn L, et al. 2004. Identification of spontaneous feline idiopathic pulmonary fibrosis: Morphology and ultrastructural evidence for a type II pneumocyte defect. Chest. 125:2278–2288.
429
CHAPTER 180
Pulmonic Stenosis Larry P. Tilley
Overview Congenital obstruction of the right ventricular outflow tract is less common in the cat than in the dog. Isolated pulmonic stenosis (PS) has been reported infrequently in the cat, with only 3% of congenital heart defects in one study. Right ventricular outflow obstruction secondary to valvular or infundibular stenosis causes right ventricular pressure overload and subsequent right ventricular concentric hypertrophy. Physical examination findings suggestive of pulmonic stenosis include a left basilar systolic ejection-type murmur, jugular pulses or distention, and sometimes evidence of right-sided heart failure such as ascites. Affected cats may be asymptomatic, may experience weakness associated with exercise, or may develop right-sided congestive heart failure. Cats with other congenital malformations may also have left basilar systolic ejection murmurs. Left-to-right shunting ventricular septal defects with significant shunting volumes demonstrate a murmur of relative pulmonic stenosis in association with the increased blood volume being ejected through the normal right ventricular outflow tract. Additionally, pulmonic stenosis is part of the tetralogy of Fallot, which is a relatively common congenital defect in the feline.
Figure 180-1 Angiography can be used to diagnose pulmonic stenosis. A catheter (open arrow) is passed through the anterior vena cava into the right ventricle. Contrast material is injected and lateral thoracic radiographs are made. The stenotic area (closed arrow) is seen in the outflow of contrast from the right ventricle into the pulmonary outflow tract.
Diagnosis Primary Diagnostics • Echocardiography: Right ventricular concentric hypertrophy, right atrial enlargement, and high-velocity systolic turbulent flow across the obstruction as demonstrated by spectral or color-flow Doppler. Doppler can be used to calculate the pressure gradient across the stenosis. Tricuspid valve regurgitation may also be present.
Secondary Diagnostics • Electrocardiography: Right-axis deviation (deep S waves in leads I, II, and III) may be present with occasional atrial and ventricular premature complexes. • Thoracic Radiography: Right atrial and ventricular enlargement, poststenotic dilation of the pulmonary artery, diminutive pulmonary vasculature, and a distended caudal vena cava may be present depending on the severity of the outflow obstruction. Angiography helps to visualize the lesions. See Figure 180-1.
Treatment Primary Therapeutics • Cardiac surgery (valvulotomy or patch-graft procedure) may be palliative in cases with severe outflow obstruction; but mortality rate is high. • Balloon catheter dilation of the obstruction may also be considered.
Secondary Therapeutics • Vasodilators may cause hypotension and are best avoided. Angiotensin-converting enzyme inhibitors may be helpful with heart failure, but low doses should be used. • Therapy for right-sided congestive heart failure (furosemide) may be indicated in some patients.
Diagnostic Notes • Electrocardiographic findings are variable. QRS complex waveform changes include deep S waves in leads I, II, III, and aortic valve flow and right-axis deviation. Pulmonary stenosis often occurs with other congenital defects.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
430
Therapeutic Notes • The primary therapeutics noted usually require referral of the patient to a specialist. • β-blockade may be cardioprotective by reducing myocardial oxygen consumption and slowing the heart rate; but this has not been studied. • Interventional procedures, such as balloon valvuloplasty and cardiac surgical procedures, are performed infrequently in the feline.
Pulmonic Stenosis
Prognosis The prognosis of pulmonic stenosis depends on the severity of the obstruction and the presence of concurrent lesions. The presence of an atrial or ventricular septal defect may allow right-to-left shunting to occur, leading to hypoxemia and cyanosis and chronic incapacitation. A severe lesion is likely if the Doppler gradient exceeds 70 to 100 mm Hg. Mild cases of pulmonic stenosis are unlikely to cause clinical disease.
Suggested Readings Fuentes VL. 2007. Pulmonic Stenosis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 227–231. Ames, IA: Blackwell Publishing. Strickland K. 2008. Congenital Heart Disease. In LP Tilley, FWK Smith, Jr., M. Oyama, et al., eds., Manual of Canine and Feline Cardiology, 4th ed., pp. 1156–1157. St. Louis: Elsevier.
431
CHAPTER 181
Pyelonephritis Gary D. Norsworthy
Overview Pyelonephritis is inflammation of the renal pelvis and parenchyma. The etiology in cats is typically bacterial, most commonly Escherichia coli, Staphylococcus spp., Proteus spp., and Enterobacter spp. However, urine cultures do not always recover an organism. Usually, the affected cat is presented for chronic renal failure after many months or years of subclinical pyelonephritis; by this time, it is abacteriuric. The infection may arise hematogenously (i.e., bacterial endocarditis, abscesses, or dental disease); however, experimental evidence favors ascension of bacteria from the lower urinary tract in most cases. Cats over 10 years of age are more likely to have bacturia. Infrequently, it may also arise secondary to metabolically induced renal uroliths. There is increased risk for cats that have an indwelling urinary catheter while receiving corticosteroids. During the time of active infection, the cat may be febrile, anorectic, and lethargic. Some cats may be presented for fever of unknown origin. The kidneys, abdomen, or lumbar area may be painful to palpation, and polyuria and polydipsia may be present. If the source of the infection is bacterial cystitis, there may be signs of lower urinary tract disease (i.e., hematuria, dysuria, or pollakiuria). However, many cases elude diagnosis because some cats are asymptomatic, the symptoms are unrecognized by the owner, or a diagnosis of lower urinary tract disease is made based on hematuria, dysuria, pollakiuria, and bacturia. Many cats showing nonspecific signs of infection are treated empirically with antibiotics without a definitive diagnosis and subsequently improve. Evidence of the disease may be found years later following the onset of chronic renal failure, abdominal ultrasound, or at necropsy, especially if it occurs unilaterally.
Secondary Diagnostics • Radiology: An excretory urogram will reveal dilation and blunting of the renal pelvis with lack of filling of the collecting diverticula, dilation of the proximal ureter, and decreased opacity of the nephrogram phase and of the contrast media in the collecting system. The kidneys are often enlarged during acute pyelonephritis and small and irregular if the disease becomes chronic . See Figures 292-60 and 292-63. • Ultrasound: Active pyelonephritis produces a dilated renal pelvis (see Figure 181-1) and proximal ureter and a hyperechoic mucosal margin line within the renal pelvis or the proximal ureter. The
Diagnosis (A) Primary Diagnostics • Clinical Signs: If the cat is presented during active bacterial infection, it will have the clinical signs as described previously. • Physical Examination: Pain in the kidneys, abdomen, or lumbar area is strongly suggestive and is consistent during the acute, bacturic phase of the disease. • Chemistry Profile: Typical findings during active infection include azotemia, hyperphosphatemia, nonregenerative anemia, and metabolic acidosis. However, cats with acute disease with more than 75% of their nephrons functioning will have normal renal values; this is not unusual. • Urinalysis: Typical findings during active infection are low specific gravity, proteinuria, bacturia, pyuria, and hematuria. Leukocyte casts are diagnostic for renal inflammation and usually result from pyelonephritis. • Urine Culture: This should be performed to document the presence of bacteria and to provide data on which to base antibiotic selection.
(B)
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
432
Figure 181-1 Ultrasonographic findings of pyelonephritis include an irregular dilated renal pelvis. It is usually a bilateral disease as seen in images A and B, but one kidney is often more severely affected and consequently smaller. Escherichia coli was cultured from this cat’s urine.
Pyelonephritis
4.0 mg/dL. Forty to 60 mEq of potassium chloride should be added to each liter of fluid, but the rate of administration should not exceed 0.5 mEq/kg per hour and serum potassium values should be monitored for hyperkalemia. If metabolic acidosis is present, sodium bicarbonate should be added to the fluids. See Chapter 190.
Therapeutic Notes
Figure 181-2 The end result of pyelonephritis is often a kidney that is small, irregular on its surface, and in failure. Both kidneys were affected in this cat. The smaller kidney likely was diseased prior to the onset of pyelonephritis with resulting compensatory hypertrophy of the other kidney.
intensity of the latter finding will diminish, but it may persist for months or years following resolution of the active infection. The kidneys are often enlarged during acute pyelonephritis and small and irregular if the disease becomes chronic. See Figure 181-2. • Renal Pelvic Aspiration (pyelocentesis): A 22-gauge needle is passed into the renal pelvis with ultrasound guidance or during a laparotomy so as to avoid the renal artery and vein. The disease is confirmed if bacteria are aspirated. This sample provides good material for culture.
Diagnostic Notes • The best way to differentiate a lower urinary tract infection and pyelonephritis is an ultrasound study or an excretory urogram. • Recurrent bacturia, even with only lower urinary tract signs, should raise the index of suspicion for pyelonephritis. An imaging study should be recommended. • Experimentally, it has been shown that bacteria may impair renal concentrating ability. A positive urine culture in a cat with dilute urine is strongly suggestive of pyelonephritis, even in the absence of azotemia.
Treatment Primary Therapeutics • Antibiotics: Specific antibiotic therapy should be given for at least 4 weeks. Some cats need 12 weeks of therapy with a rotation of antibiotics based on culture and sensitivity.
Secondary Therapeutics • Renal Support: If azotemia is present, intravenous fluids should be given until the creatinine level returns to normal or below
• Some recommend reculturing the urine after about 5 to 7 days of antibiotic therapy to be sure the correct drug is being used. • Approximately 1 week following completion of antibiotic therapy, the urine should be recultured. If it is positive, antibiotics should be reinstituted for another 4 to 8 weeks. If the first reculture is negative, the urine should be cultured again in about 1 month and anytime the cat develops fever, renal, abdominal or lumbar pain, or other clinical signs suspicious of recurrence. Recurrence or relapse is common. • Appropriate antibiotics should show sensitivity when cultured, be bactericidal, achieve good serum and urine concentrations, and not be nephrotoxic. Aminoglycosides should only be used if no other alternative exists; concurrent fluid therapy should be employed. • Colonization of the renal medulla can occur. Poor tissue penetration of antibiotics makes this an infection that may require long-term treatment. • Pyelonephritis generally causes some permanent renal damage. Affected cats should be monitored periodically for early onset of renal insufficiency or failure. • High serum and urinary antibiotic concentrations do not necessarily ensure high tissue concentrations in the renal medulla; thus, chronic pyelonephritis may be difficult to eradicate. Therefore, some cases may require antibiotic therapy for life. One effective management program is to alternate nonnephrotoxic drugs each month. • In cats with renal uroliths, resolution may require urolith removal. See Chapter 263. However, nephrotomy causes some permanent damage to the kidney. Long-term antibiotics are usually a better choice if they control bacturia.
Prognosis Prognosis varies with the stage and severity of the disease. Cats diagnosed during the early acute phase that are treated aggressively have a good prognosis. Cats that are not treated early usually have some resulting permanent renal damage, which eventually leads to chronic renal failure. However, the ensuing renal failure may not occur for many years.
Suggested Readings Adams LG. 2007. Pyelonephritis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 1160–1161. Ames, IA: Blackwell Publishing. Senior DF. 2000. Management of difficult urinary tract infections. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy, XIII, pp. 883–886. Philadelphia: WB Saunders.
433
CHAPTER 182
Pyometra and Mucometra Gary D. Norsworthy
Overview Progesterone has several significant influences on the uterus. It suppresses leukocyte response within the uterus, reduces contractility of the myometrium, and stimulates endometrial gland development. These are designed to prepare the uterus for pregnancy. However, if pregnancy does not occur, these effects can become pathologic. Exogenous progesterone administration and repeated estrus cycles without pregnancy predispose the queen to disease, beginning with endometrial hyperplasia. Mucometra occurs when the quiescent uterus becomes distended with sterile mucus. If bacterial contamination occurs, either due to ascension through the cervix or hematogenously, pyometra results. Escherichia coli is the most common isolate. Most queens that develop pyometra are at least 4 years of age. Clinical signs include abdominal distention, anorexia, and lethargy; pyrexia is a rare occurrence. Purulent vaginal discharge occurs if the cervix is open. See Figure 182-1. Unlike dogs, most cats do not have a history of polydipsia and polyuria. The history often includes an estrous cycle within 8 weeks prior to the onset of clinical signs; however, this is more variable in cats than in dogs. If uterine rupture occurs, peritonitis and septic shock occur. Queens that cycle repeatedly but are not bred are likely to develop endometrial hyperplasia and are, therefore, predisposed to development of pyometra.
Treatment Primary Diagnostics • Clinical Signs: The typical clinical signs, especially abdominal distention and vaginal discharge, in an intact female that cycled recently should raise one’s index of suspicion for pyometra. • Imaging: Radiography can detect uterine enlargement; however it is difficult to differentiate a gravid uterus from pyometra before about 48 days of pregnancy, the time at which calcification of the fetal skeleton becomes visible. Ultrasonography reveals a tubular structure containing hypoechoic material often interspersed with hyperechoic areas. See Figure 182-2. Ultrasound can differentiate intrauterine fluid from noncalcified feti about 21 days after the last breeding. • Serum Progesterone: The serum progesterone level at the time of diagnosis is typically greater than 15.9 nmol/L (5 ng/mL).
Secondary Diagnostics • Abdominal Palpation: Precise palpation can detect an enlarged uterus as a tubular structure in the mid- to caudal abdomen. However,
Figure 182-1 A purulent vaginal discharge is obvious on this cat. However, the fastidious grooming habits of most cats with pyometra keep owners from seeing the discharge.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
434
Figure 182-2 A tubular hypoechoic structure in the mid- to caudal abdomen is the typical ultrasound finding in pyometra or mucometra.
Pyometra and Mucometra
Figure 182-3 This distended uterus was removed surgically. Note the degree of distension. The segmentation could cause confusion with pregnancy based on palpation; however, ultrasound would easily differentiate.
Figure 182-4 This uterus ruptured and sent the cat into septic shock. An emergency laparotomy, ovariohysterectomy, intravenous fluids, and antibiotics were life-saving.
some uteri with infection can be segmented and simulate pregnancy. See Figure 182-3. • Complete Blood Count (CBC): Most cats have a marked neutrophilic leukocytosis with a regenerative left shift. Some have a mild anemia. • Chemistries: Hyperglobulinemia and hypoalbuminemia may occur in advanced cases.
Secondary Therapeutics
Diagnostic Notes
Therapeutic Notes
• Because of the fastidious nature of cats, a vaginal discharge may go undetected by owners.
• Prostaglandin therapy should be restricted to queens that meet all of the following conditions: (a) have significant breeding value; (b) are in stable condition (not septicemic); and (c) have an open cervix. • Prostaglandin therapy may produce intense grooming of the flanks and vulva, vomiting, vocalizing, restlessness, panting, salivation, urination, and defecation (usually diarrhea with tenesmus). These resolve within 1 to 2 hours after treatment and tend to diminish with subsequent injections. These cats should be hospitalized at least for several hours to be sure that any side effects are transient. They should be bred on the next estrus cycle. • Even if prostaglandin therapy is successful in alleviating pyometra, the prognosis for successful breeding is guarded due to underlying uterine pathology that persists. • If prostaglandin is given to a pregnant queen, abortion is highly likely.
Treatment Primary Therapeutics • Antibiotics and Fluids: Regardless of the form of therapy chosen, many of these cats are septic and azotemic. Antibiotics should be chosen based on culture and sensitivity, if possible. If not possible or pending culture results, the following antibiotics are recommended: potentiated sulfas, clavulanate-amoxicillin, ampicillin, cephalosporins, or fluoroquinolones. Clavulanate-amoxicillin and ampicillin can be combined with a fluoroquinolones. • Ovariohysterectomy: This is the treatment of choice except when valuable breeding queens belonging to a highly motivated owner are affected. See Therapeutic Notes. • Prostaglandin F2α therapy: This drug can be used in queens that are to be used for future breeding. It is dosed at 0.1 mg/kg q12h SC for 2 days then increased to 0.2 mg/kg q12h until the size of the uterus nears normal, preferably with assessment by ultrasound. Total treatment time is usually about 5 days. Transition from a purulent vaginal discharge to a clear, serous discharge is suggestive of successful treatment. A second course of treatment should be considered if the first one is not successful. Ultrasound can also be used to monitor response. Administration to a queen with a closed cervix can result in uterine rupture or retrograde movement of purulent material out the oviducts into the peritoneal cavity. See Therapeutic Notes.
• Hysterotomy and Lavage: This procedure produces mixed results but can be helpful in resolving infections so that future breeding is possible. It is indicated for closed-cervix pyometra; however, it can cause rupture of a friable uterine wall. See Figure 182-4.
Prognosis The prognosis is generally good if advanced sepsis has not occurred prior to treatment and ovariohysterectomy is performed.
Suggested Readings Potter K, Hancock DH, Gallina AM. 1991. Clinical and pathologic features of endometrial hyperplasia, pyometra, and endometritis in cats: 70 cases (1980–1985). J Am Vet Med Assoc. 198:1427–1431. Root-Kustritz MV. 2007. Pyometra and Cystic Endometrial Hyperplasia. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 1164–1165. Ames, IA: Blackwell Publishing.
435
CHAPTER 183
Pyothorax Gary D. Norsworthy
Overview Pyothorax is an accumulation of pus within the pleural cavity. It is almost always caused by a bacterial infection; Pasturella multocida and Bacteroides spp. are common isolates. Anaerobic organisms are often found, and fungi may also be causative. Traditionally the causative organism has been thought to gain entry into the pleural space through penetrating bite wounds from other cats, but foreign bodies, such as migrating plant awns, have rarely been found within the pleural space and presumed to be causative. In addition, it is thought that infections may arise from abscesses in adjacent organs, including the trachea and esophagus, or may develop from hematogenous spread. A recent study shows a strong link to oropharyngeal bacteria that may descend the respiratory tract, penetrate the lung parenchyma via abscessation, and enter the pleural space. However, in most cases, the source of the infection is not definitively identified. Presence of the organisms and their toxins leads to the systemic effects of fever, inappetence, weight loss, and dehydration. Pulmonary compression results in dyspnea and tachypnea. As with most cases of dyspnea, the owner usually reports an acute onset, even though the disease typically has been present for days to weeks.
(A)
Diagnosis Primary Diagnostics • Clinical Signs: Clinical signs include dyspnea and tachypnea; some cats may have systemic signs of illness. • Auscultation: Heart sounds are muffled; lung sounds are decreased ventrally and increased dorsally. • Radiography: Pleural effusion with pleural fissures and scalloped lung borders are typical. See Figure 183-1. • Thoracentesis: A few milliliters of fluid may be removed to confirm the presence of pleural effusion and for subsequent analysis. • Pleural Fluid Analysis: The protein content is greater than 35 g/L (3.5 g/dL), and the specific gravity is greater than 1.020. The nucleated cell count is greater than 15 × 109/L (15,000 × 103/mm3), often greater than 50,000 × 109/L (50,000 × 103/mm3), and may reach 100,000 × 109/L (100,000 × 103/mm3). • Pleural Fluid Cytology: Degenerative neutrophils, macrophages, and the causative organism are usually found. Nondegenerate neutrophils may predominate when higher bacteria, such as Actinomyces or Nocardia, are involved. See Figure 183-2. • Culture and Sensitivity of Pleural Fluid: Aerobic and anaerobic cultures are essential as many of the pathogens are anaerobic. Some organisms take 2 to 4 weeks to grow.
Secondary Diagnostics • Hemogram: Marked neutrophilic leukocytosis and anemia of chronic disease are typical. • Serum Chemistries: These are often normal, but there may be increased total protein with a decreased A-to-G ratio.
(B) Figure 183-1 Radiographs of a cat with pyothorax. Both lateral (A) and dorsal-ventral views (B) show lack of detail within the thoracic cavity due to the large amount of fluid present. These radiographs are not significantly different from pleural effusion caused by other diseases. • Urinalysis: This is usually normal. Proteinuria is present if glomerulopathy has developed.
Diagnostic Notes th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
436
• Dyspneic cats should be handled carefully because increased stress may be fatal. Extreme care should be taken when doing the physical
Pyothorax
(A)
Figure 183-2 When the pleural effusion is centrifuged, a large amount of sediment is common in pyothorax.
examination, imaging, and thoracentesis. It may be necessary to place the cat in an oxygen cage for several minutes prior to diagnostics and between diagnostic procedures. The least stressful radiographic view is the dorsoventral (DV); it may be the only view that is practical in some cases and is usually sufficient to diagnose the presence of pleural effusion. The ventrodorsal (VD) view is contraindicated because it increases dyspnea.
Treatment Primary Therapeutics • Thoracentesis: The least amount of sedation should be employed. Anesthetic agents permitting rapid recovery are preferred. These include isoflurane, sevoflurane, and propofol. Aspirate both sides of the chest, and remove as much fluid as possible. Aspirate below the costochondral junction in multiple locations beginning at the fourth to sixth intercostal space with the cat in sternal recumbency. • Antibiotics: The initial choice should include drugs likely to be effective against both aerobic and anaerobic bacteria. Amoxicillin (high dose of 40 mg/kg q8h IM or SC) plus metronidazole or a fluoroquinolone is the initial drug combination of choice. Antibiotics should be given for at least 1 month past apparent recovery based on clinical signs and radiographs and sometimes long term. The average antibiotic duration is 3 to 4 months. The choice of antibiotics should be based on culture and sensitivity. • Thoracostomy Tube: This permits continuous or intermittent chest drainage without further stress to the cat. Generally, one tube will drain both sides of the chest; however, some cases require bilateral tube placement, especially if a complete mediastinum is created due to pleural thickening. See Figure 183-3. The chest should be aspirated two to three times per day through the tube. Many clinicians flush the pleural space with warm saline solution (5–10 mL/kg) without antibiotics and allow the fluid to remain in the chest for about 1 hour. However, if dyspnea increases the fluid should be removed immediately. Heparin may be added to the lavage fluid (1,500 IU/L) to
(B) Figure 183-3 Placement of a thoracostomy tube is usually required for proper drainage of the pleural space. Generally, only one tube is sufficient. This is the cat in Figure 183-1.
reduce fibrin buildup. Parenteral antibiotics are sufficient; adding antibiotics to the lavage fluid offers no advantage. Overzealous use of certain antibiotics, especially aminoglycosides, may result in toxicity. The pleural space should be aspirated until less than 4 mL/kg of fluid is removed because this amount is usually due to the presence of the tube. In most cats, the thoracostomy tube can be removed in 1 week or less.
Secondary Therapeutics • Intravenous Fluids: Placement of an intravenous catheter and fluid administration should be delayed until thoracentesis has been performed due to the stress involved. • Thoracotomy: Cats that do not respond to 3 to 5 days of chest drainage and appropriate systemic antibiotics are candidates for this surgery. The pleural space should be probed for foreign bodies, lung abscesses, and lung lobe torsions.
437
SECTION 1: Diseases and Conditions
Therapeutic Notes • Repeated thoracentesis may be used in place of thoracotomy. However, this can be a painful procedure that may be too stressful for many cats that are fragile patients. The use of a chest drain is strongly recommended for all but the most debilitated patients. • There appears to be no advantage to adding antibiotics to the lavage fluid, and doing so complicates the calculation of antibiotic dosages. If significant fibrous tissue is present in the pleural space, absorption is difficult to determine. • The new data regarding oropharyngeal bacteria has led to stronger recommendations for the use of antibiotics following dental procedures and for upper respiratory infections that are presumed to be viral but potentially complicated with secondary bacterial infections.
Prognosis This is a serious and potentially fatal disease. However, with aggressive diagnostics and therapeutics, including a thoracotomy tube, most of
438
these cats will recover. Recurrence is likely if antibiotic therapy is discontinued too soon; otherwise, the prognosis is good. Adhesions between the lung lobes and other structures are usually permanent and will limit ventilatory capacity.
Suggested Readings Barrs VR, Allan GS, Martin P, et al. 2005. Feline pyothorax: A retrospective study of 27 cases in Australia. J Fel Med Surg. 7:211–222. Barrs VR, Beatty JA. 2009. New insights into an old problem: Part 1: Aetiopathogenesis and diagnostic investigation. Vet J. 179:163–170. Mertens MM, Fossum TW, MacDonald KA. 2006. Pleural and Extrapleural Diseases In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1272–1283. St. Louis: Elsevier Saunders.
CHAPTER 184
Pyrethrin and Pyrethroid Toxicosis Gary D. Norsworthy
Overview Pyrethrins are insecticides derived from the extract of dried Chrysanthemum (pyrethrum) flowers. Synthetic pyrethroids were developed because pyrethrins degrade due to exposure to ultraviolet light, moisture, and air. They are grouped into Type I and Type II pyrethroids on the basis of their chemical structures. The most popular Type I pyrethroids are permethrin, d-trans-allethrin, sumethrin, resmethrin, phenothrin, and tetramethrin. The most popular Type II pyrethroids are fenvalerate, fluvalinate, cypermethrin, flucythrinate, and deltamethrin. Fenvalerate plus diethyltoluamide (DEET) is used on dogs but is toxic to cats. A newer pyrethroid, etofenprox, has a favorable feline toxicity profile. Pyrethrins and pyrethroids are non-toxic to most mammals, but cats have less ability to degrade these products than other species. Toxicity occurs in an occasional cat, but it is usually not fatal with the exception of N,N-Diethyl-meta-Toluamide (DEET) toxicity. However, there is some evidence that cats less than 1 year of age may be more severely affected. Toxicity is due to prolonged sodium conductance in nerve axons resulting in repetitive nerve discharges. The toxicity is enhanced in hypothermic cats and if a pyrethrin or pyrethroid is combined with synergistic insecticides. Lethargy and profuse salivation are the mildest clinical signs. The toxicity may progress to ataxia, tremors, hyperexcitability, disorientation, hypothermia, mydriasis, vomiting, diarrhea, seizures, and, rarely, death.
Diagnosis Primary Diagnostics • History and Clinical Signs: A combination of known exposure and clinical signs is the basis for diagnosis in most cases.
Diagnostic Notes • There is no specific diagnostic test to confirm pyrethrin or pyrethroid toxicosis. Likewise, no pathognomonic gross or histopathological changes occur. • Chemical analysis for pyrethrin or pyrethroid residues on the skin or in the gastrointestinal tract may be used for confirmation.
Treatment Primary Therapeutics • Methocarbamol: This is the drug of choice and is effective for muscle tremors. It may be given IV or PO. The IV dose is 50 to 200 mg/kg. The dose should not to exceed 300 mg/kg per day. Do not exceed 200 mg/min injection rate. The PO dose is 22 to 44 mg/kg q8h.
• Diazepam: This drug is given in 0.5- to 1.25-mg increments IV to control seizures. The dosage should not exceed 20 mg/cat. • Phenobarbital: If seizures are not controlled by diazepam, consider this drug at 5.0 to 20.0 mg/kg IV to effect. • Bathing: It is important to remove remaining toxin from the skin with a noninsecticide-containing shampoo.
Secondary Therapeutics • Activated Charcoal with Osmotic Cathartic (Sorbitol 70%): This is to remove residual insecticide from the gastrointestinal tract. However, pyrethrins and pyrethroids are so rapidly absorbed from the gastrointestinal tract that activated charcoal is rarely effective. Actidose with Sorbitol (Paddock Laboratories, Minneapolis) is given at 6 to 12 mL/kg via orogastric tube. • Supportive Care: This may include correction of anorexia, dehydration, hypothermia, or hyperthermia and is important for recovery. • Emetics: They are rarely indicated because of the rapidity of toxin absorption.
Therapeutic Notes • Atropine is not an antidote for this type of toxicity. It is contraindicated because it may cause tachycardia, central nervous system (CNS) stimulation, disorientation, drowsiness, respiratory depression, and seizures. • Phenothiazine tranquilizers, such as acepromazine, are contraindicated.
Prognosis The prognosis is generally good with aggressive care with the exception of DEET toxicity or toxicity due to pyrethrin-containing insecticide combinations. In the latter cases, the prognosis will vary depending upon the other insecticide involved.
Suggested Readings Harvey JW. 2007. Pyrethrin and Pyrethroid Toxicity. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 1168. Ames, IA: Blackwell Publishing. Linnett PJ. 2008. Permethrin toxicosis in cats. Aust Vet J. 86(1–2):32–35. Sutton NM, Bates N, Campbell A. 2007. Clinical effects and outcome of feline permethrin spot-on poisonings reported to the veterinary poisons information service (VPIS), London. J Fel Med Surg. 9(4): 335–339. Valentine WM. 1990. Pyrethrin and pyrethroid insecticides. Vet Clin North Am Small Anim Pract. 20(20):375–382.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
439
CHAPTER 185
Rabies Mark Robson and Mitchell A. Crystal
Overview Rabies is caused by the rabies virus, a labile (easily destroyed by heat, ultraviolet (UV) light, and various disinfectants), single-stranded RNA virus in the family Rhabdoviridae. Rabies is acquired via a bite from an infected animal, typically a raccoon or skunk, or uncommonly, a bat, fox, or other mammal. Rarely, infection can be acquired by inhalation or ingestion. Younger cats are more susceptible to infection. Rabies virus has a predilection for nervous and salivary gland tissue. After being bitten by an infected animal, cats will undergo an incubation period without clinical signs, during which time the virus spreads to the central nervous system (CNS) by retrograde flow-up axons. The incubation period is of variable length depending on the site of the bite (i.e., shorter when closer to the CNS and in highly innervated tissue), age (shorter in younger cats), and the amount of virus introduced. The incubation period in cats is reported to be 2 to 24 weeks, although the vast majority will develop clinical signs within 4 to 6 weeks. The clinical course of rabies is generally divided into the prodromal, furious, and paralytic phases. In cats, the prodromal phase usually lasts 1 to 2 days and is characterized by anxiety, apprehension, nervousness, and increased vocalization with or without a change in voice. Friendly animals may become shy or irritable, and fractious animals may become docile and affectionate. Cats more consistently develop the furious phase of rabies, showing a wild, anxious, or blank look to the eyes, ptyalism, vicious striking movements, muscle tremors, weakness, ataxia, anorexia, depression, and seizures. The paralytic phase usually begins around day 5 of the clinical illness and is characterized by lower motor neuron paralysis that ascends from the site of the injury to the CNS, causing generalized paralysis, coma, and death. Cats occasionally develop the paralytic form directly after the prodromal phase. Death typically occurs 3 to 4 days after the onset of clinical signs, although some cases survive 10 days or more. Virus shedding generally occurs 1 to 5 days prior to development of clinical signs; thus, in cases in which euthanasia and brain testing are not required or performed, most public laws require a 10-day observation period for cats that have bitten a human. Vaccineinduced rabies has been reported secondary to the use of modified-live virus rabies vaccines. Clinical signs begin 2 weeks after vaccination and include hindlimb weakness progressing to posterior, then generalized, paralysis. Consequently, no modified-live virus rabies vaccines are currently available for use in cats in the United States. The true prevalence of rabies is underestimated as many rabid animals are never observed, and therefore, go untested and undetected. Since 1981, reported cases of feline rabies have outnumbered cases of canine rabies. In 2008 in the United States and Puerto Rico, cats made up 294 of the confirmed 6,841 cases (4.3%) of animal rabies compared with only 75 cases (1.1%) in dogs. This represents a 12% rise in feline cases since 2007. The increasing number of cases in cats may reflect the increasing prevalence of wildlife rabies and the limited vaccination of cats. As a consequence, the frequency of human rabies attributed to cats is increasing at a greater rate than dogs, although bats are still the most common
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
440
source of human rabies cases. Hawaii is the only location in North America that is rabies free. Rabies is a public health concern. Although the incidence of human rabies in developed countries is low (an average of one to two cases a year in the United States), infection is nearly 100% fatal. Therefore, early recognition and prevention are essential. Any human potentially exposed to a rabid animal is advised to consult his or her physician immediately to discuss therapy with human rabies immune globulin (unvaccinated person, 20 IU/kg infiltrated at the site of the bite on day 0; vaccinated person, no immune globulin therapy) and rabies vaccination (previously unvaccinated person, Food and Drug Administration [FDA]-approved vaccine IM in upper deltoid on days 0, 3, 7, and 14 with immunocompromised persons also receiving a fifth dose on day 28; previously vaccinated person, FDA-approved vaccine IM in upper deltoid on days 0 and 3). Individuals who are at an increased risk of exposure (e.g., veterinarians and staff, spelunkers, rabies diagnostic lab workers, animal control persons, wildlife workers, and so on) should receive preexposure rabies prophylaxis (FDA-approved vaccine 1.0 ml IM in a deltoid on days 0, 7, and 21 or 28). Booster revaccination should be based on risk group. The Center for Disease Control and Prevention (CDC) recommends evaluating titers every 2 years in persons in enzootic rabies areas who have frequent risk of exposure; the CDC does not recommend titer reassessment or booster revaccination in persons in low rabies rate areas (even in persons considered of increased risk of exposure).
Diagnosis Primary Diagnostics • Direct Immunofluorescent Antibody Test: This test performed on brain tissue will demonstrate virus in all cats excreting virus in their saliva. The entire head, chilled but not frozen, should be quickly submitted to the proper testing facility. • Quarantine and Observation: Any vaccinated cat that bites a human should be confined for observation for 10 days. Rabies vaccination should not be administered during this time. If potential signs of rabies develop, the cat should be euthanized and the head submitted to the proper authorities for rabies testing; the appropriate state public health official should be notified. The individual receiving the bite should be contacted and referred to a physician immediately.
Diagnostic Notes • There are no rapid, definitive antemortem tests for rabies. • Any unvaccinated cat that bites a human should be euthanized and the head submitted to the proper authorities for rabies testing. • Freezing of a brain to be examined for rabies will damage the tissue and destroy the virus, potentially making detection impossible. • Gloves and mask should be used when handling tissue that is potentially infected with rabies. • Containers used to ship or transport tissue that is potentially infected with rabies should be clearly marked as a biologic hazard. • Animals undergoing quarantine for rabies should be confined to a secure, limited-access area with clearly posted signs indicating suspected rabies.
Rabies
Treatment Primary Therapeutics • Euthanasia: No therapy is effective once clinical signs of rabies are present. Because rabies is a human health concern, any cat known or suspected to have rabies should be euthanized and the appropriate state public health official should be notified, followed by submission of the head to the proper authorities for rabies testing. • Vaccination: To prevent rabies, all cats should be vaccinated with an approved rabies vaccine (i.e., current options include adjuvanted killed, adjuvanted recombinant, and nonadjuvanted canary pox vectored) given IM or SC, based on manufacturers recommendations, at one location in the thigh no earlier than 3 months of age, at 1 year of age, then at the appropriate interval determined by duration of product immunity and local public health regulations. Cats are considered protected from rabies 28 days following initial vaccination and immediately following booster vaccination. • Nonvaccination Preventive Measures: Any wound from a possible cat bite should be thoroughly cleansed. Owners should be discouraged from allowing their cats to roam free in areas endemic for rabies, especially kittens under 3 months of age. Owners should be advised to immediately report any free-roaming wild or domestic animal demonstrating neurologic signs to the appropriate animal or wildlife control officials.
Secondary Therapeutics • Quarantine: Any vaccinated cat that is bitten by a known or suspected rabies-infected animal should be revaccinated, kept under owner control, and observed for 45 days. If potential signs of rabies develop, the appropriate state public health official should be notified, the cat should be euthanized, and the head submitted to the proper authorities for rabies testing. In addition, the vaccine manufacturer and the United States Department of Agriculture (USDA) Animal and Plant Health Inspection Service, Center for Veterinary Biologics should be notified (1-800-752-6255 or
[email protected]). An unvaccinated cat that is bitten by a known or suspected rabiesinfected animal should be euthanized and the head submitted for rabies evaluation; the appropriate state public health official should be notified. If the owner is unwilling to have this done, the cat should be isolated for 6 months and vaccinated on entry into isolation and 1 month prior to being released. If potential signs of rabies develop, the cat should be euthanized and the head submitted to
the proper authorities for rabies testing; the appropriate state public health official should be notified.
Therapeutic Notes • Veterinarians should educate clients on the importance of feline rabies vaccinations with regard to human health considerations. • When applicable, owners should be informed of state laws requiring rabies vaccination. • Any humans potentially exposed to rabies should be referred to their physician to discuss appropriate postexposure rabies prevention therapy. • Accidental human exposure to killed, parenteral animal rabies vaccine does not constitute a risk for rabies virus infection. Human exposure to vaccinia-vectored oral rabies vaccines should be reported to state health officials. • Rarely, rabies vaccine may induce injection site (induced) fibrosarcomas in predisposed cats. Rabies vaccines should be administered on the right hind limb, as distal as possible. • Current rabies vaccines are cross-protective against the Australian bat Lyssavirus (ABLV).
Prognosis Rabies is nearly 100% fatal in animals and humans. Due to public health concerns, cats suspected of having rabies should not be treated. Immediate euthanasia is indicated followed by proper evaluation of the head by designated authorities and notification of the appropriate state public health official. Humans exposed to potentially rabid animals should be referred to their physician for appropriate postexposure prophylaxis. Postexposure prophylaxis, when performed early, is almost always effective in preventing rabies in humans.
Suggested Readings Blanton JD, Robertson K, Palmer D, et al. 2009. Rabies surveillance in the United States during 2008. J Am Vet Med Assoc. 235(6):676–689. Fogelman V, Fischman HR, Horman JT, et al. 1993. Epidemiologic and clinical characteristics of rabies in cats. J Am Vet Med Assoc. 202(11):1829–1833. Green CE, Rupprecht CE. 2006. Rabies and other Lyssavirus infections. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 167–183. St. Louis: Saunders Elsevier. 2008 Compendium of Animal Rabies Prevention and Control, 2008. Centers for Disease Control and Prevention. MMWR 57(RR–2):1–9.
441
CHAPTER 186
Recreational Drug Toxicosis Tatiana Weissova
Overview Recreational drugs are psychoactive substances because they produce pleasurable sensations. The most popular psychoactives used worldwide are ethanol (i.e., alcohol, which is legal), caffeine (e.g., coffee and tea, which is legal legal), theobromine (i.e., chocolate, which is legal legal), nicotine (i.e., tobacco, which is legal), and cannabis (marijuana, which illegal in the majority of countries). Other psychoactives are barbiturates, benzodiazepines, opium and opioids, deliriants, dissociative anesthetics, phenethylamines, central nervous system (CNS) stimulants, indole alkaloids, inhalants, and unclassified stimulants.
Ethanol Ethanol is short-chain aliphatic alcohol. Cats usually do not like the smell or taste of alcohol but are often attracted to mixed drinks that contain milk, cream, or ice cream. They are far more sensitive to ethanol than humans; even drinking a small amount of products containing alcohol can cause significant intoxication. Ethanol is readily absorbed from the gastrointestinal (GI) tract and is metabolized in the liver by enzyme alcohol dehydrogenase (ADH). Alcohol intoxication commonly causes vomiting due to gastric irritation and CNS signs including loss of coordination, disorientation, and stupor. In severe cases coma, seizures, and death can occur. Cats that are intoxicated by alcohol should be monitored until they recover. Differential diagnoses include other alcohols (e.g., methanol, isopropanol, and butanol), abused drugs (e.g., barbiturates and marijuana), early stage of ethylene glycol toxicosis, pesticides (i.e., amitraz and macrolide antiparasiticides), and halogenated or aliphatic hydrocarbon solvents.
Treatment Primary Therapeutics • Induce emesis only with caution in depressed animals. • Fomepizole (4-methylpyrazole, Antizol-Vet®) is an effective and nonlive toxic ADH inhibitor. Initially, give 125 mg/kg IV within 1 to 3 hours post-ingestion; then give 31.25 mg/kg IV at 12, 24, and 36 hours after the initial dose. • Sodium Bicarbonate: This is used to correct metabolic acidosis according to plasma bicarbonate and base deficit with monitoring every 4 to 6 hours. If this is not possible, the dose is 5 mEq/kg per hour. • Fluid Therapy: Used to correct dehydration and electrolyte imbalances.
Secondary Therapeutics • Artificial Ventilation: to correct depressed respiratory function. • Cardiac Arrest Therapy: Give epinephrine at a dose of 0.01 mg/kg IV. Using a 1 : 10,000 concentration, give 1 mL/5 kg (11 lbs). • CNS Depression: Give yohimbine at 0.11 mg/kg IV or 0.25 to 0.5 mg/ kg SC or IM and do not administer other CNS depressants.
Therapeutic Notes • Activated charcoal is controversial. Aliphatic alcohols may not be well adsorbed by it.
Prognosis Diagnosis Primary Diagnostics: • History: Ask about evidence of exposure or possible exposure, usually in a household with teenagers who may find it fun to give alcohol to the cat. • Clinical Signs: They develop within 15 to 30 minutes on an empty stomach or 1 to 2 hours on a full stomach, depending on doses and stomach content. They include vomiting, behavioral changes, excitement or depression, ataxia, hypothermia, reduced reflexes, polyuria, and incontinence. Advanced signs include depression or narcosis, slowed respiratory rate, metabolic acidosis, cardiac arrest, and death. • Blood Ethanol Concentrations: Toxicosis in adults occurs when the blood level is greater than 1 to 4 mg/mL. • Acid-Base Evaluation: Abnormalities occur in blood gases, pH, anion gap, and plasma bicarbonate concentration due to metabolic acidosis. • Hypoglycemia: This may occur; it is necessary to monitor for it.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
442
The prognosis is always guarded in cases with acidosis and severe CNS or respiratory system depression. Most cases involving mild signs usually resolve with close monitoring and supportive care for 24 hours.
Caffeine Caffeine is methylxanthine alkaloid found in coffee, tea, cola, and chocolate and is an additive in many soft drinks, medications, and diet pills. It is used as a CNS stimulant; stimulant tablets may contain 100 to 200 mg caffeine. Although cats are slightly more sensitive than dogs, toxicosis is infrequent. The lethal dose ranges from 80 to 150 mg/kg body weight. Caffeine is quickly absorbed after ingestion and passes through the blood-brain barrier, placenta, and mammary glands. It is rapidly metabolized by the liver and is excreted by the bile. Caffeine directly stimulates the myocardium and medullary, respiratory, vasomotor, and vagal centers of the brain. Benzodiazepine receptors in the brain are competitively antagonized. Clinical signs start within 1 to 2 hours and include restlessness initially, hyperactivity, abnormal behavior, and possibly vomiting. Later signs include panting, tachycardia, ataxia, weakness, diuresis, diarrhea, hyperexcitability, hyperkinesis, and muscle tremors. Animals often are hyperthermic and dehydrated. Hypertension, cyanosis, and coma precede death from cardiac arrhythmias or respiratory failure. Differential diagnoses include convulsant or excitatory alkaloids (i.e., strychnine, amphetamine, nicotine, cocaine, or tricyclic antidepressants),
Recreational Drug Toxicosis
convulsant pesticides, toxicosis (i.e., bromethalin or fluoroacetate), cardioactive glycosides (digitalis), psychogenic drugs (lysergic acid diethylamide [LSD]), hypomagnesemia, and hypocalcemia.
Diagnosis Primary Diagnostics • History: Ask about drinking coffee (usually with milk or cream), tea, or soft drinks or eating caffeine containing pills, sweets, or cakes. • Clinical Signs: The characteristic signs are a combination of CNS excitation and severe tachycardia. • Laboratory Tests: Look for hypokalemia, hyperglycemia, or hypoglycemia; however the latter is not a reliable indicator.
Secondary Diagnostics • Electrocardiogram (ECG): This is used to confirm tachycardia, ventricular tachyarrhythmia, and premature ventricular contractions.
Treatment Primary Therapeutics • There is no antidote; treatment is supportive. • Seizures: They should be controlled with diazepam (0.1–5 mg/kg IV q10–20min up to four times). It is used to control tremors, anxiety, and seizures. If diazepam is ineffective because of the antagonism of the benzodiazepine receptors, use phenobarbital (5–20 mg/kg IV administered over 5–10 minutes) followed by pentobarbital (3– 15 mg/kg IV slowly) if necessary. • Tachycardia: Give metoprolol (2–15 mg/cat PO q8–12h) or propranolol (2.5–5.0 mg/cat PO q8–12h) while monitoring the ECG and blood pressure. Lidocaine is not recommended in cats. • Activated Charcoal: Give at 0.5–1 g/kg PO with a saline cathartic or use a product that contains a cathartic.
Secondary Therapeutics • Fluid Therapy: Give to support blood pressure, maintain urine output, and enhance excretion of caffeine. • Others: Control hyperthermia and hypoventilation (supplementation of oxygen). Avoid stress and excitement because they may cause hyperreflexia and seizures.
Prognosis The prognosis is often guarded in cats with severe seizures or arrhythmias.
Theobromine Theobromine is methylxanthine alkaloid of plant origin commonly found in a variety of foods, beverages, candy, sweets, chocolates, and cocoa bean and powder. The methylxanthines inhibit phosphodiesterases, which results in increased cyclic adenosine monophosphate (cAMP) and release of catecholamines, and antagonism of adenosine receptors. These combined actions result in cerebral cortical stimulation and seizures, myocardial contraction, smooth muscle relaxation, and diuresis. Depending on the type and amount of chocolate a cat eats, the signs can range from vomiting, increased thirst, abdominal discomfort, and restlessness to severe agitation, muscle tremors, urinary incontinence (diuresis), diarrhea, irregular heart rhythm, high body temperature, seizures, and even death. The rule for chocolate is “the darker, the more dangerous.” Dry, unsweetened cocoa powder is the most dangerous.
Differential diagnoses include convulsant or excitatory alkaloids (i.e., strychnine, amphetamine, nicotine, cocaine, or tricyclic antidepressants), convulsant pesticides, toxicosis (i.e., bromethalin or fluoroacetate), cardioactive glycosides (digitalis), psychogenic drugs (lysergic acid diethylamide [LSD]), hypomagnesemia, and hypocalcemia.
Diagnosis Primary Diagnostics • History: Ask about chocolate ingestion, usually at the time of Valentine′s day, Halloween, Christmas, or other holidays. • Clinical Signs: The systems involved are GI, nervous, and cardiovascular. • Specific Testing: Attempt chemical detection of methylxanthines in stomach contents, plasma, or urine. • Cardiac Monitoring: Perform an ECG to detect arrhythmias (especially premature ventricular contractions).
Diagnostic Notes • Laboratory Tests: There are no specific changes in biochemistry and hematology tests.
Treatment Primary Therapeutics • No antidote exists. • Gastric Lavage: This should be performed using warm water, which helps to remove melted chocolate from the gastric mucosa. Cool or cold water may actually worsen retrieval of chocolate. • Urinary Catheterization: This is used to minimize urine retention time to prevent absorption of theobromine through bladder mucosa. • Seizures: They should be controlled with diazepam (0.1–5 mg/kg IV q10–20min up to four times). It is used to control tremors, anxiety, and seizures. If diazepam is ineffective because of the antagonism of the benzodiazepine receptors, use phenobarbital (5–20 mg/kg IV administered over 5–10 minutes) followed by pentobarbital (3– 15 mg/kg IV slowly) if necessary. • Tachycardia: Give metoprolol (2–15 mg/cat PO q8–12h) or propranolol (2.5–5.0 mg/cat PO q8–12h) while monitoring the ECG and blood pressure. Lidocaine is not recommended in cats. • Activated Charcoal: Give at 0.5 to 1 g/kg PO with a saline cathartic or use a product that contains a cathartic.
Secondary Therapeutics • Fluid Therapy: Give to support blood pressure, maintain urine output, and enhance excretion of caffeine. • Others: Control hyperthermia and hypoventilation (supplementation of oxygen). Avoid stress and excitement because they may cause hyperreflexia and seizures.
Therapeutic Notes • Emesis: Inducing vomiting is not effective because chocolate has a sticky composition when melted.
Prognosis The prognosis is often guarded for cats with severe seizures or arrhythmias.
443
SECTION 1: Diseases and Conditions
Nicotine Nicotine is a poisonous alkaloid derived from the tobacco plant and is found in a variety of sources, primarily cigarettes, cigars, snuff, chewing tobacco, nicotine gum, inhalers, patches, nasal spray, and insecticides. It is readily absorbed through GI tract, skin, and mucosa membranes and is excreted via the kidneys, but its excretion is pH dependent. Excretion is decreased when the urine pH is alkaline. At low doses, nicotine mimics acetylcholine and stimulates postsynaptic nicotinic receptors of CNS, ganglia of the autonomic nervous system, neuromuscular junctions of skeletal muscles, and emetic chemoreceptor trigger zone. Because of the latter, it can initiate vomiting. At high doses the initial stimulatory effects are followed by blockade of the nicotinic receptors due to persistent depolarization. The minimum lethal dose of nicotine for cats is 20 to 100 mg; cigarettes typically contain 9 to 30 mg. Some cats are attracted to the products like chewing tobacco that are supplemented with flavors such as honey, molasses, syrups, and other sugars. Clinical signs are dependent on the amount and type of nicotine ingested and occur within 1 hour of nicotine exposure. Cats may vomit spontaneously, often are seen salivating, and experience urination, lacrimation, and diarrhea. Small doses may cause bradycardia and peripheral vasoconstriction. Patient becomes excited and hyperactive. High doses or prolonged exposure cause tremors, muscular twitches, inability to stand, and depression. Rapid shallow respiration is followed by bradypnea, tachycardia, collapse, and coma. Paralysis of the diaphragm and intercostal muscles are the cause of death. Differential diagnoses include anticholinesterase insecticide poisoning in early stages of nicotine intoxication and depressants in later stages.
Diagnosis
Marijuana Marijuana, made from the dried leaves and flowers from Cannabis sativa, is a commonly used recreational drug in humans. It is used for medical treatment under certain conditions. Prescription products include dronabinol (Marinol®) and nabinole (Cesamet®), which are used to treat nausea in cancer patients, glaucoma, multiple sclerosis, chronic pain, epilepsy, various psychiatric disorders, and to promote weight gain. Illegal marijuana is most commonly used in the form of cigarettes but may be brewed into a tea, or baked into brownies, cookies or cakes. Most animals are intoxicated by secondhand smoke or after ingestion of marijuana products. Marijuana smoke contains up to 61 different cannabinoids; the most important is tetrahydrocannabinol (THC), which is the predominant psychoactive agent. THC acts on a unique receptor in the brain that is selective for cannabinoids. Cannabinoids interact with many neurotransmitters and neuromodulators, stimulate dopamine release, enhance γ-aminobutyric acid (GABA) turnover, and may increase norepinephrine, dopamine, and 5-hydroxytryptamine formation. THC is lipid-soluble compound and is rapidly distributed to the brain and other tissue (i.e., heart, liver, fat, and kidneys). It is metabolized by the liver and excreted through the bile (65–90%) and in the urine (10–25%). Marijuana has a wide safety margin in that the lethal dose is approximately 1,000 times the effective dose, but the LD50 is not established in cats. Onset of clinical signs is delayed from the 6 to 12 minutes associated with the respiratory route to 30 to 60 minutes or longer after ingestion. Clinical signs are depression, ataxia, and bradycardia. Other signs include behavioral disturbances, agitation, vocalization, vomiting, diarrhea, hypersalivation, mydriasis, hyperesthesia, tachycardia, urinary incontinence, and hypothermia; less commonly stupor, seizures, and coma occur. Differential diagnoses include exposure to ethanol, ethylene glycol, opioids, ivermectin, barbiturates, and other CNS depressants.
Primary Diagnostics • History: Ask about ingestion of tobacco products or prolonged exposure to cigarette or cigar smoke. • Clinical Signs: Effects are on the GI, respiratory, nervous, cardiovascular, and musculoskeletal systems as stated previously. • Laboratory Testing: Nicotine levels may be determined in blood, urine, and vomitus.
Treatment Primary Therapeutics • Toxin Removal: Only induce vomiting if it can be performed within 1 hour of ingestion and if there are no clinical signs. Gastric lavage, saline cathartic, and activated charcoal may be beneficial. • Oxygen: Administer supplemental oxygen as necessary for bradypnea.
Secondary Therapeutics • Supportive Therapy: Control seizures and hyperthermia, and administer fluid therapy as needed. • Acidification of urine may enhance elimination of nicotine. This should not be attempted when the cat is acidemic (pH < 7.3).
Therapeutic Notes No specific antidote exists.
Prognosis Exposures to high levels of nicotine warrant a poor prognosis.
444
Diagnosis Primary Diagnostics • History: Ask about exposure to marijuana smoke or goods; however, the illegal nature of marijuana will often trigger denial. • Clinical Signs: The most common are ataxia, depression, and recumbency. Others are listed previously. • Urine Drug Testing: This can be confirmatory, but increased water consumption and polyuria may elicit a false-negative result.
Diagnostic Notes • Laboratory Testing: There are no specific abnormalities in routine blood panels.
Treatment Primary Therapeutics • Emesis: Induce within 30 minutes of exposure only in asymptomatic patients. • Activated Charcoal: Give 0.5 to 1 g/kg q8h PO; if the cat is recumbent use caution because of the risk of aspiration. • Diazepam: Give 0.25 to 0.50 mg/kg IV to agitated patients.
Therapeutic Notes • No specific antidote exists. • Monitoring: Monitor respiratory and cardiac function and thermoregulation carefully.
Recreational Drug Toxicosis
Prognosis The prognosis is favorable for symptomatic animals without secondary complications, such as aspiration pneumonia.
Suggested Readings Bischoff K. 2007. Toxicity of drugs of abuse. In RC Gupta, ed., Veterinary Toxicology: Basic and Clinical Principles, pp. 518–521. New York: Academic Press, Elsevier. Carson TL. 2006. Methylxanthines. In ME Peterson, PA Talcott, eds., Small Animal Toxicology, 2nd ed., pp. 845–852. St. Louis: Saunders. Donaldson CW. 2002. Marijuana exposure in animals [Toxicology Brief] Vet Med. 102(6):437–439.
Gfeller RW, Messonnier SP. 1998. Handbook of Small Animal Toxicology and Poisonings. St. Louis: Mosby. Osweiler GD. 2007. Chocolate toxicosis. In LP Tilley, FWK Smith, Jr., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 234–235. Ames, IA: Blackwell Publishing. Osweiler GD. 2007. Ethanol toxicosis. In LP Tilley, FWK Smith, Jr., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 452–453. Ames, IA: Blackwell Publishing. Plumlee KH. 2006. Nicotine. In ME Peterson, PA Talcott, eds., Small Animal Toxicology, 2nd ed., pp. 845–852. St. Louis: Saunders. Richardson JA. 2006. Ethanol. In ME Peterson, PA Talcott, eds., Small Animal Toxicology, 2nd ed., pp. 698–701. St. Louis: WB Saunders. Thrall MA, Hamar DW. 2007. Alcohols and glycols. In RC Gupta, ed., Veterinary Toxicology: Basic and Clinical Principles, pp. 608–614. New York: Academic Press, Elsevier.
445
CHAPTER 187
Rectal Disease Heloisa Justen Moreira de Souza
Overview The most common rectal diseases in cats include perineal hernia, rectal prolapse, rectal stricture, rectal tumors, rectal perforation, and rectovaginal fistulae.
Perineal Hernia Overview Perineal hernias are related to weakness of the pelvic diaphragm musculature and failure to support the rectal wall. This results in persistent distention and outpouching of the rectum and impaired defecation. The median age of onset of signs is 9 years (range 1–15). Tenesmus and constipation are the most common clinical signs. In cats with perineal hernias visible perineal swelling occurs less often than in dogs. Cats with megacolon and perineal herniation have hard stool filling the entire colon and rectum. Perineal hernias are usually bilateral, and many are associated with predisposing conditions that cause persistent straining, such as lower urinary tract diseases, chronic constipation, megacolon, perineal masses, chronic fibrosing colitis, and perineal urethrostomy. Perineal hernia with bladder retroflexion is a rare condition and may occur following a pelvic fracture resulting in stenosis of the pelvic canal and chronic constipation.
Figure 187-1 Chronic constipation in this cat resulted in tenesmus that created a perineal hernia. Fecal material can be seen just cranial to the anus in the hernia. Image courtesy Dr. Gary D. Norsworthy.
Rectal Prolapse Overview Rectal prolapse is defined as eversion or prolapse of the rectum through the anal opening caused by persistent straining because of urogenital or intestinal disease. It may be complete (entire rectum and may include part of the anus as well) or partial (protrusion of the rectal mucosa). The complete prolapse mass is cylindrical, with a depression seen in the end. The most common cause is severe enteritis or proctitis due to endoparasites, most often affecting kittens. Additional causes include foreign bodies, neoplasia of the rectum or distal colon, dystocia, urolithiasis, or sequelae of perineal urethrostomy. See Figure 187-1. Manx cats with neurologic dysfunction of the anorectum are predisposed to this disease. Rectal tissue appears edematous and hyperemic. See Figure 187-2. In longstanding cases of rectal prolapse, the tissues may be ulcerated and necrotic. Individual predisposition probably contributes to the development of a prolapse; such predispositions may include weakness of the perirectal and perianal connective tissues or musculature or uncoordinated peristaltic contractions of the rectum in association with rectal or anal inflammation.
Figure 187-2 Rectal prolapse results in a hyperemic and edematous rectal tissue protruding from the anus. Photo courtesy Dr. Gary D. Norsworthy.
Rectal Stricture Overview Rectal stricture is a decrease in size of the rectal lumen either from cicatricial contracture or from deposition of abdominal tissue extralumi-
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
446
nally. Any disease or trauma that evokes an inflammatory response in the anorectal region can cause formation of a constricting ring of scar tissue. Affected cats have persistent tenesmus, prolonged posturing to defecate, and frequent attempts to defecate, with only a narrow ribbon of feces or no feces produced.
Rectal Disease
Rectal Tumors Overview Colonic and rectal lymphomas are the most common large bowel tumor of the cat. Adenocarcinoma is rare in this location in cats but may cause an annular-type stricture of the distal colon or rectum. See Figure 187-3. The stool may be “thin” in diameter due an obstructive mass.
Rectovaginal Fistulae Overview A rectovaginal fistula connects the dorsal wall of the vagina with the ventral portion of the terminal rectum. It may result from a congenital malformation or a variety of acquired disorders. Congenital rectovaginal fistula is usually associated with concurrent type II atresia ani (i.e., rectal lumen has a blind end just cranial to imperforate anus). Kittens with rectovaginal fistula exhibit abdominal enlargement and discomfort, bulging of the perineum, lack of anal opening, passage of fluid feces through the vagina and impaction, irritation of the vulva, tenesmus, and inappetence. See Figure 187-4. Signs are usually noted after weaning.
masses, herniation, rectoanal prolapsed, or fistulas. A digital rectal examination should be performed to evaluate the pelvic diaphragmatic musculature, the diameter of the rectal lumen, the presence or lack of retained feces and the texture, regularity, and surface of the mucosa. Cats should be sedated prior to rectoanal palpation to prevent patient injury. • Clinical Signs: Hematochezia, excess mucus with normally formed feces, tenesmus, and dyschezia are the common signs. Constipation, dysuria, and stranguria are also reported. As the duration and severity of the diseases worsen, other systemic signs may be observed as lethargy, anorexia, vomiting, and weight loss. • Endoscopy: Proctoscopy is the diagnostic tool of choice for examination and biopsy. The rectal mucosa can be visualized for color, texture, friability, masses, and bleeding. Furthermore, any lesions of the terminal rectum that are identified can often be directly
Rectal Perforation Overview Rectal perforation may be associated with administration of enemas or manual extraction of impacted feces in cats and bite wounds. See Figure 187-5. It is easy to perforate the rectal wall with even a rubber catheter when the procedure is made without gentle handling. Cellulitis, abscessation, and endotoxic shock may occur.
Diagnosis Primary Diagnostics • History and Physical Examination: The close association of the anorectum and colon results in similar clinical signs of disease for these two components and creates difficulty in localizing signs to a specific region of the lower gastrointestinal tract. The perineum should be inspect carefully for evidence of inflammation, swelling, tumor
(A)
(B) Figure 187-3 This rectal stricture was caused by adenocarcinoma. The lumen (arrow) was about 25% of its normal diameter. Photo courtesy Dr. Gary D. Norsworthy.
Figure 187-4 A rectovaginal fistula connects the dorsal wall of the vagina with the ventral portion of the terminal rectum. This kitten had atresia ani. A, Fecal material can be seen exiting the vulva. B, Barium was injected into the vagina (V). It is seen going through the fistula (arrow) into the rectum (R) and colon (C).
447
SECTION 1: Diseases and Conditions
and most importantly, the predisposing cause identified and treated. Recurrent prolapses may be reduced by gentle traction on the descending colon via laparotomy. The reduction is maintained by colopexy.
Rectal Stricture • A rectal pull-through procedure is recommended for treatment of rectal strictures. Simple circular strictures may respond to bouginage, but it may be necessary to repeat this procedure several times. Rectal strictures also can be successfully dilated using balloon dilatation techniques. Balloons with a diameter of 10 to 15 mm are used for cats. Four to six dilatation procedures may be required to achieve functional success.
Rectal Tumors
Figure 187-5 This cat experienced a rupture of rectal wall associated with associated with administration of enemas. The rectal wall was perforated with a rubber catheter.
visualized by gently prolapsing the rectum and anus using tissue forceps. This technique also allows surgical removal of small polyps or masses. In cats with constricted areas of the rectum, proctoscopy demonstrates a circular band of tissue and area of narrowed lumen. • Radiography: Survey radiographs of the abdomen may reveal fecal retentions in anorectal and may demonstrate gas-filled loops of intestine in an obstructive pattern outlying a prestenotic dilation of the bowel rostral to an intestinal stricture. Contrast radiography appears to be more successful in outlining either an obstructive pattern or an intestinal mass. A barium enema is effective in outlying a mass in cats with colorectal carcinomas. Vaginography was helpful in determining the type of malformation present in rectovaginal fistula. See Figure 187-4. • Ultrasonography: In cases of rectal tumors, ultrasonography is helpful for defining the depth of the lesion in the intestinal tract and identifying enlarged regional lymph nodes; it can aid in staging the extent of metastasis. • Fecal Examination: A fecal flotation should be performed to evaluate for parasites.
Treatment Perineal Hernia • Herniorrhaphy is indicated for most cases of perineal hernia. This technique approximates the structures which form the perineal diaphragm. These structures are: the external anal sphincter medially, the levator ani and sphincter medially, the levator ani, coccygeus muscles and the sacrotuberal ligament laterally, and the internal obturator muscle ventrally. All these structures are incorporated into the reduction. However, the sacrotuberal ligament, which is incorporated in herniorrhaphy in dogs, does not exist in cats.
Rectal Prolapse • A simple, fresh prolapse with minimal tissue damage and edema may be replaced and a purse string suture inserted round the anus. An opening may be left, large enough to allow passage of soft feces but not further prolapse. Stool softeners should be given by mouth
448
• For cats with rectal lymphoma, treatment with standard chemotherapy protocols is initiated unless a mass is obstructing the rectum and debulking is necessary. A rectal pull-through procedure is recommended for treatment of rectal carcinoma. The primary indication for performing a rectal pull–through is to resect a distal colonic or midrectal lesion not approachable through the abdomen and too large or cranial for an anal approach.
Rectovaginal Fistula • The surgical correction consists of two procedures. First, the fistula is localized and excised, with reconstruction of the rectovaginal shelf. Second, a new terminal opening for the intestinal tract is established. Various postoperative complications such as fecal incontinence, wound dehiscence, constipation, and excessive scar tissue formation may occur. However, some cats have a favorable prognosis.
Rectal Perforation • Surgical intervention is mandatory. The rectal rupture must be sutured up with a simple interrupted crushing technique using nonabsorbable suture material. The tissue around the rectal perforation will be contaminated from the feces. It is necessary to flush the area liberally to keep it clean. The wound may be allowed to heal by contraction and epithelialization, or it may be necessary to use drain tubes. Systemic antibiotics are recommended.
Suggested Readings Bright R M, Bauer MS. 1994. Surgery of the digestive system. In RG Sherding, ed., The Cat: Diseases and Clinical Management, 2nd ed., pp. 1353–1401. New York: Churchill Livingstone. Corgozinho KB, Neves A, Caloeiro MA, et al. 2005. Hernia perineal em uma gata: relato de caso. Medvep. 3(10):89–92. Hedlund CS. 1997. Surgery of the perineum, rectum, and anus. In TW Fossum, ed., Small Animal Surgery. pp. 335–366. St Louis: Mosby. Kramer MR, Velde BVV, Gortz K. 2003. Retrofexion of the urinary bladder associated with a perineal hernia in a female cat. J Small Anim Pract. 44(11):508–510. Ogilvie GK, Moore AS. 2001. Tumors of the alimentary tract. In GK Ogilvie, AS Moore, eds., Feline Oncology: A Comprehensive Guide to Compassionate Care. pp. 271–294. Ohio: Veterinary Learning Systems. Popovitch CA, Holt D, Bright R. 1994. Colopexy as a treatment for rectal prolapse in dogs and cats: A retrospective study of 14 cases. Vet Surg. 23(2):115–118. Risselada M, Kremer M, Van de Velde B, et al. 2003. Retroflexion of urinary bladder associated with a perineal hernia in a female cat. J Small Anim Pract. 44(11):508–510. Zoran DL. Rectoanal disease. 2005 In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1408–1420. St. Louis: Elsevier Saunders.
CHAPTER 188
Refeeding Syndrome Karen M. Lovelace
Overview Refeeding Syndrome, or refeeding injury, refers to the constellation of sudden life-threatening metabolic derangements, including hypokalemia, hypophosphatemia, hypomagnesemia, and hyperglycemia, which occur after initial oral, enteral, or parenteral refeeding of a malnourished patient. The underlying pathogenesis of the refeeding phenomena centers around the conversion from a state of catabolism to anabolism associated with the sudden onset of carbohydrate use. When the starved patient is given food, insulin is released from the pancreas, which shifts potassium, phosphate, magnesium, water, and glucose into cells and increases protein synthesis. This shift in metabolism further promotes the release of insulin and increases the energy demands of the cell, including the demand for phosphate containing adenosine triphosphate (ATP). As catabolism ensues, cells quickly deplete the phosphorus supply from the blood, and the body can no longer meet the demand to make ATP. As a result, cells that need large amounts of ATP, such as erythrocytes, brain cells, and skeletal myocytes, are affected. This can lead to weakness, muscle injury, central nervous system signs, and intravascular hemolysis if there is not enough phosphorus to maintain erythrocyte structure. As potassium shifts intracellularly and blood stores are decreased, cats may also exhibit weakness, cervical ventroflexion, constipation, problems urinating, vomiting, listlessness, or confusion. Hypomagnesemia, which is often confused with or masked by other derangements, exacerbates hypokalemia and can cause arrhythmias, cardiac excitability, hemolysis, dysphagia, dyspnea, muscle weakness, and confusion. Hyperglycemia causes an osmotic diuresis, which worsens electrolyte depletion and contributes to weakness. Cats with hepatic lipidosis or diabetes mellitus are especially at risk for refeeding injury. Patients such as these that have been anorectic may already have electrolyte disturbances, such as hypokalemia, making the refeeding phenomenon more severe. Patients on high carbohydrate diets are also at an increased risk for refeeding injury. Onset of metabolic derangements associated with the refeeding phenomenon can occur as early as 12 hours or as late as 72 hours after refeeding is initiated, with the peak occurrence at 24 to 48 hours. The metabolic derangements associated with refeeding can be life-threatening and should therefore be treated with urgency.
Diagnosis Primary Diagnostics • History: Refeeding complications should be considered likely in any anorectic or malnourished patient, and especially in cats with hepatic lipidosis or diabetes mellitus. Overconditioned diabetic cats being fed a high carbohydrate diet have the greatest risk. • Clinical Signs: Signs of hemolytic anemia due to hypophosphatemia may include weakness, pallor, jaundice (i.e., check sclera, gums, soft palate, and pinnae, or other mucous membranes), or discolored urine due to hyperbilirubinuria. Signs relevant to hypokalemia may include cervical ventroflexion (weakness), vomiting, constipation,
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
problems urinating, or confusion. Signs due to hypomagnesemia may include dysphagia, weakness, dyspnea, or arrhythmias. Hypomagnesemia will also contribute to hemolysis. Hyperglycemia may result in polyuria, polydipsia, and increased electrolyte losses due to osmotic diuresis. Patients may have tachycardia, increased blood pressure, and retained fluid. Respiratory distress and seizures are also possible. • Chemistry Profile: Icterus in serum or plasma will occur if the total bilirubin level is at least 14 µmol/L (0.8 mg/dL), whereas jaundiced tissues will be evident when bilirubin levels are over 34 µmol/L (2.0 mg/dL). Electrolytes should be assessed. The patient is considered hypophosphatemic when the serum phosphorus concentration is below 0.80 mmol/L (2.5 mg/dL). However, clinical signs of hypophosphatemia may not be evident until the serum phosphorus level falls below 0.48 mmol/L (1.5 mg/dL). • Serial Pack Cell Volumes (PCV): A rapidly declining PCV will signal an acute hemolytic crisis. Examining PCV tubes may also reveal icterus when jaundice cannot be detected in the tissues. Finally, a PCV will help the clinician to determine if a blood transfusion is necessary. Considering the acute nature of the hemolysis, transfusion is indicated if the PCV falls below 0.2 L/L (20%). • Blood Smear: Documentation of Heinz bodies on a blood smear may help confirm hemolysis, although a small number of Heinz bodies are normal in feline peripheral blood. Diagnosis of hemolytic anemia in cats must include evidence of regeneration (such as an increase in reticulocytes or polychromasia) and either hyperbilirubinemia or hyperbilirubinuria, in addition to finding Heinz bodies. Within the first 3 to 4 days after hemolysis, the anemia will appear nonregenerative because the event is acute. The anemia, however, is truly regenerative.
Secondary Diagnostics • Complete Blood Count (CBC): The CBC can be used to confirm anemia and thrombocytopenia. Automated platelet counts are frequently unreliable. If the count is low, a stained blood smear should be evaluated.
Diagnostic Notes • Hemolysis caused by severe hypophosphatemia (less than 0.32 mmol/L [1.0 mg/dL]) in cats is most often associated with diabetic ketoacidosis (DKA). This is caused by carbohydrate loading and simultaneous regular insulin administration in a patient that was likely anorectic.
Treatment Primary Therapeutics • Correct Hypophosphatemia: Put sodium or potassium phosphate in fluids. If the patient is severely hypophosphatemic (<0.32 mmol/L [1.0 mg/dl]), add an injectable phosphate salt to a calcium-free balanced electrolyte fluid and give at a rate of 0.01 to 0.06 mmol/kg IV each hour for 6 hours (i.e. 0.06–0.18 mmol/kg over 6 hours IV). Each mL of sodium or potassium phosphate injection will contain
449
SECTION 1: Diseases and Conditions
3.0 mmol of phosphate and 4.4 mmol (4.4 mEq) of either sodium or potassium, respectively. Oral phosphorus supplementation should be initiated soon after the phosphorus begins to rise, and as soon as the patient can tolerate PO administration. Supplementation with lactose free cow’s milk, such as skim milk, or oral phosphate products such as sodium phosphate oral solution (Fleet® Phospho® Soda) should then be given at a dose of 0.5 to 2.0 mmol/kg per day. Phospho Soda comes in a concentration of 4.15 mmol/mL. Recheck the serum phosphorus level 3 to 6 hours after starting sodium or potassium phosphate therapy. Recheck the level every 6 hours thereafter until the serum phosphorus reaches 0.65 mmol/L (2.0 mg/dL), at which time the phosphate salt supplementation can be discontinued. Monitor electrolytes every 12 hours thereafter for the first several days following the initial realimentation. • Correct Hypokalemia: Administer potassium chloride (KCl) at a rate to meet the patient’s hydration needs. Never exceed a rate of 0.5 mmol (mEq)/kg per hr. If using potassium phosphate [K(PO4)3], reduce the amount of potassium chloride by the amount of potassium in the potassium phosphate. Table 188-1 lists suggested supplementation of KCl based on serum potassium levels. See Table 188-2 for a sample calculation for adding K(PO4)3 and KCl to fluids. • Correct Hypomagnesemia: Administer either 9.25 mEq/g of a 50% solution of magnesium chloride or 8.13 mEq/g of a 50% solution of magnesium sulfate IV as a 20% solution in 5% dextrose and water. Give as a constant rate infusion for 2 to 3 days at a rate of 0.75 to 1.0 mEq/kg per day, and reduce the dose to 0.3 to 0.5 mEq/kg per day for 2 to 5 days. • Transfusion: Due to the acute and immediate nature of the hemolysis, if the PCV falls below 0.2 L/L (20%), transfusion is warranted. Whole blood should be administered at a rate of 2 to 3 ml/kg per hour, for a maximum total dose of 30 ml/kg. See Chapter 295.
Secondary Therapeutics • Thiamine Supplementation: Thiamine is an essential cofactor for the metabolism of many reactions involving glucose. Thiamine (Vitamin B1) depletion may result from osmotic diuresis. Therefore, 25 to 50 mg of Vitamin B1 (or a Vitamin B complex containing 50 mg/mL of Vitamin B1) should be supplemented by adding it directly to one liter of fluids. Alternatively, 25 to 50 mg can be given twice daily SC. Vitamin B complex is light sensitive. If it is added to intravenous fluids, the bag should be protected from light. • High Protein, Low Carbohydrate Diet: Once the patient is stable, continue alimentation with a diet containing adequate levels of phosphorus. High protein, low carbohydrate diets, such as Maximum Calorie® (Eukanuba®, Dayton, OH), best meet this requirement. Do not use phosphate-poor (low protein) enteral diets for refeeding. • For Overcorrection of Phosphorus: If hyperphosphatemia develops, stop all other electrolyte supplementation and begin IV diuresis until levels are normal. Use calcium gluconate (give slowly to effect over 10–30 minutes at 1.0–1.5 ml/kg IV, using a 10% solution) if tetany develops.
TABLE 188-1: Potassium Chloride Supplementation to 500 mL Fluids Serum Potassium (mmol/L [mEq/L])
Potassium Chloride mmol (mEq) to add to 500 mL Fluids
<2.0 2.0–2.5 2.5–3.0 3.0–3.5 3.5–5.0 >5.5
25 20 15 10 2 0–2
450
TABLE 188-2: Sample Calculation for Addition of K(PO4)3 and KCl to Fluids Given
What dose of K(PO4)3 is needed?
How much (PO4)3 is in each mL of K(PO4)3? How much K(PO4)3 should be added to the bag?
How much potassium should be added to the bag?*
Summary: Add 4.2 mL K(PO4)3 and 3.26 ml KCl to 500 mL 0.9% NaCl Finally, check the amount of potassium added.
Weight = 5.0 kg (11 lb.) Fluids = 500 mL of 0.9% NaCl Serum phosphorus = 0.29 mmol/L (0.9 mg/dL) Serum potassium = 1.8 mmol/L (mEq/L) Desired fluid rate for this patient = 10 mL/hour Phosphorus supplementation rate = 0.05 mmol/kg per hour (for 6 hours) = 0.25 mmol/hour (for 6 hours, or 1.5 mmol over 6 hours) Concentration of K(PO4)3 = 3.0 mmol/mL (PO4)3 and 4.4 mmol (mEq) of K/mL Solve for “X” mmol of (PO4)3: “X” mmol/500 mL NaCl = 0.25 mmol (PO4)3/10 mL fluid rate × = 12.5 mmol (PO4)3 “X” = 12.5 mmol (PO”X” = 12.5 mmol (PO4)3 12.5 mmol (PO4)3 ÷ 3.0 mmol (PO4)3/mL K(PO4)3 = 4.2 mL K(PO4)3 First, calculate the amount of K in 4.2 ml K(PO4)3 4.2 ml K(PO4)3 × 4.4 mmol (mEq) K/mL K(PO4)3 = 18.48 mmol (mEq) K Then, subtract 18.48 mmol (mEq) K from the amount of KCl you add to your fluids: 25 mmol (mEq) KCl − 18.48 mmol (mEq) K = 6.52 mmol (mEq) KCl to 500 ml 0.9% NaCl Amount of KCl to add = 6.52 mmol (mEq) KCl ÷ 2 mmol (mEq)/ml = 3.26 ml KCl
We cannot exceed 0.5 mmol (mEq) K/kg per hour, so to check: 0.5 mmol (mEq) K × 5.0 kg = cannot exceed 2.5 mmol (mEq) K/hour Equation: mmol (mEq)/total volume in bag × fluid rate = actual mmol (mEq)/ hour < 2.5 mmol (mEq)/hour = 25 mmol (mEq)/500 mL fluids × 10 mL/hr = 0.5 mmol (mEq) total/hour < 2.5 mmol (mEq)/hour
* Note: This sample problem is calculated using the given data, but suggested total potassium requirements may differ by clinician preference.
Therapeutic Notes • Serum phosphorus may be within normal limits before refeeding begins, but hypophosphatemia may develop as the refeeding continues. • If hypophosphatemia or hemolytic anemia results from institution of insulin therapy or hyperalimentation, stop administering insulin or food temporarily (about 2 hours) while phosphorus is supplemented. • Cats with DKA may require higher doses of phosphorus (0.06– 0.12 mmol/kg per hour IV) and longer therapy (up to 24 hours). • Use caution in administering phosphorus to patients with hypercalcemia as excess calcium can result in soft-tissue mineralization. Intravenous supplementation in these patients should be avoided. Complications of intravenous phosphorus supplementation include hypocalcemia, dystrophic soft-tissue mineralization, and acute renal failure. Oral supplementation in patients with mild hypophosphatemia is therefore preferred.
Refeeding Syndrome
• Although lactated Ringer ’s solution is acceptable if no other fluid choices are available, 0.9% saline or Normosol solution is preferred to decrease the chance of calcium and phosphorus complex formation. • Hyperglycemia will usually be corrected with fluid administration. For severe hyperglycemia the fluid rate may need to be increased. • Whole blood is preferred in cases where a transfusion is needed because stored red blood cells may use serum phosphorus, further aggravating hypophosphatemia.
Prognosis Notwithstanding the resolution of any underlying disease, the complications of refeeding should resolve within several days if clinical signs are identified promptly and aggressive treatment is instituted early.
Suggested Readings Center SA, Richards, JR. 2005. Feline hepatic lipidosis. Vet Clin North Am Sm Anim Pract. 35(1): 225–269. Giger U. 2005. Regenerative anemias caused by blood loss or hemolysis. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1886–1907. St. Louis: Elsevier Saunders. Justin RB, Hohenhaus AE. 1995. Hypophosphatemia associated with enteral alimentation in cats. J Vet Inter Med. 9:228–233. Stockham SL, Scott MA. 2002. Erythrocytes. In SL Stockham, MA Scott, eds., Fundamentals of Veterinary Clinical Pathology, pp. 105–135. Ames: Iowa State Press. Stockham SL, Scott MA. 2002. Calcium, Phosphorus, Magnesium, and Their Regulatory Hormones. In SL Stockham, MA Scott, eds., Fundamentals of Veterinary Clinical Pathology, pp. 401–432. Ames: Iowa State Press.
451
CHAPTER 189
Renal Failure, Acute Sharon Fooshee Grace
Overview Acute renal failure (ARF) is a clinical syndrome (not a specific disease) marked by the sudden decline of renal function, usually as the result of a toxic, infectious, or vascular/ischemic insult. The kidneys are susceptible to various types of injury because they receive a large amount of blood flow (approximately 20–25% of cardiac output). Ischemia deprives tubular cells of oxygen needed for metabolic processes, resulting in calcium accumulation within the cells, breakdown of tubular cell membranes, and vasoconstriction. ARF failure due to nephrotoxins is common in veterinary medicine and may be caused by a variety of drugs, chemicals, and plants. Infectious agents are another significant cause of ARF in cats and dogs. When ARF occurs, the tubules or glomeruli (or both) may be injured. See Table 189-1. Causes of ARF may be characterized as pre-renal (i.e., insufficient blood flow to the kidneys, as with dehydration), intrinsic or primary renal (i.e., renal parenchymal damage caused by toxic, ischemic, and infectious insults), or post-renal (i.e., obstruction) in origin. Consideration of these categories is helpful to the clinician in managing potential risk factors so as to prevent ARF, when possible. Risk factors are additive and include pre-existing diseases of the kidney or other major organs, as well as clinical conditions (i.e., dehydration, anesthesia, nephrotoxic drugs, hypo- or hypertension, sepsis, decreased cardiac output, trauma, and electrolyte abnormalities). Dehydration and volume depletion are the most common and easily prevented risk factors for development of ARF. Acute intrinsic renal failure has three phases: initiation, maintenance, and recovery. During initiation, the kidneys are injured; vascular and cellular insults occur, leading to decreased excretion of urea and creatinine and onset of azotemia. Oliguria (or anuria) and decreased urinary concentrating ability characterize the maintenance phase. Cell swelling, cell necrosis, and sloughing of debris into the tubular lumen obstruct flow of tubular fluid. This phase may last for several days to a few weeks; many patients will die or be euthanized during this phase. The recovery (diuretic) phase, which is characterized by a solute-induced diuresis and significant polyuria, may continue for months. Some cats will recover significant renal function, whereas others will have persistent uremia despite polyuria.
Diagnosis Many disease conditions need to be considered as differentials for ARF.
TABLE 189-1: Known Causes of Acute Renal Failure Anesthetics/anesthesia Burns (severe) Cardiac disease, arrhythmias, cardiac arrest Dehydration Drugs Antimicrobials, aminoglycosides (i.e., gentamicin and paromomycin), sulfonamides, and tetracyclines Antifungals, Amphotericin B Nonsteroidal anti-inflammatory drugs Angiotensin-converting enzyme inhibitors Ethylene glycol* Hemorrhage Hypercalcemia Cholecalciferol-containing rodenticides or idiopathic causes Hypertension Hypotension Immune-mediated disease (rare) Infectious agents Pyelonephritis* Obstruction to urine flow Nephroliths or ureteroliths* Urethral obstruction (i.e., feline idiopathic cystitis) Neoplasia Especially lymphoma Pancreatitis Pigments Myoglobin and hemoglobin Plants Especially plants in the lily family* (See Chapter 170) Radiographic contrast agents Shock, trauma
Primary Diagnostics
Thromboembolism of renal artery
• History: Question the owner about (a) onset, duration, and progression of illness; (b) the cat’s environment (i.e., access to ethylene glycol, cholecalciferol rodenticide or lilies; access to medications; access to outdoors); (c) recent anesthesia and a list of all medications being administered. • Physical Examination: Clinical signs are usually non-specific and recent in onset. When the cat is examined (and prior to initiation of any therapy), it is critical to obtain an accurate baseline weight and
* Most common.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
452
to determine hydration status. The kidneys may be enlarged or painful if intracapsular swelling has occurred. • Minimum Data Base (Complete Blood Count [CBC], Chemistry Profile and Electrolytes, Urinalysis [with Sediment Examination], and Retrovirus Tests): The CBC is usually unremarkable. Creatinine and blood urea nitrogen (BUN) levels will be elevated. Hyperphosphatemia occurs because of decreased glomerular excretion of phosphates. Sodium levels are variable. Hyperkalemia occurs with oliguria/anuria. Calcium is usually normal but may be increased (cholecalciferol rodenticide) or decreased (ethylene glycol toxicity).
Renal Failure, Acute
Urinalysis usually demonstrates isosthenuria or inadequately concentrated urine (<1.035) and proteinuria; hematuria and glucosuria are also possible. Urine sediment should be examined at each collection for the presence of white blood cells and bacteria (urinary tract infection), casts (tubular damage), epithelial cells, cellular debris, and crystals (calcium oxalate crystals with ethylene glycol toxicity). • Urine Culture: This is indicated in all cats with ARF recognizing that a significant number of cats with quiet urine sediment will have bacterial growth on culture. A culture is vital if white blood cell casts or bacteria are seen in the urine sediment or the cat is febrile. Urine should be collected, preferably by cystocentesis, for culturing prior to the administration of antibiotics. • Abdominal Radiographs or Ultrasound: Radiographs are helpful for detecting radiopaque uroliths, assessing general size of the urinary bladder, and measuring the size of each kidney. The normal feline kidney is 2.0 to 2.5 times the length of the second lumbar vertebra on the ventrodorsal view for neutered cats and 2.0 to 3.0 times for intact cats. Ureteral uroliths are found much more reliably on radiographs than on ultrasound. If the patient is oliguric or anuric and appears intolerant of fluid therapy, follow-up thoracic radiographs may be beneficial in assessing for pulmonary edema or ascites. The normal ultrasonographic longitudinal measurement of the kidneys of young adult cats is 38 to 42 mm. An ultrasound study can also be helpful in cases of ethylene glycol toxicity. See Figure 70-2. • Urine Output (UOP): In ARF, UOP varies from anuria to oliguria to polyuria. Normal urine output is 1to 2 mL/kg per hour. Cats that are adequately hydrated and not producing urine are oliguric (<1 mL/ kg per hour) or anuric (no urine or <0.08 mL/kg per hour). Urine can be measured by collection in a metabolic cage, intermittent catheterization, or a closed indwelling system. Importantly, UOP cannot be accurately determined until the patient has been adequately hydrated. Once euhydration is established and the patient is normotensive, the goal is to restore UOP to a minimum of 1 to 2 mL/kg per hour.
Secondary Diagnostics • Thoracic Radiographs or Cardiac Ultrasound: These are indicated if the cat is suspected to have heart disease (e.g., cardiac murmur) because of the risk posed by rapid volume expansion with fluids. Distention of pulmonary vessels or interstitial edema signal volume overload. • Fundic Examination: Fundic examination can detect retinal hemorrhage or detachment, findings suggestive of hypertension. • Blood Pressure Determination: When mean arterial pressure drops below 70 mm Hg, renal perfusion decreases in a linear fashion. On the other hand, some cats with renal disease are hypertensive. • Central Venous Pressure (CVP): If possible, monitoring of CVP can prevent overhydration. Volume expanded patients will have a CVP of 4 to 8 cm H20; overhydrated patients approach or exceed 10 cm H20. If CVP cannot be attained, frequent assessment of body weight, auscultation of the lungs for edema, thoracic radiography, and measurement of packed cell volume (PCV) and total protein level will help gauge adequacy of hydration. Consult a critical care text for details on setting up a CVP catheter. • Ethylene Glycol Test: An in-house test is available, and a test is available at commercial veterinary laboratories. See Chapter 70 for details. • Renal Biopsy: Histopathology will not necessarily determine the cause of ARF, but it may be important in establishing the prognosis. Presence of intact basement membranes and tubules is consistent with the potential for recovery. The risk of anesthesia and potential benefit of information to be gained must be considered.
Diagnostic Notes • If it is impractical or unfeasible to monitor UOP via a closed drainage system or intermittent catheterization, place a clean, dry empty litter
box in the cage. Most cats that are able to urinate will be accepting of an empty litter box. Monitor the box frequently to collect and measure the urine volume. Be sure that the box is deep enough that it cannot easily be tipped over. • Distinguishing acute from chronic renal failure (and acute failure concurrent with chronic failure) can sometime be difficult or even impossible. Findings consistent with chronic renal failure are chronic anorexia and weight loss; poor body condition; small, irregular kidneys; nonregenerative anemia; stable azotemia; and inactive urine sediment. A PCV is the most reliable single test for differentiation; cats with ARF typically have normal PCVs. • Leptospirosis is a common infectious cause of ARF in dogs, but cats are resistant to clinical leptospirosis.
Treatment Primary Therapeutics • Managing Severe Hypovolemia: If the cat is severely hypovolemic and hypotensive, the deficit may be replaced over 1 hour by giving 40 to 90 mL/kg divided into quarters and administering until signs of hypovolemia and shock resolve. • Replace Fluid Deficits: The cat must be weighed and hydration status determined prior to starting fluid therapy. Deficits can be replaced over the first 2 to 4 hours if the cat is tolerant of additional fluid volume. Unless the cat is hyperkalemic, lactated Ringer ’s solution (LRS) is adequate for hydration; LRS has the additional benefit of mild buffering against metabolic acidosis. If the cat is hyperkalemic, use 0.9% sodium chloride. See Chapter 302 for calculation of fluid replacement. UOP cannot be determined until deficits have been corrected. • Supply Maintenance Fluid Needs: A maintenance fluid rate of 40 to 66 mL/kg per 24 hours should also be given during the period of replacement therapy. After vascular volume is re-established (see “Fluid Deficits”), continue at two to four times the maintenance rate or at a rate that assures continued diuresis. A buffered, balanced electrolyte solution is usually acceptable. If the cat is oliguric or anuric, careful attention must be given to avoiding overhydration. Frequent determination of the cat’s weight and UOP are critical. The lungs should be frequently monitored for volume overload, especially when UOP is not increasing as expected. As an alternative to calculating deficit plus maintenance needs, fluids may be initiated at two to three times maintenance needs once hypovolemic shock has been reversed. Urine output must be monitored. • Correct Electrolyte and Acid-Base Disturbances: Electrolyte abnormalities common in ARF include hyperkalemia or hypokalemia, hyperphosphatemia, and hypocalcemia or hypercalcemia. Electrolytes should be re-evaluated frequently during fluid therapy. Hyperkalemia is common in the oliguric and anuric states (Chapter 106) and is potentially life-threatening. Hypokalemia commonly develops with fluid therapy and after diuresis is initiated (Chapter 114). Hypocalcemia can be a consequence of hyperphosphatemia and will worsen the effects of hyperkalemia (Chapter 113). Hyperphosphatemia can contribute to ongoing kidney damage and, in the critical patient, is treated with fluid therapy. Metabolic acidosis often occurs with ARF but should not be corrected unless the blood pH can be determined accurately. Volume expansion, along with buffering by LRS and diuresis from fluids, will usually improve or correct acidosis. • Induce Diuresis: If the cat is already polyuric, continue with aggressive fluid therapy, monitoring of electrolytes and hydration status. If deficits have been corrected and hydration is adequate but urine production remains <1 to 2 ml/kg per hour, diuretics should be considered. The preferred initial treatment is furosemide, a loop diuretic that can be given as a bolus (2 mg/kg IV). Improved UOP should be seen within 30 minutes (maximum, 1 hour). If no improvement
453
SECTION 1: Diseases and Conditions
occurs, the dose can be doubled (4 mg/kg) and given 1 to 2 hours after the initial dose. If no improvement is noted at this time, the dose can be tripled (6 mg/kg IV). If no improvement is apparent 3 to 4 hours after the maximum dosage, an osmotic diuretic should be tried. Mannitol is an osmotic diuretic and weak renal vasodilator. It is contraindicated if the cat is overhydrated. A 20% solution (0.2 gm/ mL) should be given as a slow IV bolus (0.25–1.0 gm/kg or 1.25– 5.0 mL/kg) over 20 minutes and repeated in 1 hour if no increase in UOP is noted. If the cat is overhydrated and mannitol cannot be used, 10% dextrose solution is an alternative. An initial infusion of 2 to 10 mL/min is given over 20 minutes and the urine checked for glucose. If glucosuria is not present, dextrose should be discontinued. If glucosuria is present, a total dose of 22 mL/kg may be administered over 20 minutes. Once diuresis is established, signs of uremia are reversed and the patient is eating, fluids may be tapered slowly over 3 to 5 days. If urine flow cannot be established, the only remaining options are peritoneal dialysis or hemodialysis. At this point the prognosis is grave.
Secondary Therapeutics • Antibiotics: These are indicated in suspected cases of pyelonephritis. If bacterial infection is suspected, broad-spectrum therapy should be instituted pending culture results but only started after urine collection for culturing. • Uremic Complications If vomiting is persistent, anti-emetics (metoclopramide, chlorpromazine [only if normotensive]) and H2-blockers (cimetidine, ranitidine, famotidine) may be helpful. • See Chapter 229 for treatment of vomiting. Newer anti-emetics include maropitant (Cerenia®; 1 mg/kg q24h SC) and ondansetron (0.1–0.15 mg/kg q8–12h by slow intravenous push). • Therapy for Ingested Toxins: If a toxic agent has been ingested within a few hours prior to presentation, it may be helpful to induce vomiting, lavage the stomach, and administer activated charcoal. See Chapter 170. • Colloid Therapy Cats with hypoproteinemia are easily volume overloaded due to decreased plasma oncotic pressure. Synthetic colloids are generally preferred over plasma for improving oncotic pressure. See Chapter 302 for information on colloid therapy. • Nutritional Support: Protein and energy are needed for repair of damaged renal tissue. Syringe feeding and the use of a nasoesophageal tube can be used, but orogastric tube feeding (see Chapter 308) may be indicated in some patients. The relative stress of each must be compared to each other and to the benefit gained. • Peritoneal Dialysis: Peritoneal dialysis is indicated in cases of ARF that fail to respond to aggressive medical therapy. Availability is limited to referral centers, primarily because of the cost of maintaining supplies and the intensive care which is required to maintain the patient.
454
• Hemodialysis: ARF that does not respond to diuretic and fluid therapy is an indication for hemodialysis. Availability of this therapy is relatively limited and expensive. The most complete list of transplant centers can be found at the following weblink: http://www. felinecrf.com/transb.htm. See Chapter 327.
Therapeutic Notes • Frequent re-evaluation of weight is important, especially during the rehydration phase, to prevent volume overload. The patient’s condition and tolerance for fluids may change quickly. Signs of overhydration include tachycardia, tachypnea, increasing body weight, and crackles on auscultation. • Furosemide should not be given to hyponatremic patient; sodium depletion increases the risk for renal injury. Also, it should not be combined with gentamicin as furosemide enhances the nephrotoxicity of the drug. • Mannitol should not be used in oliguric, volume-overloaded animals because it is not metabolized, only filtered and excreted. Without adequate urine production, the patient is unable to eliminate mannitol from the body. Hypertonic glucose, which is metabolized, is an alternative to mannitol. • Dopamine is not recommended for treatment of feline ARF. Recent work has demonstrated that cats do not possess renal dopamingergic receptors. Additionally, the drug increases renal oxygen consumption and may have a depressor effect on systemic blood pressure, thus worsening ischemic insults.
Prognosis Toxin-induced renal failure may have a better prognosis than ischemiainduced failure because the tubular basement membrane is more likely to be preserved with toxins. Converting oliguric/anuric ARF to polyuric ARF does not necessarily correlate with improved outcome or survival, but if oliguria/anuria persists the cat will die. Prognosis is poor for ARF caused by lily toxicity and (without early intervention) ethylene glycol. Successful treatment usually results in renal insufficiency. See Chapter 191.
Suggested Readings Bleedom J, Pressler B. 2008. Screening and medical management of feline kidney transplant candidates. Vet Med. 103(2):92–102. Labato MA. 2001. Strategies for management of acute renal failure. Vet Clin North Amer. 31(6):1265–1286. Langston CE. 2002. Acute renal failure caused by lily ingestion in six cats. J Amer Vet Med Assoc. 220(1):49–52. Worwag S, Langston CE. 2008. Acute intrinsic renal failure in cats. J Am Vet Med Assoc. 232(5):728–732.
CHAPTER 190
Renal Failure, Chronic Gary D. Norsworthy
Overview Chronic renal disease is a continuum of renal pathology that begins in the first few years of life and progresses to the point of renal failure (RF), usually in the geriatric years. Renal insufficiency (RI) and RF are two stages of this continuum that are clinically different but interrelated. The term renal insufficiency is used to denote a cat with a creatinine value above normal and up to 440 to 530 µmol/L (5.0–6.0 mg/dL). It is equivalent to International Renal Interest Society (IRIS) Stage IIb plus Stage III. See Table 191-1. Such cats are asymptomatic or showing mild signs of renal disease including reduced appetite, mild weight loss, mild polydipsia, and mild polyuria. The latter two are often not perceptible to the owner. The term renal failure applies to a cat with a creatinine value over approximately 485 µmol/L (5.5 mg/dL) and is equivalent to IRIS Stage IV. This cat is usually anorectic, dehydrated, polyuric, and polydipsic. This chapter will address chronic renal failure (CRF). See Chapter 191 for a discussion of RI. CRF is usually the result of a series of often unrelated renal insults, including pyelonephritis, aminoglycoside administration, toxins, trauma, and so on, but the exact causes usually cannot be determined once RF occurs. The notable exception is polycystic kidney disease. Because most affected cats are geriatric, it is possible, in part, to be the result of the normal aging process. CRF is preceded by chronic RI, which may last several months. When CRF occurs, the most common clinical signs are weight loss, anorexia, lethargy, polyuria, and polydipsia. Vomiting may occur, but it is less common and occurs later in the course of disease compared to dogs. Many cats in CRF are dehydrated and emaciated and have pale mucous membranes. The kidneys are usually smaller than normal; this may be documented by palpation, radiography, or ultrasonography. Hyperthyroidism commonly occurs in cats in the same age range as cats with RI and RF. The hyperthyroid state frequently increases renal perfusion and may mask renal disease. When euthyroidism is restored, the renal disease may decompensate and become a significant clinical entity. See Chapter 109.
Diagnosis Primary Diagnostics • Clinical Signs: Geriatric cats that are anorectic, polydipsic, and polyuric and have experienced significant weight loss should be suspected of having CRF. Although these signs are typically present, many owners do not recognize them due to multiple cats in a household, outdoor habitat of the cat, and inattentiveness. • Laboratory Findings: Common laboratory findings include nonregenerative anemia, azotemia, hyperphosphatemia, metabolic acidosis, and low urine specific gravity. • Urine Culture: Because pyelonephritis is a recognized cause of renal disease that can lead to RF, a urine culture is indicated. Because primary bacterial cystitis is uncommon in cats, a positive urine culture is more likely to represent bacterial pyelonephritis. The risk
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
of bacterial urinary tract infections increases significantly after cats reach 10 years of age, especially in females. One study found that 12% of cats with chronic kidney disease will have a positive urine culture.
Diagnostic Notes • The serum creatinine level is less influenced by nonrenal factors than is the blood urea nitrogen (BUN), so it is usually more specific and the preferred test. It first elevates when about 75% of renal function is lost. When it is above 440 to 530 µmol/L (5.0–6.0 mg/dL), about 85% or more of renal function is lost. Creatinine values are significantly lowered in emaciated cats; this should be considered when evaluating the creatinine value of thin cats. In this instance, BUN values are more reflective of renal function if the cat’s hydration status is normal and other prerenal factors are eliminated. • It is important to differentiate acute and CRF. Typically, cats with CRF have a nonregenerative anemia; cats with acute RF are not anemic unless another anemia-causing disease is present. Serum potassium values may also be helpful; hyperkalemia frequently occurs in acute RF whereas hypokalemia is common to CRF. • Many cats with CRF have systemic hypertension; therefore, blood pressure determination is indicated. When hypertension is related to renal disease, long-term hypotensive therapy will be needed. See Chapter 107. • Although low urine specific gravity is expected to occur before creatinine values elevate, some cats in RF have values above 1.020. This is because the cat’s urine concentrating ability is greater than that of dogs, and they retain their urine concentrating ability much later into the course of RF.
Treatment Primary Therapeutics • Rehydration and Diuresis: This is best accomplished by placement of an intravenous catheter and administration of an isotonic, balanced fluid such as lactated Ringer ’s solution. Fluids are given at 1.5 to 2.0 times maintenance as long as overhydration does not occur. A central venous catheter is preferred because it will be needed for 3 to 7 days, and it permits repeated blood collection. See Chapter 297. Most cats with RF will need potassium supplementation in the fluids. See Secondary Therapeutics and Chapter 114. • Appetite Stimulant: Famotidine (0.5–1.0 mg/kg q12h PO) or another H2-blocker should be used to control gastric hyperacidity. Gastric hyperacidity causes nausea and results in anorexia; thus, famotidine may be helpful in any anorectic cat in RF. Mirtazapine (3.25 mg/cat q48–72h PO) and cyproheptadine (2 mg/cat q12h PO) are effective in many cats as appetite stimulants. • Enteral Feeding: Anorexia is a consistent finding, and vomiting is not; therefore, feeding a balanced diet via orogastric or nasogastric tube is desirable. Hydration status and general well-being improve rapidly when adequate nutrition is supplied. See Chapter 308. • Potassium: Hypokalemia may result from anorexia (lack of intake) and prolonged polyuria (excessive excretion); it further reduces RF. Intravenous fluid administration aggravates hypokalemia. Potassium
455
SECTION 1: Diseases and Conditions
chloride (40–60 mEq) should be added to each liter of intravenous fluids, or 4 to 8 mEq of potassium gluconate should be given orally each day. (See Therapeutic Notes.) Several forms of oral potassium are available, but potassium gluconate is the preferred form. • Phosphate Binder: Hyperphosphatemia occurs when about 85% or more of renal function is lost and is common in CRF and much less so in RI. A phosphate binder can help to normalize the serum phosphorus level. Aluminum hydroxide (50 mg/kg q12h in food; dose adjusted to effect), calcium acetate (PhosLo®, 166 mg/cat q12h in food), calcium carbonate (Epakitin®; 90–150 mg/kg per day), and lanthanum carbonate (Renalzin®; 200 mg [1 pump] q12h in food) are options. If a calcium containing product is used, monitor closely for hypercalcemia and change products if this occurs during treatment or is present prior to treatment. • B vitamins: The loss of water-soluble B complex vitamins is likely due to polyuria and anorexia.
Secondary Therapeutics • Hypotensive Agent: Systemic hypertension occurs in over 25% of cats in RF. Therefore, blood pressure monitoring is highly recommended. The drug of choice is amlodipine (0.625 mg/cat q24h PO adjusted to effect). Benazepril (0.5–1.0 mg/kg q24h PO) should be added if 3 to 5 days of treatment with amlodipine does not create normotension. If retinal lesions are present, begin concurrent treatment with nitroglycerin ointment (0.5 cm [3/16 in] q6-8h transdermally for the first 48 hours). See Chapter 107. • Erythropoietin Replacement: This is indicated when the packed cell volume (PCV) is less than 15%. It can greatly improve the cat’s appetite and energy level. Human recombinant erythropoietin (epoetin alfa [r-HuEPO; Epogen®]) and darbepoetin alfa (Aranesp®) are available. Epogen is dosed at 100 U/kg three times per week SC until the PCV reaches 30% then 100 U/kg two times per week SC until the PCV reaches 40% then either discontinued or continued at 75 to 100 U/kg q7 to 14d SC. Aranesp is dosed at 6.25 µg/cat weekly initially then maintained at q2 to 4w. Thereafter, the dosing interval is determined by the hematocrit. Both products can stimulate antibody production and both are moderately expensive. See Therapeutic Notes. • Blood Transfusion: This should be considered when the hematocrit is below 15%. It can occur simultaneously with erythropoietin injections. • Calcitriol: The active form of vitamin D is used to prevent renal secondary hyperparathyroidism. The goals for use are to increase appetite, decrease weight loss, and increase longevity, although convincing data supporting efficacy are lacking. It is dosed at 2.5 ng/kg q24h PO or 9 ng/kg q24h PO and must be compounded. Hypercalcemia, based on an increased ionized calcium level, will likely result if calcitriol is given with a calcium-containing phosphate binder. Discontinue use of calcitriol if hypercalcemia develops during its use. Calcitriol should not be used if the product of the serum calcium (in mg/dL) and phosphorus (in mg/dL) levels is greater than 70 so as to avoid the potential for intracellular calcification.
456
Therapeutic Notes • If treatment is successful, it is rare that the creatinine level returns to normal. Rather, the cat is converted from overt RF to RI. At that point, treatment should be continued accordingly. See Chapter 191. • Excessive dosing or administration rate of intravenous potassium can be fatal. Care should be taken not to administer intravenous potassium too rapidly; do not exceed 0.5 mEq/kg per hour. Orally administered potassium has a wide margin of safety not found in IV administered potassium. • Some potassium supplements for human use contain phosphates. These should be avoided. • When discharged, the cat should be put on a renal diet that is restricted in protein and phosphorus and is non-acidifying. Several commercial choices are available; trying several may be needed to find one the cat will eat well. • Aranesp is preferred to Epogen by some for treating renal-induced anemia because Aranesp is equally potent compared to Epogen, similar in treatment cost, and much safer. Antibody production is still possible but about 20% as likely as with Epogen. If antibody production occurs, the antibodies will destroy an injected erythropoietin product and endogenous erythropoietin making survival virtually impossible. • Anuric RF produces hyperkalemia. Potassium administration is contraindicated in this situation. See Chapter 189. • Renal transplantation has been performed successfully at some veterinary teaching hospitals and specialty hospitals. This is an expensive form of treatment with variable success rates, but it can be recommended for select patients. See Chapter 327 for information regarding this surgery.
Prognosis The prognosis for most cats in CRF is guarded to good. Generally, it is not possible to make a definitive prognosis on the outcome of RF treatment at the beginning of therapy. However, if the kidneys are less than one-third normal size, the serum creatinine is greater than 90 µmol/L (10 mg/dL), hyperphosphatemia is present, and if therapy for 3 to 4 days fails to achieve significant clinical and laboratory improvement, a guarded to grave prognosis is warranted. Cats with anuric RF have a grave prognosis. If response to therapy occurs and aggressive long-term maintenance therapy is provided, many cats will live 1 to 3 years while maintaining good quality life.
Suggested Readings Finco DR, Brown SA, Barsanti JA, et al. 2000. Recent developments in the management of progressive renal failure. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy, XIII, pp. 861–864. Philadelphia: WB Saunders. Nagode LA, Chew DJ, Podell M. 1996. Benefits of calcitriol therapy and serum phosphorus control in dogs and cats with chronic renal failure. Vet Clin North Am. 26:1293–1330. Polzin DJ, Osborne CA, Ross S. 2006. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1756–1785. St. Louis: Elsevier Saunders.
CHAPTER 191
Renal Insufficiency Gary D. Norsworthy
Overview Chronic renal disease is a continuum of renal pathology that begins in the first few years of life and progresses to the point of renal failure, usually in the geriatric years. Renal insufficiency (RI) and renal failure (RF) are two stages of this continuum that are clinically different but interrelated. The term renal insufficiency is used to denote a cat with a creatinine value above normal and up to 440 to 530 µmol/L (5.0–6.0 mg/dL). It is equivalent to International Renal Interest Society (IRIS) Stage IIb plus Stage III. See Table 191-1. Such cats are asymptomatic or showing mild signs of renal disease including reduced appetite, mild weight loss, mild polydipsia, and mild polyuria. The latter two are often not perceptible to the owner. The term renal failure applies to a cat with a creatinine value over approximately 485 µmol/L (5.5 mg/dL) and is equivalent to IRIS Stage IV. This cat is usually anorectic, dehydrated, polyuric, and polydipsic. This chapter will address RI. See Chapter 190 for a discussion of RF. In most cats, RI lasts for many months before the onset of chronic RF. Most affected cats exhibit a gradual decline in appetite and weight and a gradual increase in water consumption and urine output. These signs often remain undetected by owners for many months due to a combination of inattentiveness, gradual onset, and a belief by many that these signs are part of the normal aging process. When probing for the onset of polydipsia and polyuria, it is often most meaningful to ask about the quantity of wet litter in the litter box because this is something that is more easily noted by owners. Hyperthyroidism commonly occurs in cats in the same age range as cats with RI and RF. The hyperthyroid state frequently increases renal perfusion and may mask renal disease. When euthyroidism is restored, the renal disease may decompensate and become a significant clinical entity.
Diagnosis Primary Diagnostics • Clinical Signs: Geriatric cats exhibiting reduced appetite, mild weight loss, polydipsia, and polyuria should be suspected of RI. Because this is a progressive disease, the clinical signs will be more severe as the creatinine increases. Cats with creatinine values less than 265 µmol/L (3.0 mg/dL) are often asymptomatic or the symptoms are so mild that owners do not observe them. • Laboratory Findings: Common laboratory findings include creatinine values between approximately 220 and 530 µmol/L (2.5 and
TABLE 191-1: International Renal Interest Society (IRIS) Classification of Renal Disease
6.0 mg/dL), low urine specific gravity, and, possibly, a mild nonregenerative anemia. Serum phosphorus values may be low normal to mildly decreased. Hyperphosphatemia and metabolic acidosis are generally not present until the creatinine exceeds 350 µmol/L (4.0 mg/dL)
Diagnostic Notes • The serum creatinine level is less influenced by nonrenal factors than is the blood urea nitrogen (BUN), so creatinine is usually more specific and the preferred test. However, creatinine values are falsely lowered in emaciated cats; this should be considered when evaluating the creatinine value of thin cats. In this instance, BUN values are more reflective of renal function if the cat’s hydration status is normal and other prerenal factors are eliminated. The use of a body condition score system can be helpful in interpreting renal tests. See Table 153-1. • Many cats with RI are hypertensive; therefore, systemic blood pressure determination is desirable. • Urine microalbuminuria is used on dogs as a screening test for early renal disease. However, it is not specific enough to use in cats because it is elevated from many feline disorder. • Although low urine specific gravity is expected to occur before creatinine values elevate, some cats in RI have values above 1.020. This is because the cat’s urine concentrating ability is greater than that of dogs and they retain their urine concentrating ability later into the course of renal disease. • RI is commonly detected with routine geriatric blood profiles. This disease alone is justification for blood profiles in cats over 10 years of age. See Table 191-2. • It is imperative to differentiate acute and chronic RF because the prognosis is different. Typically, cats with chronic RF have a nonregenerative anemia; cats with acute RF are not anemic unless another anemia-causing disease is present. However, this rule is not reliable for cats with RI because erythropoietin production is usually adequate to main normal red blood cell production.
Treatment Primary Therapeutics • Hospitalization versus Outpatient Care: As long as the cat’s appetite is good, hospitalization is neither necessary nor desirable as most older cats do not tolerate hospitalization well.
TABLE 191-2: Incidence of Renal Insufficiency by Age* Age in Years
Percentage with Renal Insufficiency**
* As modified in Boyd LM, Langston C, Thompson K, Zivin K, Imanishi M. 2008.
12–13 14–15 16–17 18–19 20+
16.4 32.5 52.1 63.6 83.3
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
* Unpublished data. Gary D. Norsworthy. 2005. Study of 235 cats presented to Alamo Feline Health Center, San Antonio, Texas. ** Based on elevated creatinine values.
Stage
1
2a*
2b*
3
4
µmol/L mg/dL
<140 <1.6
140–210 1.6–2.4
211–250 2.5–2.8
251–440 2.9–5.0
>440 >5.0
457
SECTION 1: Diseases and Conditions
• Renal Diet: A protein restricted diet will reduce phosphate intake and nitrogenous waste production. Both result in the cat feeling and eating better. These diets are also non-acidifying, which is desirable as acidifying diets contribute to metabolic acidosis. Several commercial diets are available as prescription products. Offering more than one brand choice increases success in finding a diet that the cat will eat. Recommend canned or dry products that match the cat’s current diet. However, canned diets will better supply needed fluid intake. • Benazepril: Recent studies indicate that this angiotensin-converting enzyme inhibitor may have efficacy in slowing the progression of chronic renal disease. It is indicated to prevent excess urinary protein loss. It also dilates the glomerular efferent arteriole, which reduces glomerular pressure, thus potentially controlling renal hypertension. The presence of renal hypertension cannot be determined clinically, but if it occurs it will lead to nephron loss and declining glomerular filtration rate (GFR). It is thought to be a major cause of renal deterioration. Benazepril should be dosed at 0.5 to 1.0 mg/kg q24h PO.
•
Secondary Therapeutics • Rehydration and Diuresis: If the creatinine is above 440 µmol/L (5 mg/dL) or the cat is dehydrated fluid therapy is indicated for 2 to 4 days. This is best accomplished by placement of an intravenous catheter and administration of an isotonic, balanced fluid such as lactated Ringer ’s solution or normal saline; however, many cats do well with administration of fluid SC in the greatest quantity that can be absorbed well. Give about 150 mL in the morning. If it has been absorbed by the evening, repeat that dose. If not, reduce the evening volume. • Oral Potassium: Polyuria induced by renal disease results in excessive urinary potassium loss. Hypokalemia can cause or aggravate poor appetite and lethargy and can contribute to reduced GFR. Potassium gluconate (1–2 mEq per cat q12h PO) is the potassium salt of choice. Potassium supplementation is indicated for all cats that are hypokalemic. The author also prescribes it for cats that have a serum potassium in the low half of the normal range. Oral overdosing is highly unlikely because a dose high enough to cause hyperkalemia will likely induce vomiting. • Client Administered Fluids: Fluids administered SC (lactated Ringer ’s solution or normal saline solution) should be given one to seven times per week (average two to three times per week) based on the cat’s clinical response and serial creatinine levels. The average dose is 150 mL/cat given in the interscapular space. A subcutaneous fluid catheter (SurgiVet, Waukesha, WI) is available permitting owners to give subcutaneous fluids without a needle. It is implanted surgically and can be in place for a year or more; however, not all cats tolerate this device so needle-administered fluids is the preferred approach. See Chapter 271. • Phosphate Binder: Hyperphosphatemia occurs when about 85% or more of renal function is lost. It is common in chronic RF and may occur in the later stages of RI. A phosphate binder can help to normalize the serum phosphorus level and prevent the onset of renal secondary hyperparathyroidism. In some cats, mild hyperphosphatemia may be controlled with a renal (low phosphorus) diet. If 30 days of dietary therapy is not successful, aluminum hydroxide (50 mg/kg q12h in food), calcium acetate (PhosLo®, 166 mg/cat q12h in food), calcium carbonate (Epakitin®; 90–150 mg/kg per day), and lanthanum carbonate (Renalzin®; 200 mg [1 pump/1 ml] q12h in food) are options. The goal of therapy is to keep the serum phosphorus below 1.6 mmol/L (5 mg/dL). If a calcium containing product is used, monitor for hypercalcemia; if it occurs, change to a noncalcium containing product. • Calcitriol: The active form of vitamin D is used to prevent renal secondary hyperparathyroidism. The goals for use are to increase appetite, decrease weight loss, and increase longevity, although
458
•
•
•
convincing data supporting efficacy are lacking. It is dosed at 2.5 ng/kg q24h PO or 9 ng/kg q24h PO and must be compounded. Hypercalcemia, based on an increased ionized calcium level, will result if calcitriol is given with a calcium-containing phosphate binder. Discontinue use of calcitriol if hypercalcemia develops during its use. Calcitriol should not be used if the product of the serum calcium and phosphorus levels (expressed in mg/dl for both) is greater than 70 to avoid the potential for intracellular calcification. Erythropoietin Replacement: Erythropoietin is a hormone of renal origin. Its production declines dramatically in chronic RF and the late stages of RI. Supplementation is indicated when the PCV is less than 15%. It can greatly improve the cat’s appetite and energy level. Human recombinant erythropoietin (epoetin alfa [r-HuEPO; Epogen®]) and darbepoetin alfa (Aranesp®) are available. Epogen is dosed at 100 u/kg three times per week SC until the PCV reaches 30% then 100 u/kg two times per week SC until the PCV reaches 40% then either discontinued or continued at 75 to 100 u/kg q7 to 14 d SC. Aranesp is dosed at 6.25 µg/cat weekly initially then maintained at q2 to 4 w. Thereafter the dosing interval is determined by the hematocrit. Both products can stimulate antibody production and both are moderately expensive. Erythropoietin replacement therapy is not indicated in most cats with renal insufficiency. Hypotensive Agent: Systemic hypertension occurs in many cats with RI. Therefore, blood pressure determination is highly recommended. The drug of choice is amlodipine (0.625 mg/cat PO q24h or to effect). Benazepril (2.5–5.0 mg/cat PO q24h) should be added if 3 to 5 days of treatment with amlodipine does not create normotension. If retinal lesions are present, begin concurrent treatment with nitroglycerin ointment (6 mm [0.25 in] q6–8 h transdermally) for the first 48 hours. See Chapter 107. Appetite Stimulant: Famotidine (0.5–1.0 mg/kg PO q12h) or another H2-blocker should be used to control gastric hyperacidity. Gastric hyperacidity causes nausea and results in anorexia; thus, famotidine may be helpful in any anorectic cat in renal disease. Mirtazapine (3.75 mg/cat q48–72 h PO) and cyproheptadine (2 mg/cat q12h PO) are effective in many cats as appetite stimulants. Alkalinization Therapy: Persistent acidosis (serum bicarbonate less than 16 mEq/L) may resolve with oral administration of sodium bicarbonate [8–12 mg/kg PO q8–12 h] or potassium citrate [40–60 mg/kg PO q8–12 h].
Therapeutic Notes • Many cats receiving treatment for RI experience a decrease in the creatinine value, even into the normal range, for a few months, then it increases again. Be sure owner does not equate “normal renal values” with “normal kidneys” and discontinue therapy. • Angiotensin-converting enzyme inhibitors may cause hyperkalemia due to potassium retention. Cats taking benazepril and potassium should have their serum potassium levels checked after 2 and 4 weeks of combined therapy. If hyperkalemia occurs, discontinue or reduce the dosage of oral potassium. • Simultaneous initiation of benazepril and potassium therapy may cause anorexia. It is recommended that the cat be treated with one of these drugs for 1 week then the other one started. The order is not significant. • Some potassium supplements for human use contain phosphates. These should be avoided unless the cat is hypophosphatemic. • Erythropoietin may induce development of antibodies that will destroy both exogenous and endogenous erythropoietin, making the cat transfusion dependent. Some authorities feel that it should be discontinued as soon as possible. However, if it is used long term, it should be discontinued if the PCV exceeds 50% or if there are signs of antibody formation (i.e., fever, anorexia, joint pain, cutaneous or mucosal ulceration, or cellulitis). If the drug is given on a long-term basis iron should be supplemented with iron dextran (50 mg/cat
Renal Insufficiency
q30d IM). Alternatively, ferric sulfate can be given (50–100 mg/cat q24h PO). • A practical way to administer sodium bicarbonate is to add 17 teaspoons of baking soda to a liter of water, making a 1 mEq NaHCO3/ mL solution. One or two mL are given q12 to 24 h PO. The dose is adjusted to serum HCO3 levels. The solution is stable for up to 3 months if capped and refrigerated. • In general the author treats cats with creatinine values below 350 µmol/L (4.0 mg/dL) with a renal diet, potassium supplementation, and benazepril. If the creatinine exceeds 350 µmol/L (4.0 mg/ dL), subcutaneous fluids are added. Other medications are given on a PRN basis. • Rechecks should be performed every 3 months and include creatinine, potassium, phosphorus, and PCV levels, plus blood pressure determination. The calcium level should be monitored if calcitriol or a calcium-containing phosphate binder is prescribed. Pay close attention to weight, appetite, and overall attitude. Some cats are clinically more stable than their blood values would predict.
Prognosis With aggressive long-term home management, the prognosis of RI is good. They often live 1 to 3 years before the onset of RF.
Suggested Readings Boyd LM, Langston C, Thompson K, et al. 2008. Survival in Cats with Naturally Occurring Chronic Kidney Disease (2000–2002). J Vet Intern Med. 22(5):1111–1117. Brown SA, Brown CA, Jacobs G, et al. 2001. Effects of the angiotensin converting enzyme inhibitor benazepril in cats with induced renal insufficiency. Am J Vet Res. 62(3):375–382. Polzin DJ, Osborne CA, Ross S. 2005. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1756–1785. St. Louis: Elsevier Saunders.
459
CHAPTER 192
Restrictive Cardiomyopathy Larry P. Tilley
Overview Restrictive cardiomyopathy (RCM) is an uncommon cardiac disease characterized by myocardial or subendocardial fibrosis. There is no known cause, although myocarditis has been implicated as a precipitating condition. RCM may occur concurrently with hypertrophic cardiomyopathy or dilated cardiomyopathy. Myocardial fibrosis may result in both diastolic dysfunction (loss of compliance) and systolic dysfunction (reduced contractility), features that have caused RCM to be classified as an intermediate cardiomyopathy. Generalized congestive heart failure ensues, resulting in weakness and respiratory distress. Auscultatory abnormalities in order of incidence include gallop rhythm, arrhythmia, and murmur. Other physical findings may include ascites, hepatomegaly, muffled respiratory sounds (pleural effusion), and evidence of aortic thromboemboli.
Treatment Primary Diagnostics • Radiography: Thoracic radiographs reveal moderate-to-severe generalized cardiomegaly with variable pulmonary edema or pleural effusion. See Figure 294-19. • Electrocardiography: Ventricular premature complexes (VPCs), chamber-enlargement patterns, and intraventricular conduction defects may be present. • Echocardiography: Left atrial dilatation (enlargement) is consistently present. Other changes are variable and include ventricular dilatation, ventricular hypertrophy, and reduced fractional shortening (measure of contractility). Fibrosis is usually not evident by routine echocardiography. See Figure 294-19.
Secondary Diagnostics • Angiocardiogram: An irregular left ventricular chamber with variable filling effects is found. Hypertrophy of the papillary muscles may be evident. Thrombi may be discernible. • Doppler Echocardiography: Mitral regurgitation is evident.
Diagnostic Notes • In cats over 6 years of age, hyperthyroidism should be ruled out. • Definitive diagnosis antemortem is difficult because hallmark lesions (myocardial fibrosis) are not readily apparent during echocardiography. RCM cannot be differentiated from the other, more common, cardiomyopathies based on radiographs and electrocardiogram. • RCM is most often suspected when the degree of left atrial enlargement is greater than expected for the degree of left ventricular hypertrophy or dilatation. Cats with dilated cardiomyopathy usually have significantly lower indices of contractility (fractional shortening) than do cats with RCM.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
460
Treatment Primary Therapeutics • Reduce Stress: Take all measures to minimize any stress to cats exhibiting respiratory distress (e.g., delay radiographs and catheter placement). • Facilitate Breathing: Thoracocentesis should be performed in all dyspneic cats when pleural effusion is suspected (muffled lung sounds). With the cat placed sternally, place a 19- to 22-gauge butterfly catheter just into the pleural space (i.e., fifth to seventh intercostal spaces, just cranial to the adjacent rib), and aspirate. Use a closed system and tap both sides of the chest. Use furosemide when pulmonary edema is present. In the crisis setting, use 2 to 4 mg/kg IV initially and then 1 to 2 mg/kg q4 to 6 h IV or IM until the edema has resolved. Furosemide is often continued as needed (6.25–12.5 mg q12–24 h PO) to control edema formation. Apply nitroglycerin (6 mm [1/4 inch] to a hairless area q4–6 h) until the edema has resolved. • Oxygen: Administer via face mask, if tolerated, or oxygen cage (50% oxygen).
Secondary Therapeutics • Angiotensin-Converting Enzyme Inhibitor: Enalapril (0.25–0.50 mg/ kg q24h PO) or benazepril (0.2–0.5 mg/kg q24h PO) may be beneficial. • Aspirin: This drug may reduce the chance of thrombus formation. Give 10 mg/kg q3 to 4 d PO. In one study though, no significant difference was found in survival or recurrence rate between cats receiving the traditional dose and cats receiving low-dose aspirin (5 mg q72h PO). Recurrence of thrombi occurs at a high rate (43.5%) even with anticoagulation. Cats with left atrial enlargement, especially greater than 20 mm in diameter, are at greatest risk for aortic thromboembolism. • Thoracocentesis or abdominocentesis may be needed periodically. • Spironolactone: Give 0.5 to 1.0 mg/kg q12 to 24 h PO for heart failure (subdiuretic dose).
Therapeutic Notes • Monitor renal function if enalapril is used. • Warfarin (0.5 mg q24h PO) and low molecular weight heparin (high drug cost) may be used in lieu of aspirin but have a much greater chance of inducing a hemorrhagic crisis. Clopidogrel (18.75 mg [onefourth of a 75-mg tablet]/cat/day) is another option; it is superior to aspirin in human studies. • The dosage of diuretics and need for antiarrhythmic agents may change during the course of the disease; frequent monitoring is recommended. • Diltiazem is no longer recommended for this disease.
Prognosis The prognosis of affected cats has not been objectively evaluated. In general, cats with preserved contractility are expected to have a more favorable prognosis, whereas those with more extreme left atrial
Restrictive Cardiomyopathy
enlargement usually develop life-threatening complications (i.e., arrhythmias or thromboembolic disease).
Stepien RL. 2007. Restrictive cardiomyopathy in cats. In LP Tilley, FWK Smith, Jr., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 216–217. Ames, IA: Blackwell Publishing.
Suggested Readings Kienle RD. 2008. Feline cardiomyopathy. In LP Tilley, FWK Smith, Jr., M. Oyama, eds., Manual of Canine and Feline Cardiology, 4th ed., pp. 151–175. St. Louis: Elsevier.
461
CHAPTER 193
Retinal Disease Karen R. Brantman and Harriet J. Davidson
Overview The posterior segment of the eye is composed of the retina, choroid, sclera, and vitreous. The retina is the neurologic portion of the eye, converting light energy into electrical energy. These electrical signals are then carried to the brain via the optic nerve. The retina itself is composed of 10 layers. The outermost layer is the retinal pigmented epithelium (RPE), followed by rod and cone cells (the photoreceptor layer), the outer limiting membrane, outer nuclear layer, outer plexiform layer, inner nuclear layer, inner plexiform layer, ganglion cells, nerve fiber layer, and inner limiting membrane. The nerve fiber layer comes together to form the optic nerve. The optic nerve is normally round, gray to black in color, and non-myelinated at this level. There are three large arteriole-venuole pairs and several smaller arteries that radiate from the optic nerve head. Unlike the dog, these vessels rarely form a ring within the optic nerve. The retina is only firmly attached to adjacent structures in two places: the optic nerve head and the ora ciliaris retinae. As a result, a potential space exists between the retina and the choroid under which cells or fluid can collect; if this occurs, retinal detachment results. There are two types of retinal detachment: bullous and rhegmatogenous. Bullous detachment occurs as a result of vascular products
Figure 193-1 This is an example of bullous retinal detachment due to systemic hypertension. The cat’s systolic blood pressure was 220 mm Hg. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
462
accumulating under the retina. See Figure 193-1. Bullous detachments result from inflammation, systemic hypertension, or hematologic abnormalities. Clinically the retina may appear as a billowing structure, like a morning glory. This may be in one or more quarters of the fundus. Rhegatogenous detachment, which is uncommon in the cat, is a tear in the retina and generally occurs as a result of ocular trauma. A rhegmatogenous detachment may also develop secondarily to chronic bullous detachment. The retina becomes disinserted at the ora ciliaris retinae and falls to the ventral aspect of the eye. The choroid is part of the uveal tract and lies between the retina and sclera. It is composed of pigment, tapetum lucidum, and numerous vessels that radiate outward from the optic nerve. Tapetal cells are riboflavin-rich, helping to gather and reflect light in dark environments. They may appear yellow, green, blue, or red, giving the fundus its colorful appearance. Tapetal cells are normally found in the dorsal portion of the fundus and may not be present in all cats. In some cats, particularly color-dilute animals, there is little to no pigment within the retinal pigmented epithelial cell layer. This allows easy visualization of the choroidal vessels, which can be mistaken for hemorrhage by the inexperienced observer. The sclera is white and fibrous in nature but frequently not visible on fundic examination. It can be seen in color-dilute cats that have little pigment in the RPE cells or choroid; this gives the eye a white or creamy yellow appearance. The vitreous humor fills the posterior segment of the eye, resting directly on the retina. It is composed of water, collagen, cells, and hyaluronic acid. By maintaining its normal volume and consistency, the space-occupying nature of the vitreous holds the retina in place against the choroid. Changes to the vitreous resulting from age-related degeneration, chorioretinal inflammation, or hemorrhage, can make the fundus appear hazy and difficult to visualize. These changes may also result in retinal detachment. When detected, damage to the retina should be classified as either active or inactive to elucidate the etiology and help direct treatment and case management. Active retinal lesions are associated with systemic disease. They have indistinct borders and typically present as gray to white in color due to accumulation of vascular products or cellular infiltrates in or beneath the retina. Hemorrhage appears bright red in color with irregular margins. The retina becomes raised, resulting in bullous detachment and potential blindness. Blood vessels may be large, tortuous, and blood filled. Perivascular cuffing results if serum leaks from the vessels. The optic nerve head may be swollen, irregular, or puffy. Inactive retinal lesions are areas where previous inflammation, detachment, toxicity, or degeneration occurred. Inactive lesions are clear, flat, and well demarcated. Damaged areas in the tapetal fundus are hyperreflective due to loss of retinal tissue over the tapetum lucidum, whereas in the nontapetal fundus, lesions lack pigment or contain clumps of pigment. Blood vessels are thin, pale, or absent, and those overlying previously detached areas of retina will not contain blood. Previous hemorrhage may be dark in color with distinct edges. The optic nerve head may atrophy, becoming pale and small. Events, such as traumatic proptosis or optic nerve traction during enucleation of the contralateral eye, can also result in optic nerve head atrophy. Inactive lesions will not progress, will not respond to therapy, and are not helpful in determining a cause of systemic disease. Diseases of the retina may be congenital, inherited, or acquired. Congenital diseases are uncommon but include retinal dysplasia and
Retinal Disease
coloboma. Retinal dysplasia is an abnormal formation of the retina, which usually does not result in significant vision abnormalities. It has been found in cats that have had a perinatal vision infection, such as panleukopenia virus or feline leukemia virus. Dysplastic areas appear as gray-white lines or dots throughout the tapetal fundus. Colobomas are malformations that result in a hole or notch-like defect at the back of the eye and can involve the retina, choroid, or optic nerve. This condition has been reported in a rare number of cats and also does not appear to affect vision. Colobomas of the posterior segment have been seen in conjunction with other congenital malformations such as eyelid agenesis, persistent pupillary membranes, and retinal dysplasia. Inherited retinal diseases include progressive retinal atrophy (PRA) and the rare condition of lysosomal storage disease. PRA is characterized by photoreceptor degeneration. It is well described in the Abyssinian breed, but this condition affects the Siamese and Persian breeds as well. Other groups of domestic cats have been reported to have either a higher incidence than the normal population or direct family members affected with similar lesions, suggesting a genetic link. PRA can be broken down into two main types, early and late onset. The type seen in the United States is recessive with a typical onset of clinical signs at 2 years of age. Clinical signs are loss of night vision followed by loss of day vision. Due to the unique temperament of cats and personal interactions, cats will not typically be presented until they are completely blind. Ophthalmoscopically, the fundus will have thin to absent retinal vessels with a hyperreflective tapetum. Electroretinogram may be useful for detecting and tracking retinal dysfunction. There is no treatment for this condition. Early visual deficits will eventually progress to blindness. Lysosomal storage disorders result from inherited enzyme deficiencies in certain cell types and include mannosidosis, gangliosidosis, and mucopolysaccharidosis. Corneal cells and retinal pigmented epithelial cells are preferentially affected and swell as abnormal products are accumulated. Retinopathy or blindness may result in addition to corneal cloudiness. There is no treatment for this condition. Acquired retinal diseases may be localized ocular lesions or related to systemic disease. Dietary insufficiencies, toxin- or drug-induced retinal lesions infectious or inflammatory disease, hypertensive retinopathy, neoplasia, and glaucoma are all examples of acquired disease. Taurine is an essential amino acid in cats. It must be supplemented by diet; cats cannot synthesize it endogenously. Insufficient nutritional taurine results in retinal degeneration. Initially, the cat may have no evidence of vision abnormalities; clinical lesions may be discovered during ophthalmic examination for unrelated reasons. The classic ophthalmoscopic lesion is initially seen as a central, oval, or cigar-shaped hyperreflective area with poorly demarcated margins. If taurine is supplemented at this stage, the hyperreflective area will remain but become well demarcated. If the deficiency continues, the lesion will progress and result in a completely avascular, hyperreflective fundus. These severe cases result in blindness. This condition is no longer common in the United States due to current feline diet formulations. Toxins or drug overdose may also result in retinal degeneration. The most common drug toxicity is enrofloxacin, which can cause permanent blindness. Retinal toxicity is acute, occurring as early as 2 to 3 days after initiating antibiotic therapy. The first sign of toxicity is often mydriasis. The retina becomes hyperreflective and blindness follows. If retinal toxicity is detected early and antibiotic therapy stopped immediately, some vision may return. Enrofloxacin should be used at the lowest possible dose (not to exceed 5 mg/kg per day) for the shortest course of therapy. Twice daily dosing is preferred to once daily dosing. Rapid intravenous infusion and use in older cats with renal or liver disease should be avoided. Serial fundic examinations before and during therapy may be helpful. Other retinal toxicities include ethylene glycol, which may result in retinal detachment in nonfatal cases. Infectious Inflammatory disease of the retina, choroid, and optic nerve is caused by numerous conditions including bacterial, viral, fungal, protozoal, or parasitic disease. See Chapter 223. The same infectious agents
causing anterior uveitis can extend to the posterior segment of the eye, leading to chorioretinitis and visible fundic lesions. Bacterial septicemia, Bartonella spp., and viral diseases such as feline immunodeficiency virus (FIV), feline infections peritonitis (FIP) virus, and feline leukemia virus (FeLV) are common causes of retinal and choroidal inflammation. Fungal chorioretinitis caused by Histoplasma capsulatum, Cryptococcus neoformans, Coccidioides immitis, and Blastomyces dermatitidis should be considered in cases of severe disease or when concurrent clinical disease is present. Chorioretinitis due to Toxoplasma gondii has been reported in both clinical and experimental cases. Finally, dipteran larval migration to the fundus, such as that of Cuterebra spp., although rare, may occur. Optic neuritis is most commonly associated with FIP, toxoplasmosis, and cryptococcosis. Inflammatory retinal lesions are addressed by treating the underlying cause. Hypertensive retinopathy is most commonly seen in older cats with concurrent renal or thyroid disease. Hypertension is generally considered to be a systolic pressure above 160 mm Hg, although retinopathy occurs most frequently at pressures of 200 mm Hg and higher. Elevated blood pressure damages the fragile blood vessels of the retina, leading to leakage of blood and fluid within the retina and the choroid. See Figure 193-2. Retinal detachment and blindness results. After treatment with systemic antihypertensive agents, it is possible for the retina to reattach; some degree of vision may return. However, the previously detached area will likely become thin and hyperreflective ophthalmoscopically. See Chapter 107. Retinal hemorrhages have also been seen with diabetes mellitus, blood hyperviscosity syndrome, and anemia. Ocular lymphoma may cause cellular infiltrates within or beneath the retina, leading to detachment and/or to anterior uveitis. See Figure 1933. Ocular lymphoma is usually the result of metastatic systemic disease. Active secondary inflammation of the anterior uvea may be controlled topically whereas systemic therapy is used to control the underlying neoplastic disease. Intraocular sarcoma has also been reported to grow into and along the optic nerve. See Chapter 122. Chronic glaucoma also results in retinal degeneration. Along with the clinical appearance of chronic retinal degeneration (i.e., thin to absent
Figure 193-2 Retinal hemorrhage due to systemic hypertension often occurs prior to detachment. Focal hemorrhage is seen near one of the major retinal arteries. Image courtesy Dr. Gary D. Norsworthy.
463
SECTION 1: Diseases and Conditions
Figure 193-3 Lymphoma may cause anterior uveitis and concurrent retinal disease consisting of cellular infiltrates within or beneath the retina; it is often unilateral because it is considered a manifestation of metastatic disease. Image courtesy Dr. Gary D. Norsworthy.
vessels or hyperreflective tapetum) the optic nerve head may be cupped and undergo atrophy. See Chapter 85.
Figure 193-4 Systemic hypertension may cause retinal hemorrhage to be so severe that blood collects in the anterior chamber (hyphema). Blindness and hyphema were the presenting complaints. Both were due to retinal disease. Image courtesy Dr. Gary D. Norsworthy.
Treatment Primary Therapeutics
Diagnosis Primary Diagnostics: • Complete Ophthalmic Examination: A thorough examination of all ocular structures will help to rule out concurrent uveitis or intraocular neoplasia. Intraocular pressure readings (tonometry) will rule out uveitis or glaucoma. See Chapter 299.
Secondary Diagnostics • Blood Pressure: Systemic blood pressure should be determined in cats with retinal detachment or intraocular hemorrhage. See Figure 193-4. This test should be performed as early in the diagnostic phase as possible to prevent undue stress on the cat resulting in blood pressure elevation. Systolic blood pressure should not be greater than 180 mm Hg. See Chapter 107. • Minimum Data Base: A complete blood count (CBC), serum chemistries, and urinalysis should be completed in cats with suspected systemic disease or hypertension. Taurine plasma levels may be analyzed in cases of suspected nutritional insufficiency. Normal taurine levels should be 60–120 µmol/L. Tests for FIV, toxoplasmosis, FeLV, and Bartonella should also be considered. See Chapters 17, 75, 77, and 214. • Ocular Ultrasound: If the retina appears to be detached, an ocular ultrasound with a 10 mHz transducer may help document the degree of detachment and the possibility of intraocular neoplasia. • Electroretinogram (ERG): ERG is useful for detecting and quantifying retinal dysfunction, particularly in cases of inherited or toxic retinal disease.
Diagnostic Notes • Ophthalmic examination of the entire fundus through a dilated pupil is essential. This will allow diagnosis of retinal dysplasia, optic nerve coloboma, retinal degenerations of all types, and retinal detachments. See Chapter 299.
464
• No Treatment: There is no successful treatment for retinal dysplasia, optic nerve coloboma, or genetic retinal degeneration. Retinal degeneration secondary to glaucoma cannot be treated directly; however, glaucoma requires therapy (Chapter 85). If the cat has lost vision the owners will require counseling on how to adapt life for a blind cat (Chapter 23). • Taurine Supplementation: The diet may be altered or supplemented with additional taurine (250–500 mg/day q12–24 h PO) if taurine deficiency is identified with low plasma levels or suspected based on history and ophthalmoscopic lesions. The lesions that are present will remain, but further loss should not occur if taurine deficiency is the etiology. There will be no improvement if complete retinal degeneration is present, but taurine supplementation may prevent potential cardiovascular disease. See Chapter 56. • Retinitis Secondary to Uveitis: Systemic therapy for uveitis is necessary if the retinal disease is to be stopped or abated. Cats with acute retinal lesions should also be treated with systemic prednisolone (2.2 mg/kg q12–24 h PO for 1 week). The owners must be made aware that oral steroids may exacerbate a systemic condition; however, without anti-inflammatory treatment the cat may become permanently blind. See Chapter 223. • Optic Nerve Injury: Acute injury to the optic nerve secondary to traumatic proptosis or traction during enucleation of the contralateral eye should be treated with systemic steroidal therapy to prevent inflammation and oxidative damage to the optic nerve. Acute damage should be mitigated with systemic prednisolone (2.2 mg/kg q12–24 h PO for 1 week). • Retinal Detachment Secondary to Hypertension: Initial therapy should be aimed at the cause of systemic hypertension. See Chapter 107. The hypertensive drugs of choice are amlodipine (0.625 mg/cat q24h PO for 2 days, adjust therapy based on subsequent blood pressure readings or nitroglycerin paste (6 mm [1/4 in]) applied to the pinna q6–8 h for 2 days). Systemic steroids should be avoided, if possible, because they may reduce the efficacy of the hypertensive drugs due to fluid retention.
Retinal Disease
Secondary Therapeutics • Re-examination: Cats with retinal detachment and active retinitis should be re-examined every 48 hours to monitor blood pressure; therapy may be adjusted accordingly. • Surgical Repair for Retinal Detachment: This form of surgery is difficult so it should be considered a referral procedure. The success rate of this procedure is dependent on multiple factors including the cause of the detachment, length of detachment, and individual procedure used.
Suggested Reading Barclay SM, Riis RC. 1979. Retinal detachment and reattachment associated with ethylene glycol intoxication in a cat. J Am An Hosp Assoc. 15:719–724. Maggio F, DeFrancesco TC, Atkins CE, et al. 2000. Ocular lesions associated with systemic hypertension in cats: 69 cases (1985–1998). J Am Vet Med Assoc. 217:695–702. Wiebe V, Hamilton PJ. 2002. Fluoroquinolone-induced retinal degeneration in cats. Am Vet Med Assoc. 221:1568–1571.
Prognosis Prognosis depends on the primary disease, the severity, and the duration. Some retinal diseases have a good prognosis; others are not treatable or curable.
465
CHAPTER 194
Rodenticide Toxicosis Mitchell A. Crystal
Overview
Treatment
Next to insecticides, poison control centers receive more inquiries about rodenticide intoxicants than any other type of intoxicant. Several types of rodenticide intoxicants exist. Those commercially available are listed in Table 194-1. Other rodenticide intoxicants not covered in this chapter that are no longer used or are no longer available include thallium (still available in some Third World countries; causes neuropathies and hair loss) and alpha naphthyl thiouria (ANTU; causes pulmonary edema).
See Table 194-2.
Therapeutic Notes • See Chapters 189, 228, and 295.
Prognosis The prognosis for coumarins, indandiones, and strychnine is good to excellent for cure with early recognition and treatment. Most cats do not survive intoxication with bromethalin, cholecalciferol, or zinc phosphide.
Diagnosis See Tables 194-1 and 194-2.
TABLE 194-1: Commercially Available Rodenticides That Cause Toxicity in Cats Toxic Agent (Commercial Names)
Mechanism of Action
Toxic Dose
Onset
Clinical Signs
Bromethalin (Assault®, Clout®, Fastrac®, Gladiator®, Gunslinger®, Rampage® [must differentiate from cholecalciferol agents], Top Gun®, Trounce®, Wipe Out®, Vengeance®) Cholecalciferol (Hyperkil®, Quintox®, Rampage® [must differentiate from Bromethalin agents], Rat-B-Gone®) Coumarins and Indandiones first-generation: warfarin, pindone second-generation: bromadiolone, brodifacoum, diphacinone Strychnine (Certox®, Dog-Button®, Dolco Mouse Ceral®, Kwik-kill®, Martins Gopher Bait®, Mole Death®, Mouse Nots®, MouseRid®, Mouse-Tox®, Pied Piper Mouse Seed®, Quaker Button®, Ro-Dex®, Sanaseed®) Zinc Phosphide (Arrex®, Commando®, Denkarin®, Gopha-Rid®), Phosvin®, Ridall®, Prozap®, Zinc-Tox®, ZP®)
Uncouples oxidative phosphorylation leading to cerebral edema
300–1100 mg/kg of bait, or 0.5 mg/kg of agent
2–7 days, but may be as late as 2 weeks
Hindlimb ataxia, paresis or paralysis, depression, tremors, decerebrate posture, seizures
Hypervitaminosis D leading to acute renal failure
Exact toxic dose is unknown <1000 mg/kg of bait <10 mg/kg of cholecalciferol
Within 24 hours
Vomiting with or without blood, anorexia, lethargy, polyuria/polydipsia
Vitamin K antagonism leading to an acquired coagulopathy
warfarin 5–50 mg/kg pindone 5–75 mg/kg diphacinone 15 mg/kg brodifacoum 25 mg/kg bromadiolone 25 mg/kg 2.0 mg/kg
As early as 36–72 hours, as late as 2–4 weeks
Variable depending on location of hemorrhage (ecchymosis, hematomas, pallor, dyspnea, collapse, lameness, etc.) Nervousness, stiffness, rigidity, seizures (spontaneous or induced by stimulation), mydriasis, respiratory failure
20–50 mg/kg
Within 1–4 hours
Antagonizes the inhibitory neurotransmitter glycine at the postsynaptic spinal cord motor neuron
Acid pH in stomach releases phosphine gas leading to gastrointestinal irritation and asphyxia
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
466
Within 2 hours
Anorexia, lethargy, hemorrhagic vomiting, abdominal pain, ataxia, seizures, dyspnea
Rodenticide Toxicosis
TABLE 194-2: Diagnostic Procedures and Therapy for Rodenticide Toxicosis in the Cat Toxic Agent
Diagnosis (in Addition to History of Exposure and Clinical Signs)
Treatment (In addition to successful emesis and oral cathartic if more than 2 hours has passed since ingestion)
Bromethalin
Postmortem evidence of tissue residues
Cholecalciferol
Hypercalcemia with hyperphosphatemia with or without renal failure
Coumarins and Indandiones
Increased activated clotting time, activated partial thromboplastin time, and one stage prothrombin time; normal thrombin time; presence of proteins induced by vitamin K antagonism (PIVKA) in citrated plasma
Strychnine
Analysis of gastric contents, urine and hepatic biopsies
Zinc Phosphide
Analysis of gastric contents
Control seizures if present (diazepam or barbiturates), maintain hydration, provide nutritional support 0.9% NaCl diuresis (90 ml/kg q24h IV), prednisone 1–2 mg/kg q12h PO or SC, furosemide 1–2 mg/kg q12h SC or IV (only if on fluids) pamidronate sodium 2 mg/kg IV (repeat q24h if needed based on persistent or recurrent hypercalcemia), salmon calcitonin 4–6 IU/kg q2–3 h SC, check serum calcium levels to assess effectiveness of overall therapy Acute hemorrhage with significant anemia (packed cell volume <24%) is managed by transfusion with fresh whole blood (10–20 mL/kg over 2–4 hours IV) or plasma (10 mL/kg over 4–6 hours IV) and either packed red blood cells (5–10 mL/kg over 2–4 hours IV) or Oxyglobin® (10 mL/kg over 4–6 hours IV). Acute hemorrhage without significant anemia is managed by plasma alone. Vitamin K antagonism is managed with vitamin K1 (aquamephyton) at 5 mg/kg as an initial subcutaneous loading dose followed by 2.5 mg/kg PO q12h for 3 weeks. If the toxic agent is known to be a first-generation agent, therapy can be shortened to 1 week. Coagulation parameters should be checked 3–5 days following cessation of vitamin K1 therapy. Control tetany or seizures (diazepam, barbiturates, or propofol), 0.9% NaCl diuresis (70–80 ml/kg per day IV); endotracheal intubation and assisted/mechanical respiration is indicated if respiratory failure is present. Therapy is usually needed for 1 to 3 days. Gastric lavage with bicarbonate within 8 hours of ingestion, nothing by mouth, maintain hydration, HCO3− for acidosis if present
Suggested Readings Dorman DC, Dye JA. 2005. Chemical toxicities. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 256–261. St. Louis: Elsevier Saunders. Murphy MJ. 2009. Rodenticide Toxicoses. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIV, pp. 1117–1119. St. Louis: Saunders Elsevier.
http://edis.ifas.ufl.edu/pi115. The University of Florida IFAS Extension site containing miscellaneous rodenticide pesticide toxicity profiles. http://emedicine.medscape.com/article/818130-overview. This web site gives an overview and details on rodenticide toxins with general information and information about human exposure.
467
CHAPTER 195
Roundworms Mitchell A. Crystal and Mark C. Walker
Overview Roundworms, also called ascarids, are robust small intestinal nematode parasites. There are two types of roundworms found in the cat: Toxocara cati (most common) and Toxascaris leonina. T. cati and T. leonina are acquired via ingestion of infected paratenic hosts (i.e., mice, birds, or insects) or feces. Kittens may also acquire T. cati from ingestion of infected queen’s milk during nursing. Roundworms have a 2- to 3-week life cycle. The life cycle of T. cati involves migration through the lungs and liver and, in some cases, through somatic tissues. The life cycle of T. leonina has no extraintestinal migration. Transplacental infection does not occur with either T. cati or T. leonina. Clinical signs are more severe in kittens than in adult cats and include vomiting (with or without worms), diarrhea (with or without worms), abdominal distention or pain (kittens), weight loss or failure to gain weight (kittens), coughing (i.e., pneumonitis or pneumonia from T. cati due to larval migration), and rarely, intestinal obstruction. However, infections are often asymptomatic. Physical examination may be normal, reveal evidence of abdominal distention or pain (kittens), weight loss (kittens), or diarrhea. Unlike the canine roundworm Toxocara canis, T. leonina has limited public health significance. However, contrary to prior belief, T. cati is zoonotic because it does have potential to cause visceral and ocular larval migrans in humans who ingest embryonated eggs.
Diagnosis Primary Diagnostics • History: The owner may report seeing worms in vomitus or feces. See Figure 195-1. • Fecal Flotation: Eggs are seen on microscopic examination.
Secondary Diagnostics • Direct Saline Smear: Eggs are sometimes seen on microscopic examination. • Chest Radiographs: These may suggest verminous pneumonia.
Diagnostic Notes • Clinical signs may develop in kittens before eggs are detected in feces. • The most common cause of coughing in kittens is due to pulmonary larval migration of Toxocara.
Treatment Primary Therapeutics • Pyrantel pamoate (Strongid®, Nemex®, generic): Give 20 mg/kg PO; repeat in 2 to 3 weeks. It is also effective for hookworms. • Praziquantel/Pyrantel Pamoate (Drontal®): Give per label instructions; repeat in 2 to 3 weeks. It is also effective for hookworms and tapeworms. • Roundworm and Heartworm Prevention Combination: milbemycin oxime (Interceptor®, give per label instruction or 2 mg/kg PO once a month; also effective for hookworms); selamectin (Revolution®, apply per label instruction or 6 mg/kg as a spot-on topical once a month; also effective against hookworms, ear mites, and fleas); imidacloprid and moxidectin (AdvantageMulti for Cats®, give per label instruction or 10.0 mg/kg imidacloprid and 1.0 mg/kg moxidectin once by topical application). • Emodepside and praziquantel (Profender®): Topical therapy. Give 3 mg/kg emodepside and 12 mg/kg praziquantel. Treat at 8 and 12 weeks then 3 months later.
Secondary Therapeutics • Fenbendazole (Panacur®): Give 25 mg/kg q24h PO for 3 days; repeat in 2 to 3 weeks. It is also effective for hookworms, whipworms, Giardia, and Ollulanus tricuspis. • Ivermectin (Ivomec®): Give 200 µg/kg PO; repeat in 2 to 3 weeks. It is also effective for hookworms.
Therapeutic Notes • Treat kittens routinely or if roundworm infection is suspected, even if the fecal floatation is negative. • A second treatment is needed 2 to 3 weeks following initial therapy to kill new adults arising from eggs and larva that were initially resistant to therapy. Figure 195-1 Roundworms may be vomited or pass in the stool. These worms show the characteristic curling that they assume. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
468
Prognosis The prognosis is excellent for cure, although roundworm eggs often persist in the environment for years and lead to reinfection. This may be a problem in outdoor cats.
Roundworms
Suggested Readings Blagburn BL. 2000. A review of common internal parasites in cats. Vet CE Advisor. A supplement to Vet Med. An update on feline parasites. pp. 3–11. Blagburn BL. 2004. Expert recommendations on feline parasite control. DVM best practices. A supplement to DVM magazine. An update on feline parasites. pp. 20–26.
Hall EJ, German AJ. 2005. Helminths. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1358–1359. St. Louis: Elsevier Saunders. Reinemeyer CR. 1992. Feline gastrointestinal parasites. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XI. Small Animal Practice., pp. 1358–1359. Philadelphia: WB Saunders.
469
CHAPTER 196
Salmonellosis Mark Robson and Mitchell A. Crystal
Overview Salmonella spp. (most commonly S. typhimurium) are motile, nonsporeforming gram-negative rods of the family Enterobacteriaceae. Salmonella may infect a wide variety of mammals, birds, reptiles, and insects, leading to gastrointestinal (GI) disease, systemic disease, or asymptomatic infection. Salmonella may be isolated in up to 18% of normal cats, although two recent studies on 468 pet and shelter cats with and without diarrhea demonstrated prevalence rates of only 1%. In utero infection rarely occurs leading to abortions, stillbirths, and weak kittens. Salmonella is acquired via ingestion of infected feces, infected prey, or contaminated food or water. Seasonal bird migrations, contaminated fomites, nosocomial contact, and animal handlers may serve as sources of exposure. Glucocorticoid therapy, obesity, chemotherapy, neoplasia, pregnancy, feline immunodeficiency virus (FIV), feline leukemia virus (FeLV), and prolonged oral antibiotic administration may place cats at an increased risk of developing infection. The incubation period for Salmonella is 3 to 5 days, and shedding occurs for up to 6 weeks but can occur later as a result of reactivation of infection. Salmonella can exist for prolonged periods in the environment and is often resistant to common disinfectants, making it a potential source of nosocomial infections. Clinical signs of feline salmonellosis include acute or chronic gastroenteritis, sepsis, chronic febrile illness without GI signs, or localized tissue infections. Very young and old animals show the most severe clinical signs. Cats commonly demonstrate no clinical illness. Cats with acute gastroenteritis may have mild-to-severe small or large bowel diarrhea, vomiting, abdominal pain, borborygmus, weight loss, anorexia, and pneumonia. Cats with sepsis may present with pyrexia or hypothermia, dehydration, weakness, depression, or septic shock and may or may not have accompanying GI signs. Cats with Salmonella have been reported to present for chronic fever and nonspecific signs of illness without GI signs. Occasionally, cats may demonstrate only chronic diarrhea. Salmonella may cause focal disease such as pyothorax, meningitis, osteomyelitis, and abscesses and has been isolated from infected wounds and incisions. Salmonella-related disease is most common in young, stressed or diseased cats in poorly sanitary or overcrowded conditions. Salmonella is considered of zoonotic importance, and appropriate handling of feces should be discussed with owners and hospital staff. Immunocompromised individuals should avoid contact with infected animals. Of noted concern is the increasing frequency of antibioticresistant strains isolated from humans and animals. Resistance to ampicillin, fluoroquinolones, tetracycline, chloramphenicol, streptomycin, and sulfonamides has been documented. Antibiotic resistance is believed in part to be a result of indiscriminate antibiotic use by veterinarians.
• Culture and Sensitivity: Positive Salmonella spp. cultures from areas other than the GI tract (i.e., blood, discharge from wounds, urine, synovial fluid, abdominal fluid, and so on) indicate a definitive diagnosis of salmonellosis. • Fecal Polymerase Chain Reaction (PCR) Test: This method may have a higher sensitivity than culture and is more tolerant of suboptimal specimen shipping and handling.
Secondary Diagnostics • Complete Blood Count (CBC): Severe infections are associated with neutropenia with a left shift and toxic changes. A nonregenerative anemia may be present. Thrombocytopenia is rarely seen. A neutrophilic leukocytosis may be present in chronic or localized infections. • Chemistry Profile: Nonspecific changes such as hypoalbuminemia, liver enzyme elevation, hypoglycemia, electrolyte abnormalities, and prerenal azotemia may be present.
Diagnostic Notes • Enrichment broth (selenite or tetrathionate) or specialized transport media (Amies® transport media with charcoal) will help increase the chances of isolating Salmonella. Check with the microbiology lab for instructions prior to collection or submission of samples. • Negative cultures do not eliminate the possibility of infection, as Salmonella is difficult to isolate in the presence of other organisms and is shed intermittently. • Use of antimicrobials prior to sampling may result in false-negative culture results. • Cats with Salmonella should be screened for FeLV and FIV infections.
Treatment Primary Therapeutics • Supportive Therapy: Parenteral fluids, nutritional support, and plasma transfusion as required. • Enrofloxacin: Administer 5 mg/kg q24h PO, SC, IV for 7 to 10 days. • Other fluoroquinolones (e.g., marbofloxacin or orbifloxacin) may also be effective.
Secondary Therapeutics Diagnosis Primary Diagnostics • Fecal Culture and Sensitivity: The presence of Salmonella spp. with exclusion of other diagnoses supports but does not necessarily indicate the organism is causing disease as the prevalence of subclinical carriers is high. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
470
• Trimethoprim/sulfa: Administer 15 mg/kg q12h PO for 7 to 10 days. • Chloramphenicol: Administer 15 to 20 mg/kg q12h PO or IV for 7 to 10 days. • Lactulose: Decreases the survival time of Salmonella spp. by shortening GI transit time and creating an acidic environment. It is only to be used in unresponsive cases of acute GI salmonellosis in cats that are well hydrated. • Preventative Measures: Theoretically cats should not be fed raw or undercooked meats or eggs (cooking to an internal temperature of 74°C [165°F] will kill Salmonella organisms). Phenolic compounds and 1 : 32 bleach solutions are effective disinfectant agents.
Salmonellosis
Therapeutic Notes • Mild infections may be self-limiting and, therefore, may not require therapy. Antibiotic therapy has the potential to induce antibioticresistant strains and, thus, should be avoided if possible. In vitro antibiotic sensitivity may not correlate with in vivo activity. Cats with moderate to severe clinical signs, chronic carriers, and cats that demonstrate neutropenia should receive therapy. • Recent evidence suggests that fluoroquinolones are highly effective against active and chronic infections and may not be as likely to induce antibiotic-resistant strains. Fluoroquinolone use in young, growing kittens has the rare potential to cause cartilage defects when used for extended periods of time at higher doses. Note also the potential for enrofloxacin to cause retinal damage. • Improve sanitation conditions to help prevent reinfection. • Cats with suspected salmonellosis should be isolated. Client and hospital staff education on patient handling and sanitation is indicated.
Prognosis The prognosis for resolution of clinical signs is good, with recovery usually occurring in 1 to 4 weeks. Cats with severe septicemia have a
less favorable prognosis with death rates ranging from 10 to 60%. Cats with underlying immunosuppressive diseases also have a less favorable prognosis. The asymptomatic carrier state may be difficult to eliminate, so the zoonotic importance of this disease must be stressed to the owner. Salmonella spp. may also persist in the environment and lead to reinfection.
Suggested Readings Dow SW, Jones RL, Henik RA, et al. 1989. Clinical features of salmonellosis in cats: six cases. J Am Vet Med Assoc. 194(10):1464–1466. Foley JE, Orgad U, Hirsh DC, et al. 1999. Outbreak of fatal salmonellosis in cats following use of a high-titer modified-live panleukopenia virus vaccine. J Am Vet Med Assoc. 214(1):43–44, 67–70. Greene CE. 2006. Salmonellosis. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 355–360. St. Louis: Saunders Elsevier. Immerseel FV, Pasmans F, De Buck J, et al. 2004. Cats as a risk for transmission of antimicrobial drug-resistant Salmonella. Emerg Infect Dis. 10(12):2169–2174. Stiver SL, Frazier KS, Manuel MJ, et al. 2003. Septicemic salmonellosis in two cats fed a raw-meat diet. J Am Anim Hosp Assoc. 39:538–542.
471
CHAPTER 197
Sarcomas, Injection Site Sharon Fooshee Grace
Overview Since 1992, an association between administration of certain feline vaccines and subsequent development of connective tissue tumors has been recognized. Current thought suggests that vaccines are not the only agents capable of inducing tumor formation. Any type of injection that produces localized inflammation likely has the potential to cause sarcoma development in genetically predisposed or otherwise susceptible cats. Hence, the scientific literature now contains two terms to describe this association: the more general terminology, injection-site sarcomas (ISS), as well as the more specific vaccine-associated sarcomas (VAS). Sporadic reports of various pharmaceuticals as possible causes of tumor induction appear in the literature. However, because the association between vaccines and sarcomas is firmly established and vaccines are frequently administered to cats, VAS continues to generate the most attention. It is noteworthy that a possible association between tumor development and subcutaneous microchips has been recently described. In addition, there are several reports of individual cats developing sarcomas at different vaccine sites many months apart, further strengthening the concept that this is an individual cat problem and not a vaccine problem per se. In 1985 in the United States, modified-live rabies vaccine for intramuscular administration was abandoned in favor of killed products due to government mandate. With the addition of an adjuvant rabies vaccine could be injected SC, making vaccine administration more comfortable and less traumatic for the cat. This resulted in the interscapular space becoming the typical site of vaccine injection. A killed, adjuvanted vaccine for feline leukemia virus (FeLV) was also approved and marketed in the United States in 1985; it was widely adopted by practitioners. In the late 1980s more states mandated rabies vaccine in cats. These three events resulted in a significant increase in cats receiving vaccines. By the late 1980s, an increase in the number of interscapular mesenchymal tumors (primarily fibrosarcomas) was being reported by pathologists. An association between vaccines and the increasing numbers of interscapular soft-tissue tumors was quickly established. Despite more than a decade of intense study, the specific cause(s) and mechanism(s) of tumor induction remains elusive. It is speculated that the local inflammatory response elicited by certain vaccines may lead to uncontrolled fibroblast and myofibroblast proliferation in susceptible cats. This deranged response to injury eventually evolves into an aggressive neoplasia. However, this association currently remains unproven. The relationship of inflammation and tumorigenesis has previously been observed in cats with severe ocular trauma that later developed aggressive intraocular sarcomas. See Chapter 122. Additionally, the role of oncogenes, various growth factors, and expression of specific growth factor receptors continues to be investigated. The role of vaccine adjuvants in this process has been the subject of much investigation and speculation. Several large retrospective and prospective studies have not found a greater incidence in cats receiving adjuvanted vaccines. The Vaccine-Associated Sarcoma Task Force (VASTF), a study group formed in response to the problem, did not recommend against adjuvanted vaccines. Mandated pharmacovigilance in the United Kingdom actually found more sarcomas associated
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
472
with nonadjuvanted vaccines than adjuvanted vaccines. Each vaccine company uses a proprietary adjuvant, which must certainly differ from other vaccine companies’ adjuvants, making it incorrect to associate all adjuvants with the same likelihood of inducing tumorigenesis. The incidence of VAS is unknown and difficult to estimate due to various methods of reporting the tumors. However, it is estimated at 1 case per 1,000 to 1 case per 10,000 vaccines administered. Although rabies vaccines induce the most severe local inflammatory response, FeLV vaccine is more often implicated in tumor development in some studies. Other vaccines are also suspected of inducing tumor formation, although not as often as rabies and FeLV vaccines. The likelihood of sarcoma development increases with the number of vaccines administered in one anatomical location. Most tumors arise within a few months following an injection; however, there is evidence that this process may take years in some cats. Interestingly, insulins injected SC, some containing zinc, that are usually given twice per day in the same general area have not been associated with ISS. The most notable clinical finding in affected cats is a soft-tissue swelling at the site of a previous vaccination or other injection: hindlimb or flank, dorsolateral thorax, interscapular space, or over the scapula. See Figure 197-1. Over a few weeks the soft-tissue swelling transforms into a very hard, nonpainful mass. Over time a subcutaneous mass becomes less mobile as it attaches to tissue deep to the mass, including bone. If untreated, it may grow large and rapid enough to begin surface necrosis due to lack of vascularity. See Figure 197-2. Initially, ISS were thought to be only locally invasive with little or no risk of metastasis. This theory has been disproved because 10 to 24% will metastasize to other sites, primarily the lungs. See Figure 291-33. Importantly, injection-site sarcomas must be differentiated from an inflammatory response at a vaccine site (vaccine granuloma).
Figure 197-1 One of the most common locations for an injection-site sarcoma is the interscapular space. Photo courtesy Dr. Gary D. Norsworthy.
Sarcomas, Injection Site
• Spontaneous (non-ISS) fibrosarcomas and other sarcomas occur commonly in cats. One should not assume that all fibrosarcomas are associated with injections. The spontaneous sarcomas generally have a better prognosis than ISS. See Chapter 198.
Treatment Primary Therapeutics
Figure 197-2 This injection-site sarcoma has outgrown its blood supply, resulting in necrosis and ulceration of the outer portion of the mass. This will often happen if the mass is left untreated. Photo courtesy Dr. Gary D. Norsworthy.
Diagnosis Primary Diagnostics • Clinical Signs: Any soft-tissue swelling near an injection site or a subcutaneous microchip should raise one’s index of suspicion. • Histopathology: Cytology is not a dependable means of diagnosing sarcomas; biopsy is required. Do not try to excise the mass prior to biopsy as local recurrence is likely to occur and become increasingly aggressive with subsequent attempts at excision. A core needle biopsy or wedge (incisional) biopsy should be used to obtain enough tissue to differentiate sarcoma from a vaccine-related granuloma. If radiation therapy will be considered, the biopsy should be taken from within the likely radiation field. Alternatively, if a reasonable presumptive diagnosis of ISS is made based on clinical appearance and surgery is planned, the surgery should be aggressive with wide margins, even if bone removal is needed. See below.
• Triple Approach: Early investigations suggested that trimodality therapy (i.e., surgery, radiation, and chemotherapy) is likely to offer the most successful outcome in terms of longevity. However, overall cure rates are still disappointing. • Surgery: Surgical intervention is the cornerstone of therapy but, used alone, will not affect a cure in most cats. Wide, deep surgical margins are essential because the tumors are quite aggressive and extend far beyond the palpable mass. When possible, any bone in the area of the tumor should also be removed (e.g., dorsal scapular edge, dorsal spinous processes, and so on). Median time to first recurrence with surgery alone is variable, depending on how aggressive the surgery is and the extent of the tumor. It is not uncommon for a tumor to recur within 2 months of surgery. • Radiation: Radiation therapy may help control a tumor that extends beyond the mass and into adjacent tissue. However, radiation therapy alone will not affect a cure and must be performed in conjunction with aggressive surgery. If radiation is anticipated, a radiation oncologist should be consulted for guidance on marking the surgical bed for later identification. It is unknown whether preoperative or postoperative radiation is more beneficial. • Chemotherapy: Chemotherapy alone should not be considered definitive therapy. Preoperative chemotherapy may reduce tumor size and facilitate surgical resection. Response has been seen with various protocols involving doxorubicin, cyclophosphamide, vincristine, carboplatin, and mitoxantrone. For nonresectable tumors, chemotherapy may provide palliation and increase patient comfort.
Secondary Therapeutics • Supportive Therapy: Pain control can be offered with buprenorphine given at 0.005 to 0.01 mg/kg q6 to 12 h IM, IV, or SC; the buccal route is well tolerated by cats, and effects last up to 6 hours.
Therapeutic Notes Secondary Diagnostics • Data Base: A minimum data base should be performed to determine overall health of the cat: Complete blood count, biochemical profile, urinalysis, retroviral tests, and a T4 in geriatric cats. • Diagnostic Imaging: The affected area should be radiographed to identify bone lysis and achieve a general approximation of tumor extension along tissue planes. The chest should also be radiographed for evidence of metastasis. Computerized tomography (CT) or magnetic resonance imaging (MRI) are highly recommended because they will more precisely delineate the extent of disease compared to radiography.
Diagnostic Notes • The extent of tumor infiltration is underestimated by at least half if based on physical examination alone due to extension of “fingers” of tumor tissue in many directions. CT and MRI are far more accurate than radiographs. • Absence of visible pulmonary metastasis on radiographs does not preclude the risk of microscopic tumor spread.
• Because of the location, invasiveness, and aggression of these tumors, surgical excision alone is unlikely to offer a cure even when the first procedure is performed very aggressively (reported failure rates range from 30 to 70%). • ISS are more difficult to treat, are more likely to recur, and have a poorer success rate than other sarcomas. • To decrease the chance of vaccine-related tumor induction, avoid previous vaccination sites when giving boosters and do not give vaccines IM or on the trunk. Do not give vaccines to a cat with a history of ISS; however, rabies vaccination is mandated in most states. The VASTF recommends that the only vaccines which should be given over the right shoulder are those containing antigens for panleukopenia, calicivirus, and herpesvirus (FVRCP). Rabies vaccine should be given as distal as possible on the right hindlimb; FeLV vaccine, if warranted by risk of exposure, should be given on the distal left hindlimb. Rabies vaccines labeled for use every 3 years should not be used in states that require yearly rabies vaccination. The VASTF recommends that after a cat completes the kitten series and 1-year booster with FVRCP, this vaccine should be given every 3 years. Meticulous records should be kept regarding date and location of each vaccine given, vaccine manufacturer, and vaccine serial or lot
473
SECTION 1: Diseases and Conditions
number. Another possible risk factor in development of VAS is administering cold vaccines. It is recommended that vaccines be warmed to room temperature before administration. • Injection-site or vaccine-related granulomas that persist after 3 months should be removed and submitted for histopathology.
Prognosis Prognosis is usually guarded because of local recurrence and the locally aggressive nature of these tumors. However, one aggressive surgical excision, with or without adjunct therapy, has been curative in some cats.
Suggested Readings Daly MK, Saba CR, Crochik SS, et al. 2008. Fibrosarcoma adjacent to the site of microchip implantation in a cat. J Fel Med Surg. 10(2):202–205.
474
Davis KM, Hardie EM, Lascelles BDX, et al. 2007. Feline fibrosarcoma: Perioperative management. Compend Contin Educ. 29(12):712–732. DeMan MMG, Ducatelle RV. 2007. Bilateral subcutaneous fibrosarcomas in a cat following feline parvo-, herpes-, and calicivirus vaccination. J Fel Med Surg. 9(5):432–434. Dyer F, Spagnuolo-Weaver M, Cooles S, et al. 2006. Suspected adverse reactions. Vet Record. 160, 748–750. Kidney BA. 2008. Role of inflammation/wound healing in feline oncogenesis: A commentary. J Fel Med Surg. 10(2):107–109. Richards JR, Elston TH, Ford RB, et al. 2006. The 2006 American Association of Feline Practitioners Feline Vaccine Advisory Panel Report. J Am Vet Med Assoc. 229(9):1405–1441. Seguin B. 2002. Injection site sarcomas in cats. Clin Tech Small Anim Pract. 17(4):168–173.
CHAPTER 198
Sarcomas, Other Mark Robson
Overview Sarcomas are a group of tumors arising from mesenchymal connective tissues. These include fibrous tissue (i.e., fibrosarcoma and myxosarcoma), nerve sheaths (i.e., neurofibrosarcoma, malignant schwannoma, and hemangiopericytoma), skeletal muscle (rhabdomyosarcoma; see Figure 198-1), smooth muscle (leiomyosarcoma), bone (i.e., osteosarcoma, chondrosarcoma, and multilobular osteochondrosarcoma), fat (i.e., liposarcomas and infiltrative lipomas), lymphatic tissue (lymphangiosarcoma), vascular tissue (hemangiosarcoma; see Chapter 91), synovial tissue (synovial cell sarcoma), and fibrous-histiocytic tissue (i.e., malignant fibrous histiocytoma and malignant histiocytosis). Sarcomas in cats are uncommon, except for injection-site sarcomas (see Chapter 197); therefore, there are few published studies documenting their behavior in cats. Much of the published material is extrapolated from dogs, although there are significant differences in tumor prevalence, behavior, and prognosis between cats and dogs. More recent studies are now looking specifically at sarcomas in cats. Sarcomas tend to arise in older cats but may occur at any age. Sarcomas induced by feline sarcoma virus (FeSV) commonly occur in cats less than 3 years old. There is no breed or sex predisposition. In the majority of sarcomas there is no known underlying etiology, the exceptions being injection-site sarcomas and FeSV-induced sarcomas. Trauma or chronic
inflammation of the eye may predispose cats to develop intraocular sarcomas. Sarcomas often present as a soft to firm, slow-growing, nonpainful swelling. They are usually solitary, rarely involve regional lymph nodes, and are slow to metastasize (usually to the lungs). As a group, sarcomas tend to be locally invasive, and frequently recur after excision. The tumor often has a pseudocapsule of compressed neoplastic cells, with microscopic “tendrils” that extend well beyond the visible margins. The World Health Organization (WHO) staging system for bone tumors is presented in Table 198-1. Clinical signs are variable and often related to the location of the tumor. Clinical signs associated with intrathoracic or intra-abdominal sarcomas include dyspnea, coughing, hypertrophic osteopathy, vomiting, inappetence, diarrhea, dysuria, weight loss, and icterus. Neurological signs or pain may be seen with nerve sheath tumors or with direct compression of nervous tissue from a variety of tumor types. Lameness, pain, and pathological fractures are often associated with sarcomas originating in bone. Osteosarcomas (see Figure 198-2) in cats follow a slower clinical course in comparison to dogs. It is the most common primary bone tumor in cats (70–80%) but still only represents 1 to 6% of all feline cancers. The mean age at presentation is 8 to 11 years old; however, it may be seen in cats less than 1 year old. A recent study found that 35 to 40% of all osteosarcomas in cats were extraskeletal, with the remaining cases split evenly between axial and appendicular sites. Most extraskeletal osteosarcomas occur in the subcutaneous tissues (some may be associated with injections), and they tend to have a poorer prognosis compared with skeletal osteosarcoma. Metastasis is not usually evident at the time of diagnosis and, unlike dogs, only occurs in 5 to 10% of cases. Spontaneous fibrosarcomas (versus induced fibrosarcomas; see Chapter 197) are locally aggressive tumors that are usually found subcutaneously but may arise from almost any organ. They have a recurrence rate of up to 67% following surgical excision and metastasize in 15 to 23% of cases. FeSV-induced fibrosarcomas are highly aggressive, highly metastatic tumors that occur in young, cats that are positive for feline leukemia virus (FeLV) as multiple subcutaneous masses on the limbs and trunk. Chondrosarcomas are the second most common tumor of bone in cats. The mean age at presentation is 10 years old, and males are two times more likely to be affected than females. Seventy percent of chondrosarcomas are associated with bones (63% long bones and 37% flat bones),
TABLE 198-1: World Health Organization TNM Classification of Canine and Feline Tumors of Bone
Figure 198-1 This rhabdomyosarcoma originated from the quadriceps muscle and grew quickly necessitating amputation. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
T = Primary Tumor T0 T1 T2 Note: M = Distant metastasis M0 M1
No evidence of tumor Tumor confined within medulla and cortex Tumor extends beyond the periosteum Multiple tumors should be classified independently No evidence of distant metastasis Distant metastasis detected [specify site(s)]
T, tumor; n, (lymph) node; m, metastasis
475
SECTION 1: Diseases and Conditions
Diagnosis Primary Diagnostics
(A)
• Cytology: Fine-needle aspirates are of limited value in the diagnosis of sarcomas because these tumors usually do not exfoliate well. Although cytology is not accurate at differentiating sarcoma types, it should give an indication that it is a sarcoma and help rule out other types of neoplasia. • Histopathology: Incisional biopsies will usually give a definitive diagnosis of the type of sarcoma, which will aid with further surgical or therapeutic planning. Although biopsies of sarcomas do not increase the risk of metastasis, local seeding of neoplastic cells may occur. It is important that the biopsy be performed in such a way as to allow for complete excision of the biopsy site at a later date. • Radiographs: If the primary tumor is overlying bone radiographs are important to assess the degree of bony involvement.
Secondary Diagnostics • Tumor Staging: Staging typically involves three-view thoracic radiographs, cytology of regional lymph nodes (if possible), and abdominal ultrasound. This will help to determine the therapeutic options and prognosis. • Minimum Database: Complete blood count, serum biochemistry, urinalysis, T4 assay and retroviral tests are important to look for paraneoplastic syndromes and concurrent diseases, which may affect surgical planning, anesthetic planning, the patient’s ability to deal with chemotherapy, and long-term prognosis. • Advanced Imaging: Computerized tomography (CT) or magnetic resonance imaging (MRI) may be used to determine the extent of the tumor to plan for surgery or radiation therapy.
Diagnostic Notes • Cytological findings from sarcomas should be interpreted with caution because they may vary from the histological diagnosis. • Aspiration of bone marrow, liver, and spleen may be considered as part of the staging of malignant histiocytosis.
Therapy Primary Therapeutics (B) Figure 198-2 Lateral (A) and anterior-posterior (B) views of this foot with a firm swelling revealed the classic “sunburst” effect of osteosarcoma. The tumors characteristically do not cross joints as seen in the affected metatarsal. Images courtesy Dr. Gary D. Norsworthy.
• Surgical: Aggressive and complete surgical excision of the tumor, with 3-cm margins laterally and one fascial plane deep, is the most effective way to achieve remission with sarcomas. If the primary tumor is appendicular, then limb amputation may be the preferred option.
Secondary Therapeutics and the scapula is the most commonly affected of all bones (15%). The remaining 30% are found subcutaneously and less than 2% are found at vaccination sites. Chondrosarcomas are slow-growing, locally invasive, and rarely metastasize. Malignant histiocytosis (MH) is a rare and poorly described (in cats) tumor of morphologically atypical histiocytes. It is characterized by progressive, systemic, neoplastic infiltration of the liver, spleen, bone marrow, lung, and lymph nodes. There is no known effective treatment and the disease is rapidly fatal. Some authors recommend staging and treating cases of MH as for lymphoma. Malignant fibrous histiocytoma (MFH) is an aggressive localized tumor of histiocytes, usually found in the subcutis, and behaves similarly to fibrosarcoma.
476
• Radiation: Sarcomas typically do not respond well to radiation. Radiation is most commonly employed as adjuvant therapy in cases where there excised tumor has “dirty margins.” Studies in some canine sarcomas have documented longer disease-free intervals and survival times when radiation is coupled with surgical excision, compared with cases that do not use radiation. • Chemotherapy: Sarcomas are not highly chemoresponsive. Chemotherapy may be considered with high-grade tumors, tumors with incomplete excision, or when there is distant metastasis. Chemotherapeutic agents that have been used for soft-tissue sarcomas include doxorubicin, carboplatin, lomustine, ifosfamide, vincristine, mitoxantrone, and combinations of these drugs.
Sarcomas, Other
• Analgesia: Buprenorphine, butorphanol, codeine, fentanyl patches, and meloxicam may be considered for perioperative pain and longterm palliative therapy.
Therapeutic Notes • Sarcomas should never be “shelled-out” of their capsule because viable tumor will be left behind. • If complete surgical resection of the tumor has been achieved with clean margins, and there is no evidence of distant metastasis, adjuvant therapy with radiation or chemotherapy is probably of little benefit. • Despite aggressive surgical excision, feline fibrosarcomas frequently recur locally. • Radiation may also be used preoperatively to reduce tumor size and viability, or it may be used as palliative relief for tumors that are non-resectable. • Given the sparse clinical data regarding many feline sarcomas, consultation with an oncologist about a specific case may be appropriate to achieve the best outcome.
Prognosis The prognosis for sarcomas is dependent mainly on the ability to achieve complete surgical excision. Grading schemes for sarcomas do not result in a consistently accurate prognosis in cats, but in general, higher histological grades may be more likely to have local recurrence and distant metastasis. The prognosis for sarcomas is best with small appendicular sarcomas that do not have evidence of distant metastasis (early amputation of appendicular osteosarcomas can be curative) and poor with large, high-grade tumors that are located in areas where surgical resection is difficult.
Suggested Readings Durham AC, Popovitch CA, Goldschmidt MH. 2008. Feline chondrosarcoma: a retrospective study of 67 cats (1987–2005). J Am Anim Hosp Assoc. 44:124–130. Heldmann E, Anderson MA, Wagner-Mann C. 2000. Feline osteosarcoma: 145 cases (1990–1995). J Am Anim Hosp Assoc. 36:518–521.
477
CHAPTER 199
Scottish Fold Osteochondrodysplasia Sharon Fooshee Grace
Overview The Scottish Fold is an affectionate breed known for its gentle disposition, rounded face and eyes, and folded ears. The trait for folded ears has been perpetuated from a naturally occurring mutation first seen in a Scottish barn cat in the 1960s; hence the name “Scottish Fold.” The breed was accepted for registry in England in 1966, but pedigree status was rescinded in 1974 after discovery of a heritable cartilage defect in the breed. Scottish Folds are still not accepted for registry in the United Kingdom, although it is recognized as a pedigreed cat by the Cat Fancier ’s Association in North America. The long-haired version of the Scottish Fold is called the Highland Fold. When Scottish Fold cats are mated with Scottish-Fold type cats with straight ears, the offspring are called Scottish Shorthairs. Kittens are born with straight ears and at about 1 month of age, the ears will fold in some, but not all, of the kittens. Folded ears are caused by a cartilage defect which is transmitted as an autosomal dominant trait. Recent work has described the inheritance pattern as incompletely dominant rather than simple dominant. The folded-ear allele is designated as Fd. Folded-ear cats bred to other folded-ear cats are Fd/Fd; heterozygotes are Fd/fd. Unfortunately, the cartilage abnormality of the ears is linked to a progressive, crippling arthropathy, Scottish Fold Osteochondrodysplasia (SFOCD). When folded-ear cats are mated to other folded-ear cats, this arthropathy invariably results. Affected cats have shortened malformed legs and abnormalities of growth plates. Cats heterozygous for the folded gene (folded ear × straight ear mating) may develop arthritis, but it is at an older age than cats which are homozygous. Cats afflicted with SFOCD are painful in one or more limbs and reluctant to jump from heights. Their gait is stiff and stilted because their joints are unable to bear the weight of their fairly robust frame. Their distal extremities (the feet in particular) are shorter than expected and often misshapen, giving them a somewhat squat appearance. The tail is short, has a thickened base, and is variably rigid and inflexible. It is not uncommon for affected cats to present for lameness at a few weeks to months of age; the severity of signs worsens with age as mechanical stress on the bones and joints takes a toll.
(A)
Diagnosis Primary Diagnostics • Diagnostic Imaging: Radiographs provide the basis for diagnosis of SFOCD. Lesions are bilaterally symmetric and may be present as early as 7 weeks of age. There is irregularity in the size and shape of tarsal, carpal, metatarsal, and metacarpal bones, the phalanges, and caudal vertebrae. The hindlimbs are usually more severely affected than the fore. Physes are excessively wide, joint spaces are narrowed, and periarticular new bone is observed to progressively form, especially at insertions of tendons and joint capsules. See Figure 199-1.
Diagnostic Notes • A genetic test for the disorder is not available.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
478
(B) Figure 199-1 Lateral (A) and anterior-posterior (B) views of a cat with Scottish Fold osteochondrodysplasia show extensive irreversible bony changes with secondary degenerative joint disease. Images courtesy Dr. Richard Malik.
Scottish Fold Osteochondrodysplasia
Treatment
• There is considerable variation in the severity and rate of progression of disease in the breed.
Primary Therapeutics • Palliative Therapy: Judicious use of nonsteroidal anti-inflammatory (NSAID) medication and chondroprotective agents should be considered. The Scottish Fold is a breed known to be affected by polycystic kidney disease so NSAIDs should be used with caution if the renal status of the cat is unknown.
Secondary Therapeutics • Surgical Therapy: The disease is relentlessly progressive, and there in no practical therapy available. One report described bilateral ostectomies and pantarsal arthrodesis to alleviate the pain of tarsal exostoses.
Therapeutic Notes • Scottish Fold breeders try to circumvent the problem of arthropathy by breeding folded-ear cats to Scottish Shorthair or American Shorthair cats. However, all cats heterozygous for the trait have the potential to develop arthropathy, though it is usually at a later age than homozygous cats.
Prevention Folded-ear cats should never be bred to other folded-ear cats. For cat lovers who admire the gentle, sweet disposition and rounded face of the Scottish Fold, an alternative is the Scottish Shorthair. This breed retains the lovely disposition and rounded facial silhouette of the Scottish Fold but does have the gene for defective cartilage.
Prognosis Prognosis is guarded; treatment is symptomatic.
Suggested Readings Chang J, Jung J, Oh S, et al. 2007. Osteochondrodysplasia in three Scottish Fold cats. J Vet Sci. 8(3):307–309. Malik R. 2001. Genetic diseases of cats. J Fel Med Surg. 3(2):109–112. Malik R, Allan G, Howlett CR, et al. 1999. Osteochondrodysplasia in Scottish Fold cats. Aust Vet J. 77(2):85–92. Takanosu M, Takanosu T, Suzuki H, et al. 2008. Incomplete dominant osteochondrodysplasia in Scottish Fold cats. J Sm Anim Pract. 49(4):197–199.
479
CHAPTER 200
Seizures Sharon Fooshee Grace
Overview Seizures are defined as clinically apparent disturbances in the electrical activity of the brain. They do not represent a disease entity but indicate the presence of another underlying disorder, which may primarily or secondarily involve the brain. Primary disorders, such as epilepsy, have no underlying cause whereas secondary seizure disorders have an underlying structural or metabolic cause. Seizures occur less commonly in cats than in dogs, although they are seen on a regular basis in cats of all ages. Focal seizures originate in a discrete seizure focus of the brain, resulting in focal motor activity or a psychomotor disturbance. Generalized seizures originate in both cerebral hemispheres and normally result in tonic-clonic type seizures. Thus, the clinical appearance of the seizure may vary depending on the location and severity of the hypersynchronous electrical activity. A generalized tonic-clonic seizure is divided into three stages. Preictus is the period preceding the active seizure phase and may be inapparent or may consist of a variety of subtle behaviors, such as anxiety, pacing, seeking attention, and so on. Ictus is the active seizure phase that typically includes all or some of the following: loss or consciousness, involuntary movements (generalized muscle contractions), vocalization, salivation, urination, or defecation. Post-ictus is the period following the active seizure phase; it may last for minutes or hours and can include various actions or behaviors such as anxiety, hunger, pacing, aggression, exhaustion, sleepiness, blindness, and so on. The most common causes of seizures in cats involve structural cerebral disorders or metabolic diseases. Functional disturbances (idiopathic and acquired epilepsy) have historically been considered far less common in cats than dogs, although a recent review indicates that idiopathic epilepsy accounts for 21 to 59% of feline seizures. Cats with idiopathic epilepsy tend to be younger (3–4 years) than those with other causes of seizures (≥8 years). Epilepsy is a diagnosis of exclusion and should not be considered without an attempt to investigate other possible causes. Therefore, a thorough, complete evaluation of the patient is always recommended.
Diagnosis Differential Diagnoses Many diseases and disease conditions must be considered. See Table 200-1.
Primary Diagnostics • General History: Details should be sought that relate to the health of a queen during pregnancy and signs of illness in her kittens; a history of trauma; exposure to toxins; type of diet and relationship of the seizure to eating; travel history; source from which the cat was obtained (i.e., cattery, shelter, and so on); exposure to other animals (e.g., swine or wildlife); and recent administration of medications (e.g., insulin or metronidazole). A valid rabies vaccination history must be established.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
480
TABLE 200-1: Differential Diagnoses for Seizures. Anomalous and Congenital Diseases Hydrocephalus Metabolic storage disease (rare) Idiopathic Epilepsy (idiopathic or acquired) Hyperesthesia syndrome Infectious, Inflammatory, and Infestative Diseases Bacterial disease Fungal disease cryptococcosis and less commonly histoplasmosis, blastomycosis, coccidioidomycosis Nonsuppurative meningoencephalitis* Protozoal disease toxoplasmosis, neosporosis, Cytauxzoonosis Viral disease feline infectious peritonitis*, feline immunodeficiency virus*, rabies, pseudorabies Aberrant parasitic migration Dirofilaria immitis or Cuterebra larvae Metabolic Disease Thiamine deficiency Hypoglycemia* Hypocalcemia Hypernatremia Polcythemia Portosystemic shunt Hyperthyroidism Neoplasia Lymphoma* Meningioma* Metastatic tumor Toxicity Aspirin Ethylene glycol Lead Organophosphates* Metronidazole Trauma Significant head injury Vascular Disturbances Feline ischemic encephalopathy Hypertension* * The more common seizure diseases.
• History Related to Seizure Activity: The practitioner should be sure that the owner is describing seizure activity, not signs referable to cardiac, vestibular, or cerebellar disease, musculoskeletal disease, pain, or estrus. The description should include signs of an active seizure (see ictus). Additional information should include frequency
Seizures
of seizure activity, whether the cat is normal between seizures, time of day or night of seizure occurrence, length of the seizure, if the seizure was single or multiple (cluster), and possible precipitating events. Characteristics of the preictal and postictal period may be important in predicting future seizures or confirming that the episode was truly a seizure. • Physical Examination: A complete neurologic examination should be performed but not immediately after a seizure; the patient should first be fully recovered from a recent seizure. Cranial nerve deficits, proprioceptive deficits, lateralizing signs, and vision disturbances are just a few of the abnormalities that may help pinpoint the underlying cause. The head should be evaluated for signs of trauma or the presence of a “dome” shape or open fontanel in younger cats (suggesting possible hydrocephalus). A thorough ophthalmologic examination is essential to identify retinal lesions that might indicate infectious or inflammatory disease, hypertension, or lymphoma. A normal neurologic examination does not rule out structural brain disease. • Minimum Data Base: The seizure investigation should start with a complete blood count (CBC), chemistry profile, urinalysis, and feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) testing to assess the general health of the patient and screen for underlying causes of the seizure. Cats that are 6 years or older should be evaluated for hyperthyroidism with a total T4.
(A)
Secondary Diagnostics • Radiography: Skull radiographs do not provide meaningful information except with trauma and in rare cases of hydrocephalus. See Figure 200-1. Thoracic radiographs are helpful in screening for systemic infectious diseases and metastatic neoplastic conditions. • Serum Bile Acids: Fasting and postprandial serum bile acids are useful in identifying portosystemic shunts. See Chapter 178. Determination of bile acids may be especially appropriate for kittens and young adult cats with a history of seizures. • Blood Pressure Determination: This is useful to screen for hypertension in older cats with renal or thyroid conditions and acute onset seizures. See Chapter 107. • Serology: Appropriate serologic testing should be submitted if there is suspicion of infectious disease. In-clinic testing often includes FeLV and FIV tests. Local diagnostic laboratories may perform toxoplasmosis, neosporosis, and cryptococcal antigen serology. See Chapters 43 and 214. Feline coronavirus testing should be used cautiously due to the test limitations (i.e., lack of specificity for feline infectious peritonitis [FIP]). See Chapter 76. • Computerized Tomography (CT) and Magnetic Resonance Imaging (MRI): Specialized imaging techniques are helpful in identifying focal brain lesions. If not locally available, most veterinary teaching hospitals have a CT or an MRI unit. CT or MRI is usually indicated prior to cerebrospinal fluid (CSF) collection and analysis. • CSF Analysis: See Chapter 298 for technique. Because the fluid must be analyzed within 20 to 30 minutes and the procedure poses some risk for the patient, it often is appropriate to refer the patient to a specialist. Complete analysis includes measurement of protein content, cytologic analysis, and occasionally culture or serologic testing (e.g., cryptococcal antigen serology, bacterial culture, and so on). The CSF tap should not be performed if there is suspicion for increased intracranial pressure. • Serum Protein Electrophoresis: Serum electrophoresis may be helpful, especially when FIP is a suspected cause. See Chapter 76.
Diagnostic Notes • A complicated evaluation may not be appropriate for cats presenting with a first-time seizure because seizures are a one-time event in
(B) Figure 200-1 A, This 7-month-old kitten had a history of seizures and was diagnosed with hydrocephalus. The calvarium is markedly enlarged and abnormally shaped. B, The rim of brain tissue surrounds fluid resulting in the radiographic findings in 200-1. Image courtesy Dr. Gary D. Norsworthy.
some cats. Diagnostics should include a complete history and physical examination (general and neurologic) a fundic examination, FeLV and FIV testing, and a minimum data base (especially glucose and calcium). • If seizure activity becomes frequent, it may be helpful for the owner to keep a notebook that records pertinent comments related to the seizures (see “History”). In some cases, clues as to the underlying cause may become apparent. • If a cat with historical seizure activity requires sedation, ketamine should be avoided because it increases intracranial pressure. Phenothiazines (including acepromazine) are contraindicated because of their possible effect on lowering the seizure threshold. • Whenever a cat with unexplained neurologic signs bites a human, appropriate public health officials should be notified. Usually, local animal control officers can assist with this. If an unvaccinated cat bites a human or if a cat with neurologic signs bites a human and dies, it is important to submit the head of the cat for necropsy and rabies testing. See Chapter 185. Do not freeze brain tissue that is to be tested for rabies.
481
SECTION 1: Diseases and Conditions
Primary Therapeutics • Status Epilepticus: Calcium and glucose should be administered, if appropriate. In nonhypoglycemic or nonhypocalcemic cats that are not suspected of having a portosystemic shunt, diazepam (5 mg/mL) may be administered intravenously to effect at 0.5 to 1.0 mg/kg every 10 to 15 minutes for a total of three doses. Cats are slow to eliminate this drug, so repeated treatments should be given with caution. If more sustained anticonvulsant control is needed in-hospital, phenobarbital may be given (2–6 mg/kg IV), although it may take 10 to 20 minutes before it crosses the blood-brain barrier so the effect is not immediate. Although thiamine deficiency is uncommon, it is reasonable to administer injectable vitamin B1 or B-complex. See Chapter 210. Body temperature should be carefully monitored because prolonged seizures may cause hyperthermia. Oxygen may be supplemented. • When to Treat: A single seizure episode does not warrant long-term anticonvulsant therapy. Intervention is generally advised if more than four episodes occur within a year, if the cat has more than one seizure in a 24-hour period, if the cat experiences status epilepticus (seizure lasting more than 5 minutes or presence of multiple seizures without an intervening period of normalcy), or if the seizure results from trauma. • Maintenance Anticonvulsant Therapy: Phenobarbital is the drug of choice for most cats with multiple seizure episodes. Phenobarbital is dosed at 1.5 to 2.5 mg/kg q12h PO. Serum levels can be measured beginning 2 to 3 weeks after initiating therapy; therapeutic levels are similar to those for dogs (25–40 µg/ml, ideal range for cats 23–30 µg/ ml). Levels should be checked every six months and 2 to 3 weeks after any dosage change. In cats, the drug is not associated with hepatotoxicosis or hepatic enzyme induction, which are common problems for dogs. It may cause polyphagia with weight gain, marked sedation, cutaneous hypersensitivities, lymphadenopathy, and bone marrow suppression. • Corticosteroids: Glucocorticoids may be administered for cases of suspected cerebral edema or granulomatous meningitis. Trauma, brain tumors, and hydrocephalus may improve with corticosteroids. • Antimicrobials and Antifungals: When antimicrobial therapy is required, consideration must be given to distribution limitations posed by the blood-brain barrier. Generally, sulfas and chloramphenicol more readily penetrate the barrier than other drugs, although others may cross over when inflammation is present. Fluconazole is usually the preferred drug for fungal disease of the central nervous system. • Bathing: If historical topical toxic agent exposure exists (e.g., organophosphate) or if a suspicious odor or appearance to the haircoat suggests dermal exposure to toxins, the cat should be immediately bathed. • Surgery: Meningiomas can often be removed after the exact location is established through examination and specialized imaging techniques. This procedure should only be performed by those with specialized training in cranial surgery. Surgical ligation is indicated if a congenital portosystemic shunt is identified. See Chapter 137 and 178.
Secondary Therapeutics • Levetiracetam: This is a safe and effective anticonvulsant for feline epilepsy with benefits, which may continue even after the drug is discontinued. It is used as an adjunct to phenobarbital at 20 mg/kg q8h PO and may be given independent of feeding. Drug monitoring is still being investigated, but therapeutic ranges appear similar to those in humans (5–45 µg/ml). The dose should be decreased with
482
renal insufficiency. Its potential use as sole therapy is being studied and shows promise.
Therapeutic Notes • Zonisamide (5–10 mg/kg q12h PO) and pregabalin (2–4 mg/kg q8–12h PO) are newer anticonvulsants, which are currently under investigation for use in dogs and cats. • Therapy is considered successful if it results in a 50% decrease in seizure activity. • A changing seizure pattern may reflect inappropriate seizure control or progressive neurologic disease. • Ask owners to keep a written record of all seizure events to assist in seizure management. • See Chapters 70 and 155, respectively, for ethylene glycol toxicity and organophosphate toxicity therapy. • Potassium Bromide (KBr): This drug has been used as a maintenance anticonvulsant in cats, though it is not particularly effective and is no longer recommended. Approximately 40% of cats receiving chronic KBr therapy develop drug-related irreversible pneumonitis. Development of a cough while on this therapy warrants discontinuation of the drug, although cessation of therapy does not guarantee resolution of the cough or lung lesions. In some cases, KBr-related lung disease has been fatal. Asthma is a contraindication for use of KBr. Cats receiving KBr may have elevated chloride levels on routine chemistry screening. KBr is dosed at 15to 25 mg/kg q12h PO; serum bromide levels can be monitored (initial steady state levels require 6–8 weeks from KBr initiation or dose change due to the prolonged half life of KBr). Most cats are controlled with serum levels in the 15 to 20 mmol/L (1.2–1.6 mg/mL) range. • Diazepam: Diazepam has a long half-life in the cat, and unlike dogs, cats do not appear to develop a tolerance to it. However, oral use has been associated with a potentially fatal idiosyncratic hepatotoxicosis. In several recent reviews, neurologists strongly discourage the use of oral diazepam for feline seizure control. Intravenous formulations are not associated with hepatoxicosis. Because injectable diazepam is incompatible with lactated Ringer ’s solution as well as a number of drugs, it is best injected alone. Diazepam is dosed at 0.25 to 0.5 mg/ kg q8 to 12h PO; on average, this translates to 2 to 5 mg per cat q8h. • Once a cat is placed on long-term anticonvulsant therapy, the medication should never be abruptly terminated; this may precipitate uncontrolled seizure activity, especially with phenobarbital.
Prognosis Prognosis is entirely dependent on the identification and resolution of the underlying cause.
Suggested Readings Bailey KS, Dewey CW. 2009. The seizuring cat: Diagnostic workup and therapy. J Fel Med Surg. 11(5):385–394. Barnes HL, Chrisman CL, Mariani CL, et al. 2004. Clinical signs, underlying cause, and outcome in cats with seizures: 17 cases (1997–2002). J Am Vet Med Assoc. 225(11):1723–1726. Center SA, Elston TH, Rowland PH, et al. 1996. Fulminant hepatic failure associated with oral administration of diazepam in 11 cats. J Am Vet Med Assoc. 209(3):618–625. Schriefl S, Steinberg TA, Matiasek K, et al. 2008. Etiologic classification of seizures, signalment, clinical signs, and outcome in cats with seizure disorders: 91 cases (2000–2004). J Am Vet Med Assoc. 233(10):1591– 1597.
CHAPTER 201
Skin Parasites Christine A. Rees
Overview Skin parasites or ectoparasites are a common cause for feline dermatologic problems. Various skin parasites exist in cats. The most common ectoparasites in cats that cause dermatologic problems are mites and fleas. Different types of mites that commonly affect cats include: Demodex spp., Cheyletiella spp., Notoedres spp., and Otodectes spp. Each one of these parasites has a different treatment. Therefore, each one of these skin parasites will be addressed individually.
Demodicosis Overview Three distinct demodectic mites exist in the cat: Demodex gatoi, Demodex cati, and a “long” as yet unnamed Demodex spp. mite. Anecdotal reports suggest that D. gatoi is more commonly diagnosed in the United States than the other two species. The diagnosis of this mite appears to be a regional phenomenon because this mite is rarely reported in some areas of the country. The clinical presentation and possible underlying medical conditions associated with the presence of the mites varies between the three demodectic mites. D. gatoi causes barbed alopecia or partial alopecia anywhere on the body. This mite causes pruritus and is highly contagious among cats. One report suggests that D. gatoi may also be associated with a concurrent food allergy. Therefore, food allergy should be considered when D. gatoi mites are present. See Figure 201-1. In contrast to D. gatoi, D. cati are found most commonly on specific body locations, notably the face, eyelids, and ears. This mite causes patchy alopecia with or without scale. A ceruminous otitis may also be present. D. cati is most commonly associated with an underlying metabolic or systemic disease, typically diabetes mellitus, feline leukemia virus infection (FeLV), feline immunodeficiency virus (FIV) infection, or other causes of immunosuppression. Therefore, appropriate blood tests need to be included in the diagnostics when D. cati is found. The clinical presentation for the long unnamed Demodex spp. is poorly characterized. These mites are thought to occur anywhere on the body. Some reports suggest that this mite may be found in conjunction with D. cati.
(A)
(B) Figure 201-1 (A) Demodicosis may appear as other pruritic skin diseases that result in scratching. (B) It may also be more crusty and widespread. Photos courtesy Dr. Gary D. Norsworthy.
Diagnosis Secondary Diagnostics Primary Diagnostics • Skin Scrapings: Demodex mites can easily be found on skin scrapings. The species is determined by the microscopic appearance. D. gatoi is a short stubby looking mite with no apparent tail. See Figure 201-2. The D. cati mite looks similar to the Demodex canis mite with a “alligator appearance.” See Figure 201-3. The unnamed long demodectic mite appears similar to the D. cati but with a longer tail.
• Further Work-Up: If D. gatoi is found a food elimination trial needs to be performed. If D. cati is present a blood panel (i.e., complete blood count [CBC], serum chemistry, FeLV, and FIV) and urinalysis are indicated. No additional tests are indicated when the unnamed long demodex mite is found.
Treatment D. gatoi
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Primary Therapeutics • Lime Sulfur Dip: This is the most commonly used treatment. It is diluted at 120 mL to 3.8 liters (4 ounces to 1 gallon) of water and
483
SECTION 1: Diseases and Conditions
Prognosis The prognosis varies according to the species involved. The prognosis is good for D. gatoi if all cats in the household are treated. The prognosis for D. cati will vary according to the underlying cause that is present. The prognosis for the long unnamed Demodex spp. is unknown.
Cheyletiellosis Overview
Figure 201-2 magnification.
D. gatoi is a short stubby looking mite with no apparent tail. 1000×
Cheyletiella blakei is a feline ectoparasite that grossly appears as dandruff or scale. Close inspection with magnification reveals the mite to move thus creating the name “walking dandruff.” The most common clinical signs are the appearance of excessive dandruff or scale on the trunk with pruritus. However, asymptomatic carriers have also been reported. C. blakei is highly contagious between cats and is zoonotic. Eggs are shed in the environment and may be a source of reinfection. The adult mite is an obligate parasite that cannot live off of the host for more than 10 days. Cheyletiellosis should be a differential when owners complain about one or more family members having a pruritic skin eruption. See Figure 201-4.
Diagnosis Primary Diagnostics • Cytology: Mites or eggs may be seen microscopically from skin scrapings, acetate tape impressions, or flea combing samples. When using samples from a flea comb the collected material should be placed in a fecal floatation solution before viewing them under the microscope at 100×. See Figure 201-5. Figure 201-3 D. cati looks similar to the D. canis mite with a “alligator appearance.” 1000× magnification.
Treatment Primary Therapeutics
sponged over the cat’s body at weekly intervals for 4 to 6 weeks. This product is malodorous. All cats who come into contact with affected cat should be treated in the case of D. gatoi.
• Lime Sulfur Dip: Lime sulfur dip is mixed according to label directions (120 mL to 3.8 liters [4 ounces to 1 gallon] of water). The diluted dip is sponged over the cat’s body and allowed to dry. The dip
Secondary Therapeutics • Other Treatments: Anecdotal reports suggest that ivermectin and milbemycin may be effective for D. gatoi. Studies confirming efficacy are lacking.
D. cati Primary Therapeutics • Lime Sulfur Dip: The most common treatment for D. cati is lime sulfur dip; see D. cati “Primary Therapeutics.” Secondary Therapeutics • Doramectin: This drug is off label for cats. It is dosed at 0.6 mg/kg q7d SC. Because doramectin is a synthetic avermectin signs seen with ivermectin toxicosis (i.e., neurologic, coma, and death) may occur. • Amitraz: This drug is off label for cats. To minimize toxicity it is diluted to 125 ppm, which is half the recommended canine concentration. It is used q7 to 14 days by sponging on the cat. Because amitraz can lower blood glucose levels, it should not be used in a wellregulated diabetic cat.
484
Figure 201-4 Cheyletiella may be transmitted to humans and cause pruritic dermatitis. Photo courtesy Dr. Gary D. Norsworthy.
Skin Parasites
Figure 201-5 Cheyletiella blakei as seen at 100×. 100× magnification. Figure 201-6
Notoedres cati as seen at 100×. This is a dorsal view of a female.
should not be rinsed off. Weekly treatments for four to six dips are recommended. All cats and dogs that are in contact with the infected cat must be treated. This product is malodorous. • Topical Flea Products: Most topical flea products are effective in treating C. blakei.
Secondary Therapeutics • Ivermectin: Give a 1% ivermectin injection at 200 to 300 µg/kg SC and repeat in 2 weeks. This can be effective.
Therapeutic Notes • Because Cheyletiella is contagious to other animals. All cats and dogs in contact with the affected cat should also be treated.
Notoedres Feline scabies is caused by the Notoedres cati mite. Scabies is intensely pruritic and causes a papular and crusting dermatosis with or without excoriations. See Figure 201-6. The common locations are the ear margins and the dorsum of the head. In severe cases, the cat’s legs may also be affected. In addition, peripheral lymphadenopathy may occur. Secondary bacterial dermatitis (superficial pyoderma) may occur as a result of intense scratching. Because this mite is highly contagious, all cats in contact with the infected cat need to be treated.
(A)
Diagnosis Primary Diagnostics • Skin Scrapings: These mites are easily found on skin scrapings. See Figure 201-7. Sampling the medial and proximal margins of the pinna will increase diagnostic yield.
Treatment Primary Therapeutics • Lime Sulfur Dip: This product should be diluted according to label directions (120 mL to 3.8 liters [4 ounces to 1 gallon] of water). This dip is sponged all over the body and allowed to air dry. This dip is repeated weekly for 4 to 8 weeks. Because this mite is so contagious, all cats that come in contact with affected cat must also be treated with the dip. This product is malodorous.
(B) Figure 201-7 Notoedres causes a crusty, proliferative dermatitis. (A) The pinnae are the most commonly affected areas. (B) The face is also frequently affected. Photo courtesy Dr. Gary D. Norsworthy.
485
SECTION 1: Diseases and Conditions
• Selamectin (Revolution®): This topical insecticide is approved for cats and has been used to successfully treat feline scabies.
Fleas Overview
Secondary Therapeutics • Other treatments that have been used to treat feline scabies include: ivermectin (0.2–0.3 mg/kg twice, 2 weeks apart PO or SC), doramectin (0.2–0.3 mg/kg once SC), or dilute amitraz dips (see whole body dip, do weekly for 3 weeks).
Therapeutic Notes • All cats in the household should be treated for feline scabies because this mite is contagious. Although uncommon, feline scabies can transiently infest dogs, rabbits, and humans.
Otodectes Overview Otodectes cynotis is a common ear mite that causes feline otitis externa. Ear mites are much more likely to occur in kittens, usually transmitted from their mother. Infested ears appear to have a coffee ground material in them. These mites can be present on the skin around the ears. If this occurs, pruritus around the ears, shoulders, and neck areas can occur resulting in alopecia, papules, miliary dermatitis, and excoriations. Because Otodectes spp. mites are contagious to dogs and cats, all animals that come into contact with affected cat should be treated. See Chapter 62.
486
Fleas are a significant skin parasite problem in cats. They can be diagnosed based on the observed presence of fleas or flea dirt on the skin, finding fleas or flea dirt with a flea comb, or the presence of tapeworms around the rectum or on the surface of the stool. Inconsistent flea control practices can be a major inciting factor for cats developing flea allergy dermatitis. Therefore, it is important that owners be diligent with flea control. See Chapter 80.
Suggested Readings Blot C, Kodjo A, Bourdoiseau G. 2003. Selamectin administered topically in the treatment of feline otoacariosis. Vet Parasitol. 112:241–247. Chailleux N, Paradis M. 2002. Efficacy of selamectin in the treatment of naturally acquired cheyletiellosis in cats. Can Vet J. 43:767–770. Delucchi L, Castro E. 2000. Use of Doramectin for treatment of notoedric mange in five cats. J Am Vet Med Assoc. 216:215–216. Guaguere E, Olivry T, Delverdier-Poujade A, et al. 1999. Demodex cati infestation in association with feline cutaneous squamous cell carcinoma in situ: a report of five cases. Vet Dermatol. 10:61–67. Johnstone IP. 2002. Doramectin as a treatment for canine and feline demodicosis. Aust Vet Pract. 32:98–103. Scott DW, Miller WH, Griffin CE. 2001. Skin parasites of cats. In DW Scott, WH Miller, CE Griffin, eds., Muller & Kirk’s Small Animal Dermatology, 6th ed., pp. 18–29. Philadelphia: WB Saunders. Tackle GL, Hnilica KA. 2004. Eight emerging feline dermatoses. Vet Med. 99:456–467.
CHAPTER 202
Sporotrichosis Vanessa Pimentel de Faria
Overview
Diagnosis
Sporotrichosis is a mycotic disease of animals and humans caused by the dimorphic fungus Sporothrix schenckii. It is uncommon in cats. The organism is found worldwide and thrives best in soils that are rich in decaying plant material. Infection results from wound contamination (claws or teeth from another cat). It is most commonly identified in intact males and cats that roam outdoors. Sporotrichosis in cats, unlike in other host species, is characterized by large numbers of organisms in draining fluids and in tissue. For this reason, it represents a substantial public health hazard because infected cats may more readily transmit the disease to humans. Three clinical syndromes of feline sporotrichosis are known; these are localized or fixed cutaneous, lymphocutaneous, and multifocal disseminated. Sporotrichosis must be differentiated clinically from other opportunistic fungal infections, cryptococcosis, other systemic mycoses, feline leprosy syndrome, leproid granulomas, bacterial abscesses, foreign body reactions, sterile granuloma and pyogranuloma syndrome, reactive histiocytosis, and neoplasms. The lesions usually occur in sites commonly exposed or inoculated during cat fights: head, distal limbs, or tail base region (see Figure 202-1). Skin lesions develop at the site of percutaneous inoculation. First, fight wound abscesses, draining tracts, or cellulites appear. Second, the area becomes ulcerated, draining a purulent exudate, and forming crusted lesions. Finally, muscles and bones may be involved due to the extension of the affected area. The disease may be spread to other areas of the body via autoinoculation during normal grooming behavior. Most cats will have lymph node and lymphatic vessel involvement although not being apparent during physical examination. A history of anorexia, lethargy, and fever may occur when the disease is disseminated (see Figure 202-2).
Primary Diagnostics • Cytological Evaluation: Samples can be obtained from aspiration of abscesses or nodules, impression smears of ulcerated skin or exudate, smears of swab specimens, or skin scrapings. It is considered a simple, rapid, and inexpensive diagnostic method at all stages of the disease. No significant differences are observed between cytopathology, histopathology, and fungal culture during the different phases. The organism is often easily identified in the exudates from cats (see Figure 202-3). • Fungal Isolation: Samples of the exudates from deep within a draining tract and a sample of tissue surgically removed for a macerated tissue culture should be submitted for definitive diagnosis. S. schenckii grows on Sabouraud’s dextrose agar at 30°C. • Histopathologic Findings: The best specimens to submit are biopsy samples of newer, intact, nondraining lesions. Deep punch or wedge biopsy specimens should be obtained. In the feline lesions, organisms are frequently so numerous that they are readily demonstrated within the pyogranulomatous reaction, even on sections stained with H & E stain.
Secondary Diagnostics • Serologic Testing: A positive serologic testing result indicates exposure and not necessarily active infection. Therefore, it may be positive when cultures are negative. • Polymerase Chain Reaction (PCR) Testing: It can be used to identify the organism directly in biopsy specimens.
Diagnostic Notes • Sporotrichosis should always be suspected in cats with nonhealing, fight-wound abscesses. The possibility of sporotrichosis should be
Figure 202-1 of the tail.
This cat exhibits ulcerated lesions in the distal limbs and at the base
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 202-2 The disseminated form of the disease can be observed in this 2-year-old intact male cat.
487
SECTION 1: Diseases and Conditions
vomiting, anorexia, or depression) may occur but are less likely when compared with iodides and ketoconazole. Administration of any imidazole is contraindicated during pregnancy. Terbinafine and fluconazole may be useful alternatives when toxicities, side effects, or a poor response to treatment develop with the use of itraconazole. The treatment should be continued for at least 1 month beyond the apparent clinical cure (4–8 weeks).
Therapeutic Notes • Glucocorticoids and other immunosuppressive drugs are contraindicated both during and after the treatment of the disease. Concurrent bacterial infections should be treated for 4 to 8 weeks.
Prevention in Humans Humans handling cats with ulcerative lesions or open draining tracts should wear disposable gloves. Thereafter, they should remove the gloves and wash their forearms, wrists, and hands with povidone iodine or chlorhexidine solutions. Figure 202-3 Impression smear of exudate from an ulcerated lesion of a cat with sporotrichosis. Notice the high number of yeast-like forms of Sporothrix schenckii in macrophages and the extracellular spaces. Also note that the morphology of this sample is different from Figure 289-3 due to the pleomorphism of this organism. Diff Quick stain; 1000× magnification.
considered when the appropriate use of systemic antibiotics for a deep pyoderma or cellulitis results in minimal improvement.
Treatment Primary Therapeutics • Itraconazole is successful even in immunosuppressed cats and is the treatment of choice for sporotrichosis in cats. Capsules should be given at 5 to 10 mg/kg q 12 to 24h PO, preferably with food to increase absorption. The capsule may be opened and the contents divided into gelatin capsules or mixed into canned food. The oral solution has better bioavailability than the capsules. Side effects (e.g.,
488
Prognosis The prognosis for infected cats that are diagnosed early and treated aggressively is good; however, severely debilitated cats with advanced systemic disease have a guarded prognosis.
Suggested Readings Greene CE. 2006. Sporotrichosis. In Infectious Diseases of the Dog and Cat, 3th ed., pp. 608–612. Missouri: Saunders Elsevier. Gross TL, Ihrke PJ, Walder EJ, et al. Sporotrichosis. 2005. In TL Gross, PJ Ihrke, EJ Walder, eds., Skin Diseases of the Dog and Cat, 2nd ed., pp. 298–300. Ames, IA: Blackwell Publishing. Ferrer L, Fondati A. 1999. Deep mycoses. In Guaguère E, Prélaud P, eds., A Practical Guide to Feline Dermatology, pp. 5.2–5.4. Oxford: Blackwell Science. Scott DW, Miller WH, Griffin CE. 2001. Fingal skin disease. In DW Scott, WH Miller, CE Griffin, eds., Muller & Kirk’s Small Animal Dermatology, 6th ed., pp. 386–390. Philadelphia: WB Saunders Company.
CHAPTER 203
Squamous Cell Carcinoma, Cutaneous Bradley R. Schmidt and Mitchell A. Crystal
Overview Squamous cell carcinomas (SCC) make up 15 to 20% of feline skin tumors. Solar radiation is a contributing factor in tumor development. Affected cats usually have light or unpigmented skin; therefore white cats develop SCC approximately 13 times as frequently as do other cats, likely secondary to actinic damage from ultraviolet radiation exposure. Initially these lesions appear histologically as actinic keratosis (premalignant lesions) or carcinoma in situ (noninvasive cancers; see Figure 203-1) with subsequent development into invasive cancers over time. Siamese cats are underrepresented in most studies. Environmental tobacco smoke (ETS) exposure has been shown as a possible contributing factor in oral SCC; ETS has not been evaluated in cutaneous SCC. The mean age of cats with cutaneous SCC is 9 to 12 years. Common sites for tumor development are the nasal planum (80–90% of affected cats; see Figure 203-2), pinna (50% of affected cats; see Figure 203-3), eyelids (20% of affected cats; see Figure 203-3), and lips. Tumors generally appear as a proliferative or ulcerative, plaque-like or cauliflower-like lesion, with or without overlying crusts. Lesions are sometimes mistaken as nonhealing wounds. About one-third of affected cats have multiple facial lesions. Cutaneous SCC is locally invasive but rarely metastasizes; however, histologically aggressive tumors or advanced tumors may be associated with regional lymph node or pulmonary involvement. Differential diag-
noses include basal cell tumor, melanoma, mast cell tumor, cutaneous hemangioma or hemangiosarcoma, hair follicle tumors, sebaceous gland tumors, eosinophilic granuloma complex lesions, and panniculitis. A second form of cutaneous SCC is uncommon but has been described in cats: multicentric squamous cell carcinoma in situ (MSCCIS), also known as Bowen’s disease. MSCCIS is unrelated to sunlight; however, papillomavirus antigen has been demonstrated in 45% of affected cats. Concurrent Demodex infestation has been reported, possibly secondary
Figure 203-2 The nasal planum is the most common location for cutaneous SCC. Photo courtesy of Dr. Gary D. Norsworthy.
Figure 203-1 Carcinoma in situ is a non-invasive form of SCC as seen on the anterior aspect of this foot. Photo courtesy of Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 203-3 The pinna and eyelids are the second and third most common locations for SCC. Photo courtesy of Dr. Gary D. Norsworthy.
489
SECTION 1: Diseases and Conditions
to a local immunodeficiency state. Most cats are feline leukemia virus (FeLV) negative, but some cats were feline immunodeficiency virus (FIV) positive, possibly resulting in immunodeficiency predisposing to papillomavirus infections and Demodex infestations. It occurs most commonly in thick-haired, pigmented areas over the head, neck, shoulder, and forelimbs. Lesions appear as multiple well-circumscribed, melanotic, hyperkeratotic plaques that progress to become crusted and ulcerated and are generally painful. Lesions are confined to the epidermis, and metastasis has not been reported.
Diagnosis Primary Diagnostics • Surgical Removal or Incisional Biopsy and Histopathology: This is the most definitive means of diagnosis.
Secondary Diagnostics • Fine-Needle Aspiration and Cytology: This may reveal the diagnosis prior to surgery. Caution should be made in confirming a cytological diagnosis of epithelial malignancy when significant inflammation is present as atypical or dysplastic cells resembling neoplastic cells may accompany inflammatory lesions. • Lymph Node Fine-Needle Aspiration and Cytology: A fine-needle needle biopsy should be performed if regional lymphadenopathy is present. • Thoracic Radiographs: Although pulmonary metastasis is uncommon, thoracic radiographs should be performed prior to any aggressive therapy to evaluate for rare metastatic lesions as well as other cardiopulmonary abnormalities.
Diagnostic Notes • Diagnostic evaluation should be because early recognition is the Premalignant lesions (i.e., actinic should be managed as described malignancy.
pursued in any suspect lesion key to successful management. keratosis or carcinoma in situ) to prevent progression to overt
Treatment Primary Therapeutics • Surgery: Surgery is the mainstay of treatment in most cats with cutaneous SCC, with a favorable prognosis in most cats with smaller (less than 2 cm), superficial tumors. Surgical resection of lesions involving the pinna (see Figure 203-3) may be associated with a better prognosis (disease free intervals of greater than 1.5 years) than surgical resection of lesions involving the nasal planum because of the ability to perform a more aggressive surgery at that site. However, one study of eight cats with nasal planum SCC did report a median disease free interval of 16 months in five cats with resection of the nasal planum (nosectomy); three cats with more aggressive, invasive tumors of the nasal planum had tumor recurrence within 5 months of surgery. • Radiation Therapy: Radiation therapy is also considered a mainstay of treatment in cats with cutaneous SCC and may be considered in cats in which surgical resection is not possible or is incomplete or in cats with smaller lesions. Overall median disease-free intervals are reported to be at 12 to 16 months (range 0 to 2.7 years). Median survival times are reported at one year (range 4.5 months to 2.8 years). In cats with tumors of the nasal planum, the 1- and 5-year disease free
490
intervals were 60% and 10%, respectively. The 5-year disease free interval in cats with lesions smaller than 2 cm was reported to be 56%, suggesting tumor size was prognostic. Noninvasive plesiotherapy with Strontium 90 may be considered in cats with lesions less than 2 mm thick and may provide a 1-year disease free interval of 64 to 90% and a median survival of 946 days.
Secondary Therapeutics • Cryosurgery: Median disease-free intervals are reported at 8.5 months (range 46 days–5.6 years). Median survival times are reported at 1.9 years (range 5 months–5.8 years). In one study, cryosurgery in 102 cats with 163 lesions of the nasal planum, pinna, and eyelids achieved 1-year progression-free survival rates of 84%. This form of therapy is best for cats with tumors smaller than 0.5 cm in diameter. Cats with lesions of the nasal planum had a less favorable response. • Chemotherapy: Systemic chemotherapy with various agents has generally been unrewarding. Other reported therapies associated with some success have included intralesional chemotherapy with carboplatin or cisplatin (i.e., 73% complete response rate and 55% 1-year progression-free survival rate with intralesional carboplatin in sterile sesame oil in one study, and 64% complete response rate and a 20% partial response rate with intralesional cisplatin in a collagen matrix in another study). • Laser Surgery: Nd:YAG laser surgery was successful in treating a cat with nasal planum SCC. Four treatments were needed over 14 months. CO2 laser surgery has also been used successfully. See Figure 203-4. • Photodynamic Therapy: Laser excitation of an injected photosensitizing dye has been successful about 65 to 95% of the time with some cats achieving complete response. Success is related to minimal invasion and tumor size less than 5 cm. • The Use of COX-2 Inhibitors: These drugs, notably piroxicam, have limited potential for use in managing feline SCC. Although COX-2 is present in human and canine SCC, a study in cats demonstrated COX-2 in only 2 of 21 (9%) cats with oral SCC and in 0 of 6 (0%) cats with cutaneous SCC. No clinical reports of effectiveness are available for COX-2 inhibitors in cutaneous SCC, though a report of COX-2 inhibitor therapy (piroxicam) in feline oral SCC demonstrated 1 of 13 cats to have stable disease and 12 of 13 cats to have progressive disease.
Therapeutic Notes • Treatment of precancerous lesions (i.e., actinic keratosis, or noninvasive cancerous lesions [carcinoma in situ]) have been treated with various retinoic acids and carotenoids; however, response to therapy has not be consistently reported. Photodynamic therapy, cryosurgery, and topical treatment with imiquimod, a topically applied biological response modifier, all may offer some promise in treating non-invasive tumors (see MSCCIS). • Only a small amount of information exists on MSCCIS (Bowen’s Disease). Because the lesions are superficial, surgery often leads to local control, although lesions may develop at other sites. The lesions are variably responsive to plesiotherapy. Consistent response to chemotherapy has not been reported. A recent study evaluating 12 cats with MSCCIS treated with imiquimod, a topically applied biologic response modifier, reported that all cats initially responded to treatment, although most cats developed new lesions, which also responded to therapy. Side effects included local erythema, liver enzyme elevation, neutropenia, and gastrointestinal effects. A mean survival time of 243 days was reported in these cats. • Cats with solar radiation induced tumors should be kept out of direct sunlight.
Squamous Cell Carcinoma, Cutaneous
Prognosis Surgical resection is the primary therapy for most cats with cutaneous SCC. Tumor stage is prognostic for tumor control. Cats with smaller tumors of the pinna (less than 2 cm) have a good to guarded prognosis; fewer than half of the cats have tumor recurrence. The mean survival time for cats with larger tumors (>5 cm) is good with an average of 53 months; their tumor is likely to be controlled for a median of 9 months. The prognosis is generally unrelated to the location of the tumor, although tumors of the pinna often allow a more aggressive therapy and thus may be associated with a better outcome. Histological grade appears to be prognostic; 50% of cats with poorly differentiated tumors are likely to be euthanized within 12 weeks.
Suggested Readings
(A)
Beam SL, Rassnick KM, Moore AS, et al. 2003. An immunohistochemical study of cyclooxygenase-2 expression in various feline neoplasms. Vet Pathol. 40:4964–500. DiBernardi L, Clark J, Mohammed S, et al. 2002. Cyclooxygenase inhibitor therapy in feline oral squamous cell carcinoma. Proceedings of the Veterinary Cancer Society XXth Annual Conference, p. 19. Gill VL, Bergman J, Baer KE, et al. 2008. Use of imiquimod 5% cream (Aldara) in cats with multicentric squamous cell carcinoma in situ: 12 cases (2002–2005). Vet Comp Oncol. 6:55–64. Lana SE, Ogilvie GK, Withrow SJ, et al. 1997. Feline cutaneous squamous cell carcinoma of the nasal planum and the pinnae: 61 cases. J Am Anim Hosp Assoc. 33:329–332. Moore AS, Ogilvie GK. 2001. Skin tumors. In AS Moore, GK Ogilvie, eds., Feline Oncology, pp. 398–428. Trenton: Veterinary Learning Systems. Stell AJ, Dobson JM, Langmack K. 2001. Photodynamic therapy of feline superficial squamous cell carcinoma using topical 5-aminolaevulinic acid. J Small Anim Pract. 42(4):164–169. Vail DM, Withrow SJ. 2007. Tumors of the Skin and Subcutaneous Tissues. In SJ Withrow, EG MacEwen, eds., Small Animal Clinical Oncology, 4th ed., pp. 375–401. Philadelphia: Elsevier Saunders.
(B) Figure 203-4 (A) A CO2 laser was used one time to treat this SCC on the nasal planum. (B) Two years later there is no recurrence. Aggressive treatment of early lesions increases success. Photos courtesy of Dr. Gary D. Norsworthy.
491
CHAPTER 204
Stomach Worms Mitchell A. Crystal and Mark C. Walker
Overview Ollulanus tricuspis and Physaloptera spp. are nematode parasites of the feline stomach. Ollulanus causes gastric erosions and chronic fibrosing gastritis. Ollulanus is acquired via ingestion of infected vomitus. There is no extragastric migration; transplacental and transmammary infection do not occur. Clinical signs include vomiting, anorexia, and weight loss. Physical examination may be normal or reveal evidence of weight loss. The organism’s small size (about 1 mm) and unusual life cycle (neither eggs nor larvae are passed in the feces) make diagnosis of Ollulanus difficult. Physaloptera causes vomiting that is typically chronic and intermittent in nature; melena and anemia are rarely seen. It is acquired indirectly by ingestion of infected intermediate insect hosts (i.e., crickets, beetles, or cockroaches) or transport hosts (i.e., reptiles and small mammals). There is no extragastric migration; transplacental and transmammary infection do not occur. The developmental cycle of Physaloptera takes 131 to 156 days; the prepatent period for Ollulanus is from 33 to 37 days after ingestion of third stage larva. Physical examination may be normal or reveal evidence of weight loss.
Treatment Primary Therapeutics • Fenbendazole (Panacur®): This is felt to be possibly effective for Ollulanus and Physaloptera. Give 50 mg/kg q12h PO for 5 days. It is also effective for roundworms, hookworms, and whipworms. • Oxfendazole (Synanthic®): This is felt to be possibly effective for Ollulanus. Give 10 mg/kg q12h PO for 5 days. It is also effective for roundworms, hookworms, and whipworms. • Pyrantel Pamoate (Strongid®, Nemex®, generic): This is possibly effective for Physaloptera and Ollulanus. Give 20 mg/kg PO; even though the life cycle is long, a repeat dose in 3 weeks is recommended. It is also effective for roundworms and hookworms. • Ivermectin (Ivomec®): This may be effective for Physaloptera. Give 200 µg/kg PO. It is also effective for hookworms and roundworms. • Levamisole: This anthelmintic is believed to be effective for Ollulanus. Give as a 2.5% formulation or as a tablet at 5 mg/kg PO once. This agent is not available in the United States.
Therapeutic Notes Diagnosis Primary Diagnostics • Direct Microscopic Examination of Vomitus: Adults or larvae of Ollulanus may be seen. An emetic agent such as xylazine (0.2 mg/kg IV or SC) can be given to provide vomitus for examination. • Baermann Apparatus on Vomitus: Adults or larvae of Ollulanus are more likely to be seen because this is a concentrating technique. • Fecal Flotation: Thick walled larvated eggs of Physaloptera are sometimes seen. However, because the eggs are larvated, they often do not float during fecal examinations and may be missed.
Secondary Diagnostics • Endoscopic or Surgical Gastric Biopsy and Histopathology: Physaloptera may be seen as pink to white, stout worms, approximately 1 to 6 cm long, attached to the gastric mucosa. Ollulanus adults or larvae may be seen on histologic sections.
Diagnostic Notes • Ollulanus is a difficult parasite to identify. Histopathologic examination of three gastric mucosal sections may reveal Ollulanus in only half of the cats infected with the parasite. • Vomiting due to Physaloptera may be caused by a single worm.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
492
• Optimal therapy for naturally occurring O. tricuspis infection has not been definitively identified. This is likely a result of the uncommon incidence of the disease, the difficulty in initially identifying the parasite, and the difficulty in identifying whether the parasite is still present following therapy. • Other reports of effective therapy for Physaloptera include physical removal of worms via endoscope or at surgery.
Prognosis The prognosis for Physaloptera is good if identified and treated or removed. The prognosis for Ollulanus is uncertain (see problems noted previously). If Ollulanus leads to significant gastric fibrosis, clinical signs may persist despite effective therapy.
Suggested Readings Barr SC. 2007. Ollulanis infection. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult. Canine and Feline, 4th ed., p. 986. Ames, IA: Blackwell Publishing. Guilford WG, Strombeck DR. 1996. Chronic gastric diseases. In WG Guilford, DR Strombrek, DA Williams, et al., eds., Strombeck’s Small Animal Gastroenterology, 3rd ed., pp. 275–302. Philadelphia: WB Saunders. Jarvinen JA. 2007. Physalopterosis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult. Canine and Feline, 4th ed., pp. 1076. Ames, IA: Blackwell Publishing. Wilson RB, Presnell JC. 1990. Chronic gastritis due to Ollulanus tricuspis infection in a cat. J Am Anim Hosp Assoc. 26:137–139.
CHAPTER 205
Stud Tail Christine A. Rees
Overview Feline stud tail is due to hyperplasia of the supracaudal tail gland; this results in an accumulation of greasy material in the hair covering parts of the tail. This condition is seen mostly in intact males but can be seen in females and neutered males. A higher incidence has been reported in cage confined cattery cats or in cats with poor grooming habits. The greasy band-like strip occurs on the dorsum of the tail (proximal one-half to one-third). This can lead to the collection of dirt on the tail or matting in this area. When secondary infection occurs, the area can become painful. However, stud tail is most commonly considered a cosmetic problem.
Diagnosis Primary Diagnostics • Clinical Appearance: Stud tail is diagnosed most commonly by its distinct clinical appearance; see description. See Figure 205-1.
Figure 205-1 The typical greasy area on the dorsal aspect of the cranial 1/3 to 1/2 of the tail is the characteristic clinical presentation. The extent of the lesion is often not appreciated until the hair is shaved. Photo courtesy Dr. Gary D. Norsworthy.
Treatment Primary Therapeutics • Neutering: Castration does not resolve the condition but may stop its progression. • Isopropyl Alcohol: Isopropyl alcohol may be useful for removing sebaceous debris. • Benzoyl Peroxide: Shampoos containing this agent may be of benefit as maintenance treatment to keep sebum accumulation to a minimum, especially if the cat does not adequately groom the affected region. • Clipping: Clipping of the hairs in the affected area can be useful for more effectively applying topical medications. • Improvement of Grooming Habits: Self-grooming should be encouraged by minimizing the cat’s time in cage confinement. In addition, regular grooming and combing of the cat by the owner is also useful.
Prognosis The prognosis for stud tail is good for intact males following neutering. The prognosis for return to normal skin condition is guarded for neutered males and for females unless the treatment steps result in remission and the cat grooms adequately to control the problem. In all cases, study tail is considered a cosmetic issue.
Suggested Readings Scott DW, Miller WH, Griffin CE. 2001. Sebaceous gland diseases. In DW Scott, WH Miller, CE Griffin, eds., Muller & Kirk’s Small Animal Dermatology, 6th ed., pp. 14–29. Philadelphia: WB Saunders. Takle GL, Hnilica KA. 2004. Eight emerging feline dermatoses. Vet Med. 99:456–468.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
493
CHAPTER 206
Tail Injuries Sharon Fooshee Grace
Overview Traction or tail-pull injuries are common in cats and usually result from the tail being caught under the tire of a moving vehicle or in a closing door as the cat is running away. The tail is forcefully pulled away from the body, often resulting in separation of the sacrocaudal or caudocaudal vertebrae with concurrent trauma to the lumbar, sacral, or caudal nerve roots. Of particular concern are the pelvic, pudendal, and caudal nerves. Nerve injury may range from stretching to complete transection. Other associated injuries, may include degloving, fractures, or complete tail avulsion. Neurologic trauma is typically the issue of greatest concern and the most common reason for euthanasia. It is important to conduct a careful examination of the patient to determine the nature of all injuries. It is equally important to remember that many cats with apparent neurologic trauma from a tail-pull injury have the capacity to recover all or part of their neurologic function, given sufficient time, if there are no other lifethreatening injuries. In some cases, the patient has no detectable abnormality other than hyperesthesia over the base of the tail. The patient experiencing total fecal and urinary incontinence is at the other end of the clinical spectrum. The classification scheme used to characterize sacrocaudal fractures can be broadly applied to cats with tail-pull injuries (even if fractures are not present) as a means of systematically assessing neurologic dysfunction and approximating a prognosis. This approach is useful because cats with denervation of the tail often have some degree of denervation to the pelvic viscera. In this scheme, tail-pull injuries may be classified into four groups based on severity of clinical signs. See “Diagnostic Notes” for more information on assessment of specific pelvic nerves. Group 1: Cats in this group have some degree of analgesia and diminished motor function of the tail. Anal tone and perineal sensation are normal, and the bulbourethral and perineal reflexes are intact. These reflexes are tested by gently pinching the external genitalia and perineal skin and observing reflex contraction of the anus. There are no observed abnormalities of micturition (including posturing for micturition). Pudendal and pelvic nerves have normal function in these cats. Group 2: Cats in this group have some degree of analgesia and diminished motor function of the tail. Anal tone and perineal sensation are normal, perineal and bulbourethral reflexes are intact, and the cat can posture to urinate; these findings indicate intact pudendal nerve function. However, the cat is unable to void normally because inadequate detrusor function is coupled with inadequate urethral relaxation. Small amounts of urine may be voided voluntarily, but a large residual volume can be palpated. The bladder may empty with gentle steady manual compression or may be very difficult to express. These findings indicate damage to the pelvic nerve or its sacral roots (S1–S3). The pelvic and pudendal nerves travel together through the sacral roots, but the pelvic nerve is more fragile and can be selectively damaged. Group 3: Cats in this group have flaccid analgesic tails with diminished anal tone and perineal sensation, and decreased perineal and bulbourethral reflexes. Despite having a greatly distended atonic bladder, they do not attempt to urinate. Attempts to manually express the bladder are met with normal to increased urethral resistance caused by dyssyn-
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
494
ergia between the detrusor and sphincter muscles. Cats in this category have damage to the caudal, pelvic, and pudendal nerve fibers or segmental damage to the spinal cord. Group 4: Cats in this group have a flaccid analgesic tail, no anal tone or perineal sensation, and the bladder is easy to manually express. They have complete urinary and fecal incontinence. The caudal, pelvic, and sacral nerves have complete interruption.
Diagnosis Primary Diagnostics • Physical Examination: A thorough physical examination is necessary to identify and determine the extent of all injuries, with tail trauma usually the most obvious abnormality. Assessment should include determination of normal motor ability and ability of the cat to ambulate; presence of anal tone and perineal sensation; status of the bulbourethral and perineal reflexes; bladder tone and size; and, voluntary motor activity and sensation of the tail. • Urine Output and Color: If the patient has received fluids, urine should be produced within a few hours. The color and volume should be noted. Presence of blood indicates trauma to the urinary tract. Lack of urine production can indicate bladder rupture or displacement, ureteral avulsion, or a urethral tear. • Diagnostic Imaging: Caudal abdominal radiographs should be taken in both orthogonal planes. If the cat is lame or weak, the hindlimbs should also be evaluated. Careful attention should be given to the potential for sacral, pelvic, and femoral fractures. A positive contrast cystogram may be performed if there is concern that the bladder has ruptured.
Secondary Diagnostics • Urodynamic Studies: Specific assessment of urologic function may occasionally require referral for urodynamic studies, such as a cystometrogram and urethral pressure profiling.
Diagnostic Notes • Most cats will achieve the bulk of anticipated neurologic recovery within the first month. A few cats will continue to improve up to 8 weeks after the injury. • There is a high degree of correlation between urinary continence and fecal continence because of the interdependence between pelvic and pudendal nerve function. If decreased anal tone is present, there is a high likelihood that urinary incontinence will also be present. • Caudal Nerve Roots: Caudal nerve roots supply sensory and motor function to the tail. Damage to caudal nerve roots results in a flaccid, hypalgesic, or analgesic tail. • Pudendal Nerve: The pudendal nerve originates in the sacral spinal cord at S1 to S3 and supplies somatic (voluntary) innervation to striated muscle of the anal and urethral sphincters and sensory innervation to the perineum and genitalia. Pudendal nerve damage results in a dilated, areflexic anus, lack of perineal sensation, fecal incontinence, and an atonic external urethral sphincter. Urinary incontinence is usually incomplete if some function of the internal urethral
Tail Injuries
sphincter is retained. Function of the pudendal nerve can be determined through evaluation of anal tone and sensation to the perineum and genitalia. • Pelvic Nerve: The pelvic nerve originates in the sacral spinal cord at S1 to S3 and supplies parasympathetic motor and sensory innervation to the bladder, rectum, and genitalia. This nerve is vital for the detrusor reflex of the bladder and for maintaining normal resting tone of the colon and rectum to aid in fecal propulsion during defecation. Pelvic nerve damage results in uncoordinated, ineffectual attempts at urination and overflow incontinence. Feces may accumulate in the colon. Function may be checked by observing the cat urinate and determining the amount of residual urine. Normal urine volume should be less than 2 mL after micturition.
Treatment Primary Therapeutics • Sacrocaudal Fracture: These fractures are difficult to repair and will often stabilize with medical management alone. Most cats with a sacrocaudal fracture have an avulsive rather than a compressive injury. • Degloving of the Tail: Complete degloving of the tail necessitates amputation. Otherwise, the tail should be amputated at the level of the degloving injury. See Figure 206-1. • Lower Urinary Tract Dysfunction: For information on pharmacologic management of the lower urinary tract of cats in groups 2, 3, and 4, see Chapter 151.
Secondary Therapeutics • Fluid Therapy: Fluids should be administered as needed for cats sustaining trauma. See Chapter 302. • Manual Expression of Bladder: The bladder should be expressed several times a day until function returns. If the bladder cannot be expressed, the bladder should be catheterized at least twice a day or an indwelling catheter placed and attached to a closed collection system. It is critical that the bladder not have excess distention, which may irreversibly damage the detrusor muscle. • Constipation: Feces that accumulate in the colon will dehydrate and become difficult to pass. See Chapter 40 for management of constipation. For most cats, this is a transitory problem that can be managed with adding fiber to the diet or with the use of stool softeners.
Therapeutic Notes • Tail amputation should not be performed at the time of initial diagnosis unless it is fractured, degloved, has ischemic necrosis, becomes frequently soiled with urine or feces, or is persistently painful. Determination of blood flow can be made by making a blood pressure measurement near the distal end of the tail. Many cats recover function of the tail.
Figure 206-1 This cat has experienced complete degloving of the tail; tail amputation is indicated. Photo courtesy Dr. Gary D. Norsworthy.
• Cats with lower urinary tract dysfunction should be carefully monitored for bladder infection.
Prognosis Cats in group 1 and 2 have a good prognosis for recovery. Tail function will be recovered and most cats in group 2 will recover urinary function. About 75% of group 3 cats will recover with good medical management. Cats in group 4 have a more guarded prognosis but still have up to a 50% chance of some recovery.
Suggested Readings Flanders JA. 1991. Sacrocaudal fractures. In JR August, ed., Consultations in Feline Internal Medicine, pp. 493–495. Philadelphia: WB Saunders. Kot W, Partlow GD, Parent J. 1994. Anatomical survey of the cat’s lumbosacral spinal cord. Prog Vet Neuro. 5(4):162–166. Kuntz CA. 2000. Sacral fractures and sacrococcygeal injuries in dogs and cats. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIII; pp. 1023–1026. Philadelphia: WB Saunders. Smeak DD, Olmstead ML. 1985. Fracture/luxations of the sacrococcygeal area in the cat: A retrospective study of 51 cases. Vet Surg. 14(4): 319–324.
495
CHAPTER 207
Tapeworms Mitchell A. Crystal and Mark C. Walker
Overview Tapeworms are small intestinal cestode parasites that cause few, if any, clinical signs. Dipylidium caninum and Taenia spp. are the most common tapeworms seen in the cat. D. caninum is acquired via ingestion of infected fleas, and Taenia spp. are acquired via ingestion of infected small mammals. There is no extraintestinal migration, and transplacental and transmammary infections do not occur. The most common problem associated with tapeworm infection is the owner complaint of seeing proglottid sections within the feces or on the perianal hair. Physical examination is normal. Rarely, in the southeast United States, infection with the tapeworm Spirometra spp. occurs. This cestode is acquired by ingestion of infected small mammals and can lead to diarrhea.
Secondary Diagnostics • Proglottid Squash Preparation: A proglottid can be squashed in a drop of water between two microscope slides. D. caninum eggs are organized into an egg basket containing 20 to 30 eggs. Taenia spp. are liberated as single eggs. See Figure 207-3.
Diagnostics Primary Diagnostics • History: Clients may report seeing proglottid (small tapeworm segment) sections in the feces or on the cat’s perianal area. • Direct Examination of Feces: Proglottid sections, often moving on the surface of the stool, may be seen, although this is not consistent so a negative examination is not a rule out. See Figure 207-1. • Examination of the Perianal Area: Dried proglottid sections may be seen on hair, and moving proglottid sections may be seen near or within the anus. See Figure 207-2. Figure 207-2 Dried proglottids may be seen stuck to the hair of the perineal region. Photo courtesy Dr. Gary D. Norsworthy.
Figure 207-1 Proglottids may be seen on the surface of the stool or in mucus that accompanies a bowel movement. Photo courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
496
Figure 207-3 Rupturing a D. caninum proglottid will release egg baskets containing 20-30 eggs. Photo courtesy Dr. Gary D. Norsworthy.
Tapeworms
• Fecal Sedimentation and Floatation: Single eggs of Taenia spp. or (if the egg baskets have been ruptured) D. caninum may be seen. Single operculated eggs of Spirometra spp. may be seen, usually on sedimentation and occasionally on floatation.
Diagnostic Notes • The importance of identifying the specific type of tapeworm lies in prevention. If D. caninum is identified, flea control is needed. If Taenia spp. or Spirometra spp. is identified, prevention of ingestion of small mammals is needed.
drugs should be considered 100% efficacious so a second treatment is acceptable. • Treatment of Spirometra spp. requires higher doses (1.5 times) of praziquantel and may require treatment for several days. • Prevention (flea control for D. caninum, predatory behavior/ scavenging control for Taenia spp. and Spirometra spp.) will help stop reinfection.
Prognosis The prognosis is excellent because these worms are essentially nonpathogenic, and the anthelminthics are effective.
Treatment Suggested Readings Primary Therapeutics • Praziquantel (Droncit®): Administer 3 to 7 mg/kg PO or SC. • Epsiprantel (Cestex®): Administer 2.75 mg/kg PO. • Praziquantel/Pyrantel Pamoate (Drontal®): Administer according to label direction PO; also effective for hookworms and roundworms. • Emodepside and Praziquantel (Profender®): Topical therapy. Give 3 mg/kg emodepside and 12 mg/kg praziquantel.
Secondary Therapeutics
Hall EJ, German AJ. 2005. Helminths. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1358–1359. St. Louis: Elsevier Saunders. Jarvinen JA. 2007. Tapeworms (Cestodiasis). In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult. Canine and Feline, 4th ed., pp. 1322. Ames, IA: Blackwell Publishing. Reinemeyer CR. 1992. Feline gastrointestinal parasites. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XI. Small Animal Practice, pp. 13584–1359. Philadelphia: WB Saunders.
Therapeutic Notes • Only one treatment is necessary for D. caninum and Taenia spp. because there is no tissue migratory phase. However, none of the
497
CHAPTER 208
Tetanus Sharon Fooshee Grace
Overview Tetanus, an uncommon bacterial disease of cats and dogs, is caused by the gram-positive anaerobic spore-forming bacillus Clostridium tetani. Both cats and dogs have a natural resistance to development of tetanus. The organism is ubiquitous in the environment and part of the normal intestinal flora of humans and mammals. Clinical disease occurs when bacterial spores are traumatically introduced into tissues with low oxygen tension and subsequently convert to a vegetative, toxin-producing form. Elaborated toxins cause tissue necrosis and a local environment favorable to further bacterial growth and toxin elaboration. Tetanospasmin toxin gains entry to nerves at neuromuscular junctions and travels to the spinal cord by axonal transport. Toxin may remain at the level of the spinal cord or ascend the cord bilaterally to the brain; hematogenous spread affects distant neuromuscular junctions or can enter the brain via the ventricles. Binding of toxin is irreversible and recovery depends entirely on growth of new axonal terminals, a process requiring approximately 3 weeks. The clinical syndrome of tetanus is derived from the effects of toxin on the spinal cord and brain, neuromuscular junctions, and autonomic nervous system. Toxin binds to and is internalized by inhibitory interneurons of the brain and spinal cord, preventing release of inhibitory neurotransmitters γ-aminobutyric acid (GABA) and glycine. The result is blockage of neuronal inhibition of skeletal muscle and a dysfunctional autonomic nervous system. Generalized skeletal muscle spasm, especially of the face and extensor muscle groups of the extremities, is the finding classically associated with tetanus. Clinical signs usually manifest within 5 to 10 days following spore inoculation, though this is dependent on proximity of the injury to the central nervous system, local oxygen tension, and the amount of toxin produced in the wound. The innate resistance of cats to tetanus has been known to delay onset of signs for several weeks. Signs may be localized or generalized; localized disease may later become generalized. Cats and dogs are more often affected by localized tetanus, whereas humans typically have the generalized form. Wounds near the head result in more rapid onset and generalization of signs. Localized disease is associated with increased muscle tone in proximity to the site of infection. See Figure 208-1. With generalized disease, widespread muscle ridigity gives the patient a “sawhorse” appearance and a stiff gait. Animals unable to stand exhibit full body rigidity and opisthotonos. Other reported findings include an outstretched or elevated tail, third eyelid prolapse, enophthalmos, and elevated whiskers. Tetanic spasm of facial muscles causes the forehead to have a wrinkled appearance and the face to have a sneering expression as the lips are drawn back (“risus sardonicus”). Dysphagia and trismus result from pharyngeal and masticatory muscle spasm. Dysuria, urine retention, and constipation are caused by sphincter hypertonicity. Increased salivation and respiratory secretions, tachycardia, tachypnea, and laryngeal spasms are also common. Rectal temperature is usually increased due to muscular activity. Severely affected patients are profoundly sensitive to sensory stimulation and will respond with tonic contracture of muscles. This may culminate in seizures and death.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
498
Figure 208-1 This cat demonstrates localized tetanus of the hind limbs. In cats, localized tetanus is more common than the generalized form. (Image courtesy Dr. Vanessa Pimentel de Faria).
Differential diagnoses for generalized tetanus include strychnine toxicosis, hypocalcemia, encephalitis, and decerebrate rigidity.
Diagnosis Primary Diagnostics • Physical Examination: The presence of a penetrating injury or open wound coupled with appropriate clinical signs provides good supportive evidence for a tentative diagnosis.
Secondary Diagnostics • Electrocardiography: A variety of arrhythmias have been reported with tetanus.
Diagnostic Notes • Tetanus does not produce any characteristic abnormalities on routine bloodwork, though creatinine kinase may be elevated because of muscle activity and recumbency. • Tetanus localized to the pelvic limbs has been associated with the reproductive tract in cats and dogs.
Treatment Primary Therapeutics • Wound Debridement: The wound should be irrigated thoroughly and abscessed areas drained. Hydrogen peroxide will increase oxygen tension in the wound. Foreign material should be removed if identified. Antitoxin should be given prior to wound debridement because toxin will be released into circulation.
Tetanus
• Control of Infection: Penicillin G is the preferred drug for generalized tetanus (20,000 U/kg q4–6h IV for 10 days). It has superior activity to other forms of penicillin and their derivatives. Penicillin G may be given IV as the sodium or potassium salt or IM as the procaine salt; procaine penicillin may also be injected near the wound site. Amoxicillin (20 mg/kg q12h PO) has been used for localized tetanus. Some clinicians avoid penicillin because it is a GABAantagonist, as is the toxin itself. In such cases, metronidazole (15 mg/ kg q12h PO or IV for 7 to 14 days) is a good alternative because it has superior wound penetration and activity. It has been associated with drug toxicity (neurologic signs) at high doses. Fluoroquinolones do not have reliable activity against anaerobes such as C. tetani and should not be used. • Neutralization of Toxin: Antitoxin neutralizes only unbound circulating toxin; it has no effect on bound toxin. Therefore, it should be administered as soon as possible, though it does not necessarily speed the rate of recovery. It may not be needed for localized disease. Only a single dose is needed. Dosage recommendations have not been standardized for cats and dogs. Two products are available: human tetanus immunoglobulin, dosed 500 to 1000 IU IM in several locations proximal to the wound, and equine antitetanus serum, dosed 100 to 1000 IU IM or SC in several locations proximal to the wound or IV. Intravenous therapy is superior to intramuscular or subcutaneous administration although it is associated with a greater likelihood of anaphylaxis. Products containing thimerosal should not be given IV. A small intradermal test dose (0.1–0.2 mL) should be given 15 to 30 minutes prior to administration to test for hypersensitivity to the product. If a reaction is anticipated, the animal may be pretreated with glucocorticoids and antihistamines. Epinephrine (0.1 mg/kg diluted 1 : 10,000) should be given if anaphylaxis occurs. • Sedation: A number of sedatives have been used with success. These include diazepam (0.2–5.0 mg/kg q2–4h IV; titrate to lowest effective dose); acepromazine (0.02–0.06 mg/kg q2–4h IV); and, chlorpromazine (0.5–2 mg/kg q6–8h IV). Some clinicians prefer chlorpromazine because it works centrally on the brainstem to depress excitatory input to lower motor neurons. Phenobarbital is useful for grand mal convulsions (1–4 mg/kg q6–12h IM or PO). It may have to be given every few hours; the dose should be adjusted to severity of signs. The clinician must be observant for evidence of respiratory depression caused by the drug and the cumulative effects of all drugs given. • Muscle Relaxation: Methocarbamol is occasionally used but is hampered by a short duration of action. It may be given as a constant rate infusion with a maximum daily dose of 330 mg/kg per day. • Control of Airway Secretions and Bradycardia: Either atropine (0.05 mg/kg IV as needed) or glycopyrrolate (0.005–0.011 mg/kg IV as needed) may be used.
Secondary Therapeutics • Environment: A dark, quiet environment is essential. Treatments should be coordinated so as to disturb the patient as infrequently as possible. Cotton balls may be placed in the ears to decrease sound transmission.
• Fluid Therapy: Fluid support is indicated in severe cases. The clinician should be mindful of the beeping of fluid pumps, which can trigger tetanic spasms or convulsions. • Nutrition: Animals with tetanus are hypermetabolic. Some have difficulty eating and swallowing and others are unable to do either. Some animals have been reported to suck fluids or blenderized food through clenched teeth. If this is not possible, a feeding tube is suggested, especially with generalized disease. Small amounts should be provided frequently as reflux is common. Syringe feeding, nasoesophageal tubes, and orogastric tube feeding are contraindicated. • Bowel and Bladder Support: Enemas may be needed if constipation becomes problematic. If the bladder cannot be gently expressed, urinary catheterization may be necessary. Patients should be turned and bedding changed every few hours to avoid decubital ulcers; ideally, this is coordinated with treatment times.
Therapeutic Notes • In cats with localized tetanus, which is not progressive, all of the therapeutic steps noted may not be required. However, some reported cases of localized disease have appeared stable and then subsequently progressed. • Reported adverse reactions with antitoxin administration are anaphylaxis, anaphylactoid reactions, and serum sickness. • Animals surviving the initial phase of disease may require prolonged supportive care. • Severely affected animals may need to be placed under general anesthesia with positive pressure ventilation, a situation often requiring referral to a specialty center. Financial constraints of owners usually result in euthanasia of the animal.
Prevention Cats and dogs are not vaccinated against tetanus because of their innate resistance. Recovery from disease does not confer immunity.
Prognosis The prognosis is variable, with mild and localized disease offering the best chance for recovery. Some cats have spontaneous recovery from disease without intervention. Mildly affected animals may begin to improve in 1 to 2 weeks. In generalized disease, respiratory difficulty or respiratory arrest may lead to death.
Suggested Readings DeRisio L, Gelati A. 2003. Tetanus in the cat—An unusual presentation. J Fel Med Surg. 5:237–240. Greene CE. 2006. Tetanus. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 395–402. Philadelphia: Saunders Elsevier. Linnenbrink T, McMichael M. 2006. Tetanus: Pathophysiology, clinical signs, diagnosis, and update on new treatment modalities. J Vet Emerg Critical Care. 16(3):199–207.
499
CHAPTER 209
Tetralogy of Fallot Larry P. Tilley
Overview Tetralogy of Fallot is the most commonly occurring cyanotic heart disease in the cat. The components of tetralogy of Fallot include pulmonic stenosis, right ventricular concentric hypertrophy, a subaortic ventricular septal defect, and an overriding aorta. See Figure 209-1. A right-to-left shunt results secondary to the right ventricular outflow obstruction caused by the pulmonic stenosis. Cyanosis is a blue discoloration of the mucous membranes that usually indicates a significant amount of desaturated hemoglobin (3-5 g/dL). Pulmonary atresia represents the exaggerated form of tetralogy of Fallot, inasmuch as the distal right ventricular outflow tract is atretic and the main pulmonary artery is a thin, nonfunctioning vessel. A murmur of pulmonic stenosis is often absent in these cases.
Physical examination usually demonstrates a left basilar systolic ejection-type murmur. A soft systolic murmur associated with the ventricular septal defect may also be evident over the right hemithorax, although this finding is variable.
Diagnosis Primary Diagnostics • Echocardiography: The echocardiogram reveals right ventricular concentric hypertrophy, subaortic ventricular septal defect, overriding of the aorta, high velocity turbulent systolic flow across the right ventricular outflow tract as demonstrated by spectral or color-flow Doppler, and right-to-left shunting as demonstrated by contrast echocardiography (bubble study). Aortic regurgitation, as demonstrated by Doppler echocardiography, may also be present.
Secondary Diagnostics • Electrocardiography: Right-axis deviation is commonly present. • Thoracic Radiography: Right atrial and ventricular enlargement, dilated proximal pulmonary artery secondary to pulmonic stenosis, pulmonary vascular undercirculation, and an enlarged caudal vena cava may be present. • Nonselective Angiography: This procedure is useful in evaluating the pulmonary vascularity. • Packed Cell Volume: Polycythemia is present in most cases.
Diagnostic Notes • Cardiac catheterization and selective angiocardiography are rarely needed to substantiate the diagnosis of tetralogy of Fallot.
Treatment Primary Therapeutics • Surgical Palliation: The purpose of surgery is to create a systemic-to-pulmonary shunt to increase pulmonary flow, left atrial venous return, and arterial oxygen content. Specific procedures include the Blalock-Taussig (connection of the subclavian artery to the pulmonary artery) and Waterson-Cooley or Potts (connection of the aorta to a lobar or the main lobar pulmonary artery) operations.
Figure 209-1 The four components of tetralogy of Fallow include pulmonic stenosis (1), a subaortic ventricular septal defect (2), right ventricular concentric hypertrophy (3), and an (4) overriding aorta.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
500
Secondary Therapeutics • Periodic phlebotomy with IV fluid replacement to maintain the PCV below 62% can be effective in some cats. • Exercise: Restriction is encouraged. Beta blockade may reduce myocardial oxygen consumption, decrease heart rate, decrease right-to-left shunting by increasing left ventricular afterload, and provide a positive lusitropic effect (increased relaxation) of the right ventricle.
Tetralogy of Fallot
Therapeutic Notes • Cats may tolerate the defect for years; however, chronic hypoxia, polycythemia and hyperviscosity syndrome, exercise intolerance, or seizure-like activity commonly occur. • Sudden cardiac death is more likely to occur than congestive heart failure. • Surgical palliation can reduce clinical signs and increases survival times. • Surgical palliation is effective only if the pulmonary arteries are of sufficient diameter and available for anastomosis. Mortality is high with surgery. • The efficacy of β-blockers has not been proven in veterinary medicine.
Prognosis The prognosis of tetralogy of Fallot is guarded-to-poor. Clinical signs may be palliated with surgery. However, few facilities routinely perform the surgical procedures, and significant complications are possible.
Suggested Readings Kittleson MD. 1998. Tetralogy of Fallot. In MD Kittleson, RD Kienle, eds., Small Animal Cardiovascular Medicine, pp. 240–247. St. Louis: Mosby.
501
CHAPTER 210
Thiamine Deficiency Gary D. Norsworthy
Overview Thiamine is an essential, water-soluble B vitamin (B1) that is a co-factor in several steps in the Krebs cycle. Deficiency of thiamine blocks central nervous system (CNS) aerobic metabolic pathways due to polioencephalomalacia in the gray matter of the brain stem. Because it cannot be manufactured by the cat, it must be supplied by the diet. Thiamine deficiency occurs secondary to consumption of large quantities of uncooked fish (especially tuna or salmon) that contain thiaminase in the viscera, consumption of diets containing the meat preserver sodium metabisulfite, or diets that are thiamine deficient due to improper processing (especially over-cooked meats). Cooking destroys thiaminase in fish. After about 2 to 4 weeks of a thiamine-deficient diet, cats salivate excessively and stand over the food bowl as if to eat but eat only small amounts of food. After another 2 to 4 weeks, the cat experiences brief tonic seizures, cervical ventroflexion with rigid muscles (see Figure 2101), and the loss of righting reflexes. Bradycardia, pronounced sinus arrhythmia, bilateral dilated pupils, and retinal hemorrhages may also occur. If the cat is not treated at this stage, coma and death ensue.
• Clinical Signs: The clinical signs are listed in the Overview. The most common sign on presentation is cervical ventroflexion. • Response to Therapy: Cats treated with injectable thiamine (10– 20 mg IM) return to normal within 24 hours. Such response is diagnostic.
Diagnostic Notes • The cervical ventroflexion of thiamine deficiency differs from cervical ventroflexion due to organophosphate toxicosis or hypokalemic polymyopathy in that thiamine deficiency causes a rigid paralysis of the cervical muscles. In the other two diseases mentioned, weakness due to flaccid paralysis occurs. Thiamine deficiency also produces torticollis, head tilt, behavioral changes or seizure-like paddling or spasticity with opisthotonos. • Because thiamine is non-toxic, a test dose is indicated for cats, especially kittens, that are showing signs of cervical ventroflexion.
Treatment Diagnosis Primary Therapeutics Primary Diagnostics • Dietary History: A thiamine-deficient diet, especially consisting of large quantities of uncooked fish, is typical. Eating overcooked meats is another indicator.
• Thiamine: Cats suspected of having thiamine deficiency should be given 5 to 30 mg q24h PO or 25 to 50 mg IM. Oral thiamine should be given for at least 1 week while the diet is being corrected. • Diet Change: Affected cats should be placed on a balanced feline diet.
Therapeutic Notes • If dextrose is given to a cat with thiamine deficiency, it will be utilized quickly and undergo abnormal metabolism, leading to lactic acid buildup. If thiamine deficiency is a possibility, 25 mg of thiamine should be given IM prior to dextrose administration. • Cats that recover but refuse to eat any other diet than the thiaminedeficient one can be supplemented with 30 to 50 mg/cat q24h of oral thiamine to prevent recurrence.
Prognosis The prognosis for thiamine-deficient cats is excellent if proper treatment is rendered and the cat’s diet is changed to one with adequate thiamine.
Suggested Readings Figure 210-1 Cervical ventroflexion with rigid cervical muscles is a characteristic of thiamine deficiency. Note the wet front feet due to excessive salivation. Confirmation can be made with resolution of clinical signs within a few hours to 25 mg of thiamine given IM.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
502
Gunn-Moore D. 2006. The cat with neck ventroflexion. In J Rand, ed., Problem-Based Feline Medicine, pp. 890–905. Philadelphia: Elsevier Saunders. O’Brien DP, Kline KL. 1997. Metabolic Encephalopathies. In JR August, ed., Consultations in Veterinary Internal Medicine, 3rd ed., pp. 373–379. Philadelphia: WB Saunders. Podell M. 2006. Neurologic Manifestations of systemic disease. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 798–802. St. Louis: Elsevier Saunders.
CHAPTER 211
Third Eyelid Diseases Gwen H. Sila and Harriet J. Davidson
Overview The third eyelid, also referred to as the nictitating membrane, is located in the medial and ventral aspect of the orbit rostral to the globe. It is covered by conjunctival tissue, which lines the inside of the eyelids. Within the center of the third eyelid is a T-shaped cartilage, which provides stability. At the base underneath the cartilage is a serous lacrimal gland, which provides approximately 33% of the tear film. The third eyelid moves across the surface of the eye by passive movement. Contraction of the retractor bulbi muscle pulls the globe deeper into the orbit, which results in the third eyelid moving up and across the eye. In the cat there is a small portion of smooth muscle, which is innervated by sympathetic nerves, within the third eyelid. This muscle is extremely small and plays no significant role in its movement. The function of the third eyelid is to protect the cornea from external damage and help spread the tear film evenly. Problems that affect the conjunctiva may also affect the third eyelid. See Chapter 124. Elevation of the third eyelid is the most common symptom prompting consultation for a third eyelid abnormality. There are multiple possible causes that need to be considered. Haws is a lay term used to describe a prominent third eyelid. In some cases haws refers to a condition of bilateral prominent third eyelids and accompanying diarrhea. The cause of this syndrome is unknown but tends to be self-limiting after 4 to 8 weeks. Horner ’s syndrome is a collection of clinical signs that includes third eyelid prolapse, miosis, enophthalmos, and ptosis, or drooping of the superior eyelid. The cause of this syndrome is loss of sympathetic innervation of the eye and surrounding ocular structures. The lesion resulting in sympathetic denervation may occur at the level of the brain stem, along the spinal cord down to T1 to T3 where the nerves exit, along the vagosympathetic truck to the cranial cervical ganglia, and within tissues surrounding the ear. See Chapter 99. Systemic or ocular pain (i.e., corneal ulcer, uveitis, and glaucoma) may result in contraction of the extraocular muscles, pulling the globe deep into the orbit and resulting in prolapse of the third eyelid. A foreign body may become lodged between the globe and the third eyelid causing both active globe retraction and subsequent forward displacement of the third eyelid. General malaise or dysautonomia may result in passive movement of the third eyelid due to lack of normal extraocular muscle innervation, which allows the globe to passively sink into the orbit. Loss of orbital tissue from dehydration, fat or muscle atrophy, or fibrosis may result in the passive movement of the globe deeper into the orbit thus moving the third eyelid forward. Any space occupying mass behind the eye such as a neoplasm, abscess, or cellulitis may physically push the third eyelid forward. Prolapse of the gland of the third eyelid (“cherry eye”) may occur. Although this is an uncommon condition in cats, it has been reported in the Burmese as a suspected genetic disorder. See Figure 211-1. The connective tissue that holds the gland in place breaks down and allows the distal end of the gland to flip dorsally, while still remaining under the conjunctival tissue. This appears as a round, soft, red to pink, swelling beneath the leading edge of the third eyelid.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 211-1 The gland of the right third eyelid is prolapsed. This is thought to be a genetic disease in Burmese. Image courtesy Dr. Gary D. Norsworthy.
Diagnosis Primary Diagnostics • Clinical Signs: The prominent third eyelid will be more visible than in a normal cat. If the condition is bilateral the following etiologies should be considered: dehydration, fat or muscle atrophy, generalized pain or malaise, dysautonomia, and haws. If the condition is unilateral it is more likely caused by orbital neoplasia, infection, ocular pain, or Horner ’s syndrome. These are general statements with several notable exceptions. A prolapsed gland of the third eyelid is generally diagnosed by clinical appearance and palpation. The swelling should be digitally palpated following application of topical ophthalmic anesthetic. A prolapsed gland will generally be soft and moveable. In many cases the gland may be temporarily replaced by gently pushing it downward, between the globe and the third eyelid, with a cotton tip applicator or by pushing caudally on the dorsocranial aspect of the globe. If irregular or firm swelling of gland is present, a fine-needle aspirate may help rule out neoplasia. • Physical Examination: Examination of the face for evidence of asymmetry of the globes and eyelids should be part of a thorough physical examination. These clinical findings will help determine if there is evidence of neurologic disease, including dysautonomia or possible systemic problems. Pain on opening the mouth is a sign of postorbital disease. Swelling behind the last molar may indicate postorbital infection or neoplasia. • Ophthalmic Examination: This should include pupillary light reflexes, Schirmer tear test, fluorescein stain, intraocular pressure determination, retropulsion of the globes, and examination behind the third eyelid. These tests will help rule out certain conditions, including foreign bodies and Horner ’s syndrome, as the cause of the prominent third eyelid.
503
SECTION 1: Diseases and Conditions
(C) (A)
(B) Figure 211-2 Any retrobulbar mass can cause prolapse of the third eyelid. In the majority of cases these masses are malignant tumors, although cellulitis is another differential. This cat had a soft tissue mass in the orbit caudal to the globe as seen on ultrasound (A). The cat’s systemic blood pressure was 260 mmHg, severe retinal hemorrhage were present bilaterally, and the third eyelid was prolapsed (B). After three weeks of medication to normalize blood pressure the mass was no longer visible on an ultrasound study, and the third eyelid had returned to its normal position (C). The mass was presumed to be a retrobulbar blood clot. Retrobulbar hemorrhage is an extremely unusual finding with hypertension. Images courtesy Dr. Gary D. Norsworthy.
Secondary Diagnostics • Pharmacologic Testing: When Horner ’s syndrome is suspected, drug testing may be used to aid in localization of the lesion. Ophthalmic 1% phenylephrine applied topically will result in rapid mydriasis, loss of ptosis, and enophthalmous if the lesion is postganglionic. One percent hydroxyamphetamine has been used to confirm the lesion as preganglionic or central in origin, but this drug is no longer available. • Orbital Imaging: In cases of suspected orbital mass lesions, ocular ultrasound, magnetic resonance imaging (MRI), computerized tomography (CT), or radiographs may be necessary. Radiographs will not reveal soft-tissue lesions in the skull due to the surrounding bone density, but bony lysis associated with tooth root abscess or neoplasia may be seen. MRI is the imaging mode of choice for soft-tissue skull lesions. See Figure 211-2. • Fine-Needle Aspirate or Biopsy: Collection of cellular samples may be helpful in the determination of a mass within the orbit; however,
504
diagnostic samples can be extremely difficult to collect. Ocular ultrasound may be helpful as a guide for placement of an aspiration needle. An approach to the suspected mass can be made adjacent to the globe by inserting the needle through the conjunctiva. Alternatively an approach may be made through the mouth posterior to the last molar. The needle should be advanced slowly to avoid puncturing the globe. • Complete Blood Count (CBC): This may be helpful in cases of orbital abscess or cellulitis.
Treatment Primary Therapeutics • Treat any Underlying Condition: In cases in which a systemic disease is diagnosed, the condition should receive primary treatment. Resolution of systemic disease may improve third eyelid position.
Third Eyelid Diseases
• No Treatment: A prolapsed third eyelid is not detrimental to the cat, although it may be troubling to the owner. When no specific ocular or systemic etiology is determined the condition may be left alone to resolve. • Systemic Antibiotics: Orbital cellulitis or abscess requires broadspectrum antibiotics for a minimum of 3 weeks. Good antibiotic choices include amoxicillin-clavulanic acid and clindamycin. Some clinicians recommend anti-inflammatory doses of systemic corticosteroids as well. Orbital infection should be considered likely when there is pain on opening the mouth. Because cellulitis is more common than an abscess, it is frequently not possible to drain the infected material from the orbit. If an abscess is found or highly suspected, an attempt may be made to drain the infected material. For this procedure the cat is placed under general anesthesia. A small stab incision is made behind the last molar with a number 11 scalpel blade and then the region is gently probed with hemostats with the goal of allowing drainage of any infected material. If the abscess is successfully drained, antibiotic therapy can be terminated at 3 weeks. If draining is not attempted, or is not successful, antibiotic therapy will need to be continued for 4 to 5 weeks, assuming there has been improvement following initial therapy. If there is no improvement after 3 weeks, further diagnostics, such as MRI or CT, should be considered with possible orbital surgery. • Orbital Surgery without Enucleation: This type of surgery is required when a neoplastic mass or localized foreign body is within the orbit. This should be considered a referral surgery as the approach is complicated, and adjunctive therapy may be necessary for several forms of neoplasia. • Surgical Restoration of the Normal Gland Position: Using topical ophthalmic antibiotic and steroid combinations q8h for 1 week prior to surgery helps decrease the inflammation and improve surgical success. One commonly used procedure is called the Pocket Technique. The third eyelid is pulled forward, exposing the bulbar surface. A 1-cm (3/8-in) incision is made through the conjunctiva on either side of the gland parallel to the free edge of the third eyelid. The far edges of the two incisions are sutured together using an absorbable 6-0 suture in a continuous pattern. It is generally easier to replace the gland while suturing from medial to lateral. The gland is tucked down into the pocket as the suture line is closed. A second procedure is called the Modified Orbital Rim Tacking Technique. In this procedure double-armed nonabsorbable
2-0 to 4-0 suture is used. A 5-mm (3/16-in) skin incision is made along the ventral orbital rim, then a 5-mm (3/16-in) conjunctival incision is made inside the eyelid, matching the skin incision. The suture is passed through the skin incision, through the periosteal orbital rim and exits the conjunctival incision. The same suture is then passed through the conjunctiva and dorsal surface of the gland. The suture is then passed back into the dorsal surface of the gland and exits the conjunctiva close to the original bite. The second arm of the suture is passed through the skin incision, through the periosteal orbital rim, and exits through the conjunctival incision (same as the first suture arm). The two arms of the suture are tied together, pulling the gland downward and anchoring it to the orbital rim. Follow-up therapy of topical ophthalmic antibiotics q6 to 8 h for 2 weeks may be helpful at preventing secondary bacterial infection.
Secondary Therapeutics • Topical Ophthalmic Adrenergic Agents: The application of 1 to 5% phenylephrine or 0.1 to 0.5% epinephrine ophthalmic solution may be applied as needed to cause regression of the eyelid. However, extreme care should be used with this medication because, if it is absorbed systemically, it may have severe, potentially fatal side effects. • Tattooing: The leading edge of the eyelid can be tattooed to make the eyelid less noticeable. • Surgical Removal of the Gland: Removing the gland of the third eyelid may predispose the cat to development of keratoconjunctivitis sicca (KCS), although iatrogenic KCS has not been reported in the cat. Amputation of the exposed portion of the prolapsed gland can be performed. Sharp dissection with scissors is used to remove the gland and overlying conjunctiva; the remainder of the third eyelid, including the cartilage, is left intact. In most cases it is not necessary to close the conjunctival tissues. When a large incision is made, the conjunctiva may be closed with 6-0 absorbable suture in a continuous pattern. Closure of the wound will decrease the possibility of cartilage movement.
Suggested Readings Chahory S, Crasta M, Trio S, et al. 2004. Three cases of prolapse of the nictitans gland in cats. Vet Ophth. 6:169–174.
505
CHAPTER 212
Thromboembolic Disease Larry P. Tilley
Overview Systemic thromboembolism is a frequent and life-threatening complication of cardiomyopathy. Stasis of blood within dilated cardiac chambers and increased platelet reactivity combine to predispose cardiomyopathic cats to systemic thromboembolism. Typically, a clot lodges at the aortic trifurcation (saddle thrombus) resulting in severe ischemic insult to the rear limbs and tail. See Figure 212-1. If the thrombus is small, it may enter and obstruct one internal iliac artery and cause paralysis or paresis to only one rear leg. See Figure 212-2. Alternatively, if the thrombus travels cranially, it usually affects the right front leg. See Figure 212-3. Systemic thromboembolism, however, can also affect other organs, including kidneys, gastrointestinal tract, and brain. Vasoactive agents (i.e., prostaglandins or serotonin) released by platelets at the site of the thrombus result in constriction of collateral and regional vessels, further contributing to ischemia and reducing blood flow to terminal spinal cord segments. A saddle thrombus results in a consistent constellation of physical abnormalities, including hindlimb paresis or paralysis, absent pulsa-
tions, cyanosis of the foot pads (see Figure 212-4), and coolness of the skin. Hinblimb musculature is typically firm and painful, and sloughing of skin or musculature may occur. See Figure 212-5. Organ dysfunction may occur depending upon the location of the thrombi. Affected cats almost always have significant underlying cardiac disease, and congestive heart failure is often precipitated by the occurrence of systemic thromboembolism. However, some cats with thromboembolic disease are not in heart failure even though they have significant cardiac disease.
(A)
Figure 212-1 A large thromboembolus (T) is seen in the split terminal aorta (A) obstructing blood flow to the right and left internal iliac (II) and median caudal (MC) arteries. Photo courtesy Dr. Gary D. Norsworthy.
(B)
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
506
Figure 212-2 This cat had a small thrombus lodge in the left internal iliac artery resulting in (A) paresis and loss of conscious proprioception to the left rear leg. (B) Color flow Doppler shows normal blood flow in the right internal iliac artery (blue) and minimal in the left (red). Photo courtesy Dr. Gary D. Norsworthy.
Thromboembolic Disease
Figure 212-3 This cat had a thrombus enter the right brachial artery causing paresis and loss of conscious proprioception to the right front leg. Normal function returned after one week. Photo courtesy Dr. Gary D. Norsworthy.
Figure 212-4 Cyanosis due to a saddle thrombus can be seen in the pads of the rear foot (below). The normal pad color is seen in a front foot (above) of the same cat. Photo courtesy Dr. Gary D. Norsworthy.
Figure 212-5 Sloughing of skin occurred on the left metatarsal area of this cat with a saddle thrombus. Photo courtesy Dr. Gary D. Norsworthy.
Figure 212-6 An echocardiogram can detect a thrombus (arrow) in the left atrium (LA) as seen in this cat with asymptomatic hypertrophic cardiomyopathy. Photo courtesy Dr. Gary D. Norsworthy.
Secondary Diagnostics Diagnosis Primary Diagnostics • Physical Examination: Posterior paralysis is the most common clinical sign. The rear feet are often cold and cyanotic. Marked pain is common. • Blood Pressure Determination of Affected Limbs: Impeded blood flow will result in no or low blood pressure. It can replace echocardiography for making a diagnosis, but echocardiography is still needed to diagnose the form of cardiac disease. • Abdominal Ultrasonography: The aortic blood flow can be visualized with color-flow Doppler. The aorta is seen dorsal to the urinary bladder. See Figure 212-2B.
• Radiography: Radiographs often reveal evidence of congestive heart failure including pulmonary edema, pleural effusion, and cardiomegaly. There should be an absence of spinal lesions. • Echocardiography: This will demonstrate underlying heart disease. In some cats, a forming, unorganized thrombus (“smoke”) or a mature thrombus may be seen in the left atrium. See Figure 212-6. • Angiography: This can be used to demonstrate the location of a thrombus. There will be an absence of contrast material in affected arteries. See Figure 212-7.
Diagnostic Notes • The diagnosis usually is based on characteristic physical examination abnormalities.
507
SECTION 1: Diseases and Conditions
dose aspirin (5 mg q72h). Recurrence of thrombi occurs at a high rate (43.5%) even with anticoagulation. Cats with left atrial enlargement, especially greater than 20 mm in diameter, are at greatest risk for aortic thromboembolism.
Therapeutic Notes
Figure 212-7 thrombus.
Aortic angiography shows obstruction of flow due to an aortic
• If not previously established, the underlying heart disease should be determined.
Treatment Primary Therapeutics • Manage Congestive Heart Failure: See Chapters 56 and 110 for specific treatment guidelines. • Promote Collateral Circulation: Manually massage the muscles several times per day to promote circulation. • Prevention of More, Immediate Clots: Warfarin, a vitamin K antagonist, is the anticoagulant most widely used in humans and has been proposed for prevention of re-embolization in cats surviving an initial episode. The initial dose is 0.25 to 0.5 mg/cat q24h PO. Overlap with heparin therapy for 3 days. The dose is then adjusted to prolong the prothrombin time (PT) approximately two times its baseline value or to attain an international normalized ratio (INR) of 2 to 4. Warfarin has a much greater chance of bleeding complications. Clopidogrel (18.75 mg [one-fourth of a 75-mg tablet]/cat/day) is another option; it is superior to aspirin in human studies.
• The use of thrombolytic agents (e.g., streptokinase and urokinase tissue plasminogen activator) is prohibitively expensive and is associated with high mortality rates. • Heparin: Heparin has no effect on the established clot but can prevent further activation of the coagulation cascade. Give an initial dose of 100 to 200 units/kg IV and then 200 to 300 units/kg q8h SC. It should only be used for a few days following thrombus occurrence. • Daltaparin (Fragmin): (100 units/kg q12–24 h SC). This is an alternative to heparin and warfarin that reduces the need for patient monitoring for those at high risk of aortic thromboembolism. The drug is expensive. Cats with left atria greater than 20 mm in diameter are at greatest risk. • Anesthesia and Surgical Therapy (Embolectomy): This is also associated with a high mortality rate because of the concurrent cardiac disease that is almost invariably present. • Vasodilation with Acepromazine: Give 0.2 to 0.4 mg/kg q8h SC to promote collateral blood flow. It is contraindicated if hypotension occurs. • Nonselective β-adrenergic Blockers (e.g., propranolol) may impede the development of collateral circulation and should not be used when systemic thromboembolism is present. • Streptokinase and urokinase are significantly less expensive than newer fibrinolytic agents, but little clinical experience has been reported.
Prognosis Overall, the prognosis is guarded. Approximately 50% of affected cats do not survive the acute congestive heart failure and systemic thromboembolism crisis and die within 6 to 36 hours. Those surviving typically show steady improvement in limb function beginning within 24 to 72 hours of presentation. The prognosis is grave for cats showing no improvement over this time and in those developing gangrenous changes. Cats surviving are at risk of recurrence (43% in one series).
Suggested Readings Secondary Therapeutics • Provide Warmth: Use warm water bottles or warm water filled latex gloves; avoid intense heat (i.e., lights and electrical pads) because limbs are susceptible to thermal injury. • Sodium Bicarbonate: Give 1 to 2 mEq/kg IV slowly to correct metabolic acidosis and hyperkalemia. Administer with low-rate infusion of 0.45% saline/2.5% dextrose. Document the presence of metabolic acidosis or hyperkalemia before using sodium bicarbonate. • Analgesia: Give buprenorphine (0.01–0.02 mg/kg q8–12 h PO) or butorphanol (0.2–0.4 mg/kg IM). • Aspirin: This drug may reduce the chance of future thrombus formation: Give 81-mg tablet q48 to 72 h PO. In one study though, no significant difference was found in survival or recurrence rate between cats receiving the traditional dose and cats receiving low-
508
De Francesco TC. 2007. Aortic Thromboembolism. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 98–99. Ames, IA: Blackwell Publishing. Laste NJ, Harpster NK. 1995. A retrospective study of 100 cats with feline distal aortic thromboembolism: 1977–1993. J Am Anim Hosp Assoc. 31:492–500. Rodriguez DB, Harpster NK. 2002. Aortic thromboembolism with feline hypertrophic cardiomyopathy. Compend Contin Educ Pract Vet. 24: 478–481. Smith SA. 2003. Arterial thromboembolism in cats: Acute crisis in 127 cases (1992–2001) and long-term aspirin in 24 cases. J Vet Intern Med. 17:73–83. Smith CE. 2004. Use of low molecular weight heparin in cats: 57 cases (1999–2003). J Am Vet Med Assoc. 225:1237–1241.
CHAPTER 213
Thymoma Bradley R. Schmidt
Overview Thymoma is an epithelial tumor of the thymus infiltrated with benign, mature lymphocytes arising from the cranial mediastinum. Different histological cell types may be seen, but there appears to be no prognostic differenced between these cell types. In cats, 60% of thymomas are cystic, and squamous cell carcinoma has also been rarely documented to arise within feline thymomas. Features of benign or malignant characteristics are related to the pattern of growth of the tumor and not based on histology. Benign tumors are well encapsulated and are easily amendable to surgical resection. See Figure 213-1. Malignant thymomas are invasive and may be difficult to remove but do not necessarily metastasize. Metastasis within the thoracic and abdominal cavity has been reported to occur in 20% or less of reported cases. The median age of cats with thymoma is reported to be 9.5 years of age. Domestic short-hair cats and Siamese appear to be over represented in many studies. Although the finding of a cranial mediastinal mass may be incidental, most cats display clinical signs that may have been present for days to months prior to the definitive diagnosis. These clinical signs may be as a direct result of the tumor and associated pleural effusion or may be secondary to paraneoplastic syndromes associated with tumor. The most common clinical signs related to the direct presence of the mass or pleural effusion, includes dyspnea, regurgitation or vomiting, coughing, anorexia, choking, pitting edema of the head, neck and forelimbs secondary to lymphatic syndrome, swelling at the level of the thoracic inlet secondary to tumor extension, decreased compressibility of the cranial thoracic cavity, and thoracic pain. Clinical signs related to paraneoplastic conditions may include a nonpruritic exfoliative dermatitis with a possible coat color change; polymyositis resulting in weakness and ataxia; myasthenia gravis possibly resulting in dysphonia, megaesophagus, cervical ventroflexion, and profound weakness; and infections as many cats appear to be immunocompromised. Hypertrophic osteopathy was also described in a 6-month-old cat with thymoma. The primary differential diagnosis for a mediastinal mass is lymphoma; however, ectopic thyroid tissue and benign thymic cysts have also been described.
(A)
(B) Diagnosis Primary Diagnostics • Thoracic Radiographs: Thoracic radiographs generally reveal a large mass effect in the cranial mediastinum displacing the cardiac silhouette caudally and dorsally. Pleural effusion may also be seen. Dilation of the esophagus may be present in cases where myasthenia gravis is present. See Figure 213-2. • Thoracic Ultrasound: Thymomas generally appear as a heterogeneous mass with multiple small or large cysts. Pleural effusion may be noted as well. See Figure 213-3. • Thoracic Fluid Analysis: Pleural effusion may be chylous in nature with mature lymphocytes predominating. Additional cell types iden-
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 213-1 (A) Necropsy showed the extent of a very large thymoma (T). The heart (H), diaphragm (D), and liver (L) are marked for orientation. (B) The encapsulated thymoma was removed from the chest so its size could be appreciated in relation to the heart (H). Images courtesy Dr. Gary D. Norsworthy.
tified in pleural effusion supporting the diagnosis of thymoma include mast cells, eosinophils, and occasionally malignant epithelial cells. See Chapter 288. • Fine-Needle Biopsy and Cytology: Fine-needle biopsy and cytology of the thymoma, ideally with ultrasound guidance, generally reveals mature lymphocytes (rather than lymphoblasts generally seen with lymphoma), with mast cells, eosinophils, and malignant epithelial cells typically being seen. • Tissue Biopsy and Histopathology: Tissue biopsy is definitive in most instances. Tissue biopsies may be obtained with ultrasound guidance or may be obtained at the time of surgery. Presurgical biopsy is recommended because the primary differential diagnosis of lymphoma is generally treated with chemotherapy.
509
SECTION 1: Diseases and Conditions
(A)
Figure 213-3 This ultrasound image of a thymoma shows a homogenous mass with multiple cysts. About 60% of them are cystic. Image courtesy Dr. Gary D. Norsworthy.
•
•
• •
(B) Figure 213-2 Radiographs of the cat in Figure 213-1. (A) The lateral radiographic view reveals a large mass in the cranial mediastinum. It appears to be continuous with the cardiac silhouette. (B) The DV view shows the extent of the mass filling the anterior mediastinum. The trachea (arrow) has been displaced to the right side of the thoracic cavity. Images courtesy Dr. Gary D. Norsworthy.
creatine phosphokinase (CPK) levels may be substantially elevated. Most cats reported in the literature have been retrovirus negative based on serologic testing. Edrophonium Chloride: If myasthenia gravis is clinically suspected, edriphonium chloride may be administered (0.1–0.2 mg/kg IV) to support this diagnosis. Affected cats should show immediate improvement in clinical signs. See Chapter 143. Serum Acetylcholine Receptor Antibodies (AChRAb) level: AChRAb levels should be evaluated in cats with clinical signs relating to myasthenia gravis. Levels above 0.30 nmol/L are diagnostic for myasthenia gravis. AChRAb should also be evaluated in all cats prior to surgery because although not all cats with elevated levels are clinical, early diagnosis will allow appropriate treatment prior to surgery and may improve the chances for an uncomplicated outcome post-surgery. See Chapter 143. Skin Biopsy: In cats with thymoma-related dermatitis, all cats had histological evidence of cutaneous lymphoid cellular infiltrates. Thoracic Computerized Tomography (CT) Scan and Magnetic Resonance Imaging (MRI): Due to the large size of the tumor in many cats and the presence of pleural effusion, it may be difficult to identify rare metastatic lesions. CT scans or MRI may be superior to radiographs in the identification of these metastatic lesions; however, it has not been demonstrated that these modalities help to predict whether the tumor is amendable to surgical resection.
Diagnostic Notes
Secondary Diagnostics • Immunohistochemistry: Immunohistochemistry performed on tissue biopsy samples may be helpful in distinguishing between thymoma and lymphoma in lymphocytic-rich tumors, as most thymomas are cytokeratin positive. • Flow Cytometry and Polymerase Chain Reaction (PCR): Flow cytometry and PCR may aid in differentiating between benign thymic lymphocytes and malignant lymphoblasts. • Minimum Date Base: A complete blood count, serum biochemistry profile, urinalysis, and retroviral serology should be performed to evaluate the overall health of the patient. Anemia of chronic disease may be present. In cases in which polymyositis is present, serum
510
• Lymphoma is the primary differential diagnosis for thymoma in cats. Although lymphoma and thymoma can occur in cats of any age, thymomas are generally seen in older cats that are negative for feline leukemia virus (FeLV), and lymphoma may be more likely seen in younger cats that may also be FeLV positive by routine serologic testing.
Treatment Primary Therapeutics • Surgery is generally curative or may result in long-term survival in most cats. A median sternotomy is generally required due to the large size of most tumors.
Thymoma
Secondary Therapeutics • Thoracocentesis: Thoracocentesis should be performed prior to extensive diagnostics and treatment in any cat that appears to be unstable and pleural effusion is suspected or identified. • Radiation Therapy: Radiation therapy has been suggested to be associated with prolonged survival in some cats with unresectable thymoma. • Intravenous Chemotherapy: The role of chemotherapy in the treatment of thymoma is unclear. Treatment with vincristine, cyclophosphamide, and prednisone (COP) as described for feline lymphoma (Chapter 34) has been reported with variable responses. Most thymomas are rich with lymphocytes; therefore, it is possible that decreases in tumor size reported in cats treated with lymphoma-based chemotherapy protocols are due to a decrease in the lymphocyte population within the tumor. Because thymoma is considered an epithelial neoplasm, some advocate carboplatin, doxorubicin, bleomycin, or gemcitabine as more appropriate treatments; however, clinical data supporting the use of these agents are lacking to date. • Ultrasound-Guided Drainage of Cystic Lesions: If a large cystic thymoma is present, repeated ultrasound-guided drainage may result in palliation in select patients in which more definitive treatment is not pursued. • Therapy for Myasthenia Gravis: Therapy with neostigmine (0.04 mg/ kg q6–8 h IM) in cats not able to receive oral medication as a results of regurgitation or oral pyridostigmine (0.25 mg/kg per day initially, up to 1–3 mg/kg q8–12 h PO) may help alleviate clinical signs of myasthenia gravis and should be considered prior to surgery in cats when possible. Because cats are quite sensitive to anticholinesterase agents, careful monitoring for signs of cholinergic activity is recommended. Corticosteroids may be administered concurrently with the aforementioned agents or as a sole therapy in cases where cholinergic activity is noted; however, their use may result in weakness and may increase infection rates in some cats.
Therapeutic Notes
• In cases in which mediastinal lymphoma is treated with chemotherapy, thymoma should be considered when only a partial remission or stable disease is noted 14 days after chemotherapy is initiated.
Prognosis The prognosis in cats treated with surgical removal of the thymoma is generally favorable. Surgery is not successful in only a small number of cats due to tumor recurrence or extensive infiltration of the tumor. In these cats, additional surgery, radiation therapy, or chemotherapy should be considered. As stated previously, anecdotal responses to carboplatin and gemcitabine are reported by some, but no clinical data are available. Although megaesophagus may be associated with a poor prognosis in dogs, this correlation has not been reported in the cat. Cats with myasthenia gravis may improve with the therapy stated previously. Some cats require continued treatment for myasthenia gravis postoperatively.
Suggested Readings Lara-Garcia A, Wellman M, Burkhard MJ, et al. 2008. Cervical thymoma originating in ectopic thymic tissue in a cat. Vet Clin Pathol. 37(4):397–402. Rottenberg S, von Tscharner C, Roosie PJ. 2004. Thymoma-associated exfoliative dermatitis in cats. Vet Pathol. 41(4):429–433. Smith AN, Wright JC, Brawner Jr WR, et al. 2001. Radiation therapy in the treatment of canine and feline thymomas: A retrospective study (1985–1999). J Am Anim Hosp Assoc. 37:489–496. Vail DM, Withrow SJ. 2007. Miscellaneous tumors, section B thymoma. In SJ Withrow, DM Vail, eds., Small Animal Clinical Oncology, 4th ed., pp. 795–799. Philadelphia: Elsevier Saunders. Zitz JC, Birchard SJ, Couto GC, et al. 2008. Results of excision of thymoma in cats and dogs: 20 cases (1984–2005). J Am Vet Med Assoc. 232(8): 1186–1192.
• Supportive care, including nutritional support, intravenous fluids, antiemetics, H2 blockers, and analgesics, is recommended when indicated.
511
CHAPTER 214
Toxoplasmosis Gary D. Norsworthy and Sharon Fooshee Grace
Overview Toxoplasma gondii is a protozoal organism that infects most warmblooded animals, but domestic and wild Felidae are the only hosts in which the entire life cycle can be completed (i.e., are definitive hosts). Approximately 30% of cats and up to 50% of humans in the United States have been infected with the organism, although few of either species have clinical disease. There are three infectious forms of the parasite: (a) rapidly replicating tachyzoites, which live in body tissues, (b) slowly replicating bradyzoites, which reside in tissue cysts, and (c) unsporulated oocysts, which are excreted in feces. Some cats become infected through ingestion of sporulated oocysts. However, most cats become infected when they ingest bradyzoites, which are encysted in the tissues of an intermediate host, such as a rodent. These tissue cysts are digested, releasing bradyzoites, which penetrate the small intestinal wall. The asexual phase of development is followed by a sexual phase, finally producing unsporulated oocysts. These unsporulated oocysts pass in the feces but are not infective until they are exposed to oxygen and sporulate in 1 to 5 days. The entire life cycle can be completed within 3 days after ingestion of tissue cysts. If the life cycle begins with the ingestion of tachyzoites or oocysts, it requires about 3 weeks for completion. Following penetration of the small intestinal wall, the organism may spread to lymph nodes or to other organs via lymph and blood. If focal necrosis occurs in the target organs, clinical signs develop referable to the individual organ or organs, although most cats infected with T. gondii show no clinical signs. The lungs, eyes, and liver are commonly affected organs. Anorexia, fever, lethargy, pneumonia-related dyspnea, icterus, muscle pain, pancreatitis, and neurologic signs are consistent with a diagnosis of toxoplasmosis. Ocular manifestations include anterior uveitis, retinochoroiditis and hemorrhage, or other nonspecific signs of ocular inflammation. See Figure 214-1. About 20% of experimentally infected cats have self-limiting, small bowel diarrhea. Although some cats die from the infection, most recover and develop immunity. It is unknown why some cats die and others remain asymptomatic. The organism cannot be cleared from the body by known drugs, so recurrence of disease is always possible. Toxoplasmosis can be a serious disease in humans, especially when the patient is immunosuppressed. Because of the cat’s role in transmission, veterinarians should be aware of several important facts. Cats typically shed large quantities of oocysts for only about 1 to 2 weeks (rarely more than 3 weeks) and usually have only one shedding episode in their lifetime. Oocysts are not infectious until they sporulate, a process which takes 1 to 3 days. If shedding recurs, the number of oocysts passed is almost insignificant. Oocyst shedding is heaviest in kittens 6 to 14 weeks of age. Once in the environment, oocysts resist disinfectants, freezing, and drying. They can be killed if exposed to temperatures of 70°C (160°F) for 10 or more minutes. An episode of shedding does not correlate with antibody production. A negative immunoglobulin G (IgG) serologic test indicates either (a) lack of exposure (this cat is susceptible to infection) or (b) recent infection and the cat has not yet seroconverted (possible but less common than the first scenario). A positive IgG test indicates that a cat has probably
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
512
Figure 214-1 Ocular manifestations of toxoplasmosis include anterior uveitis and hyphema as seen in this cat’s left eye. Image courtesy of Dr. Richard Malik.
shed oocysts in the past and is thus much less likely to be a future shedder than a seronegative cat.
Diagnosis Primary Diagnostics • Antemortem Diagnosis: This can tentatively be made with a combination of the following: • Demonstration of IgG antibodies in serum that documents exposure to T. gondii. • Demonstration of an IgM titer greater than 1 : 64 or a four-fold or greater rise in IgG titer that suggests recent or active infection. • Clinical signs referable to toxoplasmosis. • Exclusion of other common causes of the aforementioned clinical signs. • Positive response to treatment.
Secondary Diagnostics • Radiographs: If the lungs are affected, radiographs reveal diffuse or patchy areas of interstitial or alveolar pneumonia. See Figure 214-2. Peritoneal effusion may be seen with involvement of the pancreas. • Histopathology: The organism can be found in affected tissues with H & E stains or immunohistochemical stains. However, the presence of tissue cysts containing bradyzoites does not necessarily correlate with active disease. It is necessary to find tachyzoites for confirmation of active disease. Note that the disease can be reactivated if bradyzoites convert to tachyzoites and re-enter the intestine, but this rarely leads to fecal shedding of oocysts.
Toxoplasmosis
• Trimethoprim-Sulfonamide: This combination has been used with success if given at a dose of 30 mg/kg q12h PO for 28 days. Some cats do not tolerate sulfa drugs well so the potential for side effects should be discussed with owners. Folinic acid (2 mg/d PO) or brewer ’s yeast (100 mg/kg per day) should be given to counteract bone marrow suppression when trimethoprim-sulfonamide drugs are given for this duration. • Azithromycin: This can be effective at 10 mg/kg PO q24h for 10 days.
Therapeutic Notes
Figure 214-2 Toxoplasmosis pneumonia is characterized by diffuse or patchy areas of interstitial or alveolar pneumonia. The diffuse form is shown in this radiograph. Image courtesy of Dr. Richard Malik.
• Clinical response should be detectable within 2 days of therapeutic initiation. If present, uveitis should be resolved within 1 week. If these do not occur, reassess the diagnosis. • Because this is a potentially zoonotic disease, personnel involved in therapy should exercise caution in handling bodily fluids and secretions from the affected cat. The disease is not thought to be transmitted by contact with the haircoat of the cat because oocysts do not stick to the hair, and cats are meticulous groomers.
Prevention of Transmission • Tests on Aqueous Humor or Cerebrospinal Fluid (CSF): Aqueous humor or CSF T. gondii-specific antibody detection and organism DNA detection by polymerase chain reaction (PCR) testing are available. These are the most accurate means for diagnosis of ocular or central nervous system toxoplasmosis. These tests are available at the Diagnostic Laboratory, College of Veterinary Medicine, Colorado State University, Fort Collins, CO, 80523, and some commercial veterinary laboratories. • Immunoglobulin M (IgM) Antibody Titers: IgM antibodies appear about 2 weeks post-infection; this typically corresponds with the onset of clinical signs. A titer >1 : 64 or a four-fold increase in IgG-toIgM titers within 2 weeks best correlate with active infection. Antibodies typically persist for up to 3 months. However, some cats do not develop detectable IgM titers, and in other cats positive IgM titers can persist for months to years after infection. Enzyme-linked immunosorbent assay (ELISA) testing is preferred. • IgG antibody titers: IgG antibodies appear by the fourth week postinfection and are usually present for life. They generally represent a previous infection unless there is a four-fold increase over a 3-week period. • Antigen: Antigen is positive 1 to 4 weeks post-infection and remains positive in active or chronically persistent infections. Therefore, this test is not superior to dual antibody testing. • PCR: This test detects organismal DNA, which is not verification of clinical disease. However, when evidence of the organisms is found in inflamed tissue, there is a high correlation with clinical toxoplasmosis. • Cytology: This rarely finds the organism in body fluids or tissues. • Fecal Examination: Examination using Sheather sugar solution may specifically identify Toxoplasma oocysts, but they are rarely present in stool during clinical disease. Routine fecal flotations may recover oocysts in asymptomatic cats, but Toxoplasma oocysts are not distinguishable from Hammondia or Besnoitia with this test.
Treatment Primary Therapeutics • Clindamycin: This is the most effective drug for cats. It is dosed at 12.5 to 25 mg/kg q12h PO or IM for 28 days or for 2 weeks following resolution of clinical signs.
• Meat Handling: Utensils and surfaces that contact uncooked meat should be washed with soap and water. Meat should be cooked at temperatures above 70°C (160°F) or frozen at minus 30°C (−22°F) for at least 24 hours before cooking. Undercooked pork is the most common source of human infection. Pork is often mixed with beef in making hamburgers. • Food Sources: Cats should be restricted from ingesting raw meat, bones, viscera, or unpasteurized milk (especially goat’s milk). Birds and rodents are likely sources, as is exposure to food-producing animals. • Pregnant Women: They should avoid contact with cat feces, litter box materials, soil, and raw meat. Cats should only be fed commercial cat food or food that has been cooked or frozen as described previously. Fecal material should be removed from litter boxes daily because oocysts require a minimum of 24 hours to sporulate and are not infectious until that time. Cats should not be allowed to hunt, scavenge raw meat, or eat dead animals. It is notable that cats generally only shed oocysts for days to several weeks after primary inoculation, and the shedding period can be shortened by administration of clindamycin or sulfonamides. Repeat oocyst shedding is rare, even in cats receiving glucocorticoids and those infected with the feline immunodeficiency virus (FIV) or feline leukemia virus (FeLV). Most IgG seropositive cats are not shedding and are not likely to shed again. Most seronegative cats would shed the organism if infected. For pregnant women, the most desirable test result in the household cat is a positive IgG titer. • Screening Cats: Veterinarians are often asked to test cats belonging to pregnant women for toxoplasmosis. A negative fecal examination has little significance because lack of oocyst shedding does not predict the likelihood of future shedding or equate to protection from shedding. Blood tests for antibodies should include IgM and IgG. The best result is a positive IgG and negative IgM; this combination best signals past (protective) exposure but no clinical disease present.
Prognosis The prognosis is generally good if diagnosis and proper therapy begin early, although some central or peripheral neurologic deficits may be permanent following clinical cure of the disease. The use of the ELISA IgM test is important in making an early diagnosis. Cats without ocular, central nervous system, and neuromuscular disease generally respond
513
SECTION 1: Diseases and Conditions
within 2 to 4 days; cats with those forms respond more slowly. However, recurrence of disease in any form is more likely if treatment duration is for less than 4weeks. Disseminated disease in immunocompromised cats has a poor prognosis.
Suggested Readings Barr SC. 2007. Toxoplasmosis. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 1350–1351. Ames, IA: Blackwell Publishing.
514
Dowers KL, Lappin MR. 2006. The pyrexic cat. In J Rand, ed., ProblemBased Feline Medicine, pp. 364–391. Philadelphia: Elsevier Saunders. Dubey JP. 1994. Toxoplasmosis and other coccidial infections. In RC Gupta, ed., The Cat: Diseases and Clinical Management, pp. 5654–581. Philadelphia: WB Saunders. Dubey JP, Lappin MR. Toxoplasmosis and neosporosis. 1998. In CE Greene, ed., Infectious Diseases of the Gog and Cat, pp. 493–509. Philadelphia: Saunders. Lappin MR. Protozoal and miscellaneous infections. 2006. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 5th ed., pp. 638–649. St. Louis: Elsevier Saunders.
CHAPTER 215
Tracheal Disease Andrew Sparkes
Overview Tracheal disease is most commonly manifested by dyspnea (usually inspiratory) because most clinically significant conditions will cause obstruction to the flow of air. However, coughing, stridor, and other signs, such as gagging and dysphagia, may also be present depending on the disease process. If the disease affects the intrathoracic trachea, expiratory rather than inspiratory dyspnea may be seen.
Infectious Causes Overview Infectious tracheitis may occur in cats, usually as part of the acute upper respiratory tract disease complex, with agents such as feline herpesvirus-1 and Bordetella bronchiseptica being implicated. Typically, upper respiratory (i.e., nasal, ocular, and nasopharyngeal signs) predominate with tracheal inflammation often being a minor component. Rarely, tracheitis may be severe, and it may contribute significantly to the disease presentation. Occasional cases have been seen with severe tracheal inflammation or edema that has caused significant respiratory compromise.
Tracheal Foreign Bodies
(A)
Overview Foreign bodies are more likely to lodge in the trachea in cats due to the relatively small size of the airways, but smaller foreign bodies, such as grass seeds, may pass lower down the respiratory tract. See Figure 215-1. Respiratory noise, dyspnea, and coughing are the main features seen with tracheo-bronchial foreign bodies. The signs are typically sudden in onset, may be progressive (especially with secondary infections), and may improve or resolve temporarily while the cat is receiving antibiotics.
Diagnosis Primary Diagnostics • Radiographs: The radiographic changes are often highly suggestive of a foreign body with a localized area of lung consolidation or a visible radiodense foreign body. Pulmonary consolidation usually involves the cranial portion of the right caudal lung lobe, which is the predilection site for foreign bodies, based on the anatomical configuration of the airways in cats. • Endoscopy: It is usually not possible to pass a bronchoscope with a diameter greater than 3.5 mm beyond the mainstem bronchi in cats; therefore, direct visualization of many foreign bodies may not be possible. Pus is frequently evident, arising from the right main bronchus. This may obscure the foreign body, even if it is within the visual range of the endoscope.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
(B) Figure 215-1 This cat had a tracheo-bronchial foreign body. (A) A VD radiograph demonstrates localized pneumonia in the right caudal lung lobe due to tracheo-bronchial foreign body. (B) This blade of grass was removed via bronchoscopy.
Diagnostic Notes • If a foreign body is suspected, a course of antibiotics before bronchoscopy may enable a clearer view.
Treatment Primary Therapeutics • Removal: Endoscopic retrieval of the foreign body using grasping forceps is usually the treatment of choice. This is often successful for tracheal foreign bodies but may be more difficult with bronchial foreign bodies due to the restricted size of the airways.
515
SECTION 1: Diseases and Conditions
Secondary Therapeutics • If endoscopy is unsuccessful in achieving a diagnosis or retrieving a foreign body, a more radical surgical approach will be required. The surgical options are either lobectomy of the affected lung lobe or bronchotomy to allow direct removal of the foreign body.
Treatment Primary Therapeutics
Therapeutic Notes
• Surgery: Excision of damaged tracheal rings and anastamosis of the two ends is generally completely successful. General anesthesia and maintenance of an adequate airway may require specialist facilities in some cases. There are approximately 40 tracheal rings in cats. Up to 25% of the trachea has been removed in some reported cases without complications.
• There may be a marked response with antibiotic therapy, often with complete resolution of the coughing; however, coughing will almost invariably recur once antibiotic treatment is withdrawn.
Therapeutic Notes
Prognosis The prognosis is good, provided the necessary surgical and postoperative care can be provided.
Tracheal Rupture Overview Intrathoracic tracheal rupture appears to occur mainly as a result of blunt trauma (e.g., dog fight or fall) causing hyperextension of the neck. Because the carina is relatively fixed, this often results in tracheal avulsion or rupture just cranial to the carina. In most cases, an airway is still maintained with a “psuedotrachea” being formed either from adventitial tissue surrounding the trachea or from the mediastinum. Over time there is inflammation and narrowing of the airway resulting in typical signs of dyspnea, but these signs may not occur until 5 to 14 days after the initial trauma. See Figure 215-2.
Diagnosis Primary Diagnostics • Radiographs: The most common finding is a loss of continuity of the trachea, often with a gas-filled diverticulum and hyperinflation of the lungs. Apparent narrowing of the trachea is also commonly observed, with the narrowed region being where the rupture has occurred. The two sites most commonly affected are close to the carina and at the thoracic inlet.
• To prevent tension on the trachea, suture tape between the mandible and the manubrium for 7 to 14 days postoperatively. This helps to prevent overextension of the neck to decrease the risk of dehiscence.
Prognosis When diagnosed and treated appropriately, the prognosis for cases of tracheal rupture is excellent.
Iatrogenic Tracheal Rupture and Stenosis Overview Tracheal rupture, tracheal stenosis, and tracheal necrosis are all potential iatrogenic injuries to the trachea that can occur following endotracheal (ET) intubation for general anesthesia. Such complications are uncommon but emphasize the need for careful anesthetic protocols. A variety of events have been postulated to cause longitudinal tears of the trachea including overinflation of the cuff causing the tear, traumatic intubation, turning of the patient during anesthesia without disconnecting the ET tube, and removal of the ET tube without deflating the cuff. Overinflation of the cuff is likely the most common cause. However, in the absence of definitive knowledge about the origin of the tears, all these should be considered possibilities, and care should be taken to observe good practice during anesthesia. Cats sustaining tracheal tears as a result of ET intubation often develop subcutaneous emphysema as the first clinical sign. This may occur within a few hours of anesthesia or may take several days to develop. Dyspnea may accompany the emphysema but is not invariably seen (30% of cases in one study). Cases of tracheal necrosis and tracheal stenosis have also been reported following overinflation of the cuff on ET tubes. Even though it is a rare occurrence, it can lead to life-threatening dyspnea typically up to 1 to 3 weeks post-anesthesia. The rostral thoracic trachea is most commonly affected with pressure necrosis occurring rather than an acute tracheal tear. Over time, necrotic material may be sloughed into the tracheal lumen causing obstruction, and there may also be stenosis as a result of inflammation and fibrosis. See Figure 215-3.
Diagnosis Primary Diagnostics
Figure 215-2 Tracheal rupture and stenosis is shown dorsal to the cranial border of the heart (arrow); it followed trauma.
516
• Radiography: This may reveal a disruption in the wall of the trachea. It also commonly reveals pneumomediastinum with subcutaneous emphysema. • Endoscopy: An endoscopic study of the tracheal lumen is usually confirmatory.
Tracheal Disease
(A)
All these conditions result in narrowing of the tracheal lumen, although this may be a dynamic event with tracheal collapse. Cases of “thickening” of the thoracic tracheal wall, presumably as a result of edema or inflammation, have been documented. The origin of this edema or inflammation is uncertain, but, when seen, it often appears to affect a large part of both the intrathoracic and extrathoracic trachea. Some cases may be associated with infectious agents (e.g., severe feline herpesvirus-1 infection), and some may be associated with upper respiratory obstructive disease with secondary tracheal swelling caused by the altered airway dynamics (e.g., rostral tracheal, laryngeal, or nasopharyngeal obstruction). In other cases it is possible that acute edema may occur as a hypersensitivity reaction. True tracheal collapse is extremely uncommon but has been described as a result of congenital malformation. It may also be an acquired condition, such as secondary to tracheal trauma or secondary to severe obstructive upper respiratory disease. The cough associated with narrowing of the trachea is typically of a “honking” nature, similar to tracheal collapse in small dogs. The coughing is likely to be acute in onset, and dyspnea may be a noticeable feature.
Diagnosis Primary Diagnostics • Biopsy and Culture: For tracheal edema, mucosal biopsy may be indicated (with or without viral isolation or polymerase chain reaction testing and bacterial culture) to attempt to make a specific diagnosis. • Radiography: Radiographs show an apparently thickened tracheal wall (edema) or a flattened trachea (collapse). • Fluoroscopy: This dynamic study is especially helpful for tracheal collapse. • Endoscopy: A 1- to 2-mm endoscope can be used to observe real-time tracheal collapse.
(B) Figure 215-3 (A) Tracheal necrosis and narrowing (arrows) occurred following over-inflation of an endotracheal tube. (B) Necrotic tracheal epithelium was removed endoscopically.
Treatment Primary Therapeutics
Treatment Primary Therapeutics • Antibiotics: Culture-driven antibiotic selection is the basis for treating a bacterial cause of tracheal edema. • Antivirals: If the feline herpesvirus-1 is diagnosed famciclovir (62.5 mg q12h PO; can be doubled) may be efficacious. • Surgery: Surgical repair of collapsing trachea offers the potential for cure or significant improvement.
• Observation: In mild to moderate cases, the tear may heal spontaneously using a conservative approach, consisting of cage rest and oxygen therapy. This approach is indicated if the cat is not dyspneic. • If emphysema or dyspnea occurs surgical exploration and repair are indicated. • Tracheal necrosis and stenosis are managed in a similar way, but lesions can be extensive and life-threatening.
Prognosis The prognosis depends largely on the extent of the lesion and whether surgical resection is feasible.
Tracheal Edema and Tracheal Collapse Overview Tracheal edema, tracheal narrowing, and tracheal collapse are rare diagnoses in cats, but they can result in significant respiratory compromise.
Figure 215-4 Radiographic appearance of tracheal lymphoma is seen in the midcervical region (arrow). The tumor was removed surgically with follow-up chemotherapy producing excellent results.
517
SECTION 1: Diseases and Conditions
Prognosis The prognosis for tracheal edema is good if an underlying cause can be found and treated. The prognosis is guarded for tracheal collapse.
Tracheal Neoplasia Overview Tracheal neoplasia is rare in cats. Lymphoma (see Figure 215-4), adenocarcinoma, and squamous cell carcinoma are the most commonly reported tumors. The treatment of choice depends on the tumor, its location, and the clinical signs. In general, surgical resection is recommended because this will alleviate signs of severe dyspnea and facilitate accurate diagnosis and prognosis. Lymphoma may be responsive to chemotherapy.
518
Suggested Readings Brown MR, Rogers KS, Mansell KJ, et al. Primary intratracheal lymphosarcoma in four cats. 2003. J Am Anim Hosp Assoc. 39(5):468–472. Culp WT, Weisse C, Cole SG, et al. 2007. Intraluminal tracheal stenting for treatment of tracheal narrowing in three cats. Vet Surg. 36(2):107–113. Fujita M, Miura H, Yasuda D, et al. 2004. Tracheal narrowing secondary to airway obstruction in two cats. J Small Anim Pract. 45(1):29–31. Jakubiak MJ, Siedlecki CT, Zenger E, et al. 2005. Laryngeal, laryngotracheal, and tracheal masses in cats: 27 cases (1998–2003). J Am Anim Hosp Assoc. 41(5):310–316. Mims HL, Hancock RB, Leib MS, et al. 2008. Primary tracheal collapse in a cat. J Am Anim Hosp Assoc. 44(3):149–153. Tivers MS, Moore AH. 2006. Tracheal foreign bodies in the cat and the use of fluoroscopy for removal: 12 cases. J Small Anim Pract. 47(3): 155–159.
CHAPTER 216
Triad Disease Anthony P. Carr
Overview Triad disease, or triaditis, refers to a combination of cholangiohepatitis (cholangitis), pancreatitis, and inflammatory bowel disease (IBD) that is seen in cats. It is not a disease per se but instead a statistical association. There has been much anecdotal information written on this topic; however, solid evidence regarding the extent of this problem is lacking. The initial and only scientific description of this entity was able to show that there was an association with cholangiohepatitis and inflammatory bowel disease (seen in 83% of cats with cholangiohepatitis) and mild pancreatitis (in 50%). This did not hold true for other forms of liver disease such as lymphocytic portal hepatitis. Roughly a third of cats with cholangiohepatitis had both IBD and pancreatitis which would be considered true triad disease. The form of IBD in the cats with cholangiohepatitis also tended to be more severe and have a suppurative component. Why these disorders are linked to each other is speculative, although possibly ascending bacterial infections from the gastrointestinal (GI) tract may be responsible. In the cat, the pancreatic duct joins the bile duct before entering the duodenum at the papilla (see Figure 216-1), which might make ascending infections of both liver and pancreas more likely. How this is linked to IBD has not been determined. Other publications since the initial description have tended to be less discriminate and claim that feline liver disease in general is associated with IBD and pancreatitis, although there is no proof to support this assertion.
Figure 216-1 The pancreatic duct (1) joins the bile duct (2) before entering the duodenum at the papilla. This creates an anatomical link between the duodenum, pancreas, and gall bladder/liver. Used with permission from Dr. L.C. Hudson and W.P. Hamilton.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
The predominant clinical implication of this syndrome is that patients with indications of liver disease should be evaluated for the concurrent presence of pancreatitis and IBD. Given the combination of disorders, if biopsies of the liver are to be obtained with laparotomy or laparoscopy, consideration should be given to biopsying the pancreas and GI tract concurrently. Clinical signs with all three of these disorders can be similar. Nonspecific signs such as lethargy, dehydration, vomiting, and anorexia are common to all three disorders. Fever and jaundice are generally not expected with IBD but can be seen with pancreatitis and cholangiohepatitis. Abdominal pain is often not present in cats, even with pancreatitis. Diarrhea is also possible with all three disorders although it tends not to be as common as the other signs.
Diagnosis Primary Diagnostics • Complete Blood Count (CBC), Biochemistry Profile, and Urinalysis (UA): Findings will be variable. With suppurative disease, neutrophilia may be present, potentially with a left shift and toxic changes. Often variable elevations of liver enzyme activities are the initial indication of disease in cats with triad disease. Hyperbilirubinemia is also possible and usually indicates more severe disease. Icterus can result from liver disease per se or can be post-hepatic in origin when pancreatic inflammation compromises bile flow. Hypocalcemia can be seen with pancreatitis. Bilirubinuria in cats is a sensitive early indicator of liver problems. • Feline Pancreatic Lipase Immunoreactivity (fPLI): This test is promising for the diagnosis of pancreatitis. It tends to be the most sensitive test for diagnosing pancreatitis; specificity is also high. An elevated fPLI test does not, however, mean that pancreatitis is the predominant issue with which the patient is dealing, although it is a good indicator of pancreatic pathology. In cats with triad disease, fPLI would be expected to be elevated, although pancreatitis is often mild and the predominant clinical problems are the concurrently present cholangiohepatitis or IBD. See Chapters 159 and 160. • Ultrasound: Ultrasound is a useful tool in cats that either have clinical signs associated with triad disease or indications of liver disease on a biochemical profile. The liver, pancreas, and GI tract can all be evaluated. Ultrasound of the liver with cholangiohepatitis can be normal or reveal nonspecific changes in echogenicity. Unfortunately, definitive diagnosis of the components of triad disease is not possible with this diagnostic tool, and in many cases no abnormalities may be seen. Ultrasound is, however, useful in obtaining fine-needle aspirates (FNA) or biopsies of the liver as well as a way to obtain bile aspirates. Indications of bile duct distension, which can indicate pancreatitis, may also be seen. • Cytology and Biopsy: In patients with triad disease, tissue biopsies of liver, pancreas, and GI tract are the only way to establish a definitive diagnosis. In the instances in which laparotomy or laparoscopy is performed, obtaining biopsies from multiple organs is indicated. FNA of the liver can be carried out; however, the accuracy of this test, especially with inflammatory liver disease, is limited though it can be helpful in diagnosing lipidosis or neoplasia. The advantages to FNA are that it can usually be carried out with mild or no sedation, whereas with laparotomy or laparoscopy general anesthesia is
519
SECTION 1: Diseases and Conditions
needed, which is associated with greater risk in a patient with significant liver disease. With chronic or severe liver disease, a tissue biopsy is always preferable to a FNA, provided the patient can tolerate a biopsy procedure. • Liver and Gallbladder Culture and Sensitivity: Infections need to be considered as a possible etiological factor for cholangiohepatitis, especially if suppurative in nature. Bile culture is more likely to be positive than culturing the liver, though ideally both would be tested. Bile can be obtained with a 22- or 25-gauge needle during an exploratory or using ultrasound guidance if the gall bladder is sufficiently full. Both aerobic and anaerobic culturing is recommended.
Secondary Diagnostics • Coagulation Profile: Coagulopathies occur frequently in cats with liver disease, especially in those that are jaundiced. These tests are indicated prior to a liver biopsy. • Bile Acids Testing: Pre- and postprandial bile acids can be determined in nonjaundiced cats. Elevations can be seen with shunting and decreased hepatic function. • Serum Cobalamin Level: It has been shown that in cats with IBD, cobalamin deficiency can occur. This is significant because the deficiency perpetuates GI signs. If cobalamin is low, parenteral supplementation is indicated.
Diagnostic Notes The occurrence of triad disease in cats does impact the ideal work-up for a cat with liver disease. In most instances liver disease will be initially diagnosed via clinical signs and biochemical testing abnormalities. If the clinical presentation and ancillary diagnostics indicate that liver biopsy is needed, consideration should be given to obtaining pancreatic and GI biopsies at the same time. More complete information on diagnosing the components of triad disease are found in the appropriate chapters: 94, 120, 159, and 160.
Treatment Primary Therapeutics • Antibiotics: These are the predominant initial therapy for suppurative cholangitis or cholangiohepatitis. Ideally therapy is directed by results of culture and sensitivity testing. If these are not available, broad-spectrum treatment is indicated that addresses both aerobes and anaerobes. In most instances multiple antibiotics are used. Common combinations include a penicillin (i.e., amoxicillin with or without clavulanate) with a fluoroquinolone. Alternatively a cephalosporin such as cephalexin can be used, possibly also in combination with a fluoroquinolone. Metronidazole can be added as well to increase activity against anaerobes. Treatment should continue for 4 to 6 weeks in most cases. • Therapy for Cholangiohepatitis: Additional therapies can be considered, although these treatments have not been evaluated for efficacy in patients with spontaneous cholangiohepatitis. Ursodiol (i.e., ursodeoxycholic acid, 10–15 mg/kg q24h PO) may limit hepatic inflammation and improves bile flow. It should not be used with biliary obstruction. S-adenosylmethionine (SAMe; Denosyl, Nutramax Laboratories) is supposed to aid in restoration of hepatic glutathione concentration, which limits oxidative injury and inflammation. Silybin (Silybin in phosphatidylcholine complex with Vitamin E; Marin for Cats, Nutramax Laboratories) has a variety of potential
520
mechanisms of action including antioxidant activity, stimulation of bile flow, and anti-inflammatory effects. Silybin and SAMe are available as a combination product (Denamrin for Cats, Nutramax Laboratories). • IBD: See Chapter 120. • General Supportive Care: In those patients that are debilitated supportive measures are vital. This can include fluid therapy and nutritional support when needed. Placement of a feeding tube may be of benefit in those patients not meeting their caloric needs. A variety of diets can be considered including those meant for patients with liver disease or those meant to help manage IBD. • Anti-Inflammatory or Immune Suppressive Therapy: The use of medications, such as prednisolone, is often considered in the treatment of feline liver disease, especially with chronic nonsuppurative cholangiohepatitis or lymphocytic cholangitis. The role these agents have to play, if any, in suppurative disease is unclear. A short course of an anti-inflammatory dose (i.e., 1 mg/kg prednisolone q24h PO) may have some benefits and would also aid in the treatment of IBD. Whether these medications are indicated will often depend on the biopsy results and how the patient responds to initial therapy with antibiotics and supportive care.
Secondary Therapeutics • Vitamin K1: This can be given by injection (5 mg/kg q24h SC for 2–3 days) to those patients with coagulopathies. In more severe cases plasma transfusions may be needed, especially if liver biopsy is planned. • Cobalamin: Supplementation at 250 µg/cat once or twice weekly for 4 to 6 weeks is indicated if cobalamin deficiency is documented.
Therapeutic Notes • In most instances treatment focuses initially on the therapy of suppurative cholangitis or cholangiohepatitis with antibiotics and supportive care. The supportive care also addresses pancreatitis. • Dietary therapy can be used to address IBD via novel protein diets or hydrolyzed diets. It is important that these diets are appropriate to patients with liver disease as well. • After initial therapy with antibiotics, if the liver disease has not resolved, additional therapy is needed. This can be via long-term use of SAMe, ursodiol, or silybin. In many cases, however, immunesuppressive drugs often are required to successfully manage the patient, especially if concurrent IBD is present.
Prognosis The prognosis is variable and is predominantly determined by the nature and severity of the liver disease. In most instances long-term control of pancreatitis and IBD is possible. With liver disease longterm survival is possible, Although some cats will survive less than a year.
Suggested Readings Caney SAM, Gruffydd-Jones TJ. 2005. Feline Inflammatory Liver Disease. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 1448–1451. St. Louis: Elsevier. Weiss DJ, Gagne JM, Armstrong PJ. 1996. Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis and nephritis in cats. J Am Vet Med Assoc. 209: 1114–1116.
CHAPTER 217
Trichobezoars Mitchell A. Crystal
Overview Trichobezoars (hairballs) can be a cause of regurgitation or vomiting in the cat. Hairballs appear as hair with or without food or gastric secretions. Occasionally, a cat will attempt to regurgitate or vomit a hairball but will be unsuccessful and produce only gastric secretions. Cats accumulate hair as a result of normal grooming habits, although hairballs may accumulate as a result of disorders causing excessive grooming (i.e., behavioral, neurologic, and dermatologic diseases) and changes in gastrointestinal (GI) structure or motility (i.e., primary motility disorders, inflammatory or neoplastic GI diseases, diverticula, or hiatal hernias). Therefore, in cats with normal grooming behaviors, regurgitation or vomiting of hairballs may be a normal phenomenon or may be an indicator of an underlying GI disease. See Figure 217-1. The signalment of cats with trichobezoars varies depending on whether the hairballs are normal or due to an underlying GI, dermatologic, or neurologic disease, although they tend to occur more frequently in long-haired young to middle-aged cats. Cats may also develop a problem from grooming other long-haired pets in the household. In the normal cat, no other clinical signs should be present aside from intermittent regurgitation or vomition of hairballs although some cats will be anorectic for 1 to 2 days following vomiting of a large hairball. If weight loss, diarrhea, anorexia, or other problems are present, a complete diagnostic evaluation should be performed to search for an underlying disease. Differential diagnoses should include diseases that cause regurgitation or vomiting. See Chapters 69 and 229.
Diagnosis Primary Diagnostics • History: Ask about grooming habits, including whether the patient grooms other pets in the household. Inquire as to whether weight loss has occurred. Ask if trichobezoars may have occurred in the past, with or without other clinical signs. • Response to Therapy: See Treatment.
Secondary Diagnostics • Contrast Radiographs: Although trichobezoars are radiolucent, barium may be absorbed by a trichobezoar leaving a barium-filled mass behind when the rest of the barium passes. See Figure 217-2. • Complete Diagnostic Evaluation: If other clinical signs are present or the problem is frequent and nonresponsive to therapy, further diagnostics are indicated. See Chapters 69 and 229.
Diagnostic Notes • Most trichobezoars elude abdominal palpation.
Figure 217-1 This 0.55 kg (1.2 pound) trichobezoar was removed from a cat that was not vomiting or retching. It was found by palpation on an annual examination. However, the cat was experiencing weight loss. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 217-2 Barium may be absorbed by a trichobezoar leaving a barium-filled mass behind when the rest of the barium passes. This one was in the cat’s stomach (arrow). Image courtesy Dr. Gary D. Norsworthy.
521
SECTION 1: Diseases and Conditions
If a gastric or intestinal obstruction occurs, an underlying GI problem should be considered. When the surgery is performed to remove the hairball, submit stomach and intestinal tissue for histopathology.
Treatment Primary Therapeutics
(A)
• Grooming: Frequent, even daily, brushing or combing may be needed to prevent ingestion of excessive hair. • Petroleum-Based Laxatives: These should be administered orally to provide lubrication and facilitate normal aboral passage. Several preparations are commercially available. Most are in the form of a flavored paste. Tastes vary between products so a cat’s rejection of one product does not mean it will reject another. Doses vary but generally are suggested at 1 to 5 mL/cat per day to effect. Overdosing may cause diarrhea although this is unlikely.
Secondary Therapeutics • Motility Enhancers: Cisapride (2.5–7.5 mg/cat q8–24h PO) or metoclopramide (0.2–0.5 mg/kg q6–12h PO) may provide support for those cats with motility disorders. • Shaving: Long-haired cats can be shaved every 2 to 4 months to minimize hair ingestion.
Prognosis
(B) Figure 217-3 Intestinal obstruction due to a trichobezoar is rare; however, it occurred in this cat. A. The dilated, hyperemic loop of bowel is typical of an obstruction. B. The resected portion of small bowel is opened to reveal the trichobezoar. Image courtesy Dr. Gary D. Norsworthy.
• Close attention should be paid to the history and physical examination because clients may assume a trichobezoar to be a serious problem or assume a serious problem to be a trichobezoar. • Although trichobezoars may rarely cause intestinal obstruction (see Figure 217-3.), most cats pass them without significant problems.
522
Cats without underlying disease are at minimal risk of becoming ill and trichobezoars mainly only create an inconvenience to the owner. Most of these cats can be controlled with therapy, although occasional episodes can be expected. The prognosis of cats with underlying disease varies depending on the disease.
Suggested Readings Barrs VR, Beatty JA, Tisdall PLC, et al. 1999. Intestinal obstruction by trichobezoars in five cats. J Fel Med Surg. 1(4):199–207. Durocher L, Johnson SE, Green E. 2009. Esophageal diverticulum associated with a trichobezoar in a cat. J Am Anim Hosp. 45(3):142–146. Twedt DC. 1994. Diseases of the stomach. In RC Gupta, ed., The Cat: Diseases and Clinical Management, 2nd ed., pp. 1181–1210. New York: Churchill Livingstone.
CHAPTER 218
Tritrichomoniasis Mark Robson and Mitchell A. Crystal
Overview Tritrichomonas foetus is a single cell, flagellated protozoan that colonizes the colon of cats, resulting in chronic large intestinal diarrhea. By light microscopsy feline T. foetus is indistinguishable from bovine venereal T. foetus and porcine enteric Tritrichomonas suis. T. foetus trophozoites are approximately 11 × 7 microns, pear-shaped organisms that have three anterior flagella and a distinct undulating membrane that runs the length of the organism. Trophozoites demonstrate vigorous rapid forward erratic motion, divide by binary fission, do not form cysts, and are resistant to antiprotozoal drugs. T. foetus persists in moist environments for up to a week and can be transmitted by vectors such as flies. Cats become infected via direct fecal-oral contamination and develop clinical signs 4 to 14 days after exposure. Tritrichomoniasis causes lymphoplasmacytic inflammation of the terminal ileum, cecum, and colon. There is no extraintestinal migration, and transplacental and transmammary infections do not occur. Clinical signs include malodorous, pasty to semiformed diarrhea, often containing blood and mucus. Flatulence and tenesmus is common. Physical examination may be normal or reveal evidence of large intestinal diarrhea. There is no sex or breed predilection for T. foetus diarrhea; however, the majority of infected cats are young. Cats living in an increased housing density are at higher risk of contracting T. foetus. In a recent study of cats attending an international cat show, the prevalence of T. foetus was 31%. Many of these cats resided in high-density housing; thus, lower prevalence is likely in feral and house cats. T. foetus is not considered of zoonotic importance. Tritrichomonas diarrhea is often misdiagnosed as giardiasis. This is likely because of the lack of familiarity with T. foetus and because of similarities in the clinical signs and causative agent. Cats with tritrichomoniasis may be co-infected with Giardia. Comparative features of T. foetus and Giardia are found in Table 218-1.
Diagnosis Primary Diagnostics • T. foetus Polymerase Chain Reaction (PCR) Test: This may be used to diagnose T. foetus with a sensitivity of approximately 95%. Samples should be shipped at room temperature preserved in 70% isopropyl alcohol (180–220 mg feces in 3–5 mL alcohol). A variety of commercial and veterinary school laboratories offer this test. • T. foetus Culture: T. foetus may be cultured (approximately 55–80% sensitive) in feces using a commercially available culture system (In Pouch TF, Biomed Diagnostics Inc., San Jose, CA). Less than 0.1 g of feces (a volume equal to that of a peppercorn) should be used to inoculate the culture system, and the system should be incubated upright at 25°C (77°F). Note that larger inoculate quantities and higher incubation temperatures lead to rapid bacterial overgrowth and less diagnostic results. The pouch contents should be examined for motile T. foetus every 48 hours for 12 days. Positive results usually occur in 1 to 11 days (median 3 days). The system does not support growth of Giardia.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
TABLE 218-1: Comparison of Tritrichomonas and Giardia
Size Microscopic trophozoite appearance
Forms of organism Motility Transmission Area of GI infected Environmental stability Response to antiprotozoal drugs
Tritrichomonas
Giardia
11 × 7 µm Pear-shaped; Single nucleus, undulating membrane runs length of organism, three anterior flagella, one posterior flagella Trophozoite Vigorous, rapid, forward, erratic Fecal-oral Large intestine
15 × 8 µm Face-like; two nuclei, concave disc, four pair of flagella
Up to a week Believed to be fair to good with ronidazole; other antiprotozoal drugs lack efficacy.
Trophozoite, cyst Sluggish, rolling leaf/tumbling Fecal-oral Small intestine ± large intestine Weeks to months (cyst form) Good
Secondary Diagnostics • Direct Saline Smear: Trophozoites are rarely (about 4–15% of the time) seen on microscopic examination at 40x magnification. See Figure 218-1. Freshly voided and diarrheic samples should be examined because the trophozoites do not survive refrigeration. Multiple samples may improve detection. • Exclusion of Concurrent Diseases: A complete blood count (CBC), serum biochemistry, urinalysis, retroviral tests, direct fecal examination, and fecal flotation should be performed. The presence of Giardia, Cryptosporidium, Coronavirus, and Clostridium should also be ruled out. Colonoscopy and histopathology may be considered. Studies have shown that coexisting intestinal infections increase the severity of the diarrhea and shedding of trophozoites.
Diagnostic Notes • It is preferable to evaluate fecal samples for T. foetus immediately. Survival of trophozoites for up to 4 days can be achieved by avoiding refrigeration, removal of all litter from the sample, and diluting the feces with saline (add 1.5 mL saline per 1 g feces). • Antimicrobial therapy will decrease the number of trophozoites present in the feces. This may lead to false-negative fecal smear results.
Treatment Primary Therapeutics • Ronidazole at 30 mg/kg q12h PO for 14 days may be efficacious in resolving diarrhea and eradicating T. foetus infection. Its use in foodproducing animals is currently banned due to human health risks. Gloves should be worn when handling ronidazole and informed
523
SECTION 1: Diseases and Conditions
(B)
(A)
(C) Figure 218-1 Trophozoites are uncommonly seen on microscopic examination. (A) This one shows the three anterior flagella (the “tri” in “tritrichomonas”). It is stained with Lugol’s solution plus Diff Quik® and seen at 40× magnification. (B) This one is stained with Diff Quik only and shows the granular nature of the cytoplasm but it does not demonstrate the flagella, axostyle, nucleus, or undulating membrane. (C) This specimen is stained with Nomarski DIC stain. (A) Courtesy of Jan Slapeta, PhD, MVDr. (B),(C) Courtesy of Drs. Heather Stockdale and Byron Blagburn. consent should be obtained from the owner. Neurotoxicosis has been reported as a side effect in cats. Neurological signs typically resolve after cessation of ronidazole therapy. Ronidazole should only be used in confirmed cases of tritrichomoniasis.
Therapeutic Notes • Clinical signs in untreated cats usually resolve within 2 years (median 9 months, range 5–24 months), though persistent infection with T. foetus following resolution of diarrhea is common. • Resolution of diarrhea may take longer in multi-cat households. • Cats managed with gastrointestinal diets usually have improvement in the severity of diarrhea but prolongation in resolution of diarrhea (i.e., diet change, median 15 months to diarrhea resolution; no diet change, median of 7 months to diarrhea resolution).
524
• Antimicrobial therapy may improve clinical signs in the short term but does not eradicate infection and may prolong the duration of diarrhea. • Frequent bathing and litter box changing did not result in improvement of T. foetus diarrhea. • Paramomycin is not efficacious in treating Tritrichomoniasis and may induce acute renal failure in cats.
Prognosis The prognosis is excellent as long as the owner is willing to tolerate a cat with diarrhea. Significant clinical illness is rare, and diarrhea usually resolves within 2 years. Chronic infection with T. foetus following resolution of diarrhea is common and relapses of clinical signs are also common. Approximately 50% of untreated cats tested with PCR between
Tritrichomoniasis
2 and 5 years after initial diagnosis were negative for T. foetus, indicating that spontaneous resolution of the disease can occur.
Suggested Readings Foster DM, Gookin JL, Poore MF, et al. 2004. Outcome of cats with diarrhea and Tritrichomonas foetus infection. J Amer Vet Med Assoc. 225(6):888–892.
Gookin JL. 2006. Trichomoniasis. In CE Greene, ed., Infectious diseases of the Dog and Cat, 3rd ed., pp. 745–750. St. Louis: Saunders-Elsevier. Gookin JL. 2009. Tritrichomonas. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIV. pp. 509–512. St. Louis: Saunders-Elsevier. Gookin JL, Copple CN, Papich MG, et al. 2006. Efficacy of ronidazole for treatment of feline Tritrichomonas foetus infection. J Vet Intern Med. 20(3):536–543.
525
CHAPTER 219
Ureteral Obstruction Rhett Marshall
Overview Ureteral obstruction is a serious urologic condition that was uncommon in cats until the last 10 years. However, ureteral obstructions are being diagnosed more frequently in cats presented for acute or chronic renal failure, providing unique challenges for veterinary practitioners, internists, and surgeons. Cats presenting with acute azotemia usually have bilateral obstructions or a nonfunctional contralateral kidney. On the other hand, many unilateral obstructions are asymptomatic and are only discovered when abdominal radiography or ultrasonography are performed for other reasons. Hence, many unilateral ureteral obstructions are not diagnosed at the time of obstruction. Obstructions can occur unilaterally or bilaterally and are further classified as intraluminal (i.e., calculi, solidified dried blood, cellular debris, and spasm of the ureter), mural lesions (i.e., neoplasia, fibrosis, congenital and acquired stricture, and polyps), or the result of extramural compression (i.e., secondary to neoplasia arising from the ureter, the bladder, or the retroperitoneal space). Cats most frequently have intraluminal obstructions with calcium oxalate and solidified dried blood being the most commonly identified ureteroliths. Urine, ureteroliths, and other particulate material move down the ureter by passive flow and ureteral peristalsis. The normal ureteral lumen in cats is tiny (0.4 mm), and, although some cats can pass 1- to 2-mm ureteroliths, many feline ureters are obstructed by the tiniest of stones. Complete urine outflow obstruction raises ureteral pressure, which ultimately causes a decrease in the hydrostatic pressure gradient across glomerular capillaries resulting in decreased glomerular filtration rate (GFR). Persistently high ureteral pressure leads to high intrarenal pressure and obliteration of renal parenchyma, a condition known as hydronephrosis. See Figure 219-1. Renal function can deteriorate by as much as 80% in several weeks, but fortunately, this deterioration is initially reversible if the flow of urine can be restored. Differential diagnoses occur in three categories. (a) Acute renal failure may be due to toxic nephropathy (e.g., drug therapy or toxin ingestion), inflammatory nephropathy (e.g., glomerulonephritis or pyelonephritis), obstructive nephropathy (urethral obstruction), and circulatory collapse (e.g., severe dehydration, hypotension, anemia, heart failure, shock, sepsis, or diabetic ketoacidosis). (b) Asymmetrical renal size or “big kidney-little kidney” syndrome may be due to polycystic kidney disease (PKD), neoplasia, compensatory renal hypertrophy, inflammatory nephropathy, and trauma (either current or previous). (c) Pancreatitis is a differential because ureterally obstructed cats with a functional contralateral kidney may have similar clinical findings to pancreatitis, such as severe abdominal pain, vomiting, and anorexia with normal renal parameters.
Diagnosis Primary Diagnostics • Clinical Signs: Clinical signs are usually dependent on the function of the contralateral kidney. Cats with a functional contralateral
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
526
kidney may have no apparent clinical signs, or they may present depressed, lethargic, anorectic, or vomiting. Behavioral changes consistent with severe abdominal or spinal pain may be present, including crouching, hiding, petting resentment, and atypical aggression or vocalization. • Physical Examination: Renal palpation often reveals asymmetrical renal size with one kidney small (end-stage or nonfunctional) and the remaining kidney large due to compensatory hypertrophy or hydronephrosis. Renal pain is usually present and is easily mistaken for spinal pain. • Laboratory Data: Biochemical abnormalities depend on the function of the contralateral kidney and range from unremarkable to severe azotemia (serum creatinine >1000 µmol/L [11 mg/dL]), hyperphosphatemia, and hyperkalemia. Bilateral obstructions usually have significant azotemia as neither kidney can function. Unilateral obstructions may have unremarkable biochemical changes if the contralateral kidney is functional, or they may have severe azotemia if the contralateral kidney is non-functional. Clinical pathology testing may demonstrate severe renal dysfunction, but it cannot differentiate ureteral obstruction from other forms of acute renal failure. • Urinalysis: This should always be performed, but urine obtained by cystocentesis often yields little information because the ureteral obstruction has prevented urine from the affected kidney from reaching the bladder. Urine aspirated from the renal pelvis (during an intrarenal pyelogram) should be analyzed and submitted for culture and sensitivity testing.
Secondary Diagnostics • Radiography: Survey abdominal radiographs can be useful in diagnosing radio-opaque uroliths, which if present, are highly suggestive of ureteral obstruction. However, only about 50% of ureteroliths are calcium oxalate, limiting its usefulness. Radiography can also be used to assess renal size and shape, urinary bladder size and shape, and the integrity of the urinary tract. • Ultrasonography: Renal sonography is a key diagnostic tool for differentiating ureteral obstruction from other causes of acute renal failure and asymmetrical renal size. Renal pelvis dilation greater than 3 mm (1/8 inch) also known as hydronephrosis, dilation of the proximal ureter also known as hydroureter, or visualization of a calculus within the proximal ureter is diagnostic of ureteral obstruction. See Figures 219-1A and 219-2. If visualization of the cause of suspected obstruction is not possible, an antegrade positive contrast pyelogram should be performed. Intravenous excretory pyelography should be avoided because urine flow is restricted and hence minimal contrast excreted and poor images obtained. • Contrast Antegrade Pyelography: This is an effective method of demonstrating ureteral obstruction and determining the location of the obstruction. See Figures 219-3 and 219-4. Under ultrasound guidance, a 22-gauge × 4-cm (1 1/2 in) needle is inserted into the dilated renal pelvis, 1 to 2 mL of urine is collected (for analysis), and a slightly larger volume of contrast carefully injected back into the renal pelvis. Plain lateral and ventrodorsal radiographs are taken immediately and the flow of contrast through the ureter assessed. Abrupt termination of the contrast column occurs where ureteral obstruction exists. In some cases, particularly those in which obstruction is secondary
Ureteral Obstruction
(A)
Figure 219-2 Renal ultrasonography of a dilated renal pelvis (hydronephrosis), dilated proximal ureter, and nephrolith (between markers).
(B)
Figure 219-3 Ultrasound guided antegrade contrast pyelogram showing renal pelvis dilation and proximal ureteral obstruction. Minor procedural leakage of contrast occurs commonly and should not be interpreted as urinary tract rupture.
(C) Figure 219-1 (A) Post-mortem dissection showing moderate hydronephrosis and dilation of the proximal ureter caused by proximal ureteral obstruction due to a ureterolith. (B) Ultrasound image of severe hydronephrosis. Minimal cortex or medulla remains. (C) The kidney seen in 219-1B showing the thin layer of cortex and medulla present. Images courtesy Dr. Gary D. Norsworthy.
to pyelonephritic debris, the obstruction may be flushed under pressure into the bladder during the pyelogram. • Advanced Imaging: Other methods of advanced imaging such as computerized tomography (CT), magnetic resonance imaging (MRI), and nuclear scintigraphy can be used to diagnose ureteral obstructions but are rarely performed in preference to contrast pyelography.
Diagnostic Notes • Diagnosis is difficult if contralateral kidney function is normal because there may be no clinical signs or biochemical changes to
527
SECTION 1: Diseases and Conditions
Figure 219-4 Ultrasound guided antegrade contrast pyelogram showing renal pelvis dilation and distal ureteral obstruction with multiple radiolucent ureteroliths (filling defects) present. Minor procedural leakage of contrast occurs commonly and should not be interpreted as urinary tract rupture.
Figure 219-5 Retrograde contrast pyelogram via nephrostomy tube shows ureteral patency and contrast reaching the bladder. An adhesive abdominal wrap securing the nephrostomy tube can be seen superimposed over the caudal abdomen.
suggest renal disease. A high index of clinical suspicion is often necessary to diagnose such cases. Similarly, renal ultrasonography should be performed in all cats presenting with abdominal or spinal pain, even if they are not azotemic.
successfully employed to remove ureteroliths with good long term outcomes, but it requires a highly experienced surgical team and the use of an operating microscope due to the small size of the feline ureter. See Chapter 275. Proximal Disease: Proximal obstructions may be removed by pyelolithotomy. See Chapter 263. Distal Disease: Distal obstructions are removed by ureterotomy or ureteral transection and re-implantation into the urinary bladder. A nephrostomy tube should be placed for 3–5 days to divert urine away from the ureterotomy site and resolve azotemia. Patency of the ureter should be confirmed after 3–5 days by performing a retrograde contrast pyelogram (through the nephrostomy tube) and should occur before nephrostomy tube is removed. See Figure 219-5. Nephrostomy Tube Placement: This is performed immediately following ureterotomy. An over-the-needle peel-away 14–16 ga. intravenous catheter (or similar) is carefully inserted into the renal pelvis from the greater curvature surface and stylet removed when urine is visualized. A 5 F polyurethane feeding tube (or similar) is inserted through the abdominal wall and guided into the renal pelvis via the catheter. The catheter is retracted and peeled away leaving the feeding tube in the renal pelvis. The tube is finger trapped to the renal capsule and skin using 3-0 silk and connected to a closed urinary collection system. See Figure 219-6. Percutaneous placement is highly discouraged due to difficulty with proper placement and with anchoring the tube to the kidney so it will not dislodge.
•
Treatment: Intraluminal Obstructions Due to Calculi or Debris • Medical Management: The aim of medical therapy is to increase urine output using intravenous fluids and diuretics while concurrently administering smooth muscle relaxants and analgesics to reduce ureteral spasm or edema, promoting passage of the obstruction to the bladder. Fluid diuresis (two to three times maintenance) may facilitate migration of small ureteroliths and is considered firstline therapy for cats with ureteral obstruction. Cats may be anuric or oliguric, so body weight and urine production should be carefully observed to avoid over hydration. Opiate analgesia should be administered as soon after diagnosis as possible. Smooth muscle relaxants (i.e., α-antagonists or calcium channel blockers), diuretics (i.e., furosemide or mannitol), steroids or nonsteroidal anti-inflammatory agents, and glucagon are theoretically useful in promoting passage of ureteral obstructions, but none have been proven to be beneficial in cats. In humans, combining the uroselective α-antagonist tamsulosin, with nonsteroidal anti-inflammatory drugs (NSAIDs) is the preferred approach to enhance passage of ureteroliths. In cats, recent various clinical reports suggest amitriptyline (1 mg/kg q24h PO) aids the passage of ureteroliths to the bladder. At present, recommendations regarding using amitriptyline are unclear, but with few side effects it should be considered in every case of feline ureteral urolithiasis without obstruction. • Hyperkalemia: Calcium gluconate and bicarbonate therapy should be used in cases of severe hyperkalemia. Nephrostomy tube placement or hemodialysis (when available) can be used to resolve azotemia and hyperkalemia. See Chapter 106. • Monitoring: Effectiveness of medical management should be assessed daily. Resolving azotemia or documenting distal progression of the obstruction on repeated imaging are indicative of successful therapy.
Surgical Management • Ureterotomy: Persistent ureteral obstructions must be removed surgically if renal function is to be preserved. Ureterotomy can be
528
• •
•
Therapeutic Notes • Ureteral stricture, persistent obstruction, and uroabdomen are the most common surgical complications and are likely to occur in 25 to 30% of patients. Complications are minimized by surgical experience, proper surgical technique, and correct nephrostomy tube placement and management. • Approximately 30% of cats with ureteral obstruction will spontaneously pass their obstruction with medical management. Surgery is indicated in all cases where medical management for 48 hours fails to resolve the azotemia or obstruction. Surgery may also be the preferred primary therapy in about 50% of ureteral obstruction cases, particularly if large ureteroliths have been identified or hyperkalemia is present on initial presentation.
Ureteral Obstruction
Prognosis The prognosis for recovery of renal function is dependent on both the degree of obstruction and the duration of the obstruction. Return of renal function is excellent after several days of obstruction; about 90% of GFR will return after 2 days. It is good after several weeks of obstruction; approximately 50% of GFR returns after 2 weeks. After 1 month of obstruction little or no return of renal function is expected. For cats that are alive after 1 month, the long-term survival is excellent with a 2-year survival rate of approximately 80%. However, recurrence of ureteral obstruction is high with about 40% of cats experiencing a repeated obstructive episode after a median time of 12 months.
Suggested Readings
Figure 219-6 Bilateral nephrostomy tubes exiting the abdomen are then connected to a closed collection system.
• Lithotripsy: Treatment of ureteroliths by shockwave lithotripsy is currently not recommended in cats because it is associated with significant morbidity, persistence of ureteral fragments, and decreased renal function over time.
Adin CA, Herrgesell EJ, Nyland TG, et al. 2003. Antegrade pyelography for suspected ureteral obstruction in cats: 11 cases (1995–2001). J Am Vet Med Assoc. 222(11):1576–1581 Hardie EM, Kyles AE. 2004. Management of ureteral obstruction. Vet Clin North Am Small Anim Pract. 34(4):989–1010. Kyles AE, Hardie EM, Wooden BG, et al. 2005. Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in cats with ureteral calculi: 163 cases (1984–2002). J Am Vet Med Assoc. 226(6): 932–936. Kyles AE, Westropp JL. 2009. Management of feline ureteroliths. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIV, pp. 931–935. Saunders Elsevier. Nwadike BS, Wilson LP, Stone EA. 2000. Use of bilateral temporary nephrostomy catheters for emergency treatment of bilateral ureter transection in a cat. J Am Vet Med Assoc. 216(12):1862–1865.
529
CHAPTER 220
Urethral Obstruction Rhett Marshall
Overview Urethral obstruction in cats is a common and serious urologic emergency that is fatal if urine flow is not restored within 24 to 48 hours. Immediate therapy is required to correct fluid, electrolyte, and acid-base derangements while simultaneously re-establishing urethral patency. Urethral obstruction causes increased intravesicular pressure that is transmitted “upstream” to the kidney and opposes forces driving glomerular filtration. Tubular concentrating ability and other tubular functions are also affected, leading to impaired sodium and water reabsorption, and impaired excretion of acids and potassium. This results in uremia, acidosis, hyperkalemia, and volume depletion. Following relief of the obstruction, renal tubular impairment may continue for several days, presumably to resolve the dramatic water and electrolyte abnormalities that have developed and is known as postobstructive diuresis. The most common causes of obstruction are urethral plug (see Figure 220-1), urolith (see Figure 220-2), urethrospasm (usually post blockage; see Figure 220-3), detrusor atony (post-blockage or neurologic lesion), urethral stricture (see Figure 220-4), neoplasia of the bladder neck or urethra, and extraluminal obstruction (see Figure 136-5). Male cats are predominantly affected, but obstruction may also occur in female cats. With correct management, most obstructions are successfully relived by catheterization and renal function restored. Difficulty voiding is common post-obstruction and may be due to reobstruction, urethral spasm, or detrusor atony. Proper technique and use of soft silicon catheters reduces urethrospasm and reobstruction. Differential diagnoses are in two categories. (a) Acute renal failure causing metabolic derangements may be due to obstructive nephropathy (ureteral obstruction), toxic nephropathy (e.g., drug therapy or toxin ingestion), inflammatory nephropathy (i.e., glomerulonephritis or pyelonephritis), and circulatory collapse (e.g., severe dehydration, hypotension, anemia, heart failure, shock, sepsis, or diabetic ketoacidosis). (b) Difficulty or inability to urinate may be due to nonobstructive feline lower urinary tract disease (FLUTD), urethrospasm, or urethroedema causing a functional obstruction (usually occurs post-obstruction), detrusor atony (post-obstruction), priapism, neurologic lesions affecting micturition, and neoplasia of the bladder neck or urethra.
Diagnosis
(A)
(B) Figure 220-1 Urethral plugs are a mixture of matrix and crystals. (A) Some form hard concretions that become lodged in the penile urethra. (B) Others have the consistency of toothpaste. Images courtesy Dr. Gary D. Norsworthy.
Primary Diagnostics • Clinical Signs: Cats may show signs of FLUTD (i.e., dysuria, stranguria, pollakiuria, or hematuria), which are often accompanied by a raucous howl, repeated grooming or licking of the penis, and reluctance or inability to walk. After 24 hours of obstruction, cats display systemic signs of lethargy, dehydration, depression, anorexia, and vomiting consistent with acute renal failure, and progress rapidly to recumbency, coma, and death if untreated. • Physical Examination: The key diagnostic feature is a large, firm, painful bladder that cannot be expressed. Cats often have severe
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
530
abdominal/bladder pain and may not allow accurate palpation. These bladders become hemorrhagic and friable and can rupture if excessive pressure is applied when palpating or trying to express. See Figure 220-5. Erythema, inflammation, or necrosis of the tip of the penis from overgrooming may be evident. Crystalline debris deposited around the penis, prepuce, and perineum may also be present. See Figure 220-6. Hypothermia and bradycardia may be present in severe cases. • Laboratory Data: Biochemical abnormalities reflect the duration of urethral obstruction and range from unremarkable to severe azotemia (serum creatinine >1000 µmol/L [11 mg/dL]), hyperkalemia, and metabolic acidosis. The severe renal dysfunction seen with urethral obstruction is indistinguishable from other forms of acute renal failure using clinical pathology testing.
Urethral Obstruction
Figure 220-2 Urethral uroliths, usually calcium oxalate, (arrow) are increasingly common causes of urethral obstruction. They incite inflammation and edema in the urethra making them nearly impossible to back flush into the bladder. Perineal urethrostomy is usually required for their removal. Image courtesy Dr. Gary D. Norsworthy.
Figure 220-4 Urethral stricture may occur due to stenosis caused by prior urethral catheterization, urethral neoplasia, or post-trauma. Image courtesy Dr. Gary D. Norsworthy.
Figure 220-5 After about 48 hours of urethral obstruction the bladder becomes hyperemic and friable. It must be handled gently to prevent rupture. Image courtesy Dr. Gary D. Norsworthy. Figure 220-3 Urethral spasm occurs in response to urethral dilation during an obstructive episode, due to the physical presence of a catheter, or due to stenosis caused by prior urethral catheterizations. Image courtesy Dr. Gary D. Norsworthy.
• Urinalysis: Urine can be collected by cystocentesis (care must be taken to avoid rupturing a distended bladder) or via urinary catheter after the obstruction is relieved and analyzed for crystals (usually struvite), blood, protein, inflammatory cells, bacteria, fungi, or cellular debris. Urine specific gravity (USG) and pH should also be determined.
Secondary Diagnostics • Radiography and Ultrasonography: These can identify most uroliths and should be considered in all cases because urolithiasis is fairly common in cats. A lateral abdominal radiograph will show a dramatic enlargement of the urinary bladder (see Figure 220-7), but the urethra must also be included in the image so it can be observed for a urolith. See Figure 220-2. Small uroliths can move back and forth
Figure 220-6 Crystalline debris deposited around the penis, prepuce, and perineum may be present at presentation. Image courtesy Dr. Gary D. Norsworthy.
531
SECTION 1: Diseases and Conditions
•
Figure 220-7 An abdominal radiograph of a cat with urethral obstruction can be dramatic. However, one must be sure to include the urethra to check for urethral uroliths. See Figure 220-2. Image courtesy Dr. Gary D. Norsworthy.
•
between the urinary bladder and urethra, making their detection more difficult. Ultrasound is more sensitive in detecting small uroliths or soft-tissue masses in the urinary bladder; radiography is more sensitive in the urethra. • Contrast Urography: This modality is not routinely required but may be necessary to investigate cases when the urethra cannot be catheterized, such as urethral stricture (see Figures 220-3 and 220-4), radiolucent urethroliths, urethral tears following trauma or surgery, and extraluminal compression. • Urethroscopy and Cystoscopy: Small (approximately 1 mm [1/32 in]) semi-rigid or flexible scopes allow direct visualization and assessment of the urethra and bladder. They may be useful after the obstruction has been relieved but provide little information beforehand.
Diagnostic Notes • Most cats have a raucous and seemingly desperate howl that is almost pathognomonic for urethral obstruction. • Hypothermia and bradycardia occur in severe cases after prolonged obstruction and are associated with higher mortality rates. • A complete urinalysis should be performed so specific therapies can be selected to minimize recurrence of urethral obstruction (e.g., acidifying urinary diet for struvite crystalluria or alkaline urine). • If reobstruction occurs, observation of voiding is particularly important to determine the quality of urine stream, bladder expressibility, and whether the bladder is emptied fully after voiding.
Treatment Primary Therapeutics • Fluid Therapy: Priority should be given to commence therapy to correct potentially fatal fluid and electrolyte deficits (i.e., azotemia, dehydration, hyperkalemia, or acidosis). Intravenous normal saline or Hartmann’s solution, administered at 10 to 60 ml/kg per hour depending on the acute fluid deficit, should be maintained for 2 to 3 hours before reducing to 6 to 12 ml/kg per hour (deficit = body
532
•
•
weight in kg × percent dehydration and is usually between 200 and 400 mL). Alternatively, 60 to 100 mL intravenous boluses of warmed fluid may be given in the first few hours to correct hypovolemia and restore circulating blood volume. After the acute fluid deficit and urethral obstruction have been resolved, fluid administration rate should be based on urine production or changes in body weight. A postobstructive diuresis is expected for 1 to 3 days and intravenous fluids should be continued to avoid dehydration. Potassium: Most cats with complete urethral obstruction will present with moderate to severe hyperkalemia. Calcium gluconate administered by slow intravenous injection provides short-term protection from the deleterious effects of hyperkalemia on the heart (i.e., bradycardia and arrhythmia). Sodium bicarbonate may be used for moderate hyperkalemia and acidosis. Once the flow of urine is restored and renal function returns, serum potassium levels can drop dramatically and cats often become hypokalemic after 4 to 12 hours. Serum potassium should be measured several times daily and potassium added to the intravenous fluids as required. Most cats require 20 to 40 mmol/L of potassium supplemented for 1 to 3 days until the postobstructive diuresis subsides. The maximum administration rate for potassium is 0.5 mmol/kg per hour (0.5 mEq/kg per hour). See Chapter 106. Urethral Catheterization: This should be performed as soon as possible. Many cats do not require chemical restraint to relieve their obstruction but, if necessary, may be sedated or lightly anesthetized IV. Cats that initially have their obstruction relieved without sedation quickly resolve their hyperkalemia and if necessary, are more safely anesthetized at a later date to suture in place an indwelling catheter. The perineum and prepuce are clipped and aseptically prepared. Using a sterile approach, the penis should first be gently squeezed and rolled between fingers because a penile plug can sometimes be “milked out” easily and allow urine to flow. If unsuccessful, the urethra should be flushed to remove the plug. With the penis extended, a 24-gauge. intravenous catheter attached to a fluid delivery device (12-mL syringe and extension line) is inserted into the penile urethra and sterile saline infused. Using a “feather touch” technique, the catheter is gently advanced in and out as obstructing material is dislodged and flushed out the urethra. Once the catheter has been advanced about 1 cm (3/8 in) up the urethra, the penis is released and the prepuce grasped dorsally and stretched caudodorsally as far as possible. This straightens the urethra, which facilitates the catheterization process, and is critical in preventing iatrogenic urethral laceration. Most plugs are in the penile urethra and can simply be removed using a 24-gauge catheter alone, but, for plugs extending higher up the urethra, a rigid polypropylene tomcat catheter is required. Bladder Drainage and Lavage: Once the obstruction is cleared the catheter can be carefully advanced into the bladder and its contents emptied. The bladder should be irrigated several times with sterile isotonic fluid to remove crystals and sediment from the bladder. The urethra can also be carefully flushed with saline as the catheter is slowly removed and is particularly helpful in cases in which the obstruction is due to a plug. Indwelling Catheterization: This should be performed if catheterization was difficult, urethral mucosal damage is suspected, there is a fine stream of urine from the penis after the bladder and urethra have been flushed, the cat reobstructs within 48 hrs, or the bladder is atonic. Although hard polypropylene catheters are useful for unblocking, if left indwelling, they can cause significant trauma to the urethra, so should be replaced with a soft silicon or Teflon® coated catheter. Red rubber catheters are frequently used successfully, but one must be careful not to insert too much of the catheter in to the bladder. See Figure 220-8. Urinary catheters can be left open or connected to a closed drainage system that consists of a fluid line bandaged to the tail and emptying into a fluid bag on the floor. In an open system, urine drips freely from the catheter through a layer of
Urethral Obstruction
•
•
(A)
•
(B) Figure 220-8 (A) If a catheter is inserted too far into the bladder, the tip can enter the urethra from the cranial end. Urine flow does not occur, and when removal is attempted, it becomes lodged. (B) This cat required a perineal urethrostomy for removal. Images courtesy Dr. Gary D. Norsworthy.
“dry bed” so cats never contact their urine. Changes in bodyweight can be used to match intravenous fluid administration with urine production. The benefits of a closed system are that urine output can be measured and the risk of ascending bacterial infection is minimized. However, closed systems can be associated with significant morbidity (i.e., severe discomfort as tubing pulls on preputial sutures, general distain cats have for bandaging applied to their body, or feces getting lodged on the catheter-tubing attachment) and should be disconnected immediately if identified. Catheters should only be left indwelling for 1 to 2 days until metabolic derangements are corrected, bladder distention resolved, urine sediment improved, and the cat is likely to void normally. Occasionally it may be necessary for a catheter to be left indwelling for up to 7 days.
Secondary Therapeutics • Cystocentesis: If catheterization is difficult, delayed or cannot be achieved, cystocentesis can be used to relieve intravesicular pressure
•
and temporarily restore the flow of urine in the upper urinary tract. A single puncture with small gauge needle attached to extension tube minimizes the chance of rupturing the bladder wall. See Figure 220-5. Detrusor Atony: This complication may occur following urethral obstruction and bladder overdistension. Affected cats have large distended bladders and are unable to urinate voluntarily, but urine can be easily expressed. Preventing excessive detrusor stretch or strain in the days following relief of the obstruction enhances recovery of normal detrusor function. Some cats can be managed with manual bladder expression if urethral resistance is low and expression is not difficult or painful. Most cats, however, are best managed with an indwelling catheter for 3 to 7 days and bethanechol (1.25–7.5 mg/cat q8–12h PO) for 1 to 2 weeks. Cats with detrusor muscle fatigue or mild atony (bladder not completely empty after urinating) can often be managed with bethanacol alone. Urethral Spasm and Edema: This is a challenging complication of urethral obstruction and causes additional urethral resistance. Cats should be administered a smooth muscle relaxant (prazosin 0.5 mg/ cat q8–24h PO or phenoxybenzamine 2.5–7.5 mg/cat q12–24h), a striated muscle relaxant (diazepam 2.5–5 mg/cat q12h PO or dantrolene 1 mg/kg q12h PO) and analgesics (nonsteroidal anti-inflammatories and opioids) for 5 to 7 days. Most cases will resolve with time, but an indwelling catheter or regular gentle bladder expression may be necessary for 3 to 5 days. Urine Diversion: If the urethra is unable to be catheterized or a perineal urethrostomy is not an option (e.g., breeding tom cat, large urethrolith lodged too far cranially to be removed during perineal urethrostomy surgery), urine should be diverted for 3 to 5 days to allow urethral inflammation and edema to subside before trying to flush the urethra again. Urine can be temporarily diverted by repeated cystocentesis (not preferred), a transabdominal Foley catheter secured in the bladder or bladder marsupialization (cystostomy). See Chapter 278. Once urethral inflammation subsides so the urethra can be catheterized, the Foley catheter is removed or bladder closed and replaced back into the abdomen. Permanent urinary diversion can be achieved by bladder marsupialization (salvage procedure) or prepubic urethrostomy and is necessary if urethral patency cannot be restored as often occurs with mid pelvic urethral tear post-trauma. Perineal Urethrostomy: This surgical procedure is indicated for cats with recurrent obstructions, urethral stricture, urethral uroliths, and distal urethral trauma. This life-saving surgery resolves urethral obstruction and prevents it from recurring; however, it predisposes to ascending bacterial cystitis and is not considered a first-line therapy. See Chapter 276.
Therapeutic Notes • Proper technique during catheterization and the use of soft silicon catheters are paramount in reducing urethrospasm. • Indwelling urinary catheters predispose to ascending urinary tract infections; however, prophylactic antibiotics do not prevent infection and should be avoided until the catheter is removed. • Ensure patency of the indwelling catheters at all times, and monitor urine output. The bladder should not distend at all while the catheter is in place. Urine production may be as much as 2 L per day for several days during the postobstructive diuresis and requires administration of similar volumes of intravenous fluids. • Management of each urethral obstruction can be expensive, and many cats with financial concerns are euthanized after one or two episodes. If long-term owner finances are expected to be limited, a perineal urethrostomy performed sooner improves their long-term survival.
533
SECTION 1: Diseases and Conditions
Prevention • The likelihood of urethral obstruction recurring is high regardless of the etiology but may be greatly reduced if appropriate preventive care is initiated following obstruction. • Cats with struvite crystalluria or mineralized urethral plugs should be managed with a struvite preventative diet. • Uroliths should be submitted for analysis and preventive strategies applied according to mineral composition; calcium oxalates are most common. • Cats with noncrystalline inflammatory plugs should be managed as for idiopathic cystitis. See Chapter 74. • If obstruction recurs despite appropriate preventative measures, a perineal urethrostomy is indicated to permanently prevent recurrence.
Prognosis With the correct initial management, the short-term prognosis for resolving the obstruction and correcting the metabolic derangements is good.
534
Longer standing obstructions generally carry a poorer prognosis than obstructions of short duration due to the life-threatening consequences of acute renal failure. Reobstruction occurs commonly, and the longterm prognosis is fair. This, however, is primarily due to the significant cost of therapy for urethral obstruction, with many owners electing euthanasia after repeated episodes.
Suggested Readings Bass M, Howard J, Gerber B, et al. 2005. Retrospective study of indications for and outcome of perineal urethrostomy in cats. J Small An Pract. 46(5):227–231. Drobatz KJ. 2008. Emergency management of the critically ill cat with urethral obstruction. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XIV, pp. 951–954. Philadelphia: Elsevier Saunders. Forrester DS, Roudebush P. 2007. Evidence-based management of feline lower urinary tract disease. Vet Clin North Am Small An Pract. 37(3): 533–558. Gerber B, Eichenberger S, Reusch CE. 2008. Guarded longterm prognosis in male cats with urethral obstruction. J Fel Med Surg. 10(1):16–23.
CHAPTER 221
Urinary Bladder Tumors Bradley R. Schmidt
Overview Urinary bladder tumors are rare in the cat. Transitional cell carcinoma (TCC) is the most common urinary bladder tumor in the cat, with squamous cell carcinoma (SCC) being the second most common tumor, followed by leiomyosarcoma. Lymphoma has also been reported in 2 cats. Leiomyoma is the most common benign tumor of the urinary bladder. Risk factors for development of urinary bladder tumors in the cat are not known. Urinary bladder tumors types are generally identified in older cats, with the mean age for cats with TCC being 13 to 15 years. Male and female cats were equally represented in all types of bladder tumors in most studies, but in one study males were over-represented. Clinical signs are similar to that seen in cats with urinary tract infections or idiopathic cystitis, with hematuria being reported in all cases of feline TCC. Other clinical findings may include dysuria, stranguria, pollakyuria, a palpably distended urinary bladder secondary to urethral obstruction, and nonspecific signs such as anorexia, weight loss, or lethargy. Azotemia may be noted and may be related to the tumor (secondary to urethral or ureteral obstruction) or may be due to concurrent chronic renal disease. In contrast to dogs, TCC in cats may arise from any region of the urinary bladder. Ureteral leiomyosarcoma has been reported in one cat, and urethral leiomyoma resulting in urethral obstruction was reported in another cat. Metastasis is uncommon at the time of diagnosis for all tumor types; however, in two series of 31 cats with TCC, 9 cats developed metastasis to the iliac lymph nodes with 2 of these cats having pulmonary metastasis as well. Extension of the tumor to the uterine stump and omentum was also noted in 2 cats. Other reported metastatic sites include the spleen, gastrointestinal tract, diaphragm, muscle, and liver.
(A)
Diagnosis Primary Diagnostics • Ultrasound: Urinary bladder masses may present as a discreet mass with arising from any region of the urinary bladder or without extensive wall thickening. See Figures 221-1 and 221-2. Mineralization of the mass may be present. Concurrent cystic calculi may also be seen. Evaluation of the entire abdominal cavity should be performed to evaluate for presence of lymph node or organ metastasis as well as to evaluate for hydronephrosis secondary to ureteral obstruction. • Urinalysis: Malignant cells may be identified on routine urinalysis, but in one study, only 2 of 15 urine samples (13%) demonstrated malignant cells. • Fine-Needle Aspiration and Cytology: Ultrasound-guided transabdominal needle biopsy may reveal the diagnosis prior to surgery, but it may not always be diagnostic. Furthermore, tracking of neoplastic cells into the peritoneum or abdominal wall may occur. • Traumatic Catheter Biopsy: A biopsy using a rigid, open-ended polypropylene, tomcat (3.5 French) catheter may result in a diagnosis in some cats. This procedure requires anesthesia.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
(B) Figure 221-1 When a TCC is diagnosed when it is small (A), surgical removal (B) is feasible and may provide many months of remission. Images courtesy Dr. Gary D. Norsworthy.
• Surgical Removal and Histopathology: Because cystoscopy is generally not possible due to the small diameter of the urethra, surgery with excisional or incisional biopsy is the most definitive means of diagnosis.
Secondary Diagnostics • Minimum Date Base: A complete blood count, serum chemistry profile, thyroid panel, and retroviral screen should be performed to evaluate the overall health of the patient prior to therapy. Azotemia may be present and may be related to the tumor or may be secondary to chronic renal changes, calculi, cortical cysts, or infections.
535
SECTION 1: Diseases and Conditions
(A) Figure 221-3 Positive contrast cystography is another means of identify and quantifying a bladder mass. This fast-growing mass, seen as a filling defect, was confirmed with histopathology to be a lymphoma. Image courtesy of Dr. Gary D. Norsworthy.
• Cardiac Ultrasound and Electrocardiogram: Because many cats with bladder tumors are geriatric, these diagnostic tests should be considered prior to any surgical procedure or prior to aggressive intravenous fluid administration in known hyperthyroid cats or in cats in which cardiac disease is clinically suspected.
Treatment Primary Therapeutics (B) Figure 221-2 When a TCC is diagnosed when it is very large (A), surgical removal is not feasible and the prognosis is grave. At this point metastasis is highly likely. (B) Necropsy shows the mass filling the lumen of the bladder. Images courtesy Dr. Gary D. Norsworthy.
• Urine Culture and Sensitivity: This should be performed to evaluate for concurrent urinary tract infections. • Thoracic Radiographs: Although pulmonary metastasis is uncommon, these should be performed to evaluate for metastasis as well as to evaluate the cardiopulmonary system. • Other Imaging: Contrast radiography (see Figure 221-3), computerized tomography (CT) scan, or magnetic resonance imaging (MRI) may be considered to determine the extent of the tumor locally and for presence of abdominal metastasis, but these diagnostic tests are labor intensive and expensive when compared to abdominal ultrasound examinations. CT may be superior to radiographs in identifying pulmonary metastasis.
• Surgery: Because many tumors of the urinary bladder may arise from the body wall of the urinary bladder and not the trigone, surgery is the mainstay of therapy, with partial cystectomy being the surgical procedure of choice. This procedure causes reduced reserve capacity initially resulting in dysuria and pollakiuria; however, the reserve capacity will increase in most cats over time. Even with aggressive surgery, however, the recurrence rate is greater than 50%. Long-term survival (18 months plus) is reported in cats with benign urinary bladder tumors.
Secondary Therapeutics • Chemotherapy and COX-2 Inhibitors: There are limited reports on the efficacy of chemotherapy, including piroxicam, in the treatment of urinary bladder tumors; however, reports have found high recurrence rates and short survival times. In cats with lymphoma of the urinary bladder, cyclophosphamide-Oncovin (vincristine)– prednisone (COP) or L-asparaginase-vincristine-cyclophosphamidechlorambucil-doxorubicin-prednisone (CHOP-based) protocols are recommended. See Chapter 34. • Intravesicular therapy has been treated in one cat, but no studies exist on the efficacy of this treatment of bladder tumors in the cat.
Diagnostic Notes • Peritoneal seeding secondary to transabdominal needle biopsy is of the most concern and should not be performed when the urinary bladder tumor is thought to be amendable to surgical removal based on ultrasound examination.
536
Therapeutic Notes • Supportive care with antibiotics for concurrent infections, amitriptyline for discomfort, nutritional support, and therapy for chronic renal disease may be indicated. See Chapters 190 and 191.
Urinary Bladder Tumors
• Surgical seeding has been reported as in the dog. To help prevent peritoneal or abdominal wall seeding, pack off and isolate the urinary bladder during the incisional or excisional biopsy procedure, lavage the abdomen well, and change gloves and surgical pack prior to closure of the abdomen. • Local recurrence is common even with aggressive surgery, likely due to the extensive nature of most tumors at the time of diagnosis. • Although metastasis is uncommon at the time of initial diagnosis, it may occur later in the course of the disease. • To date, chemotherapy as a primary treatment for bladder tumors appears not to prolong disease-free intervals or survival times; however, adjunctive chemotherapy including piroxicam or meloxicam may be considered post-surgery. • Because most patients are geriatric, monitoring for other concurrent medical conditions is recommended prior to definitive treatment.
Prognosis Although many malignant urinary bladder tumors arise away from the trigone, the local recurrence rate appears to still be high, likely due to tumor size at the time of surgery. The overall median survival in 20 was 261 days with a majority of deaths attributed to local disease progres-
sion. The prognosis for cats with other malignancies of the urinary bladder appears to be similar based on the small case samples reported. The prognosis for cats with benign tumors appears to be more favorable with surgical resection. See Chapter 130 for prognostic factors in cats with lymphoma.
Suggested Readings Brearley MJ, Thatcher C, Cooper JE. 1986. Three cases of transitional cell carcinoma in the cat and a review of the literature. Vet Rec. 118:91–94. Moore AS, Ogilvie GK. 2001. Tumors of the urinary tract. In AS Moore, GK Ogilvie, eds., Feline Oncology, pp. 311–317. Trenton: Veterinary Learning Systems. Schwarz PD, Greene RW, Patnaik AK. 1985. Urinary bladder tumors in the cat: a review of 27 cases. J Am Anim Hosp Assoc. 21:237–245. Takaqi S, Kadosawa T, Ishiquro T, et al. 2005. Urethral transitional cell carcinoma in a cat. J Small Anim Pract. 46(10):504–506. Wilson HM, Chunn R, Larson VS, et al. 2007. Clinical signs, treatments, and outcome in cats with transitional cell carcinoma of the urinary bladder: 20 cases (1990–2004). J Am Vet Med Assoc. 231(1): 101–106.
537
CHAPTER 222
Urolithiasis Gary D. Norsworthy
Overview
Diagnosis
A urolith is a stone, or concretion, formed in the urinary tract; it is also called a urinary calculus or stone. It is composed of a small amount of organic matrix (generally mucoid material) and a large amount of crystalline material (organic and inorganic crystalloids). At least four types of uroliths have been recognized in cats. Struvite (magnesium ammonium phosphate hexahydrate or triple phosphate) uroliths accounted for 32% of those found in 1999 and 49% in 2007 in the United States; calcium oxalate uroliths were present in 55% of cases in 1999 and 41% in 2007 in the United States. The balance are calcium phosphate, urate, and of mixed composition. A small percentage of struvite uroliths are induced by bacterial infections, usually Staphylococci spp. or Proteus spp. The remainder of struvite uroliths and the other types of stones are typically unrelated to bacteria, and their pathogenesis is not understood, although dietary factors are considerations in some cases. Uroliths in the kidneys are generally asymptomatic and are usually composed of calcium oxalate; uncommonly chronic or recurrent hematuria occurs with the origin of the hemorrhage being in the kidneys. See Figure 222-1. When uroliths are found in the bladder, hematuria and dysuria result. Ureteral or urethral uroliths cause severe pain, dysuria, or obstruction. Urine is commonly supersaturated with crystal-producing materials. However, the presence of crystals does not necessarily predispose the cat to urolith formation. Urine pH is an important element in crystal formation; however, it is not the only one or necessarily the most important one. Struvite, calcium carbonate, calcium phosphate, and urate are less soluble in alkaline urine. Cystine and uric acid are less soluble in acid urine. Urine pH does not appear to have a major effect on the solubility of calcium oxalate; these uroliths will not dissolve regardless of the pH of the urine, within the limits of being compatible with life. However, most calcium oxalate uroliths occur in cats with acid urine. Urinary stasis encourages urolith formation regardless of the type.
Primary Diagnostics • Clinical Signs: Clinical signs of hematuria, dysuria, or urethral obstruction are typical of urolithiasis; however, some cats are asymptomatic. Undetected pain is likely present in many cats with bladder uroliths as evidenced by the fact that many owners report their cats being more active and sociable following urolith removal. • Radiography or Ultrasound: These imaging modalities are able to identify most uroliths. Small-sized uroliths (<2 mm diameter [1/8 inch]) may elude detection, although small calcium oxalate uroliths are more likely to be visible than small struvite uroliths due to differences in radiodensities. Radiolucent uroliths may require contrast radiographic studies or ultrasound examination. See Figures 222-2 through 222-8.
(A)
Figure 222-1 Uncommonly chronic or recurrent hematuria can originate from urolithinduced irritation of the kidneys. This cat had hematuria for 6 months. The uroliths are surrounded by blood clots.
(B) th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
538
Figure 222-2 Multiple uroliths are seen in the kidneys in the (A) lateral and (B) VD radiographic views. Uroliths in the kidney are likely to be calcium oxalate.
(A) (B) Figure 222-3 (A) Renal uroliths are seen by ultrasonography as hyperechoic masses (down arrow) with shadows (horizontal arrow). (B) One of the larger uroliths is shown as it was found at necropsy.
(A)
(C)
(B)
(D)
Figure 222-4 (A) Two larger uroliths are seen in the kidneys (horizontal arrows), and three smaller uroliths are seen in the ureters (down arrows) in this lateral radiograph. (B) Uroliths are seen in the renal pelvis which is dilated due to an obstruction in the ureter. (C) When obstructed, the ureter has a larger diameter than normal so it and the urolith (arrow) are easily identified. (D) An incision is made in the ureter over the urolith just large enough for the urolith to exit. See Chapter 275.
539
(A) (A)
(B)
(B)
Figure 222-5 (A) Large uroliths in the bladder are easily seen with ultrasound. Note the prominent shadowing (arrow). (B) Struvite uroliths were removed surgically.
Figure 222-6 (A) Several uroliths less than 2 mm in diameter are seen in the kidneys and bladder. (B) These are the calcium oxalate uroliths removed surgically.
(A) Figure 222-7 urethrostomy.
540
(B)
(A) Several small uroliths are seen in the urethra (arrow). (B) One larger calcium oxalate calcium oxalate urolith and several small ones were removed via a perineal
Urolithiasis
• Quantitative analysis of the urolith is strongly encouraged. The composition of the center of the stone is the most important aspect for planning preventive measures. • If bacteria are noted within the center of the urolith, the urolith and the cat’s urine should be cultured if it has not already been done. • Interpretation of urine sediment for the presence of bacteria should be done with caution. Brownian movement may occur in cellular breakdown products. These breakdown products may have the same size, shape, and movement of bacteria. Conversely, it is not unusual for urine sediment to be read as free of bacteria but bacteria to be cultured. Urine culture is recommended.
Treatment Primary Therapeutics
(A)
(B) Figure 222-8 (A) Multiple small to medium sized uroliths are seen in the kidneys. The VD view permits sizing and counting more precisely than the lateral view. (B) If the lateral view is made to include the urethra, the cause of the obstructive crisis can be determined (arrow). Uroliths in the urethra are not typically visualized in the VD view.
Secondary Diagnostics • Palpation: Because of their size, most uroliths in the urinary bladder are not palpable. However, bladder palpation should be part of the physical examination. In some cases the urolith may not be palpated, but pain may be elicited.
Diagnostic Notes • Many uroliths in the urinary bladder are thin (“wafer-like”). Highdefinition radiographic technique may be necessary to identify them. Double-contrast (positive and negative) radiographic studies of the bladder are recommended because some are radiolucent. • Small uroliths may be passed through the urethra of females. They may lodge in the vagina or adhere to the perineal hair. These should be submitted for analysis so that appropriate treatment and preventative strategies can be formulated.
• Surgical Removal: In general, it is not advisable to surgically remove renoliths. Uroliths causing obstruction of the ureters must be removed surgically and promptly. See Chapters 220 and 275. Uroliths within the bladder can be removed by retrograde urohydropropulsion or surgically via cystotomy. It is advised that radiographs be performed immediately following cystotomy to verify removal of all of the uroliths present. Uroliths lodged within the urethra may be backflushed into the bladder for surgical removal or medical dissolution; however, most urethral uroliths must be removed by perineal urethrostomy. • Medical Management: Ureteral uroliths sometimes spontaneously move retrograde even as far back as the renal pelvis. If surgery is to be performed, a radiograph should be taken immediately prior to surgery to verify location. It has been reported that amitriptyline (1 mg/kg q24h PO for 3 days) may cause retrograde migration of ureteral uroliths, but this should not be attempted if obstruction is present. • Urohydropropulsion: This nonsurgical technique has been successful in removing small uroliths from the bladder of female cats or from male cats that have had a perineal urethrostomy. The cat is positioned so its vertebral column is vertical, directing the neck of the bladder downward. In this position gravity moves the urolith to the neck of the bladder. The bladder is manually expressed forcing the urolith down the urethra and out of the cat. • Dietary Dissolution: Many struvite uroliths located in the bladder may be dissolved with Feline Prescription Diet s/d® (Hill’s Pet Products, Topeka, KS); 2 to 4 months of exclusively feeding this diet are required. It is possible for a urolith to become small enough to pass into the urethra causing an obstruction. Dietary dissolution of other types of uroliths has not been successful. • Antibiotic Therapy: Some struvite uroliths are induced by bacteria, especially Staphylococcus spp. and Proteus spp. When culture reveals their presence in urine or within the center of a urolith, appropriate antibiotics are indicated.
Secondary Therapeutics: Prevention • Increased Water Intake: Reducing urine specific gravity (USG) is desirable because crystals must reside in the urinary tract for a sufficient time for urolith formation to occur. Canned foods can be effective in reducing USG. Some cats will consume more water if a drinking fountain, producing running water, is used or if ice cubes are placed in the drinking water. If the local drinking water has an undesirable taste, bottled water may also be helpful. Some commercial diets are designed to increase thirst and cause polyuria. • Struvite Uroliths with Infection: This is a common situation in dogs but very uncommon in cats. Culture and sensitivity serve as the basis for antibiotic selection. If medical dissolution is used, appropriate antibiotics should be continued for 2 weeks past complete resolution of the urolith. If surgical removal is chosen, antibiotics should be
541
SECTION 1: Diseases and Conditions
•
•
•
•
given for no less than 4 weeks. The urine should be cultured monthly for 2 to 3 months, then again in 6 months. The urine should also be cultured any time the urine pH exceeds 7.5. Struvite Uroliths without Infection: Struvite solubility is reduced in urine of pH greater than 6.7. Therefore, acidifying diets are beneficial. The goal is to keep the urine pH at 6.5 or less. Due to the postprandial alkaline tide, ad libitum feeding is desirable to maintain a more constant urine pH. Urinary acidifiers may also be effective in reducing urine pH. DL-methionine or ammonium chloride are most effective and are each dosed at approximately 1 g/cat q24h; the final dose is adjusted according to urine pH. In addition to urinary acidification, restriction of magnesium, phosphorus, and calcium have been recommended; magnesium restriction is probably of much less value than originally proposed. Cats using this approach should be monitored using urine pH levels and the presence of struvite crystals in the urine. However, there is not a strong correlation with crystalluria and urolith formation. A recent study found a recurrence rate of 2.7% for a first recurrence and 0.2% for second recurrence. For several reasons, these rates may be lower than actual. Calcium Oxalate Uroliths: Nonacidifying diets, that have reduced sodium and protein but are not restricted in phosphorus or magnesium, are recommended. Several such diets are commercially available. Potassium citrate (50–100 mg/kg q12h PO) is unproven, but possibly, effective because it may act as an inhibitor of calcium oxalate formation, and its alkalinizing effect may reduce bone release of calcium. However, oxalate solubility is relatively unaffected by a wide range of urine pH, which explains why dietary prevention and potassium citrate are often unsuccessful in calcium oxalate urolith prevention. Hypercalcemia is fairly common in older cats, and calcium oxalate uroliths are more common in older cats. Hypercalcemia may predispose the cat to calcium oxalate formation by providing the necessary calcium source for urolith formation. Increasing water intake is also recommended. Cats using this approach should be monitored using urine pH levels and the presence of calcium oxalate crystals in the urine. However, there is not a strong correlation with crystalluria and urolith formation. A recent study found a recurrence rate of 7.1% for a first recurrence, 0.6% for second recurrence, and 0.1% for third recurrence. For several reasons, these rates may be lower than actual. Struvite and Calcium Oxalate: Another approach at prevention is the use of a diet purported to have eliminated the key components in urolith formation (c/d® Multicare, Hill’s Pet Nutrition). It claims to have the potential to prevent all types of feline uroliths. Cats using this approach should be monitored using the presence of crystals in the urine. However, there is not a strong correlation with crystalluria and urolith formation. Urate Uroliths: Prevention centers on the use of a nonacidifying diet or a urine alkalinizing drug. Increasing water intake is also recommended. Effectiveness of allopurinol in the cat is unknown; however, it has been used with some success at a dose of 10 mg/kg q8h PO for
542
3 days then reduced to 10 mg q24h PO. This drug has not been extensively studied in cats; thus, toxicity is a potential problem. A recent study found a recurrence rate of 13.1% for a first recurrence and 4.1% for second recurrence. For several reasons, these rates may be lower than actual. • Cystine Uroliths: A nonacidifying diet is recommended. Increasing water intake is also recommended. Sodium bicarbonate should be avoided because dietary sodium may enhance cystinuria. • Calcium Phosphate Uroliths: An effective approach is not currently recognized, but the approach taken for calcium oxalate uroliths seems appropriate. If hypercalcemia is present, its cause should be diagnosed and treated, if possible.
Therapeutic Notes • Successful medical dissolution requires that the struvite urolith be bathed in urine for relatively long periods of time, so only uroliths in the kidneys or bladder are amenable to this approach. • Acidifying diets or acidifiers are contraindicated in cats with a history of renal insufficiency or failure. • Acidifying diets and urinary acidifiers should not be used concomitantly unless it is documented that such a practice is required to produce urine with a pH of 6.5 or less. It is not desirable to reduce urine pH below 5.0. • Struvite urolith prevention is generally more successful than calcium oxalate urolith prevention. No currently known method has been consistently successful in preventing calcium oxalate uroliths.
Prognosis Prognosis for urolithiasis is generally good as long as surgical intervention is permitted at the appropriate times; however, recurrence is problematic. Determination of the urolith composition is essential for selection of appropriate dietary therapy. The most successful prevention programs are for struvite urolithiasis.
Suggested Readings Albasan H, Osborne CA, Lulich JP, et al. 2009. Rate and frequency of recurrence of uroliths after an initial ammonium urate, calcium oxalate, or struvite urolith in cats. J Am Vet Med Assoc. 235(12): 1450–1455. Lulich JP, Osborne CA. 2009. Changing paradigms in the diagnosis of urolithiasis. Vet Clin North Am Small Anim Pract. 39(1):79–91. Osborne CA, Lulich JP, Kruger JM, et al. 2009. Analysis of 451,891 Canine uroliths, feline uroliths, and feline urethral plugs from 1891–2007: Perspectives from the Minnesota Urolith Center. Vet Clin North Am Small Anim Pract 39(1):183–197.
CHAPTER 223
Uveitis Gwen H. Sila and Harriet J. Davidson
Overview The uvea is the middle portion of the eye made up of the iris, ciliary body, and choroid. Uveitis may involve any one of these structures resulting in iritis, cyclitis, or choroiditis, respectively. It may also involve combinations of these structures resulting in anterior uveitis (iridocyclitis) or posterior uveitis (chorioretinitis). Uveitis may occur alone, or it may be associated with other ocular or systemic diseases. The causes of uveitis are variable, but in over 50% of the cases the disease is considered idiopathic. However, even with idiopathic uveitis there is an initiating pathologic process involved although that process may not be determined. Anything that allows systemic immunocytes access to the intraocular structures of the immune-privileged eye can lead to uveitis. This means that destabilization of the blood-aqueous barrier from trauma, intraocular surgery, systemic inflammation, or vasculitis may result in intraocular inflammation. One documented cause of uveitis is bacterial infection. This may be due to direct bacterial colonization of intraocular structures or hematogenously spread antigenantibody complexes. Anytime a severe systemic infection occurs, uveitis may develop. Bartonella spp. are examples of infectious organisms that may be present with or without systemic clinical signs that have been implicated in cases of feline uveitis. Viral causes include feline immunodeficiency virus (FIV), feline infections peritonitis (FIP) virus, and uncommonly feline herpesvirus (FHV-1). The feline leukemia virus (FeLV) can cause uveitis due to the abnormal hematologic factors that result from the viral infection. Fungal infections that cause uveitis include Histoplasma capsulatum, Cryptococcus neoformans, Coccidioides immitis, and rarely Blastomyces dermatitidis. See Figure 223-1. Toxoplasma gondii is the most common protozoal infection resulting in uveitis.
Figure 223-1 This cat has anterior uveitis due to histoplasmosis resulting in iridal swelling and iris rubeosis. A pink fibrin clot is visible adherent to the ventral cornea. Photo courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 223-2 This cat has anterior uveitis caused by lymphoma. The iris is thickened (presumably with lymphocytes) and new blood vessels are growing into the iris (iris rubeosis). Photo courtesy Dr. Gary D. Norsworthy. Ocular signs range from conjunctivitis to retinal hemorrhage; these can also be seen with or without systemic disease. Parasitic causes are uncommon although larval migration through the eye by Toxocara species (both anterior and posterior chambers) has been reported. Systemic hypertension may cause retinal detachment (see Chapters 107 and 193) sometimes resulting in severe hyphema. The presence of red blood cells and other proteins in the eye stimulates an immune response and can result in chronic uveitis. Intraocular neoplasia is an uncommon ocular finding that may be present for months before resulting in uveitis. Primary tumors of the eye include melanoma, posttraumatic ocular sarcoma, and adenoma or adenocarcinoma. See Chapter 122. Secondary intraocular tumors may result from mammary or uterine adenocarcinomas, hemangiosarcoma, or lymphoma (see Figure 223-2). Lymphoma can cause uveitis as a paraneoplastic syndrome without neoplastic cells present within the eye. See Chapter 163. Lens-induced uveitis is caused by slow leakage of proteins from a cataractous lens (phacolytic uveitis) that are seen as foreign material by the immune system, resulting in a low-grade, chronic uveitis. Rupture of the lens capsule (phacoclastic uveitis) results in rapid release of lens proteins and severe, acute uveitis that is typically non-responsive to medical therapy. Often surgical removal of the lens is necessary to save the eye. Corneal ulcers may be accompanied by uveitis due to the axonal response, where the ciliary body is stimulated by the ophthalmic nerve as it leaves the cornea resulting in a release of local inflammatory mediators. A transilluminator is critical for complete evaluation of all structures of the eye including the conjunctiva, cornea, anterior chamber, iris, pupil, and lens. Fundic examination may aid in determining the need for further diagnostic tests as well as developing a prognosis. See Chapter 299. Clinical signs are variable and seen in multiple combinations. Lesions are not pathognomonic for the underlying cause, but some clinical signs are seen more frequently with certain diseases and can aid in the formulation of a diagnostic plan. The clinical signs include:
543
SECTION 1: Diseases and Conditions
• Pain, exhibited by squinting, tearing, elevated third eyelid, or guarding the eye from the owner. • Miosis, which may be resistant to mydriatics and cause an irregular pupil shape. • Conjunctival vascular engorgement, which can be differentiated from the engorgement of the underlying scleral vessels based on movement of the conjunctiva across the surface of the globe. In more severe cases the deeper vessels may become inflamed as well. • Iris color changes may result from either an increase or decrease in melanin within the iris stroma or due to growth of new iris vasculature (iris rubeosis) and congestion of normal iris vessels. See Figures 223-1 and 223-2. • Iris texture changes result from swelling of the iris (see Figure 223-2). Cells may easily slough off and result in pigmented cells in the anterior chamber and pigment deposits on either lens capsule or corneal endothelium. Anterior synechia (adhesions from the iris to the cornea) and posterior synechia (adhesions from the iris to the lens) may result. Iris nodules, which are accumulations of lymphocytes, are sometimes seen within the stroma giving it an undulating appearance. • Irregular pupillary margins result from changes in the iris stroma and musculature as well as synechia formation. The edges of the pupil may be irregular in only one location, or the entire pupil may be irregular (dyscoria). • Aqueous flare is caused by increased protein in the anterior chamber, which gives the aqueous a hazy appearance, and the iris may look dull. This is best seen with direct focal illumination. • Thick, white wisps or strands of fibrin may be seen within the anterior chamber. See Figure 223-2. • Keratitic precipitates (KP) are inflammatory cells stuck to the corneal endothelium and are often located ventrally. See Figure 223-3. The third eyelid may obscure the view of this portion of the eye, requiring careful manipulation of the cat and the third eyelid. Large cellular accumulations or “mutton fat” KPs, are seen frequently in FIP and occasionally in FeLV disease. • Hypopyon is a collection of white blood cells in the anterior chamber, frequently in the ventral aspect.
Figure 223-4 This cat has had bilateral, chronic, and idiopathic uveitis resulting in iris rubeosis, peripheral iris swelling, and mature cataract formation. Photo courtesy Dr. Gary D. Norsworthy.
• White to pink masses in the anterior chamber, associated with the iris, may be seen with FeLV infections. • Hyphema is blood in the anterior chamber. Frequently the erythrocytes gravitate to the ventral aspect of the anterior chamber. • Cataracts may result secondary to alterations in the aqueous from chronic uveitis. Patients with cataracts that form secondary to uveitis are at higher risk for complications following cataract removal and surgery is not routinely performed on these patients. See Figure 223-4. • Vitreous haze or opacity results from protein and cellular leakage into the vitreous from the ciliary body or retinal vessels. This may obscure the view of the fundus. • Retinal edema results in a dull, mottled tapetum. • Fluid or exudate accumulations beneath the retina create raised, dull, blister-like, or white fluffy areas, respectively, in the fundus. Retinal involvement more strongly suggests systemic infection, particularly fungal. • Retinal vascular engorgement or vasculitis causes the retinal vessels to be large and irregular. They may have a shimmering appearance. • Retinal hemorrhages suggest systemic hypertension as an underlying cause. See Chapters 107 and 193. • Bullous detachment causes the retina to bow forward, making examination in one plane difficult. Systemic hypertension should be a primary rule out for this condition. See Figure 193-1.
Diagnosis Primary Diagnostics • History and Physical Examination: Because of the multiplicity of causes, a thorough history and physical examination are essential. • Thorough Ophthalmic Examination: This should be performed looking for the clinical signs listed previously.
Secondary Diagnostics
Figure 223-3 Keratitic precipitates (KP) are inflammatory cells stuck to the corneal endothelium.
544
• Complete Blood Count (CBC) and Serum Chemistries: These tests will help evaluate other systems and may provide direction for more specific diagnostic tests. Blood testing should be strongly recommended when the eye does not respond to standard therapy or if
Uveitis
• •
•
•
•
•
there are systemic abnormalities. A blood coagulation profile should be considered in cases of intraocular hemorrhage, particularly if hypertension has been ruled out. Fluorescein Stain: Corneal ulcers must be ruled out as their presence may alter therapy. See Chapter 41. Tonometry: This may support the diagnosis because uveitis usually lowers intraocular pressure. It also aids in monitoring therapy. Tonometry also helps to diagnose glaucoma, a possible sequel to uveitis. See Chapter 85. Blood Pressure Determination: Systemic blood pressure should be determined in cases of hyphema or bullous retinal detachment to rule out hypertension. See Chapter 107. Specific Tests: Feline immunodeficiency virus (FIV) antibody, feline leukemia virus (FeLV) antigen, and fungal serology should be considered, especially if systemic clinical signs are present. Testing for these diseases may also be considered when there is no improvement with standard therapy. Toxoplasmosis testing is done with paired immunoglobulin G (IgG) titers 2 weeks apart; a four-fold increase indicates recent or active disease. Immunoglobulin M (IgM) titers can be detected for at least 9 weeks following active infection. See Chapters 75, 76, 77, and 214. Diagnostic Imaging: Thoracic radiographs are indicated if auscultation reveals harsh lung sounds or if neoplasia is suspected. Abdominal ultrasound or radiographs are indicated when palpation reveals an abdominal mass. Aqueocentesis: Fluid is aspirated from the anterior chamber. Titers for toxoplasmosis or fungal disease may be performed on aqueous humor and compared to blood titers. Higher intraocular titers suggest localized production of antibodies and active intraocular infection. Cytology on a cytospun sample can be used to find neoplastic cells. Aqueocentesis can be simple, but complications may be severe so it should be reserved for when other less invasive techniques have not confirmed a diagnosis.
• Nonsteroidal topical ophthalmic anti-inflammatory drugs may be used in combination with steroids in severe cases. These include 0.03% flurbiprofen, 0.1% diclofenac, 1% suprofen, or 1% indomethacin, which may all be used q8 to 12h. These drugs should not be combined with systemic steroids. • Systemic nonsteroidal anti-inflammatory drugs may be used when treating uveitis that is a result of primary corneal ulceration. • Ophthalmic Atropine: This medication causes paralysis of the ciliary muscle, which provides pain relief. It also helps prevent synechia formation by dilating the pupil. Ophthalmic atropine should be administered q12 to 24h. Atropine has an objectionable taste that will cause cats to salivate. Ointments are preferred because they are less likely to travel down the tear duct into the mouth. Atropine may be tapered in frequency or discontinued soon after resolution of clinical signs, frequently within a few days. Mydriasis may persist for days after stopping the medication. • Systemic Antimicrobials: Antibacterials should be used when bacterial infection is either confirmed or highly suspected. Treatment for Bartonella spp. may include azithromycin (10 mg/kg q24h PO), doxycycline (10 mg/kg q12h PO), or rifampin (10 mg/kg q24h PO) for 3 weeks. Treatment for toxoplasmosis is controversial, but the most commonly recommended antibiotic is clindamycin (12.5–25 mg/kg q12h PO for 4 weeks). See Chapters 17 and 214.
Secondary Therapeutics • Re-examination: This should occur in 2 to 7 days depending on initial severity to determine if clinical signs are improving. • Transillumination: Careful examination with a transilluminator is essential to detect changes in ocular structures secondary to inflammation. • Intraocular Pressure (IOP): Measurement of IOP is important for monitoring progress and to detect developing secondary glaucoma.
Treatment Primary Therapeutics
Therapeutic Notes
• Treat the Underlying Cause: If a systemic disease is present it must be treated concurrently with its ophthalmic consequences. • Anti-Inflammatory Medications: The most important therapy is to control inflammation within the eye. The route of administration and rate of therapy are determined by the clinical signs. • Topical ophthalmic corticosteroids should be administered as initial therapy in the majority of cases, even when infectious agents are present. They may be used q4 to 12h. Dexamethasone and prednisolone acetate are the ophthalmic drugs of choice because they penetrate the cornea well and are potent anti-inflammatories. • Subconjunctival injection of corticosteroids may be used in severe cases as an adjunct to topical ophthalmic steroids. A subconjunctival injection may be challenging in the cat due to its ability to retract the eye and resist restraint. Therefore, the cat should either be sedated or expertly restrained. Topical ophthalmic anesthetic is applied to the surface of the eye. A syringe with a 25-gauge needle, bevel up, is inserted under the bulbar conjunctiva. A bleb of the medication is injected. Commonly used drugs are triamcinolone (4–8 mg) or methylprednisolone acetate (4–8 mg). • Systemic steroids should be used in severe uveitis when penetration into the choroid is needed. Oral prednisolone (1–2 mg/kg q12h PO on a decreasing dosage schedule) may be used.
• Atropine: This should be the first drug discontinued followed by any systemic anti-inflammatories once symptoms regress. • If clinical signs are improving topical anti-inflammatories should be slowly tapered over weeks to months then discontinued. • A final examination should be performed approximately 1 week following cessation of all therapy. This examination should detect any ongoing mild inflammation that may not be apparent to the owner. • If clinical signs have not improved, diagnostic tests should be instituted, and the next level of anti-inflammatory therapy should be added. • There are multiple complications that can occur if uveitis is not treated successfully, including pigmentary deposits on the lens capsule, anterior or posterior synechia, cataracts, iris atrophy, lens luxation, retinal detachment or degeneration, formation of cyclitic membranes, phthisis bulbi, glaucoma, and blindness.
Suggested Readings Ketring KL, Zuckerman EE, Hardy WD. 2004. Bartonella: a new etiologic agent of feline ocular disease. J Am Anim Hosp Assoc. 40(1):6–12. van der Woerdt A. 2001. Management of intraocular inflammatory disease. Clinic Tech Small Anin Prac. 16(1):57–61.
545
CHAPTER 224
Ventricular Septal Defect Larry P. Tilley
Overview Ventricular septal defect (VSD) is among the most common congenital heart defect found in the feline. The interventricular septum separates the left and right ventricles and is divided into membranous and muscular components. Ventricular septal defects may occur in any area of the septum but more commonly occur in the membranous portion near the base of the heart. Additionally, concurrent congenital defects may be present (i.e., tetralogy of Fallot). Intracardiac shunting of blood results when the defect is present. Clinical significance of a VSD is determined by two factors: the size of the defect and the relative pressures in the ventricles, which influence the degree and direction of the shunt. Small defects (restrictive VSDs) often are of no hemodynamic significance, whereas large defects (nonrestrictive VSDs) are usually of significant hemodynamic consequence. When left and right ventricular pressures are normal, left-to-right shunting occurs and the left atrium and ventricle become volume overloaded secondary to the increased venous return. If pulmonary vascular resistance is high either secondary to pulmonary hypertension as a result of chronic pulmonary venous hypertension or as a result of pulmonary arterial hypoplasia, right-to-left shunting may occur. Physical examination usually reveals a holosystolic regurgitant-type murmur heard loudest over the right sternal border, a left apical systolic regurgitant-type murmur of mitral regurgitation, and a systolic ejectiontype murmur at the left base consistent with relative pulmonic stenosis. Cyanosis may be present if a right-to-left shunt is present.
(A)
Treatment Primary Diagnostics • Echocardiography (see Figure 224-1): This will reveal evidence of a left-to-right shunt: left atrial and ventricular eccentric hypertrophy; VSD, most commonly located high in the septum. Contrast echocardiography (bubble study) demonstrates left-to-right shunting (i.e., no contrast enters the left ventricle). Ultrasound may also reveal evidence of a right-to-left shunt: right ventricular concentric hypertrophy; right atrial enlargement. Contrast echocardiography demonstrates right-to-left shunting (bubbles entering the left ventricle from the right ventricle).
Secondary Diagnostics • Electrocardiography: There will be variable findings that are dependent on the severity of the shunt. • Thoracic Radiography (see Figure 224-2): Variable findings are present that are dependent on the severity and direction of the shunt. Significant left-to-right shunts cause left atrial and ventricular enlargement, pulmonary vascular overcirculation, and possibly evidence of left-sided congestive heart failure. Right-to-left shunts are associated with right atrial and ventricular enlargement and pulmonary vascular undercirculation.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
546
(B) Figure 224-1 (A) The long-axis view shows a VSD (arrow) that resulted in left-to-right shunting. (B) Color flow Doppler clearly demonstrates blood shunting through the VSD (arrow). (B) is the cat in Figure 224-1. IVS = interventricular septum; LVFW = left ventricular free wall; AO = aortic outflow tract. Images courtesy Dr. Gary D. Norsworthy.
Ventricular Septal Defect
Diagnostic Notes • VSDs may exist concurrently with other congenital heart defects. • Cardiac catheterization and selective angiocardiography are rarely needed to confirm the diagnosis.
Treatment Primary Therapeutics • Medical: Medical management of left-sided congestive heart failure is employed using diuretics, vasodilators, such as angiotensinconverting enzyme inhibitors, and moderate dietary salt restriction. • Surgery: Banding of the pulmonary artery may be attempted in cats with large nonrestrictive VSD, moderate or large shunting, and congestive heart failure. However, primary repair of the defect is costly, requires specialized equipment, and is associated with significant complications.
Secondary Therapeutics (A)
• Exercise restriction is an important aspect of therapy because exercise intolerance is significant. • Periodic phlebotomy is indicated if significant polycythemia is present in right-to-left shunting VSDs.
Therapeutic Notes • The response to therapy may be quite variable. • Digoxin therapy is indicated in selected cases with obvious systolic dysfunction or arrhythmias such as atrial fibrillation.
Prognosis Cats with small-to-medium left-to-right shunting restrictive VSDs typically have a favorable prognosis, especially if they remain asymptomatic at 6 months of age. Most cats with significant lesions develop congestive heart failure within the first few weeks of life or reverse their shunt due to pulmonary hypertension. Patients with moderate-to-severe cardiomegaly have significant volume overload and are at risk for developing congestive heart failure. Cats with a large nonrestrictive VSD or right ventricular hypertrophy or evidence of pulmonary hypertension and Eisenmenger ’s physiology have a poor prognosis similar to cats with tetralogy of Fallot.
(B) Figure 224-2 On both the lateral (A) and dorsoventral (B) projection; left ventricular enlargement, left atrial enlargement, and increased pulmonary artery prominence can be seen. Right ventricular enlargement is also present and indicates that pulmonary resistance is present. Images courtesy Dr. Gary D. Norsworthy.
Suggested Reading Strickland K. 2008. Congenital Heart Disease. In LP Tilley, FWK Smith, Jr., M. Oyama, et al., eds., Manual of Canine and Feline Cardiology, 4th ed., pp. 161–163. St. Louis: Elsevier Saunders.
547
CHAPTER 225
Vestibular Syndrome Mitchell A. Crystal
Overview Feline idiopathic vestibular syndrome is a common disorder of unknown etiology. It results from dysfunction of either the peripheral vestibular receptors in the inner ear or the vestibulocochlear nerve (eighth cranial nerve). Adult cats of any age are affected, with one study of 75 cats reporting a median age of 4 years. There is no sex or breed predilection. The disease may be more prevalent in the summer and fall months. Clinical signs include an acute or peracute onset of rolling, falling, ataxia, tight circling, or head tilt. See Figure 225-1. Cats will often assume a crouched position or lean to one side and are reluctant to move. Clinical signs are always toward the side of the lesion. Other less common accompanying signs include vomiting, anorexia, and vocalizing. Clinical signs do not progress. Physical examination reveals a horizontal or rotary nystagmus with the fast phase away from the lesion and, aside from those described, no other physical or neurologic abnormalities. Conscious proprioception is normal but may be difficult to assess due to patient struggle and disorientation. Rarely, bilateral disease is present. These cats present with a wide stance and wide head excursions, a mild or no nystagmus or head tilt, and they may fall to either side; many of these cats are deaf. Differential diagnoses to consider for peripheral vestibular signs include otitis interna, nasopharyngeal polyps, neoplasia of the eighth nerve or inner ear, trauma, toxicity (aminoglycosides, furosemide), blue-tail lizard ingestion (Southeastern United States), and vas-
cular disorders (i.e., heart disease, ischemic encephalopathy, vasculitis, or coagulopathy).
Diagnosis Primary Diagnostics • History: The owner should be questioned about the possibility of trauma, any recent or current drug therapy, the rapidity of onset and progression of illness, and whether any other signs are present. • Physical Examination: Physical and neurologic examination should be normal aside from signs of peripheral vestibular disease. A careful otoscopic examination of the external ear canal, tympanic membrane, and associated structures should be performed looking for clues that might indicate significant ear disease (i.e., otitis, polyps, or neoplasia) as a cause of vestibular disease.
Secondary Diagnostics • Tympanic Bulla Imaging: Radiographs, computerized tomography (CT), or magnetic resonance imaging (MRI) evaluation will help exclude otitis interna, polyps, and neoplasia. See Figures 158-1, 158-2, and 158-4.
Diagnostic Notes • A diagnosis of feline idiopathic vestibular syndrome is based on the presence of clinical signs, lack of progression, rapid improvement, and the exclusion of other differential diagnoses. Routine laboratory tests are within normal limits.
Treatment Primary Therapeutics • Supportive Care: The cat should be placed in a quiet area with minimal stimulation. If imbalance, disorientation, or apprehension is severe, sedation with diazepam (0.1–0.5 mg/kg q6–12h IV or PO) may be helpful.
Secondary Therapeutics
Figure 225-1 The clinical signs of the vestibular syndrome include an acute or peracute onset of rolling, falling, ataxia, tight circling, and/or head tilt. Image courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
548
• Fluids and Nutrition: Fluid or nutritional support are occasionally initially needed in cats that are adipsic or anorexic. • Antiemetics: Dolasetron mesylate (0.3–0.6 mg/kg q12–24h IV or SC), ondansetron (0.5–1.0 mg/kg q8–12h IV, IM, or SC), metoclopramide (0.2–0.5 q6–8h PO, SC, or IM or 1–2 mg/kg per day constant rate intravenous infusion), chlorpromazine (0.25–0.5 mg/kg q6–8h SC or IM), prochlorperazine (0.1–0.5 mg/kg q6–8h SC or IM), or maropitant citrate (1 mg/kg q24h SC) can be used if vomiting is present.
Therapeutic Notes • Glucocorticoids do not speed recovery and are not recommended. • Tranquilizers may help in control of severe clinical signs but do not speed recovery.
Vestibular Syndrome
Prognosis The prognosis for complete or near-complete recovery is excellent and usually occurs within 2 to 3 weeks, although rare cats require several months to recover. Most cats show dramatic improvement in 72 hours and continue to gradually improve. The head tilt is often the last problem to resolve, and some cats retain a residual mild-to-moderate head tilt indefinitely. Recurrence is rare.
Chrisman CL. 2003. Head tilt, disequilibrium, and nystagmus. In C Mariani, S Platt, R Clemmons, eds., Neurology for the Small Animal Practitioner. Made Easy Series, pp. 125–144. Jackson, WY: Teton NewMedia. Cochrane SM. 2007. Vestibular disease, idiopathic—cats. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult. Canine and Feline, 4th ed., pp. 1426–1427. Ames, IA: Blackwell Publishing.
Suggested Readings Burke EE, Moise NS, De Lahunta A, et al. 1985. Review of idiopathic feline vestibular syndrome in 75 cats. J Am Vet Med Assoc. 187(9):941–943.
549
CHAPTER 226
Viral Dermatitis Christine A. Rees
Overview Dermatitis is not a common manifestation of viral infection. However, the cat has three specific diseases that have clinical relevance. Feline herpesvirus (FHV-1) can cause a distinct primary dermatitis. It typically occurs on the face, near the nasal openings, or on the dorsum
of the nose. The lesions range from vesicular to ulcerative to necrotizing with mixed inflammatory dermatitis and form plaques or nodules. They are often irregularly shaped to arciform and typically involved haired skin. They may be indolent and have a long disease course. See Figure 226-1A. Scarring usually occurs when healing is complete. See Figure 226-1B. Less frequently, oral ulceration and ulcerations on the haired skin, feet, and ventrum may be present. See Chapter 95. Unlike the FHV-1, primary skin disease associated with the feline retroviruses, the feline leukemia virus (FeLV), and the feline immunodeficiency virus (FIV) are rare. See figures 226-2 and 226-3. Most often, skin disease associated with these viruses are opportunistic and may be associated with immunosuppression. Examples include recurrent subcutaneous abscesses, treatment resistant or relapsing dermatophytoisis, systemic fungal infections, and generalized demodicosis due to Demodex cati. Multicentric squamous cell carcinoma in situ (MSCCIS), also known as Bowen’s disease, occurs uncommonly. MSCCIS is unrelated to sunlight. Papillomavirus antigen has been demonstrated in 45% of affected cats; therefore, it deserves mention in this chapter. See Chapter 203.
(A)
(B) Figure 226-1 (A) The FHV-1 causes dermatitis on the face and often located near the nares. (B) Following healing, scarring is common. Images courtesy Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
550
Figure 226-2 The FeLV can cause an immunosuppressive-type of dermatitis. This cat had an ulcerative and crusty dermatitis on the head and neck. Used by permission Elsevier Saunders. Mansell JK, Rees CA. 2006. Cutaneous Manifestations of Viral Disease. In Consultations in Feline Internal Medicine, 5th ed., Figure 2-3.
Viral Dermatitis
present in the epidermis and the adnexal epithelium. Epidermal ulceration and follicular epithelial necrosis may also be present. MSCCIS is also confirmed with biopsy and histopathology. Evidence of the papillomavirus may be found in the tissues. • FeLV and FIV Testing: These are recommended when retroviral dermatitis is suspected. However, the presence of FeLV antigens or FIV antibodies is not equivalent to immunosuppression or primary retroviral dermatitis. Diagnosis is one of exclusion so a thorough, “rule-out” type diagnostic work-up is needed.
Treatment Primary Therapeutics Herpes Dermatitis
(A)
• Imiquimod: Extralabel application of topical imiquimod (Aldara®) is typically moderately effective for herpes dermatitis lesions when used three times weekly until clinical symptoms resolve. Its success rate for MSCCIS is about 25%. Adverse effects are uncommon, although focal skin irritation may occur. Treatment with (Aldara®) is expensive. • Lysine: Lysine has been used at 250 to 500 mg q12h PO to kill the actively replicating virus. However, recent studies seriously question its efficacy in this regard. • Acyclovir: Acyclovir is an ophthalmic medication used to treat herpesvirus infections in human eyes. A study demonstrated a questionable efficacy for this medication in treating FHV-1. • Famciclovir: The antiviral drug is showing great promise for herpesvirus infections. It is moderately expensive and is dosed at 62.5 to 125 mg/cat q12h PO.
Retroviral Dermatitis
(B) Figure 226-3 The FIV can cause an immunosuppressive-type of dermatitis. (A) It frequently occurs as a crusty dermatitis on the head and pinnae. (B) It may also occur as pruritic, focal dermatitis in multiple locations on the trunk. Images courtesy Dr. Gary D. Norsworthy.
Diagnosis
• Antiviral Drugs: No currently available drugs are capable of eliminating either the FeLV or the FIV from infected cats. • Corticosteroids: If pruritus is a significant component of the disease, corticosteroids may be beneficial. However, immunosuppressive doses should not be used because both retroviruses can cause immunosuppression. Prednisolone can be used at 1 mg/kg q24h PO if it is effective at that dose.
Prognosis The prognosis for herpesvirus dermatitis is generally good, but response to treatment is slow and relapses are possible. The prognosis for retroviral dermatitis is poor because the immunosuppression caused by these viruses is difficult to reverse.
Primary Diagnostics • Clinical Findings: An ulcerative dermatitis near the nasal openings that occurs following an upper respiratory infection is typical of FHV-1 dermatitis. • Histopathology: Diagnostic confirmation for herpesvirus dermatitis requires histopathology of the affected region. Numerous eosinophils and intranuclear inclusion bodies consistent with herpesvirus inclusions may be present. These intranuclear inclusions can be
Suggested Readings Hargis AM, Ginn PE, Mansell JE, et al. 1999. Ulcerative facial and nasal dermatitis and stomatitis in cats associated with feline herpesvirus-1. Vet Derm. 10:267–274. Mansell JK, Rees CA. 2006. Cutaneous Manifestations of viral disease. In JR August, ed., Consultations in Feline Internal Medicine, 5th ed., pp. 114–15. St. Louis: Elsevier Saunders.
551
CHAPTER 227
Vitamin A Toxicosis Gary D. Norsworthy
Overview Cats have a dietary requirement for preformed vitamin A. This is one of the reasons they cannot survive on a vegetable-based diet. Vitamin A is a fat-soluble vitamin that accumulates if fed or administered in excessive quantity. It is found in large quantities in liver and cod liver oil. Cats fed large quantities of these products more than 3 months, especially if also given milk or vitamin A supplements, are subject to hypervitaminosis A. In kittens, it is characterized by poor appetite, depression, dull, dry hair coat, and exophthalmos within 4 to 6 weeks of excessive vitamin A intake. Also, gingivitis develops, and teeth loosen. These signs are not noted in adult cats. Within 1 year, skeletal lesions will form due to osteoblast and chondrocyte death. Secondary ossification centers develop, and heavy buildup of osteophytes is found around joint centers. Affected cats develop cervical vertebral spondylosis and new periosteal bone formation. Ankylosis of cervical and cranial thoracic vertebrae and elbows are classic findings. The forelimbs become painful, causing affected cats to assume a kangaroo-like sitting posture. The sternum and costal cartilages can also be involved. Eating becomes difficult because of the cat’s inability to reach the food bowl. Grooming is also impaired, so the hair coat becomes oily and matted.
Diagnosis Primary Diagnostics • Dietary History: These cats typically have a diet that is high in liver or cod liver oil or are being supplemented heavily with vitamin A. • Clinical Signs: Inability to move the neck and forelimbs due to ankylosis is classic. The kangaroo-like sitting posture is typical. An unkempt hair coat is common. • Radiographs: Radiographs of the cervical spine and forelimbs reveal exostoses and ankylosis after about 1 year of the toxicosis.
Treatment Primary Therapeutics • Dietary Change: The cat must be removed from the liver or cod liver oil diet, and vitamin A supplements must be discontinued. The cat needs to be placed on a balanced feline diet. • Pain Relief: Anti-inflammatories and analgesics may be helpful.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
552
Secondary Therapeutics • Feeding: Placing the food and water bowls on a platform may make eating and drinking easier for the cat.
Therapeutic Notes • Most bony changes are irreversible. • Cat owners should be warned of the dangers of feeding diets and supplements with excessive vitamin A. • Plasma levels of vitamin A will become normal within a few weeks of diet correction; however, liver vitamin A levels will be elevated for years.
Prognosis The prognosis is guarded. Bony changes are generally irreversible. Other symptoms will resolve over time when a proper diet is fed.
Suggested Readings Freytag TL, Liu SM, Rogers QR, et al. 2003. Teratogenic effects of chronic ingestion of high levels of vitamin A in cats. J Anim Physiol Anim Nutr. 87:42–51. Fry PD. 1989. Hypervitaminosis A in the cat. J Vet Intern Med. 1:16–31. Goldman AL. 1992. Hypervitaminosis A in a cat. J Amer Vet Med Assoc. 200:1970–1972. Morgan JP. 2003. Radiographic and myelographic diagnosis of spinal disease. In JR August, ed., Consultations in Feline Internal Medicine, 3rd ed., pp. 425–458. Philadelphia: WB Saunders.
CHAPTER 228
Vitamin D Toxicosis Gary D. Norsworthy
Overview Hypervitaminosis D is an accumulation of toxic levels of vitamin D. It is almost always due to the ingestion of vitamin D-containing rodenticides or oversupplementation with this vitamin by the owner (greater than 60,000 IU/kg q24h). It has also been called cholecalciferol toxicosis. It results in a pathologic increase in vitamin D from increased gastrointestinal absorption, bone resorption, and reabsorption of vitamin D by the renal tubules. The net result is hypercalcemia and dystrophic calcification of soft tissues. The typical clinical signs include polyuria, polydipsia, vomiting, diarrhea, anorexia, and depression. The kidneys may be painful on palpation, and gastrointestinal or pulmonary hemorrhage may occur. The clinical signs develop about 6 to 12 hours after ingestion. Commonly used vitamin D-containing rodenticides include Quintox®, Rampage®, Ortho Rat-B-Gone®, and Ortho Mouse-B-Gone®.
Diagnosis Primary Diagnostics • History: The owner should be questioned carefully to determine if the cat has exposure to vitamin D-containing rodenticides or if vitamin D supplementation is occurring. The owner should also be asked if the cat is predatory because rodents killed by vitamin D-containing rodenticides may also be a source. • Biochemical Profile: The typical findings are hypercalcemia, hyperphosphatemia (>2.6 mmol/L [>8 mg/dL]), hyperproteinemia, and azotemia. The serum calcium level may be normal for up to 24 hours following ingestion of a rodenticide, then the total serum calcium may exceed 3.1 mmol/L (12.5 mg/dL) and ionized calcium may exceed 1.7 mmol/L (6.6 mg/dL). • Renal cortical 25-hydroxy vitamin D concentration greater than 80 nmol/L is consistent with cholecalciferol toxicosis. • Biliary 25-hydroxy vitamin D concentration greater than 100 nmol/L is consistent with cholecalciferol toxicosis. • Serum 25-hydroxy vitamin D concentration is increased at least 10 times normal (normal range: 65–170 nmol/L) in cholecalciferol toxicosis. • Urinalysis: The typical findings are hyposthenuria (USG = 1.001– 1.007), proteinuria, and glucosuria.
Secondary Diagnostics • Imaging: Radiographs or ultrasound of the kidneys, gastrointestinal tract, and lung may reveal mineralization. • Electrocardiogram: Bradycardia is often present. • Currently there are no confirmatory tests for calcipotriol (Doronex™) intoxication. Serum 25-hydroxy vitamin D and calcitriol are normal. • Serum 1,25 dihydroxy vitamin D has a narrow window of being increased, so it is of limited diagnostic value.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Treatment Primary Therapeutics • Induction of Vomiting: This is appropriate for acute exposure to a rodenticide. Syrup of ipecac (2–6 mL/cat PO) and xylazine (0.4– 0.5 mg/kg IV) are usually effective. If vomiting has not occurred in 15 minutes, administration of syrup of ipecac should be repeated once. • Activated Charcoal: This drug will prevent further absorption of the toxin. • Reduce Serum Calcium: This may be accomplished by (a) pamidronate disodium (Aredia™, 1.3–2 mg/kg in 0.9% sodium chloride by slow intravenous drip over 2–4 hours and repeated once 3–4 days later) until serum calcium is normal. (b) Salmon calcitonin (4–6 IU/ kg q3–12h IM or SC; it may be increased up to 10–20 IU/kg IM or SC). (c) Diuresis with normal saline solution, which is calciuretic. (d) Furosemide (1–4 mg/kg q8–12h PO or SC). (e) Prednisolone (2–6 mg/ kg q12h IM). Note: Because renal damage is likely, the use of normal saline is recommended in all cases.
Secondary Therapeutics • Maintenance of Furosemide and Prednisolone: These drugs should be continued for several days at 1 to 4 mg/kg q12h PO and 0.5 to 1.0 mg/kg q12h PO, respectively. • If GI protection is needed, give a sucralfate slurry (1 g q6h PO) or famotidine (1 mg/kg q12h SC or IV).
Therapeutic Notes • Do not administer any calcium-containing fluids. • Salmon calcitonin can produce anorexia, anaphylaxis, and vomiting. • If using pamidronate, monitor serum calcium and blood urea nitrogen (BUN) at 24, 48, and 72 hours following exposure. If hypercalcemia is present institute fluid diuresis. If it is not successful, repeat pamidronate at 72 or 96 hours after the first dose then monitor serum calcium and BUN q48h. • Following salmon calcitonin therapy monitor serum calcium and BUN q24h; continue adjusting dose until calcium returns to normal (24–48 hours for calcipotriol or 2 to 4 weeks for cholecalciferol). • Calcipotriol causes hypercalcemia for 24 to 48 hours and severe soft tissue mineralization. Long-term aggressive therapy is required. • Serum calcium levels should be monitored for several days or weeks. Many vitamin D-containing rodenticides require several weeks of treatment.
Prognosis The prognosis is generally good if rapid, aggressive treatment is instituted and the owner permits fairly long-term therapy in some cases. However, persistent hypercalcemia despite aggressive therapy warrants a grave prognosis.
553
SECTION 1: Diseases and Conditions
Suggested Readings Dorman DC. 1990. Anticoagulant, cholecalciferol, and bromethlin-based rodenticides. Vet Clin North Am Sm Anim Pract. 20:339–352. Moore FM, Kudisch M, Richter K, et al. 1988. Hypercalcemia associated with rodenticide poisoning in three cats. J Am Vet Med Assoc. 193:1099–1100.
554
Rumbeiha WK. 2007. Vitamin D Toxicity. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult, 4th ed., pp. 1430–1431. Ames, IA: Blackwell Publishing.
CHAPTER 229
Vomiting Mitchell A. Crystal and Paula B. Levine
Overview Vomiting is the forceful, reflexive ejection of gastric contents from the stomach through the mouth. Vomiting is initiated via the vomiting center located within the medulla oblongata of the brainstem. The vomiting center receives input from humoral or neural pathways that are activated by a variety of means (i.e., blood-borne substances, central nervous system disease and stimulation of various organ and tissue receptors sensitive to stretch, osmotic and chemical stimuli, and pain). The chemoreceptor trigger zone (CRTZ) can also stimulate the vomiting center. The CRTZ is located in the area postrema in the floor of the fourth ventricle of the brain where the blood-brain barrier is limited, allowing exposure to various circulating drugs, endogenous and exogenous toxins, and acid-base abnormalities. Vomiting due to vestibular stimulation is believed to be mediated by the CRTZ. The vomiting center and the CRTZ are important in the pharmacologic control of vomiting. Prior to beginning diagnostic evaluation and therapeutic management, vomiting must be differentiated from regurgitation (i.e., the passive, retrograde expulsion of food from the esophagus). Characteristics of vomiting include the presence of nausea (i.e., ptyalism, swallowing, retching, depression, restlessness, and licking of lips), abdominal muscle contraction, and bile or digested blood or food in the vomitus. Characteristics of regurgitation include lack of nausea, lack of abdominal contractions or bile in the vomitus, and the presence of nondigested food in a tubular shape. It is also important to assess vomiting as acute or chronic and as serious or non-serious prior to considering potential causes and initiating initial diagnostic or therapeutic management. Chronic/serious, chronic/nonserious, and acute/serious vomiting warrant a complete diagnostic evaluation, whereas acute/nonserious vomiting can initially be supported without an in-depth investigation. If acute/nonserious vomiting recurs or persists, then additional, more complete evaluation is necessary. In some cases, chronic intermittent vomiting may result from trichobezoars (hairballs). This may be normal or may indicate underlying disease. In either case, further evaluation and management may be necessary. See Chapter 217. Vomiting may be caused by gastrointestinal or extragastrointestinal disease. When performing a diagnostic workup of the vomiting cat, one should evaluate common causes of extragastrointestinal disease prior to performing diagnostics to investigate for primary gastrointestinal disease. Once common extragastrointestinal diseases have been excluded, causes of vomiting from primary gastrointestinal disease can be considered.
Diagnosis
TABLE 229-1: Known Differentials for Vomiting Extragastrointestinal Disease Endocrinopathies Hyperthyroidism Diabetic ketoacidosis Metabolic Diseases Renal failure Ureteral or urethral obstruction Hepatobiliary disease Pancreatic disease Electrolyte and acid/base disorders Toxicity Less Common Disorders Neurologic disease Cardiovascular disease Heartworm disease Peritonitis Diseases associated with feline leukemia virus and feline immunodeficiency virus Extra-gastrointestinal neoplasia Behavior disorders Pain Gastrointestinal Disease Dietary Intolerance or Allergy Gastroduodenal Ulcer Disease Non-specific Infectious Toxic Gastroenteritis Gastrointestinal motility disorders Helicobacter gastritis Inflammatory bowel disease Lymphoma and other GI neoplasia Obstipation Obstruction Foreign body Neoplasia Intussusception Stricture Parasitism Roundworms Tapeworms Stomach worms
Differential Diagnoses The gastrointestinal and extragastrointestinal causes of vomiting are listed in Table 229-1.
Primary Diagnostics • History and Physical Examination: The owner should be questioned about the cat’s exposure to toxins, access to foreign bodies, or changes
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
in diet. The owner should be asked about and the cat should be examined for clinical signs and findings that might be associated with the diseases listed in Table 229-1. • Oral Examination: It is important to look closely under the tongue for a linear foreign body. See Figure 229-1 and Chapter 128. • Data Base (Complete Blood Count [CBC], Chemistry Profile, and Urinalysis): A data Base should be submitted to evaluate for diabetes mellitus (i.e., hyperglycemia, glucosuria, ketonuria, and low urine specific gravity), liver disease (i.e., hyperbilirubinemia, decreased blood urea nitrogen (BUN), increased liver enzymes, and
555
SECTION 1: Diseases and Conditions
Figure 229-1 A sublingual examination can be accomplished by inserting a finger in the intermandibular space and pushing dorsally. This lifts the tongue enough to permit visualization of a mass or foreign body. Note that a string or thread looped around the base of the tongue that has been in place for several days may be buried in the oral mucosa and no longer visible. Photo courtesy Dr. Gary D. Norsworthy. bilirubinuria), renal disease (i.e., elevated BUN and creatinine with a decreased urine specific gravity), signs of hyperthyroidism (i.e., increased liver enzymes, a mild increase in packed cell volume [PCV], and low urine specific gravity), electrolyte and acid-base derangements (i.e., changes in sodium, potassium, chloride, calcium, pH, and bicarbonate [HCO3] or total carbon dioxide [TCO2]), and signs of lymphoma (occasional cats demonstrate circulating lymphoblasts and cytopenias). Nonspecific CBC changes, such as eosinophilia (i.e., parasitism, heartworm, eosinophilic inflammatory bowel disease [IBD], hypereosinophilic syndrome, and mast cell tumor), neutrophilia (i.e., gastroenteritis of various causes and neoplasia), neutropenia (i.e., salmonellosis and retroviral-induced illnesses), hemoconcentration (dehydration) and anemia (i.e., chronic disease and gastrointestinal blood loss), may also be present. • Fecal: A fecal flotation should be performed to evaluate for parasites. • Total T4: This test is indicated in all vomiting cats over 10 years of age to evaluate for hyperthyroidism. • Feline Leukemia Virus (FeLV) and Feline Immunodeficiency Virus (FIV) Tests: These tests are not confirmatory of disease but might support vomiting from a FeLV/FIV related illness.
Secondary Diagnostics • Abdominal Radiographs or Ultrasound: Abdominal imaging may reveal abnormalities in organ size or architecture, demonstrate a foreign body, show evidence of gastrointestinal obstruction, or identify abdominal masses (neoplasia). • Feline-Specific Pancreatic Lipase Immunoreactivity (fPLI): A 12hour fasting serum sample can be submitted to evaluate for pancreatitis. Some cases of chronic or intermittent pancreatitis have normal fPLI values. See Chapters 159 and 160. • Heartworm Testing: Heartworm testing is indicated in cats with chronic vomiting that live in endemic areas when other more common causes have been excluded. Heartworm serology should be performed in conjunction with other diagnostic testing (i.e., CBC, thoracic radiographs, transtracheal wash, and echocardiogram). See Chapter 88.
556
Figure 229-2 Grass is a gastric irritant and frequently causes vomiting. Note that most of the dry food that was vomited is whole because cats swallow most of their dry food without chewing it. This is normal. Photo courtesy Dr. Gary D. Norsworthy.
• Intestinal Biopsy and Histopathology: This procedure should be performed to investigate for primary gastrointestinal diseases in cases of chronic vomiting after other noninvasive procedures have been completed. Biopsies may be collected via endoscopy laparoscopy or exploratory laparotomy. In some cases, ultrasound-guided aspiration or biopsy for cytology or histopathology can be performed. Histopathology may reveal IBD, lymphoma or other gastrointestinal neoplasia or Helicobacter gastritis. Endoscopic biopsies may have limited value in cases in which vomiting originates from mid to distal areas of the small bowel. • Assessment for Helicobacter gastritis: See Chapter 90.
Diagnostic Notes • The presence of a hypochloremic metabolic alkalosis on a chemistry profile is suggestive of a pyloric outflow obstruction and is most commonly seen with gastroduodenal foreign bodies. • If a foreign body is suspected and a complete oral (including sublingual) examination cannot be completed in the awake cat, sedation is recommended. • Grass gastritis is common in cats that eat grass because grass is an irritant to the stomach. Figure 229-2.
Treatment Primary Therapeutics • Treat Underlying Disease: Controlling the underlying condition is essential for long-term cure. Treatment of metabolic derangements and abnormalities (i.e., diabetes mellitus, renal disease, and hepatic disease) is necessary to control vomiting related to these extragastrointestinal conditions. Endoscopy or surgery may be necessary for foreign body retrieval. Chemotherapy may be indicated for neoplasia (such as lymphoma). Antibiotic therapy would be indicated for Helicobacter gastritis or other bacterial gastroenteritis. • Gastrointestinal Rest: Give the cat nothing by mouth for 24 to 48 hours. • Correct Fluid, Electrolyte, and Acid-Base Derangements: Intravenous fluids are recommended, but subcutaneous fluids can be used in some instances.
Vomiting
TABLE 229-2: Antiemetics Commonly Used in the Vomiting Cat Drug
Location of Action
Dose
Side Effects
Metoclopramide
CRTZ, GIS
Cisapride Chlorpromazine Prochlorperazine Dolasetron (Anzemet™) Ondansetron (Zofran™) Maropitant (Cerenia™)
CRTZ, GIS CRTZ, VC CRTZ, VC CRTZ, vagal afferent pathways CRTZ, vagal afferent pathways CRTZ, VC, peripheral GI receptors
0.2–0.5 mg/kg q6–8h SC or PO or 1–2 mg/kg per day constant rate intravenous infusion 2.5–7.5 mg/cat q8–12h PO 0.1–0.5 mg/kg q6–8h SC or IM 0.1–0.5 mg/kg q6–8h PO, SC or IM 0.3–0.6 mg/kg q12–24h IV or SC; 0.6–1.0 mg/kg q12–24h PO 0.5–1.0 mg/kg q24h IV, IM, SC, or PO 1 mg/kg q24h SC or PO
Diarrhea, disorientation, extrapyramidal signs* None reported Hypotension, sedation Hypotension, sedation None reported None reported Injection site pain, constipation
VC, vomiting center; CRTZ, chemoreceptor trigger zone; GIS, gastrointestinal smooth muscle. * Involuntary limb movements, torticollis, stiffness, tremors, and loss of righting reflex.
• Diet: Feed a reduced-fat, easily digestible diet. Other dietary trials (e.g., novel antigen diet for food allergy management) may also be attempted. See Chapter 82.
Prognosis The prognosis varies depending on the cause of the vomiting.
Secondary Therapeutics • Antiemetic Therapy: Anti-emetics are useful when vomiting compromises hydration, acid-base, and electrolyte status, is frequent enough to cause significant stress or discomfort, or is present in animals at risk for aspiration pneumonia. Table 229-2 lists antiemetics commonly used in the vomiting cat. • Antacid Therapy: These medications are useful in frequent or severe vomiting to reduce mucosal injury from gastric acid and to help heal gastric ulceration. Commonly used agents include famotidine (0.5 mg/kg q12h IV, SC, or PO), ranitidine (2.5–3.5 mg/kg q12h IV, SC, or PO), cimetidine (10 mg/kg q8h IV, SC, or PO), or omeprazole (0.7 mg/kg q24h PO).
Therapeutic Notes • Anti-emetics are contraindicated in cases of gastrointestinal obstruction. • Add potassium to fluids (20–30 mEq of KCl per liter of fluids) because most vomiting cats have a normal to decreased serum potassium level that worsens with continued vomiting, anorexia, or nothing by mouth status, and fluid diuresis. Intravenous potassium administration should not exceed 0.5 mmol/kg per hour (0.5 mEq/kg per hour).
Suggested Readings Guilford WG. 1996. Approach to clinical problems in gastroenterology. In WG Guilford, DA Williams, DR Strombeck, eds., Strombeck’s Small Animal Gastroenterology, 3rd ed., pp. 50–62. Philadelphia: WB Saunders. Hickman MA, Cox SR, Mahabir S, et al. 2008. Safety, pharmacokinetics and use of the novel NK-1 receptor antagonist maropitant (Cerenia™) for the prevention of emesis and motion sickness in cats. J Vet Pharmacol Therap. 31:220–229. Plumb DC. 2005. Plumb’s Veterinary Drug Handbook, 6th ed. Ames, IA: Blackwell Publishing Professional. Strombeck DR, Guilford WG. 1996. Vomiting: pathophysiology and pharmacologic control. In WG Guilford, DA Williams, DR Strombeck, eds., Strombeck’s Small Animal Gastroenterology, 3rd ed., pp. 256–260. Philadelphia: WB Saunders. Twedt DC. 2005. Vomiting. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp. 132–136. St. Louis: Elsevier Saunders. Washabau RJ, Elie MS. 1995. Antiemetic therapy. In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XII, Small Animal Practice, pp. 679– 684. Philadelphia: WB Saunders.
557
CHAPTER 230
Weight Loss Mitchell A. Crystal and Mark C. Walker
Overview Significant unintentional weight loss in a previously healthy cat is often a harbinger of significant underlying systemic disease. Weight loss occurs with decreased hydration or is secondary to negative energy balance (i.e., energy needs exceed intake). Weight loss from dehydration occurs rapidly (within hours to days) and is considered significant when it exceeds 3 to 5% of normal body weight or sooner in animals that cannot normally conserve fluids (e.g., animals with renal failure, causes of polydipsia and polyuria (PU/PD), burns, or wounds). Other signs of dehydration include dry, tacky mucous membranes, pallor, poor skin turgor, and sunken eyes. Dehydration can be associated with a great number of disease processes and, thus, may demonstrate a wide variety of additional clinical signs. Diagnostic evaluation is based on significant clinical signs. Therapy involves replacing the fluid deficit, meeting maintenance fluid requirements, and providing additional fluids for continuing losses and/or decreased fluid intake. A cat’s basal energy caloric requirement can be estimated as follows: 70 to 80 Kcal/kg or (30 × weight in kg) + 70. Active cats and those living outdoors are fed a greater amount. During growth, pregnancy, and lactation, energy requirements increase 1.1 to 3 times the basal requirements. Weight loss due to negative energy balance occurs slowly, over days or weeks to months. Negative energy balance can result from decreased energy intake (i.e., anorexia or hyporexia, decreased access to food or ability to eat, or decreased quality of food) or increased energy use/loss (i.e., increased activity, pregnancy, lactation, growth, or disease states). Weight loss becomes significant when it exceeds 10% of normal body weight (5% in kittens). The prevalence of suboptimal body condition begins to increase at about 11 years of age and increases sharply as cats further age. Anorexia, polyphagic weight loss, and other conditions leading to decreased body weight must be investigated when significant weight loss occurs. See Chapters 10 and 176. Usually, other clinical signs resulting from the underlying disease process will be present, suggesting the appropriate diagnostic approach.
Diagnosis Differential Diagnoses Many diseases and disease conditions must be considered. See Table 230-1.
TABLE 230-1: Differential List for Cats with Weight Loss Dehydration Pancreatic disease Hyperthyroidism
Esophagitis Inflammatory bowel disease Parasites
Electrolyte and AcidBase Disturbances Renal failure (glomerular and tubular Cardiovascular disease
Gastritis Megacolon Protein-losing enteropathies Neoplasia
Infections (i.e., bacterial, fungal, protozoal, and viral) Decreased access to Fever food and water Lactation Pain Pregnancy Stress
• •
• •
•
Hepatobiliary disease Diabetes mellitus Alimentary lymphoma and other gastrointestinal neoplasia Helicobacter gastritis Oral disease, including jaw fracture Lymphoplasmacytic stomatitis Environment and miscellaneous factors Increased activity Poor food quality
malities in organ size and shape and to determine if abdominal masses are present. A thorough oral examination should be completed to evaluate for abnormalities that might inhibit eating. Dental radiographs should be considered. The body condition score should be recorded. See Table 153-1. Fundic Examination: Some infectious diseases and lymphoma may cause uveitis or chorioretinitis. Database (Complete Blood Count [CBC], Chemistry Profile, and Urinalysis): This is indicated to evaluate for signs of metabolic diseases, endocrinopathies, gastrointestinal diseases, infectious diseases, and neoplasia. Fecal: A fecal flotation should be performed to evaluate for parasites. Total T4: This test is indicated in all cats over 10 years of age that are demonstrating weight loss to evaluate for hyperthyroidism. See Chapter 109. Retroviral Tests: These tests may signal the presence of other diseases.
Primary Diagnostics • History: The client should be questioned about the cat’s access to food and water, diet, diet changes, appetite, thirst and urination, activity, reproductive status, and whether any other clinical signs are present. • Physical and Oral Examination: The cat should be closely examined for findings to support the disease processes listed in Table 230-1. Careful abdominal palpation should be performed to detect abnor-
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
558
Secondary Diagnostics • Thoracic Radiographs: Thoracic radiographs should be submitted to evaluate for signs of cardiovascular diseases, infectious diseases, and neoplasia. See Chapter 291. • Abdominal Radiographs or Ultrasound: Abdominal imaging should be performed to investigate organs (i.e., size, location, contour, and architecture) and to look for masses. See Chapter 292. • Electrocardiogram (ECG) or Echocardiogram: These are indicated to evaluate for signs of cardiovascular disease if historical or physical examination findings suggest cardiovascular disease or if primary diagnostics and imaging are non-diagnostic. See Chapter 291, 318, and 319.
Weight Loss
Diagnostic Notes • Additional diagnostics should be based on specific clinical signs and initial test results. • Up to 10% of cats with hyperthyroidism present as weight loss without polyphagia and increased activity (apathetic hyperthyroidism).
Treatment
See Chapter 188. Low carbohydrate diets, such as those indicated for diabetes mellitus, are high in protein calories and may be used for helping regain weight.
Therapeutic Notes • Daily changes in weight are a good indicator of hydration status. Body weight changes over time will help assess success of nutritional management.
Primary Therapeutics • Treat Underlying Disease: This is the cornerstone of successful treatment. • Correct Fluid and Electrolyte Disturbances: This should be done within the first 24 hours. See Chapter 302.
Secondary Therapeutics • Nutritional Support: See Chapters 10, 253, 255, and 256. Determine the caloric need based on the basal energy requirement (see Overview). This should be multiplied by an illness factor, usually 1 to 1.5 depending on severity of the illness. In cats with subacute to chronic reduced food intake, gradually reintroduce food to meet the calculated volume over a few days to avoid the refeeding syndrome.
Prognosis The prognosis varies depending on the severity and cause of the weight loss.
Suggested Readings Greco DS. 1995. Changes in body weight. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 4th ed., pp. 2–5. Philadelphia: WB Saunders. Streeter EM. 2007. Weight Loss and Cachexia. In LP Tilley, FWK Smith, Jr., eds., Blackwell’s 5-Minute Veterinary Consult: Canine and Feline, 4th ed., pp. 1438–1439. Ames, IA: Blackwell Publishing Professional.
559
SECTION
2 Behavior
CHAPTER 231
Aggression toward Humans Debra F. Horwitz
Overview Aggressive behavior is a common complaint of feline owners. Complaints should be taken seriously because unresolved aggression can lead to injury or relinquishment of the cat. Numerous medical or environmental conditions can provoke aggressive responses. Therefore, a complete medical examination and thorough behavioral history are essential for diagnosis and treatment. Cat bites to humans can cause serious illness and damage; therefore, any comments on aggressive behavior must be taken seriously and addressed.
• Body Language and Posture: Detailed descriptions of body posture and facial expression and ear position of the cat before, during, and after the incident are useful for detecting aggressive triggers and preventing future aggressive episodes. Cues to the intensity of the aggressive response should be documented (i.e., hissing, swatting, growling, chasing, wrestling, biting, and scratching). See Figure 231-1. Any vocalization by the cat should be included in this description. If an owner can learn the signs of an imminent aggressive episode, then he or she can intervene, avoid, or change the sequence of events to stop escalation of the behavior.
Diagnosis Primary Diagnostics • Medical Testing with Physical Examination: Medical problems can precipitate or contribute to aggressive responses in cats. Therefore, a complete medical examination is needed in all aggression problem behavior cases. A physical examination should be accompanied by additional diagnostic tests, as appropriate, such as urinalysis, fecal examination, and screening tests for metabolic or endocrine dysfunction. In some cases, additional diagnostic procedures such as radiographs may be necessary to look for potential sources of pain. Other areas that can contribute to an increase in irritability include dental disease, gastrointestinal problems, changes in vision or hearing, hypertension, and allergies. • Complete History: All behavior cases require a thorough and complete history for accurate diagnosis. Detailed history and descriptions of aggressive incidents are essential to identify potential triggers of aggressive behavior and direct appropriate corresponding treatment. Historical questions should focus on the aggressive episodes themselves, such as when, where, to whom and how frequently aggressive episodes occur. All participants must be identified to give the best description of events. Owner responses and pet responses to owner intervention must also be explored. This should allow the formulation of a potential diagnostic category and a treatment regime. • Resources: Information regarding the daily routine, including how resources are allocated within the home, must be collected. The client should be questioned about the cat’s ability to hide, retreat, or escape from the locations where aggressive episodes occur. Resources include, but are not limited to, food, water, litter boxes, toys, hiding spots, and perching areas. When and how food is provided to the cat should be explored. Limited resources or poor placement of resources may lead to aggression. For example, if a litter box is placed in a high traffic area or in a corner, the cat may become aggressive when using the box if accidentally surprised by an oncoming owner. Multiple resources and resource locations allow cats to avoid unwanted human interaction by providing them with alternatives if one resource is perceived as unsafe due to human occupation. • Age of Onset: Age of the cat at onset of the problem should be documented. When cats reach social maturity, around age 1 to 2 years, they may become more territorial or defensive.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
(A)
(B) Figure 231-1 The posture of the ears and tongue often give an indication of the cat’s intent. A, When the ears are erect and the tongue is flat, the cat is threatening but may not attack. B, When the ears are flat against the head and the tongue is rolled, the cat is extremely aggressively aroused and may attack. Images courtesy Dr. Gary D. Norsworthy.
563
SECTION 2: Behavior
• Owner-Cat Dynamics: Any cat-owner interactions and the response of the owner to each incident should be recorded. In some situations, the owner will unknowingly contribute to, reinforce, or exacerbate a chain of events leading to the aggressive episode. Daily interactive events such as play time, grooming, or petting should also be explored.
Secondary Diagnostics • Classification: Categorical classification is often used to help develop treatment plans for aggressive cats and their victims. The common categories of aggression toward humans include misdirected predatory or play-related aggression, social status and frustration-related aggression, petting aggression, redirected aggression, fearful or defensive aggression. Other classification schemes are used including defensive or offensive aggression or using descriptive terms for the target of the aggression (e.g., stranger directed, familiar people, and children).
The Classifications • Misdirected Play-Related Aggression: The usual onset of this type of aggression is between 8 and 12 weeks of age and is associated with the normally developing play behavior. Predatory play behavior is a normal and integral part of early feline learning. Normal predatory play behavior includes attacking moving objects and, when it is directed toward people, it is a normal but unwanted response. Misdirected play-related aggression occurs when the kitten attacks or bites at body parts that are moving, such as when an owner moves his or her hand to pet the cat, or when he or she walks near the cat or moves quickly from place to place. This type of behavior may occur without prior aggressive signaling, such as growling or piloerection. The misdirected play-related behavior occurs most commonly in singleton cats less than 2 years of age, cats housed with other animals that will not play, or cats that are left alone for long periods of time. Diagnosis of this type of aggression relies heavily on the appropriate context and descriptions of the body posture of the cat during aggressive episodes. Little affective (e.g., hissing or growling) emotional aggressive arousal should be evident. Frequently, the kitten will be found hiding behind objects waiting for movement, springing out, attacking, and then running away. • Frustration-Related Aggression/Social Status Aggression: Frustrationrelated aggression and social status aggression are not well documented in the literature. Social status aggression is believed to involve elements of “control” of the social situation and is usually directed toward familiar people. Rather than a social status aggression, it is possible that the aggressive responses stem from the differences in social interaction between cats and people. Cats prefer short greetings and contact; people often prefer prolonged physical contact thus causing anxiety and perhaps fear from the cat. Both types often involve biting while petting, blocking owner access to areas, and biting when lifted or approached. Diagnosis may be difficult because other forms of aggression may also be simultaneously present. Furthermore, some cats will behave confidently or aloof, whereas others may engage in attention seeking but still show aggression. Frustration-related aggression occurs when the cat does not receive the perceived reward such as food, access to the outdoors, or even when interrupted when performing another activity. • Petting-Related Aggression: Petting-related aggression refers to a cat that will respond aggressively when petted. For some cats this may be a normal but unwanted response to prolonged physical interactions. Typically, the cat will allow petting for a certain period of time but will then turn, bite, and leave. The cat may even solicit attention initially but will end it by biting, grabbing, and running away. Usually, bites are inhibited, resulting in no serious injury, but this
564
can vary. Several factors may play a role in the aggressive response, including the cat’s threshold for attention, its internal conflict between adult and juvenile responses, and hyperesthesia syndrome and owner responses over time. • Redirected Aggression: Redirected aggression occurs when an aroused cat cannot reach the target of its aggression, and the arousal and subsequent aggressive response are, therefore, redirected toward a target that it can reach. Redirected aggression toward people arises when they interact with the cat when it is agitated by some other stimuli. Situations that can cause a cat to become agitated and then aggressive include open windows or doors (especially in the spring and fall when other cats are more likely to be roaming), new people or pets in the household, loud noises, unusual odors, and other extreme circumstances. • Fearful or Defensive Aggression: Fear-related or defensive aggression can happen both to familiar or unfamiliar people. The cat assumes a fearful or defensive posture (i.e., crouched position, flat ears, dilated pupils, piloerection, hissing, spitting, or growling) and may bite if touched. Cats without proper socialization may be at a greater risk of developing fear-related aggression toward people. In situations in which escape is denied or aggression is rewarded by cessation of the unwanted approach or stimulus, the behavior can become intensified and quite strong. Early traumatic experiences, inappropriate punishment, or reinforcement of the aggressive behavior can all contribute to the expression of the aggressive behavior. Defensive aggression can occur if the cat perceives it is cornered perhaps in a small hallway or on top of some furniture with no easy escape possible.
Treatment Primary Therapeutics • Anticipate Attacks: Owners should know where and when attacks occur to anticipate them. A journal may help identify locations and times or activities when attacks are likely. • Environmental Control: Control environmental access to areas where attacks are likely, or change the environment to prevent the attacks. Alternatively, the cat can be distracted before the attack takes place to decrease aggressive episodes. • Encourage Appropriate Alternatives to Aggression: Provide appropriate outlets for play, exercise, and human interaction to redirect the cat to appropriate responses. Determine physical interaction that the cat enjoys and tolerates. • Command-Response Training: Teach the cat to obey basic commands to receive attention, food, and play. • Stop All Punishment: Harsh physical reprimands are contraindicated and likely to increase rather than decrease aggressive episodes. • Pharmacological Treatments: Medication should only be used in conjunction with behavioral modification and are not needed in all cases. See related Chapter 239. When fear and anxiety are a large component of human-directed aggression, medication in conjunction with behavior therapy can help the cat learn new responses. Commonly used medications include selective serotonin reuptake inhibitors (SSRI) and tricyclic antidepressants (TCA). Certain conditions, however, are normal, but the responses are unwanted and should not be treated with medication. These include play-related aggression and petting aggression.
Therapeutic Notes • Misdirected Play-Related Aggression: Channel the normal playful energy of the kitten or cat toward appropriate play and discourage inappropriate play. Aerobic exercise and mental stimulation using proper toys, such as food-dispensing toys, boxes, and bags, are
Aggression toward Humans
•
•
•
•
•
useful. Play with one’s hands and wrestling are inappropriate play activities. Attacks directed toward humans should be interrupted using noise distracters that will startle the cat. Distracters should be applied early in the behavioral sequence and not associated with the owner, such as remote control noise devices. Once the cat stops the inappropriate behavior, it should be immediately redirected to an appropriate outlet such as a toy. Frustration-Related Aggression: Commands and rewards are used to remove the cat from aggression inciting situations. The owner must learn to identify signs of impending aggression and interrupt the behavior by leaving the situation. In addition, direct confrontation must be avoided or else aggression may escalate. Having predictable interactions and signals for various wanted activities can help diminish frustration and perhaps avoid aggressive responses. It is also essential to understand and comply with the desired level of interaction that the cat desires, not just with what the owner wants. Petting Aggression: An essential component to treatment is owners learning the cues (i.e., body language) that signal the cat’s threshold for an aggressive response. Then they must keep petting and physical interaction below that limit to hopefully avoid aggression. Cues, such as tail flicking, flattening of the ears, and perhaps dilation of the pupils, usually precede an aggressive response. When these cues are seen, petting should cease immediately. Determining what types of physical interactions are preferred is useful. These might be light petting on the head rather than long strokes down the back or sitting on the owner ’s lap without being touched. In some cases, cats can be conditioned to accept longer periods of contact using food rewards for good behavior. The owner pets the cat a few times staying below the irritation threshold and rewards the cat with food for good behavior. Each session tries to add in a slightly increased amount of contact and reward good behavior. Redirected Aggression: If avoidance of the eliciting stimulus is not an option, but the situation comes up infrequently, the owner can be instructed to stay away from the cat and not pick up the cat until it is calm. However, the best approach is counter conditioning and desensitization to the situations that aggravate the cat. See Chapter 236. Fear or Defensive Aggression toward People: This is best treated with a counter conditioning and desensitization program. The cat is taught to associate good things (food) with calm and quiet behavior in the presence of the eliciting stimulus. A distance and response gradient with control of the introduced stimulus must be designed so that no aggression is elicited. The cat should be slowly introduced to the stimulus at a distance that will not evoke an unwanted response. Distance between the cat and the stimulus is important in keeping the cat calm and may be initially quite large. To facilitate safety, the cat should be on a harness and leash or in a crate or carrier. If the cat is calm and no aggression is elicited, the cat should be rewarded (with petting, praise, a toy, or a treat), and the stimulus can be brought closer. It is important to move slowly and allow the cat to be calm and non-anxious or fearful during sessions. The goal of treatment is for the cat to experience proximity to the stimulus and remain calm instead of displaying fear or aggression. Play therapy may also be helpful in these cases. Confinement may be appropriate in some situations. At all times safety must be a primary concern. In homes with children, elderly, or immune-compromised individuals, some cats may
not be appropriate companions if aggression cannot be curtailed. If serious injury has occurred, it may be necessary to remove the cat from the home. In some cases it may be prudent to confine the cat away from people. Whenever injury occurs, medical attention should be sought immediately. One should be cautious about prescribing oral medications for the owner or your staff to administer, and the owner should be instructed not to put himself or herself at risk of a bite wound when attempting to administer medication.
Prevention One of the best means of preventing unwanted human directed aggression is good kitten socialization to handling, interactions with people and how to play appropriately with humans. The feline socialization period is from 6 to 9 weeks; often kittens arrive in homes close to the end of that time period. Thus, it is important to counsel owners on appropriate interactions and training for their new kitten. Kind and gentle interactions with respect for the tolerance level of the individual will go a long way toward teaching the kitten how to interact with people. Focusing play on appropriate toys rather than human hands and feet may diminish play-related problems. Offering appropriate outlets for predatory play will also help diminish the use of family members for those activities.
Prognosis The prognosis for misdirected play-related aggression and petting related aggression is usually quite good. Redirected and fear or defensive aggressive attacks can be more serious, and prognosis varies depending on the intensity and frequency of the attacks, the severity of any involved injuries, and the ability to predict and avoid aggressive encounters.
Suggested Readings Bateson P, Martin P. 2000. Behavioural development in the cat. In DC Turner, P Bateson, eds., The Domestic Cat: The Biology of Its Behaviour, 2nd ed., pp. 9–22. Cambridge: Cambridge University Press. Curtis TM. 2008. Human-directed aggression in the cat. Vet Clin North Am Small Anim Pract. 38(5):1131–1144. Frank D. 2002. Management problems in cats. In D Horwitz, DS Mills, S Heath, eds., BSAVA Manual of Canine and Feline Behavioural Medicine, pp. 80–89. Gloucester UK: BSAVA. Heath S. 2002. Feline aggression. In D Horowitz, DS Mills, S Heath, eds., BSAVA Manual of Canine and Feline Behavioural Medicine, pp. 216–225. Gloucester UK: BSAVA. Horwitz DF, Neilson JC. 2007. Aggression/Feline status related In Horwitz DF, Neilson JC, eds., Blackwell’s 5-Minute Veterinary Consult Clinical Companion Canine and Feline Behavior, 4th ed., pp.155–161. Ames, IA: Blackwell Publishing. Landsberg G, Hunthausen W, Ackerman L. 2003. Feline aggression. In DM Landsberg, W Hunthausen, L Ackerman, eds., Handbook of Behavior Problems of the Dog and Cat, 2nd ed., pp. 427–453. Philadelphia: Saunders.
565
CHAPTER 232
Catnip Effects Sharon Fooshee Grace
Catnip is renowned for its ability to evoke a variety of interesting pleasure-related behaviors in domestic cats. Exotic cats are also known to respond to catnip, and it is sometimes used in zoos as a source of environmental enrichment for captive cats. It has been suggested that tigers may not respond as do other exotic cats. In addition to catnip, a few other plants are known to induce behavioral changes in cats. These include cat thyme (Teucrium manum) and valerian (Valeriana officinalis). Catnip is derived from the herb Nepeta cataria, a member of the mint family. This plant was originally native to Africa and the Mediterranean but is now found on a worldwide basis. It is easily cultivated and can be found growing as a weed along roads and waterways. See Figure 232-1. Nepetalactone, an essential oil found in the stems and leaves, is the main constituent of catnip; but the most active constituent is a metabolic product of this, nepetalic acid. These compounds are not considered toxic to cats. The exact sensations that are elicited in the cat are unclear but have been speculated to include visual and auditory hallucinations based on
reports from people who have smoked catnip. During the 1960s, catnip was used in place of marijuana or added to it as a filler; it was reported to make people feel “happy, contented, and intoxicated.” It also experienced a protracted wave of popularity as a home remedy for a number of ailments, including asthma, scarlet fever, and measles. Catnip is sold either dried or fresh, but the dried form is considered to have the highest concentration of nepetalactone. Many cat owners also grow it themselves because cats are attracted to the fresh plant when it is contained in a planter or herb garden. Outdoor cats are known to actively seek the plant if it is available. It can be purchased as the plain dried herb or contained in a variety of fabric toys. Catnip-impregnated scratching trays are also popular. Many owners use catnip as a source of environmental enrichment, especially for indoor-only cats. There is a great deal of individual variation in the response to catnip; some cats do not respond at all, whereas others become highly aroused by it. The ability to respond is inherited as an autosomal dominant trait, and cats, which do not inherit the gene, do not respond. The majority of cats, however, do demonstrate some response. Age and experience influence the reaction to catnip, and kittens less than 2 months of age do not react to it. Most cats do not fully respond to catnip until they are about 6 months old, or about the age of puberty. It is noteworthy that cats that do not respond to catnip will sometimes respond to some of the other plants known to stimulate olfactory behaviors. It has been experimentally demonstrated that cats detect nepetalactone through the olfactory epithelium and not through the vomeronasal organ, a unique sensory organ found in the nasal cavity. When cats come in contact with the fresh plant, they will smell it and then rub their face on the plant, as well as the pot containing it. If planted in a garden, they will roll in the foliage. They have also been observed to eat and chew the fresh leaves. When exposed to the dried herb, a variety of behaviors can be observed, including rolling, salivating, vocalizing, kneading, head shaking, jumping, acting “spaced out” or “frolicsome,” and demonstrating estrous-like behavior (even male cats). The effect is transient, with the most intense response lasting only a few minutes. A period of satiation does follow this response, and some have suggested that to maintain maximal responsiveness, it should not be offered to cats more than twice a week.
Suggested Readings Figure 232-1 Cats are attracted to both fresh and dried forms of catnip. Catnip may be grown in a container or as part of a garden. Photo courtesy of Marco Nicovich, Mississippi State University Office of Agricultural Communications.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
566
Grognet J. 1990. Catnip: Its uses and effects, past and present. Can Vet J. 31(6):455–456. Hart BL, Leedy MG. 1985. Analysis of the catnip reaction: Mediation by the olfactory system, not vomeronasal organ. Behav Neural Biol. 44(1):38–46.
CHAPTER 233
Environmental Enrichment in the Home Debra F. Horwitz
Overview The domestic cat has evolved from small desert cats that lived as efficient predators and adapted to life with or without social groups and without human control. The early relationship between cats and humans was probably established because it was mutually beneficial without ties in either direction. Cats controlled rodent populations near food stores on land, on ships, and in stables and homes. Although some cats undoubtedly lived in homes and were valued as companions, the cat remained relatively independent of intensive human control for how they received food, where they lived, and how they reproduced. Over the years this has changed with selective breeding for specific physical characteristics and personality traits and in some countries a totally indoor life. Not only are they safer, but with the strides made in nutrition and health care, cats can live well into their teens and perhaps twenties. Although their circumstances and longevity have changed, the basic feline needs have not. Now more than ever it is a challenge to provide for and meet their social, environmental, physical, and mental needs. The results of not doing so may lead to undesirable behaviors. Recently the American Association of Feline Practitioners has recognized the need to incorporate feline behavior into any feline medical practice with the publication in 2005 of their Feline Behavior Guidelines.
Definitions and Rationale Enrichment has become a catch-all term for attempting to provide any animal that is unable to live in their natural surroundings with the components that allow them to meet their innate needs for exercise, social interaction, species specific mental and physical needs, and exercise and to cope with the challenges in their environment. The need for feline enrichment should be based on an understanding of the natural ecology of the cat. Cats have evolved as extremely efficient, and for their size, deadly predators. Yet, oddly enough, they are also prey for other species, and that balance between obtaining food and avoiding being food is part of their daily struggle. Because most cats generally live a solitary existence except for aggregations around food resources and for mating, each cat becomes a problem solver to address its own needs, usually not able to rely on a group to help them. Depending on the food provided to them a free-ranging cat might spend up to 46% of the 24-hour time budget of each day foraging for food, with resting (22%), grooming (15%), and sleeping (40%) taking up the remainder of the time. Cats that live within the human household, especially those without access to the outdoors, generally have a different time budget. They no longer need to forage for their food; they do not need to remain vigilant to avoid predators; they are often forced to live in close proximity to other cats and other animals; and they have very little control over the daily course of events. Each one of these changes in their life can lead to different problems including obesity, anxiety, fearfulness, destructive behaviors, anorexia, marking in unwanted areas with urine or claws, elimination in unwanted areas, and aggression. Anxiety and stress may lead to poor welfare and result in medical problems and changes in the hypothalamus-pituitary-adrenal axis over time. Several studies have indicated a correlation between stress and illness and the possibility that enrichment
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
may cause a decrease in the incidents of certain types of chronic diseases. Subtle signs of stress related disease are often missed by owners and veterinarians alike due to a misunderstanding of stress and its effect on the feline body. Often cats presented to the veterinarian for vague medical symptoms, such as mild anorexia, vomiting, hiding, overgrooming, elimination in unwanted locations, and even aggression, may in fact be suffering from stress-induced illness resulting from the inability of the environment to meet their needs. Behavior problems are also a major reason for feline relinquishment to shelters and euthanasia, yet many of the problem behaviors reported are either normal but unwanted feline behaviors that could be managed with proper environmental enrichment and attention to feline needs.
Diagnosis Primary Diagnostics Naturally, when a cat is presented with medical signs, practitioners must thoroughly evaluate the medical health of their patients. This might entail complete blood count (CBC), biochemistry analysis, and imaging tests if warranted. In the absence of any biological disorder, the veterinarian would be wise to begin to evaluate the environment, including potential sources of stress or lack of ability to engage in normal, species typical behaviors. In addition, it will be useful to attempt to assess the personality or temperament of the cat: Is this cat bold, outgoing, or shy and timid? How does the family interact with this cat, and is it in line with the temperamental needs of the individual? In other words, is this a cat that prefers to be solitary but is constantly picked up and handled by family members and rarely allowed quiet uninterrupted time alone? Alternatively, is this a social, outgoing cat spending a great deal of time without any human or other animal interactions?
Secondary Diagnostics Targeted questions are necessary to establish the baseline parameters of activities provided to the cat. In a multicat home, questions must clearly address how resources allocation within the home, how each cat is able to access those resources, which cats associate with one another, and which avoid each other. Resources not only include food bowls, water bowls, and litter boxes, but also climbing perches, hiding places, scratching posts, beds, toys, and owner attention.
Diagnostic Notes See Chapters 231, 235, 236, and 237 for additional information on providing needs within a multicat home. At times it may be necessary to educate cat owners on the species typical needs of cats so that they will understand what they should provide for their pet.
Treatment Primary Therapeutics The most stressful environment for most animals is one in which there is no control over what happens to them. This may include when they get to eat, if they can access the outdoors, how they access their
567
SECTION 2: Behavior
elimination locations, play and social interactions, the ability to rest undisturbed, and the ability to avoid social encounters that they find stressful. Therefore, as stated enrichment begins by first understanding the needs of cats in general and second the needs of the individual cat in question. Most animals desire predictable interactions and routines. Cats in particular do not like unpredictable occurrences and may find them stressful unless they have provisions of escape and coping.
Therapeutic Notes • There are many ways and categories in which to provide enrichment, but not all may be suitable or desired by every cat. • Feeding: Feral cats spend a significant amount of their time foraging for food, so increasing the complexity of obtaining food may enrich the environment for an indoor-only cat. Options include feeder toys, placing multiple food bowls throughout the home, leaving small portions in different bowls during the day, hiding treats in boxes and bags in various areas of the home, and providing food puzzles. Food bowls (at least one per cat) should be plentiful in multicat homes and arranging them at different heights and locations may keep less agile cats from accessing certain types of food while allowing more agile cats to eat undisturbed. Offer food at least two to three times a day, although many may prefer multiple small meals. Some cats prefer running water for drinking, and commercial fountains are available to provide that need. • Provision of Space: The amount of space necessary for an indoor cat to feel comfortable is not really known. Various studies have looked at how cats share space, and some have found that most of the time cats are not within each other ’s sight, but when they are, they are within 1 to 3 meters (3–10 feet) of each other. Cats also enjoy climbing and may want to conceal themselves. Therefore, the quality of the space provided is important with elevated vantage points from which they can survey the environment and plenty of vertical space for dispersal. Books are available that detail home modifications that can be made such as cat walks and cat shelves. • Resting and Hiding Areas: Cats spend a great deal of time resting and sleeping and often choose soft areas. When given a choice, it appears that some cats prefer soft materials for resting. Suggestions include chenille, wool, felt, fleece, or even paper. Many cats prefer raised locations, these can be simple structures, places on a bookshelf cleared for the cat, windowsills and window perches, commercially made cat towers, or elaborate custom-made structures. See Figure 233-1. Hiding is an important cat coping behavior, whether in response to or avoidance of people or other animals. Places to retreat may include covered cat beds, tunnels, boxes, or paper bags. See Figure 233-2. Places to get under and behind should also be provided, especially in multicat homes. There should be more resting areas than there are cats so that a choice is always available. • Social Environment: Recent research has increased our understanding of the social needs of domestic cats and that they can live within social groups. However, their ability to adapt to these groups is influenced by multiple factors. Cat to cat socialization takes place between 2 and 7 weeks of age, and sibling pairs of cats appear to have a better living arrangement than unrelated pairs of cats. Group living cats do not appear to have as many signals for diffusing conflict and reconciliation as do other species, which might contribute, to overall stress if social relationships are not harmonious. As mentioned previously and in other behavior chapters, the arrangement of the resources has a profound effect on the social environment within the home. Cats need to be able to disperse to reduce conflict yet still be able to access the things they need without fear or anxiety. Equally problematic may be cats outdoors that come to windows and doors, creating a threatening situation for cats inside. Owners should be informed that social conflicts may lead not only to behavioral problems but also to changes in other aspects of behavior including
568
Figure 233-1 Climbing towers and scratching posts of various shapes and sizes are commercially available, aid in space dispersal and provide marking, resting, and play areas in the home.
Figure 233-2 Normal household objects, such as shopping bags, laundry baskets, and boxes, may serve as hiding areas or entertainment objects for some cats.
food consumption (increased or decreased), grooming behavior (increased or decreased), vomiting, and altered interactions with the owner. Cats also may enjoy living with other animals, including dogs, providing they have been socialized to them and have had well-controlled introductions. However, in many cases, young exuberant dogs may be overwhelming for many cats and separation may be necessary for parts of the day. • Human Interaction: Another part of the social environment is human interactions with the cat. Most cats enjoy being with their caregivers. This can be simply sitting on the lap or nearby for some, whereas others enjoy petting, grooming, and even training. Owners should understand that although some cats enjoy prolonged stroking, others prefer gentle scratching around the head and neck that mimics the grooming routine of compatible cats. Time should be scheduled daily for meaningful interaction that meets both the needs of the humans and the cats. It must be emphasized that the cat should have the
Environmental Enrichment in the Home
Figure 233-4 Training a cat to wear a harness and leash is not difficult and allows for safe outdoor excursions.
Figure 233-3 The Feline Flyer® toy pictured here is a great toy to encourage aerobic exercise. This climbing tower also provides a perching and resting area for this cat.
•
•
•
•
ability to say “no” if they do want interaction at a certain time, and social interactions should not be forced on that cat because that could be stressful and have an adverse effect on the human-animal bond. Scratching Behavior: Scratching is a normal feline behavior; therefore, providing an acceptable outlet is essential. Scratching posts placed in an easily accessible area frequented by the cat are more likely to be used. Sisal is often a preferred substrate for scratching, but owners should be encouraged to experiment to find what is suitable for their cats. While scratching, the cat leaves marks with its claws and scent depositions from the glands between the digits. Multiple locations of scratching or marking posts are preferred and should encompass both common areas and places frequented by only one to two cats. Cats seem to like scratching posts at entries and exits and near sleeping and resting areas. Owners must keep in mind that scratching is a messaging system for the cat; therefore, the posts should be in visible, often utilized locations. Olfactory and Visual Stimulation: Cats have a well-developed sense of smell and vision. Some cats prefer catnip, and others may be calmed by pheromones diffused into the air. Many cats also like to look out windows and would utilize perches that give them visual access to the outdoors. Some cats do watch television and enjoy cat videos. Interactive and Manipulative Toys: Recent research indicates that rotating toys increases play and minimizes habituation of the play response. When a cat stops playing with a certain toy after only 5 minutes, removing the toy and substituting it with another will cause play to resume at a high level. Cats seem to prefer toys that are light, move easily, and can be picked up and mimic prey characteristics. See Figure 233-3. Wand-type toys may be preferred by some cats, but require owner participation. Care must be exercised to avoid toys that can be ingested. String can cause intestinal obstruction and intussusceptions and should be avoided. However, novel objects are enjoyed such as baskets, boxes, and bags. Toileting Areas: Litter boxes should be provided in private, quiet but accessible areas. Ideally they should not be close to feeding or water-
ing sights. In multicat homes, litter boxes must be provided in many locations, with at least one box per cat. It may be necessary in a multicat home to have litter boxes placed in rooms with more than one exit or entry to prevent a cat from being trapped in the area or conversely blocked out. Litter boxes may need to have varied characteristics such as different types of litters, higher or lower sides, larger boxes, covered boxes, and so on so that all cats within the home have the possibility of finding a toileting location that meets their needs. • Grooming: Most cats are quite fastidious and keep themselves quite clean. However, many cats can benefit from regular grooming to help remove dead fur, and in longhaired or obese cats, help reach areas that are not easily cared for by the cat. The best way to make regular grooming part of the routine is to begin when the cat is young. Grooming sessions should initially be quite short, have plenty of tasty food rewards involved, and stop before the cat becomes agitated. Over time most cats will learn to enjoy the grooming sessions, which not only provide a bonding time for owner and pet but also may diminish hairball formation. A cat can also learn to have its nails trimmed. Starting slowly, perhaps with only one foot and one to two nails and associating food reward with the process can help make the routine more palatable for the cat. • Indoor Only versus Outdoor Access: It is generally well accepted that in the United States most cats (60–70%) are kept indoors; however, in the United Kingdom a majority of cats have some outdoor access. Although outdoor access has certain risks, including infectious disease, vehicular accidents, fights with other cats, poisoning, attacks by other animals, and becoming lost, living totally indoors is not without risks. One author has examined the risks for totally indoor cats of developing various medical and behavioral problems. Although disorders such as feline urologic syndrome, hyperthyroidism, obesity and behavioral problems were noted, other studies do not agree. Some owners have attempted to provide secure outdoor enclosures or walks outdoors on a leash (see Figure 233-4) to allow cats to investigate their surroundings while still remaining secure and safe. Most cats do adapt to indoor only life quite well providing active attempts are made to meet their needs. • Kittens: Although, in general, the needs of the cat and the way to provide them as detailed also apply to kittens, kittens do have some unique needs that must be met. First and foremost is the need to socialize the kitten to people and other animals and to habituate them to new and novel things, noises and handling. The socialization period for a kitten is from 3 to 9 weeks and also encompasses the
569
SECTION 2: Behavior
socialization period for cat-to-cat relationships. Because many kittens do not enter the home until 6 to 7 weeks of age, it is extremely important that owners work diligently to help their kitten adjust to life in the human household. This includes gentle handling of all parts of the body, grooming, teaching the kitten how to use a scratching post, and providing an appropriately sized litter box (one with smaller sides). Introducing the cat to a carrier early in life, by keeping the carrier out and available as a resting area and a source of treats, may help diminish unwanted associations with later travel for necessary veterinary visits. Introductions to people, other animals, noises, and objects must be done slowly with attention to the intensity of the stimulus and the kitten’s reaction. Keeping the stimulus intensity low, associating the new item with either play or delectable food rewards, can help the kitten learn that new items need not be threatening. Punishment must be avoided because it may cause fear and distrust of the owner. Therefore, providing a safe area where it is less likely that the kitten could be injured or destroy items is essential. Finally, kittens are curious and playful and daily playtime must be provided or they will find ways to entertain themselves which might be unacceptable. • Senior Cats: Like a kitten, a senior cat may have additional special needs that must be met to keep it happy and healthy. Many of these needs revolve around the changing physical health and abilities as a cat ages. Research has indicated that nearly 90% of cats over 12 years of age have osteoarthritis in one or more joints. Many also suffer from other chronic metabolic disorders. Either of these can influence how the cat may access the resources they need and how they react to interactions with people. Most senior cats have limited mobility and may restrict their movement throughout the space provided for them. They also usually have areas they frequent for resting. For a more comfortable life, food, water, litter boxes, and soft comfortable resting areas should be near where the cat chooses to spend its time. Because pain or loss of sensory function may be present, owners
570
should be gentle and understanding when handling cats for social interactions and routine grooming. Careful observations of food and water intake, as well as eliminations, are necessary and allow continuous assessment of the health of the animal. This may be aided by feeding set meals multiple times daily rather than free choice where it may not be evident for several days that food or water intake amounts have been altered. Despite their advancing age, most senior cats will enjoy some time of mental stimulation whether looking out a window, short playtime with new toys, cat nip, or even new and novel scents.
Prognosis Meeting the social, exploratory, mental, and physical needs of cats is essential to providing good welfare and longevity. This is easily accomplished once the needs of cats are understood.
Selected Readings Buffington CAT. 2002. External and Internal influences on disease risk in cats. J Am Vet Med Assoc. 220:994–1002. Hall SL, Bradshaw JWS, Robinson IH. 2002. Object play in adult domestic cats: the roles of habituation and disinhibition. Appl Anim Behav Sci. 79:263–271. Hardie EM, Roe CS, Fonda RM. 2002. Radiographic evidence of degenerative joint disease in geriatric cats: 100 cases (1994–1997). J Am Vet Med Assoc. 220(5):628–632. Overall KL, Rodan I, Beaver BB. et al. 2005. Feline behavior guidelines from the American Association of Feline Practitioners. J Am Vet Med Assoc. 227(1):70–84. Westropp JL, Kass PH, Buffington CAT. 2006. Evaluation of the effects of stress in cats with idiopathic cystitis. Am J Vet Res. 67(4):731–736.
CHAPTER 234
Environmental Enrichment in the Hospital Gary D. Norsworthy and Linda Schmeltzer Overview A hospital visit can be a terrifying event, whether as an outpatient or inpatient and regardless of species, including humans. However, when a cat visits a typical small animal practice, the experience can be especially unpleasant. Many indoor cats have had no exposure to dogs and are terrified at the first and subsequent encounters, and many dogs, even those that live with a cat, find unknown cats to be objects of prey. Both of these situations are likely in a waiting room filled with canines and felines. Veterinarians, technicians, kennel personnel, and receptionists who are not particularly fond of cats only add to the cat’s anxiety. Unfortunately, these people are often found in the typical small animal practice. Procedures that are necessary, beginning with the rectal thermometer, further add to the cat’s response of self-preservation and aggression often resulting in a threatening situation for those who restrain and treat the cat. This chapter will chronicle how we have tried to minimize the unpleasantries of a hospital visit. The goals of hospital environment enrichment are to make the visit as pleasant as possible for the cat and for those who treat the cat so that minimal restraint is needed and so that quality health care can be provided. Environmental enrichment in the hospital is two pronged. First, it seeks to reduce anxiety on the cat. Second, it seeks to reduce anxiety on the owner. In the process of treating the cat, one must not forget that owners ultimately decide whether or not the cat receives the treatment you recommend and whether or not your services are sought in the future. One of the essentials to building a successful practice is making the owner glad that your services were sought so that your services are sought again in the future. Thus, this chapter directly impacts practice growth and practice income. The following ideas are offered based on our own personal experiences. A virtual tour of our hospital can be taken at www.alamofeline. com.
The Feline-Exclusive Practice The first feline-exclusive practice was established in the United States in the 1960s. Although many considered it a strange concept, it had an appeal to many serious cat owners. Over the past 40 years cats have gone from being a casual, almost disposable pet to an integral part of many families. A proliferation of feline-exclusive practices, now numbering over 300 in the United States, has accompanied the increase in feline popularity as a valued family member. The feline-exclusive concept is based largely on two premises that cat owners find appealing. First, a veterinarian who concentrates his or her professional life on one species should become more proficient. Second, the feline practice offers a dog-free environment, which automatically produces an atmosphere that is less threatening to feline patients. We practice in a feline-exclusive practice; the following procedures are used in that practice. However, most of them can also be used in a canine-feline practice either as described or with some creativity.
Staff Forty years ago many, if not most, veterinary students were male, came from rural backgrounds, and planned to treat a variety of species including farm or ranch animals and dogs. By and large these students had little interest in cats. However, the veterinary student profile has shifted dramatically in the last 15 years with a predominance of females students, many of whom anticipate working with cats with at least the same interest level as working with dogs. Although there is a feline shift occurring, there still remain many practitioners who really enjoy treating dogs and who treat cats only because “they have to.” Thus, feline patients are often handled by veterinarians and staff members who do not give the feline patient much respect. Although examinations and procedures are performed on cats, they are often performed out of a sense of duty instead of a strong desire to work with this species. The first way to enrich the hospital environment is to staff it with veterinarians, technicians, kennel personnel, and receptionists who really like cats. Otherwise, serious cat owners will not be happy with the way their cats are handled, and they will seek the services of another hospital that is feline friendly. This point cannot be overemphasized; it is the foundation for a cat-friendly environment.
Reception Area The reception area makes the first impression. It should convey the message that cats are valued as patients, and it should project cleanliness. These messages are given in the following ways: • The décor should be cat themed. The decorations in small animal practice need to have equal emphasis on cats as on the other species treated. Reception areas that have a 90% canine theme send a strong negative message to the cat owner. See Figure 234-1. • The furnishings in a feline-exclusive reception area can be livingroom quality. Most cats travel in carriers. They do not have chain leashes that are raked across the furniture. They do not paw at the furniture with claws. A nicely decorated reception area will cause your clients to rise to that level. • Odor control is vital. The smell of cat urine often pervades the reception area. Even though it may originate in other areas of the hospital, its presence in the reception area is not acceptable. Urine must be cleaned up immediately. An effective odor neutralizing product, such as Zero Odor Pet® (www.ZeroOdorStore.com) should be used immediately when urine is not contained within cat litter. Tom cat urine odor is especially pungent and pervasive. Either do not keep intact male cats overnight (our policy) or if they must stay, keep them in an isolation ward with a good exhaust system and use Zero Odor Pet frequently. Their litter boxes must be cleaned immediately after urination occurs, and the wet litter should be taken to an outdoor trash receptacle.
Examination Rooms Examination rooms are the first “medical” area. They must be efficient for patient care, and they must have appeal to clients.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• The décor is important. In our feline practice the six examination rooms each have a different theme based on a famous cat. See Figure
571
SECTION 2: Behavior
(A)
Figure 234-2 The décor of our examination rooms are each themed to a different famous cat. The examination tables are L-shaped, and a computer is located in each using a paperless system (www.avimark.com).
• The room needs to be “cat proof.” There should be no small, tight places where a cat can hide, thereby giving them the freedom to roam around the room. This is a stress reducer. • However, designated hiding places can be stress relievers. Some cats like to curl up in a sink. Others prefer a plastic pan (dish pan) or a designated cabinet. These need to be cleaned after each use. • There should be a place for cat carriers other than on the examination table. • Feliway® (www.feliway.com) can be helpful for calming nervous or aggressive cats. It can be sprayed on the examination table prior to use.
Examination Room Equipment and Procedures (B) Figure 234-1 A, B, The décor of the reception room should include a feline theme proportional to the percentage of feline patients there are in the practice. Living room quality furniture is feasible in a feline exclusive practice.
234-2. If the examination room is used for other species than just cats, its decorations should include some feline recognition. In a small animal practice, ideally one or more examination rooms should be dedicated to cats. The feline rooms do not need to be as large as those used for dogs. Their dedicated use eliminates the odors of dogs. During construction, sound board should be put in the walls to reduce or eliminate the sounds of dogs. • If one or more examination rooms in a small animal practice are designated for feline patients, ideally they should be located out of dog traffic paths. The sound of dogs walking past and sniffing at the bottom of the door will add to a cat’s level of anxiety. • Cleanliness is paramount. Every countertop, table top, and sink should be spotlessly clean when the client enters the room. There should be no cat hair on the countertops or floor. • Odor control is of equal importance to cleanliness. A cleaner that also deodorizes should be used. Zero Odor Pet should be used for any residual odor. Odoriferous materials (e.g., urine, stool, and anal sac material) should be removed from the room, not just put in a trash can in the room.
572
• The first step in the examination is to remove the cat from the carrier. In many cases, the owner has done so or the cat comes out voluntarily. However, if the cat is resistant to leaving the security of its carrier several approaches can be used. In some cases, the owner is proactive to coaxing the cat out; if not, the technician or veterinarian can remove the cat as long as the cat is reasonably willing. If not, other tactics can be employed with the goal of not inciting the cat into a defensive (or offensive) posture. The top of many plastic carriers can be removed; doing so removes the cat’s need to defend its territory. If that is not feasible, the carrier door can be opened and the cat “poured” out. This should be done by tipping the rear of the carrier upward slowly while the front of the carrier rests on the examination table. The cat will slide down to the door but still try to remain in the carrier. As the rear of the carrier approaches vertical, the cat will be forced to put one or more feet on the examination table. When either two front or two rear feet are on the table, the carrier can be lifted upward so the cat walks out. See Figure 234-3. It is important that this be done slowly so the cat is not antagonized. It is also important that you not lift the carrier away if there is one front and one rear foot on the table. If that happens, set the carrier back down on the table and begin again. • The next step in the examination (after greeting the client) is to assess the cat’s personality. Cats tend to fall into three groups: (a) friendly, (b) apprehensive or scared (see Figure 231-1A), and (c) aggressive or fractious (see Figure 231-1B). Cats in the first two categories should be greeted with an outstretched, nonthreatening hand. If you let the cat smell your index finger (see Figure 234-4A) it will usually become
Environmental Enrichment in the Hospital
Figure 234-3 The cat can be “poured” out of its carrier. As the rear of the carrier approaches vertical, the cat will be forced to put one or more feet on the examination table. When either two front or two rear feet are on the table, the carrier can be lifted upward so the cat walks out.
•
•
•
•
• •
•
less apprehensive. After it has done this, slide your finger behind the cat’s ear and give it a few strokes. Follow that with a few strokes down the back. If it shows interest in your advances, stroke it a few more times, or pick it up and cradle it in your arms like a baby. See Figure 234-4B. Some cats will let you do this and others will not. These proactive movements on your part will set the cat at ease and make it less likely to become aggressive during the exam. It will also send the two most important messages to the client: (a) you love cats, and (b) you love this cat. Aggressive or fractious cats must be handled with caution. Cat bites can create serious infections. See Chapter 310. Sedation is usually needed to proceed safely. Each of our six examination rooms is set up the same. Each is similarly equipped, and the equipment is located in the corresponding cabinets or draws. This permits efficiency when more than one doctor uses the examination rooms. It also reduces staff stress. Stressed doctors and technicians are likely to transmit anxiety to their patients. Our main restraint device is a heavy bath towel. Drawers in the examination tables contain three towels per examination room; they are located so they can be retrieved quickly by the veterinarian or the technician. Designate towels specifically for examination rooms making sure they are free of stains, holes, and frayed areas. Every cat should be weighed on every visit. We use a digital package scale (www.pelouze.com; model 4010) and place a plastic dish pan on it for the cat to stand or lie in. There is one in each examination room. It is stored in a drawer on the client’s side of the examination table; when the drawer is pulled out, the scale can be used without removing it from the drawer. A strongly made drawer with heavy duty hardware is vital for long-term use. Veterinary otoscope cones are too large for the feline external ear canal. We use an otoscope and cones made for humans. Successful feline cardiac auscultation is best accomplished using a stethoscope with a 12-mm (1/in) or 2-cm (3/4-in) bell. Feline murmurs are usually located near the sternum. The cat has a strong anal reflex. A rectal thermometer should be lubricated but not forced into the rectum. Gentle pressure will result in sphincter relaxation and less resistance from the cat. For apprehensive or scared cats, take the temperature after the physical examination is complete because this procedure can result in an aggressive response.
(A)
(B) Figure 234-4 A, When first approaching your patient, allow it to assess you by smelling of your index finger (“the cat scan”). After that, scratch it behind the ear, stroke it a few times down the back, and if the cat is willing, (B) hold it a few seconds. Going through this sequence usually makes the cat less apprehensive and more cooperative during the physical examination.
• Blood pressure should be measured in a quiet examination room with the owner present and touching (or holding) the cat. Ideally, this should be the first event of the examination because other events will affect blood pressure. • Blood collection can be a challenge. Most of our blood profiles are performed using a chemistry machine that requires less than 0.5 mL of blood (www.abaxis.com; VetScan VS2). Blood is taken from a medial saphenous vein. If a large quantity of blood is needed, a jugular collection procedure is used. See Chapter 303. If you are consistently proficient in drawing blood, it will impress the client; do so in the examination room. Another benefit is that this location allows you to avoid the areas of the hospital that contain dogs. • Urine collection should be performed with a cystocentesis. Unlike dogs, this needs to be a controlled bladder stick. If the bladder is half-full or more, put the cat in lateral recumbency, secure the bladder
573
SECTION 2: Behavior
with one hand, and aspirate it with the other using a 22-gauge needle and 6- or 12-mL syringe. If the bladder is less than half-full ultrasound guidance is preferred, if available.
The Hospital Area • Cleanliness and odor control are also important in this setting. Odors may be carried from the hospital to the examination rooms and reception area along hallways or through air conditioning or heating systems. • Hospital cages are more cat friendly if they are not made of stainless steel. Laminates are quieter, warmer, and sufficiently durable for cats. Our cages (www.clarkcages.com) have been in use for 10 years and show almost no signs of wear. • Cage size is usually a compromise between comfort, expense, and available space. Most cats are comfortable for a few days in a 24″ × 24″ × 24″ (i.e., width, height, depth) cage. Large cats and cats that are hospitalized longer do well in 30″ × 24″ × 24″ cages. • Food and water bowls should be as large on the bottom as on the top so they do not turn over easily. • We use two types of litter boxes. Small plastic ones are more appealing to cats but can consume more cage space and litter. They must be washed and disinfected between cats. Cardboard litter trays (www.clinet.com; 7” × 9” flat trays) are well accepted by most cats. They consume less litter and are disposable so disease transmission is not an issue. • Cats on intravenous fluids, with severe diarrhea, or those that are just messy do well on racks that fit into the cages (www.clarkcages.com). They allow fluids to go through while being reasonably comfortable to the cats. A small hand towel can be put on the rack for lying and sleeping. • Elizabethan collars are necessary in select situations. Use a soft collar when it is acceptable. Hard plastic collars are needed for some situations (www.kvpusa.com). • Intravenous catheters can be placed in several peripheral veins. Short catheters perform well in the cephalic veins for 2 to 3 days. Long (central venous) catheters can remain in place for up to 7 days, and blood samples can be collected through them. They can be placed in the jugular vein or in the medial saphenous vein. See Chapter 297. • Frequently, cats feel more secure when some form of seclusion is provided. Cardboard boxes can be used; they should be discarded after each use to prevent disease transmission. See Figure 234-5. Feliway can be sprayed on the boxes for added stress control. • A deep sink is a acceptable place for bathing cats. Cats usually need less restraint and are less aggressive compared to being in a bathtub. • Ultrasound studies are performed in a dedicated room. This room is themed like the examination rooms because owners are frequently invited to observe these studies. A spot light is attached to the ceiling and shines on the patient from behind the ultrasound screen. The spotlight is on a rheostat so the intensity can be adjusted as needed. Switches for the spotlight and the room lights are located next to the ultrasound table. A sink is available for rinsing ultrasound gel off of the moist towel used for cleaning the patient. Nearby drawers contain syringes, needles, microscope slides, and other equipment used during the ultrasound studies. An oxygen outlet is available when gas anesthesia is needed. See Figure 234-6. • Our ultrasound table measures 25” × 32” and is 32” high. An echocardiography table is placed on it. See Figure 234-7 for size and shape; it is on 6-in legs. Abdominal procedures are performed in a foam rubber tray that has a trough cut to fit the cat when the cat is in dorsal recumbency. It measures 18” × 24”. A plastic bag is taped in place over it to keep body fluids from getting into the foam rubber. The tray is covered with a clean bath towel when in use.
574
(A)
(B) Figure 234-5 These images show several important ways to increase patient comfort even when a major illness is present. A, The cages are fiberglass laminate, an intravnous pump hangs on the front of the cage. This cat is recovering from a urethral obstruction. His urinary collection bag is below the cage with its line entering the cage at the same point as the intravenous line. B, The cat is more comfortable in a box. A soft Elizabethan collar is used to protect the intravenous and urinary catheters. The bowls are elevated by taping them to a similar bowl so he can get food and water while wearing the Elizabethan collar. A slotted rack is used for flooring because a litter box is not being used for this patient.
• Our X-ray table is constructed from a base cabinet. A custom made top, measuring 24” × 51”, was built to accommodate the digital X-ray sensor. It is located in a corner of the room. Although it does not permit access to both ends of the table, the enclosed corner is advantageous between exposures because cats can be released but not allowed to get off of the table. See Figure 234-8.
Environmental Enrichment in the Hospital
Figure 234-6 The dedicated ultrasound room has an appropriately sized table attached to the wall, a cushioned trough for the cat to lie in for an abdominal study, a spotlight that shines on the patient but not on the ultrasound screen, light switches near the table, and an oxygen outlet for use by an anesthetic machine.
Figure 234-8 The X-ray table is made from a base cabinet with a custom made top to accommodate the digital receiving plate. It is placed in a corner of the room to help with restraint between exposures. The monitor for the digital X-ray system (www.soundeklin.com) is mounted on the back wall; the computer central processing unit and other X-ray system equipment are housed in a cabinet built on to the end of the base cabinet. The keyboard for the computer is located in one of the drawers in the table.
28”
14”
7” 7”
13½”
Figure 234-7 The dimensions of the echocardiogram table area shown in this drawing. It is padded, covered with vinyl, and placed on 6-inch legs. It is placed on the ultrasound table.
• Our surgery tables are stainless steel; the top measures 18.75” × 46”. Body temperature is preserved during surgery using one of two heated pads (www.hotdogwarming.com and www.thermogear.com) placed on the surgery table. See Figure 234-9. • Surgical monitoring is performed with a multiparameter monitor (www.vmedtech.com; PC-VetGard+) that a transmits data wirelessly from the surgery table to a computer at the front of the surgery room. The data is displayed on large monitors near the ends of each surgery table. See Figure 234-9. • Declawing is performed exclusively with a CO2 surgical laser (www.aesculight.com). We are convinced that cats have less pain and bleeding. This is especially evident when adult cats are declawed. • Finally, and perhaps as important as any other suggestion, you and your staff should open cage doors and give some personal tender, loving care to your patients. Knowing they are being cared for by caring cat lovers is reassuring to feline patients.
Figure 234-9 Surgery is monitored with a multiparameter system; the data is displayed on a large monitor at the end of the room. Body temperature is maintained with a controlled heat source under the cat.
Boarding Facilities • Boarding wards are separate from the hospital wards. • The same cages as described previously are used; however, multiple sizes are available depending on the size of the cat, the number of cats the owner wants together, and the comfort level the owner desires.
575
SECTION 2: Behavior
• Our luxury boarding area has cages with glass backs. They are placed on an outside wall with large windows so the cats can look outdoors. • Daily, cats are allowed out of their kennels, one at a time, to roam the boarding area. Climbing trees and scratching posts are provided during the cat’s exercise time. • Toys are provided unless the owner brings cat toys. The ones we provide must be washable.
576
Conclusion The goal of each item listed is to reduce patient stress and increase comfort level, even when medical procedures are performed. Thoughtfulness and planning, hopefully prior to construction, are the keys to increasing patient and owner appeal, both of which add to practice growth and income.
CHAPTER 235
Housesoiling Debra F. Horwitz
Overview Various terminologies are used when discussing elimination problems in cats. For this chapter, the term housesoiling will be used to describe urination or defecation outside of the litter box on horizontal surfaces, in essence, when the cat is choosing another toileting location. Vertical marking (spraying) behaviors are covered in Chapter 237. In behavioral referral practices, housesoiling is the most commonly reported behavioral problem of cats. This is noteworthy because elimination problems are associated with an increased risk of relinquishment of cats to humane shelters in the United States. Although underlying medical problems account for many cases of housesoiling, the majority of cases are due to behavioral causes or a combination of both medical and behavioral etiologies. Anecdotally, the morbidity of behavior related housesoiling increases with the number of cats in a household; therefore, the likelihood of behavior influenced inappropriate elimination may be highest in multicat households.
Primary Diagnostics • Medical Testing with Physical Examination: Medical problems can precipitate inappropriate elimination behavior in cats. Therefore, a complete medical examination is needed in all elimination behavior cases. A physical examination should be accompanied by additional diagnostic tests, as appropriate, such as urinalysis, fecal examination, and screening tests for metabolic or endocrine dysfunction. In some cases, additional diagnostic procedures such as radiographs and ultrasound examination of the abdomen may be necessary. Any prior history of urinary tract or gastrointestinal disorders, as well as diagnostic tests performed, should be recorded. For cases involving defecation outside of the box, history should be taken to raise suspicion of and localize gastrointestinal disease. Factors that indicate small bowel diarrhea include weight loss, increased appetite, infrequent stools (one to two per day), and normal or large volume stools. Factors indicating large bowel diarrhea include tenesmus, the presence of blood or mucus, small volume stools, and frequent stools (four times or more per day). Be careful when clients attribute straining to defecation because tenesmus and stranguria may look similar. For cases involving inappropriate urination, palpate the bladder and ask the client about the volume or size of the urine puddles. In general, small volume urine puddles and a small bladder are consistent with cystitis, whereas normal to large urine puddles and a normal to full bladder are more consistent with elimination for behavioral reasons, although this alone is not diagnostic. A urinalysis (via cystocentesis) and an ultrasound of the bladder should be performed to rule out urinary tract disease. In addition to disease of the urinary or gastrointestinal tract, common diseases that preclude normal litter box use include osteoarthritis (Chapter 156), pad or foot injuries, overgrown nails, senility, pain (see Chapter 266), and disorders causing polyuria or polydipsia. See Chapter 177. • General History: A complete understanding of litter box habits is essential if the underlying cause of aberrant behavior is to be identi-
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
fied. Any cat not using the box consistently should be identified. Duration and progression of the inappropriate behavior, how resources are allocated within the home, and all cat-cat and cat-owner interactions, including how the owner handled the problem, in the past should be collected. If the owner observed the inappropriate elimination, note how the behavior was handled or punished. If the client sought veterinary attention for this problem in the past, note the type, length, and outcome of the attempted treatment.
Secondary Diagnostics • Intercat Dynamics: Inquire about any intercat aggression. See Chapter 236 for more details. Keep in mind that aggressive interactions between cats can be covert and difficult for some owners to notice without additional information to help identify agonistic interactions. Collect information about the sleeping and resting patterns of the cats in the home and the locations and allocation of resources such as resting places, food bowls, and litter boxes. In a multicat home, information on which cats show affiliative or friendly behaviors and which cats avoid one another is useful.
Diagnostic Notes • Litter Box Usage: Litter box use can vary between reluctance to use the box and refusal to use the box. In other words, the cat will either be using the litter box inconsistently or not at all. Constructing a diagram illustrating locations of urine spots (i.e., on the floor or on the walls) or stool outside of the litter box is helpful for detecting patterns of elimination. In multicat houses, it may be a challenge to identify even one cat that is soiling outside of the box. Confinement to a room with no other cats and a private litter box may be necessary to determine which cats are eliminating outside of the box. However, if social conflicts are the impetus for housesoiling, separation may diminish conflict and soiling cease no matter which cat was isolated. An alternative method for identifying the unseen culprit is to roll several fluorescein strips into an empty capsule and administer by mouth to identify the urine of the suspected cat. However, this method can vary depending on the acidity of the urine and can result in carpet staining. Nontoxic crayon shavings added to wet food can help identify the cat defecating outside of the litter box. • Type of Elimination: The type of elimination (i.e., urine, stool, or both) is also important information. Urination on vertical surfaces (i.e., marking behavior) should be differentiated from urination on horizontal surfaces (housesoiling). • Substrate: Type of litter substrate should be noted. Common types include standard clay litter, clumping litter, compressed newspaper, and crystals. Be sure to note if the type used is plain or if it contains any perfumes or deodorants. Next, make a note of the substrates on which the cat eliminates when it does not use the box (e.g., carpet, bedding, and so on), and if the cat tends to eliminate repeatedly on similar substrates or if the elimination substrates are random. See Figure 235-1. • Litter Maintenance Routine: The client should be questioned as to the frequency that the litter is scooped and the frequency that the entire box is changed and cleaned. Be sure to make a note of what cleaning products the client uses.
577
SECTION 2: Behavior
• Litter Box Type and Dimensions: The size of the box and the height of the sides (high = 10 cm [4 in]) as well as whether or not the box is covered or self-cleaning should be documented. • Location: The location of all litter boxes should be specific. Be sure to describe access to the litter box, especially noting boxes that are along a wall, in a corner, or in a confined space such as a bathroom. Note the environment surrounding each box, such as loud appliances or heavy traffic areas. Access to and from the area should also be noted. • Number: In general, the number of litter boxes available in multicat homes should follow the “n + 1” rule; there should be one more litter box than the number of cats. Too often, clients will offer a limited number of boxes for multiple cats to share, increasing the chance of stress and conflict among cats. The client should be advised that litter boxes all in one area is really just one toileting area and can be problematic for a house of multiple cats.
Elimination Categories • Location Preference: These cats tend to show a clear preference for one location other than the litter box. Frequently, these situations arise due to household conflicts between cats, a lack of resources, a disturbance at the litter box location, or all of these. The cat may find it easier to use an alternate location than compete for a litter box or may prefer to eliminate in a quieter, safer location.
• Substrate Preference: This form entails elimination that is generally on the same substrate. It is speculated that these cats prefer an alternate substrate to litter because it has no odor (i.e., perfume or deodorant), is more comfortable to the cat’s foot pads, or has been learned through avoidance of the litter box location for other reasons. • Litter Box or Litter Aversion: This should be suspected when the cat will not defecate or urinate in the box. Frequently these are cases where the box or litter is not cleaned regularly enough to meet the cat’s standards. This also occurs when the cat does not like the odor or feel of the type of litter in the litter box or perhaps the box itself due to size, height of sides, or pain associated with entry or exit. • Location Aversion: This may identified as unwillingness to be where the litter box is placed. It may be due to household conflicts between cats (such as territorial disputes) or placement in an undesirable location, such as near a laundry machine, in a corner or a high traffic area of the home, or where the cat can be easily disturbed. • Marking Elimination Behavior: This is almost exclusively demonstrated as urination, although the marking of stool on horizontal surfaces does happen infrequently. Urine marking is actually normal (albeit unacceptable by humans) and is further discussed in Chapter 237. • Stress or Anxiety Motivated Elimination: This is more commonly seen after the cat has experienced some stressful event, such as a move or the introduction of a new baby or pet, which has disrupted litter box routine or daily routine interactions. In stress related to intercat dynamics, the cat that is housesoiling is usually kept from the litter box due to aggressive actions by another cat or is the victim of another cat’s aggressive behavior. • See Table 235-1 for a relationship of historical information and diagnostic categories.
Treatment Primary Therapeutics
Figure 235-1 A rug or towel in a litter box may be an appropriate strategy for cats that show a substrate preference for carpet.
• Treat Underlying Medical Problems: Medical problems should always be treated concurrently with behavior modification. • Confinement with a Litter Box: Limit the cat’s access to the areas where they have previously soiled by confinement with litter box, food, and water when no one is home or owners are sleeping. The time of day when elimination outside of the box is usually found is useful for determining whether or not, and when, a cat should be confined. Confinement is usually effective in getting the cat to use the litter box while confined but may not affect the housesoiling behavior when the cat is free in the house, especially if other contributing social and environmental issues are not addressed. Request
TABLE 235-1: Historical Information Related to Diagnostic Categories for Elimination Problems Diagnostic categories
Location of elimination
Relationship between cats
Use of the litter box
Location Aversion
Elimination in multiple sites other than the litter box Elimination near but not in litter box; may perch on litter box edge Elimination always on same materials
Conflicts between cats or inability to access location Unlikely to be related to social problems within the house Unlikely to be related to social problems within the house Cat restricted to one area due to social conflicts with other cats. No or limited litter box access Often related to social conflicts within the house; may also be related to cats outdoors
Cat not seen using the litter box
Litter Aversion Substrate Preference Location Preference
Elimination usually in one spot, area, or room
Urine Marking
Elimination usually on vertical surfaces; occasionally on horizontal ones
578
May use litter box for one type of elimination and not other May use litter box for one type of elimination and not other May use the litter box some of the time Usually continues to use the litter box for majority of eliminations
Housesoiling
that owners determine and record when the cat urinates and defecates. When the owner is home, the cat may be permitted to roam the house under strict supervision to prevent soiling. Although confinement is often suggested and in certain situations might be useful, most owners are unwilling to comply and many cats are stressed by being confined for long periods of time. • Do Not Punish Inappropriate Elimination: Punishment is not an effective tool for changing housesoiling behavior. The cat is more likely to associate the punishment with the owner, resulting in fear development, owner avoidance, and eventual disruption of the cat-owner bond. • Make the Litter Box User Friendly: Provide a litter box that is a preferable alternative to its current outlet. An attractive and easy to access litter box is extremely important for changing housesoiling behavior. • Clumping Litter: Research has shown that some cats prefer the clumping materials to clay litter products. When clumping type litter materials are provided, the box should be scooped daily and changed weekly. Some studies have indicated a preference for unscented litter materials, a dislike of strong odors such as floral scents and bleach, and a preference for carbon odor control substances. Products for “multicat households” are usually heavily scented and often repulsive to some cats. • Regular Cleaning: In addition to daily scooping and weekly (or more often) changing of litter material, boxes in good condition should be washed out weekly with mild soap. Old, soiled boxes should be discarded in favor of new, clean boxes. • Litter Depth: The depth of the litter material should be adequate for the cat to bury urine and feces; about 5 to 7.5 cm (2–3 in) is usually sufficient. Clumping litter is more effective for urine balling when the depth is at least 5 cm (2 in). • Litter Box Features: For some cats, changing specific characteristics of the litter box may be beneficial, such as removing the cover from a covered litter box, providing a larger box, or adding a box with lower sides. Some cats will prefer a plain box versus a mechanical or automatic scooper, which makes noise after the cat eliminates. • Litter (Substrate) Trials: If the cat will not use the litter box in confinement or if the history suggests a litter aversion, litter trials should be instituted. A litter trial consists of offering the cat a choice of litter materials either in the confinement spot or elsewhere and recording which material the cat prefers. The choice may be based on information in the history suggesting a substrate preference. • Resource Allocation: This is especially important in multicat homes. Adequate number and placement of litter boxes is crucial to encouraging litter box usage by all cats in the home. It may be necessary to establish multiple core areas or bases for food, litter, and resting to allow all cats’ equal access to important resources. This is especially critical if the history reveals problems in social interactions between household cats. Elderly or infirm cats with mobility or medical problems may need multiple litter boxes near where they spend their time to create easier access and to avoid climbing stairs, thus encouraging appropriate litter box use. See Chapter 236.
• Litter Box Additives: CatAttract Litter Additive® (Precious Cat, Inc., Englewood, CO) is an organic additive that can be safely added directly to litter and may attract cats to use the litter box. The theory is that it uses the feline’s sense recognition to draw it to the aroma of the litter additive. Alternatively, the product is included in CatAttract Litter®, available at many pet stores. No studies are available to substantiate the veracity of this claim. • Environmental Therapy: It is necessary to make the areas where the cat has urinated or defecated aversive to prevent repeat soiling in that area. Commonly used techniques include placing food bowls near the elimination site, covering the area with an aversive substance such as aluminum foil, plastic, sticky tape, and upside down carpet runners, or associating the area with a scent that is aversive to most cats, such as potpourri. Access to areas where the cat has soiled can be prevented by closing doors, administering motion sensors with alarms, or placing large pieces of furniture or gates in the way. • Neutralize Odor: Thorough cleaning of the areas that the cat previously soiled is necessary. Enzymatic products are preferred. Several safe and effective enzymatic cleaners are available. If carpet is involved, the carpet should be rolled back, the odorous pad removed and replaced, and the back of the carpet treated before being set back in place, if feasible. If that is not feasible, the neutralizing product should be poured on the area so it soaks into the carpet pad, the source of most of the odor. • Follow-up with owners is essential to assess progress and should occur at regular intervals of 1 to 2 weeks. • Pharmacological interventions are not warranted in cases of aversions or preferences. However, medication may be useful in cases in which anxiety is a major component due to intercat social interaction issues. However, if the underlying reasons for the anxiety are not addressed or the litter box issues not addressed medication will not be useful. • Using confinement alone will be unsuccessful unless problems with litter box maintenance, size, and cleanliness and social conflicts between cats and people are addressed.
Prevention Although no data exists to support preventative measures, certain considerations when providing litter boxes may be useful. • Litter boxes should be large, at least 1.5 times the size of the cat or more. • Litter boxes should be kept extremely clean, scooped of waste material frequently, emptied, washed, and refilled every 1 to 4 weeks depending on type of litter material used and number of cats within the home. Old soiled and stained boxes should be discarded and replaced yearly. • When multiple cats are in the home, several toileting sites should be provided. This will allow privacy and the ability to eliminate without being bothered. • Nonuse of the litter box may be triggered by other events and lack of access to resources. Attempts should be made to have multiple locations for food, water, and resting areas. Changes should be made slowly.
Therapeutic Notes • Feliway® Spray or Diffuser: The feline facial pheromone analogue, Feliway® (CEVA Animal Health Inc) is a synthetic cheek pheromone of cats used to calm cats and can be useful in decreasing or stopping spraying behavior and diminishing anxiety. The pheromone analog reproduces the familiarization properties normally produced by a cat when it deposits its own facial pheromones in the environment. It can be used in the areas of housesoiling but not in the litter boxes. Pheromones tend to be more effective and useful in marking behavior rather than housesoiling.
Prognosis Ongoing medical problems will usually result in treatment failure and relapse. Unresolved underlying disease should, therefore, be considered in cases that are resistant to therapy. The response to therapy can be quite variable and seems to depend on how long the behavior has been present. If the behavior has been a chronic problem (longer than 2 months), it will generally be more difficult to resolve permanently. When dealing with a long-term housesoiling case, owners should be made
579
SECTION 2: Behavior
aware that it may take time for the problem to resolve, or there may only be a decrease in the frequency of housesoiling behavior.
Selected Readings Bernstein P, Strack MA. 1996. Game of cat and House: spatial patterns and behavior of 14 Domestic cats (felis Catus) in the home. Anthrozoos. 11:25–39. Buffington CAT, Westropp JL, Chew DJ, et al.. 2006. Clinical evaluation of multimodal environmental modification (MEMO) in the management of cats with idiopathic cystitis. J Fel Med Surg. 8:261–268. Cooper LL. 1997. Feline inappropriate elimination. Vet Clin North Am Small Anim Pract. 27(3):569–600.
580
Horwitz DF. 1997. Behavioral and environmental factors associated with elimination behavior problems in cats: a retrospective study. Appl Anim Behav Sci. 52:129–137. Horwitz D. 2002. Housesoiling by cats. In D Horwitz, D Mills, S Heath, eds., BSAVA Manual of Canine and Feline Behavioural Medicine, pp. 97–108 Gloucester, UK: BSAVA. Neilson J. 2003. Feline housesoiling: Elimination and marking behaviors. Vet Clin North Am Small Anim Pract. 33(2):287–302. Neilson J. 2009. The latest scoop on litter. Vet Med. 103:140–144. Sung W, Crowell-Davis SL. 2006. Elimination behavior patterns of domestic cats (Felis catus) with and without elimination behavior problems. Amer J Vet Res. 67(9):1500–1504.
CHAPTER 236
Intercat Aggression Debra F. Horwitz
Overview Multiple causes exist for intercat aggression. In all situations, medical factors must be either ruled out or identified and treated. In otherwise healthy cats, fear, anxiety, and territorial responses all contribute to intercat aggression. Fights can occur due to a change in social interactions, a traumatic event, as the sequel to redirected aggressive behavior or another anxiety producing event, with the introduction of another cat, or due to social or environmental changes within the home. These scenarios are also responsible for fighting episodes between cats that have lived together for some time.
Diagnosis Primary Diagnostics • Medical Testing with Physical Examination: Medical problems can precipitate or contribute to aggressive responses in cats. Therefore, a complete medical examination is needed in all aggression problem behavior cases. A physical examination should be accompanied by additional diagnostic tests, as appropriate, such as urinalysis, fecal examination, and screening tests for metabolic or endocrine dysfunction. In some cases, additional diagnostic procedures, such as radiographs, may be necessary to look for potential sources of pain. Other areas that can contribute to an increase in irritability include dental disease, gastrointestinal problems, changes in vision or hearing, hypertension, and allergies. • Complete History: All behavior cases require a thorough and complete history for accurate diagnosis. Detailed history and descriptions of aggressive incidents are essential to identify potential triggers of aggressive behavior and direct appropriate corresponding treatment. In a multicat home, attempting to determine which cats historically interact with one another (by grooming or sleeping in proximity) may help identify clusters of friendly individuals and individuals with conflicts. Historical questions should pay particular attention to the aggressive episodes themselves, noting the behavior or response of every animal and person involved, especially signs of anxiety, fear, or defensiveness. Aggressive behaviors include but are not limited to blocking access to a territory, staring, hissing, swatting, growling, chasing, wrestling, biting, scratching, and vocalizing. In some cases overt aggressive signaling may be missing, but other subtle signs of intimidation and anxiety may occur. In the victim cat these might include poor grooming, hiding, and restriction of certain cats to select areas of the home and house soiling and urine spraying. Such behavioral cues along with the frequency of episodes may be helpful in offering clients a prognosis. • Resources/Environment: Information regarding the daily routine including when and where the aggressive episodes occur, which cats are involved, and how resources are allocated within the home must be collected. Resources include, but are not limited to, food, water, litter boxes, toys, hiding spots, and perching areas. Limited resources may lead to aggression over competition for perceived insufficient
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
resources, and territorial disputes may provoke aggression over resources that are not appropriately dispersed throughout the home. Fights may or may not take place at the location of the disputed or scarce resource but may be more covert such as overeating especially at night with resultant obesity or vomiting, housesoiling in unwanted areas due to limited access to litter boxes, or urine spraying to claim territory. This is especially true for cats that are the victims of aggressive encounters with another cat within the home. The client should be questioned about any participating cat’s ability to hide, retreat, or escape from the situation and the availability of resources within that retreat. If hiding areas are unavailable in a particular location or if a victim cat feels it cannot escape a threatening situation, it may become aggressive. If resources are not available in the retreat location this might lead to housesoiling. This emphasizes the fact that multiple resources and resource locations decrease conflict by providing cats with more choice. • Age of Onset: Age of the cat at onset of the problem should be documented. When cats reach social maturity, around age 1 to 2 years, they may be more inclined to compete for territory or change how they socially interact with other cats, which may explain more conflict among housemates. • Body Language and Posture: Detailed descriptions of body posture and facial expression of all involved cats before, during, and after the incident are useful for differentiating aggressors from victims. The relative location or spatial relationship of each cat to the other will often indicate which cat is in control of the episode versus which cat is responding. The cat in control is often situated higher than the other cat, such as on a perch or a chair, but this may not always be true. The “victim” will usually be the cat closer to the ground. If both cats are on the same level, the aggressor will usually have direct eye contact and upright body posture whereas the victim will show acts of attempting to avoid conflict, such as looking away and remaining crouched. • Owner-Cat Dynamics: Any cat-owner interactions and the response of the owner to each incident should be recorded. In some situations, the owner will unknowingly contribute to, reinforce, or exacerbate a chain of events leading to the aggressive episode.
Secondary Diagnostics • Diagnostic Categorization: Categorizing types of aggression may make diagnosis and the formulation of a treatment plan more manageable. • Territorial Aggression: Some studies indicate that cats do not share space equally and that within a group of cats, certain individuals appear to be in control of certain elements in the environment. Threats between cats may be more covert, blocking access to locations, staring or supplanting, although overt aggressive threats such as chasing, growling, hissing, and biting may also be evident. In territorial disputes, one cat (the aggressor) will usually chase another (the victim) accompanied by vocalizations such as hissing, growling, and yowling. The victim may live in a restricted area to keep away from the aggressor. • Social Status Aggression: Although good evidence of strict social hierarchies in cats is lacking, shifts in social relationships often precipitate aggression. Fighting may begin when a young resident cat reaches social maturity (usually at 1–2 years of age), when an
581
SECTION 2: Behavior
•
•
•
•
aged cat leaves or no longer controls spaces or resources, or when a new cat enters the home. In social status aggression, if access to resources such as litter boxes, resting places, and food bowls is adequate, there may only be occasional fighting. Redirected Aggression: Redirected aggression arises when a cat is agitated but is unable to vent that irritation toward the causative agent. Possible stimuli include the sight, sound, or odor of another cat or other animal, unusual noises, unfamiliar people, unfamiliar environments, and pain. After the first initial aggressive response due to these stimuli, fighting may result whenever cats see one another. The victim of the aggression will usually become fearful and defensive, causing him or her to run away or hide and be inactive. However, the victim may also react by growling or hissing at other cats. Behaviors directed at the other cats may result in maintenance of aggressive responses from the initial aggressor cat. Fearful or Defensive Aggression: This is common sequelae to fighting between cats. In this type of aggression, the cat exhibits fearful or defensive body language, including crouched posture, flattened ears, dilated pupils, piloerection, hissing, spitting or growling. Such behavioral responses often stimulate other cats to respond aggressively, leading to a vicious cycle of aggressive behaviors between house mates. Irritable Aggression: Irritation can result in aggression if the cat is experiencing underlying medical problems (especially pain) or has experienced changes in its home environment. If these problems are resolved, the aggressive behavior may diminish. Predatory or Play-Related Aggression: This behavior is most common in singleton cats less than 2 years of age, cats housed with other animals that will not play, or cats that are left alone for long periods of time. Cats exhibiting this type of aggression will display little emotional arousal. Episodes usually involve hiding behind objects, waiting for movement, springing out, attacking, and then running away. When directed to an older cat or one unwilling to play, fighting may ensue.
Treatment Primary Therapeutics • Review Previously Attempted Therapy: Regardless of the type of aggression displayed, the effects of previously employed treatments should be reviewed. • Resource Allocation: It is absolutely essential that the resources be distributed throughout the home in such a way as to allow easy access for all cats. The typical resources in dispute are food and watering sites, litter boxes, perching, resting, and hiding areas. It may be necessary to establish multiple core areas or bases for these items to allow all cats’ equal access to important resources by spreading them throughout the environment. Litter boxes, bowls, and so on should not be clustered together but spread throughout the environment allowing easy access for all cats. This is especially critical when there are problems in social interactions between household cats. The ideal location would have more than one exit or entry point to prevent cats from being cornered. Elderly or infirm cats with mobility or medical problems may need multiple litter boxes near where they spend their time to create easier access and encourage appropriate litter box use. As a general rule of thumb, there should be at least one more litter box than the number of cats. In some cases owner attention may be a valued resource, and owners should strive to give all cats within the home daily attention time. • Separation of Fighting Cats: If fighting is ongoing, the participants should be separated unless programmed introductions are taking place. Allowing aggressive encounters increases anxiety and stress on all participants and is not helpful for resolution of the problem.
582
• Counterconditioning and Desensitization: Counterconditioning and desensitization exercises are used to reacclimatize previously feuding cats to one another. The goal is for cats to share a space without any aggressive behaviors. Through a series of gradual reintroductions, each cat is taught to associate good things (such as food or treats, petting, praise, or play) with calm and quiet behavior in the presence of the other cat. Introductions are done slowly using food or other rewards to facilitate calm, nonanxious behavior (counterconditioning). Initially cats must be far apart so that they are relaxed (desensitization), during which they are offered a highly desired reward. For safety and control, a harness and leash is suggested for each cat. Cats too close together may not eat. If this occurs, increase the distance between them. If the cats do eat, they are allowed to remain together while they eat, after which they are again separated. The next feeding is provided at the same distance. If the cats remain calm, at the next session the dishes can be moved closer together, by approximately 15 to 20 cm (6–8 in). Two more feedings where no aggressive or anxious behaviors are expressed should be done at the same distance before the bowls are moved closer together. If the cats will not eat when they see one another, feedings should be attempted with each cat on opposite sides of a closed door. After using nonvisual introductions for a few days feeding from across the room can be tried once more. • Gradual Introductions: Introductions between new cats or previously feuding cats should always be gradual. The goal is to allow the cats to become comfortable in the presence of each other. Throughout each and every step of the process, rewards should be offered to reinforce calm behavior. First, cats should be allowed to smell or hear but not see each other. This is best achieved by housing cats in separate rooms, each with its own set of resources (i.e., litter boxes, food, and water). During this period, each cat’s cheeks (facial glands) and body should be rubbed with towels and presented to the other cat to exchange scents. Alternatively (or in addition to presenting the scentmarked towels), litter pans can be switched between cats to aid in familiarization. After several days, the cats should switch rooms to exchange odors. Next, cats are visually introduced with the use of a crate or kennel. Each cat is placed in a crate at opposite sides of a room and allowed visual contact. Having an owner sit with each cat and provide food rewards for reassurance often facilitates this step. Eventually, one cat is allowed outside of the crate; usually, the aggressor is placed in the crate while the victim is allowed loose in the room. Over time, the occupant of the crate can be switched. All interactions should be stopped if the aggressor threatens the victim. If cats are uncomfortable when one is loose, both cats can continue to be crated. A similar technique can be done using double baby gates or a screen or glass door on doorways to allow the cats to visualize each other without getting too close. • Warn Other Cats: Outfit aggressive cats with an approved cat collar with a large bell to forewarn the victim of approach, thereby increasing the victim’s chances of escape. However, this strategy may work only temporarily. • Pheromonal Therapy: Pheromones are chemical substances that have a species specific effect on behavior. Feline pheromone products are available as a plug-in diffuser or a spray and have shown some usefulness in calming cats and helping in aggressive situations. • Pharmacological Treatments: Medication should only be used in conjunction with behavioral modification. In some cases both the aggressor and the victim may need medication. Commonly used medications include selective serotonin reuptake inhibitors and tricyclic antidepressants for the aggressor and azapirone for the victim. See related Chapter 239. • Territorial Aggression: Ample resources should be provided and dispersed throughout the environment as described previously. Within a multicat household there should be multiple litter boxes, food bowls, water bowls, and resting areas located in different areas of the home. Drug therapy alone is rarely curative for this form of
Intercat Aggression
•
•
•
•
•
•
aggression over the long term. Introductions and separation of cats at times may allow for successful management. Social Status Aggression: Provide ample resources to ensure all cats have easy access to multiple locations, especially litter boxes. Attempt to make changes in the environment slowly, especially when adding a new cat. See the section on Gradual Introductions. Keep in mind that the cats within the home may not want another cat added to their environment. In some severe cases permanent separation and alternating which cats are in what parts of the home may be necessary for harmony to occur. Redirected Aggression: Make any anticipated changes to the home environment, such as adding new furniture, gradually. Keep windows and doors closed to avoid contact with outdoor cats. Use of a pheromone, such as Feliway® diffuser (CEVA Animal Health Inc), may make impending changes less stressful to residents. Provide cats with ample safe places to hide, as well as outlets for emotion and stress, such as toys. Fearful or Defensive Aggression: Treatment for fearful or defensive aggression is counterconditioning and desensitization as described previously. Cats should be separated unless in a treatment session. Irritable Aggression: Resolve underlying medical problems. If possible, maintain routines for cats, and attempt to maintain a constant spatial environment. For example, refrain from frequent rearrangement of furniture or movement of the cats’ resources. Misdirected Predatory or Play-Related Aggression: Provide appropriate play, exercise, and environmental enrichment. Some examples of environmental enrichment include toys, puzzles, and objects (such as boxes or laundry baskets) in which to hide and play. Allow older cats separate time away from an active younger cat. Play Therapy: This is designed to distract and occupy the cat or engage each cat in a mutually enjoyable activity.
• At all times safety must be a primary concern. In homes with children, elderly, or immune-compromised individuals, some cats may not be appropriate companions if aggression cannot be curtailed. If serious injury has occurred, it may be necessary to remove the cat from the home. In some cases it may be prudent to confine the cat away from people. Whenever injury occurs medical attention should be sought immediately. One should be cautious about prescribing medications for the owner or your staff to administer, and the owner should be instructed not to put himself or herself at risk of a bite wound when attempting to administer medication. See Chapter 239 on preconditioning cats to take medication.
Prevention • Owners should be advised that if they desire multiple cats in their home, adopting related female cats or adopting younger cats in pairs may help prevent fighting. Adding additional cats to the household should take into consideration the temperament of the original inhabitants and the temperament of the potential new addition. Shy, timid cats may not mix well with bold outgoing cats. Allocation of resources throughout the home may help prevent problems by allowing cats to use multiple core areas to meet their needs and thus avoid interactions with cats they wish to avoid. All introductions should be done slowly over several months to avoid increasing stress and the possibility of fighting. When one of an elderly pair of cats dies, it is not always prudent to assume the remaining cat wishes a companion.
Prognosis Therapeutic Notes • Do not allow aggressive interactions. Ongoing aggressive interactions may make resolution of future aggressive behaviors more difficult. • Meet daily needs for activity, exercise, and exploration and owner attention. Lack of access to these activities may increase frustration in some individuals and contribute to aggressive interactions. • Encourage calm behavior. Relocate agitated cats to a darkened room with food, water, and a litter box. Keep the cat in the dark until it is calm, which may take several hours or days. Only enter the room to feed and clean the litter box. If the cat approaches calmly and with a relaxed body posture, he or she may be ready to come out. However, premature or early reintroduction of the cat may cause fighting to resume and further prolong the problem. Feliway® diffuser has been shown to promote calm behavior in cats and could be placed in the room with the agitated cat. • Cats should be separated after a fight until they are calm. If aggressive episodes cannot be controlled, cats should be separated at all times to avoid injuries. If this is not possible, alternate living arrangements should be pursued. • Avoid lifting or handling a highly agitated cat because it is dangerous and may lead to personal injury. • If medication is prescribed, it is generally used for 6 to 12 weeks in conjunction with behavior modification and is rarely successful on its own. If the behavior changes, the cat is weaned off the medication by decreasing the dose 25% every 2 to 4 weeks while watching for a return of any aggressive indicators such as growling, hissing, or chasing. If aggressive behaviors return, the cat is maintained at the same dose for several weeks to see if the cat stabilizes before attempting to decrease the dose again. Drug therapy alone is rarely helpful without concurrent behavioral and environmental changes.
The prognosis when cats fight is quite variable. Some cats remain fearful and reactive and will not return to baseline. These cats may improve with medication or may not. In other situations, just correcting the distribution of resources in the home so that cats can avoid one another can result in a greatly improved social situation. In many cases the prognosis for territorial aggression is poor.
Selected Readings Bateson P, Martin P. 2000. Behavioural development in the cat. In DC Turner, P Bateson, eds., The Domestic Cat: The Biology of Its Behaviour, 2nd ed., pp. 9–22. Cambridge: Cambridge University Press. Crowell-Davis SL, Barry K, Wolfe R. 1997. Social behavior and aggressive problems of cats. Vet Clin North Am Small Anim Pract. 27(3): 549–568. Heath S. 2002. Feline Aggression. In D Horwitz, DS Mills, S Health, eds., BSAVA Manual of Canine and Feline Behavioural Medicine. pp. 216–225. Gloucester UK: BSAVA. Horwitz DF, Neilson JC. 2007. Aggression/Feline: Intercat. In Horwitz DF, Neilson JC, eds., Blackwell’s Five-Minute Veterinary Consult Clinical Companion Canine and Feline Behavior, 4th ed., pp. 125–133. Ames: Blackwell. Landsberg G, Hunthausen W, Ackerman L. 2003. Feline aggression. In GM Landsberg, W Hunthausen, L Ackerman, eds., Handbook of Behavior Problems of the Dog and Cat, 2nd ed., pp. 427–453. Philadelphia: Saunders. Levine ED. 2008. Feline fear and anxiety. Vet Clin North Am Small Anim Pract. 38(5):1065–1080. Lindell EM, Erb HN, Houpt KA. 1997. Intercat aggression: Retrospective study examining types of aggression, sexes of fighting pairs, and effectiveness of treatment. Appl Anim Behav Sci. 55:153–162.
583
CHAPTER 237
Marking Debra F. Horwitz
Overview Marking is the deposition of urine, and occasionally stool, on vertical locations and is considered a normal part of the feline behavioral repertoire. Marking behavior is sometimes referred to as spraying behavior. It is normal for both intact and neutered or spayed animals to urine mark. Urine marking is distinguished from housesoiling by body posture. A cat that is marking will be standing, not squatting. To mark, a cat will back up to a vertical surface, hold its tail erect, and expel a stream of urine backward, often while treading with the hind feet and quivering its tail. Cats that mark with urine on vertical surfaces will usually continue to use the litter box for elimination of both urine and stool. Cats mark with urine to attract mates and in response to environmental changes, stress, or agonistic interactions with cats inside and outside of the home. Cats will often mark inside the house as a territorial response to the presence of other cats outside the home. When there are multiple cats in the home, marking with urine may occur to delineate territory or due to stress. In addition to marking with urine (and occasionally stool), cats also mark with facial (cheek) glands and other various located scent glands and via clawing, but the focus of this chapter will be on urinary marking.
Diagnosis Primary Diagnostics • Physical Examination with Medical Testing: In all complaints of elimination outside of the litter box, a complete medical examination is needed. Medical problems can precipitate inappropriate elimination behavior in cats. However, elimination for the purposes of marking (i.e., communicating) is normal feline behavior and is, therefore, not commonly associated with underlying disease. One small study documented that urinary tract disease has not been associated with urine marking. Nevertheless, a complete physical examination accompanied by a urinalysis (or fecal examination if marking with stool) is warranted. In some cases, especially when it is unclear whether the elimination is a result of housesoiling or marking, laboratory screening for metabolic or endocrine dysfunction is indicated. In some cases additional diagnostic procedures, such as radiographs and ultrasound examination of the abdomen, may be necessary. The sudden onset of marking in an older mature cat should prompt a complete and thorough examination including extensive endocrine testing. • History: All behavior cases require a complete history. Be sure to obtain a description of the cat’s body posture during the elimination episodes because urine marking posture is characteristic. If the description of the episode is that the cat backs up to a vertical surface, holds its tail erect, and expels a stream of urine backward while treading with the hind feet and quivering the tail, the diagnosis is marking (spraying). Additionally, the urine will be found on a vertical surface 6 to 10 inches off the floor and draining downward. Continued use of the litter box is also consistent with a diagnosis of
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
584
marking. After marking has been differentiated from housesoiling, information should be gathered to identify the potential trigger(s) for the marking behavior. General history should include the size and location of the urine spot(s),to verify marking; the substrate on which the cat urinates, to verify vertical deposition; and the onset; duration; frequency; and progression of the behavior. • Identify Specific Stressors: Marking in cats is often categorized as either sexual or reactional and may occur in response to stress or anxiety. Ask the owner to report any possible sources of stress in the household. Try to identify subtle stressors, including anything that may elicit frustration or aggravation. Gather information about the daily routine now and in the past to pinpoint any changes in the cat’s routine. Inquire about pet-owner and cat-cat interactions to rule out aggression between cats or to humans as a potential source of conflict. Inquire about the number and distribution of resources such as litter boxes, food and water bowls, perching areas, and hiding places. Limited or poorly allocated resources may be a source of stress for housemates, especially in multicat homes. Questions about litter box husbandry should be obtained to rule out litter box issues as a potential source of stress (see Chapter 235) and document any other cats that may be marking. Constructing a diagram illustrating locations of urine spots is helpful for detecting possible environmental, visual, or spatial triggers. For example, if marking usually occurs by a window or glass door, outdoor stray cats may be a potential trigger (although such marking does not always occur where the outdoor cat was visualized).
Diagnostic Notes • Owners should provide some number of urine spraying episodes per week in the initial consultation. A decline in that number can be used to assess treatment response rather than relying on a total cessation of urine marking behavior. • In some cases a cat may urinate in a standing posture leaving large amounts of urine both on the wall and on the floor. It is speculated that these cats are not marking and may not respond to traditional treatments for urine marking behavior.
Treatment Primary Therapeutics • Treat Underlying Medical Problems: Medical problems are occasionally associated with urine marking (due to stress or pain) and should always be treated concurrently with behavior modification. • Feliway® Spray or Diffuser: The feline facial pheromone Feliway (CEVA Animal Health Inc) is a synthetic cheek pheromone of cats used to calm cats and can be useful in decreasing or stopping spraying behavior. The pheromone analog reproduces the familiarization properties normally produced by a cat when it deposits its own facial pheromones in the environment. • Confinement with a Litter Box: Limit the cat’s access to the areas where they have previously soiled by confinement with litter and food when no one is home or owners are sleeping. The time of day when urine spraying occurs should be used as a determinant of when to confine the cat. Confinement during times that the cat is more
Marking
likely to spray allows the cat to have an area all by itself without the presence of the other cats in the household. A cat might want between 4 and 6 hours of alone time daily. Confinement is usually effective in getting the cat to use the litter box while confined but may not affect the marking behavior when the cat is free in the house. Some cats benefit from a marking station placed in their confinement area. Request that owners check the cat and ascertain when the cat urinates and defecates and record the information. When the owner is home the cat may be out under strict supervision to prevent marking. • Do Not Punish: Punishment is not an effective tool for changing marking behavior. The cat is more likely to associate the punishment with the owner, resulting in fear development, owner avoidance, an increase in stress and eventual disruption of the cat-owner bond. • Make the Litter Box User-Friendly: A recent study by Pryor and colleagues revealed that urine marking behavior may decline by 50% or greater with environmental changes such as daily litter box cleaning, obtaining a new litter box and cleaning it weekly, providing one litter box per cat, and enzymatic cleaning of the sprayed areas. Provide a litter box that is a preferable alternative to its current outlet. An attractive and easy to access litter box is extremely important for changing marking behavior. • Clumping Litter: Research has shown that some cats prefer the clumping materials to clay litter products. When clumping type litter materials are provided, the box should be scooped daily and changed weekly. See Chapter 235 for additional details on litter preferences most common in cats. • Regular cleaning: In addition to daily scooping and weekly (or more often) changing of litter, boxes in good condition should be washed weekly with mild soap. Old, soiled boxes should be discarded in favor of new, clean boxes. • Litter Depth: The depth of the litter material should be adequate for the cat to bury urine and feces; about 2 to 3 inches is usually sufficient, but some cats prefer more. • Box Features: For some cats, changing specific characteristics of the litter box may be beneficial, such as removing the cover from a covered litter box, providing a larger box, or adding a box with lower sides. Some cats will prefer a plain box versus a mechanical or automatic scooper, which makes noise after the cat eliminates. • Resource Allocation: Especially important in multicat homes, adequate number and placement of litter boxes are crucial to encouraging litter box usage by all cats in the home. It may be necessary to establish multiple core areas or bases for food, litter, and resting to allow all cats equal access to important resources. This is especially critical if the history reveals problems in social interactions between household cats. See Chapter 231. • Environmental Therapy: It is necessary to make the areas where the cat has sprayed aversive to prevent repeat soiling in that area. Commonly used techniques include placing food bowls near the elimination site, covering the area with an aversive substance such as aluminum foil, plastic, sticky tape, and upside down carpet runners, and associating the area with a scent that is aversive to most cats such as potpourri. Access to areas where the cat has sprayed can be prevented by closing doors, administering motion sensors with alarms, or placing large pieces of furniture or gates in the way. • Designate an Acceptable Marking Location: An acceptable spraying spot for the cat can be designed by creating an “L” shaped litter box arrangement using two litter boxes: this arrangement uses two litter boxes; one placed vertically (standing on the short end) and one placed horizontally with litter inside placed inside the vertical one. An alternate method is to place just one box leaned against the wall at the site of urine spraying. Some cats may spray only in this area. This is an alternative solution that some owners are willing to live with. See Figure 237-1. • Limit Visibility to Outdoor Cats: Attempts should be made to limit an inside cat’s ability to visualize outdoor cats. Block visual access out windows and doors or close the cat in a room without windows.
Figure 237-1 An acceptable spraying spot for the cat can be designed by creating an “L” shaped litter box arrangement using two litter boxes: this arrangement uses two litter boxes; one placed vertically (standing on the short end) and one placed horizontally with litter inside placed inside the vertical one.
Remove furniture close to windows and modify windowsills so the cat cannot sit on them. The owner should be discouraged from feeding outside cats and remove bird feeders and other things that might attract additional cats. • Neutralize Odor: Thorough cleaning of the areas that the cat previously soiled is necessary. Enzymatic products are preferred. Several safe and effective enzymatic cleaners are available. If carpet is involved, the neutralizing product should be poured on the area so it soaks into the carpet pad, the source of most of the odor. • Litter Box Additives: CatAttract Litter Additive® (Precious Cat, Inc., Englewood, CO) is an organic additive that can be safely added directly to litter in an attempt to attract cats to use the litter box. It uses the feline’s sense recognition to draw it to the aroma of the litter additive. Alternatively, the product is included in CatAttract Litter®, available at many pet stores. Little scientific evidence is available to support the validity of these claims.
Therapeutic Notes • Follow-up with owners is essential to assess progress and should occur at regular intervals of 1 to 2 weeks. Initially a decline may be noted rather than cessation of urine marking, but that often indicates a response to therapy. • Pharmacological interventions are not warranted in cases of aversions or preferences; therefore, a diagnosis of urine spraying must be verified prior to using medication. However, medication may be useful in cases where anxiety is a major component of the urine spraying behavior. • Pharmacological Treatments: Medication should only be used in conjunction with behavioral modification. See Chapter 239. Commonly used medications include: fluoxetine (Prozac®), clomipramine, buspirone, and occasionally benzodiazepines.
585
SECTION 2: Behavior
• Confinement: Using confinement alone will be unsuccessful unless problems with litter box maintenance, size, and cleanliness and social conflicts between cats are addressed. • Surgery: Cats that are intact should be neutered. In the past additional surgeries for spraying in cats included olfactory tractotomy and bilateral ischiocavernosus myectomy, neither of which is performed with any regularity anymore.
Prognosis Marking behaviors often have a variable response to treatment. Factors such as outdoor cats and the ability to control them, social conflicts among cats within the household, and ongoing household changes may affect total resolution of the spraying behaviour. Ogata and Takuchi found that while urine marking decreased with pheromone therapy, urine marking was sustained at a higher level in households with intercat aggression. Mills and Mills found that while urine marking decreased, it often was not eradicated. However, the reduction in spraying behavior was acceptable to the clients as an outcome. A previous study by Hart on pharmacologic treatment of spraying behaviour showed that marking behaviour may persist or return after treatment with medication is stopped. Recent studies looking at control of urine marking with longterm treatment have shown no difference between fluoxetine and clomipramine for the treatment of urine marking and that cats that relapse usually respond to reinstatement of the medication. Prognosis may be improved in marking behaviors by keeping household stress to a minimum and the scent profile in the home constant. Long-term use of pheromone spray or diffuser may also be useful.
586
Suggested Readings Hart BL, Cliff KD, Tynes VV, et al. 2005. Control of urine marking by use of long-term treatment with fluoxetine or clomipramine in cats. J Am Vet Med Assoc. 226:378–382. Horwitz DF. 1997. Behavioral and environmental factors associated with elimination behavior problems in cats: a retrospective study. Appl Anim Behav Sci. 52:129–137. Horwitz DF, Neilson JC. 2007. Urine Marking Feline. In Horwitz DF, Neilson JC, eds., The 5-Minute Veterinary Clincal Companion 4th ed., pp. 505–513 Ames, IA: Blackwell Publishing. King JN, Steffan J, Heath SE, et al. 2004. Determination of clomipramine for the treatment of urine spraying in cats J Am Vet Med Assoc. 225:881–887. Landsberg GM, Wilson AL. 2005. Effects of Clomipramine on Cats presented for Urine Marking. J Am Anim Hosp Assoc. 41:3–11. Mills DS, Mills CB. 2001. Evaluation of a novel method for delivering a synthetic analogue of feline facial pheromone to control urine spraying by cats. Vet Record. 149:197–199. Ogata N, Takeuchi Y. 2001. Clinical trial of a feline pheromone analogue for feline urine marking. J Vet Med Sci. 63:157–161. Pryor PA, Hart BL, Cliff KD, et al. 2001. Effects of a selective serotonin reuptake inhibitor on urine spraying behavior in cats. J Am Vet Med Assoc. 219:1557–1561. Pryor PA, Hart BL, Bain MJ, et al. 2001. Causes of urine marking in cats and the effects of environmental management on frequency of marking. J Am Vet Med Assoc. 219:1709–1713. Tynes VV, Hart BL, Pryor PA, et al. 2003. Evaluation of the role of lower urinary tract disease in cats with urine marking behavior. J Am Vet Med Assoc. 223(4):457–461.
CHAPTER 238
Psychogenic Alopecia Debra F. Horwitz
Overview Psychogenic alopecia is a nondescript term that is often used to encompass various hair loss conditions in cats that have behavioral components. Other terms have been used including overgrooming, self-directed behaviors, displacement activities, and compulsive disorders. In the past, the term endocrine deficiency alopecia incorrectly described this condition. The common link in all of these is that most hair loss appears to be self-induced from excessive grooming often without any easily discernable skin lesions. Grooming is a normal feline activity that comprises up to 50% of nonsleeping time or 8 to 15% of the total daily time budget of the domestic cat. When done to excess, damage to the hair shaft and subsequent hair loss are possible. The supposition in the past has been because no discernable medical diagnosis could be ascertained; the problem was behavioral in origin. The possible inciting factors included underlying stress or anxiety due to environmental or social elements within the home, or conflict or frustration scenarios resulting in displacement grooming. However, recent research has begun to indicate that many problems actually have a medical condition as the sole cause or in some cases along with a behavioral component and only a small percentage are purely behavioral in origin. Those that are behavioral in origin may also be compulsive disorders that arise from underlying conflict, anxiety, or frustration and occur at a frequency and duration that interferes with daily normal functioning. Hair loss is most commonly noted on the medial forelegs, caudal area of the back legs, caudal abdomen, flanks, and lumbar areas. See Figure 238-1. Initially it is useful to ascertain the number of grooming bouts, their length, and intensity. This may be difficult to determine if punishment has been used in the past and now the cat engages in the behavior away from the owner. Because hair regrowth is typically slow, diagrams or photographs of the hair loss and any lesions and their size will be useful to assess treatment response. In most cases the hair loss occurs in areas more easily reached by the cat; sides, flanks, back of rear legs, and abdomen. Interestingly these areas correlate with studies that have shown that these areas receive the most time in the normal daily feline grooming ritual. There are five circumstances that can cause or contribute to psychogenic alopecia and overgrooming either individually, together, or with or without medical complications. • The goal of the behavioral history is to determine if the problem is a displacement activity, redirected behavior, attention seeking, a compulsive disorder, or hyperesthesia syndrome (see Chapter 105). • Intercat Dynamics: Inquire about any intercat aggression. See Chapter 236. Keep in mind that aggressive interactions between cats can be covert and difficult for some owners to notice without additional information to help identify agonistic interactions. Intercat aggression can result in a great deal of stress and anxiety for both the aggressor and the victim. • Displacement Activities: Displacement activities are behaviors that occur when an animal is confronted with an acute conflict situation. Usually these are short lived and self-limiting. If the problem situa-
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
(A)
(B) Figure 238-1 This cat with over grooming (psychogenic alopecia) exhibits hair loss on the forelegs (A), lateral abdominal wall, rear legs, and ventral abdomen (B). Note the lack of obvious skin lesions or dermatitis.
tion is not resolved, displacement activities can become chronic outlets for stress and frustration. • Redirected Behavior: When faced with a frustrating or conflict situation the animal may not be able to resolve the problem by direct interaction. In that case, the cat may resort to a displacement
587
SECTION 2: Behavior
activity as an outlet for the energy. If the original source of conflict is not alleviated, the redirected behavior may be come chronic. Redirected behaviors can also occur in an environment that does not meet the needs of the cat for play, exploration, social contact, and rest. • Attention Seeking: Animals will engage in behaviors to get owner attention even when it appears that the behavior is injurious. If grooming behavior results in picking up, holding, playing with, or feeding the cat, and if these are rewarding to the cat, then grooming behaviors might be reinforced and ongoing. However, generally attention seeking alone will not be the sole cause of the overgrooming. • Compulsive Disorder: Compulsive disorders are behaviors that are usually derived from a normal behavioral pattern (in this case grooming) but occur at a higher than normal rate, are difficult to interrupt, and interfere with the ability of the animal to function normally. Often animals that have compulsive disorders will engage in the behavior to the exclusion of most activities except eating and sleeping. It appears that compulsive disorders often begin in acute conflict situations or situations that create frustration and stress for the animal. Stress, anxiety, and frustration can occur when the social needs of the cat are not met, if there is intercat aggression, outlets for normal behaviors are not provided, the cat has no control over the outcome of events or life is too unpredictable. Over time, the behavior begins to occur in other circumstances and appears to have a lower threshold for initiation. It is unclear if performance of the behavior is calming for the animal or not.
Diagnosis
Figure 238-2 The hair loss on this cat was bilateral and appeared to be psychogenic in origin. Fungal culture and several skin scrapings were negative. There was no response to corticosteroids or a food trial. A skin biopsy found occasional Demodex gatoi deep in the hair follicles. The cat was infected with the feline immunodeficiency virus.
Secondary Diagnostics • Skin Biopsy and Histopathology: If the above tests are negative and response to psychogenic alopecia therapy is poor, a skin biopsy is warranted; if the problem is psychogenic alopecia, the histopathology should be normal. See Figure 238-2.
Primary Diagnostics • Establish Overgrooming: It is essential to establish that the cat is overgrooming instead of having spontaneous hair loss. Many cats are “closet lickers;” owners will not see this behavior because it occurs when the owner is out of the house or when the cat is out of sight. If there is doubt, a trichogram will usually differentiate. See Chapter 311. • Medical Testing with Physical Examination: Complete medical and behavioral histories are essential from the outset to identify all contributory factors in the hair loss. Only after all medical reasons for hair loss are explored should a purely behavioral diagnosis be made. Ideally a complete medical work up should include: cytological examination of skin scrapings (to determine the presence of parasites [Chapter 201]), fungal cultures, treatment with a parasiticide to rule out fleas or other skin parasites, an exclusion diet, an assessment for atopy and endocrinopathies, and a trial of steroids to rule out pruritis. • Hyperesthesia Syndrome: This is an uncommon but possible cause of over-grooming and should be explored. See Chapter 105. • Behavioral History: A behavioral work up is necessary once medical issues have been ruled out or treated and if hair loss and overgrooming remain. Compulsive licking in both dogs and cats have been correlated with conflict, stress, and frustration. The potential causes of conflict include anxiety, lack of appropriate stimulation, changes in contact with human family members, and social issues between cats in the home. Therefore, questions relating to the environment at the onset of the behavior and social interactions between the humans and the patient and the patient and other animals in the home are necessary. Resource allocation is important in a multicat home, can lead to anxiety and frustrations due to unmet needs and should be explored. The history should include questions related to intercat aggression, displacement activities, redirected behavior, attention seeking, and compulsive behavior.
588
Diagnostic Notes • Owner concerns about costs may limit initial testing and default to a presumptive diagnosis of psychogenic alopecia. If behavioral therapy does not result in resumption of hair growth medical testing is essential to determine the underlying cause. Obviously the reverse is also possible; medical treatment will not completely resolve the problem if a concurrent behavioral issue is present. • Some sources mention that Oriental breeds of cats (i.e., Siamese and Oriental Shorthairs) and those that are weaned early are at a greater risk for overgrooming behavior. Studies are limited and not conclusive, but these issues may be contributory in some cases.
Treatment Primary Therapeutics • Treat Underlying Medical Problems: Medical problems should always be treated first or concurrently with behavior modification. • Do Not Punish Grooming Behavior: Punishment is not an effective tool for changing overgrooming behavior. The cat is more likely to associate the punishment with the owner, resulting in fear development, owner avoidance, and eventual disruption of the cat-owner bond and increase anxiety. Overgrooming may continue but out of sight of the owner. • Specific Behavior Modification Tools: For anxiety-based disorders, counterconditioning and desensitization to the eliciting stimulus may be necessary. Counterconditioning consists of teaching the cat a new task incompatible with the undesirable behavior. This can be play behavior or even a trick for a food reward. Once the cat learns this task the eliciting stimulus is presented at a low level. This is desen-
Psychogenic Alopecia
•
•
•
•
•
sitization, and the goal is to gradually allow the cat to experience the stimulus without anxiety. Ideally, the cat should also be rewarded for showing relaxed, nongrooming behaviors with praise, play, attention, or a food reward to encourage the cat to remain calm. Offering Alternate or Competing Activities: Often for cats that overgroom, the addition of items to the food bowl, which increase the difficulty of obtaining food, and hence prolong eating behavior can be helpful. A common suggestion is to put large rocks or marbles (too large to be swallowed) in the bowl to increase the work of eating. The addition of roughage to the diet may also aid in treatment. Alternately, the cat can be provided with some of the daily ration in a food dispensing toy that is manipulated by the cat to produce food. Getting another cat, especially a kitten, can be a significant distraction that is effective 24 hours per day and is sometimes suggested. However, this strategy is recommended with caution and only after assessment of the temperament and needs of the resident cat. Adding another cat can increase rather than decrease tension depending on the individual, and therefore, is not always helpful. Social Relationships between Cats: It is essential that the resources are distributed throughout the home in such a way as to allow easy access for all cats. The typical resources in dispute are food and watering sites, litter boxes, and perching, resting, and hiding areas. It may be necessary to establish multiple core areas or bases for these items to allow all cats equal access to important resources by spreading them throughout the environment. Litter boxes, bowls, and such should not be clustered together but spread throughout the environment allowing easy access for all cats. This is especially critical when there are problems in social interactions between household cats. The ideal location would have more than one exit or entry point to prevent cats from being cornered. Counterconditioning and desensitization exercises are used to reacclimatize previously feuding cats to one another. The goal is for cats to share a space without any aggressive behaviors. Through a series of gradual reintroductions, each cat learns to associate good things (such as food or treats, petting, praise, or play) with calm and quiet behavior in the presence of the other cat. See Chapter 236. Allocation of Attention: Treatment should also try to determine if there is any reinforcement by giving attention for the grooming and withdrawing attention for the inappropriate behavior. If possible the owner should leave the room when the grooming bout occurs and only give the cat attention for calm, nongrooming behaviors. If the cat is on their lap and persistently grooming the problem areas, the owner should quietly and gently place the cat on the floor and leave. Creating a Predictable Environment and Meeting Daily Needs: In some cases, a change in family interactions can be helpful. Predictable interactions are calming for most cats, and daily events should be scheduled in a regular way. These include set feeding times, play time, and social interaction. Other activities can be encouraged, including climbing, perching, window watching and, for some cats, even videos. Keeping the toys in a basket and daily rotation of toys can stimulate alternate behaviors. Cats can be taught to play fetch or follow food trails to find hidden food sources to simulate foraging behaviors. See Chapter 233. Pharmacological Treatments: Medication should only be used in conjunction with behavioral modification and may not be needed in all cases. When anxiety is a large component of overgrooming, medication in conjunction with behavior therapy can help the cat learn new responses. Commonly used medications include selective serotonin reuptake inhibitors and tricyclic antidepressants. If medicating the cat will increase anxiety, then preconditioning the cat to accepting medication is prudent. Medication may often be necessary for 12 weeks or more before hair regrowth is noted. A good understanding of how large the areas of hair loss were initially will help monitor improvement. See Chapter 239.
Therapeutic Notes • If the overgrooming appears to occur when the owner is not present, a video tape of the behavior might be useful to identify any concurrent anxiety and determine the frequency and intensity of the problem. • Resource Allocation: This is especially important in multicat homes. It may be necessary to establish multiple core areas or bases for food, litter, and resting places to allow all cats equal access to important resources. This is especially critical if the history reveals problems in social interactions between household cats that might be contributing to anxiety and overgrooming behavior • Feliway® Spray or Diffuser: The feline facial pheromone analogue Feliway (CEVA Animal Health Inc) is a synthetic cheek pheromone of cats used to calm cats and may be useful in diminishing anxiety. The pheromone analog reproduces the familiarization properties normally produced by a cat when it deposits its own facial pheromones in the environment. • Restraint Devices: The use of restraint devices to discourage grooming should be avoided. If certain lesions require it, they should be used for the shortest amount of time possible. In one study (Eckstein 2000) cats without skin lesions wore an Elizabethan collar for 12 hours, and once it was removed a 67% increase in grooming was noted in the first 12 hours post-removal with both the frequency and duration of bouts increased.
Prevention • Early diagnostics and intervention whenever excess grooming is noted may be useful. • Owners are often unaware that excessive grooming may be the sign of a dermatological disorder or an anxiety disorder and may not seek help until large areas of alopecia are present. • Because of the fastidious nature of cats, external parasites may be overlooked due to grooming, yet cause enough irritation to create grooming problems. • If treatment of the medical condition does not cause improvement, the early implementation of behavioral interventions may improve resolution.
Prognosis The prognosis is good if the problem is primarily dermatologic in origin. Treating any concurrent allergies, whether atopy or food related, results in hair regrowth in most cases. The prognosis for overgrooming due to stress, conflict, and anxiety is mixed. If the social environment cannot be changed, some cats may continue to overgroom as a coping mechanism. It is also unknown whether referred pain in certain areas contributes to over-grooming behaviors. Fur regrowth does not occur quickly; it may take 3 to 4 months for the hair coat to recover. Counseling owners on the approximate time frame for regrowth and what that will look like can improve owner expectations. Having an accurate record of what the initial hair loss looked like will also allow both the practitioner and the owner to note when fur has regrown.
Suggested Readings Beaver BV. Feline grooming behavior. 2003. In BV Beaver, ed., Feline Behavior a Guide for Veterinarians, 2nd ed., pp 311–321. Philadelphia: Elsevier Saunders. Eckstein RA, Hart BL. 2000. The organization and control of grooming in cats. Appl Anim Behav Sci. 68:131–140. Landsberg G, Hunthausen W, Ackerman L. 2003. Stereotypic and compulsive disorders In GM Landsberg, W Hunthausen, L Ackerman, eds.,
589
SECTION 2: Behavior
Handbook of Behavior Problems of the Dog and Cat, pp. 217–222. Philadelphia: Elsevier Saunders. Luescher AU. 2002. Compulsive behavior. In D Horwitz, DS Mills, S Heath, eds., BSAVA Manual of Canine and Feline Behavioural Medicine, pp. 229–236. Gloucester, UK: BSAVA. Sawyer LS, Moon-Fanelli AA, Dodman NH. 1999. Psychogenic Alopecia in cats: 11 cases (1993–1996). J Am Vet Med Assoc. 214(1):71–74.
590
Seksel K, Lindeman MJ. 1998. Use of clomipramine in the treatment of anxiety-related and obsessive-compulsive disorders in cats. Aust Vet J. 76(5):317–321. Waisglass SE, Landsberg GM, Yager JA, et al. 2006. Underlying medical conditions in cats with presumptive psychogenic alopecia. J Am Vet Med Assoc. 228(11):1705–1709.
CHAPTER 239
Behavioral Pharmaceuticals Debra F. Horwitz
Overview Psychotropic medication can be helpful in the treatment of behavioral disorders but with no U.S. Food and Drug Administration (FDA) approved drugs for cats, all drug use is off label. Physical examinations, laboratory screenings for liver and kidney function, and in some cases, electrocardiograms are indicated before or throughout therapy. Signed consent and release forms are advisable. Clients should be informed of the off-label usage and potential side effects. Ideally an owner should be home to monitor their cat for the first 1 or 2 days of treatment with a psychotropic medication. Medication should only be used in conjunction with behavioral modification. Some conditions may not be responsive to medication, especially if environmental or social situations remain unchanged and continue to create stress and anxiety. Veterinarians should always have a behavioral diagnosis prior to prescribing a psychotropic medication and should not prescribe medication without a valid client-patient relationship. Clinicians should keep in mind that as the prescribing veterinarian, you are responsible for the health of your patient and should not prescribe medication based on the recommendations of others unless they are working with a board certified veterinary behaviorist. Prior to beginning medication it is prudent not only to have a diagnosis but also an accurate understanding of the behavior or behaviors targeted for change and what change will look like. Change might be either a change in the frequency, intensity, duration, or some other characteristic of the problem response. It is unlikely that the problem will just cease. Therefore, a good understanding of what change will look like will enable the clinician to gauge the response to pharmacological intervention, when to adjust dosages, and when to withdraw medication.
Drug Groups and Specific Drugs Selective Serotonin Reuptake Inhibitors • As a class of medication, these drugs act upon the reuptake of serotonin within the synaptic cleft enhancing the serotonergic effect. Selective serotonin reuptake inhibitors (SSRIs) may take 2 to 6 weeks to reach peak effect, and, therefore, behavioral change may not be noted for some time. SSRIs must be given daily, not on an “as needed” basis, to be effective. As a class of medication, they have a relatively long half-life and will remain in the system for extended periods, perhaps weeks. Common side effects include constipation, urinary retention, anorexia, gastrointestinal signs, tremors, irritability, and lethargy. Starting at a low dose for 1 to 2 weeks and gradually increasing the dose may minimize side effects. Toxicity due to serotonin syndrome is possible when more than one antidepressant is used; therefore, a combination with a tricyclic antidepressant (TCA) or monoamine oxidase inhibitor (MAOI), such as selegiline or amitraz, is not recommended.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• Fluoxetine is a SSRI that has been widely used in humans for a variety of disorders. Fluoxetine has an extremely long half-life of its active metabolite, which in humans can be 4 to 16 days. It appears to also have a long half-life in cats. Onset of action is slow, perhaps 3 to 4 weeks. It has been used for urine spraying, compulsive disorders, anxiety, and aggression problems in cats. • Paroxetine is used in humans for social anxiety disorders, depression, and panic disorders. Compared to fluoxetine, there appears to be a shorter elimination half-life and onset of action. However, some clinicians have noted anticholinergic side effects, such as urinary retention and constipation in cats.
Monoamine Oxidase Inhibitors • MAOIs have been used sporadically in cats but not for behavior problems.
Tricyclic Antidepressants • TCAs act on serotonin as well as other neurotransmitters, such as norepinephrine. Many commonly also have antihistaminic and other receptor effects. Some types may show activity relatively quickly (within days) whereas others may take weeks to reach peak effect. Possible side effects with a TCA include tachycardia, sedation, gastrointestinal upset, mydriasis, dry mouth, antidepressant, urinary and fecal retention, decreased appetite, and depression. Caution should be exercised in patients with cardiac disease due to the potential increases in heart rate. Screening with an electrocardiogram prior to use would be prudent. TCAs also are known to lower the seizure threshold. • Clomipramine is a TCA that is more selective for serotonin and with less effect on reuptake of norepinephrine. As with all antidepressants, it must be administered daily. Several studies have shown the efficacy of clomipramine for the treatment of urine spraying in cats, some compulsive behaviors, and psychogenic alopecia. It may take 2 to 4 weeks for behavioral change to be noted. • Amitriptyline has often been used in the treatment of aggression and urine spraying in cats. Amitriptyline inhibits the reuptake of norepinephrine as well as preventing the reuptake of serotonin and has mild antihistaminic effects. Amitriptyline must be given daily to be effective and can take 2 to 4 weeks to facilitate a change in behavior. Bitter taste may make dosing especially difficult. It has been used in urine spraying, aggression, and for the treatment of idiopathic cystitis.
Anxiolytics • Buspirone is an azapirone antianxiety medication that acts as a partial serotonin agonist. It may take 2 to 4 weeks to take effect and is usually given two to three times daily. Side effects include irritability, gastrointestinal effects, and occasional paradoxical increase in anxiety. To be effective it must be given a minimum of twice daily. Buspirone has been used in urine spraying and in intercat aggression when it is most commonly given to the victim because it appears to reduce fear and increase assertive behavior.
591
SECTION 2: Behavior
Benzodiazepines • These drugs have been used for urine spraying, intercat aggression, and to control anxiety. One product, diazepam, has been linked to reports of hepatotoxic reactions and should be used with extreme caution. Cats on benzodiazepines may disinhibit, causing the aggression to increase rather than diminish. Generally, this is not the first drug of choice due to its potential toxic reactions and disinhibition. Other benzodiazepines, such as oxazepam and alprazolam, have been used on a limited basis in cats and should be used cautiously. Mirtazapine is often used as an appetite stimulant; it does not appear to have an indication for behavior modification.
Medication Administration • Initial Dosing: Some cats appear to be particularly sensitive to medication and easily show side effects. Starting at a lower dose or using every 48 hours dosing can be beneficial for some individuals. A longer interval until response may be noted, but side effects may be lessened. Medication should be used for 1 to 3 months after control of the problem behavior is obtained. • Weaning: When the behavior appears changed and stable, attempts to withdraw medication can begin. The general recommendation is to decrease the dosage no more than 25% a week while watching for an increase in the targeted behavior. If problem behavior begins to surface, remaining at the lower dose for several weeks may allow stabilization. If the behavior does not stabilize, the higher dose should be instituted if that can be done safely and maintained for another 1 to 3 months before attempting weaning again. • Long-Term Therapy: Some cases may require long-term treatment, and the lowest possible dosage should be administered. Cats on longterm therapy should have routine blood chemistry screenings yearly or semi-yearly depending on the age and health of the animal. • Switching Medication: Some SSRIs have a long half-life; therefore, weaning and a wash out period of 3 to 5 weeks is recommended when switching from an SSRI to another drug. When switching from a TCA to an SSRI, a 1- to 3-week wash out is suggested. • Transdermal Administration: At the present time no long-term studies of transdermal administration of psychotropic medication has shown that this method is efficacious. Ciribassi and colleagues showed that although fluoxetine was absorbed through the skin in cats, the relative bioavailability was only 10% of that for the oral route of administration, but no transdermal dose has been established. Mealey and colleagues looked at the systemic absorption of amitriptyline and buspirone after oral and transdermal administration to healthy cats and found that systemic absorption of both drugs was poor when compared to the oral route of administration. Based on these studies and the lack of others, an appropriate dosage for transdermal administration of psychotropic medications has not yet been established. • Reformulated Preparations: No formal studies are available to assess the potency and absorption of psychotropic medications once they
have been reformulated into a liquid or some other distribution vehicle. For medication to be effective when given orally it must be soluble and stable in the stomach and intestines so it can absorbed appropriately into the blood stream. When a medication is altered by reformulation it is unclear if the absorption has been altered as well and, if so, to what extent. Medication failures may be due to lack of availability of the medication rather than unsuitability for the problem behavior.
Therapeutic Notes • Cytochrome P450 is an enzyme system critical in hormone synthesis, biotransformtion, and metabolism of many different types of medication. SSRIs are competitive inhibitors of many P450 enzymes, and when a patient is on another drug that is also metabolized by P450 enzymes, altered plasma levels and potential toxic side effects are possible. • Serotonin syndrome may occur when excessive quantities of medication that increase serotonin are ingested or administered, when two drugs that alter serotonin levels are administered together, or when two drugs taken together are not compatible in regard to serotonin metabolism. No diagnostic test is available. Diagnosis is made based on clinical signs and the complete history of all medications given to the cat, including herbal medicines. Signs and symptoms include mental changes, neuromuscular changes, and autonomic changes. The most serious signs are noted when an SSRI is combined with a MAOI (e.g., selegiline or amitraz), a serotonin receptor agonist (e.g., buspirone), a TCA, meperidine, tryptophan, or dextromethorphan. See Table 239-1 for a summary.
Administering Medication Giving medication to cats can be quite challenging for owners and distressing for the patients. Because many behavioral problems are chronic in nature and may need prolonged medication, preconditioning the cat to accept medication delivery seems prudent. The following program can be useful to acclimatize a cat to administration of medications.
Plan A • Determine a delectable food treat that is desired by your cat. This should be something other than its regular ration and available in small pieces. Some cats like cheese; others prefer fish flavored items. Gourmet cat foods should be considered. • Find an elevated surface on which you can place your cat for medicating, and use a towel on the surface for stability. • At a regular time every day, call your cat to you, gently lift and place it on the elevated surface, give it one to three of its treats, use a key phrase such as “Here’s your goody,” place it back on the floor, and allow it to leave.
TABLE 239 1: Summary of Pharmacologics for Behavior Key Drug
Drug Class
Dose Range
Frequency
Route
Indications
Fluoxetine Paroxetine Amitriptyline Clomipramine Diazepam Alprazolam Oxazepam Buspirone
Selective serotonin reuptake inhibitor Selective serotonin reuptake inhibitor tricyclic antidepressant tricyclic antidepressant Benzodiazepine Benzodiazepine Benzodiazepine Azapirone
0.5–1.0 mg/kg 0.25–0.5 mg/kg 0.5–1.0 mg/kg 0.25–0.5 mg/kg 0.2–0.4 mg/kg 0.125–0.25 mg/cat 0.2–1.0 mg/kg 0.5–1.0 mg/kg
q24h q24h q12–24h q24h q12–24h q12h q12–24h q12h
PO PO PO PO PO PO PO PO
Urine Urine Urine Urine Urine Urine Urine Urine
592
marking, marking, marking, marking, marking, marking, marking, marking,
compulsive, intercat aggression compulsive, intercat aggression intercat aggression intercat aggression, nompulsion intercat aggression (victim?) intercat aggression (victim?) intercat aggression (victim?) intercat aggression (victim?)
Behavioral Pharmaceuticals
• Once the cat is anticipating this ritual (usually within a few days), put the cat on the elevated surface, pick up the treat, and hand it to the cat. Try to get the cat to eat at least two pieces. Then allow them to leave. • When the cat is willing to allow this and before you give the treat, gently handle the head and mouth area then hand the cat the treats and release. • If this is going well, try to open the mouth, place a treat inside, and allow the cat to consume it. • Over time, try to place the treat inside the mouth, and the cat will swallow it.
Plan B • Another variation is to get the cat to eat three to four soft treats in a row on a regular basis. • Once the cat is willing to do that, medication is introduced into one of the treats in a small amount and fed to the cat. Each day placement of the treat is varied from first to middle to last so that the cat does not learn which piece holds the medication. • If this goes well, then slowly work up the dosage until the cat is receiving the full amount. • Always give at least one untainted food piece before the treat with the medication. • Should any unusual reaction occur, including but not limited to change in appetite or activity, contact your veterinarian immediately.
Plan C • If the cat will not consume treats, then a small amount of canned cat food can be used instead following the same plan as A or C. Once the cat is readily eating the offered portion, a minute amount of medication can be added. • Always wait at least 2 days before adding more medication. • If at any time the cat will not eat the offered food, attempt feeding the food without medication and begin again.
• Always provide a small enough portion that it will be eaten. • The medication laced food should be offered prior to the regular meal.
Selected Readings Center, SA. 1996. Fulminant hepatic failure associated with oral administration of diazepam in 11 cats. J Amer Vet Med Assoc. 209(3):618–625. Ciribassi J, Luescher A. 2003. Comparative bioavailability of fluoxetine after transdermal and oral administration to healthy cats. Amer J Vet Res. 64(8):994–998. Cooper L, Hart BL. 1992. Comparison of diazepam with progestin for effectiveness in suppression of urine spraying behavior in cats. J Am Vet Med Assoc. 200(6):797–801. Crowell-Davis SL. 2006. Combinations. In SL Crowell-Davis, T Murray, eds., Veterinary Psychopharmacology, pp. 234–240. Ames, IA: Blackwell Publishing. Hart BL. 1993. Effectiveness of buspirone on urine spraying and inappropriate urination in cats. J Am Vet Med Assoc. 203(2):254–258. Hart BL, Cliff KD, Tynes VV, et al. 2005. Control of urine marking by use of long-term treatment with fluoxetine or clomipramine in cats. J Am Vet Med Assoc. 226(3):378–382. King JN, Steffan J, Heath SE, et al. 2004. Determination of the dosage of clomipramine for the treatment of urine spraying in cats. J Am Vet Med Assoc. 335(6):881–887. Landsberg G, Wilson AL. 2005. Effects of clomipramine on cats presented for urine marking. J Am Anim Hosp Assoc. 41:3–11. Mealey KL, Peck KE, Bennett BS, et al. 2004. Systemic absorption of amitriptyline and buspirone after oral and transdermal administration to healthy cats. J Vet Intern Med. 18(1):43–46. Mills D, Simpson BS. 2002. Psychotropic agents. In D Horwitz, D Mills, S Heath, eds., BSAVA Manual of Canine and Feline Behavioural Medicine, pp. 237–247. Gloucester: BSAVA. Pryor PA, Hart BL, Cliff KD, et al. 2001. Effects of a selective serotonin re-uptake inhibitor on urine spraying behavior in cats. J Am Anim Hosp Assoc. 219:1557–1561.
593
SECTION
3 Dentistry
CHAPTER 240
Dental Examination R. B. Wiggs and B. C. Bloom
Overview Based on an extensive university study, oral and dental diseases are the most common diagnoses in felines in all age categories. Many oral and dental problems will be initially detected by the owner, but unfortunately, the disease may be well advanced prior to presentation to the clinician. The history, clinical signs, and diagnostic tests performed can aid in detection of the problems and may provide information about whether the disease is primary or secondary in nature. An appropriate oral examination, combined with a basic knowledge of oral and dental anatomy and physiology, is the basis for diagnosis and treatment of feline oral and dental diseases. This in turn becomes the key to developing an appropriate treatment plan.
Diagnosis Primary Diagnostics: • History: Signalment, including age, breed, and sex, is always the starting point. However, a complete history should provide vaccination status, diet, professional and home dental care, present and past disease problems and treatments, previous laboratory reports and data, exposure to infectious diseases, traumatic incidents, known allergies, eating or behavioral changes, information concerning chew toys, any sign of pain or discomfort (such as bruxing or chattering of teeth), crepitus during jaw movement, environment, and familial history. • Physical Examination: The general physical examination should never be overlooked in an impulse to examine obvious and interesting oral or dental problems. Methodically evaluate the body as a whole. • Initial Oral Survey: The initial oral survey is generally performed following physical examination but normally without the aid of sedation or anesthesia, depending on patient compliance. A systematic approach should be developed to evaluate head type and symmetry, nasal status, oral or facial swellings, draining tracts, occlusion, lips and commissures of the mouth, gingiva and mucous membranes, lymph nodes and salivary glands, jaw or temporomandibular joint (TMJ) movement, palate, tongue, and teeth. • Preanesthetic Diagnostic Tests: Tests are performed, not only to reduce the risk of pathological physiological complications during or following anesthetic induction, but also to provide insight into the overall health of the patient. The minimum database for most individuals consists of complete blood count (CBC), blood urea nitrogen (BUN), creatinine, alanine aminotransferase (ALT), and blood glucose. However, additional testing may be indicated by a patient’s history, physical examination, or initial oral survey. • In-Depth Oral Examination: An appropriate in-depth oral examination requires sedation, preferably using general anesthesia. All information discussed within the initial oral survey that could not be adequately observed should be obtained at this time. The primary tools for the oral examination are visual assessment, palpation, and
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
probing. The sulcus depth around each tooth should also be probed to evaluate the periodontium. Any sulcus depth greater than 0.5 mm is abnormal and warrants additional diagnostics. Discolored teeth and those injured by attrition or fracture require examining the surface with the sharp explorer tip to see if the pulp canal is open and to check for mobility. Transillumination, as an indication of vitality, and radiographs, to observe for internal and external changes in the tooth structure, are indicated. Mouth gags, lip retractors, magnification, and proper lighting are often necessary for thorough oral evaluation. • Oral Diagnostic Tests: Selection of diagnostic tests is directed by data collected in the above steps. Oral and intraoral radiographs (see Chapter 245), transillumination, cytology, and biopsy with histopathology are the most practical and most useful diagnostic tools currently available in feline dental medicine. Auscultation of suspect TMJ dysplasia may provide incriminating information, but magnetic resonance imaging (MRI) studies are more revealing. Thermal tooth tests, electronic vitality testers, Dopplers, and pulsed oximeters can be used on teeth for vitality determination but are generally not very reliable. Sulcal tests with crevicular thermal devices and testing of the gingival crevicular fluid (GCF), for elevated ALT, aspartate transaminase (AST), and elastase levels, can provide additional confirmation to the presence of periodontal disease, but less expensive probing and indices can be just as rewarding. Cultures of periodontal and dental discharges have generally provided poor correlation to clinical antibiotic response due to the complex nature of the oral biofilm. • Oral and Dental Charting: This is an integral part of diagnosis, treatment planning and monitoring, and the patient’s permanent health record. Any oral or dental abnormalities should be recorded on a dental chart. The charting process can be made simpler by using abbreviations from the indices described in this chapter. Additional charting abbreviations for common feline oral and dental pathology are listed in Chapter 241.
Secondary Diagnostics • Periodontal Pocketing Index (PPI or PP): The depth of the pocket is recorded in millimeters. For example, pocket depth of 5 mm would be denoted as PP5, and an 8-mm deep pocket as PP8. • Root Exposure (RE): This is recorded in millimeters and indicates the length of root exposed from the gingival margin to the cementoenamel junction (CEJ). RE and PP combined suggest the total amount of attachment loss and help determine and the periodontal disease index (PDI). • Plaque Index (PI): Plaque buildup is rated using: 0 = no plaque; 1 = thin film along gingival margin; 2 = moderate accumulation, plaque in sulcus; and 3 = abundant soft material in the sulcus. • Calculus Index (CI): Calculus buildup is rated using: 0 = no calculus; 1 = supragingival calculus extending only slightly below the free gingival margin; 2 = moderate amount of supragingival and subgingival calculus or subgingival calculus only; and 3 = abundance of supragingival or subgingival calculus. • Gingival Index (GI): The condition of the gingiva is rated using: 0 = normal gingiva; 1 = mild inflammation, slight change in color, slight edema, no bleeding on probing; 2 = moderate inflammation, redness, edema, bleeding on probing; and 3 = severe inflammation.
597
SECTION 3: Dentistry
• Sulcus Bleeding Index (SBI). The condition of each sulcus is rated using: 0 = healthy appearance, no bleeding on sulcus probing; 1 = slight bleeding from sulcus on probing; 2 = moderate bleeding on probing; and 3 = abundant bleeding on probing or spontaneous bleeding. • Periodontal Disease Index (PDI): The overall degree of periodontal disease is rated using: Stage 0 = normal tissues and no attachment loss; Stage 1 = no attachment loss, only gingivitis; Stage 2 = up to 25% attachment loss; Stage 3 = 25% to 50% attachment loss; and Stage 4 = greater than 50% attachment loss.
598
Suggested Readings Lobprise HB, Wiggs RB. 1999. Oral radiology, In HB Lobprise, RB Wiggs, eds., The Veterinary Companion to Common Dental Procedures, pp. 58–72. Denver: AAHA Press. Wiggs RB, Lobprise HB. 1997. Dental and oral radiology. In RB Wiggs, HB Lobprise, eds., Veterinary Dentistry, Principles and Practice, pp. 36–51. Philadelphia: Lippincott-Raven.
CHAPTER 241
Dental Prophylaxis R. B. Wiggs, S. L. Ruth, and B. C. Bloom
Overview Periodontal disease is the most common infectious disease in man and animals. It ranges from simple subclinical stages of gingivitis to more advanced and progressive forms of periodontal disease. Periodontal disease occurs in cyclic intervals of active destruction, or periodontitis, and inactive dormancy. Together they cause progressive attachment loss of periodontal tissues surrounding the tooth. Periodontitis, the active state of disease of the periodontium, occurs in many forms and is driven by many different causes, each developing and inducing attachment loss at variable rates according to host and other factors. Periodontitis normally develops from gingivitis but not in all cases. Studies suggest that over 70% of cats at 2 years of age exhibit positive signs of periodontal disease. Other studies have dramatically indicated that dental and oral diseases are the most commonly diagnosed disease processes in cats in all age categories. Furthermore, research has shown a close relationship between oral infections and disease of other body organs, such as the kidneys, liver, lungs, and heart.
Etiology Bacteria in the oral cavity mix with salivary proteins and adhere to the surface of the tooth. The bacteria and bacterial by-products then act as a biofilm that initiates both local and systemic host reactions. Bacteria can directly affect the attachment of the tooth by activating collagenase enzymes within the gingival tissues. In addition, the biofilm has strong antigens that stimulate the host’s immune response. As the intraoral bacteria flora shifts from a Gram-positive, aerobic, nonmotile cocci to a more Gram-negative, anaerobic, motile rods population, both endogenous and exogenous by-products and toxic metabolites progressively weaken the integrity of the gingival epithelium and deeper tissues of the periodontium, which can eventually result in tooth loss.
Clinical Signs Clinical signs vary greatly with the type and stage of periodontal disease. However, all of the following may be associated with some form of gingivitis or periodontitis: • • • • • • • • • • •
Edema and inflammation of gums (gingivitis) Plaque and calculus deposition Debris accumulation around teeth Purulent exudates from the sulcus Halitosis Ulcerations Gums that bleed easily when probed Change in architecture of gingival papillae Loss of gingival stippling Loss of bone around teeth Gingival recession
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• • • • • • • •
Gingival growths or hyperplasia Pocket formation around teeth Root exposure Furcation exposure Tooth mobility Tooth migration or new diastema formations Tooth extrusion Tooth loss
Diagnosis Primary Diagnostics • Examination and Radiographs: Most uncomplicated forms of periodontal disease are diagnosed by visual, tactile, and radiographic assessment. • Probing: The normal sulcus depth in the cat, which can be quickly measured with a periodontal probe, is typically no more than 0.5 mm. Depths greater than this typically denote attachment loss and the presence of disease. • Other Abnormalities: Root exposure, furcation exposure, discolored or injured teeth, tooth mobility, missing teeth, diseased teeth, gingivitis, calculus and plaque accumulations, and other pathology should be properly charted. A final periodontal index can then be assigned and treated accordingly.
Secondary Diagnostics • Periodontal Indices: The indices commonly used in periodontal disease are listed here. See Chapter 240. They are typically rated 0 (normal) to 3 (severe) and used to assign an overall periodontal disease index. See Table 241-1. • Plaque index (PI) • Calculus index (CI) • Gingival index (GI) • Sulcus bleeding index (SBI) • Periodontal pocket depth (PP) • Root exposure length (RE) • Degree of furcation exposure (FE) Note: Periodontal pocket depth and root exposure length are recorded in millimeters. For example, a 5-mmm deep pocket would be denoted as PP5 or a 3-mm root exposure as RE3.
TABLE 241-1: Periodontal Disease Index Stage Stage Stage Stage Stage
0 1 2 3 4
Normal tissues and no attachment loss No attachment loss, only gingivitis Up to 25% attachment loss 25–50% attachment loss Greater than 50% attachment loss
599
SECTION 3: Dentistry
TABLE 241-2: Treatment and Prognosis of the Stages of Periodontal Disease Stage
Treatment
Treatment Recheck
Reevaluation
1
Clean teeth Polish teeth with fine grit prophy paste Possible radiographs for future baseline data Possible application of fluoride Possible application of wax barrier sealant Dental charting Possible home care Prognosis: Very Good
N/A
9–12 months
2
Same as Stage 1 plus Radiographs Possible root planing Possible subgingival curettage Possible use of TAA Possible gingival surgery (grafts or ENAP) Possible antibiotics or pain meds Home care Prognosis: Good to Fair
2–3 weeks
6–9 months
3
Same as Stage 2 plus Possible osseous surgery (GTR or ARA) Possible extractions (ARA) Prognosis: Guarded
2–3 weeks
3–6 months
4
Same as Stage 3 plus Possible extractions (ARA) Prognosis: Poor
2–3 weeks
2–4 months
ARA, alveolar ridge augmentation; ENAP, excisional new appositional procedure; GTR, guided tissue regeneration; TAA, topically applied antibiotic or anti-inflammatory.
Treatment Primary Therapeutics • Grouping: Treatments are generally best grouped, rechecked, and reevaluated for retreatment according to the stage and type of periodontal disease encountered. Use Table 241-2 as a general guide. • Home Care: Home care must be customized to the individual patient. Both owner and patient compliance will partially dictate the home care prescribed. There is a large selection of dental home care products available including oral solutions, gels, toothpastes, sealants, diets, and water additives. The greater the severity of the disease or predisposition to progression of periodontal disease, the more dental home care therapies should be considered.
Therapeutic Notes • Intraoral bacterial cultures and susceptibilities have been relatively unsuccessful in guiding effective antibiotic selection. Therefore, antibiotic selection must usually be based on known success at the various stages of periodontal disease. Historically, clindamycin and amoxicillin-clavulanic acid have been most effective.
Charting Knowing correct dental formulas of both deciduous and permanent teeth as well as eruption times are essential for recognizing abnormalities such as missing teeth, supernumerary (extra) teeth, and even retained deciduous teeth, which should be extracted if the corresponding permanent tooth has erupted. Identifying the tooth type is necessary for good charting. They are abbreviated as follows: I, Incisor; C, Canine; P, Premolar; M, Molar. The feline dental formulas are as follows:
600
• Deciduous: I = 3/3; C = 1/1; P = 3/2; Total = 26 teeth • Permanent: I = 3/3; C = 1/1; P = 3/2; M = 1/1; Total = 30 teeth The Triadan tooth numbering system uses three-digit numbers without commas. See Figure 241-1. The first numeral designates the quadrant location and whether a tooth is primary or secondary. The number sequence is upper right, upper left, lower left, and lower right. The adult dentition utilizes numbers 1 to 4 and primary dentition (deciduous teeth) uses numbers 5 to 8. In each quadrant the first incisor is always 1, with incisors numbered 1 to 3, cuspids (canines) numbered 4, premolars numbered 5 to 8 (except when not present) and molars numbered 9 to 11 (except when not present). This numbering is based on a fully phenotypic dentition of (I 3/3, C 1/1, P 4/4, M 3/3) × 2 = 44, as in swine. The cat’s reduced dentition numbering is appropriately altered. upper right 1/5 | upper left 2/6 ______________|_______________ lower right 4/8 | lower left 3/7 Examples: 101 204 308 409 604 807
= = = = = =
permanent maxillary right first or central incisor permanent maxillary left canine or cuspid permanent mandibular left fourth premolar permanent mandibular right first molar deciduous maxillary left canine or cuspid deciduous mandibular right third premolar
Some common charting abbreviations are listed in Table 241-3. An excellent resource for charting is www.avdc.org/dental-charts. pdf.
Dental Prophylaxis
TABLE 241-3: Some Common Abbreviations Used in Charting
Figure 241-1 The Triadan tooth numbering system uses three-digit numbers without commas. The first numeral designates the quadrant location and whether a tooth is primary or secondary. The number sequence is upper right, upper left, lower left, and lower right.
Prognosis Prognosis varies greatly with the stage and type of disease, level of professional treatment, and compliance with home care. The prognosis for each stage of periodontal disease is found in Table 241-2.
0 (circle or zero)
missing tooth
ARM AT BAB BE BI CA CI CU CWD ED EP FE FX GH GI GP GVP: Index M LPS LX NV OM ONF OP PDI PE PI PP PRO PU R RAD RC RD RE RL ROT RPC RPO RRT RTR SBI SRP TAA TLUX TA VT X
alveolar ridge maintenance attrition bulbous alveolar bone biopsy Excisional biopsy Incisional cavity calculus index contact ulcer crowding of teeth enamel defect epulis furcation exposure tooth fracture gingival hyperplasia gingivitis index gingivoplasty gingivoplasty mobility lymphocytic plasmacytic stomatitis laceration nonvital tooth oral mass oronasal fistula odontoplasty periodontal disease index pulp exposure plaque index periodontal pocket professional prophylaxis pulpitis restoration radiograph root canal retained deciduous root exposure resorptive lesion rotated tooth root planed closed root planed open retained root tip retained tooth root sulcus bleeding index scale root plane polish topically applied antibiotic or anti-inflammatory tooth luxated tooth avulsed vital tooth extracted tooth
Suggested Readings Lobprise HB, Wiggs RB. 1999. Oral radiology. In HB Lobprise, RB Wiggs, eds., The Veterinary Companion to Common Dental Procedures, pp. 18–26. Denver: AAHA Press. Wiggs RB, Lobprise HB. 1997. Dental and oral radiology. In RB Wiggs, HB Lobprise, eds., Veterinary Dentistry, Principles and Practice, pp. 38–46. Philadelphia: Lippincott-Raven, 1997.
601
CHAPTER 242
Endodontics and Restorations R. B. Wiggs, S. L. Ruth, and B. C. Bloom
Overview Teeth with disease or injury compromising the health and vitality of the pulpal tissue often require endodontic treatment. Endodontic treatment helps stabilize the internal portion of the tooth to maintain the integrity of the external structure of the tooth and its surrounding periodontium. The periodontium, in turn, works to hold the teeth stable within the alveolus or tooth socket. The internal structure of the tooth is the pulp, which is encased within the pulp cavity. The pulp itself is a soft-tissue mass containing many specialized cells, such as odontoblasts, fibroblasts, and fibrocytes, as well as connective, vascular, lymphatic, and nervous tissues. The pulp exits the tooth through the apical delta located at the apex, or tip of the root, and connects to the periodontium. The pulp maintains the vitality of the tooth. Once the pulp dies, the tooth is considered non-vital even if it is still normally seated within its socket. The dead pulp tissue becomes the host to infections that typically manifest at the apex of the tooth and surrounding tissues. The degradation materials percolating from the apex also stimulate an immune response that results in gradual loss of tooth attachment, which can be detected radiographically as a radiolucency around the apex of the tooth. Over time the dead pulp can become a source for chronic bacteremia that may result in damage to numerous organs within the cat’s body; therefore, once a tooth becomes non-vital it must be properly addressed by either extraction or endodontic treatment. Not all tooth injuries, however, necessitate extraction or endodontic treatment. Tooth injuries vary greatly in the degree of severity, and staging them accordingly helps determine appropriate treatment options. For example, a Stage 1 injury results in loss of some of the tooth enamel only. A Stage 2 injury penetrates into the underlying dentin. A Stage 3 injury acutely exposes the pulp, but the pulp is still vital. A Stage 4 injury occurs with exposure and death of the pulp, yielding the diagnosis of non-vital. Other injuries can be of such a magnitude that the tooth is simply considered non-salvageable; in such cases extraction is typically the only treatment option. The etiology of tooth injury is widespread. Possible etiologies include trauma, underlying disease of the tooth itself such as with feline dental resorption (i.e., TR, tooth resorption), malformation of the tooth, or conditions resulting in undermineralization of the tooth predisposing it to discoloration, decay, fractures, or attritional wear. Clinical signs vary greatly, but generally, injury to the tooth results in a lost portion of the crown of the tooth and possibly exposure of the pulp cavity. See Figure 242-1. If the pulp cavity is exposed, the appearance will vary according to the state of the pulp vitality from bleeding, to red, pink, black, or an open hole into the tooth. If the pulp has been exposed, facial swelling and a facial or intraoral draining fistulous tract may be seen. Occasionally, nonvital teeth will be found with intact crowns, and the only indication of pathology is tooth discoloration. This discoloration may be pink, blue, gray, or beige, according to stage of pulp death and decay. Regardless, these are still nonvital teeth that require endodontic treatment or extraction. Even though tooth injuries and pulpal death can be quite uncomfortable, most felines do not show dramatic signs of pain. However, in some cases, the owner will notice a change in eating habits, salivation, or behavior.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
602
Figure 242-1 A Class 6, Stage 4 fractured maxillary canine tooth is being examined for a standard root canal procedure and restoration. A pathfinder is used to determine root canal depth.
Differential diagnoses for endodontic dental disease of include periodontal abscess, trauma, salivary disease, ophthalmic disease, and neoplasia.
Diagnosis Primary Diagnostics • Explorer Probe: The explorer probe can be used to gently search for an opening into the pulp cavity. The use of a Pathfinder™ (Kerr Co., Romulus, MI, 48174) or a small endodontic file may be used to gain access into smaller openings. • Transillumination: A concentrated light source can be shone through a tooth to evaluate the degree of light passing from one side of the tooth to the other side. A vital tooth allows greater passage of light, or transillumination, than a nonvital tooth. A comparison can be made to other teeth in the mouth of a similar type known to be vital. • Radiographs: Radiographs can show changes within the canal and around the tooth to indicate disease. The presence of radiolucency around the tooth apex typically indicates the loss of tooth vitality as well as apical support structures that have been resorbed. If an injury has been of a longer duration, a comparison of the size of the pulp chamber to the same tooth on the opposite side of the mouth can sometimes indicate tooth death. Vital teeth have narrower canals due to the continuous deposition of new layers of dentin within the canal.
Endodontics and Restorations
Therefore, if a notable difference can be seen between two teeth of the same type, the one with the larger canal has a greater chance of being non-vital. Note: some cats with endodontically compromised teeth (fracture with open canal) may show extensive resorption of the root apex, making endodontic therapy less likely to be successful. • Biopsy and Histopathology: In cases in which tissue swelling is obvious yet no sign of tooth injury is present, the death of the tooth may be from neoplastic disease, which disrupts the tooth’s blood supply and results in non-vitality. In suspect cases, a biopsy should be taken. However, many times these growths may be deep to the apex of the tooth, which can result in samples that fail to capture an appropriate tissue specimen and, thus, yield a false histopathology report. In cases where other treatment does not resolve the swelling, additional radiographs, blood work, and biopsies would be advisable.
Secondary Diagnostics • Other Diagnostic Tools: A Doppler or a pulse oximeter, can also be used to help determine tooth vitality, but they are highly unreliable in the cat due to the small size of the teeth and their close proximity to the gingival tissues. False-positives of vitality are common.
Diagnostic Notes • Determine if the tooth is vital or non-vital, then stage the degree of injury to the tooth based on the previously described examination process.
Treatment Primary Therapeutics • Medical: If swelling or indications of pain are present, initiation of antibiotics, pain management, and possible drainage of the swelling should be considered. • Stage 1 Tooth Injury (Injury to Enamel): This can be simply addressed by smoothing the roughened or jagged enamel surface. The enamel can then be acid etched to allow penetration of a bonding agent. Two to three layers of an enamel bonding agent, or sealant, are typically sufficient. If a dental unit and enamel bonding agents are not available, the roughened enamel can sometimes be smoothed using a diamond emery board. The smoothed surface can then be coated with fluoride to aid in sealing and strengthening the injured structure. Either avoid fluoride or use it cautiously in patients with renal insufficiency. Generally, a soft diet for 24 hours is the only recommended home care. • Stage 2 Tooth Injury (Injury into Dentin): This can be addressed somewhat similar to a Stage 1 injury. A dentinal bonding agent is required once dentin is encountered rather than the enamel bonding agent described previously. If the injury is more substantial, the application of a tooth colored composite resin may be applied and contoured to the desired shape of the defect. If a dental unit and enamel bonding agents are not available, the roughened enamel can sometimes be smoothed using a diamond emery board and treated with fluoride as previously mentioned. Generally, a soft diet for 24 hours is the only recommended home care. If the patient shows indications of discomfort, home pain management may be advisable. • Stage 3 Tooth Injury (Vital Pulp Injury): Treatment options would typically be one of the four following modalities: 1. Extraction. See Chapter 243. 2. Pulp capping and restoration: This is for cases of extremely short duration of pulp exposure in mature adult teeth in which the pulp has not sustained an injury of a magnitude that might
lead to non-vitality. Antibiotics and pain management are advisable. The procedure should be followed up with radiographs every 6 months to assure the procedure has been successful (the tooth has remained vital and healthy). If failure occurs, a standard root canal procedure or extraction is indicated. 3. Apexogenesis: This is a procedure used to keep young teeth vital so they may complete root development. If normal root formation occurs and the apex of the tooth properly closes, a decision must be made to discontinue additional treatment in hopes of the tooth remaining vital or to proceed with a standard root canal therapy to ensure maintenance of the tooth. If failure occurs and the tooth dies before normal root maturation and closure, either apexification prior to a standard root canal procedure can be attempted or extraction of the tooth will be necessary. 4. Standard Root Canal Therapy: A soft diet for 24 to 72 hours, antibiotics for 5 to 10 days, and home pain management for 1 to 3 days are recommended. • Stage 4 Tooth Injury (Nonvital Tooth): Treatment options would typically be one of the three following modalities: • Apexification: This is an option for young nonvital teeth that have not completed root formation or closure of the apex. This procedure stimulates the root apex to continue to close. Once closure is successfully obtained, a standard root canal can be performed. If failure occurs, extraction of the tooth will typically be required. • Standard root canal therapy. A soft diet for 24 to 72 hours, antibiotics for 5 to 10 days, and home pain management for 1 to 3 days are recommended. • Nonsalvageable Tooth: Extraction of the tooth is required. See Chapter 243.
Secondary Therapeutics • Antibiotics: Effective antibiotics include amoxicillin (22 mg/kg q24h PO(, amoxicillin/clavulanic acid (11 mg/kg q12h PO), and clindamycin (5.5 mg/kg q12h PO). • Postoperative Pain Management: Effective analgesics include buprenorphine (0.005–0.01 mg/kg q4–8h IV, IM, or sub-lingual), butorphanol tartrate (0.2–0.8 mg/kg q4–8h SC, IM, or IV), and fentanyl (1 ml/9 kg SC).
Therapeutic Notes • Loss of restorations is not uncommon, and owners should be advised that this may occur. If such should happen, a new restorative may be required. • Reinjury to the tooth may also occur, especially if the injury of the tooth or teeth is due to predisposing factors or behavioral habits. • Restorations near the gum line should be watched closely, because cracks or roughened margins may predispose this area to gingivitis. Timely initiation of appropriate professional and home dental care is advised. • During prophylaxis, restorations on teeth should be cleaned more gently than healthy teeth to reduce the risk of iatrogenic injury to the restoration. Extrafine prophy paste should be used to avoid scratching most restorations.
Endodontic Procedures These endodontic procedures appear relatively straight forward in theory but are far from it in terms of actual surgical execution. No two tooth injuries are exactly same, and each procedure must be customized to the individual patient and the tooth injury. Frequent repetition and regular practice of the procedures are critical to develop proficiency, minimize complications, and increase long term success with endodontic therapy.
603
SECTION 3: Dentistry
Apexogenesis (Incompletely Developed, Damaged Vital Tooth) The procedure is typically performed on exposed vital (alive) pulp tissue in immature permanent teeth (in cats less than 18–24 months of age). These immature teeth generally have poorly developed roots that commonly have an open apex, or root tip. The process of apexogenesis, when successful, maintains the tooth’s vitality and allows for the completion of the tooth’s root growth, maturity, thickening, and apical closure, which can make a future root canal procedure possible, if required. The basic steps of apexogenesis are: 1. Radiograph the tooth for full assessment of it and adjoining tissues. 2. Disinfect the oral cavity, usually with chlorhexidine solution (0.2% or less). 3. Inject local anesthesia, such as bupivicaine. 4. Smooth the fractured tooth surface with a white stone, an aluminum oxide bur, and number 1/2 or number 1 sterile round ball bur. 5. Remove 2 to 3 mm of pulp tissue with a sterile number 1/4 or number 1/2 round ball bur. • If bleeding fails to subside within 2 to 3 minutes, apply gentle pressure. If the pressure fails, apply a small amount of a hemostatic solution or powder. • If bleeding continues, remove an additional 1 to 2 mm of pulp and repeat hemostasis as outlined previously. • If all attempts at hemorrhage control fail, the pulp most likely has already sustained a nonreversible pulpitis and is in the process of dying. If this is the case, then apexification or extraction may be required. 6. Pending hemorrhage is controlled, direct pulp capping can be completed by applying either 1 mm of calcium hydroxide USP powder or mineral trioxide aggregrate (MTA) directly to the pulp. 7. Protect the pulp capping material and restore the tooth surface by applying a layer of glass ionomer such as Microspand™ Ionosit®. The restoration should be finished to conform with the immediate tooth structure. Overbuilding of the restoration only results in structures that are easily redamaged. 8. The final restoration should be acid etched and two to three coats of an unfilled resin applied to fill any defects and to help seal the margins of the restoration. • A radiograph of the tooth and its final restoration should then be taken for evaluation and future reference. See Figure 242-2. The tooth should re-examined and radiographed every 1 to 6 months according to the reason of the initial apexogenesis procedure.
Figure 242-2 A completed apexogenesis is shown in this postoperative radiograph.
Apexification (Incompletely Developed, Damaged Nonvital Tooth) This procedure is typically used for immature permanent teeth that are non-vital or have irreversible pulpitis (with an immature and incompletely developed apical root structures. The process, when successful, allows for the development of the tooth’s root structure and closure of the apex so that a standard root canal procedure can be performed to maintain the tooth and some degree of its original function. The basic procedure is to remove the nonvital debris from the pulp cavity and to replace it with materials that will stimulate the eventual closure of the tooth’s root with solid tissues. 1. Follow the first two steps for apexogenesis. 2. If the pulp canal is not exposed, make an access into the canal with a round ball bur. 3. Remove the debris from within the canal by gentle instrumentation with barbed broaches and either endodontic files or reamers and aggressive flushing with sterile saline or oral chlorhexidine solutions (0.2% or less). Avoid using bleach (sodium hypochlorite) solutions for flushing because extrusion of these solutions through an open apex
604
Figure 242-3 apexification.
This radiograph shows complete filling of the pulp cavity by
can result in intense pain, inflammation, and loss of the periapical tissues and the tooth itself. 4. Once the pulp cavity is clean, dry it with sterile paper points. 5. Fill the pulp cavity with a medicament powder or paste that will help stimulate root closure. Calcium hydroxide, the gold standard, is often mixed with a radiopaque agent such as barium to form a paste. The radiopaque agent allows for better radiographic analysis of the fill and provides confirmation of the presence or dissipation of the agents upon follow up examinations. See Figure 242-3. Once the material
Endodontics and Restorations
dissipates it will need replenishing (usually every 4–8 weeks) until the tooth root closes. The calcium hydroxide paste can be purchased in ready-to-use premixed injectable syringes. 6. Perform a surface restoration and sealant as previously described. 7. After the root apex closes, a standard endodontic root canal can be performed to help maintain the tooth long term.
Pulp Capping (Completely Developed Damaged Vital Tooth) The pulp capping procedure is identical to that for apexogenesis except it is performed on mature teeth as opposed to incompletely developed or immature teeth.
Root Canal Therapy (Completely Developed Damaged Nonvital Tooth) The standard root canal procedure is typically used to persevere and maintain endodontically compromised mature teeth with limited structural damage. 1. 2. 3. 4. 5.
6. 7.
8.
9.
Radiograph the tooth and adjacent tissues for full assessment. Disinfect the site with oral chlorhexidine solution (0.2% or less). Inject local anesthesia. Access the pulp cavity. This can usually be done via the fracture site in cats. Use a pathfinder to locate the pulp chamber and determine the full depth of the root canal (known as the working length). See Figure 242-1. Radiograph the tooth with the pathfinder at full depth to confirm proper working length of the root canal. If pulp tissue is still present, attempt to remove it by inserting a barbed broach into the canal, rotating the broach 180 to 360 degrees, and then withdrawing the broach from the canal. Repeat as necessary. Select endodontic reamers or files for use in instrumenting the canal. A complete set of K-Reamers of 31-mm length are a good selection for most feline root canals. The reamers can be used in either an upand-down movement or a rotary motion. Start with the smallest file and progress to the next larger size until the dentinal wall shavings are clean. Typically the canine teeth of most cats should be only opened to between a size 40 to 50 K-reamer. Excessive sizes can result in a weakening of the coronal portion of the tooth and increase the risk of fracture and loss of crown structure. The maximum size file that still reaches the working length is called the master file. Flush the canal each time the reamer is increased to a larger size and again following the master file using half strength bleach (avoid if an open apex is suspected) followed by sterile saline.
10. Radiograph the tooth to confirm the master file at working length. 11. Dry the canal with sterile paper points. 12. Select an apical sealer cement and coat the inside of the canal making sure there is an adequate covering of cement at the apex. There are numerous sealer cements available, so it is imperative to mix and apply the selected product specifically according to that manufacturer ’s recommendations. 13. Obturation or filling of the root canal section of the pulp cavity is then performed with gutta percha or some other obturating material. Gutta percha and other obturating materials, as with the sealer cements, come in a wide variety of shapes, textures, and working temperatures. Regardless of the product, the obturating material should thoroughly fill the root canal portion of the pulp cavity without any significant defects or voids in the material, especially at the apex. 14. Radiograph to confirm an adequate canal filling prior to applying an intermediate layer and surface restoration. 15. Once the root canal is filled an intermediate layer, usually a glass ionomer or zinc phosphate cement is placed between the root canal obturation materials and the restoration of the crown. The intermediate layer helps to seal off the filling and help protect against microleakage should the surface restoration become lost or damaged. 16. Clean the crown of the tooth and apply acid etch for 30 to 40 seconds. Rinse and gently air dry until the tooth surface appears chalky. 17. Apply one to three layers of a dentinal bonding agent and light cure the product according to manufacturer ’s instructions. 18. Select a shade of restoration composite material that closely matches the crown of the tooth. Once hardened, this can be shaped and smoothed with a white stone or polishing disk. 19. The final finished composite is then coated with one to three layers of a clear unfilled composite resin that fills in not only any minor pits or scratches on the restoration but also along the margin of the restoration to help decrease marginal leakage. 20. Final radiographs should be taken for future reference and comparison. Additional radiographs should be taken in 9- to 12-month intervals or as needed to evaluate the success or failure of the endodontic procedure. Root canals, when properly performed in appropriate candidates, have a very high rate of success (often >90%).
Suggested Readings Holmstrom SE, Fitch PF, Eisner ER. 2004. Veterinary Dental Techniques for the Small Animal Practitioner. Philadelphia: Saunders. Lobprise HB, Wiggs RB, eds. 1999. The Veterinary Companion to Common Dental Procedures. Denver: AAHA Press. Wiggs RB, Lobprise HB, eds. 1997. Veterinary Dentistry, Principles and Practice. Philadelphia: Lippincott-Raven.
605
CHAPTER 243
Extractions R. B. Wiggs, B. C. Bloom, and S. L. Ruth
Overview The most commonly performed procedure of oral surgery is tooth extraction, or exodontia, which involves not only removal of the tooth itself but also maintenance of the alveolar integrity following tooth loss. Normally the main objective in dentistry is to preserve teeth, but in many cases extraction is the treatment of choice due to the type or extent of disease. Diseased teeth can be a source of infection that poses danger to other organs of the body via bacteremia. Therefore, diseased or injured teeth should always be appropriately addressed. Over the first 3 to 18 months following extraction, the alveolar ridge of bone in the jaw can suffer dramatic atrophy. This atrophy can result in a great predisposition to jaw fractures. For this reason alveolar ridge maintenance (ARM) is best implemented at the time of extraction by placement of bone matrix implant materials in all major extraction sites. Teeth are most commonly extracted due to severe mobility or injury. In most cases, mobility results from attachment loss due to periodontal disease. Automobile trauma, overzealous activities with toys, injury during play, and other traumatic incidents frequently injure teeth beyond repair. Some congenital and developmental abnormalities, such as retained deciduous teeth, malocclusions, impacted teeth, advanced resorptive lesions, and oral tumors, may also require extraction. The most common clinical signs of dental disease include facial swelling, fistulous draining tracts, gingival or mucosal swelling, jaw fractures, malocclusions, and grossly injured, mobile, or diseased teeth.
Treatment Primary Therapeutics • Medical: Preoperative antibiotics and analgesics are suggested, especially if swelling or other indications of infection and pain are present. • Anesthesia: Appropriate anesthetic protocols include adequate analgesics and consideration of any concurrent medical conditions. Local anesthesia blocks are recommended for all extractions regardless of etiology. See Chapter 246. • Dental Exodontia (Extraction) Procedure
Overview Adequate accessibility and visibility, proper instrumentation, and basic knowledge of oral and dental anatomy are essential requirements for successful extraction procedures. It is advisable to extract only single rooted teeth, so multirooted teeth are best extracted after being resected into individual root segments. In the domestic feline, the only threerooted teeth are the upper fourth premolars; all other premolars and molars are two rooted, except for the upper second premolars and first molars, which have single roots similar to the incisors and cuspids. The following systematic approach to extractions usually provides the most favorable results.
Extraction Procedure Diagnosis Primary Diagnostics • Complete Oral and Dental Examination: Proper procedure is described in Chapter 240. • Intraoral Radiographs: These are imperative prior to extractions to determine the extent of disease or injury, the status of the tooth itself, and the condition of surrounding structures. See Chapter 245. • Oral Tissue Biopsy with Histopathology: This is indicated when tissue swelling is obvious but no sign of tooth disease or injury is present. However, in many cases oral masses may be deep to the root of the tooth, which can result in a biopsy that fails to capture an appropriate sample of disease. This in turn results in a false-negative histopathology report.
Secondary Diagnostics • Tooth Testing: Other diagnostic tools, such as a Doppler or a pulse oximeter, can also be used to determine tooth vitality. However, they are not highly reliable in the cat due to the relatively small size of the teeth and their close proximity to the gingival tissues, which can give false-positive indications of vitality.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
606
• Disinfect the oral cavity with a properly diluted oral chlorhexidine solution (0.2% or less). • Take preoperative radiographs. • Administer a local anesthesia block. • Sever the epithelial attachment at the base of the sulcus using a small scalpel blade (number 11 or number 15c), root pick, or the tip of a sharp elevator. • Lift the gingival tissue away from the tooth with a periosteal elevator, such as a number 2 Molt, for furcation exposure (if multirooted) and preservation of the gingival tissue. • Resect any multirooted teeth from the furcation through the tip of the crown; 699L burs on high speed handpieces work best in felines. Fragile, sharp spikes of the crown may be cut 3 to 4 mm above the gumline to reduce the risk of intraoperative tooth fractures. • Sever the periodontal ligament at the epithelial attachment at the bottom of the sulcus if this was not already performed by placing a winged elevator (sizes 1, 2, and 3 are most commonly used in feline extractions) between the tooth and alveolar socket and working circumferentially around the tooth. The elevator should be held firmly in the palm of the hand with the index finger kept as close to the elevator tip as possible while cradling the jaw with the opposite hand to help control the tip and reduce the risk of instrument slippage and penetration of unwanted deeper structures. Excess force should not be necessary when correct technique is used. Elevators should be properly maintained and sharpened regularly. Dull elevators only increase operator fatigue, length of procedure, and risk of complications. • Once the tooth or tooth segment loosens in the socket, small extraction forceps can be used to gently grasp the tooth and remove it. Extraction forceps should never be used forcefully in attempts at
Extractions
•
• •
•
•
tooth removal. Excessive force with extraction forceps often leads to complications such as or tooth or alveolar bone fractures, retained root segments, jaw fractures, and oronasal fistulas. Once the tooth is completely removed the empty socket should be curetted clean. Any loose bone spicules should be removed, and roughened alveolar bone should be smoothed with a bone file or high speed bur. Postextraction radiographs should be taken to confirm complete extraction of the tooth. Pack the alveolar socket(s) with an osteopromotive bone matrix implant material, such as Consil® (Nutramax Laboratories, Inc., Edgewood, MD). This ARM procedure will greatly reduce alveolar atrophy and the risk of future idiopathic jaw fractures. Close the gingiva over the extraction site using 4-0 or 5-0 absorbable suture material with a small cutting needle. The flap should have as little tension as possible on the suture line. This typically requires severing of the periosteum from the base of the flap tissue to allow it to travel enough to cover the socket. Apply three to five coats of Tincture of Myrrh and Benzoin, gently air drying each coat prior to placement of the next. This tincture is a periodontal dressing that acts as a flexible bandage during healing.
Crown Amputation Crown amputation, placement of a small amount of bone matrix material, and closing a flap over the “extraction” site should only be considered with extremely fragile teeth, such as those with resorptive lesions (tooth resorption) that may have external or internal root resorption, or ankylosed teeth in which the periodontal ligament is no longer detectable or functional and bone is growing into the tooth. However, every attempt should be made to properly and completely extract teeth with radiographically visible periodontal ligaments. Leaving diseased tissue or tooth structures may result in continued dental problems. Excessive extraction forces and pulverization of root structure with burs should be discouraged because facial pain syndromes may result.
• Postoperative Antibiotics: Effective antibiotics include amoxicillin, 22 mg/kg q24h PO; amoxicillin/clavulanic acid, 11 mg/kg q12h PO; and clindamycin, 5.5 mg/kg q12h PO. • Postoperative Pain Management: Effective analgesics include buprenorphine, 0.005 to 0.01 mg/kg q4 to 8 h IV, IM, or sublingual, and butorphanol tartrate, 0.2 to 0.8 mg/kg q4-8 h SC, IM or, IV. • Fistula: Should an oronasal or oroantral fistula occur during extraction, the site must be flapped and sutured closed appropriately, or the fistula may become chronic. If possible, bone matrix material should be placed unless the fistula is of such size or shape that material is unstable and will migrate into the nasal canal or sinus. • Wound Dehiscence: Dehiscence of the wound will occur on occasion. If this is discovered quickly, the site can be repacked and resutured. However, if notable swelling has ensued, the site will best heal as an open wound. Chronic swelling at the extraction site often indicates either misdiagnosis of the original problem or retained root structure within the site. At times, a biopsy may be necessary.
Therapeutic Notes • With more difficult extractions, removal of additional tooth support structures may ease extraction. A full-thickness mucogingival flap may be required to expose alveolar bone. Once exposed, the buccal alveolar bone plate can be removed with a bur on a high speed hand piece (number 2, 699L, 700, or 701) to the desired level.
Suggested Readings Lobprise HB, Wiggs RB. 1999. Oral radiology. In HB Lobprise, RB Wiggs, eds., The Veterinary Companion to Common Dental Procedures, pp. 68–84. Denver: AAHA Press. Wiggs RB, Lobprise HB. 1997. Dental and oral radiology. In HB Lobprise, RB Wiggs, eds., Veterinary Dentistry, Principles and Practice, pp. 69–91. Philadelphia: Lippincott-Raven.
607
CHAPTER 244
Dental Resorption R. B. Wiggs, B. C. Bloom, and S. L. Ruth
Overview Feline dental resorption (FDR) is one of the most commonly diagnosed dental diseases in domestic cats. This disease is associated with the presence of odontoclastic lesions, which is also sometimes referred to as feline oral resorptive lesions, feline odontoclastic resorptive lesions (FORL), cervical line lesions (CLL), neck lesions (NL), resorptive lesions (RL), or tooth resorption (TR). These dental resorptive lesions are most often found on the buccal surface of the teeth at or just below the gingival margin (see Figure 244-1), but they can be detected almost anywhere along the crown or root surface (see Figure 244-2) of any tooth. Initially, the lesions may not be grossly visible on a simple physical examination, but the presence of focal hyperemic, hyperplastic tissue at the gingival margin of a tooth may signal a lesion is concealed beneath. Many of the affected teeth also eventually develop root ankylosis. A proper examination requires anesthesia, probing, and radiographs for complete evaluation. A dental explorer may be gently inserted in the sulcus to palpate for irregularities on the tooth surface, which many times will elicit a twitch or other sign of discomfort even with the patient under anesthesia. It is not uncommon to find multiple lesions in various stages of development. Radiographs are essential to reveal lesions deep on the root surfaces, to evaluate the extent of demineralization, and to determine the best treatment alternatives. FDR lesions occur in approximately 30% of domestic cats. However, the exact pathogenesis and etiology remain unknown. Although these defects were originally thought to be carious, decay-type lesions, later studies have demonstrated odontoclastic involvement. It has been difficult to consistently correlate predisposing factors, such as age, breed, sex, diet, or concurrent diseases. Presenting
signs greatly vary in accordance with the lesion’s stage of development. Owners may not be aware of the lesions until they are pointed out. However, some cats exhibit signs, such as halitosis, pawing at the face, problems masticating, anorexia, ptyalism, lethargy, dysphagia, and even weight loss.
Diagnosis Primary Diagnostics • Visual Examination and Probing: Visual examination may reveal defects in the tooth. Gingival tissue may be mildly to severely inflamed, hyperemic, or even hypertrophic. As the lesions worsen, ankylosis, root resorption, internal crown resorption, or loss of the crown may occur. A simple swelling in the gingiva, with or without inflammation, where a tooth once existed may indicate possible root retention below the gumline following crown loss. • Radiographs: This is the only diagnostic tool that can provide information concerning the internal and root stages of the disease. The lesions can then be staged, typed, and categorized. See Table 244-1.
Treatment Primary Therapeutics • Staging: Although type and category should be evaluated for the most appropriate treatment plan, the stage of the lesion is the primary determinant for treatment. Early stage lesions may be saved by restorative treatments, but as the stages advance, extraction is currently the only treatment recommended. See Chapter 243 for extraction technique options.
Figure 244-1 A feline dental resorption in the maxillary third premolar is concealed by hyperemic, hyperplastic gingival tissue. Touching the lesion will elicit a pain response displayed as withdrawal or quivering of the lower jaw. Jaw quivering can often be elicited even when the cat is under anesthesia. Image courtesy of Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
608
Figure 244-2 The feline dental resorption in this tooth (arrow) occurred in the root instead at the gingival margin. Image courtesy of Dr. Gary D. Norsworthy.
Dental Resorption
TABLE 244-1: Stages, Types, and Categories of Feline Dental Resorption Lesions Stage 1 2 3 4 5
Lesion only into the enamel or cementum Lesion into the dentin Lesion into the pulp cavity Extensive structural damage Crown loss
Type 1 2
Secondary Therapeutics Primary inflammatory (LPS associated); usually in cats under 2 years of age. Secondary inflammation (Non-LPS); usually in cats over 7 years of age.
Category 1 2
retention may be the only option, but the site(s) and patient need to be monitored from that point on. If the presence of a healthy periodontal ligament is apparent radiographically, the resorption is likely not odontoclastic, and standard elevation of the entire root should be performed. • A good dental prophylaxis with a fluoride treatment of the remaining teeth is typically recommended in all stages of the disease as a part of the overall treatment of the condition. See Chapter 241.
Loss of periodontal ligament Normal PDL space
LPS, lymphocytic plasmacytic stomatitis; PDL, peridontal ligament.
TABLE 244-2: Treatment of feline dental resorptions based on the stage of the lesion Stage and Prognosis
Treatment
1. Good
Enamel bonding agents and fluoride treatment; extraction only if associated with severe LPS. Dentinal bonding agents and restoration or extraction Extraction Extraction Extraction of any crown remnants; extraction of retained roots if causing gingival irritation.
2. Fair to poor 3. Very poor 4. Unsalvageable 5. Tooth already lost
• Treatment is primarily based on the stage of the lesion. See Table 244-2. • Extractions: If the periodontal ligament is not observable radiographically, as in odontoclastic root resorption, successful elevation may be challenging. A modified extraction technique with intentional root
• Postoperative Care: If invasive procedures were performed, appropriate antibiotics, pain medications, and possibly anti-inflammatories should be prescribed for 7 to 14 days. The cat should be re-examined 2 to 3 weeks following treatment to evaluate healing and status of any restorations and again at 3- to 12-month intervals according to the degree of the problem. • Any chronic vomiting or regurgitation should also be addressed because stomach acids may exacerbate FDR. • Home Care: Dental diets, tooth brushing, oral solutions or gels, and dental water additives used alone or in combination are recommended.
Therapeutic Notes • Owners should be advised that the cause of FDR is unknown at this time, and additional lesions can usually be expected in the future. • Regular dental prophylaxis, fluoride treatments, and treatment of lesions at an early stage are advisable.
Prognosis Prognosis depends on the stage of the disease at the time of diagnosis. See Table 244-2.
Suggested Readings Lobprise HB, Wiggs RB. 1999. The Veterinary Companion to Common Dental Procedures. Denver: AAHA Press. Wiggs RB, Lobprise HB. 1997. Veterinary Dentistry, Principles and Practice. Philadelphia: Lippincott-Raven.
609
CHAPTER 245
Oral and Dental Radiography R. B. Wiggs, B. C. Bloom, and S. L. Ruth
Overview Oral and dental radiography are indispensable tools in veterinary dentistry for assisting in the diagnosis, treatment planning, and monitoring of oral disease. Intraoral dental imaging provides higher resolution of detail and improved isolation of oral and dental structures and thus, yields a more accurate assessment of pathology and potential treatment planning for problems, such as feline dental resorption, injured teeth, periodontal disease, and jaw fractures. Preoperative radiographs are essential for evaluating issues such as abnormal root or bone structures, impacted teeth, or ankylosis of roots. Intraoperative films may aid in the appropriate placement of materials or managing complications. Postoperative films attest to the success of treatment and the lack of complications such as remaining root structure or pathology. Oral and dental radiographs are also an important as well as legal part of the patient’s medical records and should be properly processed, identified, and stored for future baseline reference. Periodic full mouth dental radiographs can contribute to detecting previously undiagnosed abnormalities or pathology as well as providing a more complete baseline reference.
Image Receptors and Equipment Standard intraoral films and digital computer sensors can both be used for veterinary dental radiographs. Films or their equivalent (i.e., sensors or phosphorous plates) are commonly referred to as image receptors (IR). Each type of IR has its advantages and disadvantages. Dental films come in five different sizes (0 through 4), and their flexibility allows placement in areas where a sensor often will not fit appropriately. This size variation helps provide a good selection to fit the need of the location and type of pathology encountered. Presently, digital sensors are only available in size 1 and size 2. In addition, most sensors are non-flexible and much thicker than standard films. However, digital systems eliminate the need for film; film development systems or processors; purchasing and disposal of developing and fixing chemicals; and the need for film storage units. The actual image size, sensor thickness, and image quality varies slightly between companies but not substantially. The main difference is in the software programs, which vary greatly in ease of use, form of client presentation, printable form, and flexibility to interface with the clinic’s current software system. Most sensors are yoked to the computer by a USB wire connection, but there are some wireless sensors available. Indirect digital systems use phosphor plates that capture the image; they are processed fairly quickly into digitalize the images. These plates allows for greater plate size variation (size 0–6); they are flexible, but processing is not as rapid as direct digital. Films also come in various speeds (A through F), but only D, E, and F are currently available commercially for routine clinical dental use. A speed is the slowest of the films, and F is the fastest. Speed selection should be determined by the amount of detail and exposure time desired.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
610
Generally, Kodak® Insight™ film (F speed) will reduce exposure by at least 40% while still providing good detail.
Positioning Technique (Parallel and Bisecting Angle) Films or IRs are selected and positioned according to the area to be examined. In general, the IR should be as close to the object to be radiographed as possible to achieve reasonable dimensional accuracy. The technique used will be determined by the anatomy of the site, which limits proximity of the film to the object. There are two basic positioning techniques, parallel and bisecting angle. Parallel technique is when the IR and object, typically the tooth or root, are relatively parallel to each other, and the primary beam from the radiographic unit is perpendicular to the image receptor and object. See Figure 245-1. When appropriately performed, the image on the film should be fairly accurate both linearly and dimensionally. This accuracy normally makes the parallel technique preferred when it can be used. Bisecting angle technique is necessary when a parallel relationship cannot easily be obtained, such as when the palate or floor of the mouth interferes with a reasonably close proximity of the IR and object. The IR is placed in as close proximity as possible to the desired object. The angle formed between the tooth’s long axis and film is then bisected, and the primary beam is directed perpendicular to this bisecting line. See Figure 245-2. When properly executed, the receptor image is relatively linearly correct. However, some slight dimensional distortion of the image on the portion of the receptor the greatest distance from the tooth will occur. The precept of the bisecting angle technique is based on the geometric theory of isometric triangles. Typically, the following can be used as a guide for technique selection: • Maxillary Teeth: Bisecting angle technique • Mandibular Incisors, Canines, and Third Premolars: Bisecting angle technique • Mandibular Fourth Premolar and Molar: Parallel technique Extraoral studies may be used, both in parallel and bisecting techniques, as survey films to assess massive oral injuries, fractures, neoplasia, or temporomandibular studies. However, in dealing with specific oral structures and teeth, extraoral radiology often cannot provide sufficient detail or accuracy due to superimposition of structures or distortion, although it can be useful for the maxillary premolars.
Exposure Proper placement of the IR, combined with appropriate technique and exposure time, can provide isolation of a specific tooth with excellent detail. Exposure times are based on the location to be radiographed, speed of the film or IR, and the specifications of the individual radiographic unit being used. Check the recommendations of the film or IR and radiographic unit’s manufacturer for suggested exposure times. If no manufacturer information is available, Table 245-1 can be used with a dental radiographic unit to obtain an image, from which a technique chart can be developed.
Oral and Dental Radiography
Parallel Technique
Film or Sensor
Tooth Crown
Dental Radiographic Unit
Tooth Root
Mandible Figure 245-1 Using the parallel technique the X-ray beam strikes the tooth and the X-ray film at 90 degrees to their long axis.
TABLE 245-1: Suggested Initial Setting When Developing a Dental Technique Chart Using a Dental X-Ray Unit with Intraoral Dental Films Film Exposure
Time
D Speed (Ultraspeed™ Film) E Speed (Ultraspeed™ Film) F Speed (Ultraspeed™ Film)
0.8 seconds 0.6 seconds 0.4 seconds
TABLE 245-2: Suggested Initial Settings When Developing a Dental Technique Chart Using a Standard X-Ray unit with Intraoral Dental Films Film D Speed D Speed E Speed E Speed F Speed F Speed
Focal Film Distance (in)
mA
KVP
12 36–42 12 36–42 12 36–42
100 100 100 100 100 100
65 65 65 65 65 65
Exposure Time (sec) 1/10 to 1/15 2/5 to 3/5 1/12 to 1/20 3/10 to 5/10 1/15 to 1/30 1/5 to 2/5
Standard radiographic units can also be used with intraoral dental film and IRs. However, it will be more difficult to arrange the receptor, object, patient, focal film distance, and primary beam to obtain satisfactory images. Table 245-2 can be used and modified as needed for using standard units with intraoral dental films.
Film Development For film development, the best option is a chairside developer. Some of these are manual, and others are automatic. Most chairsides have four solution containers, which are typically the developer solution, water rinse, fixer solution, and a final water rinse. Standard and automatic radiographic development equipment, although more time consuming and complicated by having such small films in equipment designed for larger radiographs, may also be used for dental film processing.
Film Storage and Identification All dental films must be properly identified and stored as a part of the patient’s permanent record. Suggestions for identification and storage include cardboard or plastic mounts, dental envelopes, and radiographic marking pens.
611
SECTION 3: Dentistry
Bisecting Angle Technique
Dental Radiographic Unit
Maxilla Bisecting Angle Line Tooth Root
Tooth Crown
Film or Sensor
Mandible Figure 245-2 Using the bisecting angle technique the film is placed in as close proximity as possible to the desired object. The angle formed between the tooth’s long axis and film is then bisected, and the primary beam directed perpendicular to this bisecting line.
TABLE 245-3: Common Causes of Various Image Problems in Dental Radiography Image Problem
Probable Cause
Elongation, foreshortening, or overlap Magnified or fuzzy Distortions (varying object size or angulation) Cone cutting (partial images with curved exposure areas) Blurring Partial image with straight line across film Fogging Too light Too dark Clear film Multiple images Silver or gray films Yellow, brown, or green stains Finger prints
Poor bisecting angle technique Improper technique or positioning Improper technique or positioning Improper technique or positioning Movement of patient or unit during exposure Processing error Processing error, expired film, or film stored too close to processing chemicals Underexposed or underdeveloped Overexposed, overdeveloped, or light exposure prior to fixation Unexposed film or radiographic unit malfunction Double exposure Inadequate rinse of fixing solution Inadequate rinse of developing solution Chemical contamination during hand processing
612
Oral and Dental Radiography
Image Problems Image problems can be contributed to the radiographic unit settings, the positioning or technique, the film, or the film processing. Table 245-3 lists some of the most common image problems and their usual causes.
Radiation Safety Dental radiographic units are subject to registration and safety laws as determined by each state’s radiation safety regulators. Practitioners should contact the appropriate regulatory department within their state and become familiar with all appropriate regulations prior to use of such units.
Suggested Readings DeForge D, Colmery B. 2008. An Atlas of Veterinary Dental Radiology, 2nd ed. St. Louis: THEVETDENT. Dupont GA, DeBowes LJ. 2009. Atlas of Dental Radiography in Dogs and Cats. St. Louis: Saunders Elsevier. Lobprise HB, Wiggs RB. 1999. Oral radiology. In HB Lobprise, RB Wiggs, eds., The veterinary Companion to Common Dental Procedures, pp. 25–37. Denver: AAHA Press. Wiggs RB, Lobprise HB. 1997. Dental and oral radiology. In RB Wiggs, HB Lobprise, eds., Veterinary Dentistry, Principles and Practice, pp. 37–49. Philadelphia: Lippincott-Raven.
613
614
SECTION
4 Surgery
CHAPTER 246
Anesthesia: Local Ludovic Pelligand
Advantages of Local Anesthesia Multimodal analgesia is the simultaneous administration of several analgesics acting in synergy at different sites. It provides better analgesia cover with the lowest possible dose of each analgesic, hence reducing the risks of toxicity. The use of local anesthetics (LA) enables a reduction of general anesthetics requirement and spares the cardiovascular and respiratory systems perioperatively. LA techniques are easy and economical and should be carried out when possible, after evaluation of the benefit-to-risk ratio.
Pharmacology and Actions of Local Anesthetics LA abolish the transmission of nociceptive input initiated in peripheral receptors. The pain information is conducted via two types of nervous fibers: Aδ fibers (i.e., sharp localized pain; acute) and c fibers (i.e., dull, poorly localized pain; chronic). These small diameters fibers (especially the unmyelinated Aδ) are more sensitive to the action of LA than larger motor or proprioceptive fibers. LA are weak bases and belong to two families: the esters, which are rarely used (procaine type), and amides (i.e., lidocaine, mepivacaine, ropivacaine, and bupivacaine), which are the most commonly used. The
acid dissociation constant, pKa, of the LA determine the degree of ionization at physiological pH and the onset of action. The unionized soluble form of the LA drug passes through the cell membrane where it becomes ionized and blocks the internal surface of a sodium (Na+) channel in an inactive state. This results in an interruption of the propagation of the action potential. The lipid solubility determines the potency (lower concentration required for same effect), and the degree of protein binding determines the duration of action. LA are also vasodilatory. Vasoconstrictors (such as epinephrine) may be added in some preparations to prolong the duration of the block by limiting vasodilation and systemic uptake. Table 246-1 is a summary of the use of LA including their doses and recommended indications. Lidocaine (2–4 mg/kg) is a short acting LA with a short onset of action, which makes it suitable to provide rapid analgesia (i.e., biopsies or short surgeries). Procaine does not present any advantage over lidocaine. Bupivacaine (up to 1 mg/kg) has a slower onset (peak effect after 30 minutes) but longer duration of action (up to 6 hours), which is suitable for surgical blocks and postoperative pain management. Levo-bupivacaine (a pure solution of one of the enantiomers of bupivacaine) and ropivacaine were developed as a less cardiotoxic alternative to bupivacaine. The combination of lidocaine and bupivacaine in the same syringe results in the advantage of quick onset
TABLE 246-1: Clinical Use of Local Anesthetics Name ESTERS Procaine
AMIDES Lidocaine
Mepivacaine Ropivacaine
Bupivacaine
Levo-bupivacaine
Presentation*
Recommended Dose
Toxic Dose
Duration
Comment
Solution at 5% with epinephrine (approved in the United Kingdom)
4 up to 6 mg/kg
30 mg/kg IV (neurologic)
50 min
Slow onset, low potency, and short duration Do not administer with sulfonamides.
Solution at 2% with or without epinephrine EMLA cream 2.5% lidocaine (with prilocaine 2.5%) Solution at 2% (approved only in Canada) Solution at 0.2, 0.5, 0.75, 1% (not approved for cats)
2 up to 4 mg/kg
1 to 1.5 h
up to 0.8 g
12 mg/kg IV (neurologic) Unknown in cat
Reduces requirement in anesthetics Prokinetic and free radical scavenger May ease catheter placement
2 up to 4 mg/kg
Unknown in cat
2 to 2.5 h
Reduces requirement in anesthetics
up to 1.5 mg/kg
Unknown in cat
3 to 5 h
1 mg/kg
3.8 mg/kg (neurologic)
4 to 6 h
Reduces requirement in anesthetics Supposedly less cardiotoxic than bupivacaine Reduces requirement in anesthetics High cardiac toxicity
up to 1.5 mg/kg
Unknown in cat
4 to 6 h
Solution at 0.25, 0.5, 0.75% with or without epinephrine (not approved for cats) Solution at 0.75% (not approved)
Reduces requirement in anesthetics Supposedly less cardiotoxic than bupivacaine
* A 2% solution contains 2 g/100 mL (i.e. 20 mg/mL). A dose of 2 mg/kg for a 4-kg cat corresponds to a volume of 0.4 mL of the pure solution
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
617
SECTION 4: Surgery
(A)
(B)
Figure 246-1 A, Blockade of the infraorbital nerve is performed at the infraorbital foramen (IOF). The mental block is performed at the rostral mental foramen (RMF). B, The mandibular nerve is blocked at the mandibular foramen (MF).
and long duration. Beware of cumulative toxicities with two anesthetic agents combined; the combined dose should remain below 2 mg/kg as a rule of thumb. Toxicity is associated with blockade of neuronal and cardiac sodium channels. High systemic absorption of a LA can occur from the site of injection, especially following intrapleural or intercostal blocks. Signs of LA neurotoxicity include muscle twitching, restlessness, convulsion, or depression. Intravenous infusion of lidocaine has been shown to have deleterious effects on cardiac output in the cat. Therefore, the administration of intravenous lidocaine is not advised (continuous infusion or intravenous regional anesthesia) in the cat. Bupivacaine-induced cardiac toxicity can be reversed by infusion a lipid emulsion (Intralipid®) in dogs under isoflurane anesthesia, but no study has been carried out in the cat.
Specific Blocks Familiarity with key anatomical landmarks is necessary. Training can be based on palpation of landmarks on lean cats or visualization of foramina on skeletons. The skin should be clipped and surgically prepared before percutaneous injection of a LA. Aspiration should be performed before injecting a LA to avoid intravascular injection. The total volume must be calculated accurately using lean body weight and distributed among all sites. The use of 1-mL syringes and 22- to 24-gauge needles is advised for better precision. The LA solution may be diluted 1:2 without losing its efficacy. In general, a nerve block in the cat requires a volume of 0.1 to 0.2 mL per site.
Figure 246-2 An epidural block is performed by inserting the needle into the space caudal to the dorsal process of L7 and cranial to the first dorsal spinous process of the sacrum.
of the agent back out of the delivery site. The needle is inserted through the oral mucosa in a caudal direction and advanced in the canal. The needle should not be advanced beyond the medial canthus.
Major Palatine Block Head and Face The head and face blocks are very useful for dentistry. See Figure 246-1.
The major palatine nerve arises from the major palatine foramen, located between palatal cusps of the upper fourth premolar. It innervates the hard and soft palate rostral to the injection site. A bleb of local anesthetic is placed just under the mucosa at the exit of the foramen.
Infraorbital Block The infraorbital nerve is the last division of the maxillary nerve (second branch of the trigeminal nerve). It innervates the incisive bones and dental structures on each side of the maxilla. The position of the foramen is shown by the upper needle on Figure 246-1A. Digital pressure over the foramen after the block is required for 60 seconds to avoid leakage
618
Mental Block The position of the foramen is shown by the lower needle in Figure 246-1A. The foramen is located midway down the lateral aspect of the mandible between the first premolar and canine. If the block is placed inside the foramen, digital pressure is applied after injection.
Anesthesia: Local
Mandibular Block This nerve is blocked proximally before it enters the mandible on the medial side. The location of the foramen is shown by the needle in Figure 246-1B. The extraoral approach is advised in the cat, inserting the needle under the rostrally aspect of the angular process. This block anesthetizes all dental and bony structures of the mandible. A possible complication is tongue anesthesia and self-mutilation as the lingual nerve branches off just before the foramen.
Thoracic and Lumbosacral Rib Cage Analgesia An intercostal block is useful for the insertion of chest drains. The LA is administered caudally to the most cranial rib of the intercostal space of interest. An intrapleural block can be performed through the chest drain after thoracotomy. The cat is then laid on the side of the thoracotomy for 10 minutes to facilitate the diffusion of the LA. High systemic absorption occurs at these sites, and care must be exercised with dosage calculation.
Epidural Analgesia and Anesthesia LA or opioids can be injected epidurally. The drugs are diluted in sterile saline up to an injected volume of 0.1 to 0.2 mL/kg. For opioids epidural administration, see Chapter 266. Epidurals are performed in sternal or lateral recumbency. Hindlimbs must be flexed forward to open the lumbosacral space. After skin preparation and gloving, the thumb and the middle finger are positioned on the iliac wings (see Figure 246-2). The index finger localizes the gap between the dorsal processes of the last lumbar vertebrae (L7) and the first spinous process of the sacrum. A spinal needle (22 gauge, 1.5 in) is introduced in the space, aiming at the base of the first sacral spinous process (see localization of the needle in Figure 246-2). Localization of the roof of the sacrum helps to evaluate the depth at which the epidural space lies. The tip of the needle is then slightly withdrawn, rotated cranially, and advanced though the ligamentum flavum (“pop” sensation). The aspiration of a drop of saline pre-placed in the hub of the needle often confirms the correct location if the cat is in sternal recumbency due to the negative pressure of the epidural space. Place a 0.1-mL air cushion between the LA solution and the plunger; the air cushion should not be compressed but keep the same volume during the injection. Successful epidural administration of the LA is confirmed by relaxation of the anal sphincter. Unlike the dog, the spinal cord and meninges extend into the lumbosacral region in the cat. The risk of dural puncture and intrathecal administration is therefore higher. If this occurs, the procedure should be aborted or the dose and volume should be reduced by 50%. The contraindications for epidural anesthesia are local skin infection, hypovolemia, coagulopathies, pelvic trauma affecting identification of landmarks, and inflammation of the central nervous system. The complications of the use of LA epidurally include motor block (difficulty to stand) and hypotension. Hypotension occurs when the LA spreads cranially (often when volume injected is 0.2 mL/kg) causing splanchnic vasodilation and blood pooling. Urinary retention is sometimes seen when morphine is administered epidurally.
Appendicular Brachial Plexus Brachial plexus blockade can be used for surgical procedures located distal to the elbow. Good knowledge of anatomic landmarks or the use of a nerve locator facilitates accurate administration of the block. The radial, musculocutaneous, median, and ulnar nerves are blocked in the axillary space. The needle is introduced craniocaudally in a direction parallel to the spine, 1 cm (3/8 in) above the shoulder joint. The nerves are located at the level of the cervicothoracic junction, cranial to the first rib. The principal complications are vascular injection and pneumothorax. Selective blockade of the distal branches of the radial-ulnar-median nerve block can be performed for surgeries of the front paw. For the palmar aspect, the median and ulnar nerves are blocked medially and laterally (for the dorsal branch of ulnar) to the accessory carpal pad. For the dorsal aspect, the radial nerve is blocked medially and proximal to the radio-carpal joint. Preparations with vasoconstrictors should be avoided when performing the full foot block due to the risk of foot ischemia.
Intra-Articular Intra-articular blocks are occasionally performed in the cat after arthrotomy or arthroscopy but less frequently than in dogs. LA is injected aseptically into the joint after closure of the capsule.
Topical Use Eutectic Mixture of Lidocaine and Prilocaine (EMLA) Cream: The application of this cream might help intravenous catheterizations. EMLA must be applied 1 hour before and kept under occlusive bandage. Lidocaine sprays are used for laryngeal blockade for endotracheal intubation. It is advisable to use a 2% solution instead of a 5 or 10% solution to avoid high systemic absorption. Splash blocks are applied prior to surgical incision closure or during ovariectomies to anesthetize the mesovarium. An LA should also be deposited around nerves during amputation of the thoracic or pelvic limb to reduce the incidence of phantom limb pain. Proparacaine and tetracaine solutions are used for anesthesia of the cornea and conjunctiva for examination. The onset is within minutes, and the duration of action is 15 minutes with tetracaine.
Suggested Readings Tranquilli WJ, Grimm KA, Lamont LA. 2000. Analgesic techniques. In WJ Tranquili, KA Grimm, LA Lamont, eds., Pain Management for the Small Animal Practitioner, pp. 32–53. Jackson Hole, WY: Teton Newmedia. Woodward T, 2008. Pain management and regional anesthesia for the dental patient. Topics Compan Anim Med. 23(2):106–114.
619
CHAPTER 247
Anesthesia: Sedation and General Ludovic Pelligand
Overview In a recent epidemiological study on perioperative death in small animals, the risk of anesthesia or sedation-related death was 0.24% in cats overall and 1.4% in sick cats. Although feline anesthesia appears increasingly safe, further reduction of mortality could be achieved with greater patient care during and after anesthesia. A thorough clinical examination is necessary before sedation or general anesthesia. Even the healthy young cat going for “routine anesthesia” may hide subclinical congenital disease, which may become problematic during anesthesia. The proportion of the geriatric feline population is growing with the progresses of medicine; these animals may have chronic subclinical conditions.
Conditions and Drugs Affecting Anesthesia • Respiratory: Pleural effusion, diaphragmatic hernia, and pneumothorax. • Cardiovascular: Cardiomyopathy, systemic hypertension, hypovolemia, and distributive or septic shock. • Renal: Chronic kidney disease, urinary obstruction, and electrolyte imbalance. • Hepatic: Portosystemic shunt and hepatic lipidosis. • Medications: Angiotensin conversion enzyme inhibitors, diuretics, βblockers, and calcium channels blockers.
Further Preanesthetic Considerations If a cat is presented in an unstable cardiorespiratory state, a stabilization period is beneficial to the outcome of anesthesia or sedation. Laboratory analyses and diagnostic imaging are justified in the aging or traumatized cat, particularly if the results might change the anesthesia protocol. Some cats may not be amenable to minimal restraint for an examination, so an educated guess must be made regarding their suitability for sedation or anesthesia based on their clinical history, age, and apparent symptoms. Sedation for better cooperation is usually preferred to a stressful restraint that can lead to sudden collapse.
Sedation Sedation is required to facilitate a diagnostic procedure or the placement of an intravenous access. Sedation or premedication is also the first step of an anesthesia protocol, which should include analgesics (i.e., opioids and α2-agonists), hypnotics (i.e., induction agents and volatile anesthetics) and muscle relaxants (i.e., volatile agents, benzodiazepines, and α2-agonists). The choice of the most appropriate sedation protocol is influenced by the age and temperament of the patient, American Society of Anesthesiologists (ASA) status, and the degree of pain expected from the procedure. Opioids are the cornerstone of intraoperative and postoperative analgesia. See Chapter 266. Nevertheless, opioids used alone do not
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
620
generally provide good sedation in the cat. At the proposed dose (see Table 266-1), they cause, at most, slight hyperreactivity but not feline “morphine mania” as reported in old textbooks. The pure µ agonists commonly used (and their duration of action) are morphine (4–6 hours), methadone (4 hours), hydromorphone (4 hours), pethidine in Europe or meperidine in the United States (2 hours), and fentanyl (30 minutes). Their level of analgesia is dose related. Butorphanol (1.5 hours) is a κ agonist and µ antagonist. It provides good sedation but mediocre analgesia. Buprenorphine is a long-lasting partial mu agonist (6–8 hours) that may be included in a premedication protocol; however, its peak effect occurs 45 minutes after injection. See Table 247-1. Acepromazine in combination with opioids results in moderate to good sedation, which is often enough for catheter placement in calm conditions. See Table 247-1. This combination is frequently used as premedication prior to surgery. The action of acepromazine lasts 8 hours. This vasodilator should not be used in animals in shock because it may exacerbate hypotension. An efficient and reversible immobilization is obtained with α2 adrenoreceptor agonists alone or in combination with opioids. See Table 247-1. Nevertheless, they cause peripheral vasoconstriction and reflex bradycardia leading to reduction of cardiac output. They should only be administered to healthy cats, which have a normal cardiac function. Ketamine and midazolam are commonly combined in the same syringe to provide a profound sedation. See Table 247-1. This combination is preferred to the use of α2-agonists when the cardiovascular function cannot be assessed prior to sedation. Recoveries are occasionally stormy with this protocol. Quiet dark environment is essential for recovery after this protocol. Insulin syringes or 1-mL syringes should be used for accurate volume measurement of medetomidine and acepromazine. The use of a diluted stock solution in saline (1:10 v:v) is also acceptable. Patients should be monitored following administration of sedation. Food and water bowls must be removed from the kennel. Sufficient time should be allowed for the drugs to reach their peak effect (5 minutes for medetomidine, at least 30 minutes for acepromazine).
General Anesthesia Procedure Intravenous Access Placement of a peripheral catheter is mandatory for general anesthesia. The cephalic vein or saphenous veins are usually catheterized with a 22-gauge catheter after clipping and preparation of the area. Initial skin perforation with the bevel of a needle prevents catheter tip damage when catheters are placed in male cats with thick skin. A T-connector filled with heparinized saline (1 unit per mL) is attached on the Luer-lock of the catheter and taped in place. Good handling by an experienced technician and adequate chemical restraint make catheter placement easier and efficient. If intravenous access is required for more than 48 hours, placement of a central venous catheter under general anesthesia should be considered. See Chapter 297. Placement of a temporary intraosseous catheter (spinal needle) in young kittens or dehydrated cats is another option. The best sites for their placement include the trochanteric fossa of the femur and the
TABLE 247.1: Combinations for sedation and premedication in the cat Drug Dose
Route
Opioids alone
Butorphanol SC, IM 0.4 mg/kg
Buprenorphine
Pethidine
Morphine or methadone
Hydromorphone
SC, IM, IV
SC, IM
IM, IV
IM or IV
20 µg/kg
4–6 mg/kg
0.1–0.3 mg/kg
0.05–0.15 mg/kg
Alone Ketamine IM (mg/kg) and Midazolam IM (mg/kg)
3–10 + 0.2–0.3 0.025–0.05
Acepromazine SC, IM (mg/kg)
Alpha2 agonist Medetomidine IM (µg/kg) Normal cardiovacular function
Dexmedetomidine IM (µg/kg) Normal cardiovacular function
0.01–0.03
with
0.2–0.4 mg/kg
10–20 µg/kg
3–5 mg/kg
0.1–0.2 mg/kg
0.05–0.15 mg/kg
Alone with
20–40
Alone
10–20
with
10–20
Alone
5–10
with
0.2–0.4 mg/kg
0.2–0.4 mg/kg
0.2–0.4 mg/kg
Reduce butorphanol dose if given IV
10–20 µg/kg
10–20 µg/kg
10–20 µg/kg
Allow 45 min for full buprenorphine effect
3–5 mg/kg
—
—
Pethidine NEVER IV
0.1–0.2 mg/kg
0.1–0.2 mg/kg
0.1–0.2 mg/kg
Avoid morphine IV (histamine release)
0.05–0.15 mg/kg
0.1 mg/kg
—
Comments Possible hyperesthesia, increased sensitivity to stimulus and mydriasis Usually profound sedation Profound sedation, reduce dose if IV Ideal to secure intravenous access on fractious cats Moderate sedation Moderate to good sedation Reduce dose in elderly or in cardiovascularly unstable animals Profound sedation Profound sedation, cat might be recumbrent Appropriate for diagnostic imaging and non painful procedures Reversible Profound sedation Profound sedation, cat might be recumbrent Appropriate for diagnostic imaging and non painful procedures Reversible
621
SECTION 4: Surgery
flat medial aspect of the proximal tibia. Subcutaneous fluid catheter placement is described in Chapter 271.
Anesthesia Induction Agents Healthy Cats Propofol This anesthetic agent is classically formulated in a white lipid emulsion. Open vials should be discarded within 24 hours due to the risk of bacterial contamination. The dose varies depending on animal status and premedication. See Table 247-2. Propofol is given slowly to effect over 60 seconds (watch a clock). Propofol causes a marked respiratory and cardiovascular depression. Avoid repeated use of propofol in cats who are anesthetized on a daily basis due to the risk of developing Heinz body anemia and dyslipidemia. The new propofol formulation without lipid emulsion could be more appropriate. It appears as a clear liquid and contains a preservative that guaranties bacterial stability for 28 days. Thiopental Prepared as a 2.5% solution, thiopental is stable for 1 week. It should be given strictly IV; extravascular injection causes tissue necrosis. The induction dose depends on the effect of the premedication and the status
of the animal. See Table 247-2. The dose should be further reduced in cats with acidosis. Half of the calculated dose is given as a bolus, and the rest is given to effect over 1 minute to reach the desired effect. Thiopental causes marked respiratory and cardiovascular depression. It also accumulates in fat, which delays recovery, especially after repeated administration. Mask or Chamber Induction Sevoflurane is preferred to isoflurane in this case because of the quicker partial pressure equilibration and the absence of the pungent smell. Initial excitement is commonly observed in early stages of the inhalant induction. Beware of pollution of the working place with such induction techniques.
More Critical Patients Ketamine with Benzodiazepine (Table 247-2): Ketamine minimally depresses the cardiovascular system, but apnea can occur. Cranial nerves reflexes persist until the plane of anesthesia is deepened by other drugs. Ketamine provides good somatic analgesia and valuable antihyperalgesia properties for chronic pain. Ketamine should be avoided in cats with cardiomyopathy or raised intraocular pressure. Similar effects but longer duration are obtained with the combination tiletamine and zolazepam.
TABLE 247-2: Use of intravenous induction agents in the cat Veterinary licence
Dose below* depend on depth of sedation
Cardiovascular or respiratory depression
Analgesia
Accumulation
Recovery
Cost
Recommendation
Propofol
Yes
6 to 8 mg/kg (mild sed.) 2 to 4 mg/kg (deep sed.)
Marked
None
Yes if repeated or prolonged infusion
Good
Moderate
Low risk
Thiopental
No
10 to 12 mg/kg (mild sed.) 5 to 10 mg/kg (deep sed.)
Marked
None
Yes especially if young or liver disease
Good
Cheap
Low risk
Alfaxalone
Yes
3 to 5 mg/kg (mild sed.) 1 to 2 mg/kg (deep sed.)
Mild, dose dependent
None
None
Good but poss. twiches
Moderate
Moderate risk
Tiletamine and zolazepam
Depends on country
4 to 5 mg/kg (mild sed.) 1 to 2 mg/kg (deep sed.)
Mild, dose dependent
Some
Yes if kidney failure
Stormy
Moderate
Stable cat Avoid if cardiac
Ketamine (with benzodiazepine)
Yes for ketamine
5 mg/kg (mild sed.) 1 to 3 mg/kg (deep sed.)
Mild, dose dependent
Some
Yes if repeated administration
Stormy
Cheap
Moderate risk Avoid if cardiac
Etomidate
No
1 to 2 mg/kg (mild sed.) 0.5 to 1.0 mg/kg (deep sed.)
Almost none
None
None
Good
Expensive
High risk cat
Fentanyl with benzodiazepine
No
Fentanyl: 5 to 10 µg/kg Benzo.: 0.2 to 0.3 mg/kg
None for CV but severe for respiratory
Good
None
Good
Expensive
High risk cat
* Slow IV injection to effect, as animal’s requirements may be lower than the proposed dose. The doses are reducced with deep sedation in comparision to mild sedation.
622
Anesthesia: Sedation and General
Alfaxolone Alfaxolone solubilized in cyclodextrin is now available worldwide. The dose varies depending on the cat and premedication. Alfaxolone is given slowly over 1 minute and stopped once loss of consciousness has been reached. Only minor depression of respiratory and cardiovascular functions is observed at clinical doses. Anesthesia may be maintained with repeated administration or constant infusion; however, respiratory assistance may be necessary. Etomidate Given at 0.5 to 2 mg/kg IV etomidate or a combination of fentanyl (5–10 µg/kg) and midazolam (0.2–0.3 mg/kg) can also be used in debilitated cats. The quality of induction with this protocol is poor.
Endotracheal Intubation Endotracheal tubes should be placed in all cats undergoing general anesthesia. Laryngoscopy is necessary to ensure laryngeal visualisation and to limit laryngeal trauma. A short Miller laryngoscope blade should be used. Lidocaine may be applied to the arytenoids for intubation; it will also limit the risk of laryngospasm on recovery. If using a spray (not more than 2% concentration), apply only one squirt because cats are sensitive to lidocaine toxicity; allow at least 30 seconds for effect to occur. Preoxygenation is required (3–5 minutes) if a difficult intubation is anticipated to allow more time before hemoglobin saturation drops. Cuffed endotracheal tubes are preferable (i.e., high volume, low pressure if possible). Disconnect the cat from the anesthesia machine when rolling it to its other side to avoid twisting the endotracheal tube and causing laryngeal or tracheal damage. Avoid excessive inflation of the endotracheal tube cuff especially in dental patients. This can lead to ischemic mucosal damage or tracheal rupture. Place a pharyngeal pack to protect the airways during dental work. Laryngeal mask airways can be used in some cases to deliver anesthetic agent and fresh gas. Because there is no tracheal intubation, aspiration of gastric contents can occur. Positive pressure ventilation may result in bloating.
Maintenance of General Anesthesia The anesthesia machine and breathing apparatus should be checked at the beginning of each day (i.e., leaks, alarms, and oxygen supplies). In a normal setting, semi-open breathing systems such as the Bain, the “TPiece,” or the Mini Lack systems are used. Minute volume (MV) is calculated by multiplying the respiratory rate by the approximate tidal volume (10 mL/kg). MV is multiplied by a system coefficient (*2.5 for T-Piece or Bain and *1 for Mini Lack) to calculate the minimal flow to avoid rebreathing. Equipment dead space should be kept to minimum (short endotracheal tubes and connectors) to avoid rebreathing. The drug given during premedication and induction may be enough to carry out a short procedure. In other cases maintenance of general anesthesia is achieved with repeated boluses or a continuous infusion of injectable agents (e.g., alphaxolone or propofol). In both cases, the cat is connected to the anesthesia machine delivering at least 33% oxygen. In most cases anesthesia is maintained with volatile anesthetic agents carried in an oxygen-rich mixture. All volatile agents cause a dosedependent cardiovascular and respiratory depression. The minimal alveolar concentration (MAC) of isoflurane in the cat is 1.6%. Changes in depth of anesthesia are faster than with previously used halothane due to lower high blood solubility. Respiratory depression is marked around MAC levels. Because isoflurane is a vasodilator, hypotension often occurs during anesthesia, but cardiac output is better maintained. The MAC of sevoflurane is 2.6%. The cardiovascular effects are similar to those of isoflurane, but sevoflurane is a lesser respiratory depressant. Because of its lower blood solubility, changes in anesthesia depth and recoveries are faster than with isoflurane.
Desflurane is the least blood soluble of all anesthetic agents, resulting in extremely quick change of depth plane and recovery (4 minutes for extubation). The MAC of desflurane in cats is around 10%. Desflurane is equivalent to sevoflurane in terms of cardiovascular and respiratory depression. Contrary to isoflurane, sevoflurane, and desflurane are not licensed in cats. Nitrous oxide may be used to facilitate gas uptake and to possibly spare inhalant anesthetic. To reach the desired effect, it must represent at least 60% of the inhaled mixture (always keep at least 30% oxygen). Nitrous oxide is deleterious in case of gas filed internal spaces (e.g., pneumothorax). It should be discontinued 10 minutes before disconnection from the breathing system. The drug combination used during premedication and induction may reduce the requirement of the volatile agent of a given cat at sub-MAC levels, especially if α2-agonists, ketamine, or fentanyl are used.
Maintenance of Homeostasis Intravenous fluids should be administered for procedures exceeding 30 minutes unless contraindicated. Crystalloid solutions, such as lactated Ringer ’s solution or Hartmann’s solution are administered at a rate of 10 mL/kg per hour during the first hour and 5 mL/kg per hour thereafter. Intravenous pumps or drip sets (normal or pediatric) are used. If an intravenous pump is not used, a burette drip set is recommended to allow precise monitoring of fluid administration and avoid overload. Protective or lubricant gel is applied to the corneas to avoid desiccation especially after ketamine administration. Due to their large surface volume ratio, cats are prone to heat loss during anesthesia. Hypothermia increases the risk of infection, delays recovery, and requires adjustment in anesthetic agents. Proactive temperature sparing strategies should be followed soon after induction because body temperature will drop initially following the use of vasodilatory agents. A heat and moisture exchanger should be attached between the endotracheal tube and the breathing system, and bubble wrap should be applied to the extremities to limit heat loss. Warm air blankets, perfusion warmers, and lavage of body cavities with warm saline contribute to warming the cat. Great caution must be exercised with electric heating blankets or gloves filled with hot water due to the concern of skin burns.
Monitoring The senses of an experienced anesthetist can be reliable for monitoring. The depth of anesthesia is assessed by looking at eye position and pupil size (i.e., from light to very deep: eye central with palpebral reflex present; ventrally rotated; back to central position with constricted pupil; central eye with dilated pupil). Serial assessment of jaw tone is useful to monitor muscle relaxation. Estimation of tidal volume can be obtained by observing chest excursions or movements of the rebreathing bag. Qualitative information on pulse may be obtained by palpating the femoral, metatarsal, or sublingual arteries. Peripheral perfusion is assessed by capillary refill time. An esophageal stethoscope allows cardiac and pulmonary auscultation. Additional monitoring devices are useful to confirm clinical observations and to help to support vital physiological functions (see Table 247-3). Their goal is to reduce the incidence of complication and accidents. Pulse oximeters act as a pulse monitor and hemoglobin saturation monitor. The user must be aware of its technical artefacts (see Table 247-3). Due to the sigmoid shape of the hemoglobin saturation curve, they are not sensitive when 100% oxygen is administered. Nevertheless, they will detect desaturation quickly if only 33% oxygen is administered (e.g., when nitrous oxide is used). Capnography provides information on ventilation and gas exchange as well as cardiac output. Hypo- and hyperventilation must be addressed (see Table 247-3). A sudden drop of expired carbon dioxide (CO2) with constant ventilation is a warning sign of a sudden drop in cardiac output.
623
SECTION 4: Surgery
TABLE 247-3: Monitoring Information and Troubleshooting Guide Monitoring device
Pulse oximetry (hemoglobin oxygen saturation)
Reference range
Troubleshooting
Action
More than 90%
1) 2) 3) 4)
→ → → →
Movements artefacts Vasoconstriction Interruption of flow True hypoxemia
1) Increase CO2 uptake
a) Rebreathing → increase gas flow, reduce dead space b) Check for faulty breathing system c) CO2 inflation for coelioscopy
2) Hypoventilation
a) Assess anesthetic depth: reduce if possible b) Opioid or infusion related → ventilate
1) 2) 3) 4)
→ → → →
Check leak, obstruction, disconnection, or dislodgement Reduce fresh gas or change breathing system Assess depth of anesthesia and analgesia Immediate cardiovascular status check
1) Hypertension
a) b) c) d)
Supply of anesthetic? (e.g., empty vaporizer) Lack of analgesia → renew if due Check anesthesia depth → deepen if too light Consider endocrine or renal cause (clinical history)
1) Technical fault
a) Disconnection, somebody leaning on device b) Check cuff size and probe position
2) Hypotension
a) Decreased venous return (bleeding, major vessel occlusion) b) Assess anesthetic depth: reduce if possible c) If bradycardia: anticholinergics d) Assess fluid status → fluid load (crystalloids, colloids, blood) e) Inotropes and pressors
No more than 50 mmHg Capnography (CO2 partial pressure in expired gases and shape of the curve) Not less than 30 mmHg
Technical fault Mixing with fresh gas Hyperventilation Imminent cardiac arrest
No more than 160 mmHg Doppler systolic blood pressure or Oscillometric blood pressure monitor No less than 90 mmHg
A Doppler apparatus is a useful and affordable monitoring device to detect pulse and systolic blood pressure. It is a reliable noninvasive means of blood pressure monitoring in the cat. An ultrasound sensor is placed over a peripheral artery (i.e., metatarsal, palmar, or caudal). An audible signal is heard for each pulse. Contact gel is applied between the skin and the probe, which is taped in place. If hair is not shaved, alcohol and then contact gel will result in sufficient contact. A cuff, with a width equal to about 40% of the limb circumference, is applied proximally to the probe. The pressure at which blood flow is heard again after cuff occlusion and gradual deflation is equal to the systolic blood pressure (see Table 247-3). Most oscillometric monitors tend to be less accurate at the extremes of the blood pressure range and fail to read during hypotension and vasoconstriction. Invasive arterial blood pressure monitoring via an arterial catheter placed in the dorsal metatarsal artery can be achieved in feline patients. If used it should not be left in place for postoperative monitoring because, in contrast to dogs, complications with blood supply to the paw can be seen.
Recovery The cat should be taken to a quiet place where it can recover. Monitoring during the postanesthesia or postsedation period is paramount because many deaths happen during this phase. Brachycephalic cats should be monitored closely for airway obstruction.
Accidents and Complications Respiratory Most respiratory complications are detected with the use of pulse oximetry and a capnography. Respiratory obstructions are diagnosed by
624
Stop movements Alpha2-agonists, severe hypovolemia or hypothermia Move probe to another location Increase oxygen fraction; improve gas exchanges
capnography and auscultation with a stethoscope. A mucus plug is frequently the cause of airway obstruction, especially endotracheal tubes with a 3-mm or less internal diameter. Gentle suction or change of tube generally works in this case. Bronchoconstriction due to bronchospasm or anaphylactic reactions must be treated with bronchodilators (i.e., aminophylline or epinephrine, respectively). Barotrauma is damage inflicted to the alveoli when excessive airway pressure is reached. The usual scenario is when the pop-off valve is accidentally left closed. Pneumothorax and cardiovascular collapse may occur if not detected immediately. Upper respiratory obstruction and pawing of the face (risking self-trauma) on recovery is frequent in the cat. Keep the neck extended, with the mouth slightly open and tongue out (if possible) until the cat is more awake.
Cardiovascular The procedure for hypotension or hypertension is described in Table 247-3. Bradycardia may occur with large doses of opioids, hypothermia, intracranial lesions, or hyperkalemia. Hyperkalemia is frequent in cats with urinary obstruction and must be treated. See Chapter 220. The quantity of blood loss must be carefully monitored, and severe bleeding must be addressed intraoperatively. Depending on the volume lost, crystalloids, colloids, or whole blood (stored or fresh) should be used. See Chapter 295 for blood transfusion procedures. The signs of impending arrest include: (a) weak or irregular pulse or loss of pulse signal, (b) sudden deepening of the anesthesia plane, (c) sudden drop of expired CO2 level, or (d) grey mucous membranes or absent capillary refill time. Urgent assessment of the situation is needed. If cardiac arrest is confirmed, immediately discontinue anesthetic administration, give positive pressure ventilation, antagonize cardiovascular depressants, call for assistance, and start cardiopulmonary resuscitation. See Chapter 30.
Anesthesia: Sedation and General
Miscellaneous Excitement, dysphonia, or restlessness in recovery must be addressed. Express the bladder if necessary, and check the analgesic level. Sedation with small doses of acepromazine or medetomidine will be beneficial. Hypothermia and drug overload can lead to prolonged recoveries requiring active warming and support of elimination processes (increase diuresis and exhalation of volatiles). Partial or total reversal of opioids and α2-agonists should be considered, but drug reversal should not result in insufficient analgesia. Marked postanesthetic hyperthermia can
be seen in cats in association with the administration of hydromorphone or other opioids.
Suggested Readings Brodbelt DC, Blissit KJ, Hammond RA, et al. 2008. The risk of death: the confidential enquiry into perioperative small animal fatalities. Vet Anaesth Analg. 35(5):365–373.
625
CHAPTER 248
Bulla Osteotomy, Ventral Approach Don R. Waldron
Overview The ventral approach to the bulla or bullae is usually performed as a component of treatment for nasopharyngeal or otic polyps. Less commonly, drainage and culture of the tympanic bulla may be indicated in cats with otitis media. See Figure 248-1. Cats suspected of having nasopharyngeal polyps should have both oral and otic examinations before surgery to determine the extent of the disease process. Nasopharyngeal polyps may be avulsed from their attachments via an oral approach or otic polyps via the external ear canal; however, the recurrence rate following polyp avulsion without concurrent bulla osteotomy varies from 3 to 50%. Otic polyps are thought to have higher recurrence rates than nasopharyngeal polyps. Ventral bulla osteotomy is performed prior to removal of the polyp, ideally. Skull radiographs may be of use in deciding whether the left or right or both bullae should be operated. See Figure 248-2. Culture findings of cats with bullae disease are varied; however, amoxicillin-clavulanic acid is excellent for most cats until culture findings are obtained following surgery.
Figure 248-1 Purulent material can be seen exiting the opened bulla.Photo courtesy of Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
626
Special Equipment • A 2-mm (1/16-in) Steinmann pin in a Jacob’s chuck or bone trephine. • Lempert rongeurs • Small Gelpi retractors or Senn hand held retractors or Star SelfRetaining Retractor (Lone Star Medical Products, www.lsmp.com, 1-800-331-7427 or 1-281-340-6000)
Procedure • The cat is placed under general anesthesia, and the ventral cervical area is clipped and prepared for aseptic surgery. The patient is placed in dorsal recumbency with the neck extended over an elevated padded area (e.g., a small rolled towel). See Figure 248-3. • The head is secured to the operating table with adhesive tape. • In most cats, especially thin ones, the bulla can be palpated within the deep cervical area just caudal and medial to the ramus of the mandible. • A paramedian skin incision is made 2 cm (3/4 inch) lateral to the midline between the proximal trachea and the most caudal aspect of the mandible. The incision is centered on a line perpendicular to the midline at the vertical ramus of the mandible. See Figure 248-4. • The incision is continued through the subcutaneous tissues and platysma muscle. • Dissection continues between the linguofacial and maxillary veins as they converge to form the external jugular vein. See Figure 248-4. • The fascia between the masseter and digastricus muscles is incised; dorsal digital palpation aids in identification of the ventral tympanic bulla. See Figure 248-4. • The digastricus muscle is retracted laterally, and the styloglossus muscles are retracted medially to reveal the ventral aspect of the bulla. See Figure 248-5. • Blunt dissection or a gauze sponge is used to remove soft tissue from the bulla. • The hypoglossal nerve and the lingual artery may be visualized and should be carefully retracted. • An intramedullary pin or bone trephine is used to gain entrance to the ventromedial bulla cavity, and aerobic cultures of the bulla content are taken. See Figure 248-6. • Lempert rongeurs are used to remove additional bone, exposing the remainder of the ventromedial compartment. See Figure 248-7. • The dorsolateral compartment of the bulla is entered with the pin or rongeurs. Careful removal of the contents of the dorsolateral compartment is necessary to prevent recurrence of polyp disease. • The bulla is lavaged with normal saline prior to closure. • The digastricus and masseter muscles are apposed with 4-0 synthetic absorbable suture material. • The remainder of the closure is routine; however, exercise care when placing the suture needle as it is easy to penetrate the large veins in the area.
(A) (B)
(C) Figure 248-2 Thickening of the tympanic bulla is a sign of chronic otitis media. Lateral oblique views show an abnormal bulla ([A] arrows) contrasted to a normal bulla ([B] arrows) in the same cat. An open-mouth ventral-dorsal view shows the normal and abnormal bullae (black arrows). The white arrow points to the thin bony septum that separates the main chamber (ventromedial compartment) of the tympanic bulla from the craniolateral compartment (C). Images courtesy of Dr. Gary D. Norsworthy.
627
Figure 248-3 A paramedian skin incision is made lateral to the cervical trachea. Image used by permission from Smith MM, Waldron DR. 1993. Atlas of Approaches for General Surgery of the Dog and Cat. Philadelphia: WB Saunders.
Figure 248-4 The tissue plane between the masseter and the digastricus muscle is incised. Palpation of the ventral tympanic bulla aids in dissection and orientation. Image used by permission from Smith MM, Waldron DR. 1993. Atlas of Approaches for General Surgery of the Dog and Cat. Philadelphia: WB Saunders.
628
Digastricus m.
Hypoglossal n. Styloglossus m. Lingual a.
Caudal
Tympanic bulla Sternocephalicus m.
Masseter m.
Stylohyoid and tympanohyoid bones
Sublingual salivary gland duct complex
Mandibular salivary gland
Figure 248-5 Medial retraction of the digastricus muscle and blunt dissection of the other soft tissues exposes the ventral bulla, which is opened with rongeurs, intramedullary pin, or bone trephine. The lingual and hypoglossal nerves are avoided. Image used by permission from Smith MM, Waldron DR. 1993. Atlas of Approaches for General Surgery of the Dog and Cat. Philadelphia: WB Saunders.
Figure 248-6 The large ventromedial compartment is usually opened first; opening the dorsolateral compartment requires penetration of the septum dividing the two compartments. Image used by permission from Smith MM, Waldron DR. 1993. Atlas of Approaches for General Surgery of the Dog and Cat. Philadelphia: WB Saunders.
629
SECTION 4: Surgery
Figure 248-7 Ventral view of the skull. The intact tympanic bulla is marked with TB. The bony defect allows entrance to the larger ventrodorsal chamber. The arrow points to an opening into the dorsolateral compartment. Photo courtesy of Dr. Gary D. Norsworthy.
Comments • Drain placement is not necessary in cats with polyp disease unless fluid is within the bulla. Ventral drainage may be indicated in animals with otitis media. See Figure 248-8. • Compartmentalization of the tympanic bulla is unique to the cat. Ventral bulla osteotomy usually exposes only the ventromedial compartment. Thorough exploration necessitates that the surgeon enter the dorsolateral compartment by removal of the bony septum that separates the two compartments. Failure to do so may result in recurrence of the nasopharyngeal polyp, which usually originates in the lining of the dorsolateral compartment.
630
Figure 248-8 Drain tubes exit the skin following ventral bulla osteotomy for otitis media. They are anchored with 4-0 rapidly dissolving suture material near the bulla so the proximal end of the drain tube is in the bulla. They are also anchored to the skin. They are removed when the deep suture dissolves (about 5–7 days). Drain tubes are not placed when the diagnosis is inflammatory polyps unless fluid is within the bulla. Photo courtesy of Dr. Gary D. Norsworthy.
• More than 80% of operated cats have clinical signs of Horner ’s syndrome following surgery as a result of trauma to the sympathetic nerves that traverse the septum between the two compartments. These clinical signs usually resolve within 30 days. See Chapter 99.
Suggested Readings Fossum TW. 2002. Surgery of the Ear. In TW Fossum, eds. Small Animal Surgery, 2nd ed., pp. 229–253. St. Louis: Mosby.
Chapter 249
Colectomy Don R. Waldron
Definition Subtotal colectomy is the surgical excision of most of the colon. The distal incision is made in the colon just proximal to the pubis, leaving enough of the colon for surgical manipulation. The proximal incision can be made in the distal ileum or in the proximal colon. See Figure 249-1. The former procedure is described in this chapter and is technically easier although there is disparity of intestinal lumens that must be anastomosed. The ileocolic valve is removed using this procedure. There are
advantages and disadvantages to both approaches. There is some evidence that the expected postsurgical diarrhea will resolve faster if the cecum is not removed.
Special Equipment • Abdominal retractors (Baby Balfour) • Baby Doyen intestinal clamps
Proximal Colon Incision Ileocolic a. Right colic a. Middle colic a. Ileum Incision
Colon
Ileal branch of ileocecal a.
Ileum
Left colic a.
Distal Colon Incision Caudal
Urinary bladder
Figure 249-1 The ileocolic, middle colic, and left colic arteries are isolated and doubly ligated in the mesocolon, and the mesocolon is incised. Note the two possible proximal incision sites and the distal incision site (arrows). Image used by permission from Smith MM, Waldron DR. 1993. Atlas of Approaches for General Surgery of the Dog and Cat. Philadelphia: WB Saunders.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
631
SECTION 4: Surgery
Overview and Indications Medical therapy of megacolon has been effective in some cases. See Chapter 136. Despite occasional success with medical management, the episodes of constipation and obstipation tend to occur at shorter intervals over time. Subtotal colectomy is the treatment of choice for most cats with idiopathic megacolon, especially those with recurrent or chronic constipation or obstipation. It has also been used successfully in cats with colonic obstruction due to pelvic canal obstruction caused by malunion of pelvic fractures. Other causes of colonic obstruction, including neoplasia and stricture, have been treated by subtotal colectomy. Abdominal radiographs are taken prior to surgery to evaluate the cat for abdominal masses, the presence of lumbosacral disease, and pelvic canal stricture. A digital rectal examination and an examination of the perineal area are indicated to rule out perineal hernia and ensure a normal perineal reflex. Manx cats may have spinal anomalies resulting in abnormal colonic motility and loss of perineal tone. See Chapter 134. Surgery in these cats is advised only with caution because the diarrhea that follows surgery may be accompanied by severe fecal incontinence. Generalized neurologic disease such as dysautonomia may cause constipation; however, this disease is rare. Preoperative blood work, including a calcium level, is indicated. Hypercalcemia from any cause may affect neuromuscular activity, thus affecting gastrointestinal motility. Although the disease is uncommon in cats, primary hyperparathyroidism has been reported to cause constipation. The surgical procedure is classified as a contaminated procedure; therefore, use of a perioperative antibiotic regimen effective against both gram-negative and anaerobic bacteria is indicated. Either cefovecin (8 mg/kg SC) or a combination of enrofloxacin (5 mg/kg SC or IM) and ampicillin (10–20 mg/kg IV, IM, SC) should be used.
Procedure • After general anesthesia is induced, digital removal of feces within the rectum is performed. It is important not to leave fecal masses in the rectum because postoperative straining to defecate may increase tension at the anastomotic site. See Figure 249-2. • Prophylactic antibiotics as mentioned above are administered beginning at anesthetic induction and continued for the first 24 hours postoperatively.
• The abdomen is approached by caudal ventral midline celiotomy with the incision made from umbilicus to pubis. • Moistened laparotomy pads are placed to protect the abdominal wall, and baby Balfour retractors are placed to maintain visualization of the abdominal cavity. • The bladder is emptied by cystocentesis if necessary, and the blood supply to the descending colon ligated with absorbable suture material. This will necessitate ligation of the ileocolic, middle colic, and left colic arteries. See Figure 249-1. • The mesentery is divided to the level of the distal ileum, staying close to the colon. • Feces are manually “milked” from the distal colon, and a baby Doyen forceps is applied to the distal colon 2 to 3 cm (3/4 to 1 1/4 in) rostral to the pelvic pubis. A “stay suture” of 2-0 suture material is placed in the colon just distal to the Doyen clamp. The distal colon retracts when cut, and the suture provides a means of handling the colon should it slip through the Doyen clamp. It is preferable to move the feces into the portion of the colon that will be removed if space permits. Moving hard stool into the rectum may result in straining to defecate postoperatively before adequate healing of the anastamosis site has occurred. • A second Doyen forceps is applied to the distal ileum. • Moistened laparotomy pads are placed to pack off the colon and decrease abdominal contamination. • Kelly or Carmalt forceps are applied to the colon to be resected, and the colon is divided between the Doyen and crushing forceps. • Luminal size disparity between the ileum and the remaining colon is partially corrected by incising the ileum on its antimesenteric border with Metzenbaum scissors (preferred method). This increases the diameter of the distal ileum. See Figure 249-3. Alternatively, the colon may be partially closed with simple interrupted sutures of polydioxanone. See Figure 249-4. If the colon is severely dilated, a combination of the two techniques may be required. • The ileum and colon are anastomosed using simple interrupted sutures of 3-0 or 4-0 polydioxanone. Preplacement of the first two to three sutures on the mesenteric border is advised. • The anastomosis is tested by infusion of the surgical site with saline injected under mild pressure. • Following closure of the abdomen, the rectum is again digitally cleared of any fecal matter.
Figure 249-2 Failure to remove hard feces from the distal colon or rectum prior to or during surgery will result in postoperative straining to defecate that may cause dehiscence of the anamostomis. Image courtesy of Dr. Gary D. Norsworthy.
632
(A)
(C)
(B) Figure 249-3 A, There will be significant disparity between the lumen of the ileum (yellow bracket) and the colon (green bracket). B, To approximate equality the ileum is incised on the antimesenteric border, and the resulting point of the flaps is excised. C, The ileum and colon are anastamosed with interrupted sutures of polydioxanone placing the first sutures at the antimesenteric and mesenteric borders. Reprinted with permission from Bojrab MJ. 1998. Current Techniques in Small Animal Surgery, 4th ed., pp. 251,263. Baltimore: Williams & Wilkins.The forceps shown in 249-3A have Doyen-type jaws, but their length is more appropriate for use in the feline patient. They are vascular clamps made for human use.
633
Colon
Ileum
Cranial rectal a. Caudal
(A)
(B) Figure 249-4 A, An alternative to the technique illustrated in Figure 249-3 is to partially oversew the colon as depicted. B, The result is shown. Image used by permissionfrom Smith MM, Waldron DR. 1993. Atlas of Approaches for General Surgery of the Dog and Cat. Philadelphia: WB Saunders.
634
Colectomy
Notes
Figure 249-5 This cat had a subtotal colectomy 7 months prior to this radiograph. Constipation was returning so a negative contrast cologram was performed. The distal colon had stretched. A second surgery was performed. Image courtesy of Dr. Gary D. Norsworthy.
• Significant postoperative complications occur in only 2% of cats that undergo subtotal colectomy and may include stricture at the surgical site, loss of vascularity to the bowel, and anastamosis dehiscence or peritonitis. Common, transient postoperative problems include tenesmus and diarrhea. • Tenesmus usually resolves within a few days of surgery. • Diarrhea usually resolves within 6 weeks of surgery (80% of the cats in one study), although it has been documented to persist for as long as 6 months. • A small number of cats may develop constipation weeks to months following surgery, but this usually responds to medical management. • Cats with pelvic strictures benefit from this surgery, but stool softening diets and medications are often also needed long term. • Rarely the colon will stretch within 6 to 12 months postoperatively. See Figure 249-5. If intractable constipation recurs, a second surgery may be needed.
Suggested Readings Bright RM. Subtotal colectomy in the cat. 1998. In MJ Bojrab, ed., Current Techniques in Small Animal Surgery, 4th ed., pp. 272–276. Baltimore: Williams & Wilkins.
635
Chapter 250
Corneal Surgery Gwen H. Sila
Conjunctival Pedicle Graft Definition This procedure is indicated to provide mechanical support and a blood supply to a deep corneal ulcer or corneal rupture. A conjunctival pedicle graft (CPG) should be considered for ulcers that are 50% or greater depth into the cornea.
Equipment • Corneal surgery pack including fine, straight Bishop-Harmon forceps, curved needle holder such as Barraquer or Castroviejo, Stevens curved tenotomy scissors, eyelid speculum, Beaver Blade handle, and Colibri forceps. • Number 64 Beaver Blade • Cellulose sponge eye spears • Viscoelastic (i.e., sodium hyaluronate or hydroxypropylmethyl cellulose) • Operating microscope • 7-0 or 8-0 Vicryl®
Procedure • The eyelids are carefully clipped, and the eye and eyelids are flushed alternatively with saline and dilute (5%) povidone iodine solution. Care should be taken to flush the conjunctival fornices well. • A drop of 1% tropicamide then 2.5% phenylephrine are each administered 5 minutes apart. • The cat is positioned in dorsal recumbency with the plane of the cornea to be operated parallel with the floor. If the cornea is not central in the palpebral fissure due to anesthesia then neuromuscular blockade (pancuronium 0.022 mg/kg IV) is indicated as long as adequate ventilation can be maintained. • The microscope is focused on the cornea. The conjunctiva is grasped with the Bishop-Harmon forceps 2 to 3 mm from the limbus and 2 to 3 mm ventral to the ulcerated region. See Figure 250-1. Using the tenotomy scissors a small incision is made in the conjunctiva perpendicular to the limbus. • While holding the more dorsal aspect of the incised conjunctiva with the forceps, the conjunctiva is undermined using blunt dissection with the tenotomy scissors. Care should be taken to avoid undermining significant amounts of Tenon’s capsule (the thicker, white episcleral tissue) with the conjunctiva. • The conjunctiva is incised starting at the initial incision moving dorsally along the length of conjunctiva already undermined. This cut should be approximately 0.5 to 1 mm away from the limbus and follow the limbal curvature. • A second cut should be made in the conjunctiva again starting from the initial incision and moving dorsally. This incision should also follow the general curvature of the limbus and should be a distance
Figure 250-1 The dotted blue line shows the outline of the harvested graft. The graft is shown after it has been swung into position over the central cornea and sutured into place covering the deep ulcer beneath it.
•
•
• •
•
from the limbus that is 1 to 2 mm greater than the ulcer ’s horizontal diameter. This process of undermining conjunctiva and cutting is continued to the level of the dorsal cornea. Ideally the conjunctival flap should be slightly wider at its base then more distally. Once the graft is harvested, the cellulose spears are used to carefully wipe away any epithelium from the ulcer ’s edges. Care should be taken not to rupture the eye during this procedure, but if this does occur the anterior chamber should be inflated with the viscoelastic to facilitate suturing. It is important to prevent touching the iris and lens with the viscoelastic cannula. Using the Colibri forceps the conjunctival graft should be placed over the ulcer. The graft is now ready to be sutured into place. The sutures should pass full-thickness through the graft and to approximately 75% depth of the cornea. The suture bites into the cornea should be 1 to 2 mm in length. Sutures should be placed 1 to 2 mm apart from each other around the graft’s edge over the ulcerated region. A temporary tarsorrhaphy suture can be placed at the end of surgery for protection. See Chapter 72.
Postsurgical Complications The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
636
• Graft Dehiscence: This may result from excessive tension on the graft, regrowth of epithelium down into the ulcer, excessive surgical trauma to the conjunctiva, and melting of the ulcer around the graft.
Corneal Surgery
Depending on when this occurs, the graft may need to be replaced or a new graft may need to be harvested and sutured into place. • Loss of Vision: Depending on its size, the graft can interfere significantly with the visual axis. Cats are remarkable in their ability to remodel their cornea, so even a large graft can potentially thin enough with time to allow functional vision. • Loss of the Eye: In general, if corneal rupture is present less than 24 to 48 hours prior to surgery prognosis for saving the globe with a CPG is fair to good. Prognosis for vision is much more guarded as globe rupture often results in significant inflammation inside the globe and adhesions of the iris to either the cornea or lens. When globe rupture is not present, the prognosis for saving the eye is excellent, and the prognosis for vision correlates with size of the graft placed (e.g., smaller size graft has better potential for vision around the graft).
Keratectomy Definition This procedure is indicated to remove a portion of the cornea due to either the presence of a foreign body, corneal sequestrum, or because a biopsy is indicated.
Equipment • Small corneal surgery pack including fine, straight Bishop-Harmon forceps, eyelid speculum, Beaver Blade handle, and Colibri forceps. • Number 64 Beaver Blade • Corneal dissector (optional) • Operating microscope
Procedure • The eyelids are carefully clipped, and the eye and eyelids are flushed alternatively with saline and dilute (5%) povidone iodine solution. Care should be taken to flush the conjunctival fornices well.
• The cat is positioned in dorsal recumbency with the plane of the cornea to be operated parallel with the floor. If the cornea is not central in the palpebral fissure due to anesthesia, neuromuscular blockade (pancuronium 0.022 mg/kg IV) is indicated as long as adequate ventilation can be maintained. • The microscope is focused on the cornea. Four cuts are made in a rectangular shape around the lesion to be removed using the number 64 Beaver Blade. The cuts should be just deeper than the lesion itself but obviously not full thickness. • One corner of the rectangle is grasped with Colibri forceps and the Beaver Blade is used to gently undermine the corner. The undermining is continued in the same plane of cornea using either the Beaver Blade or corneal dissector until the rectangular piece of cornea is free. If the piece of cornea removed is greater than 50% depth, a CPG should be placed to provide support and a blood supply. • A tarsorrhaphy suture (see Chapter 72) may also be placed to provide protection to the cornea.
Postsurgical Complications • Corneal Infection: Because the epithelium is being removed, bacteria can invade into the corneal stroma and set up an infection. Prophylactic broad-spectrum topical antibiotic therapy is recommended at least four times daily until the corneal wound has healed. • Corneal Scarring: Because corneal stroma is removed with this procedure, fibroblasts must elaborate to fill the defect. This can create a white scar on the cornea. Additionally, blood vessels may grow into the cornea during the healing process. In most cases scarring and neovascularization will decrease with time as the cornea remodels itself. Because of the potential for latent herpesvirus reactivation, topical steroids are not recommended to speed up this process.
Suggested Readings Maggs, DJ. 2008. Cornea and Sclera. In D Maggs, P Miller, R Ofri, eds., Slatter ’s Fundamentals of Veterinary Ophthalmology, 4th ed., pp. 175–202. St. Louis: Elsevier Saunders.
637
CHAPTER 251
Cranial Cruciate Ligament Rupture Mac Maxwell
Definition The cranial cruciate ligament (CrCL) originates from the medial aspect of the lateral femoral condyle and courses cranially and distally to its insertion point on the tibia. It acts to prevent excessive cranial translation and internal rotation of the tibia relative to the femur. Rupture of the ligament can be complete or partial in cats and frequently results in acute lameness, stifle pain, and joint effusion. The lameness can vary from mild to nonweight bearing in cats. In contrast to canine CrCL ruptures, feline cruciate tears are frequently traumatic in origin and may involve other ligamentous damage (deranged stifle). Other frequent injuries in cats with polytrauma include rupture of the caudal cruciate and the medial collateral ligament. Anatomical differences do exist between species with the cranial cruciate being larger than the caudal cruciate in cats.
Surgical Management • Surgical treatment of stifle instability in cats can be performed by extracapsular stabilization via a lateral suture from the fabella to the proximal aspect of the tibial tuberosity. Intracapsular techniques have also been used in cats. Other techniques, such as tibial plateau leveling osteotomy (TPLO) have also been used successfully in cats but require specialized equipment to perform appropriately. Advanced procedures, such as the TPLO, may be more indicated in patients with excessive tibial plateau slope. Surgical management in general is primarily reserved for those patients who fail to respond to medical management or obese cats that are reluctant to ambulate.
Equipment Diagnosis • Physical Examination: The diagnosis of a CrCL rupture is mainly based on history and physical examination findings. Physical examination findings consistent with a CrCL rupture include a positive cranial drawer test and positive tibial compression test. Additional findings that may be present include joint effusion, a meniscal “click” during flexion and extension of the affected leg, and thickening of the joint capsule (medial buttress). Because a majority of feline cruciate ruptures are traumatic in origin, additional ligamentous damage may be present. Structures typically damaged within the stifle include the CrCL, caudal cruciate ligament, and medial collateral ligament. • Radiographs: Radiographs of the stifle often show joint effusion with or without signs of osteoarthritis. Additional radiographic findings include ossification of the insertion of the CrCL on the cranial aspect of the tibia as well as mineralization of the meniscus. Although mineralization occurs infrequently, it appears to be more common in the cat. • Careful palpation of the stifle should be performed under heavy sedation or anesthesia to determine the extent of ligamentous damage. Comparison to the unaffected limb may be beneficial to help determine normal for that particular patient.
Conservative Management • Conservative treatment of CrCL rupture involves activity restriction for a period of 4 to 6 weeks. Cases of nontraumatic ligament rupture occur frequently in overweight cats, and a weight reduction diet may be beneficial. The prognosis for return to normal function depends on many factors, but some cats exhibit pain-free function in 4 to 5 weeks. In patients that are overweight, have failed conservative management, or have conformational abnormalities (high degree of tibial plateau angle slope), surgical repair is indicated. Failed conservative management often leads to irreversible degenerative joint disease so this approach should be taken with informed consent of the owner. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
638
• • • •
Routine surgical pack Hohmann retractor or equivalent 1/16-in Steinmann pin in a Jacob’s chuck Number 2 nylon monofilament suture or 20-lb nylon leader line.
Procedure • After the induction of general anesthesia, the patient is clipped, aseptically prepped, and positioned in dorsal recumbency. A four-quarter draping technique, with hanging leg preparation, is also performed to allow for stifle manipulation during the procedure. • Perioperative antibiotics are given at anesthetic induction. • A skin incision, medial or lateral depending on surgeon preference, is performed followed by a lateral parapatellar arthrotomy. • The stifle joint is flushed and visually inspected, with the aid of a Hohmann retractor, to identify the cruciate ligament remnants and menisci. Remaining strands of the cruciate, as well as any meniscal tears, are removed using a mosquito hemostat and a number 11 blade. • The fascia of the biceps femoris muscle is elevated from the joint capsule to allow palpation of the lateral fabella. The fabella can be palpated just proximal and caudal to the lateral femoral condyle. • Suture is then passed around the lateral fabella taking care not to entrap surrounding soft tissue or the peroneal nerve. Once passed, the suture is tested for stability by pulling on both ends of the suture. If placed appropriately the suture should not give or slip distally beneath the fabella. • To place the suture distally, the cranial tibialis muscle is elevated from the lateral aspect of the tibial tuberosity. A hole is then drilled through the proximal aspect of the tibial tuberosity. • The suture is passed under the patellar tendon, through the hole in the tuberosity, and secured to the other end of the suture. • To tighten the suture the stifle is placed in flexion and tibia is slightly externally rotated. The suture is tied with a slip-knot followed by thee to four square knots. See Figure 251-1. • Closure is routine as the joint capsule is apposed with a simple continuous pattern followed by apposition (or imbrication) of the fascial layer. • Following surgical correction the patient should be kept indoors for 4 to 6 weeks.
Cranial Cruciate Ligament Rupture
Figure 251-1 Suture is passed around the lateral fabella taking care not to entrap surrounding soft tissue or the peroneal nerve. The cranial tibialis muscle is elevated from the lateral aspect of the tibial tuberosity. A hole is then drilled through the proximal aspect of the tibial tuberosity. The suture is passed under the patellar tendon, through the hole in the tuberosity, and secured to the other end of the suture.
Prognosis Cats managed with conservative treatment frequently return to pain free use in 4 to 5 weeks. A recent study also shows comparable, and possibly more predictable outcome, in cats treated with extracapsular stabilization.
Harasen GLG. 2005. Feline cranial cruciate ligament rupture: 17 Cases and a review of the literature. Vet Comp Orthop Traumatol. 18(4):254–257. Hoots EA, Peterson SW. 2005. Tibial plateau leveling osteotomy and cranial closing wedge ostectomy in a cat with cranial cruciate ligament rupture. J Am Anim Hosp Assoc. 41:395–399.
Suggested Readings McLaughlin R. Cranial Cruciate Ligament Injuries. 2007. In HW Scott, R McLaughlin, eds., Feline Orthopedics, pp. 222–225. London: Mason Publishing.
639
CHAPTER 252
Cryptorchidism Surgery Mac Maxwell
Definition Cryptorchidism is the failure of the testicle to descend into the scrotum shortly after birth. The incidence of cryptorchidism in cats is reported to be around 2%. Monorchidism is a rare occurrence and is reportedly 0.1%. The testicles are typically pulled through the inguinal ring early in life due to fibrosis and subsequent contraction of the gubernaculum. Testes that do not descend within the first 2 months of life are unlikely to do so. The condition can affect one or both testicles, but unilateral cryptorchism is more common. Cryptorchid testes can be located inside or outside the abdominal cavity. In one study, all cats with bilateral cryptorchism were located intra-abdominally. If located outside the abdomen, the testicle is between the inguinal ring and the scrotum. The appearance of cryptorchid testicle is usually abnormal as they are usually soft, small, and irregularly shaped. Persian cats may be predisposed to the condition.
Inguinal Testicles • Inguinal testicles are removed by a caudal ventral midline incision to allow for exploration of the inguinal area. Careful dissection should be undertaken to avoid damage to the pudendoepigastric artery and vein. Once the testicle is identified it should be removed as previously described.
Diagnosis • Physical Examination: The absence of both testes in the scrotum by 2 months of age is considered cryptorchidism. • Ectopic testes can be located in several locations. Physical examination should include careful palpation of the scrotum, inguinal area, and abdominal cavity. Because cryptorchid testicles are often atrophied and difficult to palpate, ultrasonography may be beneficial in determining the correct side and location of the teste. In cats, the large amount of inguinal fat can make it especially difficult to palpate. • A complete blood count and biochemistry panel should be performed prior to anesthesia to evaluate for other systemic problems including the potential bone marrow suppression associated with hyperestrogenism (Sertoli cell tumor).
Procedure • The treatment of ectopic testes in cats involves the removal of both testes via a surgical approach. Testes may be located in the prescrotal area, inguinal area, or intra-abdominally. The location of the affected testicle determines the surgical approach. • Caudally directed traction on the scrotal testicle during these procedures will help to lateralize the retained testicle.
Prescrotal Testicles • In thin or mature cats the testicle may be palpable. If so, incise directly over the testicle in the same manner as performed for a routine castration. Expose the testicle, vas deferens, and associated vasculature. Triple ligate the vessels and the vas deferens with 2-0 or 3-0 polydiaxanone. Incise between the two most distal sutures and remove the testicle. • Close the subcutaneous tissue and skin in routine fashion.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
640
Figure 252-1 The relevant anatomical structures for cryptorchid surgery are the urinary bladder (B), ureter (U), and ductus deferens (DD). Used with permission from Dr. L.C. Hudson and W.P. Hamilton.
Cryptorchidism Surgery
Abdominal Testicles • If the testicle is not found within the inguinal area the incision should be extended cranially and caudally to allow for a ventral midline celiotomy. • Retract the urinary bladder ventrally or caudally for identification of the ductus deferens. Follow this structure to the testicle using gentle traction. See Figures 252-1, 252-2, and 252-3. • Once the testicle is definitively identified remove as previously described. • Rarely, the testicle could be located within the inguinal ring. Careful dissection in the area to avoid the pudendal vasculature is essential. • Gentle traction applied to the testicle should allow for it movement into the subcutaneous space. • Alternatively, the inguinal ring may be widened to allow for retraction into the abdominal cavity. The removal of testes through keyhole incisions and a spay hook is not recommended due to the potential for ureteral damage. • If the testicle is not located gently pull on the ductus deferens while watching for movement in the prescrotal area. Incise over the area of movement until the testicle is located. See Figure 252-4. • Laparoscopic-assisted cryptorchidectomy has been described in cats and represents a minimally invasive approach to treating the condition.
Figure 252-3 Traction on the ductus deferens should lead to the testicle. If the testicle is intra-abdominal, it will be exposed easily for removal. If it is trapped in the inguinal ring or is outside the inguinal ring, the testicle may not be mobilized. If that occurs, trace the ductus deferens to the inguinal ring and open the inguinal ring. If the testicle is trapped in the inguinal ring, open the latter to expose the testicle.
Therapeutic Notes • Cryptorchidism is believed to be hereditary, and both testicles should be removed. Breeding of an affected cat is discouraged. • A cat with an intraabdominal testicle will be infertile in the retained testicle only due to the increased temperature within the abdomen as compared to the scrotum. • Failure to remove a retained testicle, regardless of location, will permit continued testosterone production and the development of or perpetuation of tom cat characteristics (i.e., strong smelling urine, aggression, territoriality, attraction to female cats in estrus, copulation, large cheeks and neck, and thickened skin). • Although presumably less frequent than the canine counterparts, cats have been reported to develop teratomas or Sertoli cell tumors of retained testicles.
Figure 252-4 If the testicle is outside the inguinal ring, a skin incision in the inguinal area will be needed to expose the testicle. Continued traction on the ductus deferens from within the abdomen will be helpful in identifying it.
Prognosis The prognosis for cryptorchid cats is good with surgical removal. Neoplastic conditions that affect the retained testicle can worsen the prognosis depending on the histopathological diagnosis.
Suggested Readings Figure 252-2 An intra-abdominal testicle can be located by identifying the ductus deferens on the appropriate side. The urinary bladder should be emptied then retracted or compressed to aid identification of the ductus deferens.
Birchard SJ, Nappier M. 2008. Cryptorchism. Compendium. 30:325–337. Millis DL, Hauptman JG, Johnson A. 1992. Cryptorchidism and monorchidism in cats: 25 cases (1980–1989). J Am Vet Med Assoc. 200(8): 1128–1130.
641
CHAPTER 253
Esophagostomy Tube Placement Gary D. Norsworthy
Definition The esophagostomy tube (e-tube) is a flexible tube that is placed through the skin on the left side of the neck and advanced into the esophagus. The distal end remains in the mid to lower esophagus. It is not placed into the stomach to prevent gastric acid reflux into the esophagus with resulting esophagitis. Its purpose is to permit an owner to feed an anorectic cat for prolonged periods of time. It is well tolerated by cats, requires minimal maintenance, and has few complications. It may be removed in as few as 3 days after placement, or it may remain in place for several weeks to months.
Equipment and Sources • 14 French esophagostomy tube (DVM Solutions, www.dvmsolutions. com) • Stylet the length of the e-tube • 18-cm (7-in) curved hemostatic forceps • Needle holder • Thumb forceps • Scalpel with number 10 blade • 45 cm (18 inches) of soft nonabsorbable suture material • 2.5-cm (1-in) adhesive tape • No Sting Barrier Spray™ (3M Animal Health, Minneapolis, MN)
Indications • Any disease-causing prolonged anorexia in a cat that can otherwise wholly or partially be treated at home. Examples include hepatic lipidosis, neoplasia with chemotherapy, systemic fungal diseases, oral disease, and traumatic injuries resulting in sloughing of tissue.
• If the e-tube has a closed tip, the tip is cut off so food can exit the end of the tube. • Lay the tube on the cat’s chest wall to simulate its position in the esophagus and the point at which it will exit the ostomy site. • With a black marker pen, mark the tube where it should exit the ostomy site with the tip about the level of the 10th rib. • The stylet is placed into the tube. It is important that it be placed at the distal end of the tube but that it not protrudes from it. • Hemostatic forceps are inserted through the oropharynx into the esophagus so the curved tip is pointing laterally. The tip is positioned about 2.5 cm (1 inch) cranial to the shoulder joint. An 18 cm (7 inch) hemostat is needed to reach this location in most cats. Putting cranially directed tension on the cat’s head helps to pass the forceps smoothly. See Figure 253-1. • A scalpel is used to cut over the tip of the hemostat. The jugular vein should be identified. The incision should be 1 to 2 cm (3/8 to 3/4 in) dorsal to it. An incision is made through the skin, underlying muscle, and esophageal wall, thus exposing the tip of the hemostats. The final layer of tissue is transparent and is best incised by opening the jaws of the hemostat and cutting between them. The incision should be just large enough to permit exit of the tips of the hemostat. See Figure 253-2. • The jaws of the hemostats are opened enough to grasp the distal end of the tube containing the stylet. See Figure 253-3. • The tube and stylet are pulled cranially so they are about 2.5 cm (1 in) into the esophagus. • The jaws of the hemostats are opened, and the hemostats removed from the cat.
Contraindications • Any disease in which enteral feeding is contraindicated. Examples include rupture or obstruction of the gastrointestinal tract. • Diseases of the esophagus, which would be aggravated by the presence of food or the tube in the esophagus. Examples include esophagitis, esophageal foreign body, or megaesophagus.
Procedure • General anesthesia is induced. Choose an agent that will permit rapid recovery as many of these patients recover slowly from some anesthetic agents due to their illness. Sevoflurane and isoflurane by mask or induction chamber with subsequent intubation are this author ’s choices. • The cat is placed in right lateral recumbency. • The esophagus is located off the midline to the left in the cervical region. Therefore, the hair on the left side of the neck is shaved, and the area prepped for surgery.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
642
Figure 253-1 The 18-cm (7-in) curved forceps is passed through the oropharynx down the esophagus to a point just cranial to the point of the shoulder. Its tip is under the surgeon’s right index finger. The surgeon’s left index finger points to the jugular vein.
Esophagostomy Tube Placement
Figure 253-2 A scalpel is used to cut through the skin, muscle, and esophageal wall allowing the tip of the forceps to exit the skin.
Figure 253-4 After pulling the tube into the esophagus, the forceps are released and removed. The tube is redirected caudally and advanced about 2.5 cm (1 in) before the stylet is removed and the tube advanced further into the esophagus.
Figure 253-3 The forceps are used to grasp the end of the tube and its stylet.
Figure 253-5 The tube is shown after placement. The black mark can be seen near the ostomy site.
• Traction is again placed on the cat’s head, extending the neck and straightening the esophagus. • Next, the proximal end of the e-tube/stylet is directed cranially so the distal end can rotate and become directed caudally. It is advanced about 2.5 cm (1 in) caudally in the esophagus. See Figure 253-4. • The tube is pushed caudally as the stylet is pulled cranially. This advances the e-tube into the esophagus as it removes the stylet. The e-tube is advanced until the distil tip is about the level of the 10th rib; the previously made black mark should be at the ostomy site. Generally, about 5 cm (2 in) of the tube exits the skin. See Figure 253-5. • A purse-string suture is placed through the skin and around the e-tube at the ostomy site. A knot is tied in the center of the suture material so that two long ends remain. The needle is cut off the suture material before the knot is tied.
• The two long ends of the suture material are used to make a Chinese Finger Trap around the e-tube. Three passes are adequate. • The tube is routed to the dorsal midline. Care should be taken not to bend the tube sharply. See Figure 253-6. • The plastic fitting is encircled with the adhesive tape. This is important because tape will not adhere to a silastic tube for more than a few days. • Adhesive tape is used to encircle the neck to secure the e-tube to the neck. Do not get the tape so tight that the cat is uncomfortable. It is important that all of the e-tube except the plastic fitting be covered so the cat cannot get its foot in a loop of e-tube and pull it out. See Figure 253-7. A final covering with a colored elastic bandage is often more appealing to the owner than the adhesive tape. However, do not omit the adhesive tape because the main part of the bandage needs to adhere to the skin.
643
SECTION 4: Surgery
• Instruct the owner to inject the food at 1 to 2 mL per second. If the cat appears to become nauseated, the feeding rate should be slowed. • The tube should be flushed with 2 to 3 mL of water following feeding to clear food from the tube and prevent obstruction.
Maintenance The tape (not the tube) should be changed about every 2 weeks. There may be discharge around the ostomy site that needs to be removed, and often the owner will get food on the tape. The tape is cut along the right side of the neck to avoid cutting the e-tube. It is peeled off of the hair and skin and from around the tube. The area is cleaned with hydrogen peroxide if needed. No Sting Barrier Spray™ is again applied to the nonhaired skin, and triple antibiotic ointment is applied to the ostomy site. Tape is reapplied as it was done previously.
Figure 253-6 After the purse string suture and Chinese finger trap have been created, route the tube to the dorsal midline for taping. This picture shows the beginning of the taping process.
Figure 253-7 The taping is completed when only the end of the tube protrudes from under the tape. This protects the tube from dislodgement when the cat scratches at it. The tape can be covered by other bandaging material for cosmesis, but the tape is essential for secure anchoring of the bandage
Feeding Process • Typically, one or two persons are needed to feed the cat. The most noteworthy complication is a consequence of injecting too large a food volume into the esophagus at one time. The limited distensibility of the esophagus must be recognized or there is a risk of regurgitation and aspiration of food into the lungs. Therefore, the following measures are recommended: • Dispense several 12-mL syringes for feeding. This limits the amount of food that can be injected at one time. In the time it takes to remove the empty syringe and replace it with a full one, the first aliquot of food will have a chance to enter the stomach. • Have the owner elevate the cat’s cranial end when injecting food. This may be accomplished by putting the cat’s front feet in the owner ’s hand and lifting the feet off the table 8 to 10 cm (3–4 in) while the food is being injected or by putting a rolled up bath towel under the cat’s chest with its rear feet on the table.
644
Complications • No food, water, or liquid medication should be given by mouth for two days to allow the esophageal wall to adhere to the muscle and skin thus creating a fistula that prevents food and liquids from leaking out of the esophagus into the surrounding tissues. Likewise, the tube should not be removed less than 2 days after placement. • The tube may become obstructed if the food mixture is too thick. Blenderized diets should be poured through a kitchen strainer before attempting to syringe them through an e-tube. My preferred tube feeding diet is Iams Maximum-Calorie™ (The Iams Company, Dayton, OH). With this product straining is not needed. • If an obstruction occurs within the e-tube, it is most likely in the plastic fitting because that is the narrowest part of the apparatus. This fitting can be pulled out of the e-tube and cleared without removing the e-tube. If the obstruction is in the tube itself, flushing with 2 mL of a carbonated cola drink may dissolve dried food. If not, the tube must be removed and replaced. • Food should be about body temperature. If it is cold, it will be very difficult to syringe it through the tube, and it is likely to induce vomiting. • Vomiting will occur immediately after feeding if too much food is fed at one time. If this occurs, reduce the quantity of each feeding. A cat with severe hepatic lipidosis may have a stomach capacity of as little as 15 mL. • Some cats become obsessed with the e-tube and will scratch at it violently enough to get it out. Fortunately, this is uncommon. A short Elizabethan collar can be helpful in some of these cats. If this happens and the tube has been in several weeks, there is a good chance the cat is ready to eat. Offer food for 1 or 2 days before replacing the tube. • Infection can occur at the ostomy site. If this happens, the site is cleaned with hydrogen peroxide, and a triple antibiotic ointment is applied to the site. A liquid, systemic antibiotic, such as amoxicillin, is dispensed. It can be injected down the e-tube for easy administration. • Rarely, a cat will vomit violently enough to expel the e-tube out the mouth. The distal end of the tube will be chewed off so that the cat is presented with the part of the tube in the pharynx still attached to the proximal part. It must be removed and replaced. It should be noted that properly placed e-tubes do not cause vomiting. However, many diseases being treated with this tube may do so. • If the e-tube exits the esophagus prior to passing it caudally down the esophagus, resistance will be met because there is no place for the tube to go. If there is concern about possible misplacement, inject 2 mL of an aqueous contrast material approved for intravenous use through the tube and take radiographs. Do not use barium because it causes severe inflammation if placed in the subcutaneous tissues.
Esophagostomy Tube Placement
• Rarely, the incision through the muscle will occur adjacent to a peripheral nerve. This will create pain in the left front leg, and the cat may become nonweight bearing. If this occurs, the e-tube should be removed and replaced a few days later in a different location. • When this tube was devised in the late 1980s, there was great concern about the development of esophageal strictures forming following e-tube removal. However, that has not been reported. I have placed several hundred of these tubes over 20 years and never seen an esophageal stricture related to an esophagostomy tube.
E-Tube Removal • Because an e-tube will not prevent proper swallowing, cats can eat with this tube in place. Food should be offered periodically to determine when the appetite returns. However, do not remove the tube
until the cat has been eating for at least 2 days because some cats have false starts regarding eating. • The tape and suture are cut. The tube is removed; anesthesia is not required. The ostomy is not sutured. It will granulate closed within 2 to 3 days and should not require care during that process.
Selected Readings Crowe DT. 1990. Nutritional support for the hospitalized patient: An introduction to tube feeding. Compend Contin Educ Pract Vet. 12:1711–1715. Fossum TW. 2002. Postoperative Care of the Surgical Patient. In TW Fossum, ed., Small Animal Surgery, 2nd ed., 69–91. St. Louis: Mosby. Norsworthy GD. 1991. Providing nutritional support for anorectic cats. Vet Med. 86:589–598.
645
CHAPTER 254
Frontal Sinus Obliteration Gary D. Norsworthy
Equipment • Routine surgery pack • Stainless steel intramedullary pin and driver • Penrose drain tube, approximately 1 cm (3/8 in) diameter
• If sinusitis is bilateral, the other sinus is opened and cleaned in the same manner. • The intramedullary pin is used to make a hole in the bony septum between the two frontal sinuses. See Figure 254-4.
Definition Frontal sinus obliteration is removal of the air-filled frontal sinuses because of chronic sinusitis.
Overview and Indications The paired frontal sinuses are air filled structures located within the right and left frontal bones dorsal to the eyes. They are separated by a bony septum on the midline. They communicate with the left and right halves of the nasal cavity through a pair of ostia, which permits infections or tumors that originate from the nasal cavity to ascend into the frontal sinuses. Once infected, systemic antibiotic therapy is ineffective in clearing the sinusitis because they become virtually avascular dead spaces. Frontal sinus trephination and flushing, obliteration with fat grafts, and obliteration with methylmethacrylate implants have been used to treat frontal sinusitis. Temporary response often occurs, but long-term results are usually disappointing or produce complications. The procedure presented in this chapter permits infection removal on a long-term basis without fear of implant rejection, a problem in the other techniques. Although this technique has been successful for treating sinusitis, it does not offer a cure for the often underlying chronic rhinitis; therefore the owner ’s expectations must be realistic. See Chapter 147.
Figure 254-1 The skin incision (solid line) is made midway between a line drawn between the medial origins of the pinnae and the lateral canthi of the eyes (dashed lines).
Procedure • The dorsum of the skull is prepared for aseptic surgery. • A line is drawn between the medial origins of the pinnae. Another line is drawn between the lateral canthi of the eyes. See Figure 254-1. • A 2.5-cm (1-in) skin incision is made between the above two lines. • A hole is created in the frontal bone about 0.5 cm (3/16 in) using a small intramedullary pin, such as a 0.062 K-wire. The pin should enter the frontal sinus. See Figure 254-2. • Bone rongeurs are used to enlarge the bony defect to about 0.75 cm (5/16 in) in diameter. The opening should be large enough to permit curettage with a cotton-tipped applicator and vigorous flushing. An aerobic culture should be performed on the material within the sinus. See Figure 254-3.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
646
Figure 254-2 A hole is drilled through the frontal bone directly ventral to the skin incision and about 0.5 cm (0.25 in) off the midline. There may be some anatomical variation between cats. When in doubt about the location for drilling, it is better to be too far rostral than too far caudal.
Frontal Sinus Obliteration
Figure 254-3 Rongeurs are used to enlarge the hole to permit removal of the purulent material with a cotton-tipped applicator. Aerobic and anaerobic cultures are taken from the sinus then vigorous flushing with saline is performed to remove as much purulent material as possible.
Figure 254-5 The drain tube is passed through the septal hole and out the holes in the frontal bones.
Figure 254-6
The drain tube is anchored to the skin, and the skin incision is closed.
Figure 254-4 The intramedullary pin is used to create a hole between the two frontal sinuses large enough for the drain tube.
• A Penrose drain tube is passed through the septal hole so it exits both frontal sinuses and the skin. See Figure 254-5. • The drain tube is anchored to the skin, and the skin is closed with 4-0 dissolvable suture material. See Figure 254-6.
Notes • The drain tube is removed in about 5 to 7 days. See Figure 254-7.
Figure 254-7 The drain tube is removed 5 to 7 days postoperatively. This picture shows the cat at 10 days post-operation.
647
SECTION 4: Surgery
Figure 254-8 This shows the cat at 6 weeks post-operation. The sinuses have filled with granulation tissue, and the openings through the skin have granulated closed. Hair has regrown resulting in excellent cosmesis.
• The frontal sinus fills with granulation tissue, and the skin defect granulates closed after about 4 to 6 weeks. The owner must be warned of the appearance of the cat’s head during the healing process. • Excellent cosmesis results. See Figure 254-8.
648
Suggested Readings Norsworthy GD. 1993. Selected surgical procedures. In GD Norsworthy, ed., Feline Practice, pp. 477–503. Philadelphia: J B Lippincott.
CHAPTER 255
Gastrostomy Tube Placement Don R. Waldron
Definition A gastrostomy tube is a surgically implanted feeding tube that permits short- or long-term feeding to provide the nutritional needs to the ill or anorectic cat. Gastrostomy tubes are placed surgically during ventral midline celiotomy for a primary disease process or during exploratory celiotomy, or they may be placed by a limited left lateral paracostal approach. The procedure described here is by midline celiotomy. Gastrostomy tube placement may also be performed without surgery by means of an endoscope (percutaneous endoscopic gastrostomy [PEG] tube) or with a specialized Eld™ feeding tube applicator. In many cases, esophagostomy tube placement is simpler and easier than PEG or Eld™ gastrostomy tube placement.
Indications • Gastrostomy tubes are especially useful in cats with prolonged anorexia from any cause. • Gastrostomy tubes provide the means for hospital personnel or owners to provide the ill or injured cat with its nutritional needs over time. • Gastrostomy tubes serve as a means of gastropexy for cats that have had surgical repair of hiatal hernia.
Equipment • A 16, 18, or 20-French Pezzar™ catheter, a 10- or 12-French Foley catheter, or a low profile gastrostomy tube (VIASYS Medsystems, Wheeling,Il). See Figure 255-1.
Figure 255-2 A mushroom tipped (Pezzar™) catheter has been routed through the left abdominal wall and placed through a preplaced purse-string suture in the stomach (S). The purse-string is placed mid-way between the greater and lesser curvatures of the stomach. Additional pexy sutures are placed between the gastric and abdominal walls to support the stomach. The liver (L) is seen cranial to the stomach.
Procedure • The abdomen is approached with a ventral midline incision large enough to accomplish the primary surgical procedure. • A purse-string absorbable suture is placed in the gastric fundus midway between the greater and lesser curvatures of the stomach. • The feeding tube is brought into the abdominal cavity through a small stab incision in the left ventrolateral abdominal wall caudal to the last rib. • A stab incision is made with a scalpel in the middle of the pursestring suture, and the tube is advanced into the gastric lumen. See Figure 255-2. • The purse-string suture is tied to secure the tube. • Four supporting gastropexy sutures are preplaced between the gastric and abdominal walls with absorbable or nonabsorbable suture material. • Traction is placed on the gastric tube to bring the stomach into apposition with the left lateral abdominal wall, and the preplaced sutures are tied. • The abdomen is closed in routine fashion, and the gastric tube is secured by a Chinese finger trap suture to the skin, capped, and loosely bandaged.
Notes
Figure 255-1 A low profile gastrostomy tube is seen prior to placement. The pointed tip is placed in the gastric lumen. The flared portion (grasped by the surgeon) is external and sutured to the skin. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
• The mushroom-tipped Pezzar™ catheter is preferred for its durability and ease of feeding. • Cats are fed approximately 20 to 30 mL q8h, adding 10 to 15 mL to each feeding on subsequent days until 50 to 60 mL is fed three times per day. A commercial intensive care-type diet with the consistency of baby food or blenderized cat food may be used. The cat may vomit if too much food is administered or if food is infused too quickly. Refrigerated food is warmed before administration, and the tube is
649
SECTION 4: Surgery
• •
• • •
flushed before and after each use with warm water to prevent clogging. Gastrostomy tubes should remain in place at least 7 to 10 days even if the cat begins to eat. Pezzar™ tube removal is performed under sedation. The tube is cut off 5 cm from the body wall, and a stiff metal probe is inserted into the catheter. Traction on the catheter and simultaneous advancement of the probe assists in flattening the mushroom tip, enabling removal of the tube through the body wall stoma. Low profile gastrostomy tubes are removed in a similar manner. The stoma is allowed to heal by second intention. Some cats have been fed without major complication for months to years with gastrostomy tubes. Low profile gastrostomy tubes are much less awkward and offer the patient and owner increased ease of feeding and maintenance if the feeding tube is to be maintained months or years.
650
Complications • Local skin irritation at the tube stoma is not uncommon. • Inadvertent tube slippage resulting in food infusion into the abdominal cavity and resulting peritonitis has been reported following PEG tube placement but is uncommon, especially if the tube is placed surgically. Signs of peritonitis include depression, fever, vomiting, and a distending abdomen. Abdominocentesis or administration of an aqueous iodine contrast agent through the tube should confirm tube location if leakage is suspected.
Suggested Readings Willard M, Seim HB. 2007. Postoperative care of the surgical patient. In TW Fossum, ed., Small Animal Surgery, 3rd ed., pp. 90–110. St. Louis: Mosby.
CHAPTER 256
Jejunostomy Tube Placement Don R. Waldron
• A 1 to 2-cm (3/8–3/4-in) longitudinal seromuscular incision is made on the antimesenteric border of the jejunum. See Figure 256-1A. • A stab incision is made at the aboral end of the incision into the intestinal lumen. • A 3.5 or 5 French feeding tube is inserted aborally into the intestinal lumen. Approximately 10 cm (4 in) of tube is placed into the intestinal lumen. See Figure 256-1B. • The incision is closed with several interrupted Cushing sutures of 3-0 or 4-0 synthetic suture material. This results in the feeding tube being buried in the submucosal portion of the intestine. See Figures 256-1C and 256-1D. • A stab incision is made through the ventrolateral body wall, and the remaining catheter is exteriorized. See Figure 256-2. • The enterostomy site is sutured to the peritoneal surface of the body wall with four simple interrupted sutures of 3-0 or 4-0 synthetic absorbable suture. See Figure 256-3. • The exterior catheter is secured to the skin with a Chinese finger trap suture. See Figure 256-4. • Closure of the celiotomy incision is routine.
Overview Jejunostomy tube placement is one of several methods of providing nutritional supplementation in cats. Many cats undergoing abdominal surgery are anorexic and possibly cachectic and thus benefit from nutritional supplementation. Esophagostomy and gastrostomy tube placements are more commonly performed, but jejunostomy tubes are useful in cats with acute pancreatitis and upper gastrointestinal reconstruction procedures.
Procedure • Make a celiotomy incision. • Select a mobile portion of jejunum and determine the normal flow of ingesta (i.e., oral and aboral ends). • Mobilize this portion of the jejunum so it easily reaches the ventrolateral body wall. • Moistened laparotomy pads are used to pack off the jejunal segment from the abdominal cavity.
(A) Figure 256-1 A, A 1- to 2-cm (3/8- to 3/4-in) linear incision is made in the antimesenteric border of the jejunum; the incision penetrates the seromuscular layers only. A number 15 scalpel blade is used to make a small stab incision into the aboral aspect of the intestinal lumen. Images A, B, and C modified and reprinted with permission from Fossum TW. 2002. Small Animal Surgery, 2nd ed., p. 86. St. Louis: Elsevier Saunders. Image D, courtesy of Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
651
(B)
(C) Figure 256-1 Continued B, Place the distal end of a 5 French feeding tube into the jejunum and insert approximately 10 cm (4 in) of the tube into the intestine. C, The exiting tube is placed in the seromuscular incision and several interrupted Cushing sutures of 4-0 absorbable suture are placed to create a tunnel for the feeding tube.
652
(D) Figure 256-1 Continued D, The completed tube anchoring is shown. Alternatively, a purse-string suture is placed in the antimesenteric border of the intestine and the tube placed through the purse-string prior to tightening. In either case, the jejunum is pexied to the exit site of the lateral abdominal wall with four absorbable sutures.
(A) Figure 256-2 A stab incision is made through the ventrolateral body wall, and the remaining catheter is exteriorized. Photos courtesy of Dr. Gary D. Norsworthy.
Figure 256-3 The enterostomy site is sutured to the peritoneal surface of the body wall with four simple interrupted sutures of 3-0 or 4-0 synthetic absorbable suture. A, Three of the four stay sutures have been placed and are held with individual forceps. The fourth is being placed. B, The stay sutures are anchored to the body wall securing the jejunum and the tube to the body wall. Photos courtesy of Dr. Gary D. Norsworthy.
(B) 653
SECTION 4: Surgery
Notes • Some surgeons secure enterostomy tubes with a purse-string suture in the small bowel without a submucosal tunnel. • All enterostomy tubes are secured under a body bandage. • Elizabethan collars are applied as necessary. • The rate and volume of diet administered through the tube is carefully calculated and slowly increased over a number of days so as to not cause intestinal overdistension.
Suggested Readings Willard M, Seim III H. 2007. Post-operative care of the surgical patient. In TW Fossum, ed., Small Animal Surgery, 3rd ed., pp. 90–110. St. Louis: Mosby.
Figure 256-4 The exterior catheter is secured to the skin with a Chinese finger trap suture. Photos courtesy of Dr. Gary D. Norsworthy.
654
CHAPTER 257
Laser Surgery, CO2 John C. Godbold, Jr.
Introduction Surgical lasers produce a monochromatic (single wavelength) beam of light that can be directed to a small area to cut or remove tissue. Although other lasers delivering different wavelengths of light have been used in veterinary surgery, the carbon dioxide (CO2) laser has emerged as the predominant surgical laser used by veterinarians. Carbon dioxide laser light is in the infrared spectrum (10,600 nanometers) and interacts with tissue through a photothermal effect. When CO2 laser light hits tissue, the photonic energy is absorbed by water in the tissue. The water is instantly vaporized, cells are ruptured and vaporized, and almost all of the energy applied to the tissue is released in a vapor plume. The effect on the tissue left behind is minimal, and the depth to which tissue is cut or removed can be precisely controlled. Good technique results in a minimal zone of reversible change in the edges of the tissue adjacent to the area vaporized. This zone of reversible tissue change (100–200 microns) gives the desired effects of the CO2 laser in surgery; blood vessels and lymph vessels are sealed reducing hemorrhage and postoperative swelling, and nerves and pain receptors are affected in ways that reduce postoperative pain. Reduced hemorrhage allows the surgeon to work in a clear field with better visualization of anatomical structures. Reduced postoperative swelling and pain allows patients increased comfort. Additionally, the nature of the CO2 laser tissue interaction allows for precise removal of tissue. The depth of CO2 laser tissue removal can be as deep as with stainless surgical instruments or can be adjusted to depths as shallow as 100 microns. The advantages offered by use of the CO2 laser make it applicable in many feline surgeries. In this chapter the focus will be on those procedures in which the CO2 laser offers significant advantages over more traditional surgical instruments. Attention will be given to how the CO2 laser is adapted to procedures, leaving full discussion of diagnosis, anatomy, and patient management to other contributors.
CO2 Laser Technique The importance of good CO2 laser technique has been well developed. Critical to good technique is the use of high power density. Power density is the amount of laser energy applied to an area of tissue, measured in watts/cm2. The less time tissue is exposed to laser energy, the less the amount of change produced in the tissue adjacent to the area of laser application. Higher power densities result in the best tissue effect by allowing faster hand speed and shorter exposure of the tissue to the laser energy. Hand speed should be adjusted so tissue smoothly and cleanly opens when cut. Good technique results in skin incisions made with one pass of the laser. Recommended settings vary depending on the CO2 laser delivery system and the skill of the surgeon, so in this chapter specific CO2 laser device settings are not given. Prospective laser surgeons must be properly trained in equipment use, technique, and safety. Training should include lecture and wet lab courses as well as reference to published material.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Feline Onchyectomy Feline onchyectomy was the first CO2 laser procedure to catch the attention of small animal practitioners. Early veterinary laser surgeons substituted CO2 lasers for other cutting instruments in this surgery with remarkable results. Without tourniquets and bandages, and with immediate return to function, CO2 laser declawed cats became the heralds of CO2 laser benefits. Pressure platform gait analysis has demonstrated that “cats had improved limb function immediately after unilateral laser onchyectomy compared with a scalpel, tourniquet, and bandage.” CO2 laser onchyectomy is the same procedure as a blade disarticulation of P3 using the laser for all tissue cutting. With the control of hemorrhage by the CO2 laser a tourniquet is not needed, and visualization of anatomical structures is superb. An initial laser skin incision is made over the extensor tubercle, extending medially and laterally in a curvilinear direction to where the nail meets the pad. Prior to incising the dorsal structures of the distal interphalangeal (P2–P3) joint, the proximal edge of the skin incision is retracted proximally to expose the surface dorsal to the joint space. The laser beam is defocused, reducing power density, and the visible vessels immediately medial and lateral to the extensor tendon are “painted” with laser energy to produce a nonevaporative contraction and coagulation of the tissue and vessels. The extensor tendon and dorsal structures of the joint are incised, aiming the laser beam toward P3. Good technique employs the use of “brush strokes” with the laser beam rather than constant application. After complete transaction of the dorsal structures of the joint, with clear visualization of the distal articular surface of P2, the medial and lateral collateral ligaments and joint structures are transected while continuing to aim the laser beam toward P3. With the medial and lateral joint structures transected P3 can easily be distracted from P2. While continuing to aim at P3 the flexor tendon and soft-tissue attachments between P3 and the pad are transected. The resulting defect should be a small incision in the proximal skin crypt in which the retracted nail was hidden. Closure is optional. It can be accomplished with tissue adhesive applied distal to each incision on the haired skin inside the crypt followed by lightly pressing the crypt together. Routine preoperative and postoperative analgesics are recommended. Patients are normally fully ambulatory postoperatively, and unless excessive activity results in hemorrhage, bandages are not necessary.
Dermatological Procedures The CO2 laser is excellent for skin excisions and for removal of lesions by ablation technique. Ablation is the removal of multiple thin layers of tissue over an area larger than the focused application used for an incision. With CO2 laser ablation, the depth of tissue removal can be precisely controlled; some lesions require partial skin thickness ablation and some full thickness. Ablation is achieved by using a larger diameter laser beam and moving the beam in a grid pattern over the target tissue. After each layer of tissue is ablated the area is wiped with a saline soaked nonwoven gauze sponge to remove tissue residue, known as char. Effective ablation requires high power density. The rate of ablation and depth can be
655
SECTION 4: Surgery
(A)
(C)
controlled by attenuating the laser beam in a pulsed delivery. Ablated lesions heal by granulation. For some feline dermatological surgeries the CO2 laser is a helpful tool. For others it is mandatory. Duclos states, “[i]n many cases, laser surgery is easier, more effective, and less harmful to the animal. In some cases, laser treatment is the only method to achieve adequate results.” Feline dermatological conditions for which CO2 laser ablation are indicated include actinic keratosis, carcinoma in situ (Bowen’s Disease), calcinosis circumscripta, ceruminous cystomatosis, nodular sebaceous
656
(B)
Figure 257-1 A, Squamous cell carcinoma of the left side of the face prior to CO2 laser ablation. B, After CO2 laser ablation the surgical defect is dry and free of hemorrhage and swelling. The defect heals by second intention. C, Healed appearance of ablated facial squamous cell carcinoma. The tumor recurred 9 months later. Images courtesy of Dr. Gary D. Norsworthy.
hyperplasia, pinnal tumors, plasma cell pododermatitis, squamous cell carcinoma, and viral plaques. See Figure 257-1.
Ear Procedures Digital video otoscopy is important for effective diagnosis and treatment of external ear canal and middle ear diseases. The use of hollow waveguide delivery CO2 lasers with focusing tips extending through the
Laser Surgery, CO2
working channel of video otoscopes allows surgical access to lesions in these areas in a minimally invasive way. Frequently lesions that would otherwise require lateral resection or total ablation can be successfully managed with this combination of technologies. When working with a CO2 laser through a video otoscope a pulsed delivery is required. The high lipid content of the ear canal environment results in a heavy plume production with CO2 laser application and visualization is impaired. Pulsed delivery allows opportunity for the airflow delivered through the focusing tip to purge the plume between pulses. Capability of lavage of the ear canal is mandatory for removal of laser debris and proper assessment of the surgical site. Otic lesions for which the CO2 laser used through a video otoscope are indicated include benign conditions such as basal cell tumors, inflammatory polyps, ceruminous gland adenomas, and papillomas. Malignant tumors include ceruminous gland adenocarcinomas and squamous cell carcinomas. Appropriate diagnosis prior to surgical intervention is critical and dictates the extent of tissue removal. Tissue removal in the ear canal can be aggressive, and although ablation in the ear canal frequently is accomplished with some degree of thermal insult to the tissues left behind, the external ear canal cartilage is an effective barrier preventing damage to surrounding tissue.
Figure 257-2 CO2 laser ablation of a laryngeal mass through a video otoscope (MedRX Inc., Largo, FL). The laser focusing tip is seen extending from the end of the scope in the upper center. To the right is the red endotracheal tube, and below the mass being lasered is the epiglottis. Images courtesy of Dr. Gary D. Norsworthy.
Ear Polyps Nasopharyngeal polyps that grow into the external ear canal usually arise from mucosal epithelium in the middle ear and tympanic bulla. Fifty percent of aural polyps will reoccur if the polyp’s base is not addressed surgically via a ventral tympanic bulla osteotomy. See Chapter 248. Acknowledging a 50–50 chance of success many practitioners choose to first attempt less invasive removal by mechanical traction working through the ear canal. CO2 laser ablation through a video otoscope can be helpful with polyps when mechanical removal is unsuccessful or results in obscuring hemorrhage.
CO2 laser ablation is indicated. Inflammatory tissue is ablated as aggressively as possible. When evaluating the extent of ablation the “Q-Tip test” is used. After ablation, the remaining tissue is wiped with a cotton-tipped applicator; normal tissue will not bleed after being lasered and inflammatory tissue will. Multiple monthly sessions are required and unless causative factors are successfully addressed, the lesions will recur. See Figure 257-3).
Nasopharyngeal Polyps Myringotomy Access to the middle ear is facilitated by using the CO2 laser through a video otoscope. Myringotomies can be successfully accomplished with single or multiple pulses of the CO2 laser, resulting in round openings that heal more slowly than those produced mechanically. Middle ear masses that involve the dorsolateral and ventromedial middle ear compartments are not accessible thorough scope equipment and require conventional ventral bulla ostectomy.
Nasophayrngeal polyps that grow in the pharyngeal area arise from mucosal epithelium in the Eustachian tube or the pharynx. With rostral retraction of the soft palate, the stalk of the polyp can be visualized and the origin noted. Removal by mechanical traction is indicated if the origin is in the Eustachian tube with an estimated 10% chance of reoccurrence. If the origin is pharyngeal, the CO2 laser offers an excellent modality for excision or ablation of the base of the polyp. With the soft palate reflected rostrally and gentle traction on the polyp, the base of the polyp is laser excised and followed by ablation of the foci of origin.
Oral and Respiratory Procedures CO2 laser use is particularly appropriate for use in the oral, pharyngeal, and upper respiratory areas, offering the benefits of reduced hemorrhage in vascular tissue, minimized postoperative discomfort, and the ability to shape or sculpt tissue. In the oral cavity, both excision and ablation can be used for masses and lesions. Fibrosarcomas, malignant melanomas, and squamous cell carcinomas can be palliatively debulked by excision and ablation when more aggressive surgery and treatment is not accepted by the owner. Additionally, use of the CO2 laser through a video otoscope allows visualization and access to lesions in otherwise difficult to access areas in the pharynx and upper respiratory tract. See Figure 257-2.
Stenotic Nares CO2 laser excision of the redundant and impairing portion of the alar fold offers an alternative approach to correction of feline stenotic nares. To achieve bilateral symmetry the line of excision can be marked with the laser using a pulse mode prior to beginning excision. It is critical with feline stenotic nares to perform a precise high power density excision rather than simply ablating tissue. The only tissue affected by the laser excision should be the alar fold. If a circumferential ablation is performed the nare will heal by granulation and contraction with a high probability of web formation across the nare. Because of the precision required, this procedure should be done with a small diameter focusing tip and a hollow waveguide CO2 laser. See Figures 26-2A and 2B.
Feline Gingivitis, Stomatitis, and Pharyngitis The CO2 laser can be part of a multimodality approach to the management of feline lymphocytic plasmacytic gingivitis, stomatitis, and pharyngitis. If removal of inflammatory tissue is part of the management,
Nasal Planectomy Excision of the nasal planum is a life-prolonging or life-saving salvage procedure for cats with malignancy. The CO2 laser offers significant
657
SECTION 4: Surgery
(A)
(B)
(C) Figure 257-3 A, Lesions of lymphoplasmacytic stomatitis prior to dental extractions and CO2 laser ablation. B, Appearance after extractions and CO2 laser ablation of stomatitis lesions. Aggressive ablation encourages scar tissue replacement of the inflammatory tissue. C, Appearance of lymphoplasmacytic stomatitis lesions 8 weeks after CO2 laser ablation. Images courtesy of Dr. Gary D. Norsworthy.
advantage in this procedure because of the brisk hemorrhage encountered if done with other cutting instruments. With a pulsed mode, the laser can be used to mark the line of excision of the planum prior to surgery, using the planum-skin junction as a general guide. Following an initial laser skin incision the excision of the planum starts dorsally immediately rostral to the nasal bone and extends
658
ventrally until removal is achieved. When using the laser, hemorrhage is usually not encountered. The laser can be used to ablate and sculpt any exposed portion of the turbinates. See Figure 257-4. Purse string or cruciate sutures are used to reduce the surgical defect. Mucosal to skin apposition is not necessary since healing is by second intention.
Laser Surgery, CO2
(B) (A)
(C)
Summary The CO2 laser gives the practitioner an effective tool for surgical use in the feline patient. It offers the advantages of reduced hemorrhage, swelling, and pain, increased precision, and access into otherwise inaccessible areas. With training, practice, and a good understanding of how CO2 laser light interacts with tissue, the practitioner will find application for the laser in a multitude of procedures and surgeries. Small animal CO2 laser surgery has been a practitioner developed technology, dependent on the imagination and ingenuity of practicing veterinary surgeons. Continued use will demonstrate additional applications helpful to the feline patient.
Figure 257-4 A, Squamous cell carcinoma was found on the nasal planum of this 12-year-old cat. B, This is what the cat looked like 2 weeks following CO2 laser treatment. C, Four years and two more surgeries later the cat still had good cosmesis of the nasal planum. Early treatment is essential for this disease in this location. Note the iris changes (C) typical of geriatric cats. Images courtesy of Dr. Gary D. Norsworthy.
Suggested Readings Berger N, Eeg PH. 2006. Veterinary Laser Surgery: A Practical Guide. Ames, IA: Blackwell Publishing. Duclos D. 2006. Lasers in veterinary dermatology. Vet Clin North Am Small Anim. 36(1):15–37. Godbold JC. 2010. Atlas of CO2 Laser Surgery Procedures. Jackson, TN: Southern Digital Publishing. Lewis JR, Tsugawa AJ, Reiter AM, et al. 2007. Use of CO2 laser as an adjunctive treatment for caudal stomatitis in a cat. J Vet Dent. 24(4):240–249. Peavy GM. 2002. Lasers and laser tissue interaction. Vet Clin North Am Small Anim. 32(3):517–534.
659
CHAPTER 258
Lip Avulsion Reattachment Gary D. Norsworthy
Definition This procedure is to surgically reattach of the lower lip (labium) following avulsion. Lip avulsion is usually due to trauma and usually occurs at the mucogingival junction. See Figure 258-1.
Equipment • A routine surgery pack • 3-0 or 4-0 polydioxanone (PDS®, Ethicon) surgical suture material
Procedure • The tissue should be closely inspected for dirt and other debris. All foreign material should be flushed from the tissue with copious amounts of sterile, normal saline. A 35 or 60-mL syringe and a 20gauge needle create sufficient muzzle velocity to adequately flush the tissue. • If the avulsion is more than a few hours old, it is necessary to freshen the edges of the tissue. If the lip has already adhered in its displaced position, it must be detached and the edges freshened. It may be necessary to undermine adjacent tissue to get the lip to return to its normal position.
Figure 258-2 After cleaning the tissue and repositioning it, sutures were placed around the right and left lower canine teeth.
Figure 258-3
A third suture was placed around the left lower premolar (arrow).
Figure 258-1 The lower lip was severely avulsed due to trauma. The kitten was presented within two hours of the occurrence.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
660
• Two mattress sutures are placed through the lip and anchored around the lower canine teeth. See Figure 258-2. • Other interrupted sutures are placed where possible to further attach the lip in its appropriate location. Anchoring to other teeth is sometimes possible. See Figure 258-3.
Lip Avulsion Reattachment
Complications • Complications are uncommon; good cosmesis is generally achieved. See Figure 258-4. • Inadequate suturing will permit dehiscence. The cat may be able to cause this; if needed, a restraint collar can be used for a few days . If the lower canine teeth are broken at the gum line, adequate anchoring my be very difficult. • Failure to removed foreign matter will result in poor healing. • Secondary bacterial infection is always possible. Broad-spectrum antibiotics should be used for several days postoperatively.
Selected Readings Harvey CF. 2004. Major oral surgery in cats: Management of trauma. Proceedings: Western Veterinarian Conference, Las Vegas, NV. Pavletic MM. 1999. Atlas of Small Animal Reconstructive Surgery, 2nd ed. Philadelphia: WB Saunders Co. Figure 258-4 Healing was complete and cosmetically excellent 10 days after surgery.
661
CHAPTER 259
Luxating Patella Otto Lanz
Overview It is reported that normal cats have some degree of patellar subluxation, but this does not lead to clinical signs. Patellar luxation is infrequently encountered in cats and can result from congenital malformations or trauma. Congenital patellar luxation is considered to be more common than traumatic patellar luxation. In most cases the condition is bilateral and may be associated with a shallow trochlear groove, slight medial deviation of the tibial tuberosity, and an underdeveloped medial femoral condyle. Lateral luxation occurs less frequently and is usually unilateral. Unlike the dog, in cats with patellar luxation, coxa vara, lateral bowing of the distal femur, and tibial torsion are not typically seen. In the Devon Rex, Abyssinian, and domestic shorthair cat medial patellar luxation is considered congenital and affects both male and female cats equally. Patellar luxation may also occur secondary to femoral fracture repair, surgical treatment of other stifle injuries, or congenital defects affecting the femur or tibia. There is a weak association between medial patellar luxation and hip dysplasia in cats. Both conditions may develop simultaneously or in combination, more frequently than has been reported in the past. Most cats that present for patellar luxation are less than 3 years of age, and in one report, 66% were less than 1 year of age. In the majority of cats, patellar luxation causes no clinical signs and is an incidental finding. In other cats, however, patellar luxation causes varying degree of gait abnormalities, acute lameness, locking of the limb in extension, or a crouching stance. A study involving 21 cats with patellar luxation reported that 66% were markedly lame or had obvious gait abnormalities. Cranial cruciate ligament rupture secondary to patellar luxation is rarely described in cats.
Diagnosis • Palpation: Palpation of the joint and evaluation of patellar stability is the primary means of diagnosis. Sedation is recommended to thoroughly evaluate the stifle. A grading system is used to describe the clinical severity of the patellar luxation: • Grade I: The patella is manually luxated using digital pressure, but reduces spontaneously when pressure is released. Cats with grade I luxation do not show clinical signs. • Grade II: The patella spontaneously luxates but reduces on its own and will remain in place until the limb is manipulated. Not all cats with grade II luxation show clinical signs. • Grade III: The patella is luxated at the time of the examination. It may be positioned into the trochlear groove using digital manipulation, but spontaneously reluxates. The degree of lameness is variable with grade III luxations but is often persistent. • Grade IV: The patella is permanently luxated and cannot be reduced with digital manipulation or rotation of the tibia. Grade IV luxations are uncommon in cats. • Radiographs: Patellar luxation can be identified on craniocaudal radiographic views of the stifle joint. The position of the tibial tuberosity and development of the medial femoral condyle are assessed
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
662
on lateral and craniocaudal radiographs. A skyline radiographic view may be used to assess the depth of the femoral trochlea. Radiographs of the pelvis should also be taken to assess the coxofemoral joints.
Indications: Conservative • Conservative therapy is recommended for treatment of cats without clinical signs (lameness) or if signs are mild or infrequent.
Indications: Surgical • Surgical treatment is recommended for cats with more severe luxation and those with persistent clinical signs (i.e., Grades II, III, and IV).
Soft-Tissue Procedures • In cats with Grade II luxation, soft-tissue procedures alone may be adequate to maintain patellar reduction. These are often used in combination with each other or with bony reconstructive procedures.
Capsular Imbrication • A portion of the joint capsule is excised and the edges are sutured to tighten the joint capsule. Monofilament, absorbable suture material (3-0) is often used. • The lateral joint capsule is imbricated to stabilize medial patellar luxations; the medial joint capsule is imbricated to stabilize lateral patellar luxations.
Retinacular Imbrication • Monofilament, nonabsorbable suture material (3-0) is placed in the retinacular fascia (Lembert or mattress pattern) to achieve imbrications of the biceps fascia. • An alternative approach is to remove a narrow strip of the retinacular fascia and then suture the edges. • The lateral retinaculum is imbricated to stabilize medial patellar luxations and the medial retinaculum is imbricated to stabilize lateral patellar luxations. • The retinaculum should be imbricated just distal to the stifle joint and continue proximal to the patella.
Fabellar-Tibial Antirotational Suture • An antirotational suture is used to prevent internal rotation of the tibia and maintain proper alignment of the quadriceps mechanism. • A suture is placed around the lateral fabella and through a hole drilled in the tibial tuberosity. • Monofilament, nonabsorbable suture material (2-0 to 0) is often used. • An antirotational suture is often used only if there is concurrent cranial cruciate ligament rupture.
Luxating Patella
(A)
(B)
Figure 259-1 A: This is a lateral radiograph of a stifle from a 1 year old female domestic shorthair with a Grade III/IV medial luxating patella. B: This is a ventral dorsal radiograph of the pelvis from the same cat showing bilateral Grade III/IV medial luxating patellas.
(A)
(B)
Figure 259-2 A: This is an immediate postoperative cranial caudal view of the stifle from the aforementioned patient showing adequate alignment of the patella. A block wedge recession, tibial tuberosity transposition, medial desmotomy, and lateral biceps fascia imbrications were performed. B: This is an immediate postoperative lateral view of the stifle from the above patient. Again, note the adequate positioning of the patella and proper placement of the pin and tension band for the tibial tuberosity transposition.
Fabellar-Patellar Suture • A suture is passed in a figure-eight pattern from the fabella to the patella. • The suture can be passed around the patella or placed through the patellar tendon. • The suture is tightened just enough to stabilize the patella.
Releasing Incision • A releasing incision is made through the fascia on the side opposite the luxation to relieve tension on the tissues that may lead to postoperative reluxation. • In some cases, the releasing incision is made as part of the surgical approach to the joint. Only the synovial membrane is sutured to reduce leakage of synovial fluid from the joint, but the fibrous joint capsule and retinacular fascia is left open.
Bony Reconstructive Procedures Trochleoplasty • Trochleoplasty techniques are used to deepen the trochlear sulcus and improve patellar stability. • The resultant trochleoplasty is made deep enough so that 50% of patella rest within the trochlea sulcus. • Several techniques are described, but only techniques that preserve the articular cartilage are preferred. • Sulcoplasty: The articular cartilage and subchondral bone of the trochlear sulcus are removed with a bone rasp or high speed burr. The procedure is easily performed and adequately deepens the trochlea but destroys the articular cartilage. • Trochlear Wedge Recession: A patella saw is used to excise a wedge-shaped osteochondral fragment from the trochlea, which preserves the articular surface. A small amount of bone is removed from the femoral defect using a patella saw, scalpel blade, or rongeur. The osteochondral fragment is then positioned back into the femoral defect. The replaced wedge is recessed, creating a deeper trochlear sulcus. • Block Recession Trochleoplasty: A patella saw and a small osteotome are used to remove a rectangular osteochondral fragment from the trochlear sulcus, preserving the articular surface of the
trochlea. A small section of bone is removed from the femoral defect (and from the base of the excised osteochondral block) with a rongeur prior to replacing the fragment. The advantage of a block recession trochleoplasty is that it increases the depth of the proximal sulcus and recesses a larger percentage of the articular surface when compared to a wedge recession. Care must be taken to avoid damaging the cartilage, especially in smaller cats. • Tibial Tuberosity Transposition: Transposition of the tibial tuberosity is reserved for cases of severe or recurrent luxation. Transposing the insertion of the straight patellar ligament aligns the quadriceps mechanism and patella over the trochlear groove to improve patellar stability. An osteotomy of the tibial tuberosity is performed with a small osteotome beginning just beneath the insertion of the straight patellar ligament. The osteotome is directed distally to free the tuberosity preserving the periosteum distally. Alternatively, the tuberosity can be cut with a small bone cutter. The tuberosity is then displaced laterally to correct medial patellar luxation (or medially to correct lateral patellar luxation). Alignment is confirmed by viewing the limb from its cranial aspect. In most cases, the tuberosity is only displaced a few millimeters to achieve proper alignment of the quadriceps. Two small Kirschner wires (0.035” or 0.045”) are driven through the tuberosity and into the tibia. Care is taken not to place the Kirschner wires into the stifle joint or into the soft tissues on the caudal aspect of the tibia. The use of a tension band and figure-eight wire is usually not required in the cat. See Figures 259-1 and 259-2.
Prognosis The prognosis after surgical repair of patellar luxation in cats is reported to range from good to excellent. The limb may be bandaged for 24 hours to help with postoperative swelling, though many cats resent bandages and immobilization is not necessary for a satisfactory outcome. Exercise is restricted for 4 to 6 weeks to allow healing.
Selected Readings Fossum TW. 2002. Diseases of the joints. In TW Fossum, ed., Small Animal Surgery, 2nd ed., pp. 1023–1167. St. Louis: Mosby.
663
CHAPTER 260
Mandibular Symphyseal Separation Don R. Waldron
Overview Mandibular fractures, including mandibular symphyseal separation, are common injuries secondary to facial and oral trauma. See Figure 260-1. Automobile caused head injury, direct impact injury, and falls from heights (“high-rise syndrome”) are causes of mandibular symphyseal separation or instability. The patient is stabilized with intravenous fluids prior to general anesthesia for fracture repair. Thoracic radiographs are normally performed if the cat has been traumatized to rule out conditions such as diaphragmatic hernia, pulmonary contusions, pneumothorax, and hemothorax. Mandibular separation also occurs with minor trauma and is common in cats over 12 years of age. However, it is usually not palpable when the cat is awake. Therefore, when a dental prophylaxis or other oral procedure is performed, the mandibular symphysis should be examined for separation. See Figure 260-2. Because it can occur due to overly aggressive jaw manipulation during a dental prophylaxis, the symphysis should be examined prior to other procedures. Otherwise, the client may believe that it was iatrogenic and not pre-existing. Diagnosis is by manipulation of the two halves of the mandible. It can also be detected on dental radiographs. See Figure 260-3.
Special Equipment • 16-gauge hypodermic needle • 20-gauge orthopedic wire • Reduction forceps
Procedure • The cat is induced and placed under general anesthesia with an endotracheal tube and inhalation anesthesia. • Careful examination of the oral cavity is performed for other maxillary or mandibular fractures. If other injuries are suspected, skull radiographs may be performed while under anesthesia. • The cat is placed in dorsal recumbency, and the hair is clipped on the rostroventral aspect of aspect of the mandibular symphysis; the area is prepared for aseptic surgery. • A small nick incision made on the ventral midline over the symphysis. • An 16- or 18-gauge hypodermic needle is inserted through the incision and lateral to the mandibular body to exit into the oral cavity just caudal to the canine tooth. See Figure 260-4A. • A strand of 20-gauge orthopedic wire is threaded through the needle. • The needle is repositioned on the opposite side of the mandible caudal to the contralateral canine tooth. • The wire is pulled across the oral cavity remaining caudal to the canine teeth and inserted through the needle to exit ventrally in the original incision. • Reduce the symphysis to a normal position and maintain reduction with reduction forceps or a towel clamp held by an assistant. • The wire is tightened, and the wire ends are bent over. See Figure 260-4B.
Comments • Alternatively, the wire can be placed in the described fashion using a suture needle with the wire attached.
Figure 260-1 Mandibular symphyseal fracture may occur due to trauma. The symphysis of this cat is obviously fractured. In addition, soft-tissue trauma is seen caudal to the immediate symphyseal region. Image courtesy of Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
664
Figure 260-2 Geriatric cats often experience symphyseal fracture without trauma. It is typically not detectable without anesthesia. Relaxation of the jaw allows one to manipulate the two haves of the mandible and see the separation. Image courtesy of Dr. Gary D. Norsworthy.
Mandibular Symphyseal Separation
(A)
(A)
(B) Figure 260-4 A, A 16- or 18-gauge hypodermic needle is inserted from the ventral midline lateral to the mandibles. A single piece of stainless steel cerclage wire is passed through needle and caudal to the canine teeth. The needle is repositioned so it exits lateral to the other mandible. The wire is threaded through the needle so it exits on the ventral midline. B, The ends of the cerclage wire are twisted together so the fracture is reduced and stable. The ends are bent against the skin. Reprinted with permission from Fossum TW. 2002. Small Animal Surgery, 2nd ed., p. 911. St. Louis: Elsevier Saunders.
(B) Figure 260-3 Dental radiographs clearly demonstrate mandibular separation (A) compared to normal (B). Images courtesy of Dr. Gary D. Norsworthy.
• If the patient has extensive oral or head trauma, placement of an esophagostomy tube to meet nutritional needs postoperatively may be indicated. • The wire is usually removed 4 weeks postoperatively. • It is common for a geriatric cat’s mandibular symphysis not to heal after four or 8 weeks. As long as the wire is tolerated well, it can stay in long term.
Suggested Reading Johnson A. 2006. Management of specific fractures. In TW Fossum, ed., Small Animal Surgery, 3rd ed., pp. 1026–1027. St. Louis: Mosby.
665
CHAPTER 261
Mastectomy Don R. Waldron
Overview Mammary neoplasia in the cat is a biologically aggressive malignant disease that may metastasize to lungs, lymph nodes, or liver. Early ovariohysterectomy provides protection against development of mammary tumors, similar to the canine. Siamese cats have been suggested to be at increased risk for the development of mammary neoplasia. Approximately 80 to 90% of mammary tumors in the cat are adenocarcinomas. Thoracic radiographs should be taken prior to surgery to rule out metastatic disease. The feline mammary gland consists of four pairs of mammae on the ventral thoracic and abdominal walls numbered from cranial to caudal. The cranial pair of glands (glands 1 and 2) drains to the axillary lymph node while the caudal pair (glands 3 and 4) drains to the superficial inguinal lymph node.
Indications Mammary neoplasia in the cat should be treated by regional or unilateral mastectomy. Lumpectomy consisting of local excision of mammary masses is contraindicated in the cat except when mammary neoplasia has recurred following mastectomy or if histopathology on the lump shows it to be benign.
Procedure • An elliptical skin incision is made around either the cranial or caudal pair of glands or all four mammary glands of the affected side. At least 1-cm (3/8-in) margins of healthy tissue should be attained by excision. See Figures 132-2 and 261-1. • The mammary tissue is excised by dissection of mammary and subcutaneous tissue from the external rectus muscle fascia. • In the caudal two glands, the pudendal artery and vein should be ligated as they enter gland 4. • The superficial inguinal lymph node is excised along with inguinal fat in the region of gland 4. • The axillary lymph node is excised only if it is palpably enlarged. • An intradermal pattern using 4-0 absorbable suture material is placed to initially close the mastectomy wound. • Skin sutures or staples are then placed to complete the closure. • Drains are usually not necessary unless undue dead space exists (heavier cats).
Figure 261-1 The types of mastectomy recommended for cats are either (1) regional or (2) unilateral. Reprinted with permission from Waldron DR. 2001. Diagnosis and surgical management of mammary neoplasia in dogs and cats. Vet Med. 96:946.
• Excised masses and lymph nodes are submitted for histologic diagnosis. • If malignant neoplasia is diagnosed, chemotherapy using doxorubicin as a single agent or doxorubicin and cyclophosphamide has been shown in the cat to provide increased survival times. • Because of their malignant nature, mammary masses may recur locally or metastasize. If masses recur locally, aggressive local excision (lumpectomy) is recommended.
Postoperative Care • Excision of both mammary chains (i.e., bilateral mastectomy) concurrently is not recommended. Excess tension on the surgical wound following closure of the resulting wound may predispose to dehiscence. • If masses are present bilaterally, surgery is staged at 3-week intervals.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
666
Suggested Readings Lane SE, Rutteman GR, Withrow SJ. 2007. Tumors of the mammary gland. In SJ Withrow, EG MacEwen, eds., Small Animal Clinical Oncology, pp. 619–636. St. Louis: Saunders. Waldron DR. 2001. Mammary neoplasia in the canine and feline. Vet Med. 12:9434–948.
CHAPTER 262
Nasopharyngeal Polyp or Mass Removal Gary D. Norsworthy
Definition This procedure is to remove a polyp or mass from the nasopharynx. Inflammatory polyps are firm masses composed of inflammatory cells. Most originate from the base of the auditory tube (Eustachian tube) and extend into the middle ear or into the nasopharynx. Their etiology is unknown, but there is some evidence for allergy or the feline calicivirus being involved. Other masses may originate in the nasopharynx. Most of these are neoplastic, but fungal granulomas may also create masses in this location. See Chapter 122.
Notes • Because the mass typically originates in the auditory tube, it may recur after removal via the previously described method. Some originate in the tympanic bulla and extend down the auditory tube into the nasopharynx. Radiographs or computerized tomography (CT) scans of the tympanic bullae reveal thickened walls and increased density within the affected bullae. See Figure 262-2. Ventral bulla osteotomy is indicated. See Chapter 248.
Nasopharyngeal (Inflammatory) Polyp: Oral Avulsion Approach Equipment • Allis tissue forceps • Snook ovariohysterectomy hook
Procedure • Place the cat under general anesthesia. An injectable anesthetic is preferred because an endotracheal tube may hinder access. • Hook the Snook ovariohysterectomy hook over the caudal end of the soft palate and pull the soft palate cranially to visualize the mass. • Grasp the mass with the Allis tissue forceps and twist it vigorously. It is usually attached with a thin stalk that ascends the auditory tube. When the stalk breaks, the mass will be free. See Figure 262-1.
(A)
(B) Figure 262-1 This nasopharyngeal polyp was removed by avulsing it with a pair of Allis tissue forceps. Note the stalk of tissue that ascended the auditory tube (arrow).
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 262-2 Because many nasopharyngeal polyps originate in the middle ear, the tympanic bulla of affected cats should be imaged. A, Thickening of the tympanic bulla indicates middle ear disease. The vertical arrow points to the normal tympanic bulla; the horizontal arrows point to a severely thickened tympanic bulla. B, A computerized tomography scan also reveals a tympanic bulla that is normal (R) and one that is abnormal (L).
667
SECTION 4: Surgery
Nasopharyngeal Polyp or Mass: Transpalatine Approach Equipment • Routine surgery pack
Procedure • The cat is placed in dorsal recumbency. Its mouth is held open by an assistant using gauze strips that are hooked around the canine teeth. • The location of the mass can often be determined from a high quality lateral radiograph. See Figure 262-3. A CT scan also be used to identify the mass. • Based on the imaging findings, a midline incision is made just caudal to the estimated position of the mass. See Figure 262-4A. • Curved mosquito hemostatic forceps are used to extract the mass. See Figure 262-4B. • The incision in the soft palate is closed with 4-0 dissoluble sutures using a simple interrupted pattern. See Figure 262-4C. Figure 262-3
This lateral radiograph shows a mass (arrows) in the nasopharynx (NP).
(A) (B)
(C) Figure 262-4 A, The mass is approached through a midline incision through the soft palate. The mass is seen through the incision. B, The mass is shown after removal. The diagnosis was adenocarcinoma. C, The incision through the soft palate is shown after it has been closed with four simple interrupted sutures. The cat was eating soft food within 12 hours post-operation.
668
Nasopharyngeal Polyp or Mass Removal
Notes • This approach is minimally invasive and is indicated when a mass has been identified with imaging. • The cat should be fed soft food for 1 to 3 days, and pain medication should be prescribed for 1 to 3 days. However, these incisions heal rapidly and most cats eat well within 24 hours postoperatively. However, if the cat is reluctant to eat, an esophagostomy or gastrostomy tube can be placed.
Complications • Oral Approach: If the polyp breaks in to several pieces, it may not be possible to remove it with the Allis tissue forceps. Therefore, a transpalatine approach may be needed.
• Transpalatine Approach: Excessive bleeding is possible if the incision is not made on the midline. If the mass is too far cranial, it may not be possible to reach it with the forceps for removal. Wound dehiscence may occur if careful suturing is not used in the soft palate, which can result in an oro-nasopharyngeal fistula.
Suggested Readings Hendricks JC. 1989. Brachycephalic airway syndrome. Update on respiratory disease. Vet Clin North Am Small Anim Pract. 19:1167– 1188. Parnell NK. 2006. Diseases of the Throat. In SJ Ettinger, EC Feldman, eds., Textbook of Veterinary Internal Medicine, 6th ed., pp 1196–1204. St. Louis: Elsevier Saunders.
669
CHAPTER 263
Nephrolith Removal Don R. Waldron
Overview Uroliths located in the upper urinary tract (i.e., kidney and ureter) are commonly diagnosed in the cat. Most calculi in the upper urinary tract are calcium oxalate in composition and are not amenable to medical dissolution. It is important to recognize that cats with upper urinary tract urolithiasis may be in renal failure. In some cases this is due to ureteral obstruction and secondary renal disease while in other cases renal failure is present without obstruction. It is unclear whether renal failure precedes nephrolithiasis or what role nephroliths have in causing renal failure. The mere presence of nephroliths is not an indication for surgical removal. Complete laboratory work-up and abdominal ultrasound or excretory urography are indicated prior to making the decision to perform nephrotomy. It is important to determine that it is a nephrolith located in the renal pelvis and not just mineralization within the renal parenchyma. See Figure 263-1. Bilateral nephrotomy is not advised under any circumstance; if both kidneys are affected, the second kidney can be operated in 4 to 6 weeks.
Indications • Nephrotomy may be indicated in cats with pain, fever, pyelonephritis, renal failure due to obstructive disease, or an actively growing stone. • Cats in renal failure should be diuresed with intravenous fluids preoperatively, and fluid administration should be maintained during and following anesthesia and surgery.
Special Equipment • Bulldog (noncrushing) vascular clamp for temporary occlusion of the renal artery.
Procedure • General anesthesia is induced, and the ventral abdomen is prepared for aseptic surgery. • The cat is placed in dorsal recumbency, and a ventral midline incision is made from the xiphoid process of the sternum to 3 to 5 cm (1 1/8 to 2 inches) caudal to the umbilicus. • The abdominal cavity is entered, and the appropriate kidney is exposed by retraction of the duodenum and mesoduodenum on the right side or the colon and mesocolon on the left side. • The kidney is bluntly dissected and mobilized from its peritoneal attachments. • The renal artery is located dorsal and just cranial to the large renal vein. Both vessels are surrounded by varying amounts of abdominal fat. • The artery is isolated and occluded with a bulldog clamp. See Figure 263-2. Occlusion time is noted. A goal of renal artery occlusion is less than 15 minutes.
Figure 263-1 A ventral-dorsal radiograph shows uroliths of varying sizes in both kidneys. The left kidney had experienced hydronephrosis (note renomegaly) so it was chosen for urolith removal. Image courtesy of Dr. Gary D. Norsworthy.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
670
Figure 263-2 A noncrushing (bulldog) clamp is placed across the renal artery. Image courtesy of Dr. Gary D. Norsworthy.
Nephrolith Removal
(A)
(B)
Figure 263-3 A, An incision made on the convex surface of the kidney extending approximately two-thirds the length of the kidney. The parenchyma is gently incised and B, the back of the scalpel handle used to gently and bluntly dissect to the renal pelvis. Images courtesy of Dr. Gary D. Norsworthy.
Figure 263-4 Calculi are removed from the pelvis with a scoop, and a 3.5 French urinary catheter is used for pelvic flushing and to catheterize the proximal ureter to assure patency. Image courtesy of Dr. Gary D. Norsworthy.
• A longitudinal 3 to 4-cm (1 1/8 to 1 1/2-in) incision is made on the convex surface of the kidney with a number 15 scalpel blade. See Figure 263-3A. • The incision is deepened through renal parenchyma by using the blunt end of the scalpel handle to bluntly separate parenchyma down to the renal pelvis. See Figure 263-3B. • All uroliths within the pelvis are removed and submitted for quantitative analysis. Scooping and vigorous flushing with warm saline are employed for urolith removal. See Figure 263-4. • A 3.5-French urinary catheter is used to catheterize the proximal ureter and assure patency.
• The bivalved kidney is held together (see Figure 263-5A), and the kidney incision is carefully closed with 4-0 or 5-0 absorbable suture on a tapered needle placed in a continuous pattern. The needle should engage the renal capsule and a small amount of renal parenchyma. See Figure 263-5B. • Capsular closure only is desirable; however, the capsule is so thin in the cat that it often tears unless some parenchyma is included. • After closure is complete, the bulldog clamp is released from the renal artery. • Focal areas of hemorrhage may be occluded with a cruciate suture or Gelfoam®, and direct pressure is applied to any area of hemorrhage.
671
SECTION 4: Surgery
(A)
Figure 263-6 The removed uroliths are shown. Image courtesy of Dr. Gary D. Norsworthy.
• The abdomen is lavaged with warm saline and closure is routine. • The uroliths should be submitted for analysis. See Figure 263-6.
Notes • Intravenous fluids should be continued postoperatively. There is a risk of worsening renal failure in these patients. • It is emphasized that the presence of renal calculi is not, by itself, an indication for nephrotomy. • Nephrotomy performed in normal cats usually does not significantly reduce renal function; however, the same procedure in compromised kidneys may cause acute decompensation.
Suggested Readings (B) Figure 263-5 A, The kidney incision is held closed for several minutes. B, And then a 4-0 or 5-0 absorbable suture on a tapered needle are placed through the capsule and superficial parenchyma. If the capsule can be reapposed, a simple continuous pattern is used. However, sutures easily tear through the capsule so several mattress sutures are placed through the renal cortex. The vessels in the cortex are much smaller than those in the medulla. Images courtesy of Dr. Gary D. Norsworthy.
672
King MD, Waldron DR, Barber DL, et al. 2006. Effect of nephrotomy on renal function and morphology in normal cats. Vet Surg. 35:749–758.
CHAPTER 264
Onychectomy Don R. Waldron
Definition Onychectomy (declawing) is removal of most or the entire third phalanx of the forepaws and occasionally of the rear paws also.
Equipment • Guillotine-type (Resco™) or scissors-type (White’s™) nail trimmers • Number 11 Bard-Parker™ scalpel blade on handle • CO2 laser with 0.3 to 0.4 metal tip
Indications Onychectomy is performed as an elective procedure to prevent damage to the home environment (e.g., carpets, drapes, amd furniture) or injury to the owner. Trauma or infection may also necessitate onychectomy.
Contraindications Cats that go outdoors unsupervised should not be declawed because the nails provide defense and a means to escape by climbing.
Techniques Several methods of onychectomy have been used successfully. For many years, guillotine or scissor-type nail trimmers were used exclusively for this operation. Declawing by using a scalpel blade to disarticulate P2 and P3 has also been used extensively. Onychectomy performed with a surgical laser is preferred by many. All three methods are discussed.
Procedures Nail Trimmers • The cat is placed in lateral recumbency, and a tourniquet is applied proximal to the elbow. • The entire paw is prepared with surgical scrub; however, hair clipping is not necessary. • The cutting blade of a nail trimmer is positioned between the unguicular crest and the second phalanx with care taken to exclude the digital footpad. The third phalanx may be extended with tissue forceps or by digital pressure on the footpad. See Figure 264-1. • Following excision of the phalanx with the nail trimmers, the wound should be examined, and the articular surface of the second phalanx should be visible. • A small palmar portion of the ventral unguicular crest may remain following excision with nail trimmers.
Figure 264-1 Resco® Nail Trimmer Technique: The cutting blade of a nail trimmer is positioned between the unguicular crest and the second phalanx with care taken to exclude the digital footpad. The third phalanx may be extended with tissue forceps or by digital pressure on the footpad.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
673
SECTION 4: Surgery
• Skin closure is optional, but most veterinarians use either a single absorbable suture for each wound or a drop of surgical grade cyanoacrylate tissue glue on the surface of each skin defect to close the wound. Glue should be applied only to the skin edges. Glue application into the wound will result in lameness until the glue is extruded.
• • •
Scalpel Blade • The cat is placed in lateral recumbency, and a tourniquet is applied proximal to the elbow. • The entire paw is prepared with surgical scrub; however, hair clipping is not necessary. • The nail is extended with digital pressure on the footpad or by using tissue forceps. • A number 11 scalpel blade is used to excise the entire third phalanx by severing all its ligament and tendon attachments. See Figure 264-2. • Complete excision is achieved by careful dissection, including the dorsal and ventral unguicular crest. • The digital pad should not be injured, and the articular surface of the second phalanx should be clearly visible following excision of the phalanx. • Skin closure is optional, but most veterinarians use either a single absorbable suture for each wound or a drop of cyanoacrylate tissue glue on the surface of each skin defect to close the wound. See previous glue instructions.
CO2 Laser • See Chapter 257 for further discussion of CO2 laser. • The cat is placed in lateral recumbency, and the paws are prepared for surgery with surgical scrub. Liberal amounts of water are used to
•
• • • •
remove the scrub and wet the surrounding hair. Alcohol is not used during the preparation because of its flammable nature. Tourniquets are not necessary except in cats over 2.7 kg (6 lbs). The laser is set at 4 to 6 watts, and the nail is extended with forceps of the surgeon’s choice. Onychectomy with the surgical laser is performed with the same hand movements as with a scalpel blade. The initial incision is made dorsally between P2 and P3, and then P3 is disarticulated by severing all ligamentous attachments between P2 and P3. This necessitates dissection around the ventral portion of the unguicular crest. Care is taken not to injure the digital footpad or P2 with the laser beam. A smoke evacuator is used to remove smoke and vaporized tissue debris from the surgical field. All charred tissue is wiped away before closure. Skin closure is optional; however, most veterinarians use either a single absorbable suture for each wound or a drop of surgical grade cyanoacrylate to close the wound. See glue instructions.
Postoperative Care Nail Trimmer and Scalpel Method • The tourniquet is removed after application of a snug bandage from the paw to the mid antebrachium. Excessive tension (tightening) of the bandage may compromise vascular supply to the extremity. Bandages are removed 12 to 24 hours before the cat’s discharge from the hospital. • Cats should be given an analgesic in the perioperative period. Buprenorphine is dispensed for oral administration to the cat for the first 3 to 6 days postoperatively.
Figure 264-2 Scalpel Technique: A number 11 scalpel blade is used to excise the entire third phalanx by severing all its ligament and tendon attachments. The same movements are used with a CO2 laser. (See Chapter 257.)
674
Onychectomy
• Shredded paper or recycled newspaper (Yesterday’s News™) is used in place of litter to minimize contamination for the first 7 days postoperatively.
Laser Method • Smaller cats (under 2.7 kg [6 lbs]) do not require bandaging following laser onychectomy; however, adult cats still benefit from bandaging for 24 hours. • Most cats undergoing laser onychectomy may be discharged the day after surgery; however, some cats hemorrhage as a result of excessive activity in the postoperative period because this procedure is associated with less pain than conventional declawing. For this reason, hospitalization for 48 hours following surgery is recommended with this method. • Perioperative buprenorphine is recommended for analgesia in the hospital, and it is administered at home for 3 to 6 days postoperatively. • Many veterinarians believe cats have less pain following laser onychectomy than with traditional techniques. Preliminary objective data suggests that laser onychectomy may be less painful in the immediate postoperative period (first 24 hours); however, there is no documented difference between laser and traditional methods with regard to pain after that time. • Shredded paper or recycled newspaper (Yesterday’s News™) is used in place of litter to minimize wound contamination for the first 7 days postoperatively.
• Some mature cats may be lame for up to 7 days postoperatively. • Persistent lameness may occur if too much cyanoacrylate tissue glue is placed in the wound; it should be carefully applied only to the skin edges. Ultimately it is extruded from the tissues, but prior to that it is a hard glue mass. • If the dorsal unguicular crest is not excised, partial claw regrowth may necessitate reoperation.
Laser Method • Inadvertent injury to surrounding tissue of the patient, laser operator, or assisting personnel is possible if care is not taken during laser use. • All personnel should wear appropriate protective eyewear. • The cat may have persistent lameness if too much cyanoacrylate tissue glue is placed in the wound; it should be carefully applied to the skin edges. Ultimately it is extruded from the tissues, but prior to that it is a hard glue mass.
Suggested Readings Hedlund CS. 2007. Surgery of the integumentary system. In SJ Ettinger, EG MacEwen, eds., Small Animal Surgery, 3rd ed., pp. 251–253. St. Louis: Mosby. Mison MB, Hauptman JG, Bohart GH, et al. 2000. Use of CO2 laser in feline onychectomy: a prospective, randomized clinical trial. Vet Surg. 29:470.
Complications Nail Trimmer and Scalpel Methods • Hemorrhage may occur postoperatively if the cat shakes its bandages off.
675
CHAPTER 265
Oronasal Fistula Repair Heloisa Justen Moreira de Souza
Overview An oronasal fistula is an abnormal communication between the oral and nasal cavities. Defects of the hard or soft palate allow food and liquid to pass easily into the nasal cavity. Palatal defects can be congenital or acquired. The palate separates the oral and nasal cavities. It consists of rostral and caudal parts. The rostral hard palate consists of bone covered dorsally by nasal epithelium and ventrally by the thick, ridged oral palatal epithelium. The caudal soft palate contains skeletal muscle between the epithelial surfaces; this muscle forms part of the nasopharyngeal sphincter that prevents food or fluid from entering the nose during swallowing. The right and left major palatine arteries are the main arteries to the mucoperiosteum of the hard palate. The major palatine artery passes through the caudal palatine foramen and the palatine canal. See Figure 265-1. It exits the palatine bone through the major palatine foramen and proceeds rostrally in the palatine groove on the surface of the hard palate. The palatine foramina are located medial to the maxillary fourth premolars. The major palatine vessels and nerves course rostrally in the palatine sulcus supplying the hard palate and adjacent soft-tissue structures. The palatine grooves, in which the vessels lie, are located halfway between the alveoli and the midline of the palate.
(A)
Congenital Oronasal Fistula Overview Congenital defects of the lip and palate may be inherited or result from intrauterine trauma or stress. Norwegian forest cats, Ocicat, Persian, Ragdoll, Savannah, and Siamese are breeds at higher risk. These anomalies are describes as affecting the primary palate (premaxilla and lip) and the secondary palate (hard and soft palates). Incomplete closure of the primary palate is a primary cleft or cleft lip (harelip). Defects of the secondary palate may appear as cleft hard or soft palate and are usually located on the midline. Cleft palate is a failure of the palatine processes to fuse properly resulting in a cleft or opening in the roof of the mouth. Soft palate defects without hard palate defects may sometimes be unilateral, or the soft palate may be entirely absent. Unilateral cleft of the soft palate occurs sporadically in cats.
Diagnosis Primary Diagnostics • History: A history of difficulty nursing, nasal regurgitation, and nasal discharge are common problems. The cleft is present at birth although it is not always recognized immediately. • Clinical Signs: Primary palate abnormalities rarely result in clinical signs other than an externally visible anomaly. Clinical signs of cats with secondary palate defects include failure to create negative pressure for nursing, nasal discharge, sneezing, nasal reflux, rhinitis,
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
676
(B) Figure 265-1 A, B, The major palatine arteries exit the palatine bone through the major palatine foramina (arrows) and proceed rostrally in the palatine grooves on the surface of the hard palate. The pathways of the arteries are simulated with red lines. The major palatine foramina are located approximately at the level of the fourth upper premolar teeth and midway between these teeth and the midline. Images courtesy of Prof Dr. José Miguel Farias Hernandez of University Federal Rural of Rio de Janeiro and Dra. Silvana Lima Marello.
Oronasal Fistula Repair
coughing, gagging, and poor weight gain. Abnormal respiratory sounds are auscultated if aspiration pneumonia is present. • Visual Examination: Incomplete closure of lip is noted. • Oral Examination: All kittens should be checked on initial presentation for evidence of a cleft palate. Inspection of the oral cavity reveals incomplete closure of the premaxilla, hard palate or soft palate.
Surgical correction is best performed on cats at 3 to 4 months of age; the larger the cat is at the time of surgery the better because more tissue is available for surgical manipulation. The primary goal of repairing a cleft palate is to reconstruct the nasal floor. Multiple procedures may be necessary before the entire cleft is permanently reconstructed. Secondary clefts are frequently repaired with sliding bipedicle flaps and overlapping “sandwich” flap techniques.
Diagnostic Notes • Always evaluate cats with cleft palates for other congenital anomalies.
Treatment Closure of Primary Clefts The most rostral palate and the floor of the nasal vestibule are reconstructed by creating overlapping double flaps and advancement, rotation, or transposition flaps of both oral and nasal tissue or flaps that are harvested from oral soft tissue only. Extraction of one or more incisors and also the canine tooth on the affected side 6 to 8 weeks prior to surgery will facilitate flap management. Lip repair is challenging and requires reconstructive cutaneous surgery to provide symmetry.
Surgical Procedure Sliding Bipedicle Flap • Incise the margins of the defect and make bilateral releasing incisions along the margins of the dental arcade. See Figure 265-2A. • Elevate the mucoperiosteal layer on both sides of the defect with a periosteal elevator. See Figure 265-2B. Avoid damaging the major palatine arteries. Control hemorrhage with pressure and suction. Appose the nasal mucosal edges or periosteum at the margin of the defect with buried interrupted sutures. Slide the elevated mucoperiosteal flaps across the defect and appose with simple interrupted sutures. See Figures 265-2C and 2D. • Various suture materials have been used successfully in the oral cavity. Absorbable and non-absorbable sutures usually slough within 3 to 4 weeks. • Allow the denuded hard palate near the dental arcades to heal by second intention. See Figure 265-2E.
Closure of Hard Palate Defects Management of cats with congenital defects of the secondary palate requires nursing care by the owner. In most affected cats, tube feeding of a milk substitute several times daily is necessary to avoid recurrent and eventually fatal aspiration pneumonia. Prognosis without surgical repair is grave because of the risk of lower airway aspiration.
(A)
Overlapping “Sandwich” Flap • Incise one margin of the defect separating the oral and nasal mucosa. Elevate the mucoperiosteum at this edge approximately 5 mm (3/16 in). At the opposite side of the defect create a mucoperiosteal rotational flap large enough to cover the defect with its base hinged
(B)
Figure 265-2 A, Incise the margins of the defect and make bilateral releasing incisions along the margins of the dental arcade. B, Elevate the mucoperiosteal layer on both sides of the defect with a periosteal elevator.
677
SECTION 4: Surgery
(D) (C)
(E) at the margin of the palatal defect. Begin the incision near and parallel to the dental arcade creating a flap 2 to 4 mm (1/16–1/8 inch) larger than the defect. Make perpendicular incisions at the rostral and caudal end of the incision extending to the cleft. Elevate this mucoperiosteal flap being careful not to disrupt the margin of the defect. Dissect carefully around the palatine artery to release it from fibrous tissue. • Rotate the flap across the defect. Place the edge of the flap under the mucoperiosteal flap on the opposite side. • Preplace and then tie a series of horizontal mattress sutures to secure the flaps in position.
678
Figure 265-2 Continued C, The nasal and oral mucosas are closed in separate layers. D, Allow the denuded hard palate near the dental arcades to heal by second intention. E, Healing has progressed well after 1 week.
Double Flap for Repair of Soft Palate Defects • Soft palate defects are repaired with either technique previously described. Feline tissues must be handled gently. • Incisions at the end of the hard palate are continued onto the soft palate at the junction of the oral and nasal epithelia to the level of the middle of the tonsils. These incisions are deepened by gentle blunt dissection to form a dorsal and ventral flap on each side. The dorsal flaps are sutured to appose the nasal epithelial edges, placing the suture knots on the epithelial surface to minimize scar tissue formation with the muscle tissue of the palate. The ventral flaps then are sutured together to appose the oral epithelium.
Oronasal Fistula Repair
Acquired Oronasal Fistula Overview Acquired palatal defects may occur in adult cats for various reasons, including trauma (e.g., high-rise injuries, dog bites, electrical shock, gunshot wounds, and foreign body penetration causing necrosis of the hard palate), or they can be a complication of surgery, neoplasms, radiation, or of hyperthermic treatment of oral lesions.
Diagnosis Primary Diagnostics • History: Acquired oronasal fistula should be suspected in a cat at any age with chronic rhinitis and a history of trauma or previously treated oral tumor. • Clinical Signs: Serous or mucopurulent nasal discharge and sneezing are common. Ingested food or liquid that passes through the fistula into the nasal cavity may be expelled from the nostril by sneezing. • Oral Examination: Inspection of the oral cavity reveals an oronasal fistula.
Treatment Primary Therapeutics • Small Defects: Many defects in the hard palate can be closed by some form of mucoperiosteal flap without tension and with a good blood supply. Midline palatal defects are frequently repaired with a sliding bipedicle flaps and overlapping “sandwich” flap techniques. Fractures of the hard palate are usually midline in locations and
(A)
frequently seen most commonly in high-rise syndrome. These types of injuries may vary from a barely noticeable split to a substantial gap. Most will heal spontaneously within several weeks, and surgical intervention should only be planned for severe cases and those which persist and cause clinical signs for over a month post-injury. • Large Defects: These are usually located in the caudal aspect of the palate can be frustrating to repair; postoperative dehiscence is a common complication. The application of the split palatal U-flap or advancement flap techniques may be an option for repairing acquired palatal defects located in the central and caudal aspect of the hard palate. Others methods such as free cartilage graft harvested from either the pinna (scapha) or vertical ear canal (annular cartilage) or a silastic nasal septal button can be used. For extensive rostral hard palatal defects, tongue flap may be another option. Surgical Procedures Split Palatal U-Flap • The split palatal U-flaps are used to repair acquired palatal defects located in the central and caudal aspect of the hard palate. • The patient should be placed in dorsal recumbency with the premaxilla taped to the surgical table and the mandible taped caudally in an open position. • Perform sharp debridement of the epithelial margins of the palate defect using a number. 15 Bard-Parker® scalpel blade. • A large full-thickness U-shaped mucoperiosteal flap is created anterior to the defect. The incisions begin at the level of the rostral aspect of the defect. The palatal mucoperiosteum is incised 3 to 4 mm (1/16– 1/8 in) from the maxillary arcade in each quadrant extending to the level of the second premolar. See Figure 265-3A and 3B. • Bleeding may occur when the major palatine artery at the rostral extent of the flap is transected. • A midline incision is made at the rostral aspect of the defect.
(B)
Figure 265-3 A, The split palatal U-flaps are used to repair acquired palatal defects located in the central and caudal aspect of the hard palate. B, A large U-shaped flap is created rostral to the defect. The major palatine arteries should be preserved during the creation of the U-flap. The U-flap is divided on the midline. The left side of the U-flap is rotated 90 degrees into the defect and sutured into place. C, The right side of the U-flap is also rotated 90 degrees into the defect and transposed anterior to the left flap. D, The exposed palatal bone will heal by reepithelialization within 1 to 2 months. This picture was made 4 weeks after surgery.
679
SECTION 4: Surgery
(C)
(D)
Figure 265-3 Continued
• Two equally sized flaps are created by gently and subperiosteally elevating the flap from the bone. The flaps are elevated to the level of the anterior aspect of the maxillary fourth premolar using a periosteal elevator. • Flaps with an excellent blood supply are created because the major palatine artery is located at the base of each flap. These two flaps are gently rotated 90 degrees and transposed to cover the defect. • The left flap is rotated into the palatal defects. The medial aspect of left flap is sutured to the caudal aspect of the palatal defect. The tip of left flap is then sutured to the lateral aspect of the defect. See Figure 265-3C and 3D. • The right flap is rotated 90 degrees and transposed anterior to left flap. The medial aspect and tip of right flap are sutured to the edge of left flap. • Absorbable 3-0 or 4-0 sutures (polyglycolic acid, polyglactin 910, or chromic gut) are placed in a simple interrupted pattern. • The rostral aspect of the palate from which the U-flap is harvested is devoid of a mucoperiosteal covering. The exposed palatal bone will heal by reepithelialization within 1 to 2 months. • Systemic antibiotics should be considered based on the medical status of the case. • Soft food should be given for 2 to 3 weeks or a feeding tube can be placed. Tongue Flap • The edges of the dorsal aspect of the tongue are excised and apposed to the debrided edges of the palatal defect. • Oral feeding should be prevented to avoid dehiscence or perforation of the flap separating the oral and nasal cavities postoperatively. Feeding via esophagostomy tube or gastrostomy tube should be done until the flap is removed.
680
• Approximately 4 weeks later the tongue is separated from the palate leaving enough tongue with the palate to close the defect without tension. • Alternative techniques to tongue flaps are recommended whenever possible because of the high incidence of dehiscence associated with tongue flaps. Silastic Nasal Septal Button • This technique is used to close large defects located in the caudal aspect of the palate. • The defect is obscured using a 3-cm (1 1/8-in) conical silastic nasal septal button (Hood nasal septal button with Ultra-smooth®, Hood Laboratories) with a 7-mm (5/16-in) diameter core. • The patient is placed in dorsal recumbency, and the oral cavity is prepared aseptically. See Figure 265-4A. • The transparent device is shaped by trimming before insertion and placed in the oronasal fistula. See Figure 265-4B. • One portion of the double-sided device is positioned on each side of the oronasal fistula, providing obturation of the defect in 5 minutes. See Figure 265-4C. • Patients typically tolerate the prosthetic appliance without apparent complications. The procedure of managing the traumatic fistula with the conical prosthetic device is fast, easy, and efficient, when compared to other prosthetic appliances. See Figure 265-4D. • The device should be removed and replaced with a new one in 2 years. • Note: This device should be considered after surgical treatment has failed to close the oronasal fistula. This method would appear particularly useful in similar cases for obturation of large, recurrent oronasal fistulae and as an alternative treatment for debilitated cats that cannot undergo surgical repair.
Oronasal Fistula Repair
(A)
(C)
(B)
(D)
Figure 265-4 A, A silastic nasal septal button is used to close large defects located in the caudal aspect of the palate. This fistula measured 2.2 × 1.6 cm (7/8 × 5/8 in) and was due to trauma. B, The device is shaped to fit the defect by trimming with scissors and placed in the oronasal fistula. C, Each piece of the device is positioned on opposite sides of the oronasal fistula. D, It is not necessary to suture the device. It will be fit in both cavities, closing the fistula.
Suggested Readings Beckman BW. 2006. Split palatal U-flap for repair of caudal hard palate defects. J Vet Dent. 23(4):267–269. Cox CL, Hunt GB, Cadier MM. 2007. Repair of oronasal fistulae using auricular cartilage grafts in five cats. Vet Surg. 36(2):164–169. Griffiths LG, Sullivan M. 2001. Bilateral overlapping mucosal singlepedicle flaps for correction of soft palate defects. J Am Anim Hosp Assoc. 37(2):183–186. Hedlund CS. 1997. Surgery of the oral cavity and oropharynx. In SJ Withrow, EG MacEwen, eds., Small Animal Surgery, pp. 200–232. St Louis: Mosby.
Marretta SM, Grove TK, Grillo JF. 1991. Split palatal U-flap: A new technique for repair of caudal hard palate defects. J Vet Dent. 8(1):5–8. Sager M, Nefen S. 1998. Use of buccal mucosal flaps for the correction of congenital soft palate defects in three dogs. Vet Surg. 27(4):358–363. Smith MM. 2000. Oronasal fistula repair. Clin Tech Small Anim Pract. 15(4):243–250. Smith MM, Rockhill AD. 1996. Prosthodontic appliance for repair of an oronasal fistula in a cat. J Am Vet Med Assoc. 208(9):1410–1412. Souza HJM, Amorim FV, Corgozinho KB, et al. 2005. Management of the traumatic oronasal fistula in the cat with a conical silastic prosthetic device. J Feline Med Surg. 7 (2):129–133.
681
CHAPTER 266
Pain Management Sabine Tacke
Overview Pain management in cats is a challenge. Recognition of pain is difficult, metabolism of drugs is different from dogs, and administration of medication is sometimes a problem. In this chapter only the special considerations concerning pain management in cats are described. Signs of pain in cats take many forms. Changes in behavior (e.g., crying, yowling, growling, hiding or separating itself from other cats, unusual quietness, incessant licking, lack of appetite, and urinating in unusual places), appearance, and posture or movement can signal pain. It is important to obtain as much information as possible from the owner concerning changes in behavior, especially if chronic pain is suspected. Sometimes pain is first recognized after administration of an analgesic; this can be used as a diagnostic test. Cats suffer from acute and chronic pain. Regardless of the type of pain (i.e., acute, chronic, traumatic, neuropathic, inflammatory, or neoplastic), pain management should start as soon as it is recognized. It is important to regularly assess pain levels to determine the success of treatment.
Analgesics Analgesics used in cats include opioids, nonsteroidal anti-inflammatory drugs (NSAIDs), local anesthetics, and others (e.g., ketamine, α2adrenergic-agonists). Spasmolytics, anticonvulsants (e.g., gabapentin and pregabalin), and tricyclic antidepressants are adjuvant analgesics because they can help to reduce pain in cats. It is important to realize that acepromazine, alfaxalone, barbiturates, benzodiazepines, inhalant anesthetic agents (e.g., isoflurane, sevoflurane, and desflurane), and propofol are not analgesic drugs.
Opioids Opioids are very potent analgesics (see Table 266-1). They are effective for treatment of moderate-to-severe pain and should be part of the therapy plan for trauma and surgical procedures. If opioids are given before surgery (pre-emptive) they can reduce intraoperative stress reactions, postoperative pain, and the consumption of other anesthetics (balanced anesthesia). Many adverse effects of opioids are the same in cats as in other species (e.g., bradycardia, respiratory depression, and sedation). Some of these side effects are seen at anesthetic dosages but not in conscious cats. A unique side effect of opioids in cats is mydriasis instead of miosis. However, the diameter of the pupil does not directly correspond to the analgesic effect. Mydriasis can result in aversion to bright light and inability to focus. Opioids can decrease gut motility resulting in inappetence. They can also cause an opioid-related hyperthermia resulting in body temperatures greater than 40°C (104°F). This phenomenon has been described with morphine, hydromorphone, butorphanol, and buprenorphine. Opioids should be used with caution in patients with head trauma because respiratory depression leads to an increase in PaCO2, and this
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
682
can lead to cerebral vasodilation with an increase in intracranial pressure. The antagonist naloxone (0.01–0.04 mg/kg IV or IM) can be used if significant side effects occur. Because this drug antagonizes the analgesic effects of opioids, another analgesic should be used following administration of naloxone. Nalbuphine (0.5–1.5 mg/kg IV) is an alternative antagonist that can be used to reverse undesired effects of µ agonist while permitting maintenance of some analgesia. Usually the duration of action of the antagonists is shorter than the duration of action of the agonist; therefore, repeated doses of the former could be necessary.
Nonsteroidal Anti-Inflammatory Drugs Nonsteroidal anti-inflammatory drugs (NSAIDs) have analgesic, antiinflammatory, and antipyretic activity (see Table 266-2). They are frequently used in dogs with osteoarthritis (OA). Cats have limited hepatic glucuronidation so side effects occur more frequently because drug metabolism fails to eliminate NSAIDs rapidly enough. However, some NSAIDs, like meloxicam, are metabolized via oxidation, which is efficient in cats. NSAIDs are indicated in mild to moderate, inflammatory, acute, and chronic pain. If NSAIDs are given preoperatively, sufficient perfusion of the kidneys and normal blood pressure must be sustained during surgery. One of their advantages is the long duration of analgesia; one dose may last up to 24 hours. Side effects of NSAIDs include renal, hepatic, and gastrointestinal toxicity; therefore, they should not be used in patients with pre-existing renal or hepatic disease. Hypovolemia, dehydration, shock, and hypotension are also contraindications for the use of NSAIDs. NSAIDs should not be combined with corticosteroids because NSAIDs are inhibitors of the cyclo-oxygenase, and corticosteroids are inhibitors of phospholipase A2. Both are involved in arachidonic acid metabolism, and their combination can enhance side effects. Paracetamol (acetaminophen), ibuprofen, and naproxen are toxic in cats.
Local Anesthesia The classic mode of action of local anesthetics is reversible inhibition of nerve function (see Table 266-3). This leads to a loss of sensation, analgesia, and inhibition of active mobility in the anesthetized body region. In contrast to human medicine, sedation is often necessary for administration of local anesthetics to veterinary patients. Sedation also reduces the anesthetic risk for the patient. Local anesthesia could be an effective tool in trauma and surgery patients. It provides complete analgesia with minimal side effects. Local anesthetics may be administered topically (e.g., eye or larynx), infiltrated SC, injected around nerves, intra-articularly, or epidurally. Adverse drug reactions and other complications are rarely seen if local anesthetic drugs are properly administered. There is a lag time of up to 5 minutes before the onset of action, depending on the local anesthetic administered. In addition to local infiltration anesthesia and peripheral nerve blocks, epidural anesthesia is a significant way local anesthetics are used in cats. Local anesthetics can be mixed with opioids (e.g., morphine) to potentiate the analgesic duration. The duration of the analgesic action of morphine (0.1 mg/kg epidural) is 24 to 40 hours making it effective for early postoperative pain.
Pain Management
TABLE 266-1: Commonly Used Opioids in Cats
Opioid
Dose (mg/kg)
Buprenorphine
0.005–0.01 0.005–0.04
Butorphanol
0.1–0.4
Fentanyl
0.001–0.005 0.0024–0.04/h
Route of administration IV IM, SC, or transmucosal IV, IM, or SC
Onset of analgesia (minutes)
Duration of analgesic action (hours)
30–45
Analgesic efficacy
Comment
3–4 4–12
moderate
rapid
1–4 2–6
weak to moderate
immediate
0.2–0.5
very strong
Partial µ-agonist; licensed for use in cats in United Kingdom, Germany Agonist-antagonist; visceral analgesic; hyperthermia and mydriasis common µ-agonist; before CRI give a bolus as loading dose; see important precaution in footnote1.
360–720 rapid
>72 4–6
strong
0.002–0.004/h 0.05–0.1 0.1–0.5
intravenous bolus intravenous CRI* intraoperative intravenous CRI* postoperative patch IV IM, or SC
Morphine
0.05 0.1–0.3
IV IM, or SC
20–30 45–60
1–4 4–6
strong
Oxymorphone
0.05–0.1
IV, IM, or SC
fast
2–6
very strong
0.005–0.01/h
Methadone
µ-agonist; less side effects; also acting at N-methyl-D-aspartic acid-receptors µ-agonist; after intravenous injection only 50% of the cats had detectable active metabolite µ-agonist licensed for cats in United States; hyperthermia not reported; after intravnous shorter duration of analgesic action
*CRI, constant rate infusion per hour. 1. Keep out of the reach of children. Fentanyl patches can cause injury or death in adults and children who are not already taking fentanyl to relieve chronic pain. Even after the patch has been removed, it still contains enough fentanyl to cause serious side effects and even death to children or pets.
TABLE 266-2: Commonly Used Nonsteroidal Anti-Inflammatory Drugs in Cats Nonsteroidal anti-inflammatory drug
Dose (mg/kg q24h)
Route of administration
Carprofen
2–4, maximum 3 days
IV, SC, or IM
Ketoprofen Meloxicam
1–2, maximum 3 days 0.3 once 0.1 once followed by 0.05 q24–48h
IV, SC, or IM SC perioperatively PO long term
Comment Half-life after intravenous injection ranged from 9 to 49 hours; not licensed for use in cats in United States Can alter platelet function and increase bleeding Oral formulation is palatable to most cats; licensed in several countries (not in United States) for long term use in cats with osteoarthritis
TABLE 266-3: Commonly Used Local Anesthetics Local Anesthetic
Maximal Dose (mg/kg)
Onset of Analgesia (min)
Duration of Analgesic Action (min)
Lidocaine Mepivacaine Bupivacaine
5 5 2
10–15 5–10 20–30
30–120 90–180 180–480
Local anesthetics combined with epinephrine should not be used for peripheral nerve blocks (e.g., digital nerve block for onychectomy) because epinephrine can lead to vasoconstriction and reduced tissue perfusion. A mixture of lidocaine and prilocaine in a cream formulation can be used as a topical local anesthetic for venipuncture, skin biopsy,
wound debridement, and catheter placement. It should be applied to shaved skin at least 30 to 45 minutes before the procedure is to be performed. Constant rate infusion of lidocaine is not recommended in cats because it is arrhythmogenic. For specific uses of local anesthetics see Chapter 246.
683
SECTION 4: Surgery
Other Analgesic Drugs α2-adrenoceptor-agonists Dexmedetomidine, medetomidine, and xylazine are primary acting sedative agents with some analgesic effects in cats; they also provide good muscle relaxation. Therefore, they are mostly used as sedatives in an anesthetic protocol. They are contraindicated in cats with cardiovascular disease, shock, or pre-existing hypovolemia because α2adrenoceptor-agonists can lead to cardiovascular depression and peripheral vasoconstriction. In cardiovascularly stable, healthy patients medetomidine can be used for analgesia as a constant rate infusion (1–g/kg per hour IV). Medetomidine is not licensed for use in cats in the United States, but it is in several other countries.
Ketamine Ketamine is a noncompetitive antagonist of the N-methyl-D-aspartate receptor. It is particularly effective in preventing central sensitization. Its analgesic efficacy is good, and ketamine acts against ischemic and somatic pain. It is primarily used as part of an anesthetic protocol (1, 5, or 10 mg/kg IM) to provide dissociative anesthesia. A dose of 1 to 2 mg/ kg IM provides good analgesia in cats without signs of excitation. Ketamine could be administered as a constant rate infusion during anesthesia (0.6 mg/kg per hour) and for postoperative pain management (0.12 mg/kg per hour up to 24 hours).
Gabapentin Gabapentin (5–20 mg/kg q12h PO) is useful for neuropathic pain (e.g., intervertebral disk disease or after limb amputation). Some studies indicate that gabapentin could also be used to prevent pain during surgery. The most undesirable side effect is sedation.
Corticosteroids Corticosteroids, such as prednisone (initially 1–2 mg/kg q12–-24h PO, IV, or IM then taper to q48h), prednisolone (initially 1–2 mg/kg q12–24h PO, IV, or IM then taper to q48h), and dexamethasone (0.1 mg/kg q24h SC, PO, or IV up to 5 days), can be used for inflammatory pain if other drugs, like NSAIDs, are not successful or available. Corticosteroids and NSAIDs should not be used in combination because side effects are more likely.
684
Amitriptyline Amitriptyline (2.5–12.5 mg/kg q24h PO) has been used to reduce pain caused by idiopathic cystitis with mixed results.
Multimodal Approach A multimodal approach to analgesia is based on the concurrent use of drugs that act at different levels of the pain pathway, leading to better analgesia. In addition, side effects may be reduced. For example the combination of buprenorphine (0.01 mg/kg IM) and carprofen (4 mg/kg SC) leads to a reduction in postoperative (ovariohysterectomy) pain scoring compared to buprenorphine or carprofen alone. Multimodal pain therapy can also mean the combination of analgesics with physiotherapy, casts or bandage, tender loving care, and complementary methods. In human medicine, many complementary methods are described as effective for pain therapy, but in veterinary medicine only a few scientific papers exist. Acupuncture has been shown to be effective for controlling pain during surgery and for chronic pain due to osteoarthritis.
Suggested Readings Bockstahler B, Levine D, Millis D. 2004. Essential facts of physiotherapy in dogs and cats: Rehabilitation and pain management. Babenhausen: BE VetVerlag. Hammond R, Macdonald C, Nicholson A. 2008. Opioid analgesics. In JE Madison, S Page, D Church, eds., Small Animal Clinical Pharmacology, 2nd ed., pp. 309–329. Philadelphia: Elsevier Saunders. Hellyer P, Rodan I, Brunt J. 2007. AAHA/AAFP pain management guidelines for dogs & cats. J Am Anim Hosp Assoc. 43:235–248. Lascelles BD, Court MH, Hardie EM. 2007. Nonsteroidal anti-inflammatory drugs in cats: a review. Vet Anaesth Analg. 34:228–250. Lascelles BD, Hansen BD, Thomson A, et al. 2008. Evaluation of a digitally integrated accelerometer-based activity monitor for the measurement of activity in cats. Vet Anaesth Analg. 35:173–183. Plumb, Donald C. 2008. Plumb’s Veterinary Drug Handbook. Ames: Iowa State University Press. Robertson SA. 2008. Managing pain in feline patients. Vet Clin North Am Small Anim Pract. 38:1267–1290. Steagall PV, Taylor PM, Rodrigues LC, et al. 2009. Analgesia for cats after ovariohysterectomy with either buprenorphine or carprofen alone or in combination. Vet Rec. 164:359–363.
CHAPTER 267
Perivulvar Skin Fold Removal Gary D. Norsworthy
Definition This procedure, also known as episioplasty, is to remove vertical skin folds that lie lateral to the vulva. They are often so large that the vulva is not visible. See Figure 267-1. They occur primarily in obese cats and frequently become infected due to urine pooling following urination. The dermatitis or pyoderma that begins in the skin folds may spread to the entire perineum and the ventral aspect of the tail. See Figure 267-2.
• Mirrored, elliptical, vertical incisions are made lateral to the vulva wide enough to completely remove the skin folds. At least 2 mm (1/8 in) of skin must remain lateral to the vulva to permit suturing. See Figure 267-3. • The incisions are closed with simple interrupted sutures placed approximately 2 mm (1/8 in) apart. Begin at the center of the incisions
Equipment and Sources • A routine surgery pack • Soft, absorbable 3-0 or 4-0 suture material (I prefer polyglactin 910)
Procedure • If perineal dermatitis or skin fold pyoderma is present, it must be resolved prior to surgery. Systemic antibiotic treatment and local treatment may take 1 to 4 weeks to resolve the infection. • The perineum is clipped and prepared for aseptic surgery. The cat is positioned in ventral recumbency with the tail extended over the dorsal lumbar area. A roll of gauze is inserted through the anus to prevent dropping of stool. Alternatively, a purse string suture can be used to close the anus, but it must not be pulled so tight as to distort the perianal skin. Figure 267-2 If perineal dermatitis is present, it must be resolved prior to surgery. The dermatitis may extend to the ventral surface of the tail as seen in this cat.
Figure 267-1 The abnormal skin folds (arrows) are located lateral to the vulva, which is usually not visible without moving the skin folds laterally.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 267-3 Mirrored, elliptical, vertical incisions are made lateral to the vulva (arrow) wide enough to completely remove the skin folds. At least 2 mm (1/8 in) of skin must remain lateral to the vulva to permit suturing.
685
SECTION 4: Surgery
Figure 267-4 The incisions are closed with simple interrupted sutures placed approximately 2 mm (1/8 in) apart. Begin at the center of the incisions and alternate sutures between incisions to achieve symmetry and a smooth skin contour.
Figure 267-5 When the suturing is completed the incisions will be closed, and the vulva will be clearly visible.
and alternate sutures between incisions to achieve symmetry and a smooth skin contour. See Figures 267-4 and 267-5. The ends of the sutures should be cut short so they do not encourage licking. • An Elizabethan collar is placed on the cat for 24 to 48 hours postoperatively and as needed thereafter.
• If the cat gains weight following surgery, new skin folds may form. Weight loss should be encouraged to prevent recurrence.
Complications • If the elliptical incisions are not identical, asymmetry will result. • Failure to excise adequate skin will not achieve a smooth contour needed to prevent recurrence.
686
Suggested Readings Fossum TW. 2002. Surgery of the reproductive and genital systems. In TW Fossum, ed., Small Animal Surgery, 2nd ed., pp. 610–674. St. Louis: Mosby. White RAS. 2006. Surgical treatment of specific skin disorders. In DH Slatter, eds., Textbook of Small Animal Surgery, 3rd ed., pp. 339–355. Philadelphia: Saunders.
CHAPTER 268
Physical Therapy and Rehabilitation Barbara Bockstahler and David Levine
Overview Physical therapy and rehabilitation is a rapidly growing field in veterinary medicine. To help ensure optimal treatment adequate knowledge should be obtained about the different physical modalities used but also about the pathophysiology and treatment of the underlying disease, the anatomy and physiology of the tissues and their healing processes, and the timing of introducing rehabilitative techniques to the tissues based on their strength. In this chapter a short overview of common physical therapy interventions are given. For more detailed information, there are several textbooks on physical therapy for small animals available. In contrast to dogs, the feline patient is underrepresented in veterinary physical therapy and rehabilitation. This might be a consequence of the false belief that cats are not treatable with traditional methods of physical therapy because of their behavior. Although the species-related behavior of cats makes it somewhat more difficult to handle the patient, cats have some unique characteristics that can be used in the development of a rehabilitation program.
Examination Before starting a physical therapy program, a thorough clinical examination has to be performed. Never start a rehabilitation program without a clinical diagnosis. In addition to the physical examinations special attention should be given to: • General Muscle Condition, Symmetry, and Tone: Older cats or cats that have undergone a prolonged period of immobilization, such as cage rest, often show muscle atrophy and decreased muscle strength. The muscle mass of the limbs can be easily measured using a tape measure, but it is crucial to always measure the limb circumference in the same location. In cases of neurological disorders, the muscle tone can be diminished or increased. Painful muscle spasms that often occur secondary to orthopedic and neurological disorders can also be detected. • Passive Range of Motion of Joints: This means the full comfortable motion that a joint can be moved through without resistance or signs of discomfort. The passive range of motion can be measured with a goniometer. The joint is flexed and extended through its range of motion and the values are read from the goniometer. Jaegger (2007) reported range of motion values (flexion/extension) in normal cats for the carpal joint 22 degrees /198 degrees, elbow 22 degrees/163 degrees, shoulder 32 degrees/163 degrees, tarsal 21 degrees/167 degrees, stifle 24 degrees/164 degrees, hip 33 degrees/164 degrees.
Special Recommendations • In general, cats are less tolerant than dogs, and therefore, it is more difficult to perform exercises with them. • Cats are relatively impatient and quickly bored. Therefore, the time of the session should be as short as possible and offer a variety of different activities.
• Behavioral characteristics of cats, such as playing and hunting, can be used to design active exercise. • Not all treatments are tolerated by all cats. Some cats enjoy electrotherapy or ultrasound treatment, some do not. Therefore, each therapy should be introduced carefully to avoid injuries of the patient and the therapist. • Some cats will tolerate hydrotherapy. Nevertheless, for the majority of the cats this causes high stress and should be only used as a last option.
Techniques Massage Massage has been proven as an effective treatment modality in several conditions, such as low back pain in humans, and is often recommended for rehabilitation of small animals.
Biological Effects There are many beneficial therapeutic effects of massage, such as the increase of blood flow, increasing oxygen supply, and the release of endogenous endorphins, which can be used effectively in the rehabilitation.
Methods A lot of different massage techniques are described in the literature, the most commons classic or “Swedish” ones are: • Effleurage is a superficial technique to increase blood flow and make the cat comfortable with the treatment. • Petrissage is a kneading type of massage and is effective to increase blood supply, and the mobility and length of fibrous tissues. It increases the extensibility and strength of connective tissues. • Friction is a deep form of massage that can help to restore the mobility between tissue interfaces.
Indications, Precautions, and Contraindications Indications for massage are improvement of muscle spasms secondary to musculoskeletal disorders, increasing blood flow, increasing elasticity of tendons and ligaments, improving the joint and muscle function, and to prevent tissue adhesions after surgery. Massage should not be used in case of tumors, infections, cardiac decompression, fever, or bleeding disorders.
Use of Heat Biological Effects
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Heat can be applied to increase the blood flow and the metabolic rate of tissues, relax muscles, relieve pain, and increase the extensibility of connective tissues.
687
SECTION 4: Surgery
Methods To heat tissues up to a depth of 2 cm (3/4 in), commercially available hot packs can be used. They are applied to the affected body part for about 15 to 20 minutes, one to three times daily, commonly before some activity such as range of motion and stretching.
Indications, Precautions, and Contraindications It is useful in cases of osteoarthritis, back pain due to spondylarthrosis, disc lesions or other spinal conditions, muscle spasms, and to prepare tissues such as muscles and tendons for exercise. Contraindications include acute inflammations, tumors, open wounds, severe cardiac insufficiency, and decreased sensation in the treatment area.
Use of Cold Biological Effects The application of cold (or cryotherapy) causes vasoconstriction and therefore, reduces bleeding in the area after injury or surgery. Cold also decreases the metabolism of cells, decreases nerve conduction velocity, and helps to alleviate pain.
Indications, Precautions, and Contraindications Cold is used to decrease swelling, pain, and the overall inflammatory process after surgery and exercise and reduce swelling and pain in acute stages of osteoarthritis for example. Cold should not be used in case of paresthesia and circulatory disorders.
Methods To cool tissues commercial available cold packs or ice packs can be used. They are typically wrapped in a towel and placed directly on the affected body part for about 10 to 15 minutes, one to three times daily.
the heart or in cats with peacemakers, in areas at risk for embolism, over tumors or infections, over the epiphyseal area of immature physis, and over the spinal cord after laminectomy.
Methods • The choice of the mode (continuous or pulsed) depends on the desired effects. The thermal effects are pronounced with a continuous mode; the tissue healing effects are pronounced if a pulsed mode is used. • The choice of the frequency depends on the depth of the target tissue. • The intensity for ultrasound is generally between 0.5 (little soft tissue) to 1.5 (large amount of soft tissue) W/cm2. For pulsed treatments with the goal of wound healing, specific guidelines have been developed (Millis, Levine, Taylor, 2004). • The treatment time depends on the size of the area and of the sound head. Generally 4 minutes for each sound head that fits into the treatment area (e.g., sound head size 5 cm2, treatment area 10 cm2: 8 minutes). • The treatment area must be shaped, and a suitable contact gel must be used. Hair must be clipped for effective transmission and to avoid burns. • The sound head must be slowly moved during the treatment to avoid overheating the skin.
Electrotherapy Electrical stimulation is a useful therapeutic modality and is often possible in cats; in fact, many cats like this modality. The two most common uses for electrical stimulation are for muscle strengthening and pain control.
Biological Effects For muscle strengthening, the motor nerve is stimulated, which causes a muscle contraction. For pain control, analgesia occurs due to several mechanisms such as the Gate Control Theory and the release of endogenous endorphins.
Therapeutic Ultrasound In physical therapy therapeutic ultrasound is commonly used for deeptissue heating to improve the extensibility of connective tissues, to decrease pain and muscle spasms, and to promote tissue healing and improve the quality of scar tissue. Two frequencies are used, 1.0 and 3.3 MHz; 1 MHz is absorbed at a depth of 2 to 5 cm, whereas 3.3 MHz acts more superficially at a depth of 0 to 3 cm. Two modes of ultrasound are used; continuous (100%) and pulsed (typically 20%).
• Hyperemia is caused by muscle contraction and the release of vasoactive substances.
Indications, Precautions, and Contraindications Electrical stimulation is often used for pain management, improvement of muscle spasms, prevention of muscle atrophy, and muscle strengthening. Precautions and contraindications include anesthetized areas of skin, acute inflammation, infection, and tumors.
Biological Effects Depending on the mode the biological effects of ultrasound differ: • Continuous Mode: The thermal effects are higher, and it is primarily used for tissue heating prior to stretching. • Pulsed Mode: The thermal effects are minimal, but a variety of effects may occur based on the phase of tissue repair. These include an acceleration of the inflammatory process, increased fibroblast proliferation, increasing tensile strength of healing tissues, and numerous others.
Electrodes A variety of electrodes are available (e.g. rubber, gel, and needle); with exception of needle electrodes, the skin must be clipped before treatment, and a suitable contact medium, such as ultrasound gel, must be applied. Electrodes can be placed directly on the painful area, segmentally via the nerve innervating the target tissue, over acupuncture or trigger points, and to stimulate muscle over the motor point and the muscletendon junction. See Figure 268-1.
Indications, Precautions, and Contraindications Common indications include increasing tissue temperature prior to stretching, decreasing pain, treatment of calcifying tendinitis, and the acceleration of the wound healing process. It should not be used over
688
Therapeutic Exercises Therapeutic exercises are one of the most important parts of the rehabilitation process. The design of the therapy program depends strongly
Physical Therapy and Rehabilitation
Figure 268-1 Electrotherapy using needle electrodes (PT2000, S+BmedVet) is applied to the back of this cat with lumbar pain.
Figure 268-2 on the needs of the individual patient and should ensure that the exercises can be performed safely without the risk to worsen the symptoms. The exercises should be selected based on the stage of tissue repair, and therefore, the therapist should understand the underlying pathology, the expected recovery progress, and biomechanical considerations.
Indications, Precautions, and Contraindications These are performed to achieve many goals including improving range of motion, increasing muscle mass, strength, conditioning and endurance, active pain-free range of motion and joint function, use of the limbs, coordination and proprioception, and performance and daily function. Therapeutic exercises are contraindicated if the desired movement could worsen the state of the disorders (e.g., high impact exercises in acute cases of osteoarthritis or directly after fracture stabilization).
Passive Range of Motion Passive range of motion (PROM) occurs when a joint is moved without an active muscle contraction of the patient within the available range of motion. Adding and holding additional pressure to increase the range of motion is termed stretching. RROM exercises are, therefore, performed to maintain the flexibility of joints, not to increase the flexibility, muscle strength, or endurance. Usually all joints in the affected limb are treated, starting distally and 10 to 30 repetitions can be performed two to three times daily.
Bicycling Bicycling movements are a type of PROM that involves moving all the joints in a limb through their ROM in a bicycling type of motion. It can be performed in lateral recumbency or in the standing position. The exercise is performed to train the PROM of the joints and gait patterns. The tarsal or carpal region is grasped gently, and the limb is moved smooth circular in caudal to dorsal to cranial movements. If the cat is in a standing position it should be assisted to prevent falling.
A cat is shown playing with a laser light shined on the wall.
Stretching Whereas PROM exercises are performed to maintain joint mobility, stretching is performed to increase the flexibility of joints and periarticular tissues such as the joint capsule, tendons, and muscles. The joint is flexed until a restriction is detected and the muscles and connective tissues are stretched. The stretch is held for 20 to 30 seconds. The same procedure is repeated in extension direction. Repeat for 2 to 5 repetitions, one to three times daily.
Assisted Standing This is a valuable exercise, especially after orthopedic and neurological surgery. It is useful to strengthen the patient, to train the neuromuscular function, and to improve proprioception. Usually body slings or harnesses are used to support the cat. The limbs should be placed squarely underneath the body. The cat should be allowed to bear as much weight as possible for several seconds. As soon the cat shows signs of weakness, it is lifted back into a standing position. As the cat becomes stronger, less support is provided by the therapist. Repeat for 5 to 15 repetitions, one to three times daily.
Weight Shifting If the cat is able to stand safely, this exercise is useful to improve balance, proprioception, and the use of a limb the cat does not want to put down. The therapist tries to disturb the balance by gently pushing the cat on the shoulder or the pelvis momentarily causing as loss of stability for the cat. Repeat for 5 to 15 repetitions, one to three times daily.
Playing with Laser Lights, Toys, and Treats Cats may be difficult to motivate, but some of their playing and hunting behaviors can be used to design active exercises. The use of laser lights, toys, and treats can help to motivate the cat to perform the desired exercise. For example, moving the light along the wall can motivate the cat to stretch the legs to reach the light. See Figure 268-2. Other possibilities involve playing with toys or treats.
689
SECTION 4: Surgery
Wheelbarrowing and Dancing The wheelbarrowing exercise is designed to improve the use of the forelimbs and to strengthen or stretch the forelimb muscles. The rear legs are lifted off the ground, and the cat is moved forward. Dancing is performed to improve use and muscle strength or range of motion of the hind legs. The forelimbs are lifted off, and the cat is encouraged to move several steps forward and backward. See Figures 268-3 and 268-4.
Suggested Readings
Figure 268-3
This cat’s therapy included a wheelbarrowing exercise.
Figure 268-4
The same cat as in Figure 268-3 is shown in a dancing exercise.
690
Bockstahler B, Levine D, Millis D, eds. 2004. Essential Facts of Physiotherapy in Dogs and Cats. Babenhausen, Germany: BE VetVerlag. Levine D, Millis DL, Marcellin-Little DJ. 2005. Introduction to veterinary physical rehabilitation. Vet Clin North Am Small Anim Pract. 35(6): 1247–1254. Furlan AD, Imamura M, Dryden T, et al. 2009. Massage for low back pain: An updated systematic review within the framework of the Cochrane Back Review Group. Spine. 34(16):1669–1684. Jaegger, Gayle. 2007. Validity of goniometric joint measurements in cats. Am J Vet Res. 68(8):822–826. Saunders DG. 2007. Therapeutic exercise. Clin Tech Small Anim Pract. 22(4):155–159. Saunders DG, Walker JR, Levine D. 2005. Joint mobilization. Vet Clin North Am Small Anim Pract. 35(6):1287–1316. Steiss JE, Levine D. 2005. Physical agent modalities. Vet Clin North Am Small Anim Pract, 35(6):1317–1333.
CHAPTER 269
Rhinotomy Gary D. Norsworthy
Definition A rhinotomy is used to gain access to one or both halves of the nasal cavity for sample collection for histopathology (HP), cytopathology (CP), culture for bacteria, and polymerase chain reaction (PCR) testing for respiratory pathogens; mass removal; or foreign body removal. The nasal cavity consists of two halves separated by the nasal septum. It contains thin, scroll-like conchae (turbinate bones). See Figure 269-1.
Equipment and Sources • A routine surgery pack • Bone drill with cutting burr or an intramedullary (IM) pin, such as a 0.062 K-wire, with hand chuck • Small, pointed rongeurs
Procedure • Images are made to determine if unilateral or bilateral surgery is to be performed. See Chapters 146 and 147. • A 2- to 3-cm (approximately 1-in) midline incision is made beginning about 1 mm (1/16 in) caudal to the nasal planum. • This is a vascular area so bleeders are clamped for hemostasis. Direct pressure is sufficient in many cases. • The periosteum is removed from the bone beginning to expose the nasal and frontal bones on the midline. • A drill burr or IM pin is used to make an opening about 1 mm (1/16 in) off the midline on the side or sides chosen for entry. • The drill burr, IM pin, or rongeurs are used to enlarge the opening to the desired size. Most biopsies can be made through an opening about 2 mm × 1 cm (1/8 in × 3/8 in). However, the opening can be made as large as 3 mm × 1.5 cm (3/16 × 5/8 in). See Figures 269-2 and 269-3. • Samples are collected for HP, CP, culture, and PCR testing as appropriate. See Figure 269-4. • Closure consists of suturing the skin. For best cosmesis, a subcuticular suture pattern, beginning near the nasal planum, is used. No attempt is made to close the bony defect.
Figure 269-1 The two halves of the nasal cavity are separated by the nasal septum (1). Each half communicates with the environment through the nares, with the frontal sinus (FS) through the ostium (not shown), and with the nasopharynx through the choanae (2). The nasal cavity is filled with thin, scroll-like conchae (turbinate bones) that are covered with a mucous membrane. In this specimen the conchae are seen in the right half of the nasal cavity (3) and have been removed from the left half of the nasal cavity.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 269-2 An opening about 2 mm × 1 cm (1/8 × 3/8 in) is made through the frontal bone (FB). It may extend into the nasal bone (NB) depending on the desired point of access.
691
SECTION 4: Surgery
Figure 269-3 Purulent material (arrow) in the nasal cavity can be seen through the surgical opening.
Complications • If the median septum is removed, there will be a depression over the nose. • It is possible for subcutaneous emphysema to develop, but this author has never had this complication occur.
692
Figure 269-4 cytopathology.
A cotton-tipped applicator is used to collect samples for culture or
Suggested Readings Fossum TW. 2002. Surgery of the upper respiratory system. In TW Fossum, ed., Small Animal Surgery, 2nd ed., pp. 716–759. St. Louis: Mosby.
CHAPTER 270
Sliding Skin Flaps Mac Maxwell
Overview Skin defects are common in veterinary medicine and can occur as a result of trauma or tumor removal. Regardless of the cause, a variety of techniques exist to allow for skin reconstruction. Skin flaps are classified according to the direction in which the skin is moved to cover a defect. In general, flaps that advance in a forward direction are termed advancement flaps and those rotate along the pedicle are rotational flaps. Regardless of the type of flap, each one maintains a tissue base with an intact subdermal plexus to supply the tissues blood supply. Flaps that directly incorporate an artery and vein are termed axial pattern flaps. Sliding skin flaps rely on the elasticity of surrounding skin to allow direct skin apposition and closure. Donor sites that are high motion or in areas of high tension should be avoided as this can increase the risk of flap dehiscence. In general advancement flaps are oriented in the direction of the least amount of skin tension. On the contrary, rotational flaps are oriented parallel to lines of the greatest skin tension. Skin tension can be assessed by grasping the skin between your fingers to assess tightness. Because advancement and rotational flaps rely on the subdermal plexus for its blood supply, it is recommended that the base of the flap be slightly wider than the flap itself to ensure adequate blood supply. In addition, flaps should be as short as possible to cover the defect. Wounds should be evaluated carefully with regard to the size, shape, elasticity of surrounding skin, and character of the recipient bed. Wounds present on the trunk of an animal are often amenable to local advancement flaps as described herein. Wounds located on the distal extremities are managed via releasing incisions and direct closure or mesh grafts. Prior to placement of free skin grafts the recipient bed must be free of infection and be covered with healthy granulation tissue.
• The flap is advanced and sutured into place using a simple interrupted pattern. Some recommend placement of half-buried horizontal mattress sutures in the corners to minimize circulation alterations. • Defects that require single long advancement flaps are best treated with two single-pedicle advancement flaps (H-plasty). Disadvantages of the H-plasty include increased dehiscence rates due to the intersection of the two advancement flaps.
Bipedicle Advancement Flaps Overview Bipedicle flaps allow circulation to be obtained from two directions and use local elastic skin. Orientation of the flap is usually with the long axis of the defect. Although this type of flap has blood supply from two directions, narrow flaps are at risk for central necrosis.
Surgical Technique • See Figure 270-2.
Single Pedicle Advancement Flaps Overview Single pedicle advancement flaps are the simplest of flaps and rely on the elasticity of adjacent skin. Preoperative planning for this technique involves the initial assessment of skin elasticity, and the flap is oriented in the direction of the least tension. Flap width is dictated by width of the defect. Flap length is kept to minimum to avoid possible necrosis of the tip.
Surgical Technique • See Figure 270-1. • The skin is grasped with fingers or forceps to assess the best direction for donor skin advancement. • Two parallel skin incisions are made equal to the width of the defect. Alternatively, the incision can be made in a divergent manner to ensure that the flap is wider at the base. • The flap is carefully undermined with Metzenbaum scissors until adequate mobility is obtained.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 270-1 Single pedicle advancement flap: Parallel or divergent incisions are made adjacent to the defect in the direction with most skin elasticity. The flap is undermined and sutured over the defect.
693
SECTION 4: Surgery
(A)
Figure 270-2 Bipedicle advancement flap: A skin incision is made parallel to the long axis of the wound. The flap is undermined, advanced, and sutured. The donor bed can be undermined and advanced to allow for direct closure or left to heal by second intention.
• The skin is grasped with fingers or forceps to assess the best direction for donor skin advancement. • Width and length of the flap are equal to the width and length of the defect. • A skin incision is made parallel to the long axis of the wound and curved slightly so that the concave side is toward the defect. • The flap is gently undermined with Metzenbaum scissors and advanced to cover the recipient bed. Simple interrupted sutures are used to appose the skin edges. The donor site is closed primarily via undermining and advancement. If the donor site cannot be directly closed it can be left to heal by second intention. • Alternatively two bipedicle advancement flaps can be created on either side of the defect.
Ninety-Degree Transposition Flap Overview A transposition flap is a rotating flap that relies on the subdermal plexus for blood supply. Although the length of the flap is limited when compared to an axial pattern flap, it is useful in most anatomical regions. The flap can be rotated either 45 or 90 degrees. Flaps that are only rotated 45 degrees are particularly useful for triangular defects.
Surgical Technique • See Figure 270-3. • Assess skin tension in the region adjacent to the recipient bed.
694
(B) Figure 270-3 A, B, Transposition flap: The width and length of flap are carefully measured to ensure adequate coverage of the defect. Length Y represents the length from the rotation point to the edge of the defect. X represents the length from the rotation point to the far corner of the flap. Length X should equal length Y. The skin is incised, and the flap is rotated and sutured in place over the defect.
• The flap should be created parallel to the direction of least tension and flap width and length are equal to the defect. Careful measurements should be obtained and marked on the skin prior to incision. • Incise the flap in the marked areas and gently undermined with Metzenbaum scissors. • Rotate the flap to cover the defect, and suture in a simple interrupted pattern. Any sharp points, such as corners, should be resected prior to closure to decrease the risk of necrosis.
Tension Relieving Procedures Overview In cases where the additional skin needed to close a wound is small, tension relieving procedures can be performed. These procedures include everything from simply undermining the surrounding skin to plasty procedures. Relaxing, staggered, punctate incisions can be made approximately 1 cm (3/8 in) from the wound edge and about 1 cm
Sliding Skin Flaps
(3/8 in) in length. If excessive tension still exists, a second row can be made about 1 to 2 cm (3/8–3/4 in) outside of the first. Z-plasty or V- to Y-plasty can also be performed to potentially allow for the advancement of the skin around the wound. See Figure 270-4. Skin stretchers or tissue expanders offer a different perspective and allow the dermal collagen to stretch in response to the tension. This prestretching of skin can be performed a few hours to days before primary closure of the wound occurs. Regardless of the type of tension relief employed, careful planning is required for optimal reconstruction.
Prognosis Flap survival is dependent on numerous factors including overall patient health as well as the viability of the recipient bed. Prior to graft placement, the recipient should be free of infection and have a good vascular supply. Culture and sensitivities of the wound should be taken as needed to aid in antimicrobial therapy. Graft sites should be free of tension and have no sharp edges or points. The presence of tension or points will greatly increase the risk of dehiscence. Bandages and drains may be employed on an as-needed basis depending on the mobility of the tissue and degree of dead space.
Suggested Readings
Figure 270-4 Z-plasty for tension relief: This is performed to allow advancement of skin around the wound. A Z-shaped incision is made with the central component being parallel to the direction where laxity is needed. The flaps are oriented at approximately 60-dgree angles. The two flaps of the Z are undermined, transposed, and sutured to achieve approximately a 75% gain in length.
Bosworth C. 2004. Skin Reconstruction Techniques: Z-plasty as an Aid to Tension-Free Wound Closure. Vet Med. 109(10):892–897. Gibbs A. 2004. Skin Reconstruction Techniques: Full-thickness Mesh Grafts. Vet Med. 109(10):882–891. Hedlund CS. 2007. Skin reconstruction. In TW Fossum, ed., Small Animal Surgery, pp. 193–205. St. Louis: Elsevier. Leonatti, S. 2004. Skin reconstruction techniques: Axial pattern flaps. Vet Med. 109(10):861–880. Pavletic, MM. 2006. Skin grafting. In MM Pavletic, ed., Atlas of Small Animal Reconstructive Surgery, 2nd ed., pp. 192–209. Philadelphia: Lippincott.
695
CHAPTER 271
Subcutaneous Fluid Catheter Placement Gary D. Norsworthy
Definition A subcutaneous fluid catheter is a multifenestrated catheter that is about 4 mm (1/8 in) in diameter and 20 to 25 cm (8–10 in) long. It is placed in the subcutaneous space on or near the dorsal midline. It is designed to be in place for about 1 year. It has a fitting that accepts an intravenous fluid line. This fitting is attached to the skin of the dorsal cervical area, permitting subcutaneous delivery of fluids or other medications by owners for prolonged periods of time.
Equipment and Sources • The catheter described in this chapter are sold by DVM Solutions, www.dvmsolutions.com. • A similar tube, the GIF-Tube™, is distributed by Veterinary Sales and Marketing, LLC.
Indications • Subcutaneous fluids are administered several times per week to support cats that need supplemental fluids, such as those with chronic renal disease or megacolon. • This catheter is also suitable for antibiotics or other injectable drugs intended for subcutaneous administration of several weeks to months duration.
Contraindications • The temperament of some cats is such that they will not tolerate this device. If a cat removes it within a few days of placement and the placement was performed properly, it is questionable if it should be replaced.
Postoperative Care • Antibiotics should be administered for about 48 hours following catheter placement to kill any bacteria inadvertently introduced at the time of catheter placement. Because Staphylococcus spp. are the most likely contaminants, an antibiotic should be chosen that should be effective against these pathogens. Antibiotics may be administered orally, or an injectable antibiotic, such as Cefazolin™ (SmithKline Beecham) or Baytril™ (Bayer Corporation), which can be administered through the catheter. Alternatively, one injection of Convenia™ (Pfizer Animal Health) can be administered. To get best disbursement throughout the catheter, add about 2 mL of the chosen subcutaneous fluid to the calculated dose of Cefazolin or Baytril. Give the first dose at the time of catheter placement, then every 12 hours thereafter for a total of about four doses. The owners can be instructed on the administration of the final three doses. • It is important that the first fluid treatment not be painful to the cat, or it will likely object to future treatments. Therefore, do not give the first dose of fluids for about 48 hours postoperatively. The subcutaneous tissue may be somewhat tender from the insertion process. This 48-hour delay permits the pain of placement to diminish. Administration of buprenorphine (0.005–0.04 mg/kg q8–12h SC or transmucosal) for 2 to 3 days is advised.
Likely Complications • Most cats will scratch at the catheter fitting for a day or two following insertion, much like they will scratch at a newly placed collar. Compulsive scratching will eventually result in dislodgement of the catheter. This indicates that this cat is not a good candidate for this
Procedure • General anesthesia is induced. • A 5-cm (2-in) square of hair is clipped from the dorsum of the neck, and the area is prepped for surgery. • A 1-cm (3/8-in) longitudinal incision is made in the center of the prepped area. • The catheter, containing a blunt-pointed metal stylet, is inserted through the subcutaneous tissue about 1 cm (3/8 in) off dorsal midline. It is guided with one hand and pushed with the other until the fitting is flush with the incision. • The stylet is removed. • The fitting is sutured with several soft, nonabsorbable sutures so it is well anchored to the skin. The fitting should be well anchored on both sides and at the cranial and caudal ends. If the sutures are too tight, they will ultimately cut through the skin. The success of this catheter is largely dependent on successful suturing. See Figure 271-1.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
696
Figure 271-1 The plastic fitting of the subcutaneous fluid catheter can be seen attached to the skin on the dorsal midline of this cat’s neck. It was in place 15 months before the cat died of renal failure.
Subcutaneous Fluid Catheter Placement
Figure 271-2 A bandage made of VetWrap® is helpful to prevent the cat from scratching out the catheter. It can usually be removed after about 4 days.
procedure. A bandage made of VetWrap® (3M Animal Health) and encircling the chest and neck should be applied for about 4 days so the cat can get used to the catheter without scratching it out. See Figure 271-2. • If fibrin builds up around the catheter, fluids will not flow properly. Because these catheters are foreign material, this commonly happens.
Therefore, a heparin-saline flush should be performed following each fluid treatment. Inject 5 mL of dilute heparin in saline (5 USP u/ml) through the catheter following each fluid treatment. It is important to begin this process before fibrin buildup occurs because heparin will not dissolve fibrin, only prevent its occurrence. The heparin solution is prepared by injecting 5 mL of 1000 u/mL heparin into a liter bag of normal saline. • If infection develops around the catheter, do not remove the catheter. Instead, flush about 5 mL of sterile normal saline into the catheter and aspirate. Perform a culture on the aspirated material to permit proper antibiotic selection. Administration of an antibiotic directly into the catheter puts the drug at the site of infection, optimizing the chance for a positive treatment outcome. Regular fluid therapy can continue during and after antibiotic therapy. Discuss aseptic technique with the owner, including soaking of the cap in a dilute bleach solution (150 ml/l of water [0.6 cup/pint of water]) during the infusion process followed by a sterile saline or lactated Ringer ’s solution (LRS) flush before reinserting. • The catheter may migrate cranially so that it becomes tortuous. It may be straightened in the following manner. Anesthetize the cat. Insert the original long stylet (that has been cold sterilized) into the catheter to straighten and reposition it. A dissolvable suture may be placed through the skin and into the distil end of the catheter to maintain the catheter ’s position for a few days while an adhesion forms to anchor the catheter permanently.
Suggested Readings St. Germain, MS. 2000. Use of the subcutaneous fluid administration tube. Newsletter of the American Association of Feline Practitioners. 18(1):19.
697
CHAPTER 272
Thoracostomy Tube Placement Don R. Waldron
Definition Thoracostomy tube (chest tube) placement is a temporary short-term means of providing thoracic drainage of air or fluids from the pleural space. Placement of a thoracostomy tube during thoracic surgery allows the most efficient removal of air or fluid from the pleural space postoperatively. Thoracostomy tubes placed concurrently with thoracic surgery are placed while the thorax is open during surgery. Thoracostomy tube placement may also be performed in a “closed” fashion.
• The tube is secured to surrounding skin with a “Chinese-finger trap” suture (see Figure 272-4) or a tape tag, which can be sutured to the skin. • Proper placement of the tube is verified radiographically prior to recovery from anesthesia. See Figure 272-5.
Indications • Cats undergoing thoracic surgery. • Cats with pleural effusions that may require drainage over several days, such as pyothorax or chylothorax. • In some cats with pneumothorax.
Special Equipment • Commercial thoracostomy tube and trocar (Argyle Straight Thoracic Catheter®, Sherwood Medical Products, www.dvmsolutions.com) or curved Carmalt or Kelly hemostats and a 10- to 16-French sterile red rubber catheter (Sovereign, Sherwood Medical Products).
Procedure Extreme care is taken in handling the dyspneic cat. Initial needle thoracocentesis with withdrawal of air or fluid along with preoxygenation of the cat in an oxygen cage or tank will decrease the risk of anesthesia administration. Although chest tubes may be placed in the sedated cat with local anesthesia, I prefer the use of general anesthesia unless strictly contraindicated.
Figure 272-1 A 1-cm (3/8-in) skin incision is made at the midthorax at approximately the 10th intercostal space. A curved Carmalt or Kelly hemostat is used to tunnel subcutaneously cranially several intercostal spaces. Orientation: Caudal is right. Photo courtesy Dr. Gary D. Norsworthy.
Closed Tube Placement • General anesthesia is induced, and the cat intubated. • The lateral thorax is generously clipped and prepared for aseptic tube placement. • A 1-cm (3/8-in) skin incision is made at the 10th intercostal space at or just above the mid-thorax. • The tube/trocar unit or surgical instrument is used to tunnel three to four intercostal spaces in a cranioventral direction. See Figure 272-1. • The trocar or instrument is thrust in a controlled fashion through the muscle and pleura of the intercostal space. See Figure 272-2. When using a trocar, grasp the trocar/tube unit 2 cm (3/4 in) from the thoracic wall with one hand, and use the second hand to thrust the trocar through the intercostals space. • The tube is advanced in a cranioventral direction into the rostral thorax (see Figure 272-3) and a Christmas-tree adaptor and three-way valve placed in the open end of the tube.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
698
Figure 272-2 A sterile red rubber catheter is grasped with the forceps in preparation for tube placement. Note that the tips of the forceps blades point in the same direction as the tube and will be used to make the hole in the intercostal muscles. Alternatively, a commercially available thoracostomy tube is placed using the included stylet instead of a forceps. Orientation: Caudal is right. Photo courtesy Dr. Gary D. Norsworthy.
Thoracostomy Tube Placement
(A) Figure 272-3 The forceps and tube are directed cranioventrally, and the instrument and tube are thrust through the muscle and pleura of the intercostal space in one brisk motion. Orientation: Caudal is right Photo courtesy Dr. Gary D. Norsworthy.
(B)
Figure 272-4 The tube is secured to surrounding skin with a Chinese finger trap suture. Orientation: Caudal is right. Photo courtesy Dr. Gary D. Norsworthy.
• An occlusive dressing is placed over the tube exit wound and covered by a loose bandage or stockinet. • The use of a special aspiration device can expedite fluid removal. See Figure 272-6.
Open Tube Placement (Thoracostomy) • The tube is placed through an intercostal space two spaces caudal to the primary thoracotomy incision. • Placement is identical to that described previously except final placement is easier to verify because the tube can be visualized and radiographs are not routinely taken postoperatively.
Figure 272-5 A, Lateral view of the thorax with a properly placed thoracostomy tube. Note that the tube is advanced into the cranial aspect of the chest. A, Ventral-dorsal view of the same cat. Images courtesy Dr. Gary D. Norsworthy.
Comments • In most cases, the mediastinum is perforate and only one tube is necessary; however, in cats with pyothorax or chylothorax the presence of fibrin may necessitate the use of bilateral tubes to most efficiently drain the thorax. • Intermittent manual drainage is performed two to three times daily or the tube attached to a continuous suction drainage apparatus. Feline intrathoracic pressure is not sufficient to activate a Heimlich® valve. • Thoracostomy tube placement is preferable to repeated needle thoracocentesis, which is painful and causes distress to an already dyspneic cat.
699
SECTION 4: Surgery
(A)
(B)
Figure 272-6 A: The effusion is aspirated with the smaller syringe. When this syringe is emptied, the fluid goes into the larger syringe. Two one-way valves prevent fluid from going the wrong direction during each phase of the process. (ICU Medical, Inc. www.icumed.com; AN7073 Non-DEHP Bifuse Set). B: The Bifuse Set is shown in use during a thoracentesis. It is attached to a butterfly catheter for this use.
• The tube is removed when fluid volume decreases to 2 to 3 mL/kg per day, the amount expected to be produced by the presence of the tube. • The tube can be removed in patients with pneumothorax once negative pressure has been achieved for 12 hours. • Prolonged drainage of chylothorax by tube is not recommended due to the potential of causing hypoproteinemia.
700
Suggested Readings Crowe DT, Devey JJ. 1998. Thoracic drainage. In MJ Bojrab, ed., Current Techniques in Small Animal Surgery, 4th ed., pp. 403–417. Baltimore: Williams and Wilkins. Fossum T. 2007. Surgery of the lower respiratory system: Pleural cavity and diaphragm. In TW Fossum, ed., Small Animal Surgery, 3rd ed., pp. 899–901. St. Louis: Mosby.
CHAPTER 273
Thyroidectomy Gary D. Norsworthy
Definition Thyroidectomy is the surgical removal of one or both lobes of the thyroid gland for cats with hyperthyroidism.
Anatomy • The thyroid gland has two unattached lobes separated by the trachea and located just caudal to the larynx. The sternothyroideus muscle is located lateral to the thyroid lobe. • There are four parathyroid glands. The external glands are located extracapsularily, usually on or near the cranial poles of the thyroid lobes. However, they may be located anywhere on the thyroid lobe. They may be engulfed by proliferative thyroid tissue and be difficult to locate; this is more likely with greater thyroid enlargement. The internal thyroid lobes are in random locations within the parenchyma of the thyroid lobes. • The cranial thyroid artery enters cranially, and the thyroid vein exits caudally. • The left recurrent laryngeal nerve traverses the area of the left thyroid lobe. If the lobe is significantly enlarged, the nerve may be adherent to the thyroid capsule and can be seen as a white linear structure.
Equipment and Sources • A routine surgery pack • Either iris scissors or a number 11 Bard Parker scalpel blade • Splinter forceps can be helpful for handling the parathyroid gland
Indications • A definitive treatment for hyperthyroidism.
Contraindications • A patient that is not a good candidate for anesthesia or that has a concurrent, more life-threatening condition.
Surgical Options • There are three basic approaches. Some surgeons only remove the thyroid lobe that is actively causing disease. Others prefer to remove both lobes in each patient, even if only one lobe is diseased, rationalizing that eventually the normal lobe will also become diseased. If bilateral surgery is performed, both lobes may be removed at the same time or the lobes may be removed in staged procedures, generally about 30 days apart. The latter is used to reduce the incidence of hypoparathyroidism. • There are three basic thyroidectomy techniques. • The intracapsular technique is performed by incising the thyroid capsule and removing all thyroid tissue. The capsule remains in the cat with the external parathyroid gland attached. This
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
technique has the advantage of protecting the parathyroid; however, there is increased chance of leaving abnormal thyroid tissue in the cat. If this occurs, hyperthyroidism will recur. • The extracapsular technique is performed by carefully dissecting the external parathyroid gland from the thyroid capsule, taking care to keep the parathyroid vasculature intact. The thyroid lobe is then removed. This technique is less likely to leave abnormal thyroid tissue in the cat because the thyroid capsule is not invaded. However, there is increased risk of hypoparathyroidism and resulting hypocalcemia because the parathyroid vessels may be easily severed or vasospasm may result from tissue handling. • The parathyroid transplant technique is performed as described herein. Its greatest advantage is that it virtually eliminates hypocalcemia. Another advantage is that tedious dissection of the parathyroid vasculature is not needed, making it simple enough for most veterinary surgeons to perform. Its greatest disadvantage is that two surgical procedures are required if the cat has bilateral disease.
Procedure • Isoflurane or sevoflurane is the anesthetic agent of choice. The cat is induced by facemask or anesthetic chamber and maintained via tracheal intubation. • The ventral aspect of the neck is clipped and prepped for surgery from 2 cm (0.75 in) cranial to the larynx to 2 cm (0.75 in) caudal to the xiphoid process. • The cat is placed in dorsal recumbency. It is important that a true ventrodorsal position be achieved because the midline is not obvious and is determined by positioning. A small pad (2–4 cm [0.75–1.5 in] thick) is placed under the neck. • A midline incision is made through the skin at the level of the thyroid lobe, if it is palpable. If it is not palpable, the incision should extend from 1 cm (3/8 in) caudal to the larynx to 2 cm (3/4 in) cranial to the xiphoid process. It may be extended cranially or caudally to access the thyroid lobe. • The incision is extended through both layers of muscle until the trachea is exposed. Minimal bleeding will occur if the incision is made on the midline; there will be considerable muscle bleeding if it is not. See Figure 273-1. • The largest thyroid lobe is chosen for removal by presurgical palpation or by visual inspection during surgery. The other lobe is visualized (without significant dissection) to ensure removal of the larger lobe and to determine if it is larger than normal for determination of the need for a second surgery. • The muscles and surrounding tissues are moved laterally en mass to expose the thyroid lobe. • The external parathyroid gland is identified. It is much lighter in color than the thyroid and about 1 to 3 mm (1/16–1/8 in) in diameter. See Figure 273-2. • The external parathyroid gland is excised using iris scissors or a number 11 scalpel blade. • The external parathyroid gland is placed on a gauze square and soaked with saline to keep it moist. The gland is cut in one-third and two-thirds portions. The smaller is placed in formalin and submitted for histopathology to verify that the correct tissue was transplanted. See Figure 273-3.
701
SECTION 4: Surgery
Figure 273-1 The incision is made through the skin on the midline then through two layers of muscle to expose the trachea.
Figure 273-4 A longitudinal incision is made in an adjacent muscle belly creating a pouch that receives the parathyroid gland (arrow). The pouch is closed with a single suture, which may be placed through the parathyroid gland to help secure it in place.
Figure 273-2 The external parathyroid gland (arrow) is identified on the cranial pole in this cat and removed. Figure 273-5 The thyroid lobe is exteriorized so the vessels at both ends can be ligated. Following ligation, the thyroid lobe is excised.
Figure 273-3 The parathyroid gland is placed on a gauze square that has been moistened with saline solution. For assurance that the parathyroid has been harvested, cut the tissue into one-third and two-thirds proportions and submit the smaller portion for histopathology.
702
• A 1-cm (3/8-in) longitudinal incision is made in a nearby muscle belly to produce a pouch in which the parathyroid gland is to be placed. It should be just deep enough to accommodate the gland. • The two-thirds portion of the parathyroid gland is placed in the muscle pouch using splinter forceps. The pouch is closed with 4-0 dissoluble suture material. A single suture is usually adequate; however, a mattress suture may be required if the pouch is too long. The anchoring suture may be passed through the parathyroid tissue if needed. See Figure 273-4. • The thyroid lobe is lifted so the tissue containing the artery (cranial) and vein (caudal) can be isolated. They are ligated using the same 4-0 dissoluble suture material. See Figure 273-5. • The thyroid lobe is excised and placed in formalin for histopathology. • The deep muscle layer is closed with a continuous pattern using the same 4-0 dissoluble suture material. • The superficial muscle layer is closed in the same manner.
Thyroidectomy
• The skin is closed using a subcuticular pattern. The center of the incision is anchored to the underlying muscle at one point to prevent seroma formation. • If bilateral disease is present, the second lobe is removed about 30 days later.
Complications • Hypoparathyroidism is an unlikely complication because the first transplanted parathyroid gland becomes functional prior to the second surgery, if bilateral surgery is performed. • Hypothyroidism is possible but unlikely following bilateral surgery. There are clusters of ectopic, quiescent thyroid cells from the base of the tongue to the base of the heart in almost every cat. When both thyroid lobes are removed, thyroid stimulating hormone activates the ectopic cells so they become functional and produce adequate thyroid hormone. Giving thyroxine will inhibit this compensatory response so postoperative thyroxine administration is discouraged. However, if the TT4 remains subnormal for more than 2 to 3 months
postoperatively and the cat is gaining weight rapidly, thyroxine therapy should be initiated and will likely be needed long term. It is my experience that this occurs in about 2% of cats following bilateral surgery. • Laryngeal paralysis or a change in the tone of the voice may occur if the recurrent laryngeal nerve is cut or traumatized. This nerve is generally not in the surgical field; however, I have seen a few cats in which this nerve coursed over the thyroid lobe. It is more likely to be adherent to the thyroid lobe when the lobe is large. If that is the case, it should be dissected free before the lobe is removed.
Selected Readings Norsworthy GD. 1995. Feline thyroidectomy: A simplified technique that preserves parathyroid function. Vet Med J. 90(11):1055–1063. Sheldon LP, Karen MT, Charles WL, et al. 1998. Efficacy of parathyroid gland autotransplantation in maintaining serum calcium concentrations after bilateral thyroparathyroidectomy in cats. J Am Anim Hosp Assoc. 219(34):181–264.
703
CHAPTER 274
Total Ear Canal Ablation and Lateral Bulla Osteotomy Don R. Waldron Definition Total ear canal ablation (TECA) is the excision of both the vertical and horizontal ear canals to the level of the external acoustic meatus (skull). Lateral bulla osteotomy is always performed concurrently with TECA.
Overview TECA is most commonly performed in the canine for end-stage inflammatory disease and chronic tissue hyperplasia. In contrast, in feline patients, TECA is primarily indicated for ear canal neoplasia. Thoracic and skull radiographs may be indicated in cats with suspected ear canal neoplasia to evaluate for metastasis and bony destruction of the bulla. The presence of either indicates a grave prognosis.
Special Equipment • Small Gelpi retractors or Senn handheldretractors or Star SelfRetaining Retractor (Lone Star Medical Products, www.lsmp.com, 1-800-331-7427 or 1-281-340-6000)
Procedure: Total Ear Canal Ablation • The cat is placed under general anesthesia, and the entire ear and lateral skull on the affected side is clipped and prepared for aseptic surgery. • The patient is placed in lateral recumbency with the neck extended over an elevated padded area (e.g., a small rolled towel). • A tear-drop or triangular skin incision is made to encompass the opening of the auditory tube. See Figure 274-1. • The vertical limb of the incision should extend parallel to the vertical ear canal. • The parotid salivary tissue is bluntly dissected from the vertical canal and displaced ventrally and caudally or cranially from the operative field. • Blunt dissection is performed with a mosquito hemostat making an effort to stay as close to the cartilaginous ear canal as possible. • Careful circumferential dissection to free the ear canal from surrounding tissue is performed. See Figure 274-2A. • The facial nerve exits the skull from the stylomastoid foramen, which is immediately caudal to the external acoustic meatus. See Figures 274-2B and 2C. The nerve courses laterally then cranially then dorsally as it traverses the external cartilaginous ear canal. The nerve is preserved by careful dissection and staying close to the ear canal as well as gentle tissue traction. • Complete dissection of the ear canal is performed to the level of the external acoustic meatus. • The external ear canal is carefully excised using a scalpel blade cutting from caudal to cranial while protecting the facial nerve. Care is taken to remove any epithelial remnants from the opening of the external acoustic meatus.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
704
Figure 274-1 A vertical incision is made over the lateral ear canal (arrow) and then extended around the external auditory meatus. The incision is through skin and auricular cartilage. Photo courtesy of Dr. Gary D. Norsworthy.
Procedure: Lateral Bulla Osteotomy • When the aforementioned steps are completed, Lempert rongeurs are used to open the ventrolateral bulla wall, and a small curette is used to remove epithelial lining from the dorsolateral compartment of the bulla. • After careful removal of all epithelium from the bulla and external acoustic meatus, the surgical field is liberally lavaged with normal saline.
Procedure: Closure • Deep tissues are carefully closed with 4-0 absorbable sutures taking care to not include the facial nerve in suture bites. • The skin is closed with 4-0 nylon or polypropylene sutures. • Because the dorsal portion of the incision is round, tissue sculpting may be needed dorsal to the opening to created good cosmesis. See Figure 274-3.
Comments • Drainage of the surgical field is optional depending on the reason for TECA. A 6 mm (1/4 in) Penrose drain exiting ventral to the primary incision provides adequate drainage when deemed necessary. • The feline ear, because of its upright nature, may be slightly folded following the procedure; however, most owners have not found this objectionable.
(A)
(C)
(B) Figure 274-2 A, The ear canal (arrow) is dissected from surrounding tissue by staying as close to the cartilage as possible. The arrowhead notes where it attaches to the external auditory meatus. The facial nerve is at the level of the point of the arrowhead and illustrated. B, The facial nerve (FN) exits the stylomastoid foramen (SMF) just caudal to the external auditory meatus (EAM). It courses laterally then cranially then dorsally as it traverses the external cartilaginous ear canal. C, The facial nerve (arrow) can be seen coursing around the horizontal ear canal (HC) ventral to the point where the ear canal enters the external auditory meatus. The vertical ear canal has been retracted dorsally stretching the horizontal ear canal dorsally. Photos A and C courtesy of Dr. Gary D. Norsworthy. Drawing B Used with permission from Dr. L.C. Hudson and W. P. Hamilton.
705
SECTION 4: Surgery
Complications • Facial nerve paresis or paralysis may result from neuropraxia or severance of the nerve. Lack of a “blink” reflex and drooping of the face will result. Paresis caused by neuropraxia is usually temporary and returns within 4 to 6 weeks. Eye lubrication may be necessary to prevent corneal drying during this time. • Horner ’s syndrome may also occur and consists of miosis, ptosis, and nictitans protrusion. Horner ’s usually resolves within 30 days. See Chapter 99. • Fistulation or development of a draining tract may occur weeks to months following surgery if all epithelium is not removed from the external acoustic meatus and bulla.
Suggested Readings Venker-van Haagen AJ. 1994. Diseases and surgery of the ear. In RG Sherding, ed., The Cat: Diseases and Clinical Management, 2nd ed., pp. 1999–2009. New York: Churchill Livingstone.
Figure 274-3 The vertical incision is closed following the incision around the opening to the vertical ear canal. It is often necessary to sculpt the tissue of the pinna to achieve cosmesis. Photo courtesy of Dr. Gary D. Norsworthy.
706
CHAPTER 275
Ureterolith Removal Don R. Waldron
Overview Upper urinary tract calculi have increased in prevalence in cats in the past 10 years. These calculi are located in the ureter or kidney. The causes are multifactorial, but acidifying diets introduced to decrease magnesium ammonium phosphate calculi in the lower urinary tract are thought to be a major causative factor. Calculi in the ureter or kidney of cats are almost exclusively calcium oxalate or calcium phosphate in composition, thus medical dissolution protocols are not available. Cats with ureterolithiasis or nephrolithiasis should have a complete blood count (CBC), blood chemistry, urinalysis, and urine culture as a data base. Ureteroliths may, in some cases, pass through the ureter to the urinary bladder. In other cases, the calculi may cause obstructive disease of the ureter and kidney. Ultrasound or excretory urography are indicated to assess the degree of ureteral and renal pelvic dilation in the affected cat. In many cases, affected cats are azotemic or uremic, and these patients should be treated with intravenous fluids. The only method available for clinical assessment of individual kidney function (glomerular filtration rate [GFR]) is nuclear scintigraphy, which may be available in referral institutions. Cats with chronic renal disease and obstruction caused by ureteroliths may be helped by surgical intervention, but renal function does not return to normal. The normal ureter in the cat is small, and an operating microscope is preferred by some surgeons for enhanced visualization. When the ureter is dilated due to obstruction, surgery with eye loupes is possible. Ureteral surgery in the cat has many potential complications including urine leakage and ureteral stricture, thus referral to a surgeon should be considered.
Special Equipment • • • • • •
Bishop Harmon 1 × 2 tissue forceps Derf or Castroviejo needle holders 5-0 or 6-0 synthetic absorbable suture Eye magnification 3.5 French catheter Sterile tongue depressor
Procedure • The patient is induced and placed under inhalation general anesthesia. • The abdomen is clipped and prepared for aseptic surgery, and the patient placed in dorsal recumbency. • A ventral midline skin incision is made from the xiphoid process of the sternum to 3 cm (1 1/8 in) caudal to the umbilicus. • The abdomen is entered, and the affected kidney and ureter exposed by retraction of the duodenum and mesoduodenum on the right side or the colon and mesocolon on the left side. • The ureter is carefully examined and palpated to locate the obstructing stone(s). See Figure 275-1A. • The ureter is mobilized by blunt dissection, and a sterile tongue depressor is placed dorsal to the ureter to aid the surgeon in incising the ureter. • A longitudinal incision is made into the ureteral lumen over the obstructing stone, and the stone is removed with forceps and flushing of the ureter with normal saline. If multiple stones are present, the others are milked to this incision. If that is not possible, other incisions are made. See Figure 275-2. • Once patency of the ureter is assured, the ureterotomy incision is closed with simple interrupted sutures of 5-0 or 6-0 monofilament synthetic absorbable suture. A longitudinal or transverse suture pattern may be used. See Figures 275-1B and 1C. • Alternatively, a transverse incision may be used. See Figure 275-1D. • A catheter is placed, as necessary, during closure to prevent inadvertent occlusion of the ureter. • If leakage is observed following ureteral closure, a small piece of Gelfoam® is moistened and applied to the ureterotomy site. • The abdomen is lavaged with warm saline and closed routinely.
Comments • Some surgeons prefer transverse closure of the longitudinal ureterotomy incision and believe this may reduce the risk of ureteral stricture.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
707
SECTION 4: Surgery
(A)
(B)
(C)
(D)
Figure 275-1 A, A ureteral calculus is shown obstructing the ureter causing ureteral dilatation proximal to the obstruction. B, A longitudinal ureterotomy is performed and the calculus removed. The incision is closed with 5-0 or 6-0 absorbable suture on a tapered needle. C, Alternatively, closure of a longitudinal ureterotomy incision may be performed transversely to decrease stricture formation. D, A transverse ureterotomy incision can be used. If so, it is closed in a transverse manner. Reprinted with permission from Slatter DH. 2003. Textbook of Small Animal Surgery, 3rd ed., pp. 1627. Philadelphia: Saunders.
• The cat is maintained on intravenous fluids at least the first 24 hours following surgery. • Abdominal effusion, depression, or vomiting should prompt the surgeon to repeat blood work with attention to the blood urea nitrogen (BUN) and creatinine levels. • Ureteral leakage is possible and can be diagnosed by excretory urography.
Suggested Readings Fossum TW. 2002. Surgery of the kidney and ureter. In TW Fossum, ed., Small Animal Surgery, 2nd ed., pp. 549–571. St. Louis: Mosby.
Figure 275-2 A calcium oxalate ureterolith is seen being removed from the ureter. Photo courtesy Dr. Gary D. Norsworthy.
708
CHAPTER 276
Urethrostomy, Perineal Don R. Waldron
Definition Perineal urethrostomy (PU) is a surgical method of permanent urinary diversion in which the penile urethra is excised and the pelvic urethra sutured to the perineal skin. When performed correctly, PU prevents most cases of urethral obstruction in male cats. The procedure requires neutering of the cat, so owners of breeding tom cats should be fully informed prior to surgery.
Indications • PU is the surgical procedure of choice for male cats that suffer repeated episodes of urethral obstruction as a result of feline lower urinary tract disease or urethrolithiasis. • PU is the surgical procedure of choice for male cats with urethral obstruction that cannot be relieved with urethral catheterization. • The procedure is sometimes indicated for lower urethral trauma.
Procedure • Abdominal radiographs are advisable prior to surgery to rule out cystic and urethral calculi as causes of obstruction. • Surgery should not be performed on uremic cats. Intravenous fluid therapy and correction of acid-base and electrolyte imbalances are indicated prior to surgery. The exception is the cat with an unrelievable urethral obstruction. • After induction of general anesthesia, hair is clipped in the perineal area and on the ventral surface of the tail. • A purse-string suture is placed around the anus, and the cat is positioned in sternal recumbency on the operating table. • The tail is taped in a rostral direction. • The perineal area is prepared for aseptic surgery. • A catheter is placed in the urethra. This permits identification of the urethra during the dissection described below. • An elliptical skin incision encompassing the scrotum and prepuce is made. See Figure 276-1. • The prepuce and scrotum are dissected free and excised and, if necessary, the cat is neutered. • Hemorrhage from the cranial and caudal scrotal arteries is controlled by cautery, clamping, or ligation. • The penis is isolated and dissected from surrounding fatty tissue. • The ischiocavernosus muscles are isolated bilaterally by blunt dissection and are transected close to their ischial attachments. See Figure 276-2. • The penis is retracted dorsally, and the fibrous ventral ligament is transected with scissors. • Blunt dissection is performed ventrally and laterally to free the pelvic urethra from all of its pelvic attachments. Insert your index finger ventral to the urethra and push forward to detach the urethra from the pelvic canal. • The retractor penis muscle is excised from the dorsal aspect of the urethra to the level of the bulbourethral glands.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 276-1 A purse-string suture is placed around the anus (covered by the drape), and a catheter is placed in the urethra prior to beginning surgery. An elliptical skin incision is made to encompass the scrotum and prepuce. It should be wide enough to put mild tension on the sutured urethra to help prevent stricturing of the ostomy. Photo courtesy Dr. Gary D. Norsworthy.
Figure 276-2 The subcutaneous tissue is excised, and the ischiocavernosus muscles (ICM) are isolated and incised bilaterally. The retractor penis muscle (RPM) is attached to the dorsal surface of the urethra. Photo courtesy Dr. Gary D. Norsworthy.
709
SECTION 4: Surgery
Figure 276-3 The urethra is split longitudinally on its dorsal surface to the level of the bulbourethral glands. The glands are just proximal to the ischiocavernosus muscles and are atrophied in the neutered cat. Iris scissors or a number 11 scalpel blade is inserted lateral to the catheter with the sharp blade facing dorsal. Photo courtesy Dr. Gary D. Norsworthy.
Figure 276-5 The first three sutures in the urethra are placed at 12, 11, and 1 o’clock positions, in that order. Reprinted with permission from Smith MM, Waldron DR. 1993. Atlas of Approaches for General Surgery of the Dog and Cat, p. 285. Philadelphia: WB Saunders.
Figure 276-4 The urethra is sutured to the skin edges. It is important to suture the urethral mucosa (arrow) directly to the skin without any muscular tissue between them. The urethral mucosa is a tough, white, transparent layer of tissue. Photo courtesy Dr. Gary D. Norsworthy.
• The penis is amputated, and the penile urethra is incised with iris scissors or a number 11 surgical blade (sharp side of the scalpel blade directed dorsally and inserted beside the urethral catheter) to the level of the bulbourethral glands. See Figure 276-3. • The bulbourethral glands are atrophied in cats that have been previously neutered and are just proximal to the ischiocavernosus muscle attachments. • A through-and-through mattress suture is placed in the distal penile urethra to control hemorrhage from the incised corpus spongiosum penis. • The surgeon begins the urethrostomy by suturing the urethral mucosa only (See Figure 276-4) to the skin dorsally with interrupted
710
Figure 276-6 The pelvic urethra is sutured to the skin with simple interrupted sutures. The “drain board” should be about 1 to 1.5 cm (3/8–5/8 in) long. Photo courtesy Dr. Gary D. Norsworthy.
sutures of 5-0 nylon, polypropylene, or polyglactin 910 at the 11:00, 12:00, and 1:00 o’clock positions. See Figure 276-5. • The remainder of the urethral mucosa is sutured to the skin in an interrupted or simple continuous pattern at 1-mm (1/16-inc) intervals. See Figure 276-6. • The dorsal and ventral portions of the skin incision are closed with nonabsorbable suture in an interrupted pattern. See Figure 276-7. • The purse-string suture is removed from the anus.
Urethrostomy, Perineal
• Most of the surgical dissection takes place laterally and ventrally to the urethra. • Dorsal dissection of periurethral tissues is performed close to the urethra and is minimized to prevent damage to the rectum, the external anal sphincter muscles, and the pelvic nerves. • The urethra must be incised to the level of the bulbourethral glands to ensure that the pelvic urethra has been reached. The flared end of the catheter can be used to determine the urethral diameter. • Meticulous suturing of the urethral mucosa to skin will minimize postoperative hemorrhage and stricture. • A postoperative indwelling urethral catheter is not recommended. • A restraining collar is used to prevent self-trauma for 2 days after surgery. • Shredded paper is used instead of litter until healing is complete. • The patient is sedated for suture removal to minimize trauma to the urethrostomy site 10 to 14 days following surgery. If dissoluble sutures are placed, this step is not necessary. • The cat should be monitored every 6 to 12 months for urinary tract infection and urolith development for the remainder of its life.
Figure 276-7 A completed perineal urethrostomy shows the sutures placed in the split urethra and in the skin dorsal and ventral to it. They should be placed about 1 mm (1/16 in) apart and their ends cut short. The arrow points to the new urethral opening Photo courtesy Dr. Gary D. Norsworthy.
Notes
Suggested Readings Griffin DW, Gregory CR. 1992. Prevalence of bacterial urinary tract infection after perineal urethrostomy in cats. J Am Vet Med Assoc. 200:681–684. Smith MM, Waldron DR. 1993. Approach to the perineal urethra: feline. In MM Smith, DR Waldron, TA Lawrence, eds., Atlas of Approaches for General Surgery of the Dog and Cat, pp. 284–287. Philadelphia: WB Saunders.
• It is essential to have a catheter in the urethra during surgery so the urethral lumen can be identified. If this is not possible, perform a cystotomy and antegrade the catheter out the urethra. Attach it to the prepuce with a suture or a clamp. Cut off the flared end that is inside the bladder then close the bladder and body wall.
711
CHAPTER 277
Urethrostomy, Prepubic Don R. Waldron
Prepubic (antepubic) urethrostomy (PPU) is a permanent urinary diversion technique in which the urethral-cutaneous stoma is placed on the ventrocaudal abdomen.
Indications PPU has been performed for urethral stricture, neoplasia, pelvic urethral trauma, granulomatous urethritis, failed perineal urethrostomy, and perineal skin defects that may prevent perineal urethrostomy. Survey abdominal radiographs should be taken to rule out calculi as a cause of urethral obstruction. Cystotomy may be indicated to remove calculi. If the cat has had urinary tract obstruction, preoperative stabilization by administration of intravenous fluids and electrolyte normalization is necessary.
Special Equipment • Sharp iris or tenotomy scissors are useful for spatulation of the urethra.
Procedure
• The cat is placed in dorsal recumbency, and a ventral midline incision is made form the umbilicus to the pubis. • The abdominal cavity is entered and the urinary bladder is identified. • The urethra is identified and isolated by blunt dissection of the abundant periurethral fatty tissue between the bladder and the pubis. See Figure 277-1. • A circumferential ligature is placed around the caudal urethra as it enters the pelvic canal. • The urethra is transected, and a stay suture is placed in the distal aspect of the cranial urethra to facilitate atraumatic tissue handling. See Figure 277-2. • The urethra is freed of its dorsal attachments for a short distance to aid in exteriorization of the cranial urethral segment. The urethra is exteriorized ventrally and incised longitudinally (spatulated) with sharp iris scissors. See Figure 277-3. • Urethrostomy is performed by suturing the urethra to skin of the caudal aspect of the incision with 4-0 nylon or polypropylene suture material. • The abdominal wall is closed carefully so as not to narrow the urethral lumen. • Subcutaneous tissue and skin are closed routinely.
• General anesthesia is induced, and the ventral abdomen is prepared for aseptic surgery.
Figure 277-1 The urethra is isolated in the caudal abdomen between the urinary bladder and the pubis. Reprinted with permission from Smith MM, Waldron DR. 1993. Atlas of Approaches for General Surgery of the Dog and Cat, pp. 289–293. Philadelphia: WB Saunders.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
712
Figure 277-2 The distal urethra is ligated and divided as far caudally as possible. Pubic ostectomy may be performed with rongeurs to expose additional pelvic urethra. Dissection is minimized in the area of the bladder. Reprinted with permission from Smith MM, Waldron DR. 1993. Atlas of Approaches for General Surgery of the Dog and Cat, pp. 289–293. Philadelphia: WB Saunders.
Figure 277-3 The urethra is incised on its ventral aspect. Then, it is either sutured to abdominal skin outside the primary incision as depicted here, or alternatively, sutured to the skin within the primary incision (preferred method). Reprinted with permission from Smith MM, Waldron DR. 1993. Atlas of Approaches for General Surgery of the Dog and Cat, pp. 289–293. Philadelphia: WB Saunders.
713
SECTION 4: Surgery
Comments and Complications • Excessive dissection of tissues of the dorsal periurethral area and the urinary bladder neck may result in incontinence. • The pubis may be ostectomized with rongeurs to make additional urethra available to perform the procedure. • Care is taken during urethrostomy not to kink the urethra between the bladder neck and skin. • Placement of an Elizabethan collar to prevent self-trauma of the stoma may be necessary in the postoperative period. • Urinary incontinence and peristomal skin inflammation and ulceration are the most common complications, occurring in up to 30% of cats.
714
• Stomal sutures are removed 10 to 14 days following surgery. • Cats should be monitored periodically for urinary tract infection following the procedure. • This procedure is technically easier to perform than perineal urethrostomy; however, the relatively high incidence of incontinence and skin ulceration makes it a second choice behind perineal urethrostomy for permanent urinary diversion.
Suggested Readings Baines SJ, Rennie S, White RAS. 2001. Prepubic urethrostomy: A longterm study in 16 cats. Vet Surg. 30:107–113.
CHAPTER 278
Urinary Bladder Marsupialization Gary D. Norsworthy
Definition Marsupialization of the urinary bladder, also known as a cystostomy, creates an open fistula from the bladder lumen through the skin of the ventral abdomen. It is one of several urinary diversion surgeries. A tube cystotomy achieves the same end, but a foreign body, usually a lowprofile gastrostomy tube port, is implanted through the abdominal and bladder walls. Some cats will not tolerate the foreign material for even 1 or 2 days.
Equipment and Sources • Routine surgery pack • 3-0 or 4-0 dissoluble suture material with a cutting needle • Skin protectant ointment
Indications • Unrelievable urethral obstruction (see Figure 278-1) or unresponsive bladder atony. The primary indication is when a urethral obstruction cannot be relieved in a breeding tom cat. The bladder remains marsupialized for a few days until urethral swelling and inflammation are relieved and catheterization is possible. At that time the bladder is closed and replaced into the abdomen. I have also used this for a
cat that could not be catheterized even after having had a perineal urethrostomy; the obstruction was due to multiple calcium oxalate uroliths in the urethra. If used for unresponsive bladder atony, there must be some reasonable hope of bladder recovery so the fistula does not remain permanent.
Procedure • General anesthesia is induced, and the cat is prepared for abdominal surgery. • The cat is placed in dorsal recumbency. • A celiotomy incision is made over the urinary bladder. • As much as possible, the bladder is exteriorized. See Figure 278-2. • A syringe and needle are used to remove as much urine as possible from the bladder. • A 1-cm (3/8-in) incision is made in the bladder wall on the ventral midline at the most ventral location. • Simple interrupted sutures are passed through the bladder wall to the corresponding location in the skin until the cystostomy opening is secured to the skin. The bladder lumen should open directly through the skin. See Figure 278-3. • The remainder of the bladder wall and skin incision is closed with either a simple interrupted or continuous interlocking suture pattern. See Figure 278-4.
Aftercare • A skin protectant ointment, such as used on babies for diaper rash, is applied to the skin once or twice per day to prevent urine scalding. An Elizabethan collar is used to keep the cat from licking the ointment and the urine-soaked skin.
Figure 278-1 This cat could not pass urine 4 hours following a perineal urethrostomy. Repeated attempts to back flush the urethral uroliths (closed arrow) only resulted in two uroliths being moved into the bladder (open arrow). His bladder was marsupialized for 4 days then the remaining urethral uroliths could be moved back into the bladder, at which time the bladder was closed.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 278-2
The bladder is partially exteriorized and emptied.
715
SECTION 4: Surgery
Closure • Every 24 to 48 hours urethral catheterization is attempted with the cat under anesthesia. When it is successful, a urinary catheter is sutured in place, and the cat is prepped for surgery again. The cystostomy incision is closed, and the body wall and skin are closed.
Complications
Figure 278-3 The bladder wall is sutured to the skin using simple interrupted sutures. The sutures go through the bladder wall, the muscle layer of the body wall, and the skin.
• Inadequate suturing of the urinary bladder wall to the skin may result in dehiscence of the wound. • The most common complication is urine scalding of the skin of the ventral abdomen. If the skin protectant ointment is not sufficient, frequent bathing of the skin is recommended. • If this procedure is used on a long-term basis, urine scaling and bacterial cystitis will be likely to occur. The bacteria often become antibiotic resistant over several weeks to months. After 6 to 12 months, the ostium may close so surgery is needed to recreate it. Bladder marsupialization is only recommended in this situation as a salvage procedure.
Suggested Readings Norsworthy GD. 1984. Bladder marsupialization. Fel Pract. 14(5):37–45.
Figure 278-4 The bladder empties directly to the exterior through a hole large enough to accommodate a scalpel handle. The remainder of the skin and abdominal wall incisions is closed routinely.
716
SECTION
5 Cytology
CHAPTER 279
Sample Staining Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt
Overview One of the more important steps in cytologic diagnosis of any lesion, adequate sample staining, occurs before the microscope is turned on. Romanowsky-type stains, including Wright’s and Giemsa stains, and quick stains such as Diff-Quik® (Dade Diagnostics Inc., Mississauga, Ontario, Canada), are the most commonly used cytology stains in veterinary medicine. Because Diff-Quik® and other fast stains are the most widely used in private veterinary practice; the majority of this chapter will focus on features of this stain. However, any Romanowskytype stain usually produces acceptable staining quality of cytology samples.
Preparing to Stain In general preparing cytology smears for staining with any Romanowskytype stain only requires allowing the smear to air dry; no other preparation is necessary. However in certain situations (such as staining air-dried smears of urine sediment) heat fixation is helpful to keep cells from washing off the smear. The sets of fixatives and stains included in each kit are all that are needed to stain a cytology slide. Improper heat fixing of a cytology smear (e.g., excessive passes of the smear directly over an open flame) is detrimental causing cell damage and altered cell morphology and may prohibit evaluation. If one wants to heat fix a slide, the safest method is to hold the smear at arms length and gently blow dry with a hair dryer. No additional fixatives need to be applied to the slide before staining. It is important to keep cytology smears away from formalin. Even slight exposure to formalin fumes can affect staining quality of a cytology smear. Formalin inactivates cell enzymes and alters cell membranes so that cells stain a pale homogeneous blue with Romanowsky-stains making cytologic evaluation difficult to impossible. Formalin fumes will seep out from even a tightly sealed container and fix cytology smears; therefore, do not ship cytology slides and specimens in formalin in the same package.
Staining Quick stains generally consist of three solutions: a fixative, an eosinophilic (pink) stain, and a basophilic (blue) stain. Each brand of stain will have its own manufacturer ’s recommended staining times in each of the solutions. However, these times may need to be adjusted depending on the age of the stain, smear thickness, and sample type. Highly cellular samples such as lymph node, bone marrow, spleen, liver, and hemodilute specimens, usually require a longer staining time; whereas cytology smears from low protein, low cellularity fluids may require a shorter staining time. See Table 279-1. Examine the slide on low power after staining. If the slide is understained (pale), it can be returned to the eosinophilic and basophilic stains to stain longer. Or if just one color is too pale, only that stain may need to be reapplied. Do not repeat the fixative step when restaining because this will decolorize the smear. If oil is present on a slide that needs restaining, the slide can be placed in a jar containing a solvent to remove the oil. However, using a delicate tissue paper product to gently but completely wipe the slide free of oil often is sufficient.
Other Staining Tips It is important to properly maintain a stain set. Stain should be kept in jars with tight fitting lids to help prevent evaporation, especially with the fixative, and to keep out condensation, which can cause water artifact on cytology smears. As stains become older, it will take longer to adequately stain the smears. The basophilic stain is often the first one to exhaust. If samples containing bacteria, yeast, or other organisms will be stained, it is recommended to keep two sets of staining jars. Yeast and bacteria readily grow in stain jars and will contaminate slides. By keeping one set for “dirty samples” (e.g., ear swabs, fecal smears, or infected lesions) and one set for “clean samples” (e.g., mass aspirates and blood smears), contamination will be kept to a minimum. If contamination occurs, simply empty the jars of stain, wash the jars, rinse with alcohol, allow to thoroughly dry, and then refill with new stain. Note that water is detrimental to the stains. If water is used for cleaning the jars, dry them thoroughly before refilling.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
719
SECTION 5: Cytology
TABLE 279-1: Some Possible Solutions to Problems Seen with Common Romanowsky-Type Stains Observation
Problem
Solution
Excessive blue staining (red blood cells may be blue green)
1. 2. 3. 4. 5. 6. 7. 8.
Prolonged stain contact Inadequate wash Specimen too thick Stain, diluent, buffer or wash water too alkaline Exposure to formalin vapors Wet fixation in ethanol or formalin Delayed fixation Surface of the slide was alkaline
1. 2. 3. 4. 5.
Excessive pink staining
1. 2. 3. 4. 5. 6.
Insufficient staining time Prolonged washing Stain or diluent too acidic Excessive time in red stain solution Inadequate time in blue stain solution Mounting coverslip before preparation is dry
1. Increase staining time 2. Decrease duration of wash 3. Check with pH paper and correct pH; fresh methanol may be needed 4. Decrease time in red solution 5. Increase time in blue stain solution 6. Allow preparation to dry completely before mounting coverslip
Weak staining
1. Insufficient contact with one or more of the stain solutions 2. Fatigued (old) stains 3. Another slide covered specimen during staining
1. Increase staining time 2. Change stains 3. Keep slides separate
Uneven Staining
1. Variation of pH in different areas of slide surface. May be due to slide surface being touched or slide being poorly cleaned. 2. Water allowed to stand on some areas of the slide after staining and washing 3. Inadequate mixing of stain and buffer
1. Use new slides and avoid touching their surface before and after preparation 2. Tilt slides close to vertical to drain water from the surface or dry with a fan 3. Mix stain and buffer thoroughly
Precipitate on preparation
1. 2. 3. 4.
1. 2. 3. 4.
Miscellaneous
1. Overstained preparations 2. Refractile artifact on red blood cell
Inadequate stain filtration Inadequate washing of slide after staining Dirty slides used Stain solution dries during staining
Decrease staining time Wash longer Make thinner smears if possible Check with pH paper and correct pH Store and ship cytologic preps separate from formalin containers 6. Air dry smears before fixation 7. Fix smears sooner if possible 8. Use new slides
Filter or change the stain(s) Rinse slides well after staining Use clean new slides Use sufficient stain and do not leave it on slide too long
1. Destain with 95% methanol and restain; Diff-Quikstained smears may have to be destained in the red Diff-Quik stain solution to remove the blue color: however, this damages the red stain solution 2. Change the fixative, usually due to moisture in the fixative; be sure smears have completely dried before staining.
Taken from Cowell RL, Tyler RD, Meinkoth JH, DeNicola DB. 2008. Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., p. 16. St. Louis: Mosby.
Suggested Readings Baker R, Lumsden JH. 2000. Cytopathology techniques and interpretation. In R Baker, JH Lumsden, eds., Color Atlas of Cytology of the Dog and Cat, pp. 7–20. St. Louis: Mosby. Cowell RL, Tyler RD, Meinkoth JH, et al. 2008. Sample collection and preparation. In RL Cowell, RD Tyler, JH Meinkoth, et al., eds.,
720
Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., pp. 1–18. St. Louis: Mosby. Meinkoth JH, Cowell RL. 2002. Sample collection and preparation in cytology: increasing diagnostic yield. Vet Clin North Am Small Anim Pract. 32:1187–1207. Raskin RE, Meyer DJ. 2001. The acquisition and management of cytology specimens. In RE Raskin, DJ Meyer, eds., Atlas of Canine and Feline Cytology, pp. 1–18. Philadelphia: W.B. Saunders.
CHAPTER 280
Differentiation of Inflammation versus Neoplasia Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano Common Types of Inflammation
Overview Cytologic assessment of tissue samples allows a rapid, inexpensive, relatively noninvasive, and diagnostic examination of a population of cells. General categorization of inflammatory cells versus noninflammatory cells is the initial task of cytology with further differentiation based on cytomorphologic features. Inflammatory populations can be comprised of one or more of the following cell types: neutrophils, macrophages, eosinophils, and lymphocytes. Noninflammatory populations consist of tissue cells. There are three categories of tissue cells: discrete cells (round cells), mesenchymal cells (spindle cells), and epithelial cells. Mixed populations of tissue cells and inflammatory cells are common occurrences and can cause difficulties in definitive interpretations.
Inflammation Various types of inflammation are listed here along with common causes and differentials. See Table 280-1.
• Suppurative or Neutrophilic: This is generally comprised of greater than 85% neutrophils. Bacterial infection is a common cause of suppurative inflammation, and bacteria may be observed phagocytized within neutrophils. See Figure 280-1. Degenerate changes (including nuclear swelling and decreased stain intensity) are caused by bacterial toxins and are common features of neutrophils present in bacterial infections. See Figure 280-2. Low grade bacterial involvement or concurrent antibiotic use can make identification of bacteria in a sample challenging due to low numbers. Culture may be helpful in ruling out low-grade bacterial sepsis if organisms are not seen on cytology smears. Ulcerated lesions often become secondarily infected with bacteria, which may reflect a response to the inflammation and not necessarily the primary cause. Therefore, search for a primary cause should be pursued, especially if the lesion is chronic. Noninfectious causes, including immune-mediated skin disease, steatitis, and tissue necrosis, can also elicit suppurative inflammation. However, in these cases the neutrophils are typically nondegenerate.
TABLE 280-1: Some Conditions Suggested by Certain Proportions of Inflammatory cells Inflammatory Cell Population
First Considerations
Marked predominance (85%) of neutrophils: Many neutrophils are degenerate Gram-negative bacteria Gram-positive bacteria
Second Considerations Abscess secondary to neoplasia, foreign bodies, and so on
A few neutrophils are degenerate
Gram-positive bacteria Gram-negative bacteria Higher bacteria (Nocardia, Actinomyces, and so on)
Fungi Protozoa Foreign body Immune mediated Chemical or traumatic injury Abscess secondary to neoplasia
No neutrophils are degenerate
Gram-positive bacteria Higher bacteria (Nocardia, Actinomyces, etc) Chemical or traumatic injury Panniculitis
Gram-negative bacteria Fungi Foreign body Abscess secondary to neoplasia
Higher bacteria (Nocardia, Actinomyces, and so on) Fungi Protozoa Neoplasia Foreign body Panniculitis Any resolving inflammatory lesions
Nonfilamentous Gram-positive bacteria Parasites, chronic allergic inflammation and eosinophilic granuloma if eosinophil numbers are increased
Admixture of inflammatory cells: 15–40% macrophages
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
721
SECTION 5: Cytology
TABLE 280-1. Continued Inflammatory Cell Population
First Considerations
Second Considerations
>40% macrophages
Fungi Foreign body Protozoa Neoplasia Panniculitis Any resolving inflammatory lesions
Parasites, chronic allergic inflammation, and eosinophilic granuloma if eosinophil numbers are increased
Inflammatory giant cells present
Fungi Foreign body Protozoa Collagen necrosis Panniculitis Parasites (if eosinophils are present)
>10% eosinophils
Allergic inflammation Parasites Eosinophilic granuloma Collagen necrosis Mast-cell tumor
Neoplasia Foreign body Hyphating fungi
Adapted from Cowell RL, Tyler RD, and Meinkoth JH. 1999. Diagnostic Cytology and Hematology of the Dog and Cat, 2nd ed., p. 23. St. Louis: Mosby.
Figure 280-1 Septic suppurative inflammation. Aspirate from a cutaneous lesion. Note the phagocytized bacteria within the cytoplasm of some of the neutrophils (arrows). Wright’s stain 1000×. Photo courtesy of Robin Allison, Oklahoma State University.
Figure 280-2 Pyogranulomatous inflammation. Aspirate of a subcutaneous mass. A mixed population of neutrophils and macrophages is present secondary to actinomycosis. Many neutrophils display degenerate changes and a few contain phagocytized bacteria (arrow). Wright’s stain 1000×. Photo courtesy of Robin Allison, Oklahoma State University.
• Granulomatous: Macrophages are the predominant inflammatory cell population observed in granulomatous inflammation. Simple bacterial infections usually do not incite granulomatous inflammation; however, mycobacterial infections often cause a granulomatous reaction. The presence of high numbers of macrophages should raise concern of larger, more complex infectious organisms, such as fungi or protozoa. Other stimuli for granulomatous inflammation include foreign bodies (including injection site reactions), neoplasia, steatitis, and tissue necrosis. See Figure 280-3. Parasites and insect bites can also cause granulomatous inflammation that often is accompanied by eosinophils and other inflammatory cells. Occasionally granulomatous inflammation includes the presence of multinucleated “giant cells.” These cells are formed when multiple macrophages merge together to form one large cell in an attempt to phagocytize a large
organism or foreign object or material. Cutaneous keratinous cysts (including epidermal inclusion cysts, hair matrix tumors, and so on) can also incite granulomatous inflammation, particularly when their contents rupture into the subcutis. • Pyogranulomatous: This type of inflammation is made up of a mixture of macrophages and neutrophils. See Figure 280-2. Causes include higher forms of bacteria, such as Actinomyces and Nocardia, as well as the causes of granulomatous inflammation (i.e., fungi, neoplasia, foreign body, injection site reaction, insect bites, tissue necrosis, and so on) • Eosinophilic: An inflammatory population consisting of greater than 10% eosinophils indicates an eosinophilic component in that process. See Figure 280-4. Common causes of eosinophilic inflammation include allergic or hypersensitivity responses, eosinophilic granu-
722
Differentiation of Inflammation versus Neoplasia
Figure 280-3 Granulomatous inflammation; steatitis. Aspirate from a cutaneous mass. Note the numerous clear, lipid vacuoles within several macrophages. Wright’s stain original magnification 250×. Photo courtesy of Rick L. Cowell.
Figure 280-5 Injection site reaction. Cutaneous mass from a different patient than in Figure 280-12. The macrophage contains eosinophilic adjuvant material. In this case lymphocytic inflammation is present. Wright’s stain 1000×. Photo courtesy of Oklahoma State University teaching files.
Tissue Cells If a noninflammatory population of tissue cells is identified, features of the cells usually allow classification into one of the three cell types: discrete (round) cells, mesenchymal (spindle) cells, or epithelial cells. See Table 280-2.
Tissue Cell Types
Figure 280-4 Eosinophilic inflammation. Scraping from an eosinophilic granuloma. Several eosinophils are present, and numerous free eosinophil granules are present in the background (arrows). A few neutrophils are also present indicating suppurative inflammation as well. Wright’s stain 1000×. Photo courtesy of Oklahoma State University teaching files.
loma complex, parasitic infection, and insect bites. Less commonly, foreign bodies, hyphating fungi, and neoplasia can also incite eosinophilic inflammation. • Lymphocytic: This type of inflammation is comprised primarily of small mature lymphocytes with scattered larger lymphocytes and occasionally other inflammatory cells. Variable numbers of small mature lymphocytes and plasma cells may also accompany other types of inflammatory responses. Inciting causes of lymphocytic inflammation include injection site reactions, insect bites, stomatitis, and neoplasia (such as fibrosarcoma) as well as nonspecific antigenic or immune stimulation. See Figure 280-5.
• Discrete (Round) Cells: Tumors of discrete cell origin typically yield high cellularity samples of round, small to medium sized, individually arranged cells with distinct cell borders. Examples of discrete cell tumors of cats include lymphoma, mast cell tumor, and plasma cell tumor. See Figures 280-6 and 280-7. • Epithelial Cells: These cells are medium to large in size appearing round to caudate in shape and are usually present in cohesive clusters with distinct cellular borders. Neoplastic populations of epithelial cells are termed carcinomas. Adenocarcinomas are epithelial tumors of glandular origin. See Figures 280-8 and 280-9. • Mesenchymal (Spindle) Cells: These cells typically have a fusiform or tapered shape with indistinct cell borders. Usually these cells are present individually, but they may be present in aggregates. When present in aggregates, the mesenchymal cells may appear embedded in an eosinophilic (pink), amorphous substance called matrix. See Figure 280-10. Sarcomas are malignant tumors of mesenchymal origin. Examples of sarcomas include fibrosarcoma, hemangiosarcoma, and osteosarcoma.
Evaluation of Malignant Criteria Tissue cells in a cytology sample should be evaluated for malignant potential by looking for abnormal, anaplastic features collectively called criteria of malignancy. See Figure 280-11 and Table 280-3. Malignant criteria may involve features of the nucleus or features of the entire cell. Nuclear criteria are considered more significant. Identification of three or more nuclear criteria of malignancy is strongly suggestive for malignant transformation. Less than three criteria may indicate a benign population; however, some types of malignant tumors may appear well
723
TABLE 280-2: General Appearance of the Three Basic Tumor Categories Cellularity of aspirates
Clumps or clusters common
Round to caudate
Usually high
Yes
Small to medium
Spindle to stellate
Usually low
No
Small to medium
Round
Usually high
No
Tumor type
General cell size
General cell shape
Epithelial
Large
Mesenchymal (spindle cell)
Discrete round cell
Schematic representation
Figure 280-6 Discrete (round) cell tumor. Aspirate of a cutaneous plasma cell tumor. Eccentrically placed nuclei, a perinuclear clear zone, and occasional binucleate cells are features characteristic of plasma cells. Wright’s stain. Photo courtesy of Oklahoma State University teaching files.
Figure 280-7 Discrete (round) cell tumor. Aspirate of a cutaneous mast cell tumor. Numerous pinpoint magenta granules fill the cytoplasm and commonly obscure the nucleus of mast cells. Note the free granules also present in the background. Wright’s stain 500×. Photo courtesy of Oklahoma State University teaching files
Figure 280-8 Epithelial cell tumor. Aspirate of a cutaneous mass. Epithelial cells are recognized by their large size, tendency to cluster, and distinct cell to cell junctions. These cells only display a few atypical features including moderate anisocytosis and anisokaryosis. Wright’s stain 500×. Photo courtesy of Oklahoma State University teaching files.
724
Differentiation of Inflammation versus Neoplasia
(A)
Figure 280-9 Transitional cell carcinoma. Aspirate of a bladder mass. Many epithelial cells are present with a high degree of malignant criteria. Marked anisocytosis, anisokaryosis, multinucleation, prominent angular nucleoli (arrow), and a coarse chromatin pattern are displayed by these cells. These cells are large when compared to the neutrophil present in the picture. Large cell size is a common feature of epithelial cells. Wright’s stain 500×. Photo courtesy of Robin Allison, Oklahoma State University.
differentiated with only few malignant criteria. If in doubt or when unfamiliar with tumors that behave aggressively but appear benign, confirmation should be made by submitting samples to a clinical pathologist or submitting a biopsy for histopathologic analysis of tissue architecture.
Mixed Sample of Inflammatory and Tissue Cells A cytologic sample containing both inflammatory cells and tissue cells should be interpreted with caution. Inflammation causes dysplastic changes in normal tissue cells present in the area. These cells can display significant criteria of malignancy but are not neoplastic cells. Also, tumors themselves can incite inflammation or become secondarily infected resulting in a mixture of inflammatory cells and atypical tissue cells. When faced with distinguishing an inflamed neoplastic population from an inflamed dysplastic population of cells, the inflammation should be treated and the lesion reevaluated cytologically. Often strictly inflammatory dysplasia will resolve with resolution of the concurrent inflammation.
Injection Site Reactions Vaccines and other injections can cause persistent cutaneous nodules. Aspiration of these lesions typically yields a large number of mixed inflammatory cells. The cell types present in these responses are quite variable and may be primarily lymphocytic, suppurative, granulomatous, or even eosinophilic. Mixed inflammation is also quite common. Bright pink to magenta staining amorphous material, thought to be consistent with vaccine adjuvant, may be observed extracellularly and phagocytized within macrophages. See Figures 280-5 and 280-12. Occasional spindle-shaped, atypical fibroblasts can also be observed in these lesions. As mentioned previously, these changes could represent reactive changes due to the inflammation or changes due to neoplasia. Fibrosarcomas may be associated with previous sites of vaccination; therefore, histopathology is recommended for any vaccine reaction site that fails to regress. Refer to the Vaccine-Associated Feline Sarcoma Task
(B) Figure 280-10 A, Mesenchymal (spindle) cell tumor. Aspirate of a cutaneous mass. Note the tapering shape and indistinct cytoplasmic borders characteristic of mesenchymal cells. B,) Same case as image A. These mesenchymal cells are observed producing eosinophilic matrix material (arrow). Anisocytosis, anisokaryosis, multinucleation, and prominent nucleoli are displayed by these cells. Wright’s stain 500×. Photos courtesy of Oklahoma State University teaching files. Force (VAFSTF) report for vaccine reaction details. The VAFSTF suggests that incisional biopsy of a mass that develops at an injection site be performed prior to excisional biopsy, if it meets any one or more of the following “3-2-1” criteria: if persists greater than 3 months postinjection, if greater than 2 cm (3/4 in) in diameter, or if increased growth 1 month post-injection.
Epidermal Inclusion Cysts and Hair Follicle Tumors Epidermal inclusion cysts and hair follicle tumors (such as pilomaticomas and trichoepitheliomas) are fairly common benign cutaneous tumors in cats. Aspirates from these masses have a unique cytologic appearance predominantly comprised of anucleate mature squamous epithelial cells along with a background of blue amorphous cellular debris. The squamous epithelial cells are large and have angular borders. Sometimes large, polygonal, nonstaining cholesterol crystals are also observed. See Figure 280-13. These tumors can occasionally rupture into the subcutis and cause significant inflammation. If this occurs, neutrophils and macrophages may also be present in the samples.
725
TABLE 280-3: Easily Recognized General and Nuclear Criteria of Malignancy Criteria General criteria Anisocytosis and macrocytosis
Description Variation in cell size, with some cells ≥1.5 times larger than normal.
Hypercellularity
Increased cell exfoliation due to decreased adherence.
Pleomorphism (except in lymphoid tissue)
Variable size and shape in cells of the same type.
Nuclear criteria Macrokaryosis
Not depicted
Increased nuclear size. Cells with nuclei larger than 10 µ in diameter suggest malignancy.
Increased nucleus-to-cytoplasm ratio (N-to-C)
Normal nonlymphoid cells usuall have a N-to-C of 1:3 to 1:8, depending on the tissue. Increased ratios (1:2, 1:1, and so on) suggest malignancy
Anisokaryosis
Variation in nuclear size. This is especially important if the nuclei of multinucleated cells vary in size.
Multinucleation
Multiple nucleation in a cell. This is especially important if the nuclei vary in size.
Increased mitotic figures
Mitosis is rare in normal tissue.
Abnormal mitosis
Improper alignment of chromosome
Coarse chromatin pattern
The chromatin pattern is coarser than normal. It may appear ropy or cord-like.
Nuclear molding
Deformation of nuclei by other nuclei within the same cell or adjacent cells
Macronucleoli
Nucleoli are increased in size. Nucleoli ≥5 µ strongly suggest malignancy. For reference, red blood cells are 5–6 µ in the cat and 7–8 µ in the dog.
Angular nucleoli
Nucleoli are fusiform or have other angular shapes, instead of their normal round to slightly oval shape.
anisonucleoliosis
Variation in nucleolar shape or size (especially important if the variation is within the same nucleus).
726
Schematic representation
Red blood cell See macrokaryosis
See “increased mitotic figures”
See “angular nuceoli”
Differentiation of Inflammation versus Neoplasia
(A)
Figure 280-11 Mitotic figures. Pleural fluid from a cat with metastatic mammary adenocarcinoma. One mitotic figure is present showing disorganized mitotic activity. Wright’s stain 250×. Photo courtesy of Rick L. Cowell.
(B) Figure 280-13 A, Epidermal inclusion cyst. Aspirate of a cutaneous mass. Numerous anucleate keratinized squamous epithelial cells are present. Wright’s stain 50×. B, Higher power of image A. Wright’s stain 250× Photos courtesy of Rick L. Cowell.
Suggested Readings
Figure 280-12 Injection site reaction. Aspirate of a cutaneous mass at the site of previous vaccination. Pyogranulomatous inflammation is present, and eosinophilic adjuvant material has been phagocytized by the macrophages (arrow). Wright’s stain 500×. Photo courtesy of Robin Allison, Oklahoma State University.
Baker R, Lumsden JH. 2000. Cytology techniques and interpretation. In R Baker, JH Lumsden, eds., Color Atlas of Cytology of the Dog and Cat, pp. 7–20. St. Louis: Mosby. Cowell RL, Tyler RD, Meinkoth JH, et al. 2008. Cell types and criteria of malignancy. In RL Cowell, RD Tyler, JH Meinkoth, et al., eds., Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., pp. 20–46. St. Louis: Mosby. Meinkoth JH, Cowell RL. 2002. Recognition of basic cell types and criteria of malignancy. Vet Clin North Am Small Anim Pract. 32:1209–1235. Raskin RE, Meyer DJ. 2001. General categories of cytologic interpretations. In RE Raskin, DJ Meyer, eds., Atlas of Canine and Feline Cytology, pp. 19–33. Philadelphia: W.B. Saunders. Richards JR, Starr RM, Childers HE. 2005. Vaccine-Associated Feline Sarcoma Task Force: Roundtable Discussion. J Am Vet Med Assoc. 226(11):578–601.
727
CHAPTER 281
Adenocarcinoma Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt
Overview Adenocarcinomas are malignant tumors of glandular epithelial origin. These tumors may arise from any glandular tissue including sites such as: ear (ceruminous glands), nasal, gastrointestinal, mammary, biliary, pancreatic, or subcutaneous adnexal tissue (sebaceous and apocrine glands).
Cytologic Features Glandular epithelial cells can be identified cytologically by high exfoliation, large cell size, tendency to cluster and form an acinar pattern, and by the presence of intracytoplasmic vacuoles of secretory material. Cells of glandular origin should be evaluated for criteria of malignancy as described in Chapter 280. Although adenomas will be fairly uniform in size and appearance, adenocarcinomas generally will show malignant cytological criteria such as anisocytosis, anisokaryosis, and large prominent nucleoli. See Figure 281-1. Not all adenocarcinomas have vacuolated cytoplasm or acinar arrangements, and some cannot be identified to specific gland/cell type. See Figures 281-1 and 281-2A and 2B. Additionally, well-differentiated adenocarcinomas may be fairly uniform cytologically and difficult to distinguish from an adenoma. In these cases, histopathology is needed to further characterize biological behavior and for identification of specific gland type.
(A)
(B) Figure 281-2 Metastatic mammary adenocarcinoma. Pleural fluid. A, Clusters of markedly atypical cells are displaying multinucleation, anisocytosis, anisokaryosis, coarse chromatin pattern, and nuclear molding. However, only minimal vacuolation is present to suggest glandular origin. This tumor was identified as a mammary adenocarcinoma by histopathology. Wright’s stain 250×. B, Same case as image A showing the same neoplastic characteristics. Wright’s stain 100×. Photos courtesy of Rick L. Cowell. Figure 281-1 Adenocarcinoma. Pleural fluid. Clusters of atypical vacuolated cells are present. These cells display criteria of malignancy such as marked anisocytosis and anisokaryosis, coarse chromatin pattern, multinucleation, with significant variation in nuclear to cytoplasmic ratio.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
728
Adenocarcinoma
Suggested Readings Baker R, Lumsden JH, eds. 2000. Cytology techniques and interpretation. In R Baker, JH Lumsden, eds., Color Atlas of Cytology of the Dog and Cat, pp. 32–20. St. Louis: Mosby. Cowell RL, Tyler RD, Meinkoth JH, et al. 2008. Cell types and criteria of malignancy. In RL Cowell, RD Tyler, JH Meinkoth, et al., eds.,
Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., pp. 32–35. St. Louis: Mosby. Klaassen JK. 2002. Cytology of subcutaneous glandular tissues. Vet Clin North Am Small Anim Pract. 32:1237–1266. Raskin RE, Meyer DJ. 2001. General categories of cytologic interpretations. In RE Raskin, DJ Meyer, eds., Atlas of Canine and Feline Cytology, pp. 19–33. Philadelphia: W.B. Saunders.
729
CHAPTER 282
Atypical Bacterial Infections Tara P. Arndt, Rick L. Cowell, and Amy Valenciano
Overview Atypical bacteria, including filamentous bacteria (Actinomyces and Nocardia spp.) and Mycobacterium, can cause infections in cats that can be more refractory to treatment than more common bacterial infections. Cytologic preparations from these types of atypical bacterial infections often contain more macrophages than typically seen with more common bacterial infections such as Staphylococcus and Streptococcus spp. infections, which are often neutrophilic in nature; however, filamentous bacterial infections can be noted with significant neutrophilic inflammation as well. Cytologic preparations noted with granulomatous or pyogranulomatous inflammation should prompt close evaluation for atypical bacteria as well as other causes of granulomatous or pyogranulomatous inflammation, such as foreign body reactions.
Filamentous Bacterial Infections Filamentous rod bacteria such as Actinomyces and Nocardia spp. commonly cause cutaneous infections (abscesses) resulting from penetrating wounds and bite wounds but can also associated with systemic infections including pyothorax and peritonitis. See Chapters 4 and 152. Cytology samples will often have pyogranulomatous inflammation and appear as an admixture of neutrophils (in various stages of degeneration) and macrophages. The filamentous bacteria may appear as long, slender pale blue, structures with intermittent red to blue staining beads along their length. See Figure 282-1. Occasionally, filamentous bacteria
may be seen as branching filamentous rods. See Figure 282-2. Filamentous bacteria may be found intracellularly as well as extracellularly and can be observed individually or in aggregates. Mixed bacteria (i.e., cocci, short rods, coccobacilli) may also be seen along with the filamentous bacteria reflecting a mixed bacterial infection. Note that Actinomyces and Nocardia can be pleomorphic and may form any of the aforementioned shapes mimicking a mixed bacterial infection.
Diagnosis Primary Diagnostics • Culture: Aerobic and anaerobic culture and sensitivity are recommended since Nocardia species are aerobes and Actinomyces species may be facultative or obligate anaerobes. If Actinomyces or Nocardia spp. is suspected from clinical or cytologic finding, alerting the laboratory of your suspicions assures appropriate cultures for Actinomyces and Nocardia will be set up.
Mycobacteriosis Mycobacterium spp. can cause cutaneous (lepromatous) lesions, internal organ (tuberculosis) infection, or spreading subcutaneous lesions. See Chapter 144. The cell populations in these lesions are usually granulomatous, consisting mainly of macrophages. Mycobacterium spp. do not stain with Romanowsky-type stains or quick stains (including Diff-Quik®) and may be difficult to visualize using these staining methods alone; however, “negative staining” long slender rod structures can often be seen phagocytized within macrophages or free in the background. See Figure 282-3. Acid fast staining is often helpful in identifying these organisms. See Figure 282-4.
Figure 282-1 Pyogranulomatous inflammation with filamentous bacteria found in pleural fluid. Numerous filamentous bacteria are present that have intermittent red staining beads along their length typical of species such as Actinomyces and Nocardia. Wright’s stain 1000×. Photo courtesy of Oklahoma State University teaching files.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
730
Figure 282-2 Pyogranulomatous inflammation with branching filamentous bacteria. Note the branching characteristics in this population. Wright’s stain 1000×. Photo courtesy of Rick L. Cowell.
Atypical Bacterial Infections
Diagnosis Primary Diagnostics • Staining: Acid-fast stains will stain Mycobacterium a bright red color and can be applied to cytology samples or histopathologic sections to assist with their identification. If organisms are indistinct or not found on cytology, biopsy and histopathology are recommended. • Culture: Culture may also be done to confirm mycobacteriosis; however, some Mycobacterium species are slow growing and may require 4 to 6 weeks for a positive culture. Polymerase chain reaction (PCR) testing and other molecular diagnostics on tissue specimens are also available and can hasten diagnosis.
Suggested Readings
Figure 282-3 Mycobacterium from a liver aspirate. A macrophage is present containing several nonstaining filamentous organisms. Wright’s stain 1000×. Photo courtesy of Rick L. Cowell.
Baker R, Lumsden JH. 2000. Infectious agents. In R Baker, JH Lumsden, eds., Color Atlas of Cytology of the Dog and Cat, pp. 23–38. St. Louis: Mosby. Cowell RL, Tyler RD, Meinkoth JH, et al. 2008. Selected infectious agents. In RL Cowell, RD Tyler, JH Meinkoth, et al., eds., Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., pp. 47–62. St. Louis: Mosby. Greene CE. 2006. Actinomycosis and nocardiosis. In CE Greene, ed., Infectious Diseases of the Dog and Cat, 3rd ed., pp. 451–461. Philadelphia: W.B. Saunders Company. Raskin RE, Meyer DJ. 2001. Skin and subcutaneous tissues. In RE Raskin, DJ Meyer, eds., Atlas of Canine and Feline Cytology, pp. 35–92. Philadelphia: W.B. Saunders.
Figure 282-4 Mycobacterium. Acid-fast stain from a liver aspirate. Several thin red staining filamentous organisms are noted within a macrophage consistent with Mycobacterium. Wright’s stain 1000×. Photo courtesy of Rick L. Cowell.
731
CHAPTER 283
Fibrosarcoma Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt
Overview Fibrosarcomas are malignant tumors of mesenchymal tissue origin, specifically, of fibrocytes. These tumors are invasive and recurrent, but uncommonly metastatic. They represent nearly 17% of all skin tumors in cats. Aside from the skin, fibrosarcoma can also arise in mammary tissue, the oropharynx, and intestine. Injection-site sarcoma is a specific type of sarcoma that arises at sites of previous injections of vaccines and other products. Detailed information regarding the diagnosis of suspect injection-site sarcomas established by the Vaccine-Associated Feline Sarcoma Task Force can be found at: www.avma.org/vafstf/. See Chapter 197.
Cytologic Features Most mesenchymal tumors are poorly exfoliative and hemodilute upon fine-needle aspiration. When aspirates fail to yield sufficient cells for evaluation, a nonaspiration technique should be considered. This can be accomplished by inserting the needle into the mass and redirecting without aspirating (tattoo technique). Once the needle is removed, an air-filled syringe is attached to the needle and the sample can then be expressed onto a slide. See Chapter 301. If an adequate sample still cannot be obtained, biopsy or excision with histopathology will be necessary for diagnosis. When cells do exfoliate on aspiration or nonaspiration fine-needle techniques, neoplastic fibrocytes generally have a tapered to spindle shaped appearance with indistinct cell margins. Cytoplasm can be scant to moderate and is often basophilic. Nuclei range from slender and elongate to plump and ovoid. Most cells are uninucleate, but multinucleate cells may be found in lesser numbers. See Figure 283-1. Cells may be present individually or in aggregates, and occasionally mesenchymal cells may be observed producing a bright pink amorphous to fibrillar matrix. See Figure 283-2. Cytology samples of mesenchymal tissue should be evaluated for criteria of malignancy as described in Chapter 280. See Figure 283-3. A high degree of malignant criteria is supportive of a sarcoma, with the caveat that uniform, minimally atypical cells can be seen with well-differentiated, yet malignant, neoplasms. In this case, histopathology is needed for definitive characterization of biologic behavior. Most sarcomas, including fibrosarcomas, appear similar on cytology. Thus, histopathology, occasionally with the aid of special stains, is needed to distinguish the different types of sarcomas. Special caution must be made with any cytologic diagnosis of sarcoma because nonneoplastic fibrous tissue that is reactive secondary to inflammation can display significant criteria of malignancy and be indistinguishable from a sarcoma. Biopsy and histopathology is always recommended to differentiate reactive fibrous tissue from a sarcoma, especially when atypical spindle cells are seen with significant associated inflammation cytologically. Differentiation of spontaneous versus injection-site sarcoma, both cytologically and histopathologically, can be difficult. However,
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
732
Figure 283-1 Fibrosarcoma. Aspirate of a cutaneous mass. Note numerous large multinucleate giant cells and admixed uninucleate, atypical mesenchymal cells. Wright’s stain 500×. Photo courtesy of Amy C. Valenciano.
Figure 283-2 Fibrosarcoma. Aspirate of a cutaneous mass. Large numbers of individualized, pleomorphic mesenchymal cells intimately associated with abundant bright eosinophilic, fibrillar extracellular matrix. Wright’s stain 200×. Photo courtesy of Amy C. Valenciano.
development of a sarcoma at a site of previous injection/vaccination and the presence of foreign material suggests injection association. Microscopically, the foreign material is characterized as homogenous, bright eosinophilic, variably sized globules of material present both in the extracellular space and phagocytized within macrophages. See Figure 283-4.
Fibrosarcoma
Figure 283-3 Fibrosarcoma. Aspirate of a cutaneous mass. Neoplastic mesenchymal cells with ill-defined cytoplasmic borders, moderate basophilic cytoplasm, singular ovoid nuclei with a moderate to marked degree of anisocytosis and anisokaryosis. Wright’s stain 500×. Photo courtesy of Amy Valenciano).
Suggested Readings Baker R, Lumsden JH. 2000. The skin. In R Baker, JH Lumsden, eds., Color Atlas of Cytology of the Dog and Cat, pp. 39–70. St. Louis: Mosby. Cowell RL, Tyler RD, Meinkoth JH, et al. 2008. Cell types and criteria of malignancy. In RL Cowell, RD Tyler, JH Meinkoth, et al., eds.,
Figure 283-4 Vaccination/injection reaction. Aspirate of a cutaneous mass. There is mixed inflammation, primarily composed of mature lymphocytes followed by lesser numbers of large macrophages. Note bright magenta, globular extracellular and phagocytized (within the macrophages) foreign material. Wright’s stain 1000×. Photo courtesy of Amy C. Valenciano).
Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., pp. 20–46. St. Louis: Mosby. Hauck M. Feline injection site sarcomas. 2003. Vet Clin North Am Small Anim Pract. 33:553–557. McEntee MC, Page RL. 2001. Feline vaccine-associated sarcomas. J Vet Intern Med. 15:176–182.
733
CHAPTER 284
Hepatic Lipidosis Tara P. Arndt, Rick Cowell, and Amy Valenciano
Overview Hepatic lipidosis can be a common cause of hepatomegaly in the feline patient. The mechanisms causing hepatic lipidosis in cats are discussed in Chapter 93. Fine-needle aspiration and fine-needle biopsy of the liver are quick, fairly noninvasive ways to differentiate several causes of hepatomegaly.
Normal Liver Cytology Liver aspirates generally yield variable numbers of hepatocytes in a background of peripheral blood. Hepatocytes are large, round to polyhedral shaped cells with distinct cellular borders. Hepatocytes have round to slightly oval nuclei that often contain a single, small, round nucleolus. Abundant, grainy, blue-grey cytoplasm is also a characteristic feature. See Figure 284-1. Some of the hepatocytes may contain a small amount of intracytoplasmic blue-green pigment thought to represent bile, lipofuscin, or other pigment accumulation. The finding of lipofuscin accumulation is a more common finding in older animals.
Cytologic Features of Hepatic Lipidosis In hepatic lipidosis, the cytoplasm of the hepatocytes becomes distended with numerous, microvesicular and macrovesicular clear vacuoles. These vacuoles are distinctly demarcated and defined as opposed to vacuolar degeneration in which the hepatocytes contain indistinct vacuoles. See Figure 284-2. The background is often noted with similar punctuate vacuoles. Cytologic interpretation of hepatic lipidosis is based on appreciation of large amounts of fatty vacuolar deposition in significant numbers (greater than 80%) of the present hepatocytes. Distinct lipid vacuoles must be identified within intact hepatocytes because inadvertent aspiration of normal adipose tissue, especially the falciform ligament, can also produce a background of lipid vacuoles. Care should be taken before interpreting feline hepatic lipidosis as other conditions can also cause significant lipid material to accumulate within hepatocytes including metabolic conditions such as congenital storage diseases and diabetes mellitus. For a cytologic interpretation of hepatic lipidosis, there must be marked fatty deposition within hepatocytes. Cholestasis can occur concurrently with hepatic lipidosis and is recognized by the formation of “bile casts,” which appear as ribbons of greenish-black bile pigment trapped in cannuliculi between hepatocytes. Cholestasis can contribute to elevated liver enzyme values. See Figure 284-3.
Figure 284-1 Normal hepatocytes. Liver aspirate. Large round to polyhedral shaped hepatocytes with round nuclei and a grainy, blue gray cytoplasm. Hepatocytes usually contain a single round nucleolus. Wright’s stain 500×. Photo courtesy of Oklahoma State University teaching files.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
734
Figure 284-2 Hepatic lipidosis. Liver aspirate. Hepatocytes are present which are filled with sharply demarcated microvesicular and macrovesicular lipid vacuoles. Wright’s stain 500×. Photo courtesy of Robin Allison, Oklahoma State University.
Hepatic Lipidosis
Suggested Readings Baker R, Lumsden JH. 2000. The gastrointestinal tract: Intestines, liver, pancreas. In R Baker, JH Lumsden, eds., Color Atlas of Cytology of the Dog and Cat, pp. 177–198. St. Louis: Mosby. Center SA. 2005. Feline hepatic lipidosis. Vet Clin North Am Small Anim Pract. 35(1):225–269 Cowell RL, Tyler RD, Meinkoth JH, et al. 2008. The liver. In RL Cowell, RD Tyler, JH Meinkoth, et al., eds., Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., pp. 312–329. St. Louis: Mosby. Raskin RE, Meyer DJ. 2001. The liver. In RE Raskin, DJ Meyer, eds., Atlas of Canine and Feline Cytology, pp. 231–252. Philadelphia: W.B. Saunders.
Figure 284-3 Cholestasis. Liver aspirate. A cluster of hepatocytes is present with greenish-black “bile casts” between cells (arrows). Wright’s stain 500×. Photo courtesy of Oklahoma State University teaching files.
735
CHAPTER 285
Lymph Node Disease Tara P. Arndt, Rick L. Cowell, and Amy Valenciano
Overview Lymphadenopathy can be a common finding in the feline patient, and cytologic evaluation of lymph nodes can be a useful tool to aid in differentiation of inflammatory and neoplastic causes of lymphadenopathy. This chapter serves to highlight several features and more common causes of enlarged lymph nodes including immune reactivity, inflammation, and neoplasia. The cytologic features of feline lymphoma are discussed in Chapter 286.
Normal Lymph Node Normal lymph nodes are predominantly comprised of (75–95%) small mature lymphocytes with lower numbers of intermediate sized lymphocytes and larger immature lymphocytes (often referred to as lymphoblasts). See Figure 285-1. The lymphocyte populations are differentiated on the basis of size and cellular features. A neutrophil can be used as an estimation to assist in size determination. Small mature lymphocytes are larger than a red blood cell but smaller than a neutrophil. They generally have round nuclei, densely clumped chromatin, no visible nucleoli, and a small rim of lightly basophilic cytoplasm. Large immature lymphocytes (lymphoblasts) are larger than a neutrophil and have round to polygonal shaped nuclei with a stippled chromatin pattern and a single or multiple nucleoli and a larger amount of basophilic cytoplasm. Plasma cells (transformed B lymphocytes producing antibody) may be seen in low numbers. Plasma cells have round eccentrically placed nuclei with a dense chromatin pattern and abundant basophilic cytoplasm that contains a clear, perinuclear Golgi zone. Low numbers of other cells may also be present in a normal lymph node aspirate including macrophages, neutrophils, eosinophils, and mast cells.
Figure 285-1 Hyperplastic/normal lymph node. Normal, hyperplastic and reactive lymph nodes consist primarily of small mature lymphocytes as seen here. Also pictured are scattered lymphoblasts and a single eosinophil. Wright’s stain, 1000×. Courtesy of Rick L. Cowell). The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
736
Reactive or Hyperplastic Lymph Nodes Small mature lymphocytes are the predominant cell type present in a reactive node, but the percentage of intermediate and larger immature lymphocytes will be increased and can approach 15 to 25% of the lymphoid population. Plasma cells may also be increased and Mott cells (i.e., abnormal plasma cells with defective immunoglobulin secretion) may be present. Mild increases in inflammatory cell numbers may sometimes be seen in reactive lymph nodes as well. As inflammatory cell numbers increase, the population of cells is sometimes termed lymphadenitis. See Figure 285-2. Lymphadenitis is often observed concurrently with a reactive lymphoid population and can be considered a subcategory of a reactive node. Lymphoid reactivity and hyperplasia is often noted as a response to immune or antigenic drainage from the regional areas draining to the lymph node or from systemic inflammatory reactions, both infectious and non-infectious.
Lymphadenitis Lymphadenitis is characterized cytologically by increased numbers of inflammatory cells. Neutrophils, eosinophils, or macrophages may be increased alone, or a mixed inflammatory reaction may be present. If lymphadenitis is severe and has effaced the node, aspirates may consist only of inflammatory cells with no significant numbers of lymphocytes appreciated. An increase in neutrophils greater than 5% of the nucleated cell population or an increase in eosinophils above 3% of the nucleated cell population indicates inflammation of these types. A common cause of suppurative (neutrophilic) lymphadenitis is bacterial infection in the regional drainage area to the associated lymph node, although mycobacterial infections can induce granulomatous lymphadenitis in the cat. Dental disease is a common cause of suppurative lymphadenitis of the mandibular lymph nodes. Allergic reactions, parasitic infections, and
Figure 285-2 Reactive lymph node. Plasma cells (arrows) are increased in number. A mildly increased number of neutrophils is also present indicating a mild suppurative (neutrophilic) lymphadenitis. Wright’s stain 500×. Photo courtesy of Oklahoma State University teaching files.
Lymph Node Disease
Figure 285-3 Lymph node with metastatic carcinoma. Large atypical epithelial cells with numerous malignant criteria are present in a lymph node aspirate. Increased numbers of inflammatory cells are present also (reactive lymph node). The malignant cells display large prominent nucleoli, multinucleation, and a coarse chromatin pattern. Wright’s stain 500×. Photo courtesy of Rick L. Cowell.
Figure 285-4 Normal adipose tissue. Large balloon-shaped cells with small displaced nuclei are consistent with adipocytes and perinodal lipid. Wright’s stain 200×. Photo courtesy of Robin Allison, Oklahoma State University.
feline eosinophilic granuloma complex are more common causes of eosinophilic lymphadenitis. Systemic fungal infections, such as histoplasmosis, blastomycosis, cryptococcosis, and coccidiomycosis as well as with protozoa such as Cytauxzoon felis, typically evoke a granulomatous to pyogranulomatous (increased numbers of neutrophils and macrophages) lymphadenitis. Granulomatous inflammation is also noted with paraneoplastic responses in some cases of feline lymphoma.
Lymph Node with Metastatic Neoplasia Metastatic neoplasia can be identified on cytologic evaluation of lymph node aspirates. Metastatic cells from primary neoplastic lesions may be present in lymph node cytologic preparations in variable numbers and will often display criteria of malignancy. See Figure 285-3. Refer to Chapter 280 for more information regarding criteria of malignancy. Increases in the number of cells other than lymphocytes (e.g., mast cells, plasma cells, or histiocytic cells) that are normally present in lymph nodes may cause a diagnostic dilemma because it can be difficult to determine if these cells represent metastatic cells or part of a reactive node or lymphadenitis. In any case of suspected metastasis, submission of the aspirates to a clinical pathologist or biopsy and histopathology of the affected node are recommended for confirmation.
Figure 285-5 Normal salivary gland. Highly vacuolated epithelial cells with uniformly sized nuclei are typical. Salivary glands can be difficult to distinguish from enlarged submandibular lymph nodes with palpation alone. Wright’s stain 1000×. Photo courtesy of Rick L. Cowell.
Artifacts of Inadvertent Tissue Aspiration Some lymph nodes (especially ones that are not enlarged) may be difficult to aspirate. Inadvertent aspiration of other structures, such as a salivary gland and perinodal lipid, will produce preparations with a population of cells not expected in a lymph node aspirate. Note that these cells will not exhibit significant criteria of malignancy. Adipocytes from perinodal lipid appear as large balloon-shaped cells that may form clusters or be found individually. They have a small oval-shaped nucleus that may be displaced to the margin of the cell. See Figure 285-4. Enlarged salivary glands can be mistaken for lymph nodes and aspirated. Salivary epithelial cells have small round nuclei and abundant amounts of vacuolated, pale basophilic cytoplasm. Normal salivary epithelial cells appear glandular and will not display criteria of malignancy. See Figure 285-5.
Suggested Readings Baker R, Lumsden JH. 2000. The lymphatic system: Lymph nodes, spleen, and thymus. In R Baker, JH Lumsden, eds., Color Atlas of Cytology of the Dog and Cat, pp. 71–94. St. Louis: Mosby. Cowell RL, Dorsey KE, Meinkoth JH. 2003. Lymph node cytology. Vet Clin North Am Small Anim Pract. 33:47–67. Cowell RL, Tyler RD, Meinkoth JH, DeNicola DB. 2008. Lymph nodes. In Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., pp. 180–192. St. Louis, MO: Mosby. Raskin RE, Meyer DJ. 2001. Lymphoid system. In RE Raskin, DJ Meyer, eds., Atlas of Canine and Feline Cytology, pp. 93–134. Philadelphia: W.B. Saunders.
737
CHAPTER 286
Lymphoma Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt
Overview Cytology is a rewarding method for diagnosing lymphoblastic (highgrade) lymphoma; however, the standard criteria of malignancy used for carcinomas and sarcomas do not apply to lymphoma. An entirely different set of criteria is used. Immature lymphoblasts are normal residents of lymphoid tissue, and it is impossible to distinguish a neoplastic lymphoblast from a normal lymphoblast by cytologic examination. A diagnosis of lymphoblastic lymphoma is made using the percentage of lymphoblasts present in an aspirate of lymphoid tissue (i.e., lymph nodes, or spleen). When lymphoblasts consistently exceed 60% of the population of lymphoid cells in all areas of all smears, a diagnosis of lymphoblastic lymphoma can be made. Alternatively, when there is a prominent population of lymphoblasts found on aspiration of nonlymphoid tissue (e.g., ocular, cutaneous, renal, hepatic, and gastrointestinal), a cytological diagnosis of extranodal lymphoma can be confidently made. This chapter will focus on the cytological diagnosis of lymphoma in lymph node aspirates. Further information on lymphoma can be found in Chapters 34 and 130.
Normal Lymph Node Cytology Aspirates of normal lymph nodes consist of 75 to 95% small mature lymphocytes. See Figure 286-1. Small mature lymphocytes are larger than a red blood cell but smaller than a neutrophil. They have roundish, slightly indented, eccentric nuclei with smudged chromatin, no visible nucleolus, and a small amount of lightly basophilic cytoplasm. Lymphoblasts usually comprise less than 5% of the lymphoid population. Lymphoblasts are equivalent to and often larger than the diameter of neutrophils and have round to irregularly shaped eccentric nuclei, a finely stippled chromatin pattern and a larger amount of basophilic cytoplasm compared to mature lymphocytes. Lymphoblasts have singular or multiple nucleoli. Low numbers of prolymphocytes or intermediatesized lymphocytes may also be present in normal lymph nodes. These cells resemble slightly smaller versions of lymphoblasts that are roughly the same size to slightly smaller than a neutrophil, yet lack well defined nucleoli and have more open or less compact chromatin compared to a small mature lymphocyte. Lymphoglandular bodies are small, basophilic, variably sized fragments of cytoplasm shed by rapidly dividing lymphoid cells. These fragments are usually scattered throughout the background in low numbers in aspirates of normal lymph nodes. Low numbers of other cells may be seen including plasma cells, neutrophils, macrophages, and mast cells.
gently smear the aspirated material applied to a glass slide can reduce cellular disruption. Lymph node aspirates should always be adequately stained before evaluation and usually require extra staining time due to their high exfoliation. Understaining smears causes nucleoli to be more prominent and may cause small lymphocytes to be falsely identified as lymphoblasts. Lymphoblastic lymphoma is the type commonly diagnosed by cytology. A lymph node aspirate can confidently be diagnosed as lymphoma when >60% of the lymphoid cell population in all areas of all smears are lymphoblasts. See Figure 286-2. Generally there is no increase in plasma cells with lymphoma. Some lymphomas involve neoplastic transformation of prolymphocytes (intermediate grade lymphoma) or small lymphocytes (small cell lymphoma). These types of lymphomas are difficult to distinguish from a normal or hyperplastic lymph node cytologically and usually require histopathology with the benefit of nodal architecture evaluation for a definitive diagnosis. In some cases of small cell lymphoma, cytology can be suggestive if there is a monomorphic population of small mature lymphocytes in high numbers and a lack of plasma cells or other inflammatory cells. Occasionally, atypical morphology of the neoplastic small lymphocytes can be seen as a slight increase in the amount of cytoplasm, which trails away from one end of the nucleus, forming a small cytoplasmic “tail.” This morphology is by no means specific for lymphoma but can be seen occasionally with low-grade lymphoma on cytology.
Lymphoma in Lymph Node Aspirates Lymphoid cells are fragile, and it is easy to rupture cells during smear preparation. Only intact cells should be evaluated. Ruptured cells are seen as round eosinophilic smudges that lack defined cell borders and cytoplasmic and nuclear structures. Sometimes using a cover slip to
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
738
Figure 286-1 Normal lymph node aspirate. The majority of the cells present are small mature lymphocytes with low numbers of larger lymphoblasts (closed arrow). The lymphoblasts are larger than the neutrophil in the picture (arrowhead). A few ruptured cells are present and appear large (open arrow); however, only clearly intact cells should be evaluated. Wright’s stain 500×. Photo courtesy of Oklahoma State University teaching files.
Lymphoma
(A)
Figure 286-2 Lymphoma. Lymph node aspirate. The majority of the cells are lymphoblasts. The lymphoblasts are the same size or larger than the neutrophil present in the picture (arrow). Many of the lymphoblasts also have visible nucleoli. Wright’s stain 500×. Photo courtesy of Oklahoma State University teaching files.
Other less common types of lymphoma include histiocytic lymphoma and large granular lymphoma. The neoplastic cells in histiocytic lymphoma have an abundant amount of cytoplasm and often appear similar to macrophages. In large granular lymphoma (which, in cats, often involves the intestine), the lymphoid cells contain a few to many reddish staining granules within their cytoplasm See Figure 286-3. Biopsy and histopathology are recommended for confirmation in suspected cases of prolymphocytic or small cell lymphoma or in any other equivocal case of lymphoma, such as when there are expanded immature lymphoid cells yet still maintenance of lymphoid heterogeneity (early lymphoma versus hyperplasia), or increased immature lymphocytes accompanied by increased plasma cells or other inflammatory cells. A histopathologic diagnosis of lymphoma involves looking at the architecture of the node for abnormalities such as effacement by neoplastic cells and capsular invasion. Small core biopsies do not allow visualization of architecture and are not recommended. Wedge biopsy or complete nodal excision will yield the best sample for histopathologic diagnosis.
(B) Figure 286-3 Large granular lymphoma. A, Intra-abdominal mass. Numerous lymphoid cells are present containing reddish staining granules in their cytoplasm. Wright’s stain 500×. B, Higher magnification of image A. Wright’s stain 1000×. Photos courtesy of Oklahoma State University teaching files.
Extranodal Lymphoma Lymphoma can also occur in organs other than lymph nodes, such as the gastrointestinal tract and liver. Aspirates that yield a population of lymphoid cells comprised mostly of large lymphoblasts are diagnostic for lymphoma. As in lymph nodes, prolymphocytic or small cell types of lymphoma are difficult to distinguish from a nonneoplastic lymphoid follicle or lymphocytic inflammation. These cases should be biopsied for confirmation. When evaluating possible nodules of lymphoma in the spleen, extra care needs to be taken. The spleen has a normal population of resident lymphoid cells. When undergoing stimulation, germinal centers of proliferating nonneoplastic lymphoblasts may occur. If these germinal centers are aspirated, numerous lymphoblasts may be observed resembling lymphoma. Biopsy and histopathology are recommended to confirm questionable splenic masses.
Suggested Readings Baker R, Lumsden JH, eds. 2000. Color Atlas of Cytology of the Dog and Cat. St. Louis: Mosby. Cowell RL, Tyler RD, Meinkoth JH, et al., eds. 2008. Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., St. Louis: Mosby. Raskin RE, Meyer DJ, eds. 2001. Atlas of Canine and Feline Cytology. Philadelphia: W.B. Saunders. Richter KP. 2003. Feline gastrointestinal lymphoma. Vet Clin North Am Small Anim Pract. 33:1083–1098.
739
CHAPTER 287
Mast Cell Tumors Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt
Overview Mast cell tumors are one of the discrete (round) cell tumors. Most mast cell tumors can be diagnosed easily with fine-needle aspiration due to their highly exfoliative nature. Mast cell tumors in the feline can be cutaneous (focal or multicentric) or visceral, involving the intestine, spleen, and liver. Cutaneous forms are usually not associated with systemic disease; however, simultaneous cutaneous and visceral involvement can occur. The cutaneous form is the most common form in the feline, yet less common in occurrence than in the canine. Grossly, cutaneous mast cell tumors can be nodular, plaque-like, or papular. Overlying skin is often alopecic and pink. Large lesions can be superficially ulcerated. In contrast to the dog, most feline cutaneous mast cell tumors are benign. Solitary cutaneous tumors without evidence of spread to regional lymph nodes are considered benign with surgical excision being curative. However, the diagnosis of cutaneous mast cell tumor should be followed by assessment for lymph node and visceral involvement. Multifocal cutaneous mast cell tumors, development of multiple tumors, recurrence of mast cell neoplasia, and splenic mast cell neoplasia are often associated with a guarded prognosis. Unlike in the canine, histological grade is not predictive of biologic behavior in the feline. Histologically, benign tumors are usually composed of uniform, well-differentiated cells with a low mitotic index. Poorly differentiated tumors with invasion and a high mitotic index are associated with a worse prognosis. Further information about mast cell neoplasia can be found in Chapter 135.
to stain poorly. Consider this limitation when attempting to identify any discrete cell population using these stains. Biopsy with histopathology may be needed to determine the identity of any ambiguous cells. A diagnosis of mast cell tumor is easily made when aspirates contain mostly mast cells. If mast cells are present in low numbers or accompanied by other inflammatory cells, biopsy may be needed for definitive diagnosis. Mast cell tumors should be evaluated histopathologically regardless of whether the cells are cytologically uniform, atypical, granular, or agranular.
Cytologic Features Aspirates from mast cell tumors usually exfoliate high numbers of cells containing singular, round, central nuclei, and moderate amounts of cytoplasm containing large numbers of pinpoint, magenta, metachromatic granules that often obscure the nucleus. See Figure 287-1. Mast cell granules have a high affinity for cytology stains; therefore, on occasion, the granules may uptake all of the stain entering the cell leaving the nucleus understained (pale blue). See Figure 287-2. Granules from ruptured mast cells are usually observed free in the background of the smear. Variable numbers of eosinophils and fibroblasts may also be seen in samples from mast cell tumors. See Figure 287-3. Some cutaneous mast cell tumors in the feline contain mast cells almost exclusively, with eosinophils being rare to absent. This is in contrast to canine mast cell tumors in which eosinophils are often present in high numbers. Cytologically, most neoplastic mast cells are uniform, heavily granulated, and demonstrate minimal criteria of malignancy. However, some mast cell tumors may consist of mast cells that are poorly granular to agranular, especially tumors involving the intestine. In the intestine, mucosal mast cells appear to differ from mast cells derived from the mesenchyme, and are often agranular. See Figure 287-4. Pleomorphic and agranular mast cells can be difficult to distinguish from other discrete cell tumors (i.e., histiocytic neoplasia, plasma cell neoplasia, or lymphosarcoma). Additionally, fast Romanowsky-type stains (Diff-Quik®) can sometimes fail to stain mast cell granules or cause them
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
740
Figure 287-1 Aspirate of a cutaneous mass. The mast cells are heavily granulated with granules obscuring the nucleus. Free mast cell granules are present in the background. Wright’s stain 500×. Photo courtesy of Oklahoma State University teaching files.
Figure 287-2 Aspirate of a cutaneous mass. In this case the mast cell granules are taking up most of the stain leaving the nuclei understained. Wright’s stain 500×. Photo courtesy of Oklahoma State University teaching files.
Mast Cell Tumors
Figure 287-3 Aspirate of a cutaneous mass. Some of the mast cells present in this lesion are poorly granulated. A large fibroblast (arrow) is also present; they are commonly seen in mast cell tumors. Wright’s stain 500×. Photo courtesy of Oklahoma State University teaching files.
Figure 287-4 Aspirate of an intestinal mass. There are large numbers of poorly granular neoplastic mast cells with fewer associated eosinophils and lesser numbers of nondegenerate neutrophils. Wright’s stain 1000×. Photo courtesy of Amy C. Valenciano.
Suggested Readings Baker R, Lumsden JH, eds. 2000. Color Atlas of Cytology of the Dog and Cat. St. Louis: Mosby. Cowell RL, Tyler RD, Meinkoth JH, et al., eds. 2008. Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., St. Louis: Mosby. Raskin RE, Meyer DJ, eds. 2001. Atlas of Canine and Feline Cytology. Philadelphia: W.B. Saunders.
741
CHAPTER 288
Pleural Effusions Amy C. Valenciano, Rick L. Cowell, and Tara P. Arndt
Overview
Characteristics of Various Forms of Effusions
There are five mechanisms responsible for the formation of pleural effusion: increased venous or capillary hydrostatic pressure; decreased capillary oncotic pressure due to hypoalbuminemia; increased capillary membrane permeability; lymphatic obstruction or spillage and hemorrhage. (Hemothorax is disputably included as a form of effusion.) Cats of any age, breed, or sex may be affected. Many cats are reported to have an acute onset of dyspnea or tachypnea. However, most causes of pleural effusion are not peracute. The cat’s ability to conceal disease until the crisis stage is reached prevents many owners from detecting disease in the early stage. Many cats with pleural effusion will have a history of lethargy and anorexia of 1 to several days duration. Some will also have weight loss.
Transudate Transudative effusions are clear to pale yellow and are of low protein content and low cellularity. Because of the low cellularity, direct smears are often acellular, necessitating review of sedimented and cytospin concentrated slides. Cytologically, there is an absence of hemodilution, with few mononuclear cells. Most of the cells are uniform mesothelial cells, with lesser admixed mature lymphocytes and macrophages. Neutrophils should be uncommon to absent. The primary differential for a pure transudate is decreased oncotic pressure from hypoalbuminemia usually caused by protein-losing nephropathy, protein-losing enteropathy, or hepatic insufficiency. Increased hydrostatic pressure from early cardiac disease is also a mechanism.
Evaluation of Pleural Effusion After the detection and removal of a pleural effusion, initial evaluation of the fluid should include assessment of volume and gross observation of color and turbidity followed by measurement of protein and specific gravity via refractometry. Next, red blood cell and nucleated cell counts are performed either via manual (hemacytometer) or automated methods. Because many effusions (specially neoplastic effusions and effusions with large numbers of reactive mesothelial cells) can have dense clusters and sheets of cells, correlation of cell counts with cytological assessment of a direct smear is important. Occasionally, low cell counts obtained by manual and automated means can be obtained with effusions that are actually highly cellular, if the majority of the cells are in aggregates and sheets. Finally, cytological examination of the fluid is performed. Ideally, direct, sedimented or concentrated smears, buffy coat smears for hemodilute specimens, and concentrated cytospun slides should be reviewed. This complete fluid analysis will allow categorization of the effusion as a transudate, modified transudate, nonseptic exudate, septic exudate, chylous effusion, hemorrhagic effusion, or neoplastic effusion. See Table 288-1 for categorizing and interpreting the fluid analysis.
Modified Transudate This effusion is a transudate that has been modified by the addition of cells or protein. Color may range from yellow to pink to orange. There is increased turbidity compared to the clear appearance of a transudate. Protein or cell counts are higher than for a transudate; however, similar to a transudate, cytological examination is fairly unremarkable with a predominance of mesothelial cells, mature lymphocytes, and macrophages with lesser numbers of nondegenerate neutrophils, eosinophils, and plasma cells with a mild to moderate degree of hemodilution. Differentials can include disorders such as cardiac disease and nonexfoliative neoplasia.
Nonseptic Exudate Nonseptic exudates are of moderate to high protein content and often quite cellular. Thus, their appearance can range from yellow to pink to orange to red/brown, and they are turbid. Inflammatory cells predominate. Typically neutrophil percentages are fairly high, and neutrophils
TABLE 288-1: Interpretation of Pleural Fluid Analysis Effusion type/ Characteristics Color
Transudate
Modified transudate
Nonseptic exudate
Septic exudate
Chylous effusion
Hemorrhagic effusion
Yellow to pink to orange Cloudy
Yellow to orange to tan Cloudy and turbid
White/milky
Red
Opaque
>3.0
2.5–6.0
Similar to peripheral blood >3.0
>5,000
Variable
Mild to moderate
Mild to moderate
Turbidity
Colorless to pale yellow Clear
Protein (g/dL)
<2.5
Yellow to pink to orange Clear to slightly cloudy 2.5–7.5
Nucleated cells/µL
<1,500
1,000–7,000
>3.0 Feline infectious peritonitis: >4.5 >5,000
Hemodilution
Minimal
Mild to moderate
Mild to moderate
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
742
Similar to slightly higher than peripheral blood Marked
Pleural Effusions
are the primary cell type with admixed macrophages. Cytophagia can be seen, and mesothelial cells may be present and reactive. Reactive mesothelial cells show increased cytoplasmic basophilia, a prominent eosinophilic fringe border may be evident, and there is a mild to moderate degree of anisocytosis and anisokaryosis. Often, there is a clear background and good cellular preservation with a lack of identifiable extracellular or phagocytosed infectious agents. All nonseptic appearing exudates should be cultured for bacterial and fungal organisms to rule out an infectious cause even when not demonstrated cytologically. Differentials for nonseptic exudates can include: inflammation of visceral organs, inflamed or necrotic nonexfoliative or poorly exfoliative neoplasia, and feline infectious peritonitis (FIP).
Feline Infectious Peritonitis Effusions secondary to FIP are characterized by a high protein content, often 4.5 gm/dL or more, rarely as low as 3.6 gm/dL. The high protein content lends a viscous nature to the fluid. Effusions secondary to FIP can have quite a range in cellularity, with cell counts occasionally dipping into the modified transudate range, to very cellular specimens containing 20,000 cells/µL or greater. Cytologically, there is a characteristic basophilic, stippled, proteinaceous fluid background with a near equal mix of nondegenerate neutrophils, foamy, cytophagic macrophages, and mild to moderate accompanying hemodilution. The inflammatory cells are generally well preserved and infectious agents are not observed. See Figure 288-1.
Chylous Effusions Chylous effusions have a characteristic homogenous white, milky appearance. Protein content is often high, and cellularity is moderate to high with a predominance of small, mature lymphocytes. Lesser numbers of macrophages, nondegenerate neutrophils, plasma cells, eosinophils, and mesothelial cells are present. Hemodilution may be absent or mild or moderate. See Figure 288-3. In the case of hemodilution, the fluid will appear pink and milky. If the effusion is of long duration, an increase in the numbers and percentages of nondegenerate neutrophils and macrophages will be evident; however, still, mature lymphocytes are a prominent cellular population. Macrophages, which have scavenged lipids, have a foamy, highly vacuolated appearance cytologically. Special note should be made in the case of a lymphocytic effusion. If the patient is anorectic, the effusion may lack a milky appearance due to the absence of chylomicrons. Yet, cytologically, there is still a predominance of
Septic Exudates Septic effusions are of moderate to high protein content and are one of the most cellular fluid specimens. Thus, grossly the fluid is yellow and quite turbid. There is often a marked predominance of degenerate neutrophils and a range from few to large numbers of extracellular and phagocytosed bacteria. See Figure 288-2. Etiology is often from penetrating wounds or foreign bodies into the thoracic cavity with seeding of bacteria. Rupture of an internal abscess and extension from pneumonia are uncommon etiologies. Aerobic and anaerobic bacterial culture of the fluid is essential.
Figure 288-1 Effusion associated with feline infectious peritonitis. Note prominent basophilic, stippled highly proteinaceous background with mix of pyknotic and nondegenerate neutrophils and macrophages, rare mature lymphocytes, and few red blood cells. Wright’s stain 500×. Photo courtesy of Amy C. Valenciano.
Figure 288-2 Septic effusion. Several moderately to severely degenerate neutrophils and few macrophages. Some neutrophils contain phagocytosed bacilli. Wright’s stain 1000×. Photo courtesy of Amy C. Valenciano.
Figure 288-3 Chylous effusion. Large numbers of small mature lymphocytes and few foamy macrophages which appear lipid-laden. Wright’s stain 1000×. Photo courtesy of Amy C. Valenciano.
743
SECTION 5: Cytology
Figure 288-4 Effusion. Aggregate of macrophages which are erythrophagic, contain intracellular dark blue globular hemosiderin and few small and one large golden hematoidin crystals. The findings indicate evidence of chronic hemorrhage. Wright’s stain 1000×. Photo courtesy of Amy C. Valenciano.
Figure 288-5 Effusion associated with thymoma. Predominance of mature lymphocytes and rare heavily granulated uniform mast cell. Neoplastic epithelial cells may not be present in effusions associated with thymoma. If a triad of atypical epithelial cells, low-to-moderate numbers of mast cells and mature lymphocytes are found in an effusion, and if a mediastinal mass is evident, thymoma can be confidently diagnosed on cytology of the fluid. If only mature lymphocytes and mast cells are found, the diagnosis of thymoma is only tentative. Wright’s stain 1000×. Photo courtesy of Amy C. Valenciano.
mature lymphocytes. The differentials for a chylous and lymphocytic effusion are identical and can include: cardiac disease or disruption or compression of lymphatics (i.e., inflammation or neoplasia).
Hemorrhagic Effusion The accumulation of whole blood in the pleural space constitutes a hemorrhagic effusion and can be acute or chronic. If acute, gross appearance is consistent with blood. Chronic hemorrhage has a red/brown, turbid appearance. Direct smears and buffy coat smears are the most cytologically useful specimens. The ratio of red blood cells to white blood cells of the peripheral blood is often similar to that of the effusion. However, the addition of macrophages and neutrophils, which increase with chronicity, and the presence of mesothelial cells often make the effusion more cellular than peripheral blood. Cytologically, peripheral blood leukocytes are present in numbers and proportions comparable to the patient’s blood cell differential. Mesothelial cells can be infrequent to present in moderate numbers. If the effusion is acute, platelets can be seen, and there is an absence of erythrophagia, hemosiderin, and hematoidin crystals. Evidence of the later and absence of platelets suggests chronic hemorrhage. Hemosiderin pigment is most often found phagocytosed within macrophages and has a chunky, round to slightly illdefined dark blue-black appearance. Hematoidin crystals can be free in the extracellular space or phagocytosed within macrophages. Hematoidin forms diamond-shaped crystals that are a bright, clear yellow. See Figure 288-4. Differentials for a hemorrhagic effusion can include: primary or acquired coagulopathy; trauma; or internal bleeding lesions (neoplastic or non-neoplastic).
Neoplastic Effusions Many neoplastic conditions that involve the thorax result in an effusion, and if neoplastic cells exfoliate into the fluid, cytological assessment can prove diagnostic. Various types of primary and metastatic neoplasms can involve the mediastinum, intrathoracic lymph nodes, lungs, pleural and pericardial linings, and heart. Round cell neoplasms (notably lymphoma) and carcinoma or adenocarcinomas most often result in cytologically diagnostic effusions. Mesenchymal neoplasms uncommonly
744
exfoliate neoplastic cells and, instead, typically result in modified transudates or hemorrhagic effusions. As in any cytological specimen, for a diagnosis of neoplasia, neoplastic cells need to be in high numbers, well preserved, and demonstrate cytological criteria of malignancy. Especially in the case of epithelial neoplasia, if there is significant accompanying inflammation distinguishing between epithelial neoplasia, epithelial hyperplasia or dysplasia, and mesothelial reactivity can be very difficult. In these cases, biopsy with histopathology of any masses identified on thoracic radiographs or ultrasound are necessary for diagnosis.
Lymphoma The presence of large numbers of lymphoblasts in a pleural effusion is diagnostic for high-grade lymphoma. Young (less than 2 years of age), feline leukemia virus antigenic cats with the mediastinal form of lymphoma often present with such a neoplastic effusion. For review of lymphoblast morphology, see Chapter 286.
Thymoma Thymoma is a neoplasm of the thymic epithelium and occurs as a large mass in the cranial mediastinum. Aside from the neoplastic epithelial component, thymomas can contain lymphoid follicles and variable numbers of mast cells and can be cystic, necrotic, and inflamed as well. Thymomas may result in a chylous effusion, and occasionally, may manifest as a diagnostic neoplastic effusion when a triad of large numbers of small mature lymphocytes, few well-differentiated mast cells, and few sheets of mildly pleomorphic epithelial cells are present cytologically and are correlated with identification of a mediastinal mass. See Figure 288-5. Frequently the neoplastic epithelial cells are absent in the fluid, mimicking a lymphocytic effusion. The presence of few mast cells may help guide the clinician to rule out thymoma. In this case, if a mediastinal mass is identified, fine-needle aspiration or biopsy may be performed to achieve diagnosis.
Pleural Effusions
Carcinoma or Adenocarcinoma Both primary (pulmonary and bronchial) and metastatic (i.e., mammary gland adenocarcinoma, and pancreatic or intestinal adenocarcinoma) epithelial neoplasms may result in a cytologically diagnostic effusion. These effusions are cellular, with many clusters and sheets of neoplastic cohesive cells demonstrating criteria of malignancy. See Chapter 281.
Suggested Readings Baker R, Lumsden JH, eds. 2000. Color Atlas of Cytology of the Dog and Cat, St. Louis: Mosby. Cowell RL, Tyler RD, Meinkoth JH, et al., eds. 2008. Diagnostic Cytology and Hematology of the Dog and Cat. 3rd ed., St. Louis: Mosby. Raskin RE, Meyer DJ, eds. 2001. Atlas of Canine and Feline Cytology, Philadelphia: W.B. Saunders.
745
CHAPTER 289
Systemic Fungal Diseases Tara P. Arndt, Rick L. Cowell, and Amy Valenciano
Overview Several different types of fungi cause cutaneous and systemic disease in cats. Most fungal organisms provoke a pyogranulomatous (mixture of neutrophils and macrophages) or granulomatous (mostly macrophages) inflammatory response. The presence of inflammation on cytology aspirates should prompt a focused search for infectious agents, including fungal organisms. Fungi that infect cats include bimorphic fungal yeasts and hyphal fungi. See Chapters 22, 38, 43, 97, and 202 for further information regarding presentation, therapy, and prognosis of various fungal infections.
Cryptococcosis Cryptococcus neoformans (see Chapter 43) is often pleomorphic in appearance. The organisms are round, clear to pale pink staining, and vary in size from 4 to 15 µm in diameter without the capsule. The “smooth” form has a thick clear capsule surrounding the organism, whereas the “rough” form may only have a very capsule. Narrow-based budding is usually observed. Granulomatous inflammation is often seen with cryptococcosis; however, due to the large size of the organisms phagocytosis may not be appreciated in some aspirates. See Figure 289-2. With the smooth form of Cryptococcus the organisms may outnumber the inflammatory cells, and on occasion, no inflammatory cells may be observed.
More Common Systemic Fungal Infections Histoplasmosis Histoplasma capsulatum (see Chapter 97) organisms are round to oval and measure 2 to 4 µm in diameter. They are surrounded by a clear thin halo and have an eccentric pink to purple nucleus that is usually crescent shaped. This type of fungal yeast typically causes pyogranulomatous inflammation. Organisms are present in variable numbers and are usually observed phagocytized by macrophages and occasionally by neutrophils as well as free in the background. Budding organisms may sometimes be found. See Figure 289-1.
(A)
Figure 289-1 Histoplasmosis. Lymph node aspirate. Macrophages contain numerous Histoplasma organisms which have crescent shaped, eccentric nuclei and a thin clear halo. Wright’s stain 250×. Photo courtesy of Rick L. Cowell.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
746
(B) Figure 289-2 A, Cryptococcosis. Nasal swab. Numerous Cryptococcus organisms are present; they vary in size and have a thick clear capsule. Narrow based budding is also present. Wright’s stain 125×. B, Higher magnification Wright’s stain 250×. Photos courtesy of Rick L. Cowell.
Systemic Fungal Diseases
Figure 289-4 Blastomycosis. Several thick-walled, deep blue Blastomyces organisms are present within a macrophage. Note the broad based budding. Wright’s stain 250×. Photo courtesy of Rick L. Cowell. Figure 289-3 Sporotrichosis. Cutaneous lesion. Pyogranulomatous inflammation and numerous Sporothrix organisms are present. Note the round to fusiform shape and thin clear halo. Wright’s stain 500×. Photo courtesy of Oklahoma State University teaching files.
Sporotrichosis Sporothrix schenckii (see Chapter 202) organisms, like Histoplasma organisms, measure about 2 to 4 µm in diameter and have an eccentric pink to purple nucleus and a thin clear halo. Sporothrix organisms vary from the classical cigar (fusiform) shape to slightly round. Cutaneous sporotrichosis lesions in cats usually have numerous organisms providing relatively easy identification. This type of fungal yeast typically incites a pyogranulomatous inflammatory response. Organisms are usually present phagocytized within macrophages and occasionally neutrophils but also may be noted free in the background of the smear. Exudate from wounds of an infected cat usually contains high numbers of organisms and poses a potential zoonotic risk to anyone handling the cat; this is especially important in immunocompromised persons. Disposable gloves and thorough hand washing (as well as owner consultation with their primary care physician) are recommended when handling a cat suspected of having sporotrichosis given the zoonotic potential. See Figure 289-3.
Less Common Systemic Fungal Infections
Figure 289-5 Coccidioidomycosis. A single large, blue, thick walled Coccidioides organism is present and filled with numerous small, round endospores. Wright’s stain 250×. Photo courtesy of Cowell RL, Tyler RD, Meinkoth JH. 2008. Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed. St. Louis: Mosby.
Blastomycosis Blastomyces dermatitidis (see Chapter 22) organisms are deep blue staining, round to oval in shape, and 8 to 20 µm in diameter. They are thick walled and may display broad based budding. Pyogranulomatous inflammation is typically associated with blastomycosis. Organisms are not often phagocytosed due to their large size. See Figure 289-4.
Coccidioidomycosis Coccidioides immitis (See Chapter 38) organisms are usually present in low numbers on cytology preparations and therefore, difficult to identify. Organisms are clear to blue staining, round, and measure 20 to 200 µm in diameter (may be over 10× larger than a neutrophil). These organisms are thick walled, and larger organisms may be filled with numerous small (2–4 µm diameter), round endospores. Pyogranulomatous to granulomatous inflammation is typically associated with coccidioidomycosis. Figure 289-5.
Hyphating Fungi Occasionally hyphating fungi can cause infections in cats and are often localized in nasal or cutaneous infections. Systemic infections can also occur, most commonly affecting the respiratory tract. Cytology samples of infected areas may contain visible hyphae. Depending on the type of fungi, branching or distinct septae may be observed. Some fungi do not stain with commonly used cytology stains and only a “negative image” may be visible when the unstained hyphae is surrounded by stained cells and cell debris. See Figure 289-6. Several different species of hyphating fungi can infect cats; however, they cannot be reliably differentiated on cytomorphologic features alone, and fungal culture is often required to identify the various species. A mixed inflammatory response typically accompanies these types of fungal infections. Numerous neutrophils, macrophages, and eosinophils are commonly present.
747
SECTION 5: Cytology
Suggested Readings Baker R, Lumsden JH, eds. 2000. Color Atlas of Cytology of the Dog and Cat, St. Louis: Mosby. Cowell RL, Tyler RD, Meinkoth JH, et al., eds. 2008. Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., St. Louis: Mosby. Greene CE, ed. 2006. Infectious Diseases of the Dog and Cat, 3rd ed., Philadelphia: W.B. Saunders. Kerl ME. 2003. Update on canine and feline fungal diseases. Vet Clin North Am Small Anim Pract. 33:721–47. Raskin RE, Meyer DJ, eds. 2001 Atlas of Canine and Feline Cytology. Philadelphia: W.B. Saunders.
Figure 289-6 Hyphating fungi. Lymph node. Note the staining fungal branching hyphae present with prominent septae that are surrounded by mixed lymphocytes. Wright’s stain 250×. Photo courtesy of Cowell RL, Tyler RD, Meinkoth JH. 2008. Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed. St. Louis: Mosby.
748
CHAPTER 290
Transtracheal Wash Hemosiderosis Tara P. Arndt, Rick L. Cowell, and Amy C. Valenciano
Overview Transtracheal wash (TTW) samples are a common diagnostic test in evaluating feline respiratory disease. Hemosiderin-containing macrophages (hemosiderophages) have been found in a variety of underlying pathologic conditions in the feline patient. Classically hemosiderophages were referred to as “heart failure cells”; however, hemosiderophages have recently been reported to not be consistent in all cases of feline cardiac disease and pulmonary hypertension. Airway hemosiderophages have been associated with a diverse variety of other diseases including feline asthma syndrome, complicated and uncomplicated rhinitis, pulmonary neoplasia (primary or metastatic), primary or concurrent heart disease, pneumonia of varied causes, trauma, pulmonary embolism or infarction, lung lobe torsion, as well as neurologic disease. Alveolar hemorrhage can be attributed to several mechanisms including enhanced diapedesis secondary to increased pulmonary vascular congestion due to cytokine effects and microtrauma secondary to low-grade irritation due to coughing.
Cytologic Features of Transtracheal Wash Hemosiderosis Pathologic hemorrhage is often characterized by erythrophagocytosis, hemosiderin laden macrophages (hemosiderophages), and hematoidin crystals. See Figures 290-1, 290-2, and 290-3. Iatrogenic or inadvertent
Figure 290-1 Recent hemorrhage. Note that the erythrocytes (arrows) have been phagocytized by the central macrophage (erythrophagocytosis) indicating recent hemorrhage. There is also hemosiderin present (dark blue to black staining intracellular material within the macrophages/hemosiderophages). Wright’s stain 100×. Photo courtesy of Rick L. Cowell.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 290-2 Hemosiderophages. Note the alveolar macrophage with dark blue to black staining, fine to globular pigment consistent with hemosiderin. Wright’s stain 100×. Photo courtesy of Rick L. Cowell.
Figure 290-3 Hematoidin crystals. Note the macrophages containing erythrocytes, dark staining hemosiderin material, and a golden polygonal hematoidin crystal. This constitutes evidence of the erythrocyte breakdown product and signifies recent and previous hemorrhage. Wright’s stain 100×. Photo courtesy of Rick L. Cowell.
749
SECTION 5: Cytology
hemorrhage from sample collection must be differentiated from pathologic hemorrhage. Differentiation is based on the presence or absence of erythrophagia and break down products of erythrocytes (i.e., hemosiderin and hematoidin crystals). With pathologic hemorrhage, erythrophagia or red blood cell (RBC) breakdown products are present; they are absent with iatrogenic hemorrhage occurring at the time of sample collection. The presence of iron within macrophages can be assessed using special staining techniques (i.e., Prussian Blue stain) to rule out other material within the macrophage population that can appear similar to hemosiderin cytologically. Generally it takes several hours for macro-
750
phages to phagocytose erythrocytes, which is a useful guide to rule out iatrogenic hemorrhage.
Suggested Readings Cowell RL, Tyler RD, Meinkoth JH, et al. 2008. Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., St. Louis: Mosby. DeHeet HL, McManus P. 2005. Frequency and severity of transtracheal wash hemosiderosis and association with underlying disease in 96 cats: 2002–2003. Vet Clin Path. 34(1):17–22.
SECTION
6 Imaging
CHAPTER 291
Imaging: The Thorax Merrilee Holland and Judith Hudson
The Mediastinum Normal Findings: Mediastinum • The mediastinum can be divided into the cranial, middle, and caudal mediastinum. The borders in cats are not easy to distinguish.
Cranial Mediastinal Mass • Mediastinal masses in cats are usually cranioventral. Lymphosarcoma can produce a noncompressible mass in the cranioventral thorax. Mediastinal cysts can be found cranial to the cardiac silhouette along the sternum.
Radiographs of Cranial Mediastinal Mass
(A)
• Roentgen signs of cranioventral mediastinal masses include an increase in soft-tissue opacity cranial to the heart. The trachea may be displaced dorsally or to the right. Larger mediastinal masses may compress the trachea and may silhouette with the cranial border of the heart. There may be varying amounts of pleural and pericardial effusion. The cranial lung lobes may be displaced caudally.
Ultrasound of Cranial Mediastinal Mass • Ultrasound allows a quick and easy way to rule out a mediastinal mass when pleural effusion is present. If a mass is present, ultrasoundguided aspiration can be safely done in sedated patients. • Locate the heart, and then move craniad one intercostal space directing the transducer cranially and dorsally toward the thoracic inlet. The normal mediastinum contains large vessels surrounded by varying amounts of hyperechoic fat. See Figures 291-1 through 291-3.
Mediastinal Cyst • Mediastinal cysts are rare findings that have similar radiographic findings to cranial mediastinal masses. The cystic nature of these lesions can be determined with ultrasound. Coughing is often the presenting clinical sign. See Figure 291-4.
Hilar Lymphadenopathy • Enlargement of the hilar lymph node can cause a mass effect in the cranial mediastinum. Lymphadenopathy is usually in response to local infection. See Figure 291-5.
Caudal Thoracic or Mediastinal Mass • Masses in this location are usually neoplastic. See Figures 291-6 and 291-7.
(B) Figure 291-1 A, B, Mediastinal mass: There is marked enlargement of the cranial mediastinum with a soft-tissue opacity mass, which extends to the level of the eighth rib. The lungs are retracted away from the thoracic walls due to pleural effusion.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
753
(A)
(B) Figure 291-2 A, B, Mediastinal mass post-radiation: Radiographic images were obtained following radiation therapy for mediastinal lymphoma (same patient as 291-1).
754
(A)
(B)
(C) Figure 291-3 A, B, Mediastinal mass: There is a large, soft tissue, lobulated mass measuring 4 × 5 cm located in the cranial mediastinum cranial to the cardiac silhouette. This mass silhouettes with the cardiac shadow along its left cranial margin. C, The patient is in dorsal recumbency during the computerized tomography. An irregular slightly nonhomogenous soft-tissue opacity mass is present in the cranioventral mediastinum. The mass was surgically excised and the final diagnosis was a thymoma.
755
(A)
(B)
(C) Figure 291-4 A, B, Mediastinal cyst: Radiographs of the thorax reveal the presence of an ill-defined, roughly circular soft tissue opacity in the cranial mediastinum dorsal to the sternum. C, An anechoic structure can be seen in the mediastinum on ultrasonography, confirming the diagnosis of a mediastinal cyst.
756
(A)
(A)
(B) Figure 291-5 A, B, Hilar lymphadenopathy due to disseminated cryptococcus: A well-defined oval soft tissue opacity is visualized dorsal to the heart over the trachea on the lateral view. On the ventral-dorsal view, the mass can be seen superimposed over the cardiac silhouette.
(B) Figure 291-6 A, B, Caudal mediastinal mass: Radiographs show a soft tissue mass extending from the heart base to the diaphragm. Notice the enlarged kidneys on the portion of the abdomen included on the thoracic radiographs. The kidneys show changes consistent with lymphosarcoma or feline infectious peritonitis on ultrasound examination. Aspiration of the right kidney revealed large cell lymphoma.
757
SECTION 6: Imaging
(A)
(B)
(C) Figure 291-7 Caudal thoracic mass: A, B, Radiographs of the thorax reveal an increased opacity in the caudodorsal thorax. In the ventrodorsal view, this increased opacity is on midline. On esophagography (not shown), there was ventral and left lateral displacement of the esophagus. C, On the post-contrast computerized tomography, there is marked enhancement at the periphery of the mass. The mass caused partial obstruction of the esophagus and extended to the level of the diaphragm. Biopsy of the mass revealed a poorly differentiated sarcoma.
The Pleura
Pleural Effusion
Normal Findings: Pleura
Roentgen Signs of Pleural Effusion
• In normal animals, the pleura closely covers the thoracic wall. In obese animals, the pleural space can have fat accumulation causing slight retraction of the lung from thoracic wall. • The parietal pleural covers the thoracic wall and associated structures. The visceral pleura contacts the lung lobes. The parietal pleura is supplied by the systemic circulation, and the visceral pleura is supplied by the pulmonary circulation. Because the systemic circulation is under higher pressure, flow is from the parietal to visceral pleura.
• On the lateral projection, lung lobes appear retracted away from the chest wall. The margins of the lung lobes have a scalloped appearance. A silhouette sign may occur, obscuring the cardiac borders. The trachea can be elevated with pleural effusion alone or by pleural effusion concurrently with a mediastinal mass. The interlobar fissures are widened with clear demarcation of the peripheral lobar margins. The ventral portion of the cranial mediastinum appears more radiopaque than usual. The vascular structures can still be visualized.
758
Imaging: The Thorax
(A)
(B)
(C) Figure 291-8 A, B, Pleural effusion: Thoracic radiographs show pleural effusion predominately within the right hemithorax. Air bronchograms are present within the right cranial lung lobe. C, Ultrasound examination shows multiple masses attached to the pleural surface extending to the diaphragm. The final diagnosis was a malignant tumor.
• On the dorsoventral view, the cranial mediastinum appears widened. Silhouetting of the heart is more noticeable because the apex of the heart is surrounded by fluid. On the ventrodorsal view, there is increased width and opacity of the caudal mediastinum due to fluid accumulation in the paravertebral gutters. On the dorsoventral and ventrodorsal views, the interlobar fissures are widened with clear demarcation of the peripheral lobar margins. • In stable patients with pleural effusion, horizontal beam radiography can be done with the patient held erect to rule out a mediastinal mass. Gravity will cause small amounts of pleural effusion to accumulate in the caudal thorax above the diaphragm. False-negatives can occur in cases of chronic pleural effusion if areas that have walled off and formed pockets are misinterpreted as a cranial mediastinal mass. • Pleural effusion alone can cause dorsal displacement of the trachea without a mass being present. Ultrasonography can be a quick way to rule out a cranial mediastinal mass without causing stress to a compromised patient.
Ultrasound Findings with Pleural Effusion • Pleural effusion without mediastinal mass will cause dorsal elevation of the trachea in the cranial thorax. A sample of fluid can be collected via ultrasound guidance. In cases of chronic pleural effusions, walled-off areas or pockets of pleural effusion can be seen in the thorax. The pericardium in response to pleural effusion can appear thicker than normal. The significance of this finding can be incidental. According to the literature, restrictive pericarditis has not been documented in a cat. See Figures 291-8 through 291-11. • The type of pleural effusion can be classified as hemothorax, chylothorax, hydrothorax, and pyothorax. Thoracocentesis and fluid analysis is required to determine the type of fluid. • The pleural space is visualized with filling of the pleural space with fluid, cellular material, or gas, thickening of the pleura by fibrous tissue or mineralization, or lung lobe consolidation allowing visualization of the lung lobe margins or pleural surface. • Other causes of disruption or alteration of the pleural surface include pneumothorax, masses, foreign bodies, diaphragmatic hernia, and peritoneopericardial diaphragmatic hernia.
759
(A)
(B) Figure 291-9 A, B, Pleural effusion: Abdominal effusion and a heart murmur were present. On the thoracic radiographs, the lung lobes are retracted away from the body wall with blunting of the costophrenic angle due to pleural effusion. Air bronchograms are noted in both cranial lung lobes and the right middle lung lobe. There is poor serosal detail and hepatomegaly visible in the cranial abdomen. The patient was suspected to have feline infectious peritonitis.
760
Imaging: The Thorax
(A)
(B)
(D)
(C) Figure 291-10 A, B, Pleural effusion: Positional radiographs were performed to determine if the pleural effusion was “walled-off.” C, The patient was held in an upright position and an erect horizontal view of the thorax was obtained. A distinct fluid line can be visualized in the right hemithorax at the level of the 10th rib. The cranial lung lobes on this view appear normal. D, The ultrasound of this mass shows a thick walled structure containing echogenic fluid. An abscess was confirmed at surgery.
Pneumothorax • A pneumothorax indicates air is present in the pleural space. The lungs may appear to have a more pronounced interstitial pattern because the lungs are not able to completely inflate. The common causes of a pneumothorax include trauma, spontaneous rupture of a pulmonary cyst, or thoracocentesis (iatrogenic pneumothorax). There are three types of pneumothorax: simple, in which the pressure of gas within the pleural space does not exceed atmospheric
pressure; open, which is caused by a chest wound; and closed, in which air in thorax occurs because of leakage from the lung. A tension pneumothorax occurs when there is a flap type injury to the lung, (i.e., the injury acts like a one-way valve allowing air to enter on inspiration but preventing air from leaving on expiration). Emergency decompression is required because the pressure in the pleural space increases, thus exceeding the atmospheric pressure, the lungs become more atelectatic, and venous return is compromised. The diaphragm flattens and the thorax appears barrel shaped and over expanded.
761
(A)
(B)
(C)
(D) Figure 291-11 A, B, Pleural effusion: A right-sided mediastinal shift was noted. Pleural effusion is noted in the right cranial thorax. C, A ventrodorsal image of the thorax is done after the computerized tomography examination to document the shift of the cardiac silhouette to the left hemithorax. D, The computerized tomography was done with the patient in dorsal recumbency. An increase in soft-tissue opacity and focal irregular gas opacities are present in the right cranial lung lobe. The cardiac silhouette is shifted into the left hemithorax. Fluid is present dorsally within the thoracic cavity. The final diagnosis was lung lobe torsion with secondary pleural effusion.
762
Imaging: The Thorax
(A)
(A)
(B) Figure 291-13 A, B, Pneumomediastinum/pneumothorax due to dog bite: Radiographs show a pneumothorax, pneumomediastinum, and a large volume of subcutaneous air. Air can be seen extending into the retroperitoneal space surrounding the kidneys. The structures within the mediastinum are outlined by an air opacity. A fracture of the fifth rib is present.
(B) Figure 291-12 A, B, Pneumothorax due to trauma: The cardiac silhouette appears elevated from the sternum on the lateral image with retraction of the caudal dorsal lung with air accumulation in the pleural space. The left caudal lung lobe is partially collapsed. The diaphragm appears flattened on the lateral view. Tenting of the diaphragm is noted more significantly on the left side on the ventrodorsal view. There is reduced serosal detail in the cranial abdomen.
Roentgen Signs of Pneumothorax • Retraction of the lungs occurs with a relative increase in opacity. Interlobar fissures appear widened and black. Loss of vascular markings occurs in the periphery of the thorax. The cardiac silhouette appears elevated from the sternum, but the heart is actually displaced
away from the sternum toward the dependent side of the thorax and the cassette. • In tension pneumothorax, the thorax will appear barrelshaped on the ventrodorsal and dorsoventral view, the diaphragm will be flattened, and severe atelectasis will be present. Tenting of the diaphragm may also be present. See Figures 291-12 and 291-13.
Extrapleural Masses • The extrapleural space is a potential space between the parietal pleura and the chest wall; therefore, a lesion of the chest wall can displace the parietal pleura. Examples of extrapleural masses include: neoplasm of the ribs, fractured ribs with hematoma formation, and multiple cartilaginous exostoses. • The roentgen signs depend on the shape, margins, and diameter of the mass and the degree of involvement of the pleural space and adjacent ribs. See Figure 291-14.
763
SECTION 6: Imaging
(A)
(A)
(B) (B) Figure 291-14 A, B, Sternal lymph node: Thoracic radiographs reveal a cavitary-like mass in the right caudal lung lobe and a smaller mass within the left caudal lung lobe. Sternal and hilar lymphadenopathy are present. Necropsy revealed a bronchogenic carcinoma with metastasis to the distal extremities and eyes.
Disease of the Diaphragm Diaphragmatic Hernia due to Trauma • Radiographic diagnosis of diaphragmatic hernia is suggested by loss of the normal diaphragmatic border, detection of abdominal viscera in the thoracic cavity, and varying amounts of pleural effusion. With large amounts of pleural effusion, displacement of the lung lobes cranially from the diaphragm may be the only indicator of abdominal viscera within the thoracic cavity. • Ultrasound examination of the thorax following thoracic radiographs can help to confirm a diagnosis of diaphragmatic hernia. When the
764
Figure 291-15 A, B, Diaphragmatic hernia: A cat presented with labored respiration following being hit by car. The cardiac silhouette is displaced to the left and dorsally. There is a soft-tissue opacity structure within the right ventral thorax. The diaphragm cannot be fully visualized. The stomach axis is displaced cranially. The final diagnosis was a diaphragmatic hernia with cranial displacement of the liver into the thorax.
liver enters the thoracic cavity, it can sometimes be difficult to distinguish the liver from a collapsed lung lobe. Both the liver and collapsed lung will appear hyperechoic. The key is to try to follow the organ and vascular structures cranially and toward the midline (allowing recognition of the organ as collapsed lung) or caudally through the diaphragm (allowing recognition of the organ as herniated liver). Usually pleural effusion of varying amounts will be present with a diaphragmatic hernia. See Figure 291-15.
Peritoneopericardial Diaphragmatic Hernia • The cardiac silhouette appears enlarged. On the lateral view, a dorsal mesothelial remnant can sometimes be visible between the dia-
Imaging: The Thorax
(A)
(B)
(C) Figure 291-16 A, B, Peritoneopericardial diaphragmatic hernia: The cardiac silhouette is greatly enlarged and appears globoid. The diaphragm can not be visualized in its central portion. The gastric axis is shifted cranially and decreased liver volume is present within the abdomen. C, Ultrasound confirms the presence of liver adjacent to the cardiac silhouette within the pericardium.
phragm and the caudal aspect of the cardiac silhouette. The ventrocaudal border of the cardiac silhouette may be indistinct from the diaphragm on the lateral projection. See Figure 291-16.
Hiatal Hernia • Hiatal hernia can be sliding or paraesophageal. Sliding hiatal hernias are typically seen in younger animals. Paraesophageal hernias are usually static. An esophagram is needed to differentiate abnormalities of the esophagus. See Figures 291-17 and 291-18. • Tenting of the diaphragm can be seen in normal feline patients at maximum inspiration. Figure 291-19.
Normal Findings: Feline Cardiac Silhouette • On the lateral projection, the normal heart is longer and more elliptical than the dog. The size of the ventricular area covers two to two and a half intercostal spaces. In most feline patients less than 12 pounds, the cardiac silhouette will be less than two intercostal spaces. In larger cats, the cardiac silhouette can normally be greater than two and a half intercostal spaces. In the normal aged feline patient, the heart may have a more supine position. There is typically more distance from the heart to the diaphragm on both the lateral and ventrodorsal projections than in a dog.
• On the ventrodorsal or dorsoventral view, the feline heart is more elongated than that of a dog. The dorsoventral projection causes the cardiac silhouette to appear more rounded. The shape of the thoracic cavity will appear shorter on the dorsoventral projection. The borders of the heart on the ventrodorsal view are similar to those in dogs, with the exception that the left auricle and atrium are located between the 1 and 2 o’clock positions. The main pulmonary artery may be craniad or may not be visualized. The apex of the heart can be more variable in the feline patient. The relative size of the normal cardiac silhouette on the ventrodorsal projection occupies up to 67% of the thoracic cavity. • All four sets of pulmonary vessels should be evaluated. The cranial lobar vessels, the artery and vein should be similar in size, with the borders of the artery slightly more distinct. On the ventrodorsal projection, the width of the caudal lobar vessels should be less the width of the ninth rib.
Aortic Knob and Aortic Undulation • Uncoiling of the aorta creates an undulating appearance of this vessel. It is associated with aging, hyperthyroidism, and hypertension. The “aortic knob” seen in the dorsoventral or ventrodorsal view was once incorrectly considered to be an aortic aneurism. See Figure 291-20.
765
SECTION 6: Imaging
(A) (A)
(B) (B) Figure 291-17 A, B, Hiatal hernia: On the lateral view of the thorax, notice the displacement of the stomach cranially. On the ventral-dorsal view, the stomach returns to a more normal position.
Normal Findings: Lung Lobes • The lung lobe divisions are right cranial, right middle, right caudal, accessory, left cranial (cranial and caudal segments) and left caudal. The normal trachea has an angle of 15 degrees relative to the spine as it approaches the heartbase. The lung regions can be divided into perihilar (hilar), middle, and peripheral regions.
766
Figure 291-18 A, Suspect hiatal hernia. B, The barium swallow confirmed that the mass in the left caudal lung lobe was not involving the esophagus.
“Three-View Thorax” • Pulmonary disease, especially metastatic disease and pneumonia, is best evaluated with a “three-view thorax” exposing a left lateral recumbent and right lateral recumbent view with either the ventrodorsal or dorsoventral view. • Remember the non-dependent or “up” lung is better inflated so there will be more air for contrast.
Imaging: The Thorax
(A)
(A)
(B) Figure 291-19 A, B, Notice on the lateral images the diaphragm is flattened and caudally displaced. Tenting of the diaphragm (arrows) is best seen on the ventrodorsal views of the thorax.
(B)
Lung Abnormalities
Figure 291-20 A, B, Aortic undulation: Radiographs of the thorax show the cardiac silhouette lying along the sternum and prominence and uncoiling of the aorta.
Questions to Ask • Are the lungs normal or abnormal? • Is the lesion in the lung field on both views? • Are there radiographic signs that are pathognomonic for lung disease? • Is there evidence of pleural or thoracic wall disease suggesting lesions outside lung? • General questions about lung abnormality: size, shape, position, density, margination, and number.
Lung Patterns of Disease Vascular Lung Pattern • The vascular pattern can be evaluated by measuring the size of the pulmonary vessels. On the lateral projection, the artery and vein should be about the same size. On the ventrodorsal projection, the caudal lobar vessels should not exceed the width to the ninth rib.
767
SECTION 6: Imaging
(A)
(A)
(B)
(B)
Figure 291-21 A, B, Heartworm disease suspect: An increased soft-tissue opacity is noted in the region of the right middle lung lobe indicating collapse or alveolar infiltrates. The right caudal lobar artery is enlarged. Heartworm testing was negative on antibody and antigen testing.
Figure 291-22 A, B, Heartworm disease: Bronchial marking are prominent. The caudal lobar arteries are enlarged. The left ventricular border appears mildly elongated. Heartworm testing was positive on antibody and antigen testing.
Remember that in cardiac disease, not all four sets of vessels are equally enlarged, so you are obligated to examine all four sets. In patients that are volume depleted or on diuretic medication for cardiac diseases, the pulmonary vessels may appear smaller than normal.
may present with gastrointestinal signs, especially vomiting and diarrhea. The most pronounced radiographic changes associated with feline heartworm disease in cats are found associated with the caudal lobar arteries. The pulmonary artery becomes enlarged and less consistently shows signs of tortuosity and truncation. Increased lung opacity in the lung parenchyma ranges from interstitial to bronchial. The cardiac silhouette may show mild cardiomegaly. The main pulmonary arterial segment is not prominent as seen in canine patients. See Figures 291-21 and 291-22. • The right caudal lobar artery is most commonly affected.
Feline Heartworm Disease • Clinical signs are highly variable in feline patients with heartworm disease. Patients may be asymptomatic, dyspneic, tachycardia, or
768
Imaging: The Thorax
(A) (A)
(B) (B) Figure 291-23 A, B, Asthma: This patient presented with a history of a chronic hacking cough. The lung pattern is a heavy bronchial pattern. There are multiple small areas that appear to be nodules; these may represent mucous plugging of bronchial structures. The diaphragm is flattened and displaced caudally most likely from increased respiratory effort. Heartworm testing was negative.
Bronchial Lung Pattern • A bronchial pattern can normally be seen in the perihilar region as a normal aging change. In disease states, the bronchial markings extend out into the periphery. The bronchial walls appear thickened due to cellular infiltrates in or around the wall. The bronchial walls appear as donuts in transverse section and as railroad tracks in longitudinal section.
Feline Asthma • The most common example of bronchial disease in cats is feline asthma. Bronchitis is only visible radiographically when it progresses
Figure 291-24 A, B, Volume Overload: A cat presented for anorexia and dehydration. This patient was placed on intravenous fluid therapy. A diffuse heavy interstitial pattern is present. The cardiac silhouette is greatly enlarged. The thoracic radiographs show enlargement of the pulmonary vasculature and caudal vena cava. A small amount of pleural effusion is present.
from acute to chronic. Other signs associated with asthma include tenting of the diaphragm, aerophagia, and atelectasis of the right middle lung lobe. Patients with chronic bronchitis can be predisposed to pneumonia. See Figure 291-23.
Hypervascular Lung Pattern • A hypervascular pattern affecting the veins may be seen with leftsided heart disease. In cases of overhydration, both the artery and vein may be enlarged. See Figures 291-24 and 291-25. • A hypervascular pattern affecting both the arteries and veins may be seen in left-to-right congenital heart conditions.
769
SECTION 6: Imaging
•
•
• •
•
(A)
grams (i.e., air-filled alveoli surrounded by fluid-filled alveoli), lobar sign (i.e., contrast of air-filled normal lobe adjacent to lobe with alveolar disease), silhouette sign (i.e., border or silhouette can not be seen because now the same radiographic opacities are adjacent), and fluffy, coalescing densities when alveoli rupture and fluid flows from one alveolar space to another. See Figures 291-26 through 291-30. Differentiation of etiology can be assisted by history, extrapulmonary radiographic information such as size of cardiac silhouette and pulmonary vasculature, and the location in lung. Pneumonia tends to be cranial and ventral. The right middle lung lobe is commonly involved in aspiration pneumonia. See Figure 291-26. Pulmonary edema in cats can be highly variable not always presenting in a dorsal and perihilar location. Neurogenic pulmonary edema is usually dorsally distributed but can extend farther out into the periphery than is seen with cardiogenic causes. Pulmonary hemorrhage is highly variable depending on where the trauma occurred.
Interstitial Lung Pattern The interstitial pattern can be divided into structured or unstructured forms. In the structured form, there may be solitary or multiple nodules. The borders can be smooth and well demarcated. “Fuzzy” nodules occur when an inflammatory component is present. Differentials include: (a) primary neoplasia, (b) metastatic neoplasia, (c) pulmonary abscess, (d) mycotic or granulomatous pneumonia, (e) traumatic pneumatocele, and (f) hematoma or cysts.
(B) Figure 291-25 A, B, A fluid overload was suspected immediately following surgery. Alveolar opacities are in the right and left caudal lung lobes primarily in the hilar region. Patchy alveolar opacities are noted in the right middle lung lobe. The cardiac silhouette and pulmonary vascular appear enlarged. Radiographic signs were consistent with volume overload.
• A single well-demarcated nodule indicates a slowly expanding disease without an inflammatory component. Differentials include primary lung tumor, walled-off abscess, and metastatic neoplasia. • Primary pulmonary neoplasia is rare in feline patient. The appearance is highly variable in distribution and numbers of nodules. Additional radiographic signs associated with primary neoplasia include dystrophic mineralization, pleural effusion, and intrathoracic lymphadenopathy. See Figures 291-31 and 291-32. • A single poorly defined nodule indicates that the expanding lesion has an inflammatory component. Differentials include abscess, parasitic granuloma, and mycosis. • Multiple well-demarcated nodules usually represent neoplasia especially if the nodules have different sizes more consistent with metastatic neoplasia. The nodules may be variably sized with borders that are either well defined or ill defined depending on tumor type. Dystrophic mineralization may be present with metastatic neoplasia. See Figures 291-33 through 291-38. • Multiple poorly defined small-sized nodules with hazy blurred margins indicate an active inflammatory component. A miliary pattern is most likely to be granulomatous or mycotic pneumonia. Cats have been reported to have blastomycosis and histoplasmosis. Paragonimus can have varying numbers of ill-defined nodular opacities in the lungs. Aelurostrongylus can produce ill-defined nodular opacities, and in later stages, increased bronchial markings. See Figures 291-39 and 291-40.
Hypovascular Lung Pattern • A hypovascular pattern affecting both the arteries and veins can be caused by a right-to-left shunt, outflow obstruction (e.g., pulmonic stenosis), and systemic circulatory disturbance such as hypovolemic shock.
Alveolar Lung Pattern • Roentgen signs of alveolar disease include air bronchograms (i.e., air-filled bronchus surrounded by fluid filled alveoli), air alveolo-
770
Unstructured Interstitial Lung Pattern • An unstructured interstitial pattern results from fluid or cellular infiltrates within the interstitium or fibrous tissue proliferation. • Roentgen signs include an increased interstitial opacity, generalized with blurring of the pulmonary vascular margins. An increased interstitial opacity can be seen with age, pulmonary fibrosis, lymphosarcoma, early stage of pulmonary edema, pneumonia, hemorrhage, and thromboembolic disease. See Figures 291-41 and 291-42.
(A) (A)
(B)
(B) Figure 291-27 A, B, This patient did not properly recover from general anesthesia done earlier in the week. Alveolar disease is present in the right cranial and left cranial lung lobes. A small amount of pleural effusion is present adjacent the consolidated cranial lung lobes. The diagnosis was bronchopneumonia.
(C) Figure 291-26 A, B, C, Aspiration pneumonia: This patient presented with severe stomatitis and pharyngitis. An alveolar opacity is present in the right middle lung lobe and the caudal aspect of the left cranial lung lobe. Pneumonia was confirmed on necropsy.
771
(A)
(A)
(B) Figure 291-28 A, B, Pneumonia and pneumomediastinum: All cats in this household had recently developed an upper respiratory infection. This cat presented for coughing and dyspnea. Thoracic radiographs show an alveolar opacity is present in the right middle lung lobe, caudal segment of the left cranial lung lobes, and a patchy area in the accessory lung lobe. Air can be seen outlining the cranial mediastinum structures indicating a pneumomediastinum. Notice the moderate amount of air in the stomach most likely from aerophagia due to respiratory distress.
(B) Figure 291-29 A, B, The right middle lung lobe appears collapsed on the ventraldorsal view. An increase in soft-tissue opacity is present in the cranial aspect of the left cranial lung lobe. A small amount of pleural effusion is noted adjacent to the left cranial lung lobe. There is an ill-defined mineralized opacity within the cranial mediastinum. Mycoplasma was found from the transtracheal wash.
772
(A)
(C) (B)
(D)
Figure 291-30 A, B, Thoracic radiographs reveal fluid in the pleural space worse on the left with rounding of the dorsal caudal lung lobe consistent with a chronic response. C, Ultrasound images show free fluid within the pleural space and suspected fluid pockets within the left caudal lung lobe. D, Computerized tomography while in dorsal recumbency suggests atelectic edge of the right caudal lung lobe and accessory lung. The left caudal lung lobe shows a mass effect. Pleural effusion is noted along the left lateral thoracic wall. The final diagnosis on cytology was an inflammatory process.
773
(A)
(B) Figure 291-31 A, B, A single large soft tissue nodule is present in the right caudal lung lobe (arrow). It was a suspected metastatic lesion from a nerve sheath tumor found on the hard palate.
774
(A)
(B)
(C) Figure 291-32 A, B, Thoracic radiographs show an ill-defined, lobulated soft-tissue mass approximately 3.4 cm in length lateral to the tracheal bifurcation in the caudal segment of the left cranial lung lobe. An additional soft-tissue mass is seen in the right caudal lung lobe. C, Computerized tomography was performed in dorsal recumbency and a biopsy guided by computerized tomography of the larger mass revealed a carcinoma.
775
(A)
(C)
(B) Figure 291-33 A, B, C, Fibrosarcoma with metastatic disease: There is a mineralized soft-tissue mass dorsal to the cervical and cranial thoracic tissues. There are multiple welldefined variable sized nodules within all lung fields.
776
(A) (A)
(B)
(B) Figure 291-35 A, B, Neoplasia: Thoracic images show multiple masses within the lung. A cavitated air filled mass is present in the right caudal lung lobe. Cytology of the pleural fluid was consistent with a carcinoma.
(C) Figure 291-34 A, B, Metastatic disease from anal sac adenocarcinoma: There are diffuse well-defined variable shaped nodules within the lung parenchyma. C, Computerized tomography in dorsal recumbency shows diffuse multiple well defined masses.
777
(A)
(B)
(C) Figure 291-36 A, B, Neoplasia round cell tumor: Thoracic radiographs show a mediastinal shift to the left. The borders of the cardiac silhouette are not well defined on the ventral-dorsal view. Increased soft-tissue opacity is present in the region of the caudal aspect of the left cranial lung lobe. Faint mineralization can be seen overlying this area of lung. C, Computerized tomography in dorsal recumbency show atelectasis of the left cranial lung lobe with focal mineralization within the left cranial and caudal lung lobes. Cytology obtained from a ultrasound guided aspiration of this mass revealed an undifferentiated round cell tumor.
778
(A)
(B)
(C) Figure 291-37 A, B, Thoracic radiographs show signs of a chronic pleural effusion by the rounding of the lung borders worse in the right hemithorax. The lungs have a heavy interstitial pattern with focal areas of mineralization. C, Ultrasound shows pleural effusion with rounded lung tissue. Fine-needle aspiration of the lung confirmed neoplastic cells.
779
(A) (A)
(B) Figure 291-38 A, B, There are multiple, ill-defined and well-defined variable sized pulmonary nodules in this obese patient. Moderate amount of pleural effusion is present. Cytology of an enlarged lymph node and a sample of the abdominal effusion had malignant cell consistent with carcinoma.
(B) Figure 291-39 A, B, Aelurostrongylus: Examination of the thoracic radiographs reveals a generalized increase in peribronchial interstitial opacity. There are several focal patchy alveolar opacities distributed in the caudal lung fields.
780
(A)
(B) Figure 291-40 A, B, Fungal pneumonia is characterized by multiple poorly defined small sized nodules with hazy blurred margins, typical of an active inflammatory component. A miliary pattern is most likely to be granulomatous or mycotic pneumonia. This cat had histoplasmosis.
781
SECTION 6: Imaging
(A)
(A)
(B) Figure 291-41 A, B, Interstitial pattern: Thoracic images show a diffuse interstitial pattern with bronchial marking in the hilar region. The findings were consistent with an aging change.
Mixed Lung Patterns • These can be seen in our older patients. An interstitial pattern can be found as a normal change or in obese patients. Other lung parenchyma changes can occur along with an interstitial pattern depending on the etiology. See Figure 291-43. • Technical problems can make the lungs appear denser when radiographs are made during expiration or the technique is underexposed.
Suggested Readings Fox PR, Sisson D, Moise NS. 1999. Radiology: Role of radiology in diagnosis and management of thoracic disease. In PR Fox, D Nisson, NS
782
(B) Figure 291-42 A, B, Thoracic radiograph were obtained following completion of radiation therapy for a fibrosarcoma on the left thoracic wall. A heavy interstitial pattern is present. Pulmonary fibrosis from the previous radiation therapy is the most likely differential.
Moise, eds., Textbook of Canine and Feline Cardiology, 2nd ed., pp. 107– 129. Philadelphia: WB Saunders. Suter PF, Lord PF. 1984. Thoracic Radiography: A Text Atlas of Thoracic Diseases of the Dog and Cat, pp. 1–45. Wettswil, Switzerland: Peter F. Suter. Thrall DE. 2007. Esophagus. In DE Thrall, Veterinary Diagnostic Radiology, 5th ed. pp. 495–511. Philadelphia: WB Saunders. Thrall DE. 2007. Heart and pulmonary vessels. In DE Thrall, Veterinary Diagnostic Radiology, 5th ed. pp. 568–590. Philadelphia: WB Saunders. Thrall DE. 2007. Interpretation paradigms for the small animal thorax. In DE Thrall, Veterinary Diagnostic Radiology, 5th ed. pp. 462–485. Philadelphia: WB Saunders.
Imaging: The Thorax
(A) (B)
(C)
(D)
Figure 291-43 Bronchointerstitial with bronchiectasis: A, B, Thoracic radiographs reveal a bronchointerstitial pattern is present. C, D, A computerized tomography performed in sternal recumbency reveals diffuse bronchiectasis with mild interstitial infiltrates. In the caudal lung fields there are areas of lucency which has been described as a honeycomb pattern.
Thrall DE. 2007. Larynx, pharynx, and trachea. In DE Thrall, Veterinary Diagnostic Radiology, 5th ed. pp. 489–494. Philadelphia: WB Saunders. Thrall DE. 2007. Radiographic anatomy of the cardiopulmonary system. In DE Thrall, Veterinary Diagnostic Radiology, 5th ed. pp. 486–488. Philadelphia: WB Saunders. Thrall DE. 2007. The canine and feline lung. In DE Thrall, Veterinary Diagnostic Radiology, 5th ed. pp. 591–608. Philadelphia: WB Saunders.
Thrall DE. 2007. The diaphragm. In DE Thrall, Veterinary Diagnostic Radiology, 5th ed. pp. 525–540. Philadelphia: WB Saunders. Thrall DE. 2007. The mediastinum. In DE Thrall, Veterinary Diagnostic Radiology, 5th ed. pp. 541–554. Philadelphia: WB Saunders. Thrall DE. 2007. The pleural space. In DE Thrall, Veterinary Diagnostic Radiology, 5th ed. pp. 555–567. Philadelphia: WB Saunders. Thrall DE. 2007. The thoracic wall. In DE Thrall, Veterinary Diagnostic Radiology, 5th ed. pp. 512–524. Philadelphia: WB Saunders.
783
CHAPTER 292
Imaging: The Abdomen Judith Hudson and Merrilee Holland
Imaging of the Peritoneal Space Radiography of the Normal Feline Peritoneal Cavity • The amount of normal peritoneal fluid is too small to be radiographically apparent. Fat surrounding abdominal organs allows serosal surfaces to be seen radiographically.
Celiography (Peritoneography) • Celiography is used for examination of the peritoneal cavity, particularly in cases in which abdominal herniation is suspected. • A sterile iodinated contrast medium (nonionic products such as iopamidol and iohexol are preferred, particularly in debilitated cats) are used. Injection should be made into the peritoneal cavity taking care to avoid the falciform ligament, which would result in an unsuccessful study. • Barium is harmful to the peritoneum and should not be injected into the peritoneal cavity. • The procedure may fail to detect herniation in which herniated solid organs or other tissue prevents movement of the contrast medium outside the peritoneal cavity. • In a normal celiogram, radiopaque iodinated contrast will be seen outlining the intestinal loops and other abdominal organs. Margins of the contrast should be smooth.
peritoneal cavity (see Figure 292-3). Inflammation of peritoneal surfaces and seeding of the peritoneum by neoplasia (carcinomatosis) can also decrease serosal detail. • The abdomen is said to be “fluid opaque” when the loss of serosal detail involves the entire abdomen (see Figure 292-1). In other cases, the loss of detail is regional, occurring, for example with peritonitis secondary to pancreatitis. • On ultrasonography, some fluid will be anechoic (see Figure 292-4). In other cases, the fluid may appear cellular with hypoechoic echoes swirling within the fluid (see Figure 292-5A). Fluid with a cellular nature suggests a high protein content, hemorrhage, or infection. • Ultrasound-guided aspiration can be done to determine the type of fluid (e.g., hemorrhage, chyle, purulent discharge, modified transudate, and urine).
Ultrasonography of the Normal Peritoneal Cavity • The interface between the diaphragm and lung is shown as a smooth hyperechoic line. Mirror image artifact can cause the liver to appear to be located cranial to the lung–diaphragm interface. Care should be taken to avoid interpreting this artifact as a diaphragmatic hernia or peritoneopericardial hernia. • A small amount of free anechoic fluid can be present, particularly in kittens. No free gas should be seen unless there has been recent abdominal surgery.
Figure 292-1 Ascites: A total loss of serosal detail (“fluid-opaque abdomen”) is caused by free peritoneal effusion. Gas and ingesta is seen in the gastrointestinal tract.
Abnormal Fluid in the Peritoneal Cavity • On radiography, decreased visualization of serosal surfaces can indicate the presence of abnormal fluid accumulation in the peritoneal cavity. • Causes of free fluid (see Figure 292-1) include ascites from hepatic or cardiac disease, peritonitis, neoplasia, hemorrhage, rupture of a hollow organ (i.e., urine, bile, and intestinal contents), and recent surgery. • It is important to realize that loss of serosal detail occurs because fat is no longer providing sufficient contrast between soft-tissue structures in the abdomen. Loss of serosal detail occurs not only when fluid is present but also when there is minimal fat (see Figure 292-2) or when the fat is obscured because of a mass or masses in the
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
784
Figure 292-2 Radiograph of the abdomen with a complete loss of serosal detail caused by emaciation. Radiopaque streaks over the caudal abdomen and legs were caused by a wet hair coat. A small radiopacity in the dorsocaudal abdomen (arrow) was caused by mineralization in a mass involving the colon.
Figure 292-3 Loss of serosal detail was caused by a large (approximately 9 × 13 cm) mass in the midabdomen. Fat remains visible in the cranioventral abdomen (arrow). Spindle cells were found on cytology of fluid obtained by ultrasound-guided aspiration.
Figure 292-4 Anechoic free fluid is seen cranial to the urinary bladder. This is another way to document ascites.
(A)
(B)
(C) Figure 292-5 A, Free cellular fluid (FF). B, On the ventral-dorsal view, gas can be seen surrounding the stomach and liver lobes, allowing better visualization of the margins of these organs. C, Exposing a lateral view of the abdomen using a horizontal beam is helpful to confirm the presence of free gas in the peritoneal cavity, particularly when gas is not obvious in other projections. In this cat, considerable gas can be seen outlining the gastrointestinal tract (arrows) and spleen (Sp). Intraluminal gas can be seen in the stomach and small intestine.
785
SECTION 6: Imaging
Free Gas in the Peritoneal Cavity • Causes of free gas include rupture of the gastrointestinal tract, a penetrating wound, infection with gas-producing organisms, and recent surgery. • On radiography, a significant amount of gas can increase visualization of serosal surfaces. Loops of intestine surrounded by gas appear brighter than when normally seen. Abnormal gas patterns can be diagnostic. Intraluminal gas will have smooth circular or oval borders. Extraluminal gas outlining bowel and other organs will have sharp angular margins. See Figure 292-5B. Gas is sometimes seen between the liver and diaphragm. • Small amounts of gas can be diagnosed by using a horizontal beam while the patient is placed in left lateral recumbency or dorsal recumbency. These positions allow gas to rise where it can be visualized with the horizontal beam. See Figure 292-5C. • On ultrasonography, gas is hyperechoic with deep reverberation artifact Small amounts of gas are difficult to identify. Care must be taken so that gas in bowel or lung is not mistaken for free peritoneal gas.
(A)
Abdominal Herniation • Intestines and other abdominal organs can herniate through the diaphragm or abdominal wall. See Figure 292-6. Peritoneo-pericardial herniation is a congenital problem in which abdominal contents herniate into the pericardial sac. See Figure 292-7. Disruption of the diaphragm or abdominal wall might be apparent on survey radiography. In some cases, intestinal gas allows visualization of displaced bowel. • Gastrointestinal contrast agents can be used to help localize the intestines, but there can be herniation of solid organs (i.e., liver, spleen, mesentery, or falciform fat) without simultaneous herniation of bowel. Abnormal cranial displacement of the gastrointestinal tract might be visible in some of these cases, particularly if barium is administered. • Celiography can be useful to demonstrate interruption of the diaphragm and abdominal wall and to outline abdominal organs. • Herniation can also occur in other locations such as the inguinal ring or perineal region. These areas should also be examined for a break in the peritoneum or the presence of abdominal organs outside the abdominal wall. An upper gastrointestinal series may be useful to identify displaced intestine. Similarly, cystography can be used to determine the location of the urinary bladder when an inguinal or perineal hernia is present. • Ultrasonography can be useful to detect herniated contents.
(B) Figure 292-6 A, Radiograph of a ventral hernia subsequent to exploratory surgery for chronic vomiting. Gas can be seen within bowel loops in the hernia (arrows). B, Ultrasonography confirmed herniation of bowel. Cursors show thinning of the abdominal wall near the rent in the body wall. A loop of small intestine (arrows) can be seen extending into the hernia.
Imaging of the Body Wall • The body wall can be examined with radiography or ultrasonography to determine integrity (see Abdominal Herniation) or evaluate involvement of the body wall in cases with neoplasia. • Computerized tomography (CT) is also valuable for determining the extent of neoplasia. See Figure 292-8.
Imaging of the Liver and Gall Bladder Radiography of Normal Feline Liver and Gall Bladder • The normal feline liver has smooth margins. The caudal edges of the ventral lobes appear sharp. In the lateral view, the liver appears elevated away from the ventral abdominal wall because of the falciform ligament. • The normal feline gall bladder has fluid opacity and is not seen separately from the liver. • Abnormalities in the liver should be described in terms of size, shape, margination, opacity, and location.
786
Figure 292-7 Sonogram of the thorax showing a peritoneo-pericardial hernia. The heart (arrows) is seen immediately adjacent to the liver.
Imaging: The Abdomen
•
•
(A)
•
•
•
(B) Figure 292-8 A, Computerized tomography of the cranial abdomen and body wall of a cat with injection-site sarcoma. B, Iodinated contrast was given intravenously, allowing improved visualization of the neoplasm (arrow) invading the body wall and adjacent spleen (Sp). LK, left kidney; RK, right kidney.
•
the large amounts of fibrous and fatty tissue that surround the vessels. Normal liver has a coarse echogenic pattern and smooth sharp margins. The sonographic appearance resembles falciform fat, but the falciform ligament is usually coarser and more echogenic. The relationship in echogenicity between the liver and falciform ligament is not a reliable indicator of disease. In some obese cats, the falciform fat is close in echogenicity or hypoechoic to the liver. The normal gallbladder is located ventrally to the right of the midline. A longitudinal image can be obtained by placing the transducer at the tip of the xiphoid cartilage with the ultrasound beam pointed cranially to the right of the midline. Both longitudinal and transverse images should be obtained. The wall should be smooth and uniform, but measurement may not be possible because the wall is usually isoechoic to the liver parenchyma. Normal wall thickness is approximately 1 to 2 mm, varying with the degree of distension. The gall bladder will be larger if the animal is anorexic or has been fasted. Normal bile is generally anechoic, but echogenic material is frequently seen (biliary sludge). Repositioning the cat will cause echogenic material to become suspended within the gall bladder. The gallbladder is generally not empty. Visualization of an extra feline gall bladder is common, but the gall bladders usually share a single cystic duct (bilobed gall bladder). True duplication with duplication of the cystic duct is rare. Refraction artifacts result in black streaks that originate at the curved surfaces of the gallbladder and extend into liver parenchyma deep to the gallbladder. Distal acoustic enhancement (or “through transmission”) can occur deep to the gallbladder. Sound is not attenuated by fluid in the gallbladder so that tissues deep to the gallbladder appear hyperechoic in comparison to adjacent tissues. The cystic duct communicates with the neck of the gallbladder. The hepatic ducts drain bile from the liver lobes. The cystic duct is joined by the first hepatic bile duct to form the common bile duct, which enters the duodenal wall near the pancreatic duct. The common bile duct measures up to 4 mm wide and can be often followed to the duodenum. The intrahepatic bile ducts are not normally visualized.
Ultrasonography of the Normal Liver and Gall Bladder • The gastric fundus is located at the left caudal border of the liver. A hyperechoic curvilinear echo will be seen at the cranial border marking the interface between the liver and diaphragm or lung. • Mirror artifact may cause the liver to appear to be located on both sides of the diaphragm. • Divisions between lobes are more obvious when peritoneal fluid is present. • The extrahepatic portal vein is clearly seen entering the liver at the porta hepatis, carrying blood from the spleen, pancreas, and most of the gastrointestinal tract. It is formed by the cranial and caudal mesenteric veins and is subsequently joined by the splenic vein. Normal portal velocity is 10 to 18 cm/sec. The hepatic artery is visible only with ultrahigh resolution transducers or color Doppler imaging. • The hepatic vein enters the caudal vena cava on the right side near the diaphragm. Excessive transducer pressure easily collapses the thin-walled caudal vena cava. In longitudinal images, both the caudal vena cava and aorta appear as well-defined anechoic tubes, but the aorta is more dorsal, is located on the left side, and is less compressible. Pulsations may help to distinguish the aorta, but pulsations can also appear to be present in the caudal vena cava because of vibrations within the tissues. • Intrahepatic branches of the hepatic vein appear as anechoic linear structures with poorly delineated walls. Intrahepatic portal veins have hyperechoic walls because of the orientation of wall fibers and
Radiography of Hepatomegaly • Diffuse hepatomegaly (see Figure 292-9) displaces the stomach and other abdominal organs caudally, centrally, and dorsally. Margins of the caudal liver lobes may appear rounded. • Focal hepatomegaly causes displacement of organs adjacent to the affected area. • Pedunculated masses can “wrap around” the stomach and may appear to have originated caudal to the stomach. • Masses near the margins of the liver may cause the liver to have a “lumpy” appearance. See Figure 292-10. • Small masses that do not distort the liver margins may not be visible radiographically. Ultrasonography is useful to detect these masses. • Large gastric or splenic masses may also appear to be associated with the liver. An enlarged gall bladder may also masquerade as a focal enlargement of the liver.
Abnormal Opacity in the Liver Region on Radiographs • Sometimes mineral opacities are seen associated with hepatic lesions such as parasitic granulomas and neoplasms. • Mineralization of the bile ducts or hepatic vessels may appear in a tree-like pattern as an incidental finding. • Air may occur in the hepatic vessels uncommonly due to air emboli.
787
SECTION 6: Imaging
(A)
Figure 292-10 Lateral radiograph showing a large irregular mass extending caudal to the stomach. Ultrasonography revealed that the mass extended from the left side of the liver. At surgery, there was torsion of the caudal portion of the left lateral liver lobe, which contained the mass. On histopathology, the mass was diagnosed as a biliary cystadenocarcinoma.
(A)
(B) Figure 292-9 Images showing hepatomegaly. A, Lateral projection shows that the liver (arrows) is enlarged with rounded caudal margins. The stomach (St) is displaced dorsally. Small intestinal segments are mildly distended with gas. “Flowing” spondylosis is apparent in the cranial lumbar spine. B, Ventral-dorsal projection shows caudal displacement of the intestines. Arrow marks the caudal aspect of the liver.
Ultrasonography of Diffuse Liver Lesions • Diffuse liver disease can be hyperechoic, isoechoic, hypoechoic, or mixed. Size is variable. • Diffuse hyperechoic disease (see Figure 292-11A) can be caused by increased levels of fat (hepatic lipidosis, normal obese cat), fibrosis,
788
(B) Figure 292-11 A, Sonogram showing the diffuse hyperechoic pattern that can be caused by increased levels of fat, fibrosis, or glycogen, steroid hepatopathy, other drugs or toxins, or infiltrative disease, including neoplasia. B, Longitudinal sonogram of the liver with multicentric T-cell lymphoma, showing a mixed pattern of liver disease. The liver has a mottled appearance with poorly defined hyperechoic areas intermingled with areas of decreased echogenicity (arrows).
Imaging: The Abdomen
(A)
(B)
Figure 292-13 Anechoic nodules (arrows) in the liver can be associated with benign cysts but can represent neoplasia particularly if there is altered echogenicity of surrounding tissue. Radiography of this cat is shown in Figures 292-10. Biliary cystadenocarcinoma was diagnosed on histopathology of the surgically excised mass.
or glycogen (diabetes mellitus), steroid hepatopathy, some drugs (e.g., phenothiazine) or toxins, or infiltrative disease (e.g., lymphoma and mast cell tumor). • Diffuse hypoechoic disease can be caused by lymphoma, amyloidosis, acute hepatitis, passive congestion among other causes. Amyloidosis can be familial in Siamese and Abyssinian cats. • Diffuse liver disease can also have a mixed pattern with intermingled areas of increased and decreased echogenicity giving the liver a mottled appearance. Diseases listed as creating a diffuse hyperechoic or hypoechoic liver pattern can also present with a mixed appearance. See Figure 292-11B).
Ultrasonography of Focal Liver Lesions
(C) Figure 292-12 A, Sonogram showing a hyperechoic mass in the liver. Spindle cells were found on cytology. B, Hypoechoic nodules were caused by metastatic mast cell tumor. Hypoechoic focal lesions can be caused by neoplasia, hematomas, granulomas, or less commonly, abscesses, infarcts, or hyperplastic nodules. C, Target lesions in the liver and spleen are associated with a high probability of neoplasia. This cat had gastric adenocarcinoma with metastasis to the liver.
• Hyperechoic focal lesions (see Figure 292-12A) can be caused by primary or secondary neoplasia, hematomas, granulomas, or less commonly, abscesses, infarcts, or hyperplastic nodules. • Hypoechoic focal lesions can be caused by lymphoma or other neoplasms, abscesses, hyperplastic nodules or hematomas. (See Figure 292-12B). • “Target” lesions are described as nodules with a hyperechoic center and hypoechoic rim. These have been associated with metastatic neoplasia. See Figure 292-12C. • Anechoic focal lesions with deep acoustic enhancement can be caused by benign cysts. Hepatic cysts may be present with polycystic renal disease. Although hepatic cysts may replace a significant amount of liver parenchyma, they may also occur as an incidental finding without clinical implication. Complicated cysts may resemble an abscess because of hemorrhage or cellular material within the cyst. Additionally, coalescing anechoic foci of variable size can be associated with biliary cystadenocarcinoma (see Figure 292-13) arising from intrahepatic bile ducts. Altered echogenicity of surrounding liver tissue may be a clue to the presence of neoplasia. • Focal lesions may have mixed or complex echogenicity. For example, neoplasms may have areas of hemorrhage, necrosis, or inflammation that contribute to this pattern of echogenicity. • Abscesses are uncommon, but may appear solid (hyperechoic or hypoechoic) or may have echogenic material moving within cavitary areas. Parasitic cysts can also occur.
789
SECTION 6: Imaging
Figure 292-14 Lateral projection of an operative mesenteric portogram in a cat showing microhepatica. Air (arrows) can be seen between the liver and stomach. Gas in the abdomen also surrounds the intestinal loops. Iodinated contrast medium was injected into a jejunal vein and could be seen traveling directly from the portal vein to the caudal vena cava confirming portosystemic shunt.
Specificity of Hepatic Ultrasonography • Note that sonography of liver lesions is non-specific. For example, lymphoma can be focal or diffuse and hypoechoic, hyperechoic, or isoechoic. Other neoplasms, hemorrhage, nodular hyperplasia, and abscesses also have variable echogenicity. • Fine-needle aspiration or biopsy is necessary for definitive diagnosis.
(A)
Microhepatica • With decreased liver size, the stomach is located closer than normal to the diaphragm. Causes include cirrhosis, portosystemic shunts, or microvascular dysplasia. History and clinical presentation can be useful in differentiating these conditions.
Portography • Contrast radiography (see Figure 292-14) can be used to investigate the portal system when the presence of a portosystemic shunt is suspected. • Contrast can be introduced at various locations. In one technique, the patient is anesthetized, and a laparotomy is performed to allow access to a jejunal vein. The jejunal vein is catheterized and sterile water-soluble iodinated contrast medium is injected into the vein. A series of rapid radiographs are obtained using a fast film changer or digital radiography. The radiographs are examined to determine if there are one or more shunts between the portal system and the systemic circulation. • Alternatively, contrast can be injected into the splenic parenchyma or directly into the splenic vein. • On ultrasonography, the liver in chronic hepatitis or cirrhosis is usually hyperechoic. Portal hypertension may cause reduced or reversed blood flow velocity. • Careful evaluation of the portal and systemic circulations with ultrasonography may lead to detection of a shunt vessel.
Gall Bladder Disease • Biliary sludge can occur in animals without liver disease. • On radiography, mineral opacity in the area of the gall bladder can occur as the result of choleliths. See Figure 292-15. These may occur as an incidental finding but may be associated with cholecystitis or biliary obstruction. Air opacity in the gall bladder is less common but can occur due to emphysematous cystitis. Abnormal opacity in the
790
(B)
(C) Figure 292-15 Radiopacities in the cranial abdomen are choleliths (black arrowhead) in the gall bladder. A, An abdominal mass is seen (arrows) caudal to the stomach. See also Figure 292-29. B, Sonogram of choleliths (arrow) in the gall bladder. The choleliths were removed surgically. C, Sonogram of the dilated common bile duct. CD, common bile duct; GB, gall bladder.
Imaging: The Abdomen
Figure 292-16 Cholecystitis may be seen as a thickened, irregular gall bladder (GB) wall and the presence of biliary sludge.
gall bladder may be interpreted erroneously as hepatic opacity. Ultrasonography is helpful in these cases. • On ultrasonography, choleliths are usually hyperechoic with deep acoustic shadowing. See Figure 292-15B. Mucoceles occur rarely in cats and are usually associated with disease such as cholecystitis. These are hypoechoic, may have spiky borders, and have been described as resembling kiwi fruit. • Obstruction can occur secondary to calculi in the bile ducts, pancreatitis, abscesses, mucocele formation, or neoplasia. Initially the gallbladder enlarges followed by the common bile duct and then, the intrahepatic bile ducts. Color-flow Doppler imaging or pulsed Doppler can be used to differentiate dilated bile ducts from dilated vessels. Obstruction cannot be excluded solely on the basis of ultrasonography. • Sonographic signs of cholecystitis (see Figure 292-16) are variable but include thickening of the gallbladder wall, the presence of biliary sludge, mucoceles, calculi, or gas (in emphysematous cystitis) and irregularity of the gallbladder wall. Echogenicity of the gall bladder wall may be altered. The wall has been described as having a “doublerim” sign in acute cases. Polyps, fibrosis (preventing gallbladder distension), and mineralization are additional findings that can occur in chronic cases.
Imaging of the Spleen Radiography of the Normal Feline Spleen • The feline spleen is best seen in the ventrodorsal view in which the proximal extremity appears as a triangular opacity located laterally between the stomach and left kidney. The proximal extremity is held in place at the caudolateral margin of the stomach by the gastrosplenic ligament. The distal extremity or tail may extend caudally along the left body wall. • The tail of the spleen is not likely to be seen on the lateral view, but in some fat cats, it may be visible dorsally, cranial to the left kidney.
Ultrasonography of the Normal Feline Spleen • The proximal extremity (head) of the spleen is located caudal to the gastric fundus held in place by the gastric fundus (see Figure 292-17). In normal cats, the spleen is found dorsally against the left lateral body wall. Scanning should be performed with the probe against the lateral body wall in a dorsal and cranial location.
Figure 292-17 Longitudinal sonogram showing a normal spleen. The normal feline spleen is tongue shaped, smaller, and less echogenic than the spleen of a dog. The stomach can be seen cranial to the spleen. The edge of a pancreatic mass can be seen deep to the spleen (arrows). Sp, spleen; St, stomach.
• The feline spleen tends to be smaller and less echogenic than the canine spleen. It is nonsinusoidal, and there are no direct arteriovenous connections (unlike in the canine spleen). Splenomegaly, other than that caused by drugs, tends to be more significant in cats than in dogs. Splenic disease in cats is more frequently neoplastic compared to splenic disease in dogs. • The splenic veins exit along the splenic hilus as branching anechoic vessels (“staghorn” appearance). The main splenic vein can be followed into the portal vein on the left side deep to the spleen. • Compared to the liver, the feline spleen has a finer, more uniform echotexture. Echogenicity is similar to that of the liver. • There is a well-defined hyperechoic capsule that appears as a fine echogenic line when imaged perpendicular to the long axis of the ultrasound beam.
Diffuse Splenic Enlargement • Diffuse enlargement of the spleen is less likely to be physiologic in cats than in dogs. • Causes of diffuse splenomegaly include infiltrative disease (i.e., lymphoma, mast cell tumor, lymphoid hyperplasia), splenitis including granulomatous splenitis associated with feline infectious peritonitis, systemic fungal disease, extramedullary hematopoiesis, parasitic infection, and torsion. • On radiography, margins of an enlarged spleen may appear rounded. See Figure 292-18A. On the lateral view, the spleen may appear as a poorly defined fluid opaque mass extending from dorsal to ventral. In some cases, the tail might appear as a triangular opacity located in the ventral abdomen as it crosses the midline. On the ventrodorsal view, the spleen will appear thicker than normal. • On ultrasonography, the enlarged spleen may be increased, decreased, or normal in echogenicity. See Figure 292-18B.
Focal Splenic Enlargement • Causes of focal splenomegaly include hemangiosarcoma and other neoplasms (such as those listed for diffuse splenomegaly), and hematoma. • Some splenic masses may distort the borders of the spleen. (see Figure 292-19).
Ultrasonography of Diffuse Splenic Change • Diffuse disease may more difficult to recognize than focal disease. Echogenicity can be decreased, increased, or normal. The spleen may be enlarged or normally sized.
791
SECTION 6: Imaging
Figure 292-19 Sonogram of a focal splenic mass. The cat had numerous subcutaneous masses that were found to be mast cell tumor on aspiration. Arrows indicate the margins of the spleen.
(A)
Figure 292-20 Sonogram of the spleen with lymphoid hyperplasia. The spleen is enlarged with a “moth-eaten” appearance affecting all of the spleen.
(B) Figure 292-18 A, Radiograph of a cat with splenomegaly. The spleen (arrows) can be seen caudal to the stomach and extending along the left body wall. B, An enlarged spleen is seen on sonography. Splenectomy was performed following histologic confirmation of mast cell tumor in the spleen.
• Splenic enlargement with diffuse decreased echogenicity (see Figure 292-20) can be seen in lymphoma, myeloproliferative disease, mast cell tumor, lymphoid hyperplasia, and extramedullary hematopoiesis. The spleen may have a moth-eaten or mottled appearance in some cases. These diseases can also cause splenic enlargement without altered echogenicity. Enlarged spleens with normal echogenicity have also occurred in cats with pyogranulomatous splenitis secondary to feline infectious peritonitis. One cat with granulomatous splenitis had an enlarged mottled spleen. • Splenic torsion can cause splenic enlargement. In dogs, resultant areas of infarction or necrosis have been described as having a “lacy” or “heteroechoic” appearance. If available, Doppler examination of the spleen is useful in splenic torsion to document interruption of blood flow. • Thrombosis of the splenic vein can also occur and may be nonsymptomatic or can lead to infarction.
792
• Splenic enlargement with diffuse increased echogenicity (as opposed to decreased echogenicity) has been reported to occur rarely with mast cell tumors.
Ultrasonography of Focal Splenic Change • Diseases that caused diffuse enlargement with decreased echogenicity can also cause focal hypoechoic nodules with or without splenic enlargement. Hypoechoic nodules and diffuse decreased echogenicity can occur concurrently. • Causes of focal hypoechoic or anechoic nodules include abscesses, hematomas (see Figure 292-21), and various neoplasms such as mast cell tumor, sarcomas, metastatic carcinomas, and cysts. • “Target” lesions can occur in both the spleen and liver as noted previously. • Hemangiosarcoma (see Figure 292-22) tends to cause complex (i.e., mixed anechoic, hypoechoic, or hyperechoic) focal lesions similar to those seen in dogs. Abdominal effusion is common with hemangiosarcoma but also occurs with other neoplasms. Hematomas can be anechoic but can also appear complex. Hemangiosarcomas and hematomas cannot be differentiated solely by their sonographic appearance. • Hyperechoic focal masses can be caused by fat, especially when found around the splenic veins, mineral, especially when acoustic
Imaging: The Abdomen
(A)
Figure 292-21 Sonogram of the spleen of a cat with a splenic hematoma. Color-flow Doppler imaging was used to differentiate cystic areas from blood vessels. On cytology, there was evidence of previous hemorrhage with macrophage clean up.
(B) Figure 292-23 A, Sonogram showing poorly defined hyperechoic nodules in the spleen of a cat. The spleen was mildly enlarged. B, A fine-needle biopsy (arrows) was used to obtain cells for cytology. (See Chapter 301.) Cytology confirmed splenic mast cell tumor. Figure 292-22 Sonogram of a large mass in the spleen. The mass bulges from the splenic capsule and is surrounded by free cellular fluid. Hepatic masses were also present on ultrasonography. The appearance is consistent with hemangiosarcoma.
Radiography of Lymph Nodes Normal Feline Lymph Nodes
shadowing is present, granulomas, and hematomas. Although hyperechoic focal masses are usually considered to be benign, neoplasms can present as hyperechoic focal masses. Notably, mast cell tumor has been reported in cats with enlarged nodular spleens in which the nodules were hyperechoic. Poorly defined hyperechoic nodules have also been found to be mast cell tumor on aspiration. See Figure 292-23.
Differentiation of Disease • Fine-needle biopsy should be performed on all splenic nodules because lesions cannot be diagnosed on the basis of the sonographic appearance. Significant hemorrhage is unlikely when using a 25gauge needle. See Chapter 301. • Remember to evaluate other organs. Abdominal effusion is frequent with hemangiosarcoma and other neoplasms (including lymphoma and mast cell tumor) but can also occur with benign disease such as hematoma. Mesenteric or retroperitoneal lymphadenopathy is much more common in lymphoma than in other diseases including mast cell tumor. Intestinal masses can occur simultaneously with either splenic lymphoma or mast cell tumor. Lymphoma can also affect other organs such as the kidney, spinal cord, brain, thymus gland, and eye. Hepatic disease is often present when splenic disease exists. Metastasis to the peritoneal surface and extra-abdominal organs (i.e., heart or bone) can also occur.
• Normal feline radiographically.
lymph
nodes
are
not
usually
visible
Ultrasonography of the Lymph Nodes Normal Feline Lymph Nodes • Normal nodes are smooth and may not be apparent when surrounded by mesenteric fat. Mesenteric lymph nodes are more likely to be visible in kittens or thin cats, particularly if a high frequency transducer is used.
Lymphadenopathy • Enlargement of visceral or parietal lymph nodes may occur due to lymphoma, mast cell tumor, or metastatic disease. Lymphadenopathy may also be a reaction to infection or may occur as the result of metastatic disease. Regional lymph nodes should always be evaluated when neoplasia is suspected or confirmed. • Enlarged mesenteric lymph nodes may be seen radiographically if sufficiently large. Usually they appear as a poorly defined opacity in the central abdomen. Rarely, there may be enlargement of a solitary lymph node. In the retroperitoneal space, enlarged sublumbar lymph nodes appear as fluid opacities. See Figure 292-24A.
793
SECTION 6: Imaging
• Other abdominal organs, such as the liver, spleen, kidneys, intestines, and lymph nodes, may be affected and should be evaluated. The thorax should be examined for further evidence of lymphadenopathy. A cranial mediastinal mass might be present particularly with lymphoma. The spine should be evaluated for the presence of lytic lesions consistent with osseous lymphoma. • Enlargement as the result of lymphoma or mast cell tumor cannot be differentiated from that caused by infection or metastasis solely by the radiographic or sonographic appearance. Aspiration may be helpful and can be guided using sonography.
Lymphoma in Lymph Nodes
(A)
• Although affected lymph nodes are characteristically large, round, and hypoechoic with a smooth border (see Figure 292-24B), they can be heterogeneous and misshapen.
Reactive Lymph Nodes • Reactive lymph nodes tend to be larger than normal. • Usually enlargement is less severe than with lymphoma and echogenicity is more normal.
Lymph Nodes with Inflammation • Inflamed lymph nodes may be enlarged and vary in size, echogenicity, and shape. • Abscesses can be present. These can be difficult to differentiate from hypoechoic, almost anechoic, nodes typical of lymphoma, but in some cases, cellular fluid may be visible in the affected nodes. See Figure 292-24C.
(B)
Metastasis to Nodes • Metastasis can occur in nodes draining organs affected by neoplasia. Metastatic nodes tend to be enlarged with increased or decreased echogenicity. They are sometimes irregular or misshapen. Suspect lymph nodes should be aspirated. • Remember that disease can be present even when the sonographic appearance is normal.
Imaging of the Pancreas Normal Feline Pancreas • The right lobe and body of the normal feline pancreas lie in the mesoduodenum. The left lobe is located in the greater omentum along the greater curvature of the stomach. • The normal feline pancreas is not visible radiographically.
Ultrasonography of the Normal Feline Pancreas
(C) Figure 292-24 A, Radiograph of enlarged medial iliac (arrows) and inguinal (arrowheads) lymph nodes in a cat with mast cell tumor. B, Sonogram showing a mesenteric lymph node in a cat with gastric lymphosarcoma. The node is enlarged, rounded, and hypoechoic. C, Sonogram in a cat with hyperthyroidism. Cellular fluid could be seen in the nodes. Aspiration revealed purulent material within the lymph nodes.
794
• The thin right lobe is located dorsomedial to the descending duodenum in the mesoduodenum. The distal tip of the right extremity has a cranial bend. The left extremity is shorter, thicker, and is located between the stomach and transverse colon. The body is found in the angle between the stomach and descending duodenum. See Figure 292-25. • The pancreatic duct runs centrally through the pancreas presenting as an anechoic tube with thin hyperechoic walls. Doppler examination can be helpful to differentiate the duct from vascular branches. • The upper limit for pancreatic duct size is about 0.13 cm (average 0.8 cm), but the duct may be larger in older cats. The duct enters the duodenum, approximately 3.0 cm distal to the pylorus, at the major
Imaging: The Abdomen
Figure 292-25 In this sonogram of a normal cat, the pancreas can be seen deep to the duodenum. The ultrasound transducer has been placed on the ventral abdomen. The pancreaticoduodenal vein (PV) is ventral to the pancreatic duct (PD).
duodenal papilla with the common bile duct. In about 20% of cats, an accessory pancreatic duct may enter the duodenum more distally at the minor duodenal papilla. • The pancreaticoduodenal vein forms a normal vascular landmark but is not seen in all cats. It is located ventral to the pancreatic duct and is a much larger structure. • The pancreas is difficult to image because of its size, proximity to gas, and echogenicity similar to surrounding mesentery. In addition, the pancreas is isoechoic or only slightly hyperechoic compared to adjacent liver. It is hypoechoic compared to the spleen. Identification of a normal pancreas may not be possible but is more likely with a high-resolution transducer. The area of the pancreas should be investigated.
Pancreatitis • Acute necrotizing and chronic nonsuppurative pancreatitis cannot be differentiated on the basis of sonographic, radiographic, historic, currently available blood tests, or examination findings.
(A)
(B) Figure 292-26 A, Sonogram of the pancreas of a cat with history of chronic vomiting that was becoming more frequent. The pancreas was enlarged and hypoechoic with hypoechoic nodules scattered throughout. Hypoechoic nodules can be pancreatic pseudocysts, complicated cysts, abscesses, hyperplasia, or neoplasia. Pancreatitis and neoplasia cannot be differentiated solely on the basis of sonography. B, Calipers have been placed to measure one of the nodules in the pancreas of the cat in image A. BOP, body of pancreas.
Radiographic Signs • Pleural effusion is visible on radiographs in about 20% of cats with acute necrotizing pancreatitis and 35% of cats with chronic nonsuppurative pancreatitis. • Decreased serosal detail is present on abdominal radiography in about 50% of cats with either form of the disease. • Concurrent disease in other organs is common in both forms of pancreatic disease but may be more frequent in chronic nonsuppurative pancreatic than in acute necrotizing pancreatitis. • Other radiographic changes include gas-filled intestine and hepatomegaly. A mass effect may be present in some cases. • Many cats with pancreatitis have normal abdominal radiographs.
Sonographic Signs • Sonography can be normal in approximately 50% of animals with acute or chronic pancreatitis. • Sonographic changes can include a hypoechoic pancreas, hyperechoic mesentery, abdominal effusion, and increased hepatic echogenicity. See Figure 292-26A. Adjacent intestine may have a corrugated or spastic appearance, may be thickened, or may have altered echogenicity because of localized inflammation. Extrahepatic bile duct obstruction has been reported in at least two cats with chronic pancreatitis.
• Dilation of the pancreatic duct can indicate pancreatitis but can also be seen in animals without clinical indication of pancreatitis. In one study, there was no statistical correlation between duct size and the presence of clinical pancreatitis. Doppler ultrasonography can be used to differentiate an enlarged pancreatic duct from a normal pancreaticoduodenal vein. • Pancreatic pseudocysts (see Figure 292-26) may be associated with pancreatitis. These may be the result of secretion into areas of necrosis. In comparison to true cysts, pancreatic pseudocysts tend to be hypoechoic rather than anechoic and their walls tend to be thicker. Ultrasonography cannot reliably differentiate pseudocysts, cysts, and abscesses, however. Hypoechoic nodules can also be hyperplastic or neoplastic. • Ultrasound can be used to guide aspiration of peritoneal effusion or fluid collections within the pancreas.
Pancreatic Masses • Pancreatic masses may not be radiographically apparent. • Free fluid or enlargement of the pancreas may be seen with both pancreatitis and neoplasia. Displacement of adjacent organs may accompany pancreatic enlargement.
795
SECTION 6: Imaging
(A)
(A)
(B) Figure 292-27 Longitudinal sonogram of a pancreatic mass found in a cat following surgical removal of gastric carcinoma. A, The pancreaticoduodenal vein can be seen cranially (arrow). A, Sonogram of a cat with a 2-week history of lethargy and inappetence. A mixed echogenicity mass is seen in the area of the pancreas. A gastrointestinal stromal tumor was diagnosed on histology following surgical biopsy of the pancreas. PAN, pancreas; RL, right liver.
• Icterus may result if there is obstruction of the bile duct. • Pancreatic neoplasia is uncommon, but pancreatic adenocarcinoma has been reported to cause anorexia, depression, vomiting, and weight loss. Apudomas, gastrinomas, and insulin-producing tumors occur rarely. Free fluid may be present in the abdomen. Icterus may be present if bile duct obstruction occurs. Acute or chronic pancreatitis, exocrine pancreatic insufficiency, and diabetes mellitus can also be present in severe cases. • On ultrasonography, pancreatic neoplasms may be hypoechoic or more complex. See Figure 292-27. Differentiation from pancreatitis is not possible on the basis of sonographic appearance; aspiration or biopsy is necessary. • Adenocarcinoma and other neoplasms may metastasize to the liver and may invade adjacent portions of the gastrointestinal tract. Insulinomas may not be visible sonographically. • Mycotic disease in the pancreas may appear similar to neoplasia or pancreatitis. See Figure 292-28.
796
(B) Figure 292-28 Images of a cat with a mass in the cranial abdomen. At surgery, the mass was found to be involving the pancreas, liver, adjacent small intestine, and local lymph nodes. Cytology confirmed blastomycosis. A, Ventral-dorsal projection with arrows indicating the mass caudal to the stomach. B, Sonogram showing a primarily hypoechoic mass involving the pancreas. Some poorly defined hyperechoic areas are seen in the mass. LK, left kidney; RK, right kidney; Sp, spleen.
• Peripancreatic masses may appear to be within the pancreas. See Figures 292-15A and 292-29. • Nodular hyperplasia in older cats may occur as isoechoic or hypoechoic nodules and will appear similar to neoplasia or complicated cysts.
Pancreatolithiasis • A calculus in the pancreatic duct was reported to be a hyperechoic structure with deep acoustic shadowing. The same cat also had a pancreatic pseudobladder with additional hyperechoic calculi that had deep acoustic shadowing.
Imaging: The Abdomen
• Nonionic organic iodinated contrast is preferred over ionic iodinated products for esophagography in cats because of the risk of pulmonary edema with ionic iodinated products. • In a normal esophagram, there are thin longitudinal lines running from the cricopharyngeus caudally to the area of the heart base. The caudal one-third of the esophagus has a “fish bone” or “herring bone” pattern caused by transverse lines in the area of smooth muscle. • A radiograph is a snapshot in time. A small area of dilation can occur as a bolus of contrast is being swallowed. Serial radiography should show the bolus is traveling distally.
Ultrasonography of the Normal Feline Esophagus
Figure 292-29 Sonogram of a cat presented for removal of choleliths in the gall bladder. Radiographs (see 292-15A) showed the choleliths and a mass caudal to the stomach. A peripancreatic mass (arrows) was removed surgically. DUOD, duodenum.
Imaging of the Feline Esophagus and Gastrointestinal Tract Radiography of the Normal Feline Esophagus • The normal esophagus blends into other fluid opaque structures in the neck and dorsal mediastinum. Portions of the esophagus may be visible because of normal air or fluid that is being swallowed. Serial radiography should show a change in opacity as the air or fluid travels down the esophagus. • Radiopaque ingesta may also indicate the location of the esophagus.
Radiography of the Normal Feline Esophagus • The normal thoracic esophagus blends into other fluid opaque structures in the dorsal mediastinum. Portions of the esophagus may be visible because of normal air or fluid that is being swallowed. Serial radiography will show a change in opacity as the air or fluid travels down the esophagus. • Radiopaque ingesta may also indicate the location of the esophagus.
Esophagography • Barium paste is used for routine examination of the esophagus because it provides optimal coating of the esophagus. • However, barium paste is thick, and therefore, should not be used if aspiration is likely. • A “barium burger” (a mixture of liquid barium and canned food) can be used after barium paste to evaluate how solids are handled. • Nonionic water soluble iodinated products provide poorer coating of the esophagus than barium but are more likely to show a small perforation. • Liquid barium coats the esophagus better than liquid iodinated products but not as well as barium paste. Liquid barium is more likely to flow around esophageal foreign bodies than barium paste. • The main complication associated with esophagography is aspiration. Barium is inert and does not usually create problems when a small amount is aspirated. A large amount placed with a stomach tube is likely to be lethal. • Ionic water-soluble iodinated products can cause pulmonary edema when aspirated and should be avoided if aspiration is likely to occur (e.g., in cases in which there is radiographic evidence of alveolar disease that likely represents aspiration pneumonia).
• Endoscopic ultrasonography is not commonly done in cats. With conventional ultrasonography, the cervical esophagus is seen inconsistently and is a poorly defined structure. The thoracic esophagus cannot be seen because of air in the lungs. Visualization can be facilitated using an esophageal stethoscope in an anesthetized cat. If the cat is awake, the sonographer can watch for swallowing. In transverse images, the esophagus has a hyperechoic, star-shaped center caused by intraluminal mucus and air.
Common Esophageal Lesions • Foreign bodies can be seen in survey radiography if they are radiopaque or if they are outlined by gas in the esophagus. Sharp foreign bodies present a risk for perforation. Chronic foreign bodies that distend the esophagus can cause pressure necrosis and may also result in perforation. Foreign bodies often cause a filling defect within the radiopaque contrast medium on esophagography. See Figure 292-30A. • If perforation of the esophagus is present, there may be air in the periesophageal cervical tissues, the mediastinum, or pleural space. Pleural effusion can also be present secondary to perforation of the thoracic esophagus. Nonionic iodinated contrast medium may show extravasation through a small tear. • Strictures can occur secondary to esophageal foreign bodies or other inflammatory conditions. Esophagography is useful to delineate the strictured area. See Figure 292-30B. • Esophagography can be performed to determine whether the esophagus is involved when a cranial mediastinal mass or caudodorsal opacity is seen in the thorax. • Megaesophagus (see Figure 292-31) can occur as a congenital problem or may be acquired. On esophagography, there is an enlarged contrast-filled esophagus. • Vascular ring anomalies (see Figure 292-32) may cause dilation of the esophagus cranial to a constricted area caused by the anomaly. Dilation caudal to the constriction may also be present. In persistent right aortic arch, the trachea may be displaced to the left by the right aortic arch. The right aortic arch may appear as an area of increased opacity. • Regurgitation due to an esophageal problem can result in aspiration pneumonia. Thoracic films should be evaluated for evidence of alveolar disease. • Motility problems that result in dysphagia can be difficult to diagnose. See Figure 292-33. Fluoroscopy can be helpful in these cases.
Radiography of the Normal Feline Gastrointestinal Tract • The normal feline stomach has been described as “J-shaped.” The pylorus is located on the midline or just to the right of the midline. • The diameter of the normal small intestine should be less than twice the height of the middle of the body of the fourth lumbar vertebra.
797
SECTION 6: Imaging
(A)
(A)
(B) Figure 292-30 A, Esophagography on a mixed breed cat showing retention of barium caused by a porous foreign body in the thoracic esophagus. Arrows indicate the abnormal region of esophagus. A normal fish bone pattern is seen in the caudal thoracic esophagus. B, Lateral projection showing esophagography on a kitten presented for regurgitation and previous episodes of aspiration pneumonia. An esophageal stricture was diagnosed by a barium swallow and endoscopic examination of the esophagus.
(B) Figure 292-32 Esophagography on a 3-month-old cat with regurgitation. There is a constriction (arrow) in the area of a vascular ring anomaly. Note that these cases typically have enlargement of the esophagus cranial to the constriction; enlargement caudal to the constriction may also be present. A,Lateral projection. B, Ventral-dorsal projection. Figure 292-31 A cat was presented with a history of regurgitation. Survey radiography showed increased opacity in the cranial mediastinum. Esophagography confirmed megaesophagus. Motility was decreased cranial to the heart base but was normal more caudally.
• A variable amount of gas outlines the mucosal surfaces. Fat allows visualization of serosal surfaces. • The normal colon is smoothly marginated. The cecum is shaped like a comma.
798
Upper Gastrointestinal Series (“Barium Series”) • Barium should not be used if perforation is suspected; an iodinated product should be used instead. If aspiration is also a concern, a nonionic iodinated product should be chosen. • Liquid barium sulfate (30% weight/volume of micropulverized barium solution) is recommended for routine use in cats. Barium creates a better study than water-soluble iodinated products because there is optimal coating of the mucosa. Also, barium does not become
Imaging: The Abdomen
Figure 292-33 Esophagography on a 6-month-old kitten presented with generalized weakness and ataxia. Decreased motility was seen in the proximal two thirds of the esophagus.
•
•
•
•
•
•
diluted because it is isotonic to blood unlike ionic iodinated contrast media. Barium is inert, inexpensive, and is not absorbed. In some cases, there may be alleviation of clinical signs following the use of barium. Barium is contraindicated if perforation is suspected because it causes severe peritonitis. Aspiration of small amounts of barium does not usually cause clinical problems, but barium will remain visible in subsequent radiography of the thorax. Barium has a slower transit time than iodinated products. Iodinated contrast media are less commonly used because they cause poorer coating of the mucosa. Vomiting is a common side effect in cats especially when ionic products are used. Ionic products are hypertonic and may cause dehydration or hypovolemic shock. Hypertonicity also leads to dilution of the contrast degrading the quality of the study. Ionic products should not be used if aspiration is likely because hypertonicity can result in pulmonary edema. These problems can be alleviated by the use of nonionic rather than ionic iodinated products. Iodinated products should be used if perforation of the intestine is likely (e.g., when sharp or string foreign bodies are suspected or if there is poor serosal detail). Iodinated contrast media have a shorter transit time than barium and may be preferred if faster results are needed. Administration of sedation can adversely affect motility and alter the appearance of the upper gastrointestinal series. Nevertheless, sedation may be necessary in some individuals. Sedation with ketamine and diazepam or with acepromazine has been recommended for these patients. Pneumogastrography can be performed by placing a stomach tube with the tip in the stomach and injecting room air. Enough air is injected with a syringe to mildly distend the stomach. This procedure is useful to positively identify the stomach or to outline gastric foreign bodies. Double contrast gastrography can be useful for identifying ulcers and neoplasia. Fasting is necessary to ensure an empty stomach, thereby avoiding artifactual filling defects in the barium contrast medium. A small amount of barium is administered followed by inflation of the stomach with a syringe. Foreign bodies, ulcers, and masses may be coated with barium or outlined with gas using this technique. Iodinated contrast media can be injected into gastrostomy tubes. With correct placement, contrast will be seen entering the intestine. If the gastrostomy tube is abnormally located, contrast will enter the peritoneal cavity giving an appearance similar to that seen with gastrointestinal perforation. See Figure 292-34. Barium impregnated polyethylene spheres (BIPS) can also be used to examine the gastrointestinal tract for possible obstruction and to assess motility. These spheres can be given with food but have the disadvantage of providing no information about the mucosal surface.
Figure 292-34 Iodinated iodide contrast medium instilled into a gastrotomy tube to check for correct placement of the tube. Iodide contrast can be seen extravasating into the peritoneal cavity. Barium should never be used for this procedure because it causes severe, usually fatal, peritonitis.
• On ventrodorsal view of a normal barium series (see Figure 292-35), the cat’s stomach takes the shape of a “J.” The pylorus is positioned either on or to the right of the midline. • On the right lateral recumbent view, barium fills the pylorus. On the left lateral recumbent view, air may be present in the pylorus. • Segmental contractions give the duodenum a “string of pearls” appearance in approximately 30% of cats. This appearance can occur in dogs but is more pronounced in cats. • Barium usually reaches the colon in 30 to 60 minutes. Most should be in the colon by 90 minutes. • The cecum of the cat is comma shaped whereas the dog’s cecum has a corkscrew shape (“pig’s tail”).
Pneumocolography • Pneumocolography (see Figure 292-36A) can be used for diagnosis of ileocolic intussusception, identification of the colon, especially where there is a distended loop that could be either small or large intestine, and screening for strictures. Care should be taken to avoid overreading of narrowed areas, which may be due to normal contraction. • This procedure is preferred over the barium enema (see Figure 29236B) because the latter requires extensive preparation and anesthesia. Pneumocolography is performed by simple injection of room air into the rectum using a conventional syringe.
Ultrasonography of the Feline Gastrointestinal Tract • Both transverse and longitudinal images should be obtained. Regional lymph nodes and the vascular supply should be examined. Doppler ultrasonography is helpful if available.
799
SECTION 6: Imaging
(A)
(C)
(B) Figure 292-35 Normal upper gastrointestinal series. A, Lateral projection 15 minutes after administration of oral barium solution. The “string of pearls” appearance of the duodenum (arrows) is normal. Normal contractions can be differentiated from the “accordion-like” appearance caused by linear foreign bodies by checking for symmetry. The normal appearance is symmetrical. B, Ventral-dorsal projection of the cat in 292-34A, 15 minutes after administration of oral barium solution. C, Barium has reached the colon and can be seen in the comma-shaped cecum (arrow). Little contrast remains in the stomach. LK, left kidney.
• Gastrointestinal walls, contents, and motility should be evaluated. The appearance varies with degree of distension and contents. • A higher resolution, 7.5- to 12-MHz transducer is preferred. • Scanning is best after fasting and before enema (less gas but one study found no difference). A previous barium study will not interfere with ultrasonography unless considerable air is given with the barium contrast. • The gastrointestinal tract has five “layers” that are visible with ultrasonography (see Figure 292-37): • Inner hyperechoic = mucosal-luminal interface • Inner hypoechoic = mucosa
800
• Central hyperechoic = Submucosa (poorly defined, extends into rugae) • Outer hypoechoic = muscularis propria • Outer hyperechoic = subserosa, serosa • Wall measurements should be made from the outside edge of the serosa to the outside edge of the mucosal-luminal interface. • Gas is hyperechoic and strongly reflective. Reverberation artifact obscures visualization of structures deep to the gas. Both the mucosalluminal interface and gas are hyperechoic so that no interface is apparent between them.
Imaging: The Abdomen
(A)
(B) Figure 292-36 Colon Studies: A, Ventral-dorsal projection showing pneumocolography on a 6-year-old mixed-breed cat with a history of chronic vomiting. The colon and cecum are distended with gas. Black arrow, cecum; white arrows, ascending colon; DC, descending colon, TC, transverse colon. B, Barium enema: This barium enema clearly shows a distended cecum (C) and colon in a cat with megacolon. The junction of the ileum and cecum (arrow) can be seen. • Luminal fluid is anechoic or hypoechoic and allows visualization of deeper structures. The mucosal-luminal interface appears as a separate layer. A large amount of luminal fluid may result in acoustic enhancement of deeper tissues. • An empty stomach has a “star-shaped” or “wagon wheel” appearance because of gas and ingesta between the rugal folds. Submucosa extending into rugal folds is also hyperechoic. • The thickness of the stomach is highly variable depending on degree of distension. The mucosal layer is the thickest layer. • The thickness of the gastric wall varies depending on the degree of distension and the placement of the calipers (between rugal folds or on a rugal fold). In one study, thickness of the normal gastric wall was 2 mm between rugal folds and 4.4 mm at the rugal folds. • The ileum has a more prominent wall and may be thicker than other segments of small intestine. There is a prominent hyperechoic submucosa and a hypoechoic, almost anechoic, muscularis. See Figure 292-38. Goggin and colleagues describe the terminal ileum as having a wagon wheel appearance in transverse section. In the area of the ileocolic junction, the mucosa projects into the lumen. • The small intestine should be “sampled” at multiple sites in the abdomen. In a recent study, the difference between wall thickness of
•
•
• •
the duodenum and jejunum was not statistically significant in cats, unlike dogs. The degree of distension also affects the thickness that averages 2.1 mm. The wall of the large intestine is thinner than that of the small intestine (averaging 1.7 mm) because the mucosa is thinner. See Figure 292-37C. The colon usually contains a large amount of gas so that the colon is characterized by obvious reverberation artifact, sometimes referred to as a “dirty acoustic shadow.” Close observation reveals the thin near wall. Occasionally, fecal material and the far wall will be visualized. The normal stomach and proximal duodenum have 4 to 5 contractions per minute. The small intestine in the central abdomen has one to three contractions per minute. Contractions are not often seen in the large intestine.
Gastrointestinal Foreign Bodies • Gastrointestinal foreign bodies occur commonly and are not always associated with clinical signs. Foreign bodies located in the pyloric region of the stomach are more likely to result in vomiting than
801
SECTION 6: Imaging
(A)
(A)
(B) (B)
Figure 292-38 Longitudinal (A) and transverse (B) sonograms of the normal ileum. The ileum has a prominent hyperechoic submucosa and a hypoechoic, almost anechoic, muscularis layer. The ileum may be thicker than other segments of small intestine. Arrows indicate the muscularis layer.
•
•
(C) Figure 292-37 A, Longitudinal sonogram showing the normal stomach of a cat. The stomach is empty and has a “wagon-wheel” appearance. The layers are similar to those of the small and large intestine. B, Longitudinal sonogram showing the normal small intestine of a cat. The wall measured 0.34 cm in thickness. 1, serosa (hyperechoic) of the near wall; 2, muscularis mucosae (hypoechoic) of the near wall; 3, submucosa (hyperechoic) of the near wall; 4, mucosa (hypoechoic) of the near wall; 5, mucosal/ luminal interface of the near wall + muminal contents + mucosal/luminal interface of the far wall (merge to form a single hyperechoic band); 6, mucosa (hypoechoic) of the far wall; 7, submucosa (hyperechoic) of the far wall; 8 = muscularis mucosae (hypoechoic) of the far wall; 9 = serosa (hyperechoic) of the far wall. C, Longitudinal sonogram showing the normal colon. The wall layers are the same as those for the small intestine, but the mucosa is much thinner. Only the near wall can be seen in this image. When gas is present, reverberation artifact prevents visualization of the far wall.
802
•
•
foreign bodies located elsewhere in the stomach. The presence of a foreign body does not exclude a metabolic cause of vomiting. Some foreign bodies will be of metal or mineral opacity and will be readily apparent on radiographs. See Figure 292-39. Some (such as corncobs) may trap gas and have a characteristic appearance. Some may be fluid opaque but may be outlined by gas. See Figure 292-40A. In other cases, the foreign body may not be visible, but its presence is indicated by dilation or corrugation of bowel. See Figure 292-40B. Linear foreign bodies (see Figure 292-41) include string, thread with or without an attached needle, ribbon, yarn, Easter basket grass, and Christmas tree tinsel. Intestinal loops are described as being gathered along the foreign object in an accordion-like fashion. There is a real danger of perforation because a linear foreign body can cut into the mesenteric side of the intestine. In one study (Felts et al.), three or more eccentric bubbles of gas tapered at one end were considered diagnostic of linear foreign body. Free gas or fluid suggests that perforation has occurred. Perforation is most commonly associated with linear foreign bodies, sharp foreign bodies, or chronic obstruction that has resulted in pressure necrosis. Barium should never be used if perforation is suspected. Water soluble iodine (preferably non-ionic) should be used in these cases if confirmation is needed before surgery. Contrast helps to show the gathered, accordion-like appearance of the intestine. See Figure 292-42.
Imaging: The Abdomen
(A)
(A)
(B)
(B) Figure 292-40 Some foreign bodies are visible because of air surrounding the foreign body. A, Lateral projection showing a hairball (arrows) in a cat’s stomach outlined by gas. B, Some foreign bodies are not visible radiographically, but dilation of the intestines is apparent indicating mechanical ileus. A dilated loop of small intestine (arrows) indicates obstruction that was caused by an acorn foreign body.
(C) Figure 292-39 Some gastrointestinal foreign bodies are radiopaque. A,Lateral radiograph of a cat that had eaten the owner’s shoelaces. The shoelaces are visible as radiopaque foreign bodies in the colon. B, Radiograph of the shoelaces found in the feces. C, Lateral radiograph of a kitten show a metallic fish hook protruding from the rectum.
• A small amount of barium can be used to coat gastric foreign bodies. • An upper gastrointestinal series can be used to identify gastrointestinal foreign bodies in the stomach or intestine. Some foreign bodies might show as a filling defect or obstruction might be apparent. See Figure 292-43. Porous foreign bodies (such as fabric and hairballs) might absorb barium and become visible after most of the barium has passed distally. See Figure 292-44. • Foreign bodies may not be obvious on ultrasonography particularly if a lot of gas is present. Prior radiography can be useful to identify
suspicious areas of intestine. Scanning from underneath the animal can help to avoid gas. • Foreign bodies in the stomach or intestine may create a distinct black or “clean” acoustic shadow unlike the “dirty” acoustic shadow that occurs because of gas. The composition of the foreign body will cause a variable amount of sound to be transmitted or reflected, however. For example, some rocks will have a reflective near interface. These present with a hyperechoic near border and a clean deep acoustic shadow. Some rubber toys will attenuate sound with minimal reflection. These will not exhibit a hyperechoic near border but will cause acoustic shadowing. The shape of the near interface can help identify an object. See Figure 292-45. An acorn might have a semicircular near interface. The shape of the entire object might be apparent if there is enough transmission of sound. Hairballs can create an irregular hyperechoic interface and strong acoustic shadowing. • When obstruction is present, the intestine may be dilated with a thinned wall and reduced motility. See Figure 292-45.
803
(A)
(B) (C) Figure 292-41 Linear (string) foreign body. Gathered loops of small intestine are seen on both the lateral (A) and ventral-dorsal (B) projections. The gathered loops were also visible on ultrasonography (C). During real-time ultrasonography, hyperechoic linear structures could be seen in the lumen. Linear foreign bodies are frequently hyperechoic.
(A)
(B)
Figure 292-42 Lateral (A) and ventral-dorsal (B) projections showing a barium upper gastrointestinal series on a cat that had swallowed yarn. The barium passed all the way to the colon but the jejunum has a three-layered appearance suggesting uptake of barium by remaining yarn. Water soluble iodinated contrast media should be used instead of barium if gastrointestinal perforation is suspected.
804
Imaging: The Abdomen
(A) (A)
(B) Figure 292-43 Barium upper gastrointestinal contrast study on a cat with a duodenal foreign body. Radiographs were made 18 hours after oral administration of barium. The stomach is distended. Barium remains in the stomach and proximal duodenum. A, Lateral projection. B, Ventral-dorsal projection.
• Linear foreign bodies can cause the intestine to become gathered in an accordion-like fashion. On ultrasonography, the bowel may appear plicated; the foreign body is usually hyperechoic. See Figure 292-41C. • Ultrasonography can reveal free air or fluid indicative of perforation. Reverberation artifacts or “comet tails” between the nondependent abdominal wall and organs such as the liver or stomach are characteristic of free gas. In one study, cats with perforation also had changes that included regional bright mesenteric fat, fluid in the peritoneal cavity, fluid-filled stomach or intestines, loss of wall layering, regional lymphadenopathy, reduced motility, pancreatic changes, and corrugated bowel.
Gastric Dilatation and Volvulus • Although gastric dilatation and volvulus (GDV) is commonly considered to be a problem of large breed dogs, both dilatation and volvulus (torsion) can occur in cats.
(B) Figure 292-44 Barium upper gastrointestinal contrast study on a cat with a history of anorexia and vomiting. Barium can be seen in the colon but also is retained in the stomach. Retention of barium in this manner is usually due to a porous foreign body such as cloth. (A) Lateral projection. (B) Ventral-dorsal projection.
• In a study by Bredal and colleagues, 5 of 10 cats with gastric dilatation had gastric torsion; 5 had simple dilatation. Three of the 10 cats (2 with gastric torsion, 1 with dilatation) also had diaphragmatic hernia. • Radiographs show a distended, gas-filled stomach. When torsion is present, the pylorus may be displaced dorsally and cranially in the lateral view and toward the left side in the ventrodorsal view. See Figure 292-46. The right lateral recumbent view has been shown to be helpful in dogs. In this view, the pylorus should be fluid opaque and located ventrally. With torsion, the pylorus (if rotation causes the pylorus to become located dorsally on the left side) will be gas-filled and located dorsally. • Contrast radiography is usually not necessary or desirable.
805
SECTION 6: Imaging
(A)
(B)
(D) (C) Figure 292-45 Sonograms of the cat with intestinal obstruction shown in Figure 292-40B. Obstruction was caused by an acorn. A, The acorn had a curved hyperechoic surface and exhibited deep acoustic shadowing. B, The small intestine was dilated and fluid-filled proximal to the acorn (arrows). C, The acorn was removed from the intestine. D, A radiograph obtained after removal of the acorn shows that the acorn is fluid opaque.
Infiltrative Diseases Including Neoplasia • Infiltrative disease includes neoplasia as noted previously, mycosis, and plasmacytic-lymphocytic enteritis. • Lymphoma is the most common intestinal neoplasm in cats. Siamese cats are overrepresented in cases of adenocarcinoma. • On survey radiography, a thickened gastric wall and abnormal gas pattern can occasionally be seen with gastric neoplasms, See Figure 292-47. Care must be taken to avoid confusing a thickened gastric wall with a gas bubble superimposed over a fluid-filled stomach. In some cases, the mass may protrude into the lumen and become outlined by gas. See Figure 292-48. Gastrointestinal neoplasia is not always apparent on survey (or even contrast) radiography. • On an upper gastrointestinal series, there may be a filling defect or mural thickening. Pyloric outflow obstruction may occur when the neoplasm involves the pylorus. • Sonographic signs include thickening of the gastric wall and alteration of echogenicity. Although most gastric neoplasms (see Figure 292-47) are hypoechoic, some are hyperechoic or have variable echogenicity. See Figure 292-48. Frequently, there is destruction of normal wall layers (especially when neoplasia is advanced). This is termed loss of wall layering.
806
• The gastric wall should be imaged in more than one plane to ensure that a normal collapsed gastric wall is not mistaken for neoplasia. • A fluid opaque mass can sometimes be seen with intestinal masses and some intestinal masses will cause obstruction. The most common intestinal neoplasms are lymphoma, mast cell tumor, and adenocarcinoma. A mass can be seen on radiographs in about 40% of these cats. Mineralization may occur in some neoplasms and may be visible on survey radiography. See Figures 292-49 and 292-50. • On contrast radiography, infiltrative diseases can cause irregular size (i.e, narrowing or dilation) of the lumen and irregularity of the mucosal surface. • On ultrasonography of intestinal neoplasia (see Figure 292-51), the most significant sign is a loss of wall layering. Thickening that may be asymmetric, decreased echogenicity, and localized lymphadenopathy are other important signs. Suspected intestinal masses should be examined in multiple planes and traced back to normal intestine. Mesenteric lymph nodes should be examined for evidence of involvement. • Rarely, neoplasms can result in perforation and the presence of gas or intestinal contents in the peritoneal cavity. Sonographic signs of free gas are discussed aforementioned.
Imaging: The Abdomen
Figure 292-47 Radiograph of the stomach of a cat with a gastric wall mass is compared to a sonogram showing the thickened gastric wall. The irregular gas bubble in the stomach allows the thickened gastric wall to be visualized radiographically.
• Surgical or fine-needle biopsy may be necessary for definitive diagnosis.
(A)
Intestinal Trauma • Trauma to bowel can occur from such things as encounters with cars and dogs. • Free fluid or gas can indicate perforation as noted previously. Small tears may not be radiographically apparent and may require diagnostic peritoneal lavage to be confirmed. • Gas can be seen in the gastrointestinal wall after trauma or as an incidental finding. See Figure 292-52. Although gas frequently resolves spontaneously, the abdomen should be monitored because perforation can occur if the gastrointestinal wall is severely compromised. On ultrasonography, reverberation artifact caused by gas will be seen originating from the wall of the stomach or bowel rather than from the lumen. • Abdominal radiographs may be normal, and clinical signs may be delayed with severe crushing injuries to bowel. • In cases of suspected perforation, iodinated contrast agents should be used. Although there are ionic iodinated products designed particularly for gastrointestinal use, nonionic iodinated products are preferred if the cat is debilitated or dehydrated. Extravasation of contrast into the peritoneal cavity confirms perforation. The contrast shows as increased opacity highlighting serosal surfaces.
Pyloric Outflow Obstruction
(B) Figure 292-46 A, The stomach of this cat was dilated following removal of a gastric hairball. The stomach is positioned normally as can be seen in the ventrodorsal projection. B, Ventral-dorsal projection of a cat with gastric torsion. Radiographs revealed marked distension of the stomach with malpositioning of the pylorus on the left side of the abdomen. Surgery confirmed gastric torsion. Courtesy of Shelley Merbitz, Furr Angels website (http://www.furr-angels.com/ gastricdv.htm) and Dr. Lee Bolt (Sweeten Creek Animal and Bird Hospital, Asheville, NC).
• Obstruction at the pylorus can be seen secondary to gastric foreign body, neoplasia, inflammation, or hypertrophy. Congenital pyloric stenosis can also occur. • Radiography may reveal a large fluid-filled stomach with a variable amount of gas. • An upper gastrointestinal series can be performed to confirm delayed gastric emptying. Barium is commonly used and can help confirm the presence of a foreign body or neoplasm as noted previously. • Ultrasonography may also be helpful in recognizing retention of fluid in the stomach, reduced motility, and the presence of a mass or foreign body. See Figure 292-53.
807
SECTION 6: Imaging
(A)
(A)
(B)
(B)
Figure 292-49 A, Lateral radiograph of the abdomen of a cat with a 1-month history of weight loss and anorexia showing mineral opacity (arrow) associated with an intestinal loop. B, Ultrasonography confirmed that the mineral was located within the intestinal wall. A loss of wall layering is also present.
Figure 292-48 A, Ventral-dorsal radiograph of the abdomen of a 12 year-old American domestic shorthair. The abnormally thickened gastric wall (arrows) could be seen as it protruded into the gastric lumen. B, On ultrasonography, the gastric wall (arrows) is greatly thickened, mildly hyperechoic, and exhibits a loss of wall layering. Gas in the lumen is hyperechoic with reverberation artifact causing acoustic shadowing. The diagnosis was B-cell lymphoma.
Ileus • Ileus can be functional (see Figure 292-54) occurring as the result of trauma or inflammation in or surrounding the intestine. Pancreatitis is frequently associated with decreased motility in the adjacent bowel. • Mechanical ileus is present when there is physical obstruction of the bowel. Etiologies include intestinal foreign body, neoplasia, volvulus, and intussusception. • The classical sign of obstruction is dilation of the intestine proximal to the source of the obstruction. It may not always be possible to identify the cause of the obstruction and determining which part of the bowel is proximal may be problematic.
808
Figure 292-50 Ultrasonography of the cat in Figure 292-2 shows that the mineral opacity (arrowhead) seen on radiographs is located within the wall of the colon. The colon wall (arrows) is greatly thickened and exhibits a loss of wall layering. Adjacent colon (pictured on the left side of the image) is normal.
Imaging: The Abdomen
(A) (A)
(B) Figure 292-51 A, Sonogram showing a concentric mass involving the intestine of a cat with a history of weight loss. The intestinal wall is hypoechoic and exhibits a loss of wall layering. B, Mesenteric lymph nodes were mildly enlarged and hypoechoic. LN, lymph node.
• The terms stacked bowel and hairpin turns have also been used to describe the manner in which dilated loops of bowel appear in the abdomen. • An upper gastrointestinal series using barium can be performed to confirm obstruction. There may be persistent dilation in the area of ileus. Barium may fill proximal loops and stop abruptly at the area of obstruction. The source of obstruction could create a filling defect in the barium contrast or may be outlined by barium. Porous foreign bodies can retain barium and may be visible once other portions of the bowel have emptied. The use of BIPS has also been recommended for detection of obstruction. • Sonographic signs include distension of the lumen and thinning of the gastrointestinal wall. Segmental contractions are decreased or absent. The cause of obstruction (e.g., foreign body or neoplasia) might be apparent. Plication of bowel might be apparent with string foreign bodies.
Inflammatory Bowel Disease • Inflammatory Bowel Disease (IBD) is a condition causing chronic enteritis. Various types of inflammatory cells can infiltrate the intestinal wall. See Chapter 120.
(B) Figure 292-52 Radiographs of a cat with pneumatosis coli. Gas (arrows) can be seen in the wall of the colon. Air in wall of the gastrointestinal tract may resolve spontaneously, but rupture can also occur. These patients should be surgically explored or monitored carefully. A,Lateral projection. B, Ventral-dorsal projection.
• In one study (Baez et al.), all nine cats had normal survey radiographs. An upper gastrointestinal series in two of three cats showed a slightly irregular wall. • In the absence of ulceration, inflammation may cause little or no changes on an upper gastrointestinal series. Nonspecific changes include irregularity of the contrast column, lack of uniformity of the contrast column, and mild narrowing of the contrast column.
809
SECTION 6: Imaging
Figure 292-53 Sonogram of a cat that presented with a 4-month history of vomiting and an acute onset of diarrhea of 3 days’ duration. A hyperechoic mass is seen in the area of the pylorus. Normal duodenum is seen distal to the mass. Ultrasound-guided aspiration was performed, and cytology revealed mast cells in the mass and in adjacent lymph nodes. A bypassing gastro-duodenostomy (Jaboulay anastomosis) was performed 2 cm distal to the mass. Histologic diagnosis was fibroplasia with well-differentiated mast cells and eosinophils, consistent with feline gastrointestinal eosinophilic sclerosing fibrosis.
Figure 292-55 Sonogram of a 10-year-old American domestic shorthair with inflammatory bowel disease. The wall of the intestine is thickened between the calipers and exhibits altered wall layering.
• Lymphoma of the spine can cause neurological problems in this area and also result in obstipation. • Strictures secondary to neoplasia or inflammation can obstruct defecation. Pelvic fractures can also cause obstruction. • Other causes include congenital disease and parasitic infection with trypanosomes. • On radiographs, the colon will be distended with a large amount of fecaloid material that has increased opacity. See Chapter 136. • Strictures might be visible on survey radiography, pneumocolography, or after administration of a barium enema. Radiography should include the pelvis and pelvic canal. • There may be other evidence of neurological disease, such as enlargement of the urinary bladder because of problems with micturition. Alternatively, the urethra can be compressed by a obstipated colon causing obstruction and bladder distention.
Intussusception
Figure 292-54 Lateral radiographs of a cat with a 6-month history of gas distended intestines and constipation. The intestines are gas-filled and moderately distended. The cause of generalized ileus was not determined. • Studies show that ultrasonographic findings correlate better with histological grade than endoscopic or radiographic findings. • Sonographic findings include poor intestinal wall definition, focal thickening, enlarged mesenteric lymph nodes, and decreased echogenicity of mesenteric lymph nodes. See Figure 292-55. The mucosa can be abnormally hypoechoic or hyperechoic and may be infolded. There may be a diffuse increase in wall echogenicity. The muscularis may be thickened. • Although a loss of wall layering is usually associated with neoplasia, severe inflammation and necrosis can also result in altered wall layering or a loss of wall layering. • Biopsy is necessary to rule out other causes of disease. • Inflammation may also occur associated with parasites, uremia, pancreatitis, ingestion of toxins or chemicals, or other disease.
Obstipation and Megacolon • Obstipation is usually a sign of megacolon, a disease of the colonic muscle. See Chapter 136.
810
• Intussusception can involve invagination of any part of the gastrointestinal tract into another including stomach into esophagus, small intestine into small intestine, ileum into colon, or colon into colon. Complete or partial obstruction can occur. • Gastroesophageal intussusceptions cause displacement of the stomach into the esophagus. On survey radiographs, the stomach shows as a fluid or gas opacity in the esophagus but rugal folds are not always visible. Barium can be used to confirm that the stomach has become abnormally located. • Ileocolic and small intestinal intussusceptions are most common. A mass effect might be apparent. Distension of small intestine with gas or fluid might be seen proximal to obstruction caused by the intussusception. • On an upper gastrointestinal series, the intussusceptum (the portion of the bowel telescoped into another loop) appears as a filling defect. • Pneumocolography might be helpful to outline ileocolic intussusception (ileum within colon). With ileocolic intussusception, air fills the colon (the intussuscipiens) and the ileum (the intussusceptum) is fluid opaque. • On ultrasonography, the presence of intestine telescoped within another loop of intestine causes the appearance of alternating hyperechoic and hypoechoic lines (i.e., concentric in transverse images and parallel in longitudinal images). The appearance varies with the luminal contents of the bowel, the degree of edema in the intestinal wall, and the imaging plane used. A “bull’s eye” appearance might be seen in transverse images.
Imaging: The Abdomen
Strictures of the Colon • A stricture may show as a narrowed region outlined by air. This appearance should be repeatable in several films to ensure that the narrowed region is not artifactual (e.g., due to contractions). Ultrasonography could be performed for further evaluation.
Imaging of the Adrenal Glands Normal Feline Adrenal Glands • Each adrenal gland is an oval structure located cranial to the ipsilateral kidney adjacent to the caudal vena cava. The phrenicoabdominal vessels are closely related to the ipsilateral adrenal gland with the artery passing dorsal and the vein passing ventral to the adrenal gland. • About 30% of older cats have dystrophic mineralization of the adrenals without abnormal clinical signs. • Normal adrenal glands are not usually visible radiographically. Even mineralization is not always recognizable radiographically. • On ultrasonography, the adrenal glands are oval, hypoechoic organs. The central portion may be more echoic than the central region. In our lab, feline adrenal glands commonly measure 3 to 4 mm in width and 10 to 13 mm in length. • The left adrenal gland is easily imaged with the cat in right lateral recumbency with the probe on the left side of the abdomen angled so that the beam passes in a ventrolateral-dorsomedial direction. The left adrenal gland is found cranial to the left kidney or the left renal artery. • See Figure 292-56. • The right adrenal gland can also be found with the cat in left lateral recumbency, and the probe is placed on the right side. The right adrenal gland is best found by first locating the right kidney and caudal vena cava in the sagittal plane and then scanning in a sagittal plane between the caudal vena cava and the right kidney. The right adrenal gland will be cranial and medial to the right kidney, closely associated with the caudal vena cava. • Mineralization is hyperechoic with deep acoustic shadowing. See Figure 292-57B. • Both adrenal glands are usually located more cranially than the respective adrenal gland in a dog.
Adrenal Gland Masses • Adrenal masses are uncommon in cats. Adenomas, carcinomas, and pheochromocytomas have been reported. • On radiography, a soft-tissue opacity cranial and medial to a kidney suggests the presence of an adrenal gland mass. See Figure 292-57. Some masses will contain areas of mineralization. • Many adrenal masses are too small to be radiographically apparent. A mass with variable size and echogenicity is apparent on ultrasonography. The caudal vena cava and adjacent tissues should be examined for evidence of local invasion.
(A)
(B) Figure 292-56 A, Sonogram of a normal adrenal gland. They are typically hypoechoic and oval in shape. They may be more hyperechoic centrally. They usually measure about 10 to 13 mm in length and 3 to 4 mm in width. B, Mineralization of the adrenal gland is common in older cats without clinical signs. In this sonogram of an older cat, the mineralized right adrenal gland is seen adjacent to the caudal vena cava (CVC). The adrenal gland is hyperechoic with deep acoustic shadowing. Calipers have been placed to measure the adrenal gland.
• The normal cat kidney is about 2.4 to 3.0 times the length of the second lumbar vertebra. • Normal kidneys are fluid opaque, smoothly marginated, and surrounded by fat.
Enlarged Adrenal Glands
Use of Excretory Urography
• Hyperadrenocorticism (Cushing’s Disease) occurs in cats but less commonly than in dogs. One or both adrenal glands may be affected. Enlargement with pituitary dependent hyperadrenocorticism tends to be less severe than enlargement caused by primary adrenal neoplasia. See Chapter 101.
• Ionic or nonionic contrast media can be given IV for evaluation of the kidneys and ureters. The newer nonionic contrast media have fewer side effects because they have a lower osmolality (are less hypertonic) than ionic contrast media, and they do not dissociate into ions. These media also appear to have reduced chemical toxicity and are less likely to cause allergic reactions. • Vomiting is a common complication in cats. • Other complications include dehydration, pulmonary edema, allergic reaction, and contrast induced renal failure. • Persistence of a nephrogram (see Figure 292-58) with absence of a pyelogram is indicative of renal failure, which could be contract induced. Intravenous fluids and diuretics should be given.
Imaging of the Kidneys Radiography of the Normal Feline Kidney • Feline kidneys are more moveable than those of dogs. The cranial pole of the right kidney is not buried in the liver as is the case in dogs.
811
SECTION 6: Imaging
(A)
(B)
(C) Figure 292-57 A, Lateral radiograph of a cat presented for cardiac disease. A somewhat circular fluid opacity (arrows) can be seen dorsally cranial to the kidneys. The mineral opacity (black arrowheads) is caused by dystrophic calcification of fat (Bates body). B, Ventrodorsal radiograph showing the fluid opacity (arrows) cranial to the right kidney. Ultrasonography showed that the opacity was an adrenal gland mass. C, Sonogram showing the adrenal gland mass with calipers placed for measurement. Color-flow Doppler imaging was turned on to evaluate blood flow.
Normal Findings on Excretory Urography
Ultrasonography of the Normal Feline Kidney
• There are four phases in a normal excretory urogram. • The arteriogram phase is not usually seen and is present briefly while iodine is in the arterioles and arteries. • The nephrogram phase starts immediately, is quickly at maximal opacity, and gradually fades over 1 to 3 hours. It occurs whereas iodinated contrast is in the proximal renal tubules. • The pyelogram phase begins within a few minutes of the injection of contrast and has maximal opacity during the initial 20 minutes. Contrast is present in the renal diverticula and pelvis and the ureter. • The cystogram phase begins when contrast becomes visible in the urinary bladder. The nephrogram and pyelogram phases are still visible. • Compression with a band around the abdomen just caudal to the kidneys (over the ureters) improves visualization of the renal diverticula and pelvis. The diverticula are usually less than 1 to 2 mm; the proximal ureter measures less than 2 to 3 mm. • Ureteral peristalsis causes the line of contrast in the ureters to appear interrupted.
• Ultrasonography has the advantage over excretory urography in that it is non-invasive, there is no ionizing radiation, and the possibility of contrast reactions is avoided. Ultrasonography can be performed even when renal function is not present. Unlike cystography, the ureters or urethra do not have to be patent. In cases where excretory urography is needed, the prior use of contrast will not affect the quality of the sonogram. The general appearance of the feline kidney is similar to that described for dogs. • As with other organs, the kidney should be scanned in multiple planes. The plane of the mid-dorsal image corresponds to the plane in which a kidney is sectioned for pathologic examination. In middorsal images (see Figure 292-59A), the lateral border of the kidney is closest to the transducer and the renal hilus and hilar vessels are directed dorsally. • Longitudinal sagittal images have a variable appearance depending whether the plane of the beam is near the lateral or medial aspect of the kidney. In lateral sagittal images (see Figure 292-59B), the kidney has a “watermelon” appearance caused when the medulla is divided by the hyperechoic renal diverticula. The mid-sagittal image (see
812
Imaging: The Abdomen
there may be poor corticomedullary definition. Cellular material might be seen in the pelvis representing purulent debris or blood clots.
Large Kidneys: Hydronephrosis
Figure 292-58 Excretory urography 2 hours after administration of iodinated contrast medium. The right renal pelvis is dilated. There is a persistent nephrogram bilaterally.
Figure 292-59C) contains two parallel bars centrally. These represent the ventral and dorsal branches of the renal pelvis separated by the renal crest. In medial sagittal images (see Figure 292-59D), the cortex surrounds the less echogenic medulla, and the medulla appears as two hypoechoic circles separated by fat surrounding the renal pelvis. Transverse images are images made along the short axis of the kidney. In mid-transverse images, the renal pelvis appears as a hyperechoic C surrounding the renal crest (see Figure 292-59E). • The renal cortex should always be hyperechoic compared to the medulla. Increased fat in the renal cortical epithelium of cats increases cortical echogenicity. • Younger animals have better corticomedullary definition than older animals, and cats have better corticomedullary definition than dogs. • Normal kidneys measure approximately 3.8 to 4.4 cm. The size of the kidney can also be compared to the length of a vertebra measured sonographically or to the diameter of the abdominal aorta.
Small Kidneys • In cats with chronic renal disease (e.g., chronic interstitial or glomerular nephritis and chronic pyelonephritis), the kidneys tend to be small and sometimes irregular on both radiography and ultrasound. See Figure 292-60. Corticomedullary definition may be poor on ultrasonography. Compensatory hypertrophy may result in enlargement of one kidney when the other is missing or functioning poorly (or not at all). Excretory urography shows a normal nephrogram and pyelogram in the large kidney and variable abnormalities in the smaller abnormal kidney. Calculi are present in some cases. • Dysplastic kidneys are usually small and irregular with pyelectasia and poor or negligible corticomedullary definition. Cysts may be present, and it is sometimes difficult to recognize the kidney because of the abnormal appearance. Renal dysplasia has been reported in feti affected with panleukopenia. • Amyloidosis may be familial in Abyssinian and Siamese cats resulting in small kidneys. • Chronic pyelonephritis can also result in a small and irregular kidney. Excretory urography may reveal dilation of the renal pelvis and possibly the proximal ureter. Blood clots, cellular debris, purulent material, or calculi can cause filling defects. On ultrasonography,
• Hydronephrosis (see Figure 292-61) causes variable enlargement of the kidneys and is the result of partial or complete obstruction in the ureter or bladder. • Causes of obstruction include ureteral calculi, ureteral strictures, ectopic ureter, ureteral neoplasia (uncommon), neoplasia obstructing the trigone of the urinary bladder, and iatrogenic ligation of the urinary bladder. • On survey radiography, the kidneys are variably enlarged. Renal or ureteral calculi may show as opacities in the area of the kidneys or in the retroperitoneal space. • On excretory urography, the renal pelvis is dilated and the diverticula are distended with sharp margins. The ureter may also be dilated, and the source of obstruction may be visible distally. In severe hydronephrosis, the renal cortex may be reduced to a thin band surrounding a large pocket of fluid. This tissue band may increase in opacity during contrast radiography. The fluid-filled pelvis may not opacify if there is no remaining glomerular filtration. • On ultrasonography (see Figure 292-61C), the dilated pelvis will appear as an anechoic region separating borders of the pelvis. With severe hydronephrosis, the pelvis can become dilated until the cortex remains as only a thin hypoechoic shell surrounding a “bag” of anechoic or echogenic contents, which can be seen swirling around within the kidney on ultrasonography. (See Figure 292-62). Remnants of the pelvis will show as radiating hyperechoic lines.
Large Kidneys: Inflammation • Acute inflammation (including granulomatous nephritis caused by feline infectious peritonitis and pyelonephritis) can cause renal enlargement, but the kidneys may also appear normal on survey radiography. • Irregular margination may be present in some cases. • Pyelonephritis and mild hydronephrosis appear similar on excretory urography. The diverticula, pelvis, and proximal ureters are variably dilated. The diverticula tend to appear sharper with hydronephrosis but are more likely to be rounded and contain filling defects with pyelonephritis. • Although pyelonephritis and mild hydronephrosis cannot be definitively differentiated sonographically, the diverticula tend to less sharp and the degree of dilatation less severe with pyelonephritis. See Figure 292-63. Echogenic material might be visible within the renal pelvis.
Large Kidneys: Polycystic Kidneys • In feline idiopathic polycystic kidney disease (see Figure 292-64), multiple cysts develop from abnormal tubules and gradually enlarge to replace functional renal tissue. The disease can be inherited particularly in Persian and Persian related cats. See Chapter 174. • The radiographic appearance varies with the size and number of cysts but as the disease progresses, there is usually bilateral enlargement with irregular margination. • On excretory urography, there are filling defects in the nephrogram in the areas of the larger cysts. Distortion of the nephrogram, persistence of the nephrogram, and the presence of a poor pyelogram have also been reported. • On ultrasonography, in early cases, the kidneys may appear to be normal or only slightly enlarged on survey radiography, but the cysts
813
(A)
(B)
(B)
(C) (D)
(E) Figure 292-59 Sonograms of normal feline kidneys. A, Middorsal image. The lateral border of the kidney is closest to the transducer and the renal hilus and hilar vessels are directed dorsally. B, Lateral sagittal image. The kidney has the appearance of a watermelon. C, Midsagittal image. The ventral and dorsal branches of the renal pelvis appear as two hyperechoic lines (arrows) separated by the renal crest (RC). D, Medial sagittal image. The medulla appears as two hypoechoic circles separated by fat (F) surrounding the renal pelvis. The cortex is seen in the periphery. E, Transverse image. The kidney is somewhat circular. The margins of the pelvis (arrows) form a hyperechoic C around the hypoechoic renal crest. Urine shows as a black area within the margins. This is the most sensitive view for detection of mild pyelectasia.
814
(B)
(A)
Figure 292-60 A, Lateral radiograph showing that the right kidney is small and round. The left kidney is wider than normal. Mineral opacities are visible in the area of both kidneys and the urinary bladder. The glomerular filtration rate was calculated using nuclear scintigraphy. Total glomerular filtration rate was 0.15 ml/min per kg (normal > 2.5) with the workload being similar for both kidneys (49% and 51%). B, Sonogram of another cat with chronic renal disease and elevated BUN and creatinine. The left kidney is small and irregular. The cortical surface had a marked depression (arrow), likely caused by previous infarction.
(A)
(B)
(C) Figure 292-61 Radiographs show mineral opacity in the area of the kidneys and ureters. The left kidney (arrows) is enlarged. A, Lateral projection. B, Ventral-dorsal projection. C, Ultrasonography revealed a markedly dilated renal pelvis and diverticula consistent with hydronephrosis.
815
SECTION 6: Imaging
(A) Figure 292-62 Sonogram showing massive hydronephrosis. Only a thin rim of renal parenchyma remains. Cellular fluid could be seen swirling during sonography. Small hyperechoic lines are seen peripherally representing remnants of the renal diverticula. Adhesions involving the ureter were found at surgery. Histology showed ureteral fibrosis.
(B)
Figure 292-63 Sonogram of a 7-year-old mixed-breed cat with diabetes and pyelonephritis. Pyelectasia tends to be less severe with pyelonephritis than with hydronephrosis.
Figure 292-65 Images of the abdomen of a cat with lymphoma in the kidneys and gastrointestinal tract. A, On radiography, both kidneys are moderately enlarged. B, Ultrasonography revealed irregularity of the margins of the kidneys and poor corticomedullary definition. A hypoechoic rim around the kidney could represent fluid, but this has been shown to most likely be solid tissue in cases of lymphoma.
will be visible on ultrasonography. See below for details under parenchymal changes. In severe cases, the kidneys will be enlarged and distorted, appearing masslike on radiographs.
Large Kidneys: Neoplasia
Figure 292-64 Polycystic kidney disease: There are large cysts displacing most of the renal parenchyma.
816
• The classic appearance of a neoplastic kidney is a mass located dorsally with no visualization of a normal renal shadow (apart from the mass). • Perirenal pseudocysts can also create a mass effect and masquerade as renal enlargement. • Lymphoma is the most common renal neoplasm in cats (see Figure 292-65), usually presenting as bilateral renomegaly on survey radiography. Margins of the kidney are frequently irregular. On ultrasonography, the kidneys are usually enlarged with altered echogenicity. There may appear to be fluid surrounding the kidney, but this has been shown to be solid tissue in many cases. In some cases, renal architecture remains relatively undisturbed, but in others the kidneys are barely recognizable on ultrasonography. Renal lymphoma is often metastatic, not primary. It may be seen in the alimentary form of lymphoma along with involvement of mesenteric lymph nodes and bowel, so the patient should be examined carefully for evidence of intestinal disease.
Imaging: The Abdomen
• Renal adenocarcinomas are more likely than lymphoma to occur unilaterally and result in more distortion of normal renal parenchyma. Malignant histiocytoma, transitional cell carcinoma, and hemangiosarcoma have also been reported. • On excretory urography of various renal masses, focal and multifocal nonuniform opacification of the nephrogram has been reported. There may be distortion, deviation, or dilation of the pelvis and diverticula in the pyelogram. • Renal masses present with variable sonographic signs. There may be disruption of the renal parenchyma or diffuse infiltration. A complex or solid mass may be present. Solid masses can be hypoechoic, isoechoic, or hyperechoic. Other possible changes include distortion of the margins of the kidney, dilation of the renal pelvis, and enlargement of the kidney. • Differentials for neoplasia include abscesses, granulomas, and hematomas. Biopsy is necessary for definitive diagnosis and to determine cell type.
chyma. Fluid will reoccur after aspiration unless the renal capsule is surgically resected, but the renal disease is usually progressive and fatal. See Chapter 167. • On survey radiography, there is apparent enlargement of the kidney. See Figure 292-66. As with neoplasia, the fluid opacity remains dorsally located but may extend to the floor of the abdomen if the pseudocyst is large. A normal renal silhouette will not be seen on the same side separate from the mass. • Excretory urography usually shows a small irregular nephrogram representing the chronically diseased kidney. The surrounding cystic fluid usually remains fluid opaque. In some cases, the fluid may opacify during excretory urography. • On ultrasonography, anechoic fluid is present surrounding the kidney. See Figure 292-66C. The kidney is usually small with poor corticomedullary definition and irregular margins.
Renal Calculi Enlarged Renal Silhouette: Perirenal Pseudocyst • Perirenal pseudocysts affect one or both kidneys and are usually secondary to chronic renal disease in which transudate or modified transudate is found between the renal capsule and the renal paren-
• Renal calculi are common occurring in about 5% of cats that form calculi. See Figure 292-67. Calculi most commonly consist of oxalate, apatite, or a combination. Renal calculi can be unilateral (especially on the left) or bilateral.
(A)
(B)
(C) Figure 292-66 Images of a cat that presented with history of abdominal distension. Lateral (A) and ventrodorsal (B) radiographs reveal large circular fluid opacities in the area of the kidneys. The kidneys are not visible separate from the opacities. Ultrasonography shows that the opacities are perirenal pseudocysts (C). The left kidney is shown to be small and irregular with poor corticomedullary definition.
817
SECTION 6: Imaging
(A)
Figure 292-68 A distinct medullary rim sign is seen in this cat with chronic renal disease.
Renal Mineralization • Mineralization can be dystrophic occurring secondary to infarcts, neoplasms, or other renal lesions or may be metastatic associated with disease in other organs causing altered blood levels of calcium or phosphate. • Excretory urography is useful to differentiate calculi and parenchymal mineralization in the area of the pelvis and diverticula.
Ultrasonography of Diffuse Parenchymal Disease (B) Figure 292-67 Images of a 7-year-old castrated male cat with a 48-hour history of vomiting. Blood urea nitrogen was 200 mg/dL. A, Lateral radiograph shows irregular mineral opacities in the area of the renal pelves. B, Numerous small calculi are visible in the renal pelvis on ultrasonography.
• Radiopacity of renal calculi is dependent on size and composition. Larger calculi (greater than 3 mm) and calculi made of calcium oxalate, magnesium ammonium phosphate, or silica are more likely to be radiopaque. Smaller calculi or calculi made of cystine or ammonium urate are more likely to be radiolucent. In a large study of almost 3,500 cats, calculi in kidneys were more often made up of calcium oxalate than magnesium ammonium phosphate. • Calculi may be larger than they appear to be on survey radiography. • Because iodine contrast media have a greater opacity than calculi, calculi usually cause a filling defect in the pyelogram on contrast radiography regardless of whether they were radiolucent or radiopaque on survey radiographs. However, small radiopaque calculi may be hidden within a large amount of contrast medium. • Excretory urography is helpful to differentiate parenchymal mineralization from calculi. Parenchymal mineralization will not create a filling defect in the pyelogram. • On ultrasonography, calculi are usually hyperechoic. See Figure 29267B. In some cases, only the surface can be seen. In other cases, the shape of the calculus can be discerned. Acoustic shadowing is usually present deep to the calculus. Pyelectasia may be present. • If calculi have moved distally into the ureter, significant hydronephrosis may be present.
818
• Examination of the kidney for diffuse disease includes evaluation of cortical echogenicity, cortical thickness, medullary echogenicity, and corticomedullary definition. • Corticomedullary definition is greater in cats than in dogs. Renal disease can cause decreased corticomedullary definition, which can be almost non-existent. • The medullary rim sign (see Figure 292-68) is a linear area of increased echogenicity that can occur in the outer zone of the medulla parallel to the corticomedullary junction. This can occur in normal cats and may be related to mineralization of the basement membrane. The medullary rim sign has also been reported in multiple diseases including ethylene glycol toxicity, acute tubular necrosis, hypercalcemic nephropathy, granulomatous nephritis due to feline infectious peritonitis, and chronic tubulointerstitial nephritis. • The renal medulla and cortex should be equally thick in lateral sagittal images. In disease, the cortex can be too thick or too thin. Increased cortical echogenicity can have multiple causes including glomerular nephritis, interstitial nephritis, acute tubular necrosis, nephrosis, end-stage renal disease, lymphoma, feline infectious peritonitis, mycotic infection (see Figure 292-69), and nephrocalcinosis. Ethylene glycol toxicity can cause an extremely hyperechoic cortex. The medullary rim sign in this disease is a poor prognostic indicator.
Ultrasonography of Focal Parenchymal Disease: Decreased Echogenicity • Small cortical cysts are frequently seen without causing clinical signs. In other cases, cysts may displace a large number of renal tubules, resulting in significant clinical signs. • Sonography shows circular anechoic areas with a distinct far wall and deep acoustic enhancement. See Figure 292-64. • If echogenic contents are seen within the cysts, consider concomitant infection or other disease, such as hematoma or neoplasia.
Imaging: The Abdomen
Figure 292-69 Sonogram of the left kidney of a cat with renal cryptococcosis. The kidney is enlarged with poor corticomedullary definition.
(A)
Figure 292-70 This kidney is small and irregular. The triangular hyperechoic area at the edge of the kidney is likely a renal infarct (arrows).
• Acute renal infarcts have been reported as hypoechoic (almost anechoic) lesions.
Ultrasonography of Focal Parenchymal Disease: Increased Echogenicity • Renal mineralization may occur as small pinpoint areas or large areas. Areas of mineralization may be hyperechoic. Acoustic shadowing may be present depending on the composition of the mineral. • Chronic renal infarcts (see Figure 292-70) are usually hyperechoic focal lesions. The classical infarct is usually triangular with the base at the renal surface. We have also seen acute infarcts present as a hyperechoic lesion. • Other hyperechoic lesions include hemorrhage, fibrosis, gas, fat, and neoplasia.
Renal Failure • Excretory urography can provide a crude evaluation of renal function. Failure of the kidneys to opacify or persistence of the nephrogram is an indication of renal failure. (See Figure 292-71). • Renal scintigraphy is preferred over excretory urography for the determination of renal function. A radionuclide, labeled for the kidney, is injected IV. The kidneys are imaged during elimination of
(B) Figure 292-71 Images of a cat with a 5-year history of renal disease. On survey radiography (not shown), the right kidney was mildly enlarged. The left kidney was small and round. A, On excretory urography, there is persistence of the nephrogram two hours after intravenous administration of iodinated contrast medium. Minimal contrast is seen in the pelvis, indicating poor glomerular filtration. B, Sonogram of the left kidney (LK) shows a small irregular kidney with numerous cysts. the radionuclide, allowing quantitative evaluation of function for each of the kidneys.
Congenital Disease: Renal Ectopia • Renal ectopia is a rare congenital condition in which one or both kidneys becomes abnormally located during embryologic develop-
819
SECTION 6: Imaging
ment. Fusion with the other kidney can occur (fused renal ectopia). Fused kidneys are referred to as “horseshoe” kidneys when fusion results in the kidneys being fused by a narrow band of tissue so that they have a horseshoe shape. These conditions are rare but have been reported in cats. • On survey radiographs, one or both may not be apparent in the normal location. An apparent mass elsewhere located in the caudal abdomen represents the ectopic kidney(s) that may be fused. • Excretory urography can be used to localize the abnormally located kidneys(s) and characterize the collecting system.
Congenital Disease: Renal Agenesis • One of the renal silhouettes will not be visible on survey radiography. • Excretory urography or ultrasonography can be used to confirm renal agenesis and rule out renal hypoplasia or renal dystrophy. • There may be compensatory hypertrophy of the solitary kidney.
(A)
Imaging of the Ureters Normal Feline Ureters • Normal ureters are not radiographically apparent on survey radiography. • On excretory urography, normal feline ureters are approximately 1 to 2 mm in diameter. They are smoothly marginated and appear interrupted because of peristalsis.
Ruptured Ureter • Ruptured ureter is usually secondary to trauma. • On survey radiography, there is usually a loss of detail in the retroperitoneal space. • Excretory urography shows positive contrast “spilling” into the retroperitoneal space. • Excretory urography is better than ultrasonography for diagnosis of ruptured ureter and ureteral ileus.
Enlarged Ureter • Ileus secondary to inflammation or trauma can cause the ureters to be enlarged. On excretory urography, the iodine contrast column will be continuous rather than interrupted because of a lack of normal peristalsis. • Enlarged ureters may also be the result of hydroureter with or without hydronephrosis as the result of obstruction caused by ureteral calculi, neoplasia, or strictures or bladder neoplasia near the trigone. • Excretory urography or ultrasonography can be used to confirm enlargement of the ureter and possibly to identify the source of obstruction.
Ureteral Calculi • On survey radiography, small mineral opacities might be apparent in the retroperitoneal space. See Figure 292-72. Small calculi or calculi composed of cystine or ammonium urate may not be radiographically apparent (see Renal Calculi). Enlargement of the affected ureter might be apparent proximal to the calculus. • Ureteral calculi can be bilateral and can occur concurrent with renal calculi. • Be careful not to confuse material in the gastrointestinal tract or on the body wall with calculi. The deep circumflex iliac arteries can also appear as circular radiopacities when viewed end on.
820
(B) Figure 292-72 Images of a cat with renal, bladder, and ureteral calculi. A, A calculus (arrow) can be seen in one of the ureters. B, Excretory urography shows that the ureteral calculus is obstructing the ureter resulting in hydronephrosis.
• On excretory urography, the ureter may appear dilated in the pyelogram phase. See Figure 292-58. The calculus may present as a filling defect in the iodine contrast column. • On ultrasonography, ureteral calculi (see Figure 292-61) are usually hyperechoic and may or may not exhibit deep acoustic shadowing. Obstruction may cause dilation of the ureter (hydroureter) proximal to the calculus. Distal to the calculus, the ureter will be normal.
Congenital Conditions: Ectopic Ureter • Ectopic ureter (see Figure 292-73) is a bilateral or unilateral condition that uncommonly occurs in cats (usually females) and in which the ureter terminates abnormally in the bladder or urethra. • Survey radiographs are usually non-diagnostic. • Excretory urography can help identify the site at which the ureters enter the urinary tract particularly if negative contrast (or double contrast) cystography is performed simultaneously. • On ultrasonography, urine can sometimes be seen swirling into the urinary bladder at the ureteral papillae (“ureteral jet”) in normal individuals. Color Doppler ultrasonography might be helpful to locate the ureteral jet, ruling out ectopic ureter. Lack of visualization of a normal ureteral jet and the presence of a dilated ureter (a common
Imaging: The Abdomen
If the bladder was relatively empty at the time excretory urography was performed, the ureterocele may not be as apparent because it will similar in opacity to the bladder contents. Filling the bladder with negative contrast will improve visualization of the contrast filled ureterocele. If positive contrast cystography is performed without concurrent excretory urography, the urine-filled ureterocele will appear as a filling defect within the contrast-filled urinary bladder. • On ultrasonography, an ureterocele will appear as a cystic structure within the bladder.
Imaging of the Urinary Bladder and Urethra (A)
Radiography of Normal Feline Urinary Bladder and Urethra • The feline bladder is described as having the shape of a teardrop or ellipse. • The intra-abdominal urethra of the cat is long compared to that of the dog so the bladder is more cranially located.
Cystography
(B) Figure 292-73 A, Lateral projection of an excretory urogram in an 8-month-old cat with urinary incontinence since 8 weeks of age. There is right hydronephrosis and hydroureter secondary to ureteral ectopia. A normal left ureter (arrow) enters the bladder and a dilated right ureter (arrowhead) enters the urethra. B, Ventrodorsal projection. Arrow , dilated right ureter.
sequel of ectopic ureter) supports the diagnosis of ectopic ureter. Remember, however, that a normal ureteral jet is not always detectable. Following a dilated ureter past the bladder may also be possible.
• Cystography is used for evaluation of the urinary bladder wall and contents. Cystography is preferred over ultrasonography for confirmation of a ruptured urinary bladder. • Ionic organic iodinated contrast media are used for positive contrast cystography. If there is a possibility of extravasation of contrast into the peritoneal cavity, nonionic contrast media could be used to reduce possible side effects including dehydration. Air is usually used for negative contrast cystography. Carbon dioxide is less convenient (and less commonly used) but is more soluble in blood and is thus, less likely to cause embolism. A combination of positive and negative contrast media is used for double contrast cystography. • On positive contrast cystograms, the bladder contour is smooth. The contrast is uniform with no radiolucencies seen. • On negative contrast cystograms, the air should smoothly outline the mucosal surface of the bladder if all urine has been removed. If the urine is not removed, the air forms a bubble above the urine. Measurement of wall thickness will not be accurate because the urine silhouettes with the wall, making the wall appear thicker that it is in reality. • On double contrast cystograms, contrast smoothly coats the mucosal surface of the bladder and forms a puddle in the dependent side of the bladder. Air surrounds the contrast puddle. • Common causes of a poor double contrast study include dilution of the positive contrast by urine left in the bladder, air bubbles, and an incorrect amount of positive or negative contrast. • Vesicoureteral reflux occurs in normal animals. Consequently, air or contrast medium may be seen in the kidneys during positive or double contrast cystography. • The most common complication is infection secondary to catheterization. Other complications include rupture, kinking of the catheter, and trauma to the urethra or bladder caused by the catheter.
Congenital Conditions: Ureterocele • Ureterocele is dilation of the terminal ureter causing it to become a cystic structure located between the serosal and mucosal layers of the bladder. Hydroureter and possibly hydronephrosis on the affected side may result. • Excretory urography will show hydronephrosis and hydroureter (if present). The dilated terminal ureter (ureterocele) will fill with contrast. The ureterocele may appear more radiopaque than the surrounding bladder if the bladder contains both urine and contrast.
Ultrasonography of the Normal Feline Bladder and Urethra • The normal feline urinary bladder has a smooth regular wall. The inner and outer layers are hyperechoic; the middle mucosal area is hypoechoic. See Figure 292-74. The lumen is anechoic. The normal urethral wall is hypoechoic. • A catheter appears as two parallel hyperechoic lines. • Ultrasonography is useful to guide needle placement for cystocentesis. See Figure 292-74.
821
SECTION 6: Imaging
Figure 292-74 Sonogram showing cystocentesis to obtain urine for urinalysis. The inner and outer layers (arrow) are hyperechoic; the middle muscular layer is hypoechoic. The needle appears as a hyperechoic linear structure.
(A)
Bladder Calculi • Urinary cystic calculi vary in size and number from one large calculus to numerous small calculi or crystals. Calculi are more likely to be radiopaque when they are larger than 3 mm and when they are composed of calcium oxalate or phosphate, magnesium ammonium phosphate, or silica. See Figure 292-75. Cystine and ammonium urate uroliths are usually radiolucent. Cats with urolithiasis associated with portosystemic shunts usually have calculi composed of ammonium urate. • Double contrast cystography is preferred over positive contrast urography for detection of calculi and evaluation of the bladder wall for thickening or other change. • Calculi appear radiolucent in double contrast and positive contrast cystograms. See Figure 292-76. If the calculi are small, they may not be obvious with positive contrast cystography. • On cystograms, calculi can be differentiated from air bubbles because air bubbles are more likely to have smooth, bright margins and be located at the periphery of the contrast “puddle.” Calculi are more likely to be irregular and less well marginated. Gravity will cause them to be located centrally in the lateral recumbent view. Blood clots can be more difficult to differentiate. • On ultrasonography, hypoechoic material in the lumen can represent blood cells, clots, cellular debris, or fat droplets. Calculi (see Figure 292-75) in the lumen are usually hyperechoic and will be present in the dependent side of the urinary bladder, although uncommonly calculi will adhere to the bladder mucosa and not move as expected. They are variable in size and number and may exhibit deep acoustic shadowing. Small calculi or crystals may become suspended in the lumen of the bladder.
(B) Figure 292-75 Images of a cat with obstruction of the urethra. Radiopaque calculi are seen in the urinary bladder. A, Lateral radiograph. B, On sonogram, one calculus is seen to be hyperechoic with deep acoustic shadowing; the bladder wall is moderately thickened.
Ruptured Bladder • Rupture of the urinary bladder can result from trauma or obstruction. • Survey radiography shows decreased serosal detail resulting from urine free in the peritoneal space. See Figure 292-77A. The amount of time elapsed since trauma and the size of the tear will determine how much urine is present in the peritoneal cavity. The degree of serosal detail remaining also depends on how much fat is present in the abdomen. A normal bladder silhouette may or may not be present.
822
Figure 292-76 Double-contrast cystography clearly shows a calculus as a filling defect in the contrast puddle. The calculus is less radiopaque than the iodinated iodide contrast medium.
Imaging: The Abdomen
•
• • •
(A)
or chronic. The mucosa may also be irregular. Large projections into the lumen can be seen in neoplasia or polypoid cystitis. An urachal diverticulum can cause a bulge in the cranial margin of the bladder. This may be more obvious on excretory urography; it may be induced when too much contrast material is infused during positive cystography. It may or may not be associated with clinical signs. A nondistensible bladder wall may occur in chronic cystitis. Vesicoureteral reflux occurs in normal cats and either air or contrast can be present in the kidneys after double contrast cystography. On ultrasonography, the urinary bladder wall is often thickened and sometimes irregular. When evaluating the bladder wall, remember to consider the degree of distension because an empty bladder could appear thickened. Conversely, disease could be missed in an overly distended bladder. In emphysematous cystitis, gas may appear hyperechoic with deep reverberation artifact.
Bladder Neoplasia
(B) Figure 292-77 Images of a cat with a ruptured bladder secondary to obstruction by a urethral calculus. A, Lateral projection showing a fluid opaque abdomen. A radiopaque calculus can be seen in the urinary bladder (arrow). B,Positive contrast cystography confirms rupture of the urinary bladder.
• Positive contrast cystography using water-soluble iodine contrast is preferred over negative or double contrast cystography for the diagnosis of ruptured bladder because small amounts of air are difficult to appreciate in the peritoneal cavity. On positive contrast cystography (see Figure 292-77B), iodine contrast will be seen extruding from the bladder. Serosal surfaces will seem brighter than normal. If the mucosa is intact but herniated, contrast remains within confines of the bladder but a contrast-filled protrusion will extend from the bladder. • Ultrasonography can be useful to visualize free fluid in the abdomen but the tear will not likely be seen. Positive contrast cystography is more likely to be diagnostic.
• Transitional cell carcinoma is the most common neoplasm found in the feline urinary bladder. Other neoplasms include squamous cell carcinoma, adenocarcinoma, leiomyoma or leiomyosarcoma, hemangiosarcoma or hemangioma, fibroma, rhabdomyosarcoma, and primary or secondary lymphoma. • Survey radiography usually shows a normal bladder unless dystrophic mineralization is present. Sublumbar lymphadenopathy may be present if there is metastatic disease in regional lymph nodes. Metastasis could also be seen in the thorax or bones. The kidneys or ureters may be enlarged if there is hydronephrosis or hydroureter associated with a mass at the trigone. • On double contrast cystography, bladder masses in the dependent side of the bladder show as a filling defect in the contrast puddle. Bladder masses on the nondependent side are coated with contrast. • Ultrasonography is usually used instead of double contrast cystography for diagnosis of mural masses. Bladder neoplasia causes a thickened, irregular wall. Polypoid masses may protrude into the bladder lumen. See Figure 292-78. A similar appearance is seen with polypoid cystitis although most large masses are usually neoplastic. Biopsy is necessary for definitive diagnosis. In evaluating bladder masses, the extent of mural involvement, the location of masses, and urethral involvement should be recorded. Determination of whether or not the masses are full thickness is important for staging of disease. Masses at the apex of the bladder are more likely to be resectable while those at the trigone cannot be resected without removal of the bladder. Hydroureter or hydronephrosis can result from masses obstructing the ureter at the trigone. The prognosis is poor when neoplasia extends distally into the urethra. • Regional lymph nodes should be evaluated when imaging the abdomen. The medial iliac lymph nodes may be enlarged when inflammation or neoplasia is present in the bladder. On ultrasonography, inflamed lymph nodes may be mildly enlarged. Irregularity and altered echogenicity are more likely to occur with neoplasia. Abnormal lymph nodes can be aspirated to assess for possible metastasis, taking care to avoid the aorta and other vessels. In addition, the lungs should be evaluated for possible metastasis. Other organs with clinical evidence of disease should also be checked for metastasis.
Bladder Inflammation • Cystitis is not visible in survey radiography except when gas is present in the lumen. Gas is present in the lumen, bladder wall, or bladder ligaments with emphysematous cystitis and may also be present following recent cystocentesis or catheterization. • Double contrast cystography is the preferred contrast procedure for evaluation of the bladder wall. Thickening of the bladder wall is the most common radiographic sign particularly when cystitis is severe
Localization of the Urinary Bladder • On survey radiographs, the masses in the caudoventral abdomen may be difficult to differentiate from the urinary bladder. An overfilled urinary bladder could also be erroneously believed to be an abdominal mass. • Ultrasonography or cystography can help identify the urinary bladder.
823
SECTION 6: Imaging
(A)
Figure 292-79 Radiopaque urethral calculi (arrows) are apparent in radiography of cat with difficulty urinating.
(B) Figure 292-78 A, Sonogram of a female cat with a leiomyosarcoma in the urinary bladder. Involvement of the muscular layer of the bladder is apparent. B, Sonogram of a blood clot in the bladder of a cat with immune mediated hemolytic anemia. Care must be taken not to confuse blood clots with neoplasia. Repositioning the patient will dislodge some blood clots.
Figure 292-80 Urethrogram showing a urethral stricture in a 4-year-old cat with partial obstruction. A portion of the urethra is narrowed and irregular.
• Sterile ionic or nonionic organic iodinated contrast medium can be placed by catheter into the urethra. If catheterization is not possible, iodinated contrast medium can be injected into the urinary bladder, and the bladder can be expressed to allow a voiding urethrogram to be obtained.
• On urethrograms, filling defects (i.e., radiolucencies in the contrast column) can be calculi, bubbles, or blood clots. Calculi tend to be asymmetrically located, irregular with indistinct margins, and may distend the urethra. Air bubbles usually have sharper, smooth margins, and are round or oval. Blood clots appear similarly to calculi (i.e., irregular, indistinct margins), but they do not distend the urethra. Large calculi can cause obstruction, hydroureter, and hydronephrosis. • On ultrasonography, urethral calculi are usually hyperechoic with or without deep acoustic shadowing. • In cases of partial or complete obstruction, check for evidence of bladder distension and possible hydroureter or hydronephrosis.
Urethral Calculi
Urethral Strictures
• On survey radiography, radiopaque calculi may be visible in the urethra. See Figure 292-79. • Urethrography can be performed to identify calculi that were radiolucent on survey radiographs, strictures, or other lesions.
• Strictures (Figure 292-80) may cause an irregular area of narrowing in the urethral contrast. Urethral spasm can create a similar appearance. Lidocaine can be injected through a catheter into the urethra to avoid spasm. Severe strictures may result in complete obstruction.
Imaging of the Urethra Urethrography
824
Imaging: The Abdomen
Ruptured Urethra • Survey radiography may show increased opacity and indistinct margins in the periurethral region. • Urethrography with iodine contrast may show extravasation of contrast into the periurethral region.
Urethral Neoplasia • Transitional cell carcinomas and squamous cell carcinomas are the most common urethral neoplasms. Primary urethral neoplasia is rare. • Survey radiographs may show a mass associated with the urethra. Metastasis to the regional lymph nodes can result in sublumbar lymphadenopathy. There may also be lysis or proliferative bone affecting the caudal lumbar vertebrae. • Urethrography may reveal irregular mucosal margins, mural thickening, and intraluminal masses. • The thorax should be radiographed to check for the presence of pulmonary nodules indicative of metastasis. • On ultrasonography, the most common observation is increased thickness of the urethral wall. The wall may also become heterogeneous with neoplasia.
(A)
Imaging of Feline Reproductive Organs Radiography of Normal Feline Reproductive Organs • Normal ovaries and the normal nonparturient uterus are not radiographically visible. • In pregnant cats, survey radiographs may show uterine enlargement at about 25 to 35 days of gestation. Mineralization of the fetal skeletal can be seen at about 36 to 45 days of gestation. (See Figure 292-81A).
(B) Figure 292-81 A, Radiograph of a cat in late pregnancy. B, Sonogram of the uterus of a cat 23 days after breeding showing several feti in the uterine horns.
Ultrasonography of Normal Feline Reproductive Organs • The ovary and uterus are best visualized during estrus or pregnancy. See Figures 292-81B and 292-82. • Uterine enlargement begins in some cats at four days of gestation. The gestational sac appears as a small anechoic structure at about 11 days of gestation. Cardiac movement is seen between 16 to 20 days. Limb buds and heads are seen at about 1 month. • Pregnancy can be detected earlier with ultrasonography than with radiology, but radiology is more accurate in counting the number of kittens present. • During estrus, follicles are seen as anechoic circular structures (see Figure 292-82); the uterus is a hypoechoic tubular structure.
Problems in Pregnancy • Radiography or ultrasonography can be done to ensure that all feti have been delivered. • On radiographs, fetal death can be recognized by gas in the fetal tissues or uterus, loss of flexion of the fetus, and overlapping of skull bones. Radiology is also useful to ensure that all kittens have been delivered and to determine that the fetus is not large for the size of the queen. See Chapter 60. • On ultrasonography, fetal death is recognized by the absence of a fetal heartbeat and fetal movement. Gas may be recognized in the fetal tissues or uterus. • Ultrasonography is also useful following parturition to make sure that normal involution occurs.
Pyometra • On radiography of cats with pyometra (see Figure 292-83A), the classical radiographic sign is the presence of tortuous, tubular opacities originating from the caudal abdomen between the colon and bladder. Uterine enlargement must be greater than the diameter of the small intestine to be recognized. Enlarged fluid-filled small intestine has a similar appearance, but the clinical presentation is different. Differentials for an enlarged uterus include early pregnancy, mucometra, and neoplasia. • On ultrasonography, pyometra (see Figure 292-83B) presents as an enlarged uterus, variably sized and containing anechoic or swirling, echogenic fluid. • Anechoic fluid in an enlarged uterus may also be seen with hydrometra. Cellular fluid may also be seen with mucometra.
Miscellaneous Bates Bodies • Bates bodies are small radiopaque structures (see Figure 292-57) that are not uncommonly found in the peritoneal cavity of cats and dogs. These are not clinically significant, apparently resulting from dystrophic mineralization of fat. • On ultrasonography, there is a hyperechoic surface with a strong deep acoustic shadow. See Figure 292-84.
825
SECTION 6: Imaging
(B)
(A) Figure 292-82 A, Sonogram of the ovary of a cat in estrus. A follicle can be seen in the ovary. B, Close-up of the ovary.
(B)
(A)
Figure 292-83 A, Lateral radiograph of a cat that was missing for 1 week showing markedly enlarged uterine horns suggesting pyometra or mucometra. Ovariohysterectomy was performed. B, Sonogram of a cat with pyometra. Cellular material could be seen swirling in the uterus during ultrasonography. UB, urinary bladder.
Aortic Thrombosis • Ultrasonography is useful for evaluating the aorta and other vessels for formation of thrombosis. Gray scale sonography shows an irregular hypoechoic structure in the normally anechoic vessel. • Pulsed and color Doppler ultrasonography are valuable for confirmation of obstruction of flow. See Figure 292-85.
Additional Imaging
Figure 292-84 Sonogram of the Bates body of the cat pictured in 292-57. The Bates body has a hyperechoic surface with deep acoustic shadowing.
826
• Computerized tomography and magnetic resonance imaging are becoming more available for cross-sectional imaging of the abdomen. In particular, these modalities are useful for investigation of abdominal masses. See Figure 292-86.
Imaging: The Abdomen
(A)
(A)
(B) Figure 292-85 Sonograms of the abdominal aorta in a cat that presented with cold hindlimbs and that was unable to stand. A, No blood flow is detected with pulsed Doppler imaging of the abdominal aorta just proximal to the origin of the external iliac arteries. B, A normal arterial waveform is recorded more cranially.
Suggested Readings Baez JL, Hendrick MJ, Walker LM, et al. 1999. Radiographic, ultrasonographic, and endoscopic findings in cats with inflammatory bowel disease of the stomach and small intestine. J Am Vet Med Assoc. 215:349–354. Boysen SR, Tidwell AS, Penninck DG. 2003. Ultrasonographic findings in dogs and cats with gastrointestinal perforation. Vet Radiol Ultrasound. 44:556–564. Cuccovillo A, Lamb C. 2002. Cellular features of sonographic target lesions of the liver and spleen in 21 dogs and a cat. Vet Radiol Ultrasound. 43:275–278. Ferrari JA, Hardam E, Kimmel SE, et al. 2003. Clinical differentiation of acute necrotizing from chronic nonsuppurative pancreatitis in cats: 63 cases (1996–2001). J Am Vet Med Assoc. 223:469–474. Goggin JM, Biller DS, Debey BM, et al. 2000. Ultrasonographic measurement of gastrointestinal wall thickness and the ultrasonographic appearance of the ileocolic region of healthy cats. J Am Anim Hosp Assoc. 36:224–228.
(B) Figure 292-86 Computerized tomography of the abdomen. A, On the initial scan without contrast, there is an irregularly marginated mass involving the liver. The mass had nonhomogeneous soft-tissue opacity. B, After intravenous administration of iodinated contrast medium, there was nonhomogenous enhancement of the abnormal portion of the liver. Changes are consistent with neoplasia. L, liver; Sp, spleen; St, stomach. Hanson JA, Papageorges M, Girard E, et al. 2001. Ultrasonographic appearance of splenic disease in 101 cats. Vet Radiol Ultrasound. 42:441–445. Hecht S, Penninck DG, Mahony OM, et al. 2006. Relationship of pancreatic duct dilation to age and clinical findings in cats. Vet Radiol Ultrasound. 47(3):287–294.
827
CHAPTER 293
Imaging: The Head and Spine Merrilee Holland and Judith Hudson
Skull Views Purpose • Evaluation of the skull for trauma, nasal and sinus disease, nasopharyngeal polyps, periodontitis, otitis media, staging of neoplasia, neurologic disorders, and temporomandibular joint disease.
Clinical Indications • Trauma to the temporomandibular joint • Nasal disease including intranasal neoplasia, chronic rhinosinusitis, foreign body, and neoplasia • Nasopharyngeal polyps • Tympanic bullae-otitis media and neoplasia • Periodontal disease (see Chapters 240 and 245) • Neurologic disorders
Figure 293-1 A 7-week-old kitten presented for seizures. The calvarium was markedly enlarged and abnormally shaped. Radiographic signs are suggestive of hydrocephalus.
Technique • General anesthesia required. • Symmetrical positioning is critical for proper evaluation of subtle changes. • Lateral and dorsoventral views of the skull are standard. • Additional views needed for complete evaluation of skull such as frontal view, open mouth ventrodorsal view, intraoral doroventral view, lateral oblique view, and oblique views of upper and lower arcade for dental evaluation (see Chapter 245). • Temporomandibular joints are readily viewed on the dorsoventral projection. Oblique views of the feline skull require rotation of the skull 20 degrees from ventrodorsal. • Nasal disease requires symmetrical views of the skull including open mouth ventrodorsal, frontal view, intraoral dorsoventral, and lateral oblique views. See Chapter 146. • Nasopharyngeal polyps can be visualized most consistently from the lateral projection. See Chapter 149. • Tympanic bullae can be visualized on open mouth rostrocaudal, left dorsal 20-degree right ventral oblique, and right dorsal 20-degree left ventral oblique views. • Evaluation of periodontal disease and odontoclastic resorption requires open mouth views with the head obliqued between 30 and 45 degrees from lateral to isolate each arcade of the maxilla and mandible. Intraoral radiographs of the canine and maxillary fourth premolar teeth may help in complete identification of dental disease. See Chapter 245.
Common Lesions Hydrocephalus Hydrocephalus occurs rarely in cats. See Figures 293-1 and 293-2. On radiographs, the shape of the calvarium may appear domed with the
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
828
Figure 293-2 A kitten was presented following being stepped on by the owner. There is severe hydrocephalus presented with symmetric dilation of both lateral ventricles found on transverse ultrasound imaging.
bones of the calvarium thinning. The loss of normal skull markings results in a homogenous appearance to the calvarium.
Traumatic Luxation or Subluxation of the Temporomandibular Joints Traumatic luxation or subluxation of the temporomandibular joints can be unilateral without concurrent mandibular or symphyseal fracture being present. See Figures 293-3, 293-4, and 293-5.
(A)
(A)
(B) (B)
Figure 293-4 Temporomandibular subluxation: A, B, Subluxation of the left temporomandibular joint with fracture fragments is noted associated with the medial aspect of the condyloid process of the mandible in this kitten following trauma.
Figure 293-3 Temporomandibular degenerative changes: A, Bilateral degenerative changes of the temporomandibular joints are present with more severity on the left side. The right temporomandibular joint space is widened. The condylar and retroarticular processes of the mandible are flattened. B, The rostral aspect of the mandible is displaced to the left.
829
SECTION 6: Imaging
(A)
Figure 293-6 Chronic rhinitis: A cat presented for history of sneezing and gagging with an occasional purulent nasal discharge. On this transverse computerized tomography image, soft-tissue opacity is present within both nasal passages. The nasal turbinates lack their normal symmetrical scrolling and appear deformed. The nasal septum deviates slightly to the right. No conclusive areas of lysis can be identified. A chronic suppurative rhinitis was diagnosed from a biopsy sample.
However, definitive diagnosis of chronic rhinitis requires biopsy of affected tissues. See Chapter 146 and 148. • If available in your area, CT can provide a more sensitive method for evaluation of diseases of the nasal cavity, tympanic bullae, and temporomandibular joints. A higher incidence of bilateral nasal opacity was found on CT in feline patients regardless of etiology. The extent of change to the nasal cavity and paranasal structures can be more completely evaluated by CT. Magnetic resonance imaging may also be helpful. See Figures 293-6 through 293-9.
Neoplasia (B) Figure 293-5 A, B, Vehicular trauma. On computerized tomography transverse and dorsal images in a soft-tissue window, there is malalignment of the maxilla and mandible. Multiple fractures are noted in both orbits, left maxillary bone, and cribriform plate, the pterygoid, zygomatic arch, and left medial orbital wall. Increase in soft-tissue opacity is noted throughout the nasal passages and frontal sinuses.
The most common cause of nasal cavity neoplasia is lymphoma. In one study of CT of nasal disease found neoplasia had more severe turbinate disruption, osteolysis of bone surrounding the nasal cavity, destruction of the nasal septum, and soft-tissue extension beyond the nasal cavity. Unilateral nasal disease has a higher incidence of neoplasia over other causes of rhinitis. Bilateral nasal disease has a similar incidence of neoplasia compared to rhinitis. See Figures 293-10 and 293-11.
Nasopharyngeal Polyps Rhinitis • Radiographic changes associated with rhinitis in cats can be variable or absent. Nasal disease from neoplasia, chronic rhinitis, and foreign body show radiographic changes of unilateral or bilateral opacification of nasal passages or frontal sinus, soft-tissue mass, dental changes, erosion of the nasal septum, deviation of nasal septum, and erosion of the nasal conchae. Chronic rhinitis can be a sequel of previous viral infections that can result in long-term carriers. Damage to the nasal cavity from the viral infection can lead to bacterial infections. Computerized tomography (CT) is a much more sensitive imaging modality for evaluation of the skull than radiography.
830
Cats with nasopharyngeal polyps can present with signs ranging from chronic rhinitis to dysphagia. Nasopharyngeal polyps appear as a softtissue mass located in the nasopharynx. Concurrent chronic disease of the tympanic bullae should be ruled out. See Chapter 149 and Figures 293-12 and 293-13.
Vestibular Disease Cats present with variable signs related to vestibular disease. Differentiation of peripheral and central vestibular disease requires proper interpretation of clinical signs. Central vestibular disease requires evaluation of the brainstem best accomplished by magnetic resonance
(A) (A)
(B) Figure 293-7 Sinusitis: A, B, A cat previously with a history of epistaxis, herpes virus infection, and anorexia. New physical examination findings include head tilt and recent history of falling. On the magnetic resonance T2- weighted images viewed in transverse and dorsal planes, there is increased signal intensity present in the right frontal sinus and dorsal caudal nasal passages. Biopsy of the right frontal sinus revealed chronic necropurulent sinusitis.
(B) Figure 293-8 Rhinitis: A 9-month-old kitten presented for nasal discharge. This patient was positive for feline herpes. A, B, On dorsal and transverse computerized tomography images in a bone window a cavitated appearance to the right nasal passage with loss of normal turbinates is found. Biopsy showed rhinitis with gram positive bacteria possibly predisposed from atresia of the nasal turbinates.
831
SECTION 6: Imaging
(A) (A)
(B) Figure 293-9 Fungal rhinitis: A, B, A cat presented with a persistent nasal discharge. On transverse and dorsal computed tomography images using a bone window a softtissue mass is present within the right frontal sinus with bony proliferation and focal area of lysis. The right frontal sinus has an abnormal contour and bulges dorsally. There is lysis of the dorsal aspect of the medial orbital wall. Biopsy of the frontal sinus found a pyogranulomatous sinusitis and fungal hyphae from aspergilloma.
imaging (MRI). Peripheral vestibular signs can be related to changes in the middle ear or idiopathic vestibular disease. Tympanic bullae disease can be identified on radiographs by change in the shape, bone density, or soft-tissue opacity. Radiographic evidence of the middle ear disease occurs later in the disease process. Radiographs fail to detect otitis media in 25% of the cases. The tympanic bullae changes can be detected more consistently with CT or MRI. Neoplasia of the middle ear has been most commonly associated with squamous cell carcinoma. See Chapter 158 and Figures 293-14 through 293-20.
(B) Figure 293-10 Neoplasia-lymphosarcoma: A, B, A cat presented with nasal deformity, open mouth breathing, and oral ulceration. On transverse and dorsal computerized tomography images, a large soft tissue mass is seen within both nasal cavities and expands laterally with lysis of both medial orbital walls. The globes are displaced. There is lysis of the hard palate with extension of the mass ventrally into the oropharyngeal region. Nasal biopsy revealed immunoblastic type lymphoma.
Myelography Purpose • Evaluation of spinal cord disorders
Clinical Indications Brain Imaging Imaging of the brain can be done using CT and MRI. Typically lesions involving the bone can be more clearly imaged with CT. When the brain tissue needs to be evaluated MRI is the imaging modality of choice. The most common brain tumor is a meningioma. See Figures 293-21 and 29322. Penetrating foreign bodies can also be evaluated. See Figure 293-23.
832
• Paresis, paralysis, pain, and proprioceptive deficits • Survey radiographs are negative for identification of spinal cord lesion • Need to identify specific location for surgical intervention • Need to identify extent of lesion • Multiple sites are suspected on survey radiographs
Figure 293-11 Neoplasia-adenocarcinoma: An older domestic shorthair presented with a 6 month history of epistaxis. On the transverse computerized tomography scan in a bone window an increase in soft-tissue opacity is noted within the right nasal passage. There is marked thickening of the turbinates on this side. Lysis is noted within the medial orbital wall. Biopsy findings of the right nasal passage were consistent with a nasal adenocarcinoma.
(A)
Figure 293-12 Nasopharyngeal polyp: A cat presented for inspiratory stridor. On the postcontrast transverse computerized tomography image there is a ringlike enhancement of the soft-tissue mass consistent with a nasal polyp. Increased opacity is noted in the right tympanic bulla.
(B) Figure 293-13 Nasopharyngeal polyp: An adult cat presented for vestibular signs and upper respiratory signs since 5 months of age. A, B, On transverse and dorsal post-contrast computerized tomography images, a large well-defined elongated ovoid mass is present in the nasopharyngeal area. There is moderate peripheral contrast enhancement of this mass. Moderate hydrocephalus is present. Biopsy confirmed a nasopharyngeal polyp.
833
SECTION 6: Imaging
(A)
Figure 293-15 Chronic inflammation: A cat was presented for chronic pruritus of the left ear for 2 years duration. The transverse computerized tomography image in bone window shows normal tympanic bullae with thickening of the left external ear canal. Chronic inflammation was suspected on computerized tomography.
Normal Findings • The normal myelogram consists of thin parallel columns of contrast medium in the subarachnoid space outlining the spinal cord. • The spinal cord normally widens in the caudal cervical and caudal lumbar regions due to the brachial and lumbar intumescences. • In normal myelograms, the cervical spine cord of a cat appears proportionally wider than that seen in dogs. The contrast columns are comparatively narrower.
Common Lesions
(B)
(C) Figure 293-14 Normal: A, On magnetic resonance imaging, the T1 transverse postcontrast image shows normal bilateral tympanic bullae. B, C, The same patient has a normal study of the tympanic bulla on transverse computerized tomography image one in a soft tissue window (B) and one in a bone window (C). Notice the apparent thickening of the tympanic bulla when viewed on a soft tissue window.
834
• Inflammatory diseases caused by feline infectious peritonitis, toxoplasmosis, and cryptococcosis can cause abnormal neurological signs in cats. Myelography and MRI studies may be normal. • Infrequent problems in cats include intervertebral disc disease, spinal cord trauma, lymphosarcoma, and spinal cord infarction. In one MRI study, neoplasia was the most common spinal cord disease. • Lesions can be categorized as intramedullary (within the cord), extramedullary intradural, and extradural. • In intervertebral disc disease, myelographic signs (see Figure 293-24) reflect extradural compression and include narrowing of the disc space with or without mineralization of the disc, dorsal displacement of the ventral contrast column in the lateral view, and thinning of the contrast columns in the ventrodorsal view. The contrast columns may be displaced lateral in the ventrodorsal view. An intramedullary pattern may be present if there is significant cord swelling. • Similar findings will be present on MRI with narrowing of the intervertebral disc space, dorsal displacement of the ventral spinal cord on the sagittal image, and variable degree of ventral to lateral compression on the transverse image. See Figures 293-25 and 293-26. • Lymphosarcoma can invade either the vertebral column or nervous system or both. There may be involvement of the spinal cord or the neoplasm may involve intradural or extradural structures. In survey radiography, there may be lysis of one or more vertebrae. See Figures 293-27 and 293-28. • Dilation of the central canal or hydromyelia (see Figure 293-29) can occur as a congenital or acquired lesion. Acquired causes include neoplasia, infection, trauma, and cord atrophy. In some cases, hydromyelia is an incidental finding unrelated to abnormal neurological signs. • Malformations of the spine can occur following trauma or can be the result of congenital disease. Myelography can be used to determine if there is resultant compromise of the spinal cord. See Figures 293-30 and 293-31.
(A)
Figure 293-17 Neoplasia: A cat presented for mass in the right ear canal. Transverse computerized tomography image post-contrast shows the right tympanic bulla filled with soft-tissue material. Increased soft tissue is noted in the mid and distal portions of the external ear canal. The biopsy results were consistent with a plasma cell tumor.
(B) (A)
(C) Figure 292-16 A cat presented with 6-month duration of ear infection and more recently a head tilt. A, Ventrodorsal image of the skull shows an increase in soft-tissue opacity within the left tympanic bulla. B, C, Transverse computerized tomography images in bone and soft-tissue windows show increased soft-tissue opacity present in the medial and lateral compartment of the left tympanic bulla. The left bulla appears thickened in the bone window. An inflammatory process was diagnosed from the computerized tomography examination.
(B) Figure 293-18 Neoplasia: A cat presented with a mass in the left ear canal. A, B, On transverse computerized tomography images, in soft tissue and bone windows there is a large soft tissue swelling that has a heterogeneous opacity and that is associated with the left external ear canal. Increased opacity is present in the left tympanic bulla. There is lysis of the caudal aspect of the tympanic bulla. A neoplastic process was suspected from the computerized tomography, and the biopsy confirmed a squamous cell carcinoma.
835
(A)
(B) Figure 293-19 Fungal otitis: A cat presented with a history of ear infections with vestibular signs. A, Magnetic resonance image in transverse plane on the postcontrast T1 fatsat weighted image shows thickening of the left tympanic bullae. In addition, a mass is seen extending into the brainstem adjacent to the left tympanic bulla. Marked atrophy of the left temporalis muscle is present. B,On the sagittal magnetic resonance imaging postcontrast enhancement shows the dorsal extension of the mass. Biopsy of the left ear canal revealed fungal otitis media most likely Aspergillus.
Figure 293-21 Neoplasia: A cat presented with an eight month history of a nasal mass and draining tract. (A),(B) On transverse and dorsal computerized tomography scans in a bone window, there is a large mineralized mass with soft tissue occupying the majority of the left nasal passage. This mineralized mass extends into the medial aspect of the left orbit causing lateral displacement. The frontal sinus has a moth eaten appearance with some soft tissue opacity. The biopsy of the mass was consistent with multilobular tumor of bone.
Figure 293-20 Neoplasia: A, A cat presented with peripheral vestibular signs. On the T1 transverse postcontrast image there is increased signal present along the lateral aspect of the calvarium. Increase signal is noted in right tympanic bulla. There appears to be destruction of the portion of the calvarium associated with the right tympanic bulla. Biopsy of the mass was consistent with a squamous cell carcinoma.
836
(A)
(B) Figure 293-22 Neoplasia: A cat presented for weight loss, intermittent blindness, and ataxia. A, Radiographic images of the skull show increased thickness of the cortical bone consistent with osteopetrosis. B, On the magnetic resonance postcontrast T1 weighted dorsal image there is nonuniform contrast enhancement of the mass. The mass is peripherally located within the left cerebrum and extends to the parietal lobe. The large contrast enhancing mass most likely would be a meningioma. This patient died and a meningioma was diagnosed.
837
(A)
(B)
(C)
(D) Figure 293-23 Arrow: A cat presented with an arrow shot through its head. A, B, Radiographs show a metallic tube extending from the right nasal cavity through the skull and exiting the right lateral neck adjacent to C1–C2. There are fractures of the right frontal bone and right lateral tympanic bulla. C, D, On transverse and dorsal computerized tomography, the arrow extends from the nasal cavity into the cervical region. The arrow extends into the right tympanic bulla with multiple fractures in this area. A portion of bone is displaced dorsally into the calvarium immediately rostral to the right tympanic bulla. This patient made a successful recovery after the arrow was removed.
838
(A)
(B) Figure 293-24 Myelography was performed on a 10-month-old cat with a history of progressive paresis. The injection of contrast was made in the caudal lumbar region. A, In the lateral projection, both the dorsal and ventral contrast columns stop at the level of L1–L2. Only a small amount of contrast is seen more cranially. B, In the ventrodorsal projection, the right contrast column extends to the level of L1–L2, but the left contrast column stops more caudally at about L2–L3. Radiographic changes suggest left-sided extradural compression at the level of L2.
839
SECTION 6: Imaging
(A) Figure 293-25 A six-month-old Maine Coon presented for an acute onset of paraparesis. On survey radiographs, the T13-L1 disc space is narrowed (arrow).
(B) Figure 293-27 A cat presented for lameness of the left rear leg. A, Lateral projection suggesting an expansile lesion in the vertebral body of L4. B, On myelography, there is thinning of both the ventral and dorsal contrast columns. The dorsal column was displaced dorsally; the ventral contrast column was displaced ventrally. Similar changes were present in the ventral-dorsal view, indicating an intramedullary lesion at L4. The final diagnosis was lymphosarcoma.
(A)
• Osteopetrosis occurs rarely in cats. Osseous lesions are found in the axillary and appendicular skeleton. Affected bones exhibit a diffuse increase in medullary opacity and are hard resisting penetration by biopsy needles. Because osteopetrosis in humans results in bones that are fragile and brittle, the term diffuse osteosclerosis has been suggested for the problem that occurs in cats. Although these lesions are often considered to be incidental, many of the affected cats later succumb to a variety of diseases including myeloproliferative disorders, lymphoma, C-cell tumor, and systemic lupus erythematosis. See Figures 293-32.
(B) Figure 293-26 Magnetic Resonance Imaging of the cat shown in Figure 293-25. A, Sagittal T2 weighted image. B, Transverse T1 weighted post-contrast image. Arrows indicate a mass within the ventral spinal canal at T13-L1. Radiographic and MRI findings are consistent with an extruded intervertebral disc.
840
Additional Comments • CT and MRI are useful to further evaluate the spine and extraskeletal structures and are available in some areas. These modalities are useful in staging cancer patients. See Figures 293-33 through 293-41.
(A)
(A)
(B) Figure 293-28 A cat presented for emergency paraparesis. A, On the T2-weighted sagittal and transverse images, there is increased signal in the spinal cord at L5. B, On the transverse image this increased signal is present in the mid and ventral two-thirds of the cord. An intramedullary lesion within the spinal cord is suspected with neoplasia such as lymphosarcoma as top differential.
(B) Figure 293-30 Congenital: A, B, A 4-month-old cat presented for 1-month history of diarrhea. There is an abnormal appearance to the sacrum and caudal vertebrae. There appears to be spina bifida associated with the caudal aspect of the sacrum and caudal vertebra.
Figure 293-29 A cat presented for progressive weakness in the rear limbs. The myelogram has filling of the central canal (hydromyelia). Hydromyelia can be congenital or can occur secondary to neoplasia, infection, trauma, and cord atrophy. Notice the decrease in bone opacity of the vertebral spine, with loss of visualization of the spinous processes.
Figure 293-31 Congenital: A 9-month-old cat presented for dragging his rear limbs since 6 weeks of age. There is marked dorsal deviation of the spinal canal in the midthoracic area. There is shortening and malformation of the vertebral bodies of T6–T8. The neural canal is markedly deviated over the malformed vertebrae.
841
(A)
(B) Figure 293-32 A cat presented with a history of renal failure. Radiographs of the lumbar spine show increased opacity in the medullary region of the vertebral bodies consistent with osteopetrosis. A, Lateral projection. B, Ventral-dorsal projection.
842
(A)
(C)
(B) Figure 293-33 A 12-week-old kitten presented for ataxia. This kitten was only being fed cooked chicken. On spinal radiographs (A, B) and transverse computerized tomography image (C) in a bone window there is an overall decrease in bone opacity.
843
(A)
(B) (C) Figure 293-34 A 10-year-old mixed-breed presented for chronic back pain. A, B,Spinal radiographs show ventral spondylosis at L6–L7. The intervertebral disc space appears narrowed at L6-L7. New bone formation is noted at the caudodorsal margin of L6 and craniodorsal margin of L7. C,On transverse computerized tomography scan there is increased soft-tissue opacity in the spinal canal. There is an unusual oval shape to the spinal canal in the sacral region. Degenerative changes along with suspect fibrous tissue or disc material was present at the lumbosacral junction.
844
(A)
(B)
(A)
(C) Figure 293-36 A cat presented with a 3 week history of ataxia in the rear limbs. A, On spinal radiographs the L1 vertebral body shows lucency in the caudal aspect of the lamina, pedicle, and articular processes (arrows). This lytic area has an expansile appearance. B, On the sagittal T2-weighted STIR magnetic resonance imaging, a decreased signal is present within the spinal canal at L1–L2 (arrows). C, On the T1weighted transverse image with contrast, there is a mass effect displacing the spinal cord to the left side (arrows). This mass is uniform and contrast enhancing. Based on the spinal radiographs and magnetic resonance imaging findings the differential diagnoses were osteosarcoma, chrondrosarcoma, or lymphoma.
(B) Figure 293-35 A, B, A cat presented for 6 week history of ascending paralysis. A, On the transverse computerized tomography done in a bone window the lamina and pedicle on the right side of T1-T2 is less opaque. This suggests some erosion of bone due to a mass extending from the spinal canal. B, On the post contrast T1 weighted magnetic resonance image, there is contrast enhancement distal to the intervertebral foramen on the right side. This patient was euthanized and a peripheral nerve sheath tumor was diagnosed on histopathology.
845
(A)
(B) Figure 293-37 A cat presented with a history of removal of a fibrosarcoma from the right rear leg 1 year ago and removal of a fibrosarcoma from the left rear leg 10 days ago. Three days ago he became paraparetic in both rear limbs. On the sagittal (A) and transverse (B) T1 postcontrast magnetic resonance imaging of the spine, a mass was seen within the spinal canal (arrows). An extradural mass and extraspinal mass were found consistent with metastatic disease.
Figure 293-38 A 7-year-old cat presented for a progressive ataxia. On the T2-weighted sagittal magnetic resonance imaging, there is increased signal within the dorsal spinal canal from the caudal cervical to thoracic spine (arrows). Hyperintensity in the dorsal column may represent inflammation or infiltrative neoplasia. The cerbrospinal fluid was consistent with an inflammatory process.
Figure 293-39 A cat presented for a recurrent fibrosarcoma. On the T1-weighted postcontrast magnetic resonance imaging, there are multiple mildly contrast enhancing multilobulated mass caudal and dorsal to the scapula (arrows).
846
(A)
(B) (C) Figure 293-40 A cat presented for a mass near the scapula. A, B, Radiographic images show a mass associated with the proximal humerus and scapulohumeral joint. C, The transverse computerized tomography image shows a mass of decreased opacity associated with the humerus. (arrows). The biopsy was not diagnostic of the etiology of the mass.
847
SECTION 6: Imaging
Suggested Readings
(A)
(B) Figure 293-41 A cat presented for recheck of a previously diagnosed myxosarcoma. A, There is a large mass present within the right pelvic canal causing left lateral displacement of the colon. B, There is marked nonhomogenous contrast enhancement of this mass.
848
Bischoff MG, Kneller SK. 2004. Diagnostic imaging of the canine and feline ear. Vet Clin Small Anim Pract. 34:437–458. Gonçalves R, Platt SR, Llabre’s-Diaz FJ, et al. 2009. Clinical and magnetic resonance imaging findings in 92 cats with clinical signs of spinal cord disease. J Feline Med Surg. 11:53–59. Henderson SM, Bradley K, Day MJ, et al. 2004. Investigation of nasal disease in the cat-a retrospective study of 77 cases. J Feline Med Surg. 6:245–257. Knipe MF, Vernau KM, Hornof WJ, et al. 2001. Intervertebral disc extrusion in six cats. J Feline Med Surg. 3:161–168. Lamb CR, Richbell S, Mantis P. 2003. Radiographic signs of cats with nasal disease. J Fel Med Surg. 5:227–235. LeCouteur RA. 2003. Spinal cord disorders. J Feline Med Surg. 5(2):121–131 Muilenburg RK, Fry TR. 2002. Feline nasopharyngeal polyps. Vet Clin Small Anim. 32:839–849. Mukaratirwa S, van der Linde-Sipman JS, Gruys E. 2001. Feline nasal and paranasal sinus tumours: clinicopathological study, histomorphological description and diagnostic immunohistochemistry of 123 cases. J Feline Med Surg. 3:235–245. Schoenborn WC, Wisner ER, Kass PP, Dale M. 2003. Retrospective assessment of computed Tomographic imaging of feline sinonasal disease in 62 cats. Vet Radiol Ultrasound. 44(2):185–195. Schwarz T, Weller R, Dickie AM, Konar M, Sullivan M. 2002. Imaging of the canine and feline temporomandibular joint: a review. Vet Radiol Ultrasound. 43(2):85–97.
CHAPTER 294
Imaging: Cardiovascular Disease Merrilee Holland and Judith Hudson
Roentgen Signs of Cardiac Enlargement • The earliest change on the lateral projection will be a bulge along the left ventricular border indicating left ventricular enlargement. The left atrium (LA) will not bulge until later stages of heart disease. In some severe cases, the heart appears folded due to the presence of the atrioventricular groove between the enlarged LA and left ventricle (LV). See Figure 294-1. • On the ventrodorsal projection, the LV appears elongated with or without widening at the heart base (atrial enlargement). See Figure 294-2. Remember that the LA normally creates the border at the 1 to 2 o’clock position, not at the typical location of the atrium and auricle seen in dogs. • Primary right-sided heart disease in feline patients is rare. Rightsided heart disease does not give a “reverse D” appearance in cats that is seen in dogs. The ability to visualize the right ventricular border does not indicate right heart enlargement.
Echocardiographic Signs of Cardiac Disease
and extends their cooperation time. The examination is usually begun by obtaining the right parasternal short-axis view at the level of the papillary muscles to make the measurements of the right ventricle (RV) and left ventricle (LV). When performing the examination with the cat in sternal recumbency, it may be helpful to place the transducer closer to the sternum, attempting to be relatively perpendicular to the body wall. The cutout in the cardiac table can facilitate transducer placement closer to the sternum without retraction of the limb. It is best not to maintain retraction of the front limbs because eventually the patient will resist being handled. Usually, minimally handling the scruff allows most patients to permit the examination. In the more uncooperative patient, restraining the patient in lateral recumbency will still allow a complete examination. Removing extraneous noises from the examination area can promote a more calming environment. If the examination is impossible to perform without it, sedation for cardiac examination can be done; however, sedation will significantly alter measurements. A standard published sedation protocol with known echocardiographic values needs to be followed to properly evaluate the results.
• The standard views of an echocardiogram include right parasternal short-axis and long-axis views. All the standard measurements done on the right parasternal views can be achieved while most feline patients are in sternal recumbency. Cats are best allowed to be in sternal recumbency on a cardiac table to minimize stress. This enables a portion of the examination to be performed with minimal restraint
Figure 294-1 Enlarged left ventricle: This cat presented with a history of hyperthyroidism. Notice on the lateral image of the thorax the rounded appearance of the left ventricular border (arrows).
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 294-2 Enlarged left atrium: This cat presented in respiratory distress. Notice on the ventrodorsal view the widened heart base along with an enlarged left ventricular border. The left atrium is located at the 1–2 o’clock position (arrows).
849
SECTION 6: Imaging
• Ideally patients should not have echocardiograms while dehydrated or on fluid therapy. Either scenario will alter the cardiac measurement and may hinder a proper diagnosis. • In severe cases of hypertrophic cardiomyopathy, finding a window between the papillary muscles can be challenging from the short-axis view. Nevertheless, the short-axis views are preferred for M-mode measurement of the RV and LV because it can be difficult to achieve the longitudinal views without tilting the plane of the heart. In a repeat echocardiogram, it may be more difficult to reproduce similar images from the longitudinal plane.
Helpful Tip: Right Ventricle and Left Ventricle M-Mode • To accurately measure the interventricular septum (IVS) in the standard right parasternal short-axis view, a small portion of the right ventricular chamber needs to be visualized permitting the right ventricular free-wall (RVFW) and IVS to be measured separately. Solutions are to move the transducer cranially one or two intercostal spaces at the same level or slightly more dorsal.
Helpful Tips: M-Mode Measurements, Normal Values • Diastolic measurements of the IVS and left ventricular freewall (LVFW) greater or equal to 6 mm can indicate cardiac disease. The LA enlarges in response to myocardial disease. The normal size of the LA has been highly disputed; however, as a rule of thumb, the LA size should not be greater than 1.5 cm in systole when measured from two-dimensional and M-mode images made at the heart base from the right parasternal short-axis view. Measurement of the LA from the right longitudinal plane may further document LA size over time. Fractional shortening (FS) in normal cats usually ranges from 45 to 55%; some studies have found 40 to 60%. If the patient is overly excited the FS can be elevated; it will be decreased when the cat is sedated or anesthetized. If the patient’s heart rate slows during the examination, it may be helpful to measure the FS again. If the ultrasound machine is capable of performing spectral Doppler, the normal velocities should be approximately 1.0 m/sec. Sequential echocardiograms may be helpful to determine the significance of baseline echocardiograms if clear evidence of heart disease cannot be determined (e.g., left atrial enlargement is not present but thickening of the IVS or LVFW is present).
Echocardiographic Examination • A complete two-dimensional evaluation of the heart includes visual inspection of the size and shape of all the valves, myocardium echogenicity and motion, pericardium, pleural cavity, and even the degree of lung interference. The relative size of the RV and LV from the twodimensional image of the heart should show that the LV size is three times the size of the RV. The normal right-sided heart appears as a small crescent surrounding the LV. The standard examination should include M-mode measurements of the RV and LV. Typically this measurement is done twice to ensure proper positioning of the cursor. The FS should be within 5% at each time point. If variability of the FS goes above this 5%, a third measurement should be made. Careful attention to the measurements of the IVS and LVFW should be done in the feline patient. Typically, electrocardiogram (ECG) leads are not well tolerated. Even the tips of the mitral valves cannot be present for M-mode evaluation of the RV and LV because the interventricular septum will be flattened at this level causing a significant drop in the FS. The aorta-to-left atrium (Ao : LA) ratio is measured at the heart base from two-dimensional and M-mode images, although the actual size of the LA may be more useful. Doppler of the pulmonic valve can be performed at the heartbase. By tipping the transducer up toward the heart base, the pulmonary arteries can be examined for
850
size and to visualize the occasional heartworm. A longitudinal measurement of the LA can be made as another method to document LA size that may be important in sequential evaluation of cardiac diseases. A visual inspection of the left ventricular outflow tract (LVOT) should be done from the right parasternal longitudinal view and will give indication of septal hypertrophy and potential outflow obstruction. M-mode of the mitral valve from the right parasternal longitudinal view can further document hypertrophic changes by demonstrating systolic anterior motion (SAM) of the mitral valve. • Because the majority of the examination has been done in sternal recumbency, most feline patients will allow a short restraint time in left lateral recumbency to Doppler the mitral, tricuspid, and aortic valves. Doppler examination of the aortic, mitral, and tricuspid valves is best achieved while the patient is in left lateral recumbency. The aortic valve should be mapped with Doppler ultrasound to document changes in velocity in the LVOT compared to the aortic valve. In cases of hypertrophy of the IVS, an increase in velocity can be noted in the LVOT due to outflow obstruction. The transducer is placed along the sternum angled toward the heart base with the beam parallel to the sternum to obtain the left parasternal longitudinal-axis view. It may be helpful to view the thoracic radiographs to determine the degree of sternal contact of the heart. Due to the location of the heart in the aged patients, the position of the transducer may need to be more parallel with the spine to obtain cardiac images that will be parallel to flow, which is critical in proper Doppler evaluation.
Helpful Tips • Doppler imaging of the heart from the left parasternal longitudinal axis may be easier to obtain just cranial to the liver. Just move up one or two intercostal spaces cranial to the liver between the sternum and costochondral junction. When attempting to perform a Doppler study too cranially, especially in the aged or diseased patient, it will be difficult to obtain the proper cardiac images for Doppler evaluation.
Left-Sided Heart Failure: Radiographic Signs of Pulmonary Edema The Three Stages of Pulmonary Edema • See Figures 294-3 and 294-4. 1. Pulmonary venous engorgement: remember to assess all four sets of vessels. 2. Interstitial edema: fluid in the perivascular tissues causes blurring and haziness of the pulmonary veins especially in the perihilar region; easier to visualize on the ventrodorsal or dorsoventral views. 3. Alveolar edema: distribution in feline patients is highly variable.
When Heart Failure Advances to Biventricular Failure • End-stage heart failure can lead to additional signs of right-sided heart failure: enlargement of the caudal vena cava, hepatic enlargement, varying degrees of ascites, pleural effusion, and pericardial effusion. See Figure 294-5.
Pericardial Effusion • Pericardial effusion in cats can be hemorrhage, infrequently serous effusion (as seen with heart failure), purulent material (as seen with feline infectious peritonitis), or rarely neoplastic exudates (as reported with lymphosarcoma). • Radiographic findings will be determined by the amount of pericardial effusion, not by the nature of the fluid. In those cases with small volumes, the cardiac silhouette may appear normal. With moderate
(A) (A)
(B) Figure 294-3 A, B, Pulmonary edema: This cat presented following two episodes of respiratory distress. This patient has been receiving a diuretic for the last 4 days. The cardiac silhouette appears severely enlarged. There is a diffuse severe heavy interstitial to alveolar pattern noted consistent with pulmonary edema. Soft-tissue opacity can be seen dissecting between the lung lobes with blunting of the costophrenic angles indication a small volume of pleural effusion.
(B) Figure 294-4 A, B, Pulmonary edema: There is a diffuse patchy interstitial to coalescing alveolar pattern. A moderate amount of pleural effusion is present. The liver is greatly enlarged. The diaphragm appears flattened on the lateral image most likely from the respiratory distress.
851
SECTION 6: Imaging
(A)
(B) Figure 294-5 A, B, Biventricular failure: This cat presented in respiratory distress, this is the same patient that presented months previously with cardiac enlargement and pulmonary edema in Figure 294-4. A moderate amount of pleural effusion is present. The diaphragm cannot be clearly visualized. The liver appears enlarged and the intestines are gas filled consistent with dyspnea and aerophagia. On the ventral-dorsal view, a mass effect (hepatomegaly) is noted in the left cranial abdomen with decreased abdominal detail noted in this quadrant due to peritoneal effusion.
to large accumulations of pericardial effusion, the cardiac silhouette may appear rounded or globoid. • Pericardial effusion can accompany heart disease (see Figures 294-6 and 294-7) or infiltrative disease (see Figures 294-8 and 294-9).
Acquired Heart Disease in Cats • The prevalence of acquired heart disease in cats has not been clearly identified because of the finding of concurrent myocardial disease.
Cardiomyopathies • The type of feline cardiomyopathy (hypertrophic cardiomyopathy [HCM], dilated cardiomyopathy [DCM], or restrictive cardiomyopathy [RCM]) cannot be distinguished on survey thoracic radiographs. Echocardiography is required to differentiate between the different
852
types of cardiomyopathy. Critical evaluation of thoracic radiographs in the feline patients with heart murmurs allows earlier diagnosis and treatment of these patients. Subtle changes in the shape and size of the cardiac silhouette may be the earliest change in patients with feline cardiomyopathy or thyrotoxic cardiomyopathy (TCM). See Chapter 109. A classic valentine shaped heart may be seen in endstage heart failure; however, our goal should be to diagnose feline heart disease much earlier than heart failure.
Feline Hyperthyroidism Causing Secondary Cardiomyopathy • Radiographic signs of thyrotoxic cardiomyopathy can be seen with varying degrees of enlargement of the left-sided heart. If left untreated, some cats may progress to congestive heart failure (CHF). See Figure 294-10.
(A)
(B)
(C) Figure 294-6 A, B, Pericardial effusion: A cat presented following radiation therapy for a mandibular squamous cell carcinoma. There is generalized cardiomegaly. The cranial and caudal lobar veins are enlarged. C, Ultrasound confirms the presence of a moderate amount of pericardial effusion associated with advanced myocardial failure.
853
(A) (B)
(C) Figure 294-7 Pericardial and pleural effusion: A, B, A cat presented for recurrent urinary obstruction. The cardiac silhouette is enlarged. C, A small amount of pericardial effusion and moderate amount of pleural effusion are found during the echocardiogram.
854
(A)
(B) (C) Figure 294-8 A, B, Lymphoma: The cardiac silhouette is greatly enlarged and has a globoid appearance. Pleural effusion is present. Multiple soft tissue nodules are present. C, Pericardial and pleural effusion are present. The myocardial wall is heteroechoic and thickened. The final diagnosis was anaplastic lymphosarcoma within the heart and lungs. HT, heart.
855
SECTION 6: Imaging
(A)
(B)
(C) Figure 294-9 A, B, Right atrial mass: A recent thoracocentesis to remove some of the pleural effusion has resulted in small air pockets within the thoracic cavity. The cardiac silhouette is enlarged and rounded. The increase opacity within the cranial lungs (atelectic lungs) is most likely secondary to the pleural effusion. C, A small volume of pericardial effusion is present. A hypoechoic mass appears to be originating from the right atrial wall. A neoplastic process was suspected.
Hypertrophic Cardiomyopathy • See Chapter 110. • Radiographic changes on the lateral projection include dorsal elevation of the trachea and prominence of the LA. In advanced stages of heart failure, pulmonary edema or pleural effusion may be present. On the ventrodorsal projection in advanced stages, the cardiac apex may appear smaller than the base due to atrial enlargement giving a “valentine” shape to the heart. • Nonselective angiography can reveal marked thickening of the LVFW and IVS in the concentric type of HCM. In cases of asymmetric hypertrophy, obstruction of the LVOT occurs because of IVS hypertrophy. A significant decrease in volume will be noted in the LV. A large filling defect can be seen in cases of papillary muscle hypertrophy. The LA is greatly enlarged. The pulmonary veins are enlarged and may be tortuous.
Cardiac Ultrasound Applications in the Thorax Hypertrophic Cardiomyopathy • The diagnosis of concentric HCM requires finding hypertrophy of the IVS and LVFW greater or equal to 6 mm. In asymmetric forms of
856
HCM, the standard M-mode plane may not document segmental hypertrophy. The two-dimensional image may be a more accurate method to document segmental hypertrophy. The LA will enlarge to greater than 1.5 cm if hypertrophy is clinically significant. The left ventricular chamber becomes decreased because left ventricular wall thickening is on the chamber side of the walls. One form of asymmetric HCM can be suspected from the two-dimensional image when narrowing of the LVOT is observed from the right parasternal longitudinal axis. Doppler confirmation of increased velocity in the LVOT greater than the velocity at the level of the aorta indicates outflow obstruction. The LA will enlarge due to LVOT obstruction. In concentric or asymmetric HCM, the FS will typically be elevated. In HCM, M-mode of the mitral valve may show SAM of the mitral valve. • It is important to rule out hyperthyroidism or hypertension to make a final diagnosis of HCM. Feline patients with hyperthyroidism exhibit thickening of the LVFW, variable changes of the IVS, left atrial enlargement, hypercontractility (elevated FS), and variable degrees of left ventricular dilation. These echocardiographic findings should resolve following treatment of hyperthyroidism. Echocardiographic changes associated with systemic hypertension are highly variable. • End-stage HCM can be difficult to distinguish from other forms of cardiomyopathy, especially if there is only one time point. Echocardiographic findings include increased left ventricular
Imaging: Cardiovascular Disease
(A)
(B) Figure 294-10 Hyperthyroidism: A, Echocardiogram has concentric thickening of interventricular septum (0.6 cm) and left ventricular free wall (0.6 cm). B, The left atrium is still within normal limits (1.43 cm; normal < 1.5 cm).
chamber in diastole or systole, left atrial enlargement, normal to decreased FS, normal to hypertrophied IVS and LVFW, and varying amounts of pericardial and pleural effusions. See Figures 294-11 through 294-13.
Systolic Anterior Motion See Figure 294-14.
Aortic Outflow Obstruction See Figures 294-15 and 294-16.
Dilated Cardiomyopathy • See Chapter 56. • Radiographic findings: On the lateral projection, the heart is enlarged causing dorsal elevation of the trachea. Concurrent pleural effusion, and to a lesser degree, pulmonary edema can be found. On the ventrodorsal projection, the heart has generalized enlargement. Retraction of the lung lobes may be noted on the ventrodorsal projection because of pleural effusion.
• Angiography: In patients with DCM, the LVFW and IVS appear thinner than normal. The chamber of the left ventricle is dilated due to increased volume. The surface of the endocardial margins may appear smooth. The left atrium may be enlarged.
Dilated Cardiomyopathy • The typical echocardiographic findings in DCM include dilated left ventricular chamber in diastole and systole, decreased to normal FS dependent on the stage of disease, normal to thin IVS and LVFW, left atrial enlargement, variable findings of right atrial and right ventricle enlargement, pericardial effusion and pleural effusion. The septum or free wall may not have normal motion. M-mode of the mitral valve will show an increase in the E point septal separation above normal. References use less than 0.2 cm or less than 0.4 cm for normal values. See Figures 294-17 and 294-18.
Restrictive Cardiomyopathy • See Chapter 192. • Radiographic signs may show biatrial enlargement on the ventrodorsal view. Depending on the stage of disease, varying degrees of
857
(A)
(B) (C)
(D) Figure 294-11 Concentric hypertrophy due to hypertrophic cardiomyopathy with left atrial enlargement and congestive heart failure: A, B, Thoracic radiographs taken on presentation because of a history pleural effusion and lethargy. The thoracic radiographs show an enlarged cardiac silhouette. Pleural effusion is present indicated by retraction of the lung lobes from the body wall and blunting of the costophrenic angles. There is silhouetting of the cardiac shadow along the left cranial border. A diffuse heavy interstitial to patchy alveolar pattern is present. C, The interventricular septum and left ventricular free wall are 0.7 cm and 0.7 cm, respectively. D, The left atrium at the heart base is 1.79 cm (normal < 1.5 cm).
858
(A)
(C)
(B)
(D) Figure 294-12 Valentine heart: A and B. Lateral and ventrodorsal radiographs of the thorax show a cardiac silhouette that is markedly enlarged. There is marked biatrial enlargement with rounding of the ventricle. The heavy interstitial pattern in the hilar region, slightly worse in the right hemithorax, is consistent with pulmonary edema. C, The left atrial size is 2.23 cm at the heart base. Notice the increased echogenic “strands” within the left atrium, this will appear as smoke on the real time image and can be a precursor to a thrombus. D, The interventricular septum and left ventricular free wall are both thickened in diastole at 0.9 cm (normal < 0.6 cm). The final diagnosis was end-stage concentric hypertrophy cardiomyopathy since the FS had dropped down to 36%.
859
(A)
(C)
(B)
(D) Figure 294-13 A, B, Concentric hypertrophic cardiomyopathy: The cardiac silhouette appears to be greatly enlarged with a widened heart base and elongation of the left ventricular border. The apex of the heart is shifted to the right hemithorax. A patchy interstitial lung pattern is present, consistent with pulmonary edema. C, The interventricular septum is 0.9 cm and the left ventricular free wall is 1.0 cm in diastole. D, The left atrium is 2.37 cm at the heart base (N < 1.5 cm).
860
Imaging: Cardiovascular Disease
(A) Figure 294-14 Systolic anterior motion of the mitral valve: On the M-mode of the mitral valve, the E-point of the mitral valve closely approximates the septum. The motion of the mitral valve toward the septum (arrow) prior to the E point shows the systolic anterior motion of the septal leaflet of the mitral valve.
generalized cardiomegaly will be present. Pleural effusion, pericardial effusion, and pulmonary edema can be seen in this form of cardiomyopathy. • Angiography of restrictive forms of cardiomyopathy may show left atrial enlargement or biatrial enlargement. The chamber of the LV is close to normal and the IVS and LVFW may be normal to mildly hypertrophied.
Restrictive Cardiomyopathy • The textbook case of RCM has echocardiographic findings of dilated LA, varying dilation of the RA, normal left ventricular chamber with an irregular-shaped lumen, normal to thickened IVS and LVFW, normal to decreased FS, and varying degrees of pericardial and pleural effusions. The walls of the IVS or LVFW can have inhomogeneous echogenicity with alteration in the motion noted on twodimensional image or documented on M-mode if in the standard plane of measurement. This form of cardiomyopathy can be suspected but may be more difficult to diagnose due to the overlap of echocardiographic findings at different stages of cardiac disease. The hallmark of this form of cardiomyopathy is left atrial or biatrial enlargement with relatively normal FS and wall thickness. The endocardium of many older feline patients has a hyperechoic appearance without evidence of significant myocardial disease. See Figure 294-19.
(B) Figure 294-15 Left ventricular outflow tract obstruction: When scanning from the right parasternal longitudinal axis, the left ventricular outflow tract should be imaged. A, In this example, significant narrowing of the left ventricular outflow tract is visualized on the two-dimensional image (arrow). B, The velocity at the level of the aortic valve is compared to the left ventricular outflow tract while scanning from left parasternal longitudinal view. In this example, the velocity was elevated in the left ventricular outflow tract to 5.8 to 6.0 m/s pressure of 135 to 149 mm Hg.
Arrhythmogenic Right Ventricular Cardiomyopathy • On thoracic radiographs, the right-sided heart shows significant enlargement. In some cases, the LA may be enlarged. Radiographic signs of right-sided heart failure may be present.
Left Atrial Thrombus • In the early stage of left atrial embolus, “smoke” can be visualized within the lumen of the LA. It is best to use the highest frequency transducer available to image “smoke” or thrombus formation. It is important to try to image the LA and left auricle in multiple planes because an embolus can be “hiding” in the left auricle. See Figure 294-20.
Unclassified Cardiomyopathy • When the myocardial disease does not follow into a specified category it is ruled as an unclassified form. See Figure 294-21.
Arrhythmogenic Right Ventricular Cardiomyopathy • On an echocardiogram, varying degrees of right ventricular enlargement and right atrial enlargement are present. Variable changes are noted in the LA and LV. See Figures 294-22 and 294-23.
Bacterial Endocarditis • Bacterial endocarditis has been described involving aortic, mitral, and tricuspid valves. Some patients may have concurrent infections involving the aortic and mitral valves. Patients may present with signs of heart failure depending on which side of the heart was involved. See Figure 294-24.
861
SECTION 6: Imaging
(A)
(B)
(C)
(D)
Figure 294-16 Left ventricular outflow tract obstruction and systolic anterior motion. A, Note the narrowing of the left ventricular outflow tract on the two-dimensional image when scanned from the right. B, Systolic anterior motion of the mitral valve is present. C, D, The velocity in the left ventricular outflow tract is 2.0 m/s compared to 1.1 m/s at the aortic valve indicating mild outflow obstruction.
Congenital Heart Diseases Ventricular Septal Defect • Radiographic signs associated with a ventricular septal defect depend on the size of the defect. With a small defect, radiographs may show enlargement of the RV, LA, and subtle enlargement of the pulmonary arteries. Radiographic signs with larger defects show prominent right ventricular enlargement, left ventricular enlargement, overcirculation of the lungs, inconsistent enlargement of the pulmonary arterial segment, and eventual right-sided heart failure with larger shunts. • Angiography shows that ventricular septal defects in cats are usually high within the IVS. Injection of contrast within the left ventricle results in contrast immediately entering the right ventricle. • On 2D echocardiogram a ventricular septal defects usually occur high in the membranous septum. The size of the defect will determine the changes in the left-sided and right-sided heart. A small defect may not be visualized on the two-dimensional image and
862
Doppler ultrasound will be required to identify the location of the ventricular septal defect. See Figure 294-25 and 294-26.
Patent Ductus Arteriosus • In a left-to-right patent ductus arteriosus (PDA), the LV and LA are enlarged on radiographs. Overcirculation of the lungs is present. Echocardiography is the primary method of confirmation of a PDA. Doppler flow studies show retrograde blood flow in the pulmonary artery. Although not present in left-to-right PDA in dogs, some changes in the right-sided heart can be seen in the feline patient. See Figure 294-27.
Heartworm Disease • See Chapter 88. • Heartworms have been visualized most consistently in the pulmonary arteries on the echocardiogram; they may also be seen in the RV. They are seen as two parallel lines. Be careful not to confuse them with chordae tendonae in the RV. See Figure 294-30.
(A)
(C)
(D)
(F)
(B)
(E)
Figure 294-17 Dilated cardiomyopathy: This cat acutely was unable to use both rear limbs within the last 24 hours. A, B, There is enlarged cardiac silhouette and evidence of a small volume of pleural effusion. The cardiac silhouette is shifted to the left hemithorax most likely due to prolong recumbency. A heavy interstitial lung pattern is present. C, The interventricular septum and left ventricular free wall are 0.3 cm. The chamber of the left ventricle is enlarged in systole and diastole. The fractional shortening is severely lowered to 5%. D, E, Within the enlarged left atrium, a thrombus can be visualized with the left auricle. F, The E point septal separation is increased to 0.55 cm.
863
(A)
(B)
(C) Figure 294-18 Dilated cardiomyopathy: Thoracic images and 2D ultrasound image are seen in Figure 294-6 showing a patient with pericardial effusion. A, The interventricular septum is 0.3 cm and the left ventricular free wall is 0.5 cm. The fractional shortening is decreased to 32%. B, The left atrium is increased to 2.08 cm. C, Notice on the longitudinal view of the heart, the right atrium can be seen collapsing; this indicates some degree of cardiac tamponade and would be an indicator that the pericardial fluid needs to be removed.
864
(A)
(C)
(D)
(B)
(E)
Figure 294-19 Restrictive cardiomyopathy: A, B, This cat presented for respiratory distress. Pleural effusion and cardiomegaly are present on the thoracic radiographs. The apex of the cardiac silhouette is shifted to the right hemithorax. Alveolar opacities were present in the right cranial and middle lung lobes. C, Echocardiogram show thickening of the interventricular septum and left ventricular free wall of 0.7 cm. The fractional shortening is decreased to 26%. D, There is biatrial enlargement and focal thickening within the septum from the two-dimensional image. E, M-mode of the aorta and left atrium show the left atrium to be 2.53 cm. Necropsy finding confirmed severe myocardial fibrosis consistent with restrictive cardiomyopathy.
865
(A)
(B)
(C) Figure 294-20 Left atrial thrombus: A cat presented with a chylous effusion. A, While scanning the left atrium initially “smoke” was visualized. Further interrogation of the enlarged left atrium and auricle revealed multiple thrombi. B, The left ventricle is dilated with a decreased frastional shortening of 22%. Notice the severe decreased movement of the left ventricular free wall. C, The E point septal separation is 0.45 cm. An end-stage hypertrophic cardiomyopathy was suspected.
866
(A)
(B)
(C)
(E)
(D) Figure 294-21 Unclassified cardiomyopathy. A, B, There was marked enlargement of the cardiac silhouette. C, The fractional shortening was decreased with an increase in the size of the left ventricular chamber. D, The left atrium was enlarged to 2.43 cm. E, Doppler studies of each of the valves showed a marked regular variability to the waveforms. The aortic valve has been shown as an example. The electrocardiogram showed an abnormal rhythm that was classified as bigeminy.
867
(A)
(B)
(C)
(D) Figure 294-22 Arrhythmogenic Right Ventricular Cardiomyopathy. A cat presented for abdominal distension and depression. A, B, The cardiac silhouette is greatly enlarged with dorsal elevation of the trachea noted on the lateral projection. The caudal vena cava appears enlarged. Severe loss of detail is present in the abdomen. C, The cross-sectional image of the right ventricle and left venticle from a right parasternal view shows the right-sided heart to be greatly enlarged. The interventricular spetum was displaced resulting in a decrease in the left ventricle chamber size. D, The right atrium was greatly enlarged measuring 2.7 cm. Notice the displacement of the atrial septum due to the right atrial enlargement.
868
(A)
(B)
(C)
(D) Figure 294-23 Arrhythmogenic Right Ventricular Cardiomyopathy. A, B, Thoracic radiographs shows a mediastinal shift to the left. Faint air bronchograms are present in the caudal aspect of the left cranial lung lobe. There is generalized cardiomegaly present. The pulmonary vessels appear enlarged. C, Echocardiogram shows an enlarged right ventricle with normal fractional shortening of 45%. D, On the two-dimensional image of the right and left ventricles note the enlargement of the right ventricle and mild flattening of the septum. Notice the increase in lung interference surrounding the cardiac silhouette. The electrocardiogram was interpreted as a bundle branch block. The final diagnosis was an arrhythmogenic right ventricular cardiomyopathy.
869
(A)
(B)
(C)
(D) Figure 294-24 Endocarditis suspect: This cat presented for fever of unknown origin following amputation of the right rear limb for an injection site fibrosarcoma. A, B, Thoracic images showed an increased interstitial pattern with mild cardiac enlargement. C, Echocardiography was performed and shows thickening on the aortic valve leaflet (arrow). D, Aortic insufficiency is documented on continuous wave Doppler ultrasound. The final diagnosis was suspected endocarditis of the aortic valve.
870
(A)
(B) (C)
(D)
(E)
Figure 294-25 Ventricular septal defect: A, B, A 1-year-old cat presented for a heart murmur. The cardiac silhouette is enlarged. The caudal lobar artery and vein appear enlarged on the ventral-dorsal view. C, The echocardiogram reveals a defect in the interventricular septum. The left-sided heart subjectively seems volume overloaded with a normal appearing right heart. D, Note the abnormal shape of the aorta when viewed at the heart base. E, The velocity of the flow across the septal defect is 4.2 m/s.
871
(A)
(B)
(C)
(D)
(E) Figure 294-26 Ventricular septal defect and tricuspid dysplasia: A, B, Generalized cardiomegaly with enlargement of the pulmonary vasculature is consistent with a left-to-right shunt on the thoracic radiographs in this 10-month-old kitten. C, A small defect (arrow) can be visualized within the interventricular septum. D, Echocardiography documents a small ventricular septal defect with a velocity of 6.5 m/s. E, The right atrium appears enlarged and the tricuspid valve had a shortened thickened septal leaflet and clubbed shaped free wall leaflet consistent with tricuspid dysplasia.
872
(A)
(B) Figure 294-27 Patent ductus arteriosus: A 6-month-old cat presented for heart murmur. A, B, The radiographs reveal a generalized cardiomegaly. The pulmonary vasculature is enlarged most notably involving the caudal lobar vessels. A significant increase in peribronchial interstitial opacity is noted. On the ventral-dorsal view, increased soft-tissue opacity is noted at the heart base at the level of the aorta or main pulmonary arterial segment. On the lateral view, this increased density is noted at the level of the aorta at the heartbase. Hepatomegaly is present. A left to right shunt is suspected because of the hypervascular lung field and generalized cardiac enlargement. A patent ductus arteriosus was confirmed on a echocardiogram.
873
(A)
(C)
(B)
(E) (D) Figure 294-28 Tetralogy of Fallot: A, B, Thoracic radiographs show enlargement of the cardiac silhouette. The aortic arch appears enlarged. The pulmonary vasculature appears decreased. C, The two-dimensional image of the heart shows hypertrophy of the right ventricular free wall and enlargement of the right ventricular chamber. D, A large septal defect is present in the interventricular septum (arrows). E, The aorta is enlarged and has overriding with the interventricular septum. See Chapter 209.
874
(A)
(B)
(C)
(D) Figure 294-29 Mitral dysplasia: A, B, Thoracic radiographs demonstrate enlargement of the cardiac silhouette with prominence of the left ventricular border. C, Echocardiogram shows hypertrophy of the left ventricle, free wall and papillary muscles. D, The mitral valves are attached to the interventricular septum and left ventricular free wall near the apex of the heart indicating mitral dysplasia. See Chapter 141.
875
SECTION 6: Imaging
(A) (B)
(C) Figure 294-30 Heartworm disease: A, B,This cat presented for anemia and elevated liver enzymes. The caudal lobar arteries are enlarged. There are moderate bronchial markings in all lung lobes. C,Notice the “equal” signs (hyperechoic outer borders with a hypoechoic central region) indicating the presence of heartworms within the right caudal lobar artery.
Suggested Readings Bonagura JD. 2000. Feline echocardiography. J Feline Med Surg. 2:147–151. Boon JA. 1998. Congenital heart disease In JA Boon, ed., Manual of Veterinary Echocardiography, pp. 410–418. Baltimore: Williams and Wilkins. Boon JA. 1998. Acquired heart disease In JA Boon, ed., Manual of Veterinary Echocardiography, pp. 328–331. Baltimore: Williams and Wilkins. Ferasin L, Sturgess CP, Cannon MJ, et al. 2003. Feline idiopathic cardiomyopathy: a retrospective study of 106 cats (1994–2001). J Feline Med Surg. 5:151–159. Fox PR, Sisson D, Moise NS. 1999. Congenital heart disease. In PR Fox, D Nisson, NS Moise, eds., Textbook of Canine and Feline Cardiology, 2nd ed., pp. 471–535. Philadelphia: WB Saunders.
876
Fox PR, Sisson D, Moise NS. 1999. Feline cardiomyopathies. In PR Fox, D Nisson, NS Moise, eds., Textbook of Canine and Feline Cardiology, 2nd ed., pp. 621–628. Philadelphia: WB Saunders. Henik RA, Stepien RL, Bortnowski HB. 2004. Specturm of M-mode echocardiographic abnormalities in 75 cats with systemic hypertension. J Am Anim Hosp Assoc. 40:359–363. Malik R, Barrs VR, Church DB, et al. 1999. Vegetative endocarditis in six cats. J Feline Med Surg. 1:171–180. Reisen SC, Kovacenic A, Lombard CW, et al. 2007. Prevalence of heart disease in symptomatic cats: an overview from 1998 to 2005. Schweiz Arch Tierheilkd. 149(2):65–71.
SECTION
7 Clinical Procedures
CHAPTER 295
Blood Transfusion Sharon Fooshee Grace
Definition A blood transfusion is defined as the introduction of whole blood or blood components into the blood stream. Although blood component products (e.g., fresh frozen plasma or packed red blood cells) are available at a few blood banks, most cats seen in the private practice setting, as a practical matter, receive whole blood transfusions. Whole blood is easy to collect and administer although feline blood components are limited in availability and must usually be shipped from a supplier. The relative scarcity of feline blood components is, in part, due to the difficulty in separating blood fractions given the small volume, which can be collected from cats. Until recently, it was thought that domestic cats have one blood group system with three possible types: A, B, and rarely, AB. However, in 2005, a new and apparently common feline erythrocyte antigen, the Mik (pronounced “Mike”) antigen, was reported by the University of Pennsylvania. It is likely that other feline erythrocyte antigens, which impact transfusion therapy, will be discovered with continued investigation into feline blood compatibilities. Human blood group antigens are labeled as ABO, but these are not serologically related to the AB blood group system of cats. Unlike dogs, cats have clinically significant, naturally occurring antibodies against foreign blood group antigens, including the Mik antigen, regardless of previous transfusion history. Presence of these preformed antibodies dictates that all cats be blood typed before transfusion (including the first transfusion) and receive only type-compatible blood. Type B cats have high levels of naturally occurring anti-A alloantibodies. Transfusion of less than 1 mL of type A blood into a type B cat results in systemic anaphylaxis, which is potentially fatal. Type A cats have weak antibodies against type B blood. When given type B blood, they may develop a mild transfusion reaction, but it is not life-threatening; however, the transfused erythrocytes will have a significantly shortened lifespan (2 days). The rare type AB cat should be given AB blood, if available; otherwise, type A should be given. Recent discovery of the Mik red cell antigen may explain the unusual situation in which crossmatch incompatibilities or unexpected transfusion reactions have occurred in typed, blood group compatible donor/recipient pairs. It is important to note that because of these pre-existing antibodies, there is no universal donor blood type in cats. Worldwide, type A is the most common blood type. Domestic shorthair cats are more often type A, as are Siamese and their related breeds (i.e., Oriental Shorthair, and Tonkinese). British breeds (i.e., British Shorthair, Devon Rex, and Maine Coon) have a higher frequency of type B blood. However, it should never be assumed that any particular breed will possess a certain blood type. Also, the proportion of blood types can vary considerably depending on specific geographic location. Inheritance of AB blood type occurs in a simple dominant fashion via two alleles at the same gene locus. Type A is completely dominant over type B. Cats expressing blood type A may be genotypically homozygous (A/A) or heterozygous (A/B). Cats expressing blood group B are always homozygous (B/B) because type B is recessive to type A. The rare type AB cat expresses both A and B erythrocyte antigens but does not possess naturally occurring alloantibodies against either type; both antigens are
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
recognized as self-antigens. Mode of inheritance of the Mik antigen is unknown at this time.
Indications • Life-threatening blood loss • Bone marrow failure • Hemolysis
Equipment and Supplies • Sixty mL syringe • Intravenous catheter • Butterfly catheter, preferably 21-gauge or central venous catheter, preferably 20 gauge • In-line microthrombi filter • Citrate phosphate dextrose adenine (CPDA-1) anticoagulant • Sedatives • Replacement fluids for donor • Note that the Association of Veterinary Hematology and Transfusion Medicine maintains a web site with links to blood banks and sources for transfusion supplies: http://www.vetmed.wsu.edu/orgAVHTM/links.asp
Procedure Screening and Maintenance of Donor Cats • Blood Typing of Donor: Blood typing is performed to determine the nature of blood group antigens on the erythrocyte membrane. Blood may be sent to a commercial laboratory for typing but, when time is limited, in-house blood typing may be done with affordable, reliable, user-friendly kits. See Figure 295-1. Recipient cats must always receive type-specific blood from the donor (i.e., type A recipient cat must receive type A donor blood; type B recipient must receive type B donor blood; type AB cats should receive type AB donor blood or, if none available, type A donor blood). Therefore, the blood type of the donor cat must be known and compatible with that of the recipient. Also, note that breeding toms and queens should be blood typed; breeding pairs must be of the same type to prevent kitten loss due to neonatal isoerythrolysis. Specific testing for the new Mik antigen is available in the Hematology and Transfusion Lab at the University of Pennsylvania (phone: 1-215-73-6376). • Donor Selection and Yearly Evaluation: Donor cats should be of good temperament and adequate body size (usually >5 kg [11 lbs]) to facilitate phlebotomy. Lean body condition is desirable to facilitate access to the jugular vein. Donors should be neutered and have no history of health problems or need for medications. They should undergo frequent physical examinations and receive vaccinations as indicated by risk assessment. Lab work should be performed once or twice yearly: complete blood count, biochemical profile, urinalysis, screening for infectious agents (i.e., feline leukemia virus, feline immunodeficiency virus, Mycoplasma haemofelis [previously Hemobartonella felis], Bartonella, and Dirofilaria immitis [in endemic areas]). If a donor colony is maintained, records should be kept that note the date and amount of each collection to avoid excessive collection from any individual cat.
879
SECTION 7: Clinical Procedures
to screen cats for the Mik antigen, which can cause transfusion reactions in blood-type compatible cats.
Collection of Whole Blood
Figure 295-1 Blood typing of this cat resulted in a type A result. The control and B pads show no agglutination. Agglutination is obvious in the A pad. • Parasite Control: Donor cats should receive regular deworming for intestinal parasites and heartworm prevention in endemic areas. A strict program of ectoparasite control should be maintained to prevent the donor from becoming infected with Bartonella and other arthropod-borne parasites. • Environment: Donor cats should reside indoors only and have no contact with cats that have access to the outdoors. • Collection from the Donor Cat: Most donors can safely give 10% of their blood volume (66 mL/kg of body weight = 1 blood volume) with no adverse effect every 4 to 6 weeks. Up to 20% of blood volume may be collected if the donor is supplemented with intravenous fluids to combat hypovolemia. Note that published ranges for maximum donation volumes are 11 to 13 mL/kg body weight. For the average size cat, donation of one “unit” translates to ≤50 ml of blood. The donor packed cell volume (PCV) should be checked prior to every collection. Iron supplementation is suggested for cats donating at least once a month (10 mg/kg twice weekly, PO). The donor should not be used if its PCV is less than 35%.
• Precollection PCV of Donor: Occasionally, the donor will have an undetected illness, resulting in anemia. Thus, it is always advisable to determine the donor PCV prior to collection to avoid a potential disaster. • Sedation: Most cats need to be sedated prior to blood collection. Ketamine/diazepam or ketamine/midazolam combinations are often used. Gas anesthetics (i.e., isoflurane and sevoflurane) are also acceptable. Acepromazine and xylazine should be avoided due to the risk of causing hypotension. • Selection and Preparation of the Vein: Alternate between the left and right jugular veins with each collection, and indicate the vein used for each collection in the donor record book. An aseptic technique is essential. The area over the jugular vein should be clipped and surgically prepared prior to collection. • Collection: Using a 21-gauge butterfly catheter, which has been primed with a small amount of CPDA-1 anticoagulant, penetrate the jugular vein and collect blood into a 60-mL syringe. The syringe should contain approximately 1 mL CPDA-1 anticoagulant for each 9 mL of blood to be collected. Gently mix the blood in the syringe as it is collected. Do not allow air to enter the collection line as the needle is withdrawn because this may allow bacteria to enter the blood; clamping the butterfly line with a hemostat can minimize this risk. The standard feline blood donation from cats greater than 4 kg is 45 to 50 mL. An easy method for keeping the blood-to-anticoagulant ratio proportional is to collect 44 mL of blood into 6 mL of anticoagulant for a total volume of 50 mL. • Replacement Fluids: Following collection, the donor cat should receive intravenous crystalloid fluids, such as lactated Ringer ’s or 0.9% saline, over 30 minutes. The volume should be approximately two to three times the amount of blood donated. • Storage: If the blood is needed primarily for erythrocytes, it can be refrigerated and stored for three to four weeks with CPDA-1 anticoagulant. If the blood is needed for maximum effect of clotting proteins and platelets, it should be administered within 6 hours of collection. Blood, which is collected in heparin, must be used immediately; it is not suitable for storage. • Blood Bags: Small blood collection bags suitable for cats are an alternative to syringe collection and are ideally suited for keeping blood on hand in a closed system, thus minimizing the risk for bacterial contamination. • Cardiocentesis: This can be used for blood collection; however, this procedure is likely to cause significant myocardial or valvular damage, and the donor is prone to shock because blood collection can be so rapid. Use of cardiocentesis is strongly discouraged except under the direst of circumstances.
Major and Minor Crossmatching • Cross-Matching: Cross-matching is performed to detect the presence of significant levels of antibody against erythrocyte antigens. Ideally, both blood typing and cross-matching should be performed. Crossmatching is especially indicated for any cat that has been previously transfused or in which the previous transfusion history is unknown. Major cross-match is the most important of the two types of crossmatches and determines the effect that recipient antibodies have on donor erythrocytes. Minor cross-match determines the effect of donor antibodies on recipient erythrocytes. Fortunately, desktop major and minor cross-match kits are now available. These offer the advantage over traditional cross-match methods of avoiding autoagglutination in the setting of immune-mediated hemolytic anemia. Note that a major cross-match is the only in-house means available
880
Administration of Whole Blood • Blood Typing of Recipient: See Blood Typing of Donor. • Pretransfusion Baseline Data: Record recipient vital signs (i.e., pulse, temperature, and respiration rate) prior to starting the transfusion, and repeat every 15 to 30 minutes during the transfusion. • Route: The intravenous route of administration (i.e., peripheral or central) is preferred, although the intraosseous route is an acceptable alternative if venous access is not possible. Small catheters do not cause hemolysis during transfusion but will slow the rate of administration. A microthrombi filter should be placed in the line between the blood and the cat, depending on type of administration set used. The blood should be not be cold; it should be warmed or allowed to rise to at least room temperature.
Blood Transfusion
• Volume of Whole Blood to Transfuse: Volume needed for transfusion can be calculated with the following formula: Volume ( mL ) =
70 × Wt ( kg ) × (desired PCV − recipient PCV ) PCV of donated blood
• The recipient PCV does not need to return to the normal range; in most cases, a PCV of 20 to 25% is quite acceptable. If the recipient is transfused to over 25%, the bone marrow may not receive adequate stimulus to respond to the anemia. In general, no more than 20 ml/ kg per day should be transfused unless the cat has severe ongoing hemolysis or blood loss. • Rate of Administration: In stable cats, administer whole blood at ≤1 mL/min to observe for acute transfusion reactions. If no reaction is noted after a few minutes, administer the remainder of the blood at 5 to 10 mL/kg per hour. Cats with cardiovascular disease should be transfused at a slower rate (4 ml/kg per hour). The transfusion should be completed in less than 4 hours to minimize bacterial growth on the blood. If the recipient cat has experienced massive blood loss, the cat should receive blood as quickly as possible (up to 60 ml/kg per hour). No medications or fluids (other than 0.9% saline) should be added to blood products or administered through the catheter during the transfusion. • Hemoglobin Solutions: Administration of Oxyglobin® (5–15 ml/kg IV) may be useful if whole blood or blood products are not available. Oxyglobin® is currently limited in availability and is expensive. It has the potential to cause volume overload in cats so slow infusion rates of 0.5 to 5 mL/kg per hour are recommended. Although it may increase the amount of oxygen carried by blood, the oxygen may not be effectively delivered to tissues due to vasoconstriction and reduced cardiac output caused by the drug.
Possible Complications • Volume Overload: Except in the situation of acute blood loss, the recipient cat will be deficient in erythrocytes but not plasma (i.e., has
normal blood volume). Because of this, whole blood transfusion can easily volume overload the recipient cat. Great care must be given to monitoring for volume overload through attention to lung sounds (pulmonary edema), respiratory rate (tachypnea), and if necessary, thoracic radiographs. • Transfusion Reaction: Transfusion of incompatible blood can result in sudden death of the recipient cat. Immediate transfusion reactions are the most life-threatening. Initial signs include hemoglobinemia, hemoglobinuria, vocalization, bradycardia or tachycardia, pallor, weak pulses, lateral recumbency, vomiting, dilated pupils, salivation, opisthotonos, collapse, and death. If a transfusion reaction is suspected, the transfusion should be stopped immediately and normal saline administration should be initiated or continued. Treatment for disseminated intravascular coagulation and shock may be indicated, requiring administration of glucocorticoids, epinephrine, or antihistamines.
Suggested Readings Castellanos I, Cuoto CG, Gray TL. 2004. Clinical use of blood products in cats: A retrospective study (1997–2000). J Vet Intern Med. 18(4):529–532. Haldane S, Roberts J, Marks SL, et al. 2004. Transfusion medicine. Compend Contin Educ. 26(7):502–518. Klaser DA, Reine NJ, Hohenhaus AE. 2005. Red blood cell transfusions in cats: 126 cases (1999). J Am Vet Med Assoc. 226(6):920–923. Knottenbelt CM. 2002. The feline AB blood group system and its importance in transfusion medicine. J Feline Med Surg. 4(2):69–76. Wardrop KJ, Reine N, Birkenheur A, et al. 2005. ACVIM Consensus Statement: Canine and feline blood donor screening for infectious disease. J Vet Intern Med. 19(1):135–142. Weinstein NM, Blais MC, Harris K, et al. 2007. A newly recognized blood group in domestic shorthair cats: The Mik red cell antigen. J Vet Intern Med. 21(2):287–292.
881
CHAPTER 296
Bone Marrow Aspiration Mitchell A. Crystal
Definition Bone marrow aspiration is the collection of bone marrow cells by needle aspiration from the bone marrow cavity followed by expression and spread onto a microscope slide for cytologic evaluation. Common bone marrow cavity sites used for aspiration include the humeral head (preferred; technically easier) and the femoral trochanteric fossa.
•
Indications • Evaluation of cytopenias or cytophilias not readily explained by history, physical examination, or clinical pathologic testing. • Evaluation or staging of neoplastic processes, especially lymphoid neoplasia. • Evaluation of suspected systemic infectious diseases (e.g., histoplasmosis and toxoplasmosis). • Evaluation of hyperglobulinemias.
• • •
Illinois Sternal/Iliac, or similar style needles. They are available from most veterinary or human medical supply companies. Most are disposable. Two mL of 2 to 3% ethylenediaminetetra-acetic acid (EDTA) solution; purchase from commercial lab or supply company. One source is MWI Veterinary Supply, 1-800-824-3703. Alternatively, prepare as follows: put 0.35 mL of sterile isotonic saline into a 7-mL EDTA tube; this produces 0.35 mL of 3% EDTA if the original tube contained EDTA powder or 0.42 mL of 2.5% EDTA if original tube contained EDTA liquid. Petri dish or watch glass. Microhematocrit tube. Several clean, new, frosted-end microscope slides.
Procedure Via Humeral Head
Contraindications • If anesthesia is contraindicated.
Equipment and Supplies • • • • • •
See Figure 296-1. Supplies and materials for anesthesia and sterile site preparation. Sterile gloves. Sterile drape. 12-mL syringe. Bone marrow aspirate needle. Options include 18-gauge, 1-in Rosenthal; 18-gauge or adjustable 1/16-in to 1 7/16-in Jamshidi,
Figure 296-1 Supplies needed to perform a bone marrow aspirate include a bone marrow aspirate needle (Illinois Sternal needle pictured), 12-mL syringes with 2 mL of 2 to 3% ethylene diamine tetraacetic acid (EDTA), microhematocrit tube, a Petri dish (or watch glass), and several clean frosted end microscope slides. Anesthesia supplies and sterile drape and gloves are not pictured.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
882
• See Figure 296-2. • Anesthetize and place the patient in lateral recumbency. • Have an assistant outwardly rotate (abduct) the forelimb so that the cranial aspect of the limb is facing upward. It will be parallel with the table. The limb will be held in this position until the procedure is completed. • Palpate the proximal cranial aspect of the humeral head about 1 cm (3/8 in) distal to the scapulohumeral joint to detect a small notch or divot. Clip and sterilely prepare a 3 × 3-cm (1.25 × 1.25-in) area over this site. • Place the sterile drape over the limb with a hole cut over the prepared site.
Figure 296-2 Bone marrow aspiration, humeral head: With the patient in lateral recumbency, the forelimb is abducted, and the bone marrow needle is advanced at a 90-degree angle into the notch/divot of the humeral head located about 1 cm (3/8 in) distal to the scapulohumeral joint. Once the needle is seated into the humeral head, marrow fluid is aspirated into a 12-mL syringe containing 2 mL of 2 to 3% ethylene diamine tetraacetic acid (EDTA). The sterile drape has been removed in this picture to allow visualization of technique.
Bone Marrow Aspiration
Figure 296-3 A successful aspirate results in nonclotted blood with lipid droplets and bony spicules. A microhematocrit tube is used to collect a few spicules to transfer to a glass microscope slide.
• Using sterile technique, aspirate 2 mL of EDTA into a sterile 12-mL syringe. Keeping the syringe sterile, set it aside for later use. • Place the bone marrow needle (with stylet in place) onto the notch/ divot at a 90-degree angle to the humerus. Slowly advance the needle 0.5 to 1.0 cm (3/16–3/8 in) by slowly rotating it clockwise and counterclockwise and applying moderate forward pressure. • Confirm that the needle is firmly seated into the humeral head, remove the stylet (keeping it sterile in case further needle repositioning is necessary), attach the 12-mL syringe containing the EDTA, and aspirate several times. A positive result appears as slightly thick, lipid droplet-containing blood filling the syringe. Stop aspirating once 2 to 3 mL of bone marrow fluid is retrieved. If no fluid is retrieved, remove the syringe, replace the stylet, reposition (advance or retract) the needle, and reaspirate. • Once bone marrow fluid is retrieved, remove the entire needle (syringe still attached) from the humeral head and quickly expel its contents into the Petri dish or watch glass. A successful aspirate will appear as blood containing tiny lipid droplets and bony spicules, most noticeable as opaque/gray flecks when gently rocking the Petri dish or watch glass. If these are not seen, repeat the aspirate. • Once successful aspiration is complete, use a microhematocrit tube to draw up three to six spicules by capillary action; gently tilt the Petri dish to allow the blood to drain to one side, usually a few bone marrow spicules will adhere to the bottom of the dish; touch one end of the microhematocrit tube to three to six of these. See Figure 296-3. Tap or blow the spicules out onto a microscope slide toward the frosted end, then use the microhematocrit tube to draw up excess blood from the slide, being careful to avoid the spicules. Once the spicules are left with only minimal blood, use a second slide placed flat and at 90-degree angle on the spicule-containing slide to smear the spicules toward the nonfrosted edge. See Figure 296-4. A light amount of pressure will be necessary to make a uniformly smeared slide. Rapidly dry the slide by waving it in the air or using a slide drying device such as a blow drier or cup warmer. • Repeat the slide preparation to make several slides. Label the frosted end of each slide with a pencil for laboratory submission (unstained) or for in-house staining and microscopic review. Be sure to hold two or three slides unstained for potential other use (e.g., feline leukemia virus test by immunofluorescent antibody [IFA], and special staining for fungi).
Figure 296-4 Once bone marrow spicules have been transferred to a microscope slide, a second slide is used to smear the spicules. A uniformly smeared specimen is accomplished by using slight pressure with the second slide placed on top and at a 90-degree angle to the first.
Figure 296-5 Bone marrow aspiration, femoral trochanteric fossa: With the patient in lateral recumbency, the hindlimb is grasped with the index finger on top of or lateral to the femur and pointing toward the trochanteric fossa. The bone marrow needle is introduced medial to the greater trochanter in the trochanteric fossa and advanced along the shaft of the femur. Once the needle is seated into the femoral shaft, marrow fluid is aspirated into a 12-mL syringe containing 2 mL of 2 to 3% ethylene diamine tetraacetic acid (EDTA). The sterile drape has been removed in this picture to allow visualization of technique.
Via Femoral Trochanteric Fossa • See Figure 296-5. • Anesthesia, patient and material preparation, sterility, aspiration, and slide preparation are the same as for aspiration at the humeral head. • Position the patient in lateral recumbency. Place a drape over the leg and lumbar area; cut a hole in the drape over the trochanteric fossa region.
883
SECTION 7: Clinical Procedures
• Grasp the leg with the left hand (opposite for left-handed individuals) such that the index finger lies on top of or lateral to and parallel to the femur with the tip of the finger pointing toward the trochanteric fossa. • Place the bone marrow needle medial to the greater trochanter so that it is slightly below and parallel to the index finger grasping the femur. The goal is to advance the needle through the trochanteric fossa and into and along the length of the marrow cavity of the femur. Slowly advance the needle 1 to 2 cm (3/8–3/4 in) by slowly rotating it clockwise and counterclockwise and applying moderate forward pressure. • Confirm that the needle is firmly seated into the humeral head by moving the femur forward and backward; the needle should move with the femur. Proceed as mentioned previously.
884
Possible Complications • Nondiagnostic sample (no spicules from either poor technique or poor sample/disease [“dry tap”, e.g., fibrotic or neoplastic tissue packed marrow]) • Fracture • Damage to the sciatic nerve
Suggested Readings Tyler RD, Cowell RL, Meinkoth JH. 2008. The bone marrow. In RL Cowell, RD Tyler, JH Meinkoth, et al., eds., Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., pp. 422–450. St. Louis: Mosby Elsevier.
CHAPTER 297
Central Venous Catheter Placement Mitchell A. Crystal
Definition Central venous catheter placement is the placement of a catheter into a central/large vein. Jugular veins are most commonly used, though other central sites are also available via advancing longer catheters from peripheral to central veins (e.g., cephalic to axillobrachial, omobrachial, or jugular vein; lateral saphenous to femoral vein). Please note that while the definitions, indications, contraindications, preparation, and approach to the site presented in this chapter are universal to central venous catheter placement, the equipment, supplies and technique are described for a through-the-needle catheter system; some changes in technique would be required for other types of catheters (e.g., peel away, Seldinger or J-wire).
• • • • •
with small veins, a 19-gauge/5-cm [2-in] needle with a 22-gauge/ 20-cm [8-in] catheter may be used). I recommend Intracath™ catheters by Becton Dickinson, available through many veterinary supply companies. Syringes containing heparinized saline. Adhesive tape, 2.5 cm (1 in). T-port preinfused with heparinized saline and with injection cap on end. Roll gauze bandage material. Roll nonadhesive bandage material (e.g., Vetrap® and Coflex®)
Procedure Indications • • • • •
To allow intravenous fluid or blood product administration. To allow intravenous medication administration. To allow repeated blood collection. To allow central venous pressure measurement (jugular vein). To assist in diagnostic testing procedures (e.g., iohexol clearance testing and intravenous urography).
Contraindications • Coagulopathy • Lesions over vascular site (neoplasia, infection, inflammation, trauma, edema, and hematoma)
Equipment and Supplies
• Jugular placement is described; cephalic or lateral saphenous sites may also be used with slight variations in technique. • Sedation or anesthesia should be used if necessary. • Clip and sterilely prepare an area over the jugular vein. • Restrain the patient in lateral recumbency. If using the right jugular vein, position the patient in left lateral recumbency with the legs extending toward you (away from you if you are left handed); if using the left jugular vein, position the patient in right lateral recumbency with the legs extending away from you (toward you if you are left-handed). • Occlude the jugular vein at the thoracic inlet with the left hand (right hand if left-handed). • Insert the needle bevel up through the skin and into the jugular vein beginning at the proximal one-third of the neck. The needle should be aimed toward the thoracic inlet. See Figure 297-2. • When blood flashes back into the catheter, continue to advance the needle another 3 to 5 mm (3/16–3/8 in) and then stop.
• Supplies and materials for sterile site preparation. • Through-the-needle intravenous catheter (a 17-gauge/5-cm [2-in] needle with a 19-gauge/20-cm [8-in] catheter is preferred [Figure 297-1]; for smaller or significantly dehydrated patients or for patients
Figure 297-1 Through-the-needle intravenous catheter (a 17-gauge, 5-cm [2-in] needle with a 19-gauge, 20-cm [8-in] catheter is preferred.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 297-2 Insert the needle bevel up through the skin and into the jugular vein beginning at the proximal one-third of the neck. The needle should be aimed toward the thoracic inlet.
885
SECTION 7: Clinical Procedures
Figure 297-3 To advance the catheter through the needle, firmly grasp the short, hard plastic tube at the top of the soft plastic sleeve with the left thumb and index finger (reverse hand roles for left-handed individuals). Using the right hand, push the catheter within the soft plastic sleeve through the needle and into the vein. Figure 297-5 Withdraw the needle from the skin, place the needle guard over the needle, and snap the needle guard closed. Be careful to orient the needle guard in the correct direction. There is a notch for the needle hub. Avoid pinching the catheter when closing the needle guard.
Figure 297-4 Firmly hold the plastic catheter tip and remove the wire stylet. Be sure to hold the plastic catheter tip and not the needle, or removing the stylet will also remove the catheter/entire device from the patient. Place a heparinized saline primed T-port in the catheter opening after the stylet has been removed. Figure 297-6 Check the catheter prior to final bandaging by aspirating at T-port injection cap to confirm return of blood then flushing to confirm easy flow. • To advance the catheter through the needle, firmly grasp the short, hard plastic tube at the top of the soft plastic sleeve with the left thumb and index finger (reverse hand roles for left-handed individuals). Using the right hand, push the catheter within the soft plastic sleeve through the needle and into the vein. See Figure 297-3. To seat/snap the catheter into place, firmly push the plastic tip of the wire stylet into the hard plastic tube at the top of the soft plastic sleeve; the hard plastic tube with the attached soft plastic sleeve will disconnect from the needle. • Firmly hold the plastic catheter tip and remove the wire stylet. See Figure 297-4. Be sure to hold the plastic catheter tip and not the needle, or removing the stylet will also remove the catheter/entire device from the patient. • Place the T-port/injection cap into the catheter and flush catheter with heparinized saline. • Withdraw the needle from the skin, place the needle guard over the needle, and snap the needle guard closed. Be careful to orient the needle guard in the correct direction. There is a notch for the needle
886
•
• •
• •
hub. Also, avoid pinching the catheter when closing the needle guard. See Figure 297-5. Position the needle guard/catheter/T-port so that it is accessible at the craniodorsolateral aspect of the neck, caudal to the base of the ear. Use adhesive tape to affix the catheter/T-port to the needle guard and to affix the needle guard/catheter/T-port to the neck. Check the catheter prior to final bandaging by aspirating at the T-port injection cap to confirm return of blood then flushing to confirm easy flow. See Figure 297-6. Apply roll gauze bandage material (light to moderate tightness) followed by nonadhesive bandage material (very light tightness). Perform final catheter check by aspirating at T-port injection cap to confirm return of blood then flushing to confirm easy flow.
Central Venous Catheter Placement
Possible Complications • During placement: hemorrhage, hematoma, subcutaneous catheter placement, pinching of catheter within needle guard, or catheter breakage. • Following placement: catheter occlusion/breakage, thrombophlebitis, infection, catheter dislodgement to subcutaneous site with subcutaneous fluid/medication administration, or positional catheter flow.
Suggested Readings Beale MW. 2005. Placement of central venous catheters, Seldinger technique. North American Veterinary Conference Clinician’s Brief. 3(10):7–10. www.vetmed.wsu.edu/resources/Techniques/jugcath.aspx. This Washington State University, College of Veterinary Medicine web site provides images and instruction on Intracath™ and Intrafusor™ catheter placement in the jugular vein of a dog.
887
CHAPTER 298
Cerebrospinal Fluid Collection Mitchell A. Crystal
Definition The retrieval of cerebrospinal fluid (CSF) from the subarachnoid space for laboratory evaluation.
Indications • To determine the general nature of central nervous system disorders; however, only on occasion does CSF collection and evaluation reveal a specific diagnosis. • To further investigate fever of unknown origin once common causes have been eliminated.
Contraindications • Increased intracranial pressure; clinical signs may include anisocoria, mydriatic or nonresponsive pupils, dull mentation or altered state of consciousness, rigid paresis, altered respiratory patterns and heart rhythms (especially bradycardia), or coma • Coagulopathy
Equipment and Supplies • • • •
Supplies and materials for anesthesia and sterile site preparation Sterile gloves Butterfly catheter, 23-gauge Red top tube
Procedure • See Figure 298-1. • Anesthetize the patient. • Clip and sterilely prepare a 4 × 4-cm (1.5 × 1.5-in) area on the dorsal cervical midline between the occipital protuberance and the dorsal spinous process of C2 (the axis). • Place the patient in right lateral recumbency with the nose and feet positioned away from the collector and with the nose parallel to the table and the head ventroflexed to open the atlanto-occipital space. (Left-handed individuals may prefer to reverse the position of the patient and the role of each hand.) The shaved area should be positioned so that it extends just off the edge of the table. • Kneel or sit in front of the patient so that the shaved area is at eye level. Wearing sterile gloves, place the middle finger and thumb of the left hand on the cranial aspects of the left and right wings of the atlas, respectively, and place the index finger on the cranial aspect of the dorsal spinous process of the axis. • Insert the needle (using the right hand, bevel facing cranial for lesions cranial to the foramen magnum and caudal for lesions caudal to the foramen magnum) on the midline just in front of the left index finger placed on the dorsal spinous process of the axis; this facilitates insertion of the needle in the caudal area of a triangle formed by the cranial
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
888
Figure 298-1 Atlanto-occipital cerebrospinal fluid collection. The patient is positioned in lateral recumbency with the nose parallel to the table, the head ventroflexed, and the shaved and prepared area positioned just off the table. The needle of a 23-gauge butterfly catheter is slowly inserted on midline just in front of the dorsal spinous process of the axis and directed toward the tip of the nose. Once fluid appears in the tubing, the needle is held still and the fluid is collected into a red top tube.
•
•
•
•
•
aspects of the wings of the atlas and the occipital protuberance. Aim the needle toward the tip of the nose. Slowly advance the needle until fluid is seen entering the clear tubing attached to the catheter. Sometimes a popping sensation can be felt when the needle penetrates the dura mater, at which point forward needle motion should be temporarily stopped to see if fluid flows into the catheter tubing. If the needle strikes bone during insertion, slightly redirect the needle cranial or caudal to attempt to enter the atlanto-occipital space. In this case, success is usually only achieved by withdrawing the needle, reassessing landmarks, and repeating the procedure from the beginning. Collect about 1.0 mL of CSF fluid in the red top tube. If the CSF drips at an extraordinarily slow rate, bilateral jugular vein compression can be attempted to hasten flow. Once sufficient fluid has been collected, the needle is removed and any fluid remaining in the catheter is allowed to drip into the collection tube. The CSF sample should be processed within 30 minutes of collection because low CSF protein levels lead to rapid deterioration of cells. Minimum analysis should consist of a total nucleated cell count, a total red cell count, a differential cell count and cytological review, and a protein concentration level. Total cell counts can be completed by loading CSF directly onto a hemocytometer and separately counting the number of leukocytes and erythrocytes on all nine large squares. The number of cells counted is multiplied by 1.1 to get the total cell count (total red cells/µL and total white cells/µL). With practice, red and white blood cells can be differentiated on unstained specimens. An inhouse staining technique can be used, if needed. A small amount of new methylene blue stain is drawn into a microhematocrit tube. The
Cerebrospinal Fluid Collection
paper so it is the size of the microscope slide, then cut a hole in the center of this rectangle just larger than the diameter of the barrel of the tuberculin syringe. Place the paper on the slide and the syringe (cut side up/away from the slide) on the paper/slide so that the barrel aligns over the hole in the filter paper. Clamp the syringe down so that it and the slide/paper device are stable in this alignment. CSF (0.2 to 0.3 mL) is placed in the barrel of the syringe and allowed to stand for 30 to 60 minutes for sedimentation and fluid wicking. The slide is then submitted to the lab (unstained) for review or stained for in hospital evaluation. • Protein concentration can be determined by sending the remaining CSF in the red top tube to the lab; protein levels in CSF are relatively stable and can be reliably assessed the next day. Clinically useful protein determinations can be performed in house using the protein pad of a urine chemistry dipstick; protein levels may be slightly underestimated via this method as dipsticks are relatively insensitive to globulins.
Possible Complications Figure 298-2 An in-house cell concentrating device can be constructed to facilitate rapid preparation and evaluation of cerebrospinal fluid samples. The sample should be processed within 30 minutes because low cerebrospinal fluid protein levels lead to rapid cell deteriora.
tube is then tilted to move the dye to the middle of the tube. A small amount of CSF is drawn into one end of the tube, creating a column of CSF and new methylene blue separated by an air pocket. The tube is gently rocked back and forth so that the two columns move from side to side but do not directly contact each other. The tube is then left undisturbed for 10 minutes. This results in a slightly stained, undiluted CSF sample that can be used for cell counts via hemocytometer as described previously. • A differential cell count and cytological review should be completed following a concentration technique because CSF is typically of extremely low cellularity. This can be performed by most labs on a 0.5-mL sample preserved in 40% ethanol (check with lab in advance). Alternatively, an inexpensive in house concentrating device can be constructed using a tuberculin syringe, a piece of filter paper (coffee filter paper will do), a glass microscope slide, and two small paper clamps. See Figure 298-2. Discard the syringe plunger, and cut and discard the hub end of the syringe at the 0.5-mL mark. Cut the filter
• Hemorrhage noted during CSF collection is usually a result of needle penetration into a blood vessel or the vertebral sinus and is rarely a result of disease-induced subarachnoid space hemorrhage. If this occurs, collection should be reattempted with a new needle as an initial hemorrhagic tap does not necessarily lead to blood contamination on subsequent attempts. This complication is rarely, if ever, a health concern for the patient. • Brain herniation can occur if increased intracranial pressure is present at the time of CSF collection. Indications of herniation may include nystagmus, changes in pupillary size, changes in respiration patterns, and reflex abnormalities. Therapy for increased intracranial pressure is immediately warranted (e.g., hyperventilation, mannitol, or corticosteroids). • Spinal cord puncture can occur from CSF collection if increased intracranial pressure is present or from advancing the needle too deeply; however, this is uncommon with the butterfly catheter technique. Signs and management are per brain herniation above.
Suggested Readings Desnoyers M, Bédard C, Meinkoth JH, et al. 2008. Cerebrospinal fluid analysis. In RL Cowell, RD Tyler, JH Meinkoth, et al., eds., Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., pp. 215–234. St. Louis: Mosby Elsevier.
889
CHAPTER 299
Eye Examination Karen R. Brantman and Harriet J. Davidson
Overview The techniques of ophthalmic examination are not complicated, but they do require practice to perform easily on a cat. First, a complete history of the cat’s eye problems, health problems, and potential familial problems should be taken. Next, perform the ophthalmic examination before any other type of manipulation to maximize cooperation. The examination room should be dark and quiet to prevent distraction and allow greater visualization of intraocular structures. Finally, perform a complete physical examination.
Examination of Head and Face • The face should be carefully evaluated prior to restraining the cat. Touching the cat’s face or stressing the cat may mask the true position of ocular and periocular structures. • Evaluate for symmetry and evidence of neurologic problems such as head tilt, ear droop, or loss of muscle mass. • Evaluate eyelids for conformation prior to touching the face. The eyelid margin should be visible along all edges. • Evaluate the eyes to determine if they are both tracking and are of equal size. Viewing the globes over the surface of the head helps to determine if one eye is further forward than the other. Place your face behind or above the cat’s ears and look across the superior eyelid.
Pupillary Light Reflexes • Note the size of the pupils with the room lights on and off. Note the size of the pupils relative to each other, as well as compared to normal. Stressed cats may have large pupils that are slow to respond. Patience and a bright light will aid the response. • Direct: Shine the light in one eye and watch that eye for pupillary constriction. This tests cranial nerves II and III. • Indirect (consensual): Shine the light in the eye and watch the opposite eye for pupillary constriction. This tests cranial nerves II and III, including the retina, optic chiasm, and optic tracts. • Keep in mind that it is possible to have positive pupillary light reflexes (PLR) and no vision, as well as vision and no PLR.
Restraint • Adequate visualization of the eye is crucial; this makes proper restraint of the cat exceptionally important. • The cat’s head usually fits easily in one’s hand, allowing manipulation of the head while maintaining exposure of the eye. See Figure 299-1. • Frequently the third eyelid is passively prolapsed due to retraction of the eye. This can be rectified by putting the cat’s rear quarters higher than its head, scratching the hind quarters, whistling, or moving the cat to the extreme edge of the examination table. This startles the cat so that it contracts its extraocular muscles, allowing
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
890
Figure 299-1 When the cat’s head is held as shown, one can control the eyelids during the ophthalmic examination.
the third eyelid to move downward. Elevating the hind quarters is best accomplished by someone holding the cat’s hind feet with one hand and the front feet with the other. The cat’s front and rear quarters can be easily moved independently.
Retrobulbar Palpation • This technique tests the orbit to determine if there is a mass posterior to the globe. • Place one’s hands over both eyelids and gently push the eyes into the orbit, feeling for pressure preventing the globes from moving deeper into the orbit.
Transilluminator This bright light source allows further examination of the eyelids, conjunctiva, cornea, anterior chamber, iris, pupil, and lens (i.e., anterior capsule/anterior cortex/nucleus/posterior cortex/posterior capsule). A magnification loop or glasses helps highlight small structures. Varying the position of the transilluminator relative to the examiner ’s line of sight emphasizes different ocular structures and makes lesions more easily identified. • Direct Illumination: View the eye from the same direction as the light. A diffuse light source is held far from the eye. A focal light source is held close (approximately 1 cm; 3/8 in) to the eye. • Transillumination: Shine the light across the eye and view from a 90-degree angle. • Retroillumination: Reflect the light off the fundus to illuminate intraocular structures. • Slit Beam of Ophthalmoscope: The slit beam highlights changes in shape or location of structures. A head loop or pair of magnification
Eye Examination
glasses used in conjunction with a slit beam creates a form of slitlamp biomicroscopy.
Schirmer Tear Test • Normal values vary depending on the source of information; however, 12 mm/min is generally considered normal. • It is not uncommon for stressed cats to have a low tear test. Prior to making a diagnosis of sicca (dry eye), the eye should be evaluated for clinical signs of disease. If no other clinical signs are noted, the test should simply be repeated at a later date. • The test is completed by bending the strip at the notched mark, placing it in the lower conjunctival sac, and holding it gently in place for one minute.
Lacrimal Duct Flush • This test evaluates the patency of the lacrimal puncta. This test should be used when epiphora is present without concurrent signs of ocular irritation. • This procedure can be difficult to perform on an awake cat. Topical anesthetic is applied to the ocular surface to prevent the cat from feeling the procedure. However, sedation is usually required. • The puncta are located 5 mm (3/16 in) from the medial canthus near the eyelid margin on both the superior and inferior lids. • A lacrimal cannula or soft and flexible intravenous catheter (23 gauge or smaller) may be used. The flexible catheter may be cut shorter to allow easier handling; a bevel on the end may help in sliding the catheter into the puncta. • A 1- or 3-mL syringe filled with eye wash, saline, or sterile water is attached to the cannula or catheter. • The cannula or catheter is slid along the inner lid edge until it slides into the puncta. • Fluid is injected into the duct until it is seen exiting the nose or the cat swallows excessively. It may also be seen bubbling out of the puncta of the apposing lid. • Fluorescein dye may be added to the eye wash to make the fluid easily visible. However, excess spillage of the dye solution can be difficult to clean up.
Fluorescein Stain • This test stains the corneal stroma and detects corneal ulceration. It can also be used to determine the depth and diameter of the lesion. • Both fluorescein stain strips (which must be moistened before use) and premade stain solutions are available. • To use a stain strip, moisten it with eyewash solution and touch the strip to the sclera. Alternatively, eyewash may be drizzled onto a strip held above the eye, allowing the stained drops to fall into the eye. • Rinse the eye well. Excess stain may be held by mucus strands or an uneven corneal surface, resulting in a false-positive test. Hold cotton balls or tissue under the eye to catch excess stain as it is rinsed. • Stain can be mixed with eye wash or topical anesthetic and sprayed on the corneal surface. Do not store this solution due to likely bacterial contamination. • The stain can be viewed with a normal light source or a cobalt blue filter which aids in fluorescence; a positive stain is green. • To access the depth of the ulcer, view across the corneal surface.
Bacterial Culture • Use small swabs to prevent contamination. To improve results, the swab should be premoistened by breaking the ampoule prior to sample collection.
• Topical ophthalmic anesthesia should be avoided because of the possibility of decreasing bacterial sample growth; however, in some cases it cannot be avoided. • Samples may be taken from eyelid, conjunctiva, or cornea and processed in a routine manner. • The longer the swab is held at room temperature, the poorer the sample quality for culture. Thus, any samples should be placed in the refrigerator immediately after collection. • Samples for Chlamydophila and Mycoplasma require special media because they are obligate intracellular organisms.
Cytology or Special Laboratory Testing • Samples may be collected from the eyelids, conjunctiva, or cornea. • A topical ophthalmic anesthetic is applied to the ocular surface to increase patient cooperation. • A cytobrush allows for the best sample collection, but a small blunt instrument of any kind, including the back side of a scalpel blade, may be used. • The area to be sampled is lightly abraded then smeared on a glass slide. • Routine staining procedures are then followed for cytology. • Samples for polymerase chain reaction (PCR) or indirect fluorescent antibody (IFA) are submitted following the instructions of the testing laboratory.
Intraocular Pressure Measurement • The intraocular pressure (IOP) should be measured in all cases of suspected glaucoma, uveitis, or lens position shift. • Normal IOP is 15 to 25 mm Hg. • Do not restrain the eyelids too tightly or restrict jugular venous flow. Struggling on the part of the cat or any pressure around the patient’s neck may result in false pressure elevations.
Schiotz Tonometry • This instrument measures IOP by corneal indentation. • The 5.5-gm weight load is standard when the instrument is assembled. • Numb the cornea first with a topical anesthetic such as proparicaine. Place the cornea in a horizontal position (i.e., tip the cat’s nose upward). • Place the footplate of the tonometer on the clear cornea. False readings may be obtained if the footplate rests on the sclera or third eyelid. • Record the scale reading, repeat two times, and figure the average of the three. • Convert the scale reading to mmHg using the chart that comes with the instrument. • Normal is 3 to 7 mm Hg on the scale when the 5.5-gm weight is loaded. • If scale reading is less than 0, add weight to the tonometer and repeat the procedure.
Tonopen® • This instrument measures by applanation. It uses ultrasound to measure the pressure required to flatten, or applanate, a specific area of the cornea. • A light touch while using the Tonopen is extremely important. • The cornea is numbed with a topical anesthetic and the cat’s head is held in a normal forward position. The instrument is gently touched to the corneal surface. The instrument will beep as readings are taken. • The value is reported in mmHg with 5% percent error.
891
SECTION 7: Clinical Procedures
Tono-Vet® • This instrument measures by rebound. It measures the return force of a small pin bounced on the corneal surface. • The cat’s head is held in a normal forward position, and again, topical anesthetic applied to the cornea. The instrument is held in front of the eye (a portion of the instrument indicates how far to hold from the eye), and a button is pushed to release the pin. The button is pushed six times to allow for an average to be calculated. The result is reported in mm Hg.
Ophthalmoscopy There are several methods of ophthalmoscopy or fundus examination with advantages and disadvantages for each. It is helpful to dilate the eye with tropicamide prior to examination to view the entire fundus. The optic nerve head should be evaluated for its size, shape, and color, normally being black or gray. Next identify the blood vessels for their caliber, color, and degree of branching. There are commonly three artery and vein pairs with additional arteries coming from the optic nerve head. The tapetal color varies with the coat color of the cat ranging from green to yellow to orange.
Direct Ophthalmoscopy • Place the brow rest of the instrument on your own eyebrow, hold the instrument a few inches from the cat’s eye, and look directly into the eye. • The instrument can be used to evaluate all levels of the eye. Dialing the central wheel of the instrument changes the diopter setting. Red numbers are negative with white or green numbers being positive. The 0 reading has no diopter correction. • The various diopter settings allow examination of the different structures of the eye: +20 (white or green) focuses on the cornea, conjunctiva, and lids; +12 focuses on the anterior lens capsule; +8 focuses on the posterior lens capsule; and 0 to −2 (red) focuses on the fundus. If you wear corrective glasses and remove them prior to using the ophthalmoscope, you will need to make your own corrections to these numbers. • The front of the instrument has variable aperture settings to allow different types of illumination: small spot, large spot, slit beam, and variable color filters. • The advantage of this instrument is simplicity. The disadvantages are the small visible area and the closeness of your face to uncooperative or fractious cats.
Panoptic® Direct Ophthalmoscopy • This instrument allows for greater viewing size when compared to a regular direct ophthalmoscope. It also allows for aperture and diopter setting changes.
892
Figure 299-2 The indirect ophthalmoscope is operated as follows: Hold the light source at eye level; create a line of light from your eye to the cat; and place the lens perpendicular to the line of light, approximately one hand’s distance from the eye.
• To view the fundus, set the aperture setting (horizontal dial on instrument) to the green bar. Hold the instrument to your eye and, with the room lights on, view an object at approximately 5 feet. Use the diopter setting (the vertical, thumb-operated dial) to focus on the object. Turn off the room lights and place the instrument 2 cm (3/4 in) from the patient’s eye (fill the pupil with light), and view the cat’s fundus. • The advantage is simplicity; the disadvantage is a small to moderatesized visible area.
Indirect Ophthalmoscopy • This instrument views a virtual image of the fundus. It requires a focused light source and a lens (20D or 28D are recommended). • Hold the light source at eye level. Create a line of light from your eye to the cat, capturing the tapetal reflection. Place the lens perpendicular to the line of light, approximately one hand’s distance from the eye. See Figure 299-2. • The advantages are visualization of a large area of the fundus and placement of the examiner at a distance from the cat. The disadvantage is the learning curve needed to develop expertise in the use of this instrument.
Suggested Readings Ollivier FJ, Plummer CE, Barrie KP. 2007. Ophthalmic examination and diagnostic procedures. In KN Gelatt, ed., Veterinary Ophthalmology, 4th ed., pp. 438–483. Ames, IA: Blackwell Publishing.
CHAPTER 300
Euthanasia Amanda L. Lumsden and Gary D. Norsworthy
Introduction Although one of the kindest and most compassionate gifts veterinarians can offer their clients, euthanasia is multifaceted and can be one of the most challenging processes faced in practice. The veterinarian is in a unique position to be able to guide clients and their cats through what is often the most difficult time period in the life of the cat and, if handled well, can leave a positive lasting impression with the client. However, if not handled well, years of goodwill between the client and the veterinarian can be severed.
Medical Aspects There are several methods of euthanasia set forth by the American Veterinary Medical Association (AVMA). Approved techniques within the guidelines “should result in rapid loss of consciousness followed by cardiac or respiratory arrest, and ultimate loss of brain function …” with the emphasis on providing the most painless and distress-free death as possible.
Client Relations Why It Must Be Done Properly Clients often struggle with the decision of ending their pets’ lives, and they must ultimately be comfortable with their decision to avoid later feelings of guilt. The veterinarian’s role in this process is to be supportive and honest with the client regarding the timing and medical condition of the cat. The way in which the euthanasia is handled will be the last memory the client has of the veterinarian and his or her interaction with both the family members and the cat. If there is a high level of trust and a strong bond between the client and veterinarian and proper logistics, the euthanasia experience will be a much less painful memory and the client is more likely to return with another cat. However, some clients will have difficulty returning to the hospital where their cats were euthanized due to the association of the hospital and the death of their cat. There are ways the veterinarian and the staff can offset some of these negative associations.
Communication Inhalant Anesthetics, Carbon Dioxide, and Carbon Monoxide Inhalant anesthesia and carbon dioxide (CO2) cause hypoxia due to depression of the cardiac and respiratory centers in the brain stem. If inhalant anesthesia is used, it can take considerable time because the inhaled gas has to reach a lethal level in the alveoli to be effective; thus there is increased exposure to personnel. This method is not recommended if an owner wants to be present for the euthanasia. The addition of potassium chloride to the protocol will facilitate the process by inducing fatal arrhythmias, but this is not the best euthanasia choice either. The use of CO2 requires a separate cylinder, and because it has been reported in humans to be a noxious stimulus to the nasal mucosa, it is not an ideal method. Carbon monoxide (CO) is a colorless, odorless gas that blocks the uptake of oxygen by the hemoglobin molecule of the erythrocyte thereby resulting in fatal hypoxemia. The risks associated with having a cylinder in the hospital far outweigh any benefits of using it as a euthanasia agent.
Barbiturates Use of barbiturates, primarily in the form of sodium pentobarbital, produces the most rapid and reliable method of euthanasia. It is the method of choice set forth by the AVMA guidelines. Unconsciousness from deep anesthesia occurs quickly, progresses to apnea due to depression of the respiratory center in the medulla of the brain stem, and is followed by cardiac arrest. Beuthansia-D® solution, the only currently available drug approved by the Food and Drug Administration for euthanasia, also contains phenytoin sodium, which exerts additional cardiotoxic effects during the deep anesthesia phase, therefore hastening the stoppage of electrical activity of the heart.
When recommending euthanasia, use the terms death, die, euthanasia, or put to sleep. Put down is a commonly used term by veterinarians and breeders, but many cat owners do not know that put down means euthanasia. This can be the source of a tragic and irreversible miscommunication.
Location within the Hospital Ideally, the room used for euthanasia should either be designated for euthanasias (e.g. a “quiet room”) or the least-used examination room. In larger practices, the use of an examination room not typically used by that particular veterinarian is beneficial because it help alleviate any negative associations with that room. Marking the client’s record to indicate an examination room used for euthanasia can help avoid the use of that room in the future, if possible. A towel should be laid out on the counter to create a comfortable place for the cat to be placed. An additional small towel near the hind end of the cat is also good to cover and minimize odors from any bladder or bowel release. Clippers and alcohol should be on the counter, if the euthanasia solution is going to be given in the medial saphenous vein. Once the veterinarian enters the room, there should be no interruptions. The client expects and deserves the complete attention of the veterinarian. Efforts should also be made to ensure that conversations or laughter from other parts of the hospital are not audible because this can be both distracting and upsetting to the client. If there is a delay before the injection is to be performed, it is important to direct the conversation in a positive direction. We frequently ask, “Did you get Fluffy as a kitten?” Regardless of the answer, the client usually recalls a time when the cat was young and healthy.
The Euthanasia Procedure The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Some clients prefer to be present during the procedure; others prefer not to be present. To some, not being present is a form of abandonment. Others wish to remember the cat alive. Regardless of preference, the
893
SECTION 7: Clinical Procedures
client’s desire should be clearly determined. We frequently ask, “Do you want to be with (cat’s name) when I give the injection?” When performing euthanasia with the client present, it is important that the procedure go smoothly. Listening to the client while stroking the cat acknowledges both and will help the client remember the veterinarian as being caring. Sometimes the client needs reassurance that this is the correct and most compassionate decision; other times the client just needs to remember the cat as a younger, healthier part of their family. Either way, active listening is critical at this stage and will form the lasting impression of the veterinarian and his or her interaction with the cat. When the client is ready, it is important to explain what is about to occur. Many owners are concerned that it will be painful or take an extended time to completion. Conversely, if not prepared death may occur so rapidly that they do not have a chance to say goodbye. Explain that the drug used is an anesthetic that rapidly stops “everything.” We usually state that “everything” will be stopped within 15 seconds. It is often helpful to use the analogy that the cat will go to sleep as if for surgery but will not awaken. Informing owners of the possibility of an agonal gasp is suggested. State that it is a reflex resulting of anoxia in the brain. It is important that the client be prepared for this so that it is not interpreted as pain or awareness. Many clients do not realize that a cat’s eyelids do not close at the time of death. If not forewarned, they can become distressed and even think that death has not occurred yet. Informing the client that urination and defecation may occur due to relaxation of muscles will also help prepare him or her for what to expect. A generous dose of euthanasia solution should be used to increase rapidity of its action. The effects of the euthanasia solution are not always as smooth and rapid as desired. Adding one part of ketamine, a neuromuscular blocking agent, to four parts of Beuthanasia-D solution virtually eliminates the agonal gasp and results in an overall smoother and more pleasant experience for the cat and the owner. There are several intravenous options for the site of euthanasia injection. The preferred site is the one with which the veterinarian is most proficient. The cephalic vein is preferred by many. The medial saphenous vein is preferred by others and allows the owner to be near the cat’s head during the procedure. It also puts the cat in a more relaxed position. With this site, the veins tend to be quite small so a 25-gauge needle is preferred by most. By holding one’s thumb over the tip of the needle while slowly injecting, there is less chance of the needle and the euthanasia solution coming out of the vein. Another option is advanced placement of an intravenous catheter, especially if the cat has poor peripheral veins. This is also beneficial in taking the pressure off of the veterinarian to have a successful venipuncture on the first try. However, this often requires taking the cat to “the back” if the cat has not been hospitalized, which can be distressful for the owner. Another option, especially in the event of a fractious cat, is to administer a sedative prior to the euthanasia. There are a number of medications and combinations that can be used. See Chapter 247. They induce relaxation and sedation and facilitate the injection process. However, this is not optimal for use in cats with poor peripheral circulation because it will take longer for the euthanasia solution to circulate to the brain. The use of a Leur-Lock® syringe is highly recommended. Beuthanasia-D has high viscosity and is slippery. If it gets between the syringe and needle hub, it is likely that the needle will detach during the injection. Although an intravenous injection is the preferred route, alternatives to this route are sometimes needed. An intracardiac injection will produce rapid distribution of the drug and rapid death. An injection into the pleural space or the peritoneal cavity will result in drug absorption, but it will occur over several minutes. Injection into a highly vascular abdominal organ, such as the liver or kidneys, has been used by some. Clients often ask to hold the cat during euthanasia. If you agree to permit this, it is imperative that you still have clear access to the vein, which is unlikely unless a catheter is placed. It is also imperative that
894
the client not be bitten or scratched by the cat, so good judgment should be used in granting this request. Following the injection of the euthanasia solution, it is imperative that you convince or assure the owner that the cat is dead. The easiest and most convincing way is to auscultate the heart. This allows you to make an official pronouncement of death and provides final closure to the client. As a side note, there have been rare reports of euthanized animals “waking up.” This is quite distressing to both the owner and the veterinarian, and especially has implications if the owner has taken the cat to be buried at home. The best way to ensure this does not happen is to use a liberal dose of euthanasia solution. Once death has been pronounced, many clients will want to spend a few moments alone in the room with the cat’s body. Others want the body removed immediately. The clinician should either ask or ascertain from the client’s body language which is preferred. In either case, the client should be allowed to stay in the room for a few minutes to gather composure. Whether the cat’s body is removed before or after the client leaves the room, it should be wrapped in a towel and carried cradled in the arms of the veterinarian or technician as if it is still alive. This is often the final memory the client will have of their cat, and they will notice the way in which their cat was handled. Even if the client has left the room, they may still be in the building so their cat should continue to be handled with the same respect as if it were alive.
Professional Fees Euthanasia is a legitimate professional service with the veterinarian incurring some direct costs, such as the drug used and the staff ’s salaries, and in some cases, the costs for burial or disposal of the body. If the client has not already paid for the services and is visibly upset, it may be best to state that a bill will be sent in the mail rather than request payment at the time. Many clients greatly appreciate this gesture, and collection problems rarely occur if the euthanasia and billing are handled in a professional manner. Sending the bill 1 week from the date of the euthanasia should be an adequate amount of time for them to be past the immediate grief period. However, doing so for new clients or in situations in which the cat’s illness or trauma occurred suddenly carries greater risk of non-payment. Some clients prefer to clear the account before leaving as part of the closure process. If so, it is important to relay the needed information to the receptionist quickly so that the transaction is not prolonged. Having the client pay the bill prior to the euthanasia is ideal.
Disposition of Body There are several options available for final disposition of the cat’s body; local and state laws must be observed. Cremation is the most popular in large cities. Most companies offer cremation with return of the cat’s ashes or cremation with scattering of the ashes. Other alternatives include burial in a pet cemetery, burial by a municipal agency, or the owner burying the cat on his or her property. It is advisable to discuss the options with the client prior to the euthanasia procedure. One’s euthanasia permit can include these options. This ensures that the client’s wishes are followed without confusion. If the euthanasia occurs unexpectedly, the owner may not be prepared to make an immediate decision; in such cases, the practitioner should offer to store the cat’s body until a decision is made.
Follow-Up and Memorials An expression of sympathy is both appropriate and appreciated by clients. A sympathy card inscribed with a handwritten message from the veterinarian and mailed in a hand-addressed envelope is perceived as being both thoughtful and sincere. Clients genuinely appreciate this
Euthanasia
expression of concern and support by the clinician, and it is a way to bring final closure to the loss of the cat for both parties. An appropriate inscription may follow these lines: Dear Ms. Jones, I am sorry for your loss of Fluffy. I know she was a special part of your family. She was fortunate to have such a wonderful and loving home. Although your decision was a difficult one, you made the most humane and compassionate choice. Thank you for allowing me to be part of her care. You are in our thoughts at this time of sadness. Personally signed The choice of the card is important, and there are several companies that make cards with inscriptions and pictures that are suitable. The sympathy card should be mailed within 2 days of the euthanasia. If the client did not pay at the time of euthanasia, the bill for services should be sent after the sympathy card to ensure the two do not arrive on the same day. A record should be made of the specific card sent and personal inscription because if another cat belonging to the same owner is euthanized within a few weeks or months, the client is likely to recognize a duplicate card or inscription. Phone calls are another way to express sympathy and are personal. They are especially warranted if the cat was taken to an emergency facility and not euthanized in the practice. The call should be made within 1 day of receiving notice from the other facility. Clients often feel touched by the effort made by the practitioner. It not only gives them the opportunity to ask any questions, but it also allows the practitioner to explore what happened with the cat, especially if it was unexpected. We advise ending the conversation with an offer to talk again if further questions or feelings arise. Letting the client know that calls are welcome keeps the lines of communication open and lets the client know that the cat, as
well as themselves, are an important part of your practice. They are more likely to return with a new cat if they feel validated and cared for by the veterinarian. Other memorials to consider are Clay Paws® or clipping some hair from the cat. These are tangible memories of the cat and may even be requested by some clients. For other clients, it may be too painful for them to have a memento. These can be offered at the time of euthanasia verbally or as part of the requests on the sheet for disposition of the body. Some practitioners make a donation in honor of the cat to a fund for homeless animals or a veterinary college. In this case, the foundation receiving the donation often sends a card letting the client know that a donation has been made in the cat’s name.
Conclusion Euthanasia is a complex and delicate situation. There are many factors to be considered throughout the entire process. However, by being prepared and professionally handling the procedure from the onset, the practitioner can ensure that it is a relatively pleasant experience for the owner and the cat, and, in doing so, continue to keep the client as they begin a new journey with a new cat.
Suggested Readings Anonymous (2009). “What to do if a euthanized animal wakes up?” DVM Newsmagazine. 1:38–40. Norsworthy GD, Norsworthy LA. 1993. Euthanasia and grief management. In GD Norsworthy, ed., Feline Practice, pp. 69–74. Philadelphia: JB Lippincott. AVMA Guidelines on Euthanasia. 2007. www.avma.org/resources/ euthanasia.pdf.
895
CHAPTER 301
Fine-Needle Biopsy Mitchell A. Crystal
Definition
Procedure
A fine-needle biopsy is a collection of biologic material, usually fluid or cells, using a small gauge needle via a nonaspiration technique followed immediately by expression and spread onto a microscope slide for staining and cytologic review. This technique maximizes diagnostic yield by providing increased needle control and minimizing hemodilution. In addition, less time and manipulation are required for sample expulsion/ slide preparation, thus decreasing sample desiccation and further enhancing diagnostic yield.
Indications • To obtain a diagnosis, identify a disease process, establish a prognosis, or help define a subsequent plan of action for mass lesions or for organ and lymph node and tissue lesions, enlargements, or infiltrates.
Contraindications • Severe coagulopathy
Equipment and Supplies • See Figure 301-1 • Syringe, 12 mL • Needle, 22 gauge (length depends on depth of lesion); 1-and 1.5-in needles used most commonly • Several clean, new, frosted-end microscope slides
• Place needle onto syringe. • Fill syringe with 10 to 12 mL of air. • Hold syringe near the 2- to 3-mL mark like a pencil, as if the needle were the writing end. • Stabilize the lesion to be aspirated with the opposite, free hand (peripheral lymph node, abdominal mass, kidney, etc.) or identify the lesion to be aspirated via ultrasonography holding the probe in the opposite, free hand (liver, abdominal lymph node, mediastinal mass, etc.). See Figure 301-2A. • Advance the needle into the lesion and rapidly move the needle back and forth within the lesion 6 to 10 times, redirecting the needle prior to each third or fourth thrust forward. It is common and desirable to not see material enter the syringe or needle. • Remove the needle from the lesion (after 6–10 thrusts or sooner if any material is seen to enter the needle hub) and quickly expel the contents onto a clean microscope slide. See Figure 301-2B. • Rapidly smear the contents using minimal to no pressure, and dry the slides via waving them in the air or using a slide drying device (such as a blow drier or cup warmer). See Figures 301-2C and 2D. • If a large amount of material is expelled, multiple thin smears can be achieved by lightly touching a second slide to the expelled material on the first slide. The material picked up on the second slide is then quickly smeared (use minimal to no pressure) onto a third slide. The remaining expelled material on the first slide can then be smeared using the same spreader (second) slide. • Label the frosted end of each slide with a pencil for lab submission or for staining and microscopic review.
Figure 301-1 The equipment and supplies needed for nonaspiration fine-needle tissue biopsy include 12-mL syringes, 22-gauge needles (length depends on depth of lesion), and several clean or new frosted-end microscope slides.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
896
Fine-Needle Biopsy
(A)
(B)
(C)
(D) Figure 301-2 To perform a nonaspiration fine-needle tissue sampling or biopsy: A, The lesion is stabilized with the opposite free hand. The syringe, prefilled with air and with needle attached, is held like a pencil, and the needle is advanced and moved rapidly back and forth within the lesion. Alternatively, as shown here, an intravenous extension set can be attached between the needle and the syringe. B, After redirecting the needle two to three times and completing multiple back and forth thrusts after each redirection, the contents of the needle are immediately expelled onto a microscope slide. C, D, The sample is immediately spread onto a microscope slide for staining and cytologic review.
• Note: An alternative set up for those who prefer holding the needle directly includes attaching an extension set between the needle and the syringe. Some find that this modification gives better control for directing the needle.
Possible Complications • Nondiagnostic sample • Hemorrhage
Suggested Readings Crystal MA. 1996. Cytological sampling techniques: Getting the diagnosis. In Proceedings of the Fourteenth Annual Veterinary Medical Forum, pp. 385–387. San Antonio, Texas. Meinkoth JH, Cowell RL, Tyler RD, et al. 2008. Sample collection and preparation. In RL Cowell, RD Tyler, JH Meinkoth, et al., eds., Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed., pp. 1–19. St. Louis: Mosby Elsevier.
897
CHAPTER 302
Fluid Therapy Sharon Fooshee Grace
Contraindications and Cautions
Definition
• Heart Failure: In particular, saline solutions should be used with great caution in cats with heart failure. Other fluids may similarly lead to problems with heart failure because of decreased pumping efficiency of the heart and sodium retention. • Alkalosis: Lactated Ringer ’s solution (LRS) should not be used in conditions of metabolic or respiratory alkalosis. • Dextrose 5% Solution: This fluid should not be used in the hypokalemic cat unless potassium chloride can be supplemented. It is rarely used as the sole fluid therapy because it is unbalanced.
Fluid therapy is one of the cornerstones of small animal practice. The ability to support hydration, modulate the electrolyte content of the body, maintain blood pressure for delivery of life-sustaining oxygen and nutrients to tissues, and adjust acid-base disturbances renders this one of the most useful tools available to the practitioner. Because cats are easily volume overloaded as compared to dogs, the feline patient needs a carefully devised fluid therapy plan. A basic understanding of body water is critical for selection of the proper fluid, calculation of the volume to administer, and determination of the rate and route of delivery. More than half of a cat’s total weight (60%) is made up of water. This volume of water, also known as total body water (TBW), is comprised of two compartments: intracellular fluid (ICF), which is two-thirds of TBW, and extracellular fluid (ECF), which is one-third of TBW. ECF is further divided into interstitial and intravascular compartments. The electrolyte concentrations vary among these different compartments. There are a number of indications for fluid therapy; however, restoration of normal hydration is perhaps the most common reason for providing fluid support to the feline patient. Prior to institution of fluid therapy, the patient should be weighed and baseline lab tests obtained, especially packed cell volume (PCV), total protein (TP), and urine specific gravity (USG). This is a critical step because once fluid delivery has begun, without this data, it is impossible to determine in retrospect what the baseline parameters might have been.
Fluid Type: Selection of Appropriate Fluid • Types of Fluids: There are two primary types of fluids used routinely in small animal practice: colloids and crystalloids. Colloid fluids are a mix of small molecules, which can penetrate the capillary membrane, and large molecules, which are retained in the vascular compartment to increase osmotic pressure of the blood; these are addressed in Chapter 112. Crystalloids consist primarily of water with a sodium or glucose base, along with electrolytes or buffers. They are capable of entering all body compartments to varying degrees. They are generally designed for replacement (correction of TBW deficits) or maintenance (normal ongoing losses) fluid needs. LRS, physiologic saline (0.9% saline), and dextrose 5% in water (D5W) are commonly used crystalloids. See Table 302-1. Every small animal practice should maintain a supply of fluids dedicated to meeting the replacement and maintenance needs of feline patients. These are two distinct types of fluids (see Table 302-1); therefore, at least two different fluids should always be stocked. • Replacement Fluids: Replacement fluids are used to replenish body water and electrolytes; they do not leave the vascular compartment as readily as maintenance fluids, although only about 25% of infused replacement fluids remain within the intravascular space after 1 hour. LRS, Ringer ’s solution, and 0.9% saline are the most commonly used replacement fluids. LRS is more physiologic (i.e., balanced) than saline because it more closely approximates the electrolyte content of ECF. Also, when metabolized, lactate has a mild buffering effect.
Indications • • • • • • • •
Maintenance of venous access. Maintenance of normal hydration. Maintain or correct electrolyte balances. Maintain normal acid-base status. Correction of dehydration. Nutritional support. Promotion of diuresis. Correction of hypovolemia or blood loss.
TABLE 302-1: Common Commercially Available Fluids
Lacted Ringer’s solution Ringer’s 0.9% saline 2.5% Dextrose with 0.45% saline Dextrose 5%
Maintenance (M) or Replacement (R)
Sodium+ (mEq/L)
Potassium+ (mEq/L)
Chlorine− (mEq/L)
Glucose (g/L)
Tonicity
Osmolarity (mOsmo/L)
R R R M
130 147 155 77
4 4 0 0
109 156 155 77
0 0 0 25
Isotonic Isotonic Isotonic Isotonic
273 310 308 280
0
0
0
50
Hypotonic
253
R
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
898
Fluid Therapy
Ringer ’s solution is similar to LRS except that it lacks lactate, making it a better choice for dehydration with alkalosis. LRS is a good general choice when doubt exists about the best fluid to use. However, both Ringer ’s solution and LRS are generally inadequate because electrolyte replacement solutions often need additives, such as potassium chloride. Normal saline is inferior to LRS in that it contains supraphysiologic levels of sodium and chloride; it also has mild acidifying properties, which can be undesirable. Normal saline is primarily designed for volume expansion (especially rapid volume expansion), correction of hyponatremia, and correction of metabolic alkalosis (when used with potassium chloride). Replacement fluids should not be used for long-term maintenance of fluid and electrolyte requirements of the patient. If inappropriately used for maintenance, they often lead to hypernatremia and hypokalemia. Most veterinary hospitals stock smaller volumes of normal saline (0.9%) as compared to LRS or Ringer ’s solution. • Maintenance Fluids: Maintenance fluids are used to support ongoing daily fluid and electrolyte needs. They are designed to maintain both the intravascular and extravascular compartments, although they primarily hydrate the interstitial and intracellular compartments. At least partial replacement of any deficits should be achieved before a cat is switched from a replacement fluid to a maintenance fluid. As compared to plasma, maintenance fluids are lower in sodium and chloride and higher in potassium. Dextrose 2.5% in 0.45% saline is a
•
•
• •
useful maintenance solution when supplemented with potassium chloride and is the fluid of choice when sodium must be restricted. Maintenance fluids should not be used to treat hypovolemia because their composition differs greatly from normal plasma electrolyte values. Inappropriate use of maintenance fluids for replacement needs can result in hyponatremia and, depending on the fluid, hyperkalemia. Dextrose 5% in Water: D5W is rarely used alone but has specific application as a part of a fluid therapy plan. It is entirely devoid of electrolytes and is considered “unbalanced.” Following administration, it becomes hypotonic to plasma because dextrose is metabolized to CO2 and water. Therefore, it is essentially the same as providing “free water” because it readily redistributes throughout the body. D5W should not be used to expand plasma volume because most of the fluid enters the intracellular (i.e., extravascular) compartment. Its primary use is in replacing a pure water deficit. It is also inadequate to supply daily calorie needs of the patient and should not be given SC. Electrolyte disturbances: Great care must be given to ongoing evaluation of electrolytes when administering fluids. Consult the following for specific information on electrolytes: Chapters 103, 106, 113, 114, 115, and 116. For fluid therapy in the hypoalbuminemic cat, see Chapter 112. Fluid selections for select clinical situation are listed in Table 302-2.
TABLE 302-2: Recommended Fluids for Select Clinical Situations* Condition
Recommended fluid and additives
Comments
Diabetes Mellitus,Uncomplicated Diabetes Mellitus, Complicated
—
Fluid therapy usually not needed
0.9% saline
Diarrhea, Acute Diarrhea, Chronic Hepatic Lipidosis
Lactated Ringer’s solution‡ Lactated Ringer’s solution 0.9% saline
Hypercalcemia Hyperkalemia Hypokalemia
0.9% saline 0.9% saline (Lactated Ringer’s solution acceptable second choice) lactated Ringer’s solution
Hypernatremia Hyponatremia Pancreatitis
lactated Ringer’s solution 0.9% saline lactated Ringer’s solution
Renal Failure, Acute Renal Failure, Chronic
Lactated Ringer’s solution Replacement: Lactated Ringer’s solution or 0.9% saline Maintenance: Lactated Ringer’s solution or 0.45% saline in 2.5% dextrose Lactated Ringer’s solution
Glucose, phosphorous, and potassium must be monitored after insulin is started. “Whole body” potassium depletion is common, even if serum values normal.† If potassium level unknown, add 40 mEq potassium chloride per liter of fluid and monitor as possible. If the cat is severely hyperosmolar (i.e., depression or confusion), rehydrate with caution over first 12 hours due to risk of cerebral edema. Potassium supplementation may need to be aggressive Correct any electrolyte or acid-base abnormalities ≥20 mEq/L potassium chloride needed in most cases; monitor potassium and phosphate levels; do not use Lactated Ringer’s solution or dextrose-containing solutions unless warranted by lab test results Induces diuresis; monitor potassium If hyperkalemia is severe, addition of dextrose with or without insulin may be beneficial; if life-threatening, calcium gluconate is indicated Avoid sodium bicarbonate, insulin, and glucose-containing fluids when possible. Refractory hypokalemia may be due to hypomagnesemia. Correct hydration deficits slowly Correct hydration deficits slowly Monitor potassium and supplement as needed; give 20 mEq/L if unsure of serum level Monitor urine production carefully so as to avoid volume overload Monitor potassium and supplement as needed; give 20 mEq/L if unsure of serum level
Vomiting, Acute Vomiting, Chronic
0.9% saline if acid-base unknown; Lactated Ringer’s solution if acidotic
IV fluids usually not needed; SC and fasting (NPO for 24 hours) usually adequate Potassium supplementation usually needed; if potassium level unknown, add 20 mEq/L to fluids for replacement and maintenance
*For each patient, selection of the appropriate fluid and additives must be based upon the history, physical examination, and laboratory findings. †Hypokalemia is likely; serum value should be determined and potassium chloride supplemented, as needed with a maximum rate of 0.5 mmol/kg per hour (0.5 mEq/kg per hour). ‡Lactated Ringer’s solution can buffer mild acidosis through conversion of lactate to bicarbonate.
899
SECTION 7: Clinical Procedures
Fluid Route • Available routes of fluid delivery include oral, subcutaneous, intraperitoneal, intravenous, and intraosseous (IO). In debilitated animals, the intravenous, subcutaneous and, occasionally, IO routes are preferred and are the focus here. • Intraosseous: IO administration is sometimes used in kittens if venipuncture is impossible; it may be used in adult cats when blood pressure is low. This route may be painful but has the advantage of being a safe, effective route of fluid delivery. The bone marrow has direct access to the systemic circulation and fluid will be rapidly absorbed. Blood and some medications may also be given by the IO route. • Subcutaneous: The subcutaneous route is convenient, rapid, and easy, but absorption may be limited when peripheral perfusion is poor. This route usually does not meet the daily fluid needs of most animals and is contraindicated for severely dehydrated or hypovolemic animals and those that are hypothermic. Only isotonic (or nearly isotonic) fluids should be given SC. Fenestrated subcutaneous catheters are ideal for delivery of supplemental fluids over a long term. See Chapter 271 for more information on these catheters. • Intravenous: The intravenous route is preferred over others for cats that are ill and require more than moderate fluid replacement. Either a peripheral (cephalic) or central (jugular or posterior vena cava via the medial saphenous catheters) vein may be used for catheter placement. Some patience and practice are required to master the technique for placement of central venous catheters (see Chapter 297); however, they offer the advantage of unhindered venous access, sampling of venous blood through the catheter, prolonged placement (1 week), and measurement of central venous pressure. • Intraperitoneal: When venous access is limited, crystalloid fluids may be administered into the peritoneal cavity. This route is especially helpful when the patient is hypothermic because warm fluids may help to normalize core body temperature.
Fluid Quantity • Assessment of Hydration: Physical assessment of hydration status (TBW) is based on clinical findings. A cat must lose approximately 5% of its body weight in water before signs of dehydration are noted (e.g., skin tenting when skin lifted over the shoulders fails to returns to its resting position slowly). See Table 302-3 for information on assessment of dehydration. The ongoing assessment of hydration includes serial monitoring of body weight, central venous pressure, and, where possible, measurement of colloid osmotic pressure (primarily referral centers). Unfortunately, lab tests (PCV, TP, blood urea nitrogen [BUN] are not significantly more sensitive in detecting dehydration than is a good physical examination. • Volume to Administer: The most convenient way to determine fluid volume needed is to estimate needs over a 24-hour period. Three
TABLE 302-3: Estimation the Degree of Dehydration Dehydration Level
Findings
5%
Tacky, dry mucous membranes; skin slowly returns to normal after tenting (mildly decreased skin turgor); otherwise normal Mild to moderate decrease in skin turgor; dry mucous membranes Marked decrease in skin turgor; tachycardia; slow capillary refill time; depression; sunken eyes
6–8% 10–12%
900
•
•
•
•
•
•
types of needs must be considered: (a) estimated deficits (dehydration), if any; (b) maintenance needs (i.e., urinary, fecal, cutaneous, and respiratory losses); and (c) ongoing losses (i.e., vomiting, diarrhea, fever, and wound drainage). Note that 1 L of water is equal in weight to 1 kg. Therefore, fluid needed in 24 hours = deficit + maintenance + ongoing losses. Dehydration: Dehydration may be estimated by physical examination (see Table 302-3). Example: A 4-kg cat is 10% dehydrated 4 kg × 0.10 = .04 kg = 400-mL deficit Maintenance requirements: Maintenance fluid requirements are estimated at 40 to 60 mL/kg per day. Some critically ill cats may not be able to tolerate the upper end of this range. Example: 4 kg cat × 50 ml/kg per day = 2000 mL/day Ongoing losses: The volume of fluid lost as vomitus or diarrhea over a 24-hour period is estimated in millileters. Example: 4-kg cat vomits 30 mL of fluid 4 times per day 30 mL × 4 = 120 mL Total 24 hour requirement: 400 mL dehydration + 200 mL maintenance + 120 mL ongoing losses 720 ml needed for first 24 hours Hourly rate: The hourly rate is calculated as the total daily need divided by 24. Example: 720 mL/24 hours = 30 ml/hour Subcutaneous Fluids: Most adult cats can tolerate 100 to 200 mL of fluid administered SC in the interscapular space. Fluid may initially appear “pocketed” in this area but will be absorbed systemically over several hours.
Fluid Rate • When subcutaneous fluids are given, the rate of fluid delivery is guided by patient comfort. Drip sets are usually more comfortable than injecting fluid with a syringe. • With severe volume depletion or shock, a maximum of one “blood volume” of fluid may be given safely over 1 hour if no complicating conditions exist (e.g., pulmonary or cerebral edema, or heart failure). In cats, a “blood volume” is approximately 66 mL/kg (30 mL/lb). • Mild to moderate dehydration is best corrected over 24 hours to allow time for fluid equilibration between all fluid compartments. • Severe dehydration may need to be corrected over less than 12 hours. • To deliver fluids over 24 hours, the hourly rate (mL/hr) is calculated as the total daily need (in milliliters) divided by 24. • When using a fluid pump, the mL/hour may be accurately delivered. When gravity flow and a pediatric drip set must be used, delivery is less complicated if mL/hour are converted to drops/min. (Adult drip sets are not recommended for use in cats.) Pediatric (minidrip) administration sets deliver 60 drops/mL. Drops/min = Total ml/total hrs × 1 hour/60 min × drops/ml • If intravenous fluids are to be given by gravity flow, it is best to use both a small bag of fluids and a pediatric drip set to minimize the chance of large volume of fluids being infused accidentally. However, the use of a pediatric drip set prolongs delivery time significantly.
Possible Complications • When a cat has both renal failure and congestive heart failure, fluid therapy is extremely complicated because the need for diuresis must be weighed against the inability of the heart to handle an extra fluid load. Such patients must be carefully monitored.
Fluid Therapy
• LRS can complicate situations of volume overload or fluid retention, pre-existing pulmonary edema, cerebral edema, or congestive heart failure. • Excessive volumes of fluid may cause hemodilution. • Long-standing dehydration should be corrected cautiously because of the potential to create cerebral edema.
Suggested Readings Mazzaferro EM. 2009. Intraosseous catheterization: An often underused, life-saving tool. North Am Vet Conf Clinic Brief. 7(5):9–12. Mensack S. 2008. Fluid therapy: Options and rational administration. Vet Clin North Amer. 38:575–586.
901
CHAPTER 303
Jugular Blood Collection Gary D. Norsworthy
Introduction Blood is commonly collected from the jugular vein when several milliliters are needed for testing. However, the conventional method generally requires shaving of the hair and placing the cat in an uncomfortable position. If owners observe this process, they often develop negative attitudes toward the veterinarian about perceived cruelty to their cat. To avoid this, many veterinarians take the cat “to the back” for blood collection, often creating another form of client apprehension. The following method of blood collection does not require shaving of hair and does not place the cat in an uncomfortable position. In addition, over 90% of my feline patients do not struggle during the process; owners are generally impressed.
• Have one technician hold the cat’s head. Its neck should be extended, and the chin turned about 45 degrees away from the jugular vein that will be used. • Have another technician hold the cat’s front feet against its abdomen with one hand and the cat’s rear feet with the other hand. See Figure 303-1A. • Wet the skin over cat’s jugular vein with isopropyl alcohol. See Figure 303-1B. When you put pressure on the vein at the thoracic inlet (with your left thumb), the vein should be readily visible. If not, use your right index finger to briskly rub across the skin over the vein
Equipment • The equipment includes a 6-mL syringe, 20-gauge needle (for blood) and a 12-mL syringe, 22-gauge needle (for urine), isopropyl alcohol, and appropriate submission tubes for blood and urine.
Indications • The indication is blood collection from most feline patients. This includes kittens and adults.
Contraindications • Cats that are fractious or resist the restraint necessary should be sedated for this method or should have blood collected using an alternative method. However, many cats that appear unruly will be amazingly cooperative for this method. • This technique is not suitable for cats with respiratory compromise because dyspneic cats have increased breathing difficulty when lying in dorsal recumbency.
(A)
Procedure • This procedure is described for a right-handed person. • Remove most of the urine from the urinary bladder with a cystocentesis. This gives you a urine sample and protects you should the cat urinate during the procedure. • Sit on a counter top or examination table with your legs together and your knees elevated. If this is not feasible, sit in a chair with your feet resting on a stool about 30 cm (1 ft) off the floor or sit on the floor. Your legs and knees should be in the same position as if you were sitting on a table. • Lay the cat on its back with its head at your knees and its rear feet resting against your abdomen. It will be apprehensive at first, but you should be able to get it to relax quite well in a few seconds. However, if the cat is determined not to lie in this position, the procedure must be abandoned. The uncooperative cat is subject to needle trauma to vital areas.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
902
(B) Figure 303-1 A, Sit on a counter top or an examination table with your legs together and knees up. The cat lies in dorsal recumbency with its head near your knees. One technician restrains the cat’s head, and a second restrains the legs. B, The hair is not clipped over the jugular vein. Instead, it is wet with alcohol. A 20-gauge needle on a 6 ml syringe is used to make the venipuncture.
Jugular Blood Collection
Figure 303-2 The hair was shaved from the ventral aspect of the neck of this cat in preparation for thyroid surgery. Note the venous distention created by having the cat lying in dorsal recumbency, even though the jugular veins have not been occluded.
• •
• •
• •
going from medial to lateral. Doing this several times often causes the vein to become prominent. See Figure 303-2. Bend the needle slightly at its base. Make the venipuncture holding the syringe with your right hand. Be aware that the needle will usually enter the vein as soon as it goes through the skin. Threading it up the vein may result in it penetrating the other side of the vein. Draw the desired amount of blood. You will usually be able to fill a 6-mL syringe within 5 seconds. Remove the needle from the vein while placing your left thumb over the venipuncture site. After handing the syringe to your technician, use your right hand to lift the cat against your chest. This position is comfortable to the cat and will allow you to keep pressure on the venipuncture site for 1 to 2 minutes. Owners are usually impressed with your compassion. Your technician should be filling the appropriate blood tubes as you are putting pressure on the venipuncture site. Hand the cat to its owner, and then get off the table.
Figure 303-3 This technique works well with kittens. A 1-mL syringe and 25-gauge needle are used for blood collection. Two technicians are usually needed for restraint.
Likely Complications • With correct restraint and technique, over 90% of cats will permit collection of blood in this manner. • Many cats that seem like they will struggle will not do so once they are on their backs and resting comfortably, especially if their owner is nearby. • If the cat struggles and you persist in using this technique, it would be easy to stab the cat in the neck with the needle. Do not use this technique for struggling cats.
Note • This technique works well with kittens also. The kitten is held in dorsal recumbency in the palm of your hand, and the jugular vein is used for venipuncture. It takes a second person, and possibly a third person, to hold the kitten’s head and feet. See Figure 303-3.
903
CHAPTER 304
Lung Aspiration Karen M. Lovelace
Definition Transthoracic pulmonary needle aspiration (lung aspiration) is the collection of cells from pulmonary parenchyma or interstitium for cytological analysis or to obtain a sample for bacteriological culturing.
Indications • For simple, fast, and inexpensive identification of diffuse pulmonary interstitial or alveolar disease, especially neoplasia and systemic fungal disease. • For identification of masses or disease localized next to the body wall, such as primary or metastatic neoplasia. • When attempts at obtaining cell samples via bronchoscopy are not productive. For example, lung aspiration has been used to successfully diagnose eosinophilic lung disease and pulmonary infiltrates with eosinophils (PIE).
Contraindications • • • •
Limited pulmonary function or pulmonary hypertension Coagulopathy Suspected pulmonary abscess, cyst, or bulla Organ failure (i.e., hepatic and renal) where the risk of anesthesia outweighs the benefit of diagnostic sampling
Equipment and Supplies • Sterile gloves. • Winged infusion set (butterfly) needle attached to a three-way stopcock valve. 25 gauge × 2 cm (3/4 in). If a butterfly is not available, a 25-gauge needle no longer than 1.5 cm (5/8 in) is preferred so that deeper structures are avoided. • Syring, 3, 6, or 12 mL. • Several microscope slides.
Procedure • Obtain appropriate imaging information (e.g., radiographs, ultrasound, and fluoroscopy) necessary to plan the side and location for sample collection. If radiographs are taken, it is important to include both lateral views along with a dorsoventral or ventrodorsal view. In one study, blind or ultrasound-guided technique yielded diagnostic samples in 20 out of 25 cats. • Anesthetize the patient. In select cases, the patient may be tranquilized. However, lung laceration is minimized by being able to freeze respiration at the time of the aspiration, so anesthesia with a cuffed endotracheal tube is preferred. The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
904
• Clip and prepare a sterile 4- × 4-cm (1.5- × 1.5-in) area overlying the area where the lesion was best visualized on the appropriate side of the thorax as indicated by imaging. Care should be taken that the location for aspiration is planned away from the heart or great vessels. If possible, choosing a location caudal to the eighth rib space is preferred. In planning needle insertion, it is best to avoid a location just caudal to any rib because nerves and vessels are closely associated with the caudal aspect of each rib. • Place the patient in sternal recumbency if the patient has previously shown any signs of dyspnea. In select cases, lateral recumbency may be acceptable, although the “up” lung may slightly fall away from the body wall during the procedure. • The prepped area should be covered with a surgical drape to maintain sterility. However, some clinicians find that this makes it more difficult to determine the appropriate location. • For tranquilized cats, a local block to the skin using 0.25 mL of 2% lidocaine can be inserted over the aspiration site through the skin and subcutaneous tissue down to the pleura. • A 25-gauge, 2-cm (3/4-in) butterfly needle is then attached to a 3, 6, or 12-mL syringe via closed three-way stopcock. • Just caudal to the selected site of aspiration, the needle is advanced through the skin layer in a cranial direction to create a short tunnel for preventing air escape. The needle is then held ready at a 90-degree angle to the chest. The patient’s lungs are gently held inflated with the bag on the anesthetic machine while the needle is inserted. It is important to keep the lungs inflated to reduce movement around the needle. The pop-off valve can be closed to assist with inflation, but it should be opened as soon as the aspiration is finished. • With the lungs still inflated, the stopcock valve is opened to the patient and the attached syringe is quickly aspirated several times through a single lung puncture. • Pressure is released on the syringe, the lungs are allowed to deflate, the stopcock is closed, and the entire needle, tubing, and syringe are removed. The syringe should never be detached from the needle or tubing while in the body because this could allow air into the lung spaces or pleura, causing pneumothorax. • The syringe can then safely be removed, filled with air, and reattached to the needle. The syringe contents are forcefully expelled onto a clean slide, gently smeared, air dried, and stained for analysis.
Aftercare • The patient should be observed for several hours after the procedure. • Thoracic radiographs should be taken if bleeding or pneumothorax is suspected. • The patient should be kept indoors for at least 24 hours after the procedure. • Analgesic medication, such as buprenorphine can be given at a dose of 0.005 to 0.01 mg/kg IM or SC or 0.01 to 0.02 mg/kg PO.
Lung Aspiration
Possible Complications • Complications are rare (<5%). Sterile technique will avoid iatrogenic infection. • Pneumothorax. • Hemothorax or pulmonary hemorrhage, although bleeding usually resolves spontaneously.
Suggested Readings Nelson RW, Cuoto CG. 1998. Diagnostic rests for the lower respiratory tract. In RW Nelson, CG Cuoto, eds., Small Animal Internal Medicine, 2nd ed., pp. 265–306. St. Louis: Mosby, Inc. Ogilvie GK, Moore AS. 2001. Respiratory Tract Biopsy. In CK Ogilvie, AS Moore, eds., Feline Oncology, pp. 19–22. Trenton, NJ: Veterinary Learning Systems.
905
CHAPTER 305
Nasal Sampling Gary D. Norsworthy
Overview Sampling of pathologic material from the nasal cavity is useful in diagnosing cats with chronic or acute rhinitis or rhinosinusitis. Collecting samples from within the nasal cavity instead of discharges that exit the nares are more likely to be representative of the true etiology. This chapter describes two methods for so doing. Skull radiographs are necessary to determine if nasal sampling is indicated and to determine the appropriate area in which to perform sample collection. General anesthesia is necessary for correct positioning and imaging of the nasal cavity. The most useful view is an open mouth ventrodorsal radiograph. See Figures 146-1 and 147-1. Increased opacity in the nasal area indicates the need for aspiration. See Figure 305-1. In this cat if nasal aspiration is chosen, it should be performed at the level of the arrow about 2 mm (1/8 in) off the midline. If nasal flushing is chosen, the left nasal cavity should be flushed.
Nasal Aspiration Nasal aspiration involves the use of a small gauge needle to aspirate material from within the nasal cavity. The described technique uses a transpalatine approach.
Figure 305-1 An open-mouth ventrodorsal radiograph of the nasal cavity is used to choose the site for nasal aspiration. In this cat, the needle should enter the nasal cavity at the level of the arrow about 2 mm [1/8 in] off the midline.
Procedure Once the area and need for aspiration has been determined, the cat is placed in ventral recumbency. It is important that a cuffed endotracheal tube be in place. A 22-gauge disposable needle and a 6- or 12-mL syringe are used. The needle insertion point is determined based on the radiograph. Dentition and the distance off of the median septum are used to position correctly. A drilling motion is used to penetrate the hard palate. See Figure 305-2. Once the needle has passed into the nasal cavity, make several aggressive aspirations with the syringe to obtain a sample. When the sample is collected the needle is withdrawn. Pressure should be applied to the biopsy site if bleeding occurs. Occasionally, a few drops of blood will exit the nares. The sample is expressed onto a clean slide, and a smear is made. The slides should be stained and evaluated for cellular content then submitted to a veterinary pathologist. If only blood is present the procedure should be repeated. Some of the sample should also be reserved for aerobic and or anaerobic bacterial culture and sensitivity. Another portion should be placed on a sterile dacron-tipped applicator and submitted for polymerase chain reaction (PCR) testing for viral respiratory pathogens.
Notes • Vigorous aspiration will yield a better quality sample. There is little chance of causing damage to the nasal cavity. Unlike the dog, hemorrhage is rarely a problem.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
906
Figure 305-2 A 22-gauge disposable needle and a 6- or 12-mL syringe are used. The needle insertion point is determined based on the radiograph. • If osteolytic disease is present in the nasal cavity the hard palate may be easily penetrated with a needle. This increases the likelihood of neoplasia. • The hard palate in some cats is thick and dense enough so a 22-gauge disposable needle will not penetrate it. If this happens, use a 20gauge disposable needle. Alternatively, a 22- or 20-gauge spinal needle with stylet may be used, but this is rarely needed. • Aspiration can be made dorsal to ventral through the nasal bone using the same equipment and techniques described. However, landmarks for site selection are more difficult to determine.
Nasal Sampling
Figure 305-3
A gauze square is placed in the pharynx using a hemostatic forceps.
Figure 305-5 The material flushed from the nasal cavity is retained on the gauze square. Samples are used for cytology, bacteriological culturing, and polymerase chain reaction testing.
vigorously flushed through the nasal cavity. It will exit the choanae, traverse the nasopharynx, and pass through the gauze square in the pharynx. The gauze square is removed using the hemostatic forceps. Some of the material filtered by the gauze square is placed onto a clean slide, and a smear is made. See Figure 305-5. The slide should be stained and evaluated for cellular content then submitted to a veterinary pathologist. Some of the sample should also be reserved for aerobic and or anaerobic bacterial culture and sensitivity. Another portion should be placed on a sterile dacron-tipped applicator and submitted for polymerase chain reaction (PCR) testing for viral respiratory pathogens.
Notes
Figure 305-4 A 3.5 French catheter is passed about 2 cm [3/4 in] into the nasal cavity. Twelve to 35-mL of sterile saline are vigorously flushed through the catheter.
• The sample quality using this procedure is often inferior to the nasal aspiration because pharyngeal contamination may occur. This can affect cytology, bacterial culture, and PCR testing results. • This technique may be used in an attempt to dislodge foreign material from the nasal cavity.
Interpretation Nasal Flushing Nasal flushing involves the antegrade passage of a catheter into the nasal cavity to recover material for appropriate testing.
Nasal samples should be evaluated by a pathologist. However, determination of sample cellularity before submission will ensure better results. Several commercial veterinary laboratories offer appropriate feline respiratory profiles using PCR testing.
Procedure The cat is anesthetized, and a cuffed endotracheal tube is placed. A gauze square is positioned in the pharynx using hemostatic forceps. See Figure 305-3. A lubricated 3.5 French catheter is passed through the nostril and directed ventrolaterally until it passes about 2 cm (3/4 in) into the nasal cavity. See Figure 305-4. Twelve to 35 mL of sterile saline is
Conclusion These procedures are useful for the diagnosis of chronic nasal disease. In most cats, good cytological samples can be obtained for diagnostic and prognostic purposes. Bacteriological culturing and viral testing by PCR are also of value in determining etiology and directing treatment.
907
CHAPTER 306
Necropsy of Kittens Michele Fradin-Fermé
Overview Making a definitive diagnosis on a very young dying kitten is difficult because symptoms are not specific and usually include hypothemia, agitation, crying, dyspnea, or cyanosis. Blood analysis is not easily done due to the limited quantity of blood and the difficulties of collection. A properly performed, thorough necropsy can allow a diagnosis by observation of gross lesions and performance of numerous laboratory analysis. Necropsy is most helpful to breeders because they usually want to know if there is an infectious or a genetic disease occurring in their breeding colony. Gross necropsy and sample collection are performed at the veterinary hospital when pathology laboratories prefer to receive samples of organs rather than a whole kitten. Necropsy of kittens should be performed as often as possible to become proficient in the procedure and to recognize normal kitten anatomy. The heart and liver are prominent in a normal kitten compared to an adult cat. There is always some fluid in the body cavities of a newborn kitten after it has been frozen then defrosts; this is not pathological or ascites. See Figure 306-1. It is helpful to understand the causes of illnesses or deaths of other kittens from the same household or cattery. This allows you to more specifically select the right organs for analysis. Get the owner ’s written permission for the necropsy, and determine if the owner wants the body returned. If so close the body cavities at the end of necropsy, and unless essential, avoid dissection of the head for cosmetic reasons.
Preservation of the Body Necropsy must be conducted on a well-preserved kitten; a dying kitten can be sacrified so fresh tissue is available. The body can be refrigerated for up to 2 days at 4°C (39°F). Freezing should be avoided because it destroys most cellular tissue.
History Events concerning the queen during gestation (e.g., vaccinations, nutrition, trauma, and diseases) and parturition (dystocia) should be recorded. History of the kitten should also be recorded including the kitten’s weight curve, history of trauma or domestic accidents, and death of siblings. The most common causes of mortality in purebred kittens based on the age of the population are presented in Table 306-1.
Procedure A systematic procedure should be employed so vital information is not overlooked. • Instrumentation: A scapel, forceps, and a pair of scissors are usually sufficient. The small skull can be easily opened with scissors. Gloves and a mask should be used for personal protection. Pictures, notes, and record of the list of samples should be kept during the examination. Because of the small size of the patient it is recommended to
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
908
Figure 306-1 There is always a small amount of fluid inside the body cavities of a kitten that has been frozen then defrosts; this is not ascites or an indication of disease.
TABLE 306-1: Common Causes of Death in Kittens Perinatal period (first 24 hours) Frequency = 5.0–8.2% Neonatal period (1–14 days) Frequency = 5% First 8 days more critical.
Preweaning period (15–34 days) Postweaning period (35–112 days) High mortality rate
50% Traumatic (usually dystocia) 50% Idiopathic Congenital defects Isoerythrolysis (See Chapter 150.) Maternal neglect Infectious diseases due to bacteria (i.e., umbilicus, skin wounds, bites, abscesses, peritonitis, or septicemia) Viral diseases are less frequent (i.e., herpesvirus or calicivirus) Mainly due to viral infections (i.e., calicivirus, herpesvirus, parvovirus, or coronavirus) because of loss of maternal antibodies, loss of weight during weaning, movement into a new and larger environment. Cardiac and nervous congenital defects leading to euthanasia. Bacterial pneumonia; uncommon Intussusception during weaning (mainly for Oriental breeds) Anemia (nursing kittens with fleas) Parasitic diseases (i.e., toxoplasmosis and intestinal worms) Nutritional disorders; rare
perform a necropsy using magnification and good lighting. Necropsy is more difficult on a newborn kitten weighting 100 g (0.25 lb or 4 oz) than on a 3-month-old 1.5-kg (0.75-lb) kitten. • Gross Examination: Weigh the kitten and take pictures and notes. Look for wounds (e.g., skin tears, bruises, and injection sites), signs of disease, including nasal or ocular discharges; diarrhea on the
Necropsy of Kittens
Figure 306-4
Figure 306-2 A cleft palate is the most common intraoral congenital defect of newborn kittens.
The kitten’s organs are removed in bloc.
TABLE 306-2: Tissues That Should be Collected Lungs, heart, and mediastinum. Stomach, small intestines, and large intestines. Internal and peripheral lymph nodes. Liver, spleen, and kidneys. Peritoneum and mesentery. Brain and eyes. Any tissue that appears abnormal.
• Sampling: The submission vials and cassettes should be prepared before opening the body. Sampling should be done in a systematic order. Collect more than you think will be needed. This permits a later decision regarding what is sent first and what is kept for further analysis. Collection should be done for cytologic, histologic, bacteriologic, serologic, and polymerase chain reaction (PCR) analysis. See Table 306-2 for a list of organs to be sampled.
Figure 306-3 This shows the extensive skin incision that should be made during a kitten necropsy. perineum; swollen, infected, or inflamed anus or umbilicus; swollen joints; dehydration; discolored mucous membranes; and anatomical defects (i.e., hydrocephalus, cleft palate [Figure 306-2]); exencephaly; umbilical hernia; and so on. • Dissection Technique: The kitten is positioned in dorsal recumbency with its legs extended and the feet facing the operator. A skin incision is made beginning under the chin, progressing to the right side of the rib cage, then to the right flank down to the right leg, then horizontally under the umbilicus. The right mandible is cut, and the tongue, esophagus, and trachea are removed together to the level of the thoracic inlet (see Figure 306-3). The thoracic cavity is opened; the presence of fluid is recorded, and a sample taken. The abdominal cavity is opened; fluid is recorded and sampled. Organs are inspected. All the attachments are severed and organs removed en bloc from the tongue to the rectum (see Figure 306-4). The kidneys, bladder, reproductive tract, and adrenal glands are removed. Finally, all of the organs are dissected, and samples are taken.
Notes • There are some technical limits. The size of some organs is small. For example the heart is about 1.5 cm (5/8 in) longitudinally. It is quite difficult to identify a cardiac defect on a newborn kitten. Cardiac anatomy is better examined on a formalized heart than on a fresh heart. • Before beginning, your laboratory should be questioned regarding appropriate submission vials and preservatives. • Lungs should always be sampled because gross lesions are often absent in newborn kittens, even in case of pneumonia. • In contrast to necropsy of an adult cat, a kitten necropsy is a short procedure.
Suggested Readings Cave TA, Thompson H, Reid SWJ, et al. 2002. Kitten mortality in the UK: A retrospective analysis of 274 histopathological examinations (1986 to 2000). Vet Rec. 151(10):497–501. Schlafer DH. 2008. Canine and feline abortion diagnostics. Theriogenology. 70(3):327–331.
909
CHAPTER 307
Neurologic Examination Stephanie G. Gandy-Moody
Overview The neurological examination is the most important tool in diagnosing and confirming a nervous system disorder and locating the site(s) of involvement. Although some feline patients may be difficult, a complete examination can usually be performed in 15 to 20 minutes.
• Evaluation of the menace response: Move your hand quickly toward the eye in question being careful not to touch the whiskers. Look for a normal blinking response. This not only evaluates the optic nerve (afferent pathway) but also the facial nerve, which is responsible for eliciting the blink (efferent pathway).
Cranial Nerve 3: Oculomotor Nerve Supplies Needed and Recommended • • • • • • • •
Reflex or percussion hammer Hemostatic forceps Cotton-tipped applicator Food (i.e., canned, dry, or treats) Focal beam light source Tongue depressor Cotton ball Laser pointer
Procedure Mental Status and Locomotion • While collecting information about the history of your patient also use this time to evaluate your patient from a distance. Pay close attention to the way the cat responds and moves around the examination room. Is the patient highly aware of its surroundings? Is it curious, frightened, or aloof?
Examination of the Cranial Nerves Cranial Nerve 1: Olfactory Nerve • For evaluating the sense of smell. • This nerve can be evaluated by placing an opened can of food (i.e., canned cat food, tuna, or sardines) near the nasal openings. If the patient smells the food they will typically respond by turning away or sniffing the food. A response as subtle as contraction of the facial muscles may occur so observe the patient closely. • Severe nasal congestion or infection may affect the assessment of this test. • Disorders of the sense of smell do exist; however, they are relatively rare.
• For evaluating pupillary constriction and oculomovement. Review of Definitions • Mydriasis: larger than normal pupil size. • Miosis: smaller than normal pupil size (usually occurs with bilateral, severe, cerebrocortical disease). • Anisocoria: resting inequality in pupil size. • Horner ’s Syndrome: Miosis, drooping of the upper eyelid, enophthalmos, protrusion of the third eyelid, vasodilation on side of the head. See Chapter 99. Pupillary Light Reflex • Using a bright light source, shine the light directly into one eye. Both pupils should constrict as this nerve is responsible for constriction of the pupil. • Direct Response: constriction of the stimulated eye. • Consensual Response: constriction of the opposite pupil.
Cranial Nerve 3 (Oculomotor), Cranial Nerve 4 (Trochlear), and Cranial Nerve 6 (Abducens): • These three nerves are often evaluated concurrently because these nerves function together resulting in ocular movement. • To assess the motor function of the oculomotor nerve, observe the position of your patient’s eyes. Gently move your patient’s head laterally while observing the eyes. A normal response results in the patient’s eyes attempting to maintain looking straight ahead resulting in a slow drift of the eyes in the direction opposite the movement. A quick movement of the eyes in the direction of the head movement will occur as the head is continuing to be moved laterally. The extraocular muscles (influenced by the vestibular system) are responsible for this response. This slow/quick eye movement is known as induced vestibular nystagmus. Strabismus is a deviation of the eye from the normal position. A lateral or ventral strabismus may be present if there is a lesion of this portion of the nerve as well as ptosis, which occurs from paralysis of the levator palpebrae muscles.
Cranial Nerve 2: Optic Nerve • For evaluating vision • There are three ways to assess vision. • Watch the patient ambulate around the examination room. • A cotton ball may be dropped in the visual field of the patient or a laser pointer may be used to catch the cat’s attention.
Cranial Nerve 4: Trochlear Nerve • Isolated lesions of this nerve are extremely rare. • If there is a problem with this nerve in your patient, the dorsal aspect of the vertical pupil would be deviated laterally.
Cranial Nerve 5: Trigeminal Nerve The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
910
• Responsible for facial sensation and movement of the muscles for mastication. • The three branches of this nerve need to be assessed independently.
Neurologic Examination
Ophthalmic Branch • Assessed by testing for a palpebral reflex and corneal reflex. To test the palpebral reflex the medial canthus is touched, and the patient should quickly close the eye. To test the corneal reflex touch the cornea. The eye should retract into the orbit and the patient should blink. This reflex is important to maintain corneal epithelium. Maxillary Branch • Assessed by touching the external nasal mucosa. One is directly stimulating the trigeminal nerve causing a reflexive muscle movement (via the facial nerve) and then a conscious movement of the head away from the stimulus. If your patient has a lesion of the maxillary branch of the trigeminal nerve, it will not have a facial reflex or be able to consciously respond to the stimulus. If your patient has a forebrain lesion, the reflex component will be intact; however, there will be no conscious response to the stimuli. Mandibular Branch • Assessed in three parts. • By pinching the skin over the mandibular area with a hemostat. This should result in the patient pulling its head away. • Assessing for muscle atrophy of the temporal and masseter muscles by visual assessment and palpation. • Opening the mouth and assessing for jaw closure and tone. • A patient with bilateral mandibular nerve disease will have a dropped jaw and be unable to close its mouth. • Dysfunction of all three branches (unilaterally) of this nerve will be associated with a lesion outside of the brainstem.
Cranial Nerve 6: Abducens Nerve • Isolated lesions of this nerve are uncommon. • The patient’s eyeball would not be able to be abducted fully and may be not be able to be retracted within the orbit resulting in a ventromedial strabismus. Note that Siamese cats can have strabismus caused by congenitally abnormally visual projection pathways.
• To assess your patient’s hearing ability, create a loud noise (such as a quick, loud, single hand clap), and observe the response of the patient to the stimuli.
Cranial Nerve 9: Glossopharyngeal Nerve • Responsible for pharyngeal sensation and movement with Cranial Nerve 10 (vagus nerve), salivation, and taste. • A tongue depressor may be held and placed in the caudal aspect of the patient’s pharynx. The patient should immediately gag pushing the tongue depressor out of the area with the caudal aspect of the tongue. • If your patient has a lesion of this nerve it will have difficulty swallowing and pharyngeal muscle abnormalities.
Cranial Nerve 10: Vagus Nerve • Responsible for laryngeal sensation, laryngeal movement, salivation, and other autonomic functions • To assess function of the vagus nerve your patient should be anesthetized. With a laryngoscope observe movement of the arytenoid folds during respiration; a normal response results in abduction of the folds during inspiration.
Cranial Nerve 11: Spinal Accessory Nerve • Responsible for motor innervation to the trapezius muscle. • If a lesion is present with this nerve your patient will demonstrate atrophy of the trapezius muscle and decreased resistance to lateral passive movement of the head and neck contralateral to the side of the lesion.
Cranial Nerve 12: Hypoglossal Nerve • Responsible for motor to the tongue. • The tongue will be weak or paralyzed when palpated. • Atrophy may occur on the affected side.
Cranial Nerve 7: Facial Nerve • Responsible for motor to the muscles of facial expression, taste, salivation, and skin sensation inside the ear. • A patient suffering from facial nerve damage will have paresis or paralysis of the facial muscles resulting in facial asymmetry. • Testing the palpebral reflex is the best way to test your patient’s facial nerve motor function; if a lesion exists the patient will not close the palpebral fissures. • The menace response will also be decreased or absent even though your patient has normal vision. • The parasympathetic function of the facial nerve is primarily responsible for lacrimal gland secretion. • If a lesion exists with this nerve your patient may demonstrate clinical signs of keratoconjunctivitis sicca (KCS) or dry eye. • Salivation may be assessed by palpating the buccal mucosa. • When assessing taste one may use an atropine-soaked cotton tipped applicator and touch the patient’s tongue with it. The patient should salivate and pull away from the stimulus.
Cranial Nerve 8: Vestibulocochlear Nerve • Responsible for equilibrium, balance, and hearing. • Clinical signs of vestibular disease are: • Ataxia. • Head tilt (usually directed toward the side of the lesion). • Nystagmus. • Eye deviations.
Postural Reflexes • This is the cat’s ability to know where its limb is in space, relative to its body, and to correct an abnormal position. • This is examined by the following techniques.
Conscious Proprioception • With the cat in standing position turn one paw so that the top of the paw contacts the table or ground surface. Assess the time it takes for the cat to return the paw to normal position. This should be performed for all limbs. • In a normal cat the paw position should be corrected immediately; any delay would indicate neurological disease.
Wheelbarrowing • With the cat in standing position raise either the front or rear end of the patient so that the weight is placed on either both pelvic or both thoracic limbs. When testing the thoracic limbs force the cat to move its body forward. When testing the pelvic limbs force the cat to move backward. • This test is helpful in testing for subtle thoracic limb paresis, especially if the head is concurrently held and extended by the examiner. • In a normal cat, the limbs that are touching the table or ground surface should make normal walking movements.
911
SECTION 7: Clinical Procedures
Hemistanding and Hemiwalking • With the cat standing hold up the forelimb and hindlimb of the same side. First assess whether or not the cat can stand balancing with the limbs of one side. Next, force the patient to walk forward or sideway. • This will determine the functional integrity of the motor cortex and spinal cord. • A normal cat will position the limbs to achieve balance.
Hopping • With the cat standing, three of the limbs should be held up by the examiner, leaving the limb in question on the table surface or ground. • When the cat is moved forward and to each side the normal response is for the cat to hop on the down leg to keep the limb under the body to support its weight.
Spinal Cord Reflexes and Muscle Tone • This is used to test the peripheral nerves and the segment of the spinal cord where each nerve originates. At this time, when the cat is in lateral recumbency, muscle tone should be assessed.
Thoracic Limb Reflexes Biceps Reflex • Musculocutaneous C6–T1: • With the cat in lateral recumbency place your finger on the biceps tendon and tap your finger with the reflex hammer. The biceps tendon is located on the craniomedial aspect of the elbow. A normal response results in a slight flexion of the elbow. Triceps Reflex • Radial, C6–T2: • With the cat in lateral recumbency place your forefinger or thumb on the triceps tendon and tap either your forefinger or thumb with the reflex hammer. The triceps tendon is located proximal to the olecranon. A normal response results in slight extension of the elbow. Extensor Carpi Radialis Reflex • Radial, C6–T2 • With the cat in lateral recumbency tap the belly of the muscle just distal to the elbow. A normal response results in extension of the carpus. Withdrawal or Flexion Reflex • Axillary, C7–C8; musculocutaneous, C6–T1; and median and ulnar, C7–T2: • Initially start with a gentle pinch (slowly increasing the intensity) and observe your patient for a response, such as crying out, looking at the limb, or a change in facial expression or respiratory rate. • This test does not require cerebral input; therefore, withdrawal of the limb does not indicate if the cat can consciously feel the stimulus.
Pelvic Limb Reflexes Patellar Reflex • Femoral, L4–L6 • With the cat in lateral recumbency and the pelvic limb relaxed (semiflexed), tap the patellar ligament with a reflex hammer.
912
• This is the most reliable tendon reflex in cats. • Normal Response: quick extension of the stifle joint. Gastrocnemius Reflex • Tibial, L7–S1, and minor contribution from L6: • With the cat in lateral recumbency place your forefinger over the gastrocnemius tendon and tap your forefinger with the reflex hammer. • Normal Response: Extension of the hock Cranial Tibial Reflex • Common peroneal, L6–L7, and minor contribution from S1: • With the cat in lateral recumbency tap the belly of the muscle just distal to the tibia. • Normal Response: slight flexion of the hock. Withdrawal or Flexion Reflex • Sciatic, L6–S1: • Initially start with a gentle pinch (slowly increasing the intensity) and observe your patient for a response, such as crying out, looking at the limb, or a change in facial expression or respiratory rate. • This test does not require cerebral input; therefore, withdrawal of the limb does not indicate if the cat can consciously feel the stimulus.
Other Spinal Cord Reflexes Anal Reflex • Pudendal, S1–S3: • Using a hemostat first gently pinch the perianal region. If no response is elicited gently increase the force of which the pinch is applied. • Anal contracture, moving away from the stimulus (tucking the tail over the anal area), head turning facing the stimulus, and growling or hissing are a few normal responses elicited by a patient. • Abnormalities include areflexia or hyporeflexia. Panniculus Reflex • Sensory: spinal nerves; motor: thoracodorsal nerve, C8–T2: • Starting over the lumbosacral region of the cat gently pinch the skin over the dorsal midline with a hemostat moving cranially to the thoracolumbar region. • A normal response is contraction of the subcutaneous musculature at the point of stimulation (usually elicits a bilateral response). • Typically absent in patients with cervicothoracic lesions such as a brachial plexus avulsion. Defecation and Micturition Reflexes • Pelvic, S1–S3: • It is important to note whether or not your patient can voluntary urinate and defecate.
Suggested Readings August JR. Performing the neurological examination. In JR August, ed., Consultations in Feline Internal Medicine, 5th ed., pp. 449–461. St. Louis: Elsevier. Braund KG. 1994. Neurological examination. In KG Braund, ed., Clinical Syndromes in Veterinary Neurology, 2nd ed., pp. 1–36. Philadelphia: Mosby. Radostits OM, Mayhew IGJ, Houston DM. 2000. Clinical examination of the nervous system. In OM Radostits, IGJ Mayhew, DM Houston, eds., Veterinary Clinical Examination and Diagnosis, pp. 493–534. Philadelphia: Saunders.
CHAPTER 308
Orogastric Tube Feeding Gary D. Norsworthy
Definition Orogastric tube feeding involves passing a feeding tube through the oropharynx, down the esophagus, and into the stomach. A syringe containing food having the consistency of a thick milkshake is attached to the tube, and the contents are expelled through the tube into the stomach. This permits feeding a substantial quantity of high quality food in a few seconds.
are held in a similar fashion with the other hand, placing the index finger between the hocks and closing the hand. See Figure 308-1. The second person faces the first person and holds the cat’s head with the nondominant hand using the other hand to place the mouth speculum, pass the tube, and empty the syringe. See Figure 308-2. About 10% of cats struggle enough or are strong enough that a third person
Indications • Orogastric tube feeding is for hospitalized anorectic patients. It can be easily mastered by veterinary technicians; however, I do not advise trying to equip and train clients to perform this procedure. • The orogastric tube technique is also appropriate for administering barium for a gastrointestinal series or activated charcoal for treating toxicosis.
Contraindications • Any condition that requires nothing by mouth (NPO) treatment (e.g., gastrointestinal obstruction or rupture, and acute pancreatitis). • Cats with respiratory distress (e.g., severe upper respiratory disease, diaphragmatic hernia, pleural effusion, pulmonary edema, and pneumonia). • Fractious cats.
Equipment • An 18 French soft tube about 40 cm (15 in) long. Tubes of this nature are sold by DVM Solutions (www.dvmsolutions.com) and Sovereign (Feeding Tube and Urethral Catheter). • A syringe, tipped with a 60-mL catheter (Monoject). • Feline Mouth Speculum: DVM Solutions (www.dvmsolutions.com). • Food with high caloric density that is syringable. I prefer Maximum Calorie (The Iams Company, Dayton, OH). The stressed or ill 4-kg (8.8-lb) cat requires about 100 mL of this food per 24 hours. Gradual onset feeding should begin with about 30 mL once or twice on the first day, 45 to 50 mL twice on the second day, and 80 to 100 mL twice on the third day. If vomiting occurs shortly after feeding, the quantity should be reduced and the daily increases in amount fed reduced also.
Figure 308-1 The first technician holds the cat vertical securing the front legs with one hand and the rear legs with the other.
Procedure • Two persons are generally required. The first person holds the cat so the dorsal midline of the cat is vertical and against the person’s chest. This person holds the cat’s front legs by inserting an index finger between the carpi and closing the hand, wrapping the thumb around one leg and the other three fingers around the other leg. The rear legs
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 308-2 The second technician places the mouth speculum, passes the tube into the stomach, and empties the syringes.
913
SECTION 7: Clinical Procedures
• •
• •
•
is needed to stabilize the cat’s head and neck to prevent its head from being dislodged from the second person’s grasp. If two syringes of food are to be administered, both are loaded before feeding begins. The tube is passed into the stomach. Reaching the stomach (instead of the tracheal bifurcation) is assured by noting how much tube exits the cat’s mouth. If it is in the stomach, there will be no more than 8 cm (3 in), including the flared part of the tube, of tube exiting the mouth. If it is in the trachea and stops at the bifurcation, there will be 16 cm (6 in) exiting the mouth. These rules apply to a 4- to 5-kg (9- to 12-lb) cat. If the cat is considerably larger or smaller measure from the last rib to the nose, and mark the tube accordingly. If the tube is in the trachea, the cat cannot vocalize. Vocalization is virtual assurance of proper tube placement. The first syringe is attached to the tube by the second person. The base of the plunger is placed against the second person’s sternum. That person leans forward pushing the plunger into the barrel. It is important not to pull the barrel back to the plunger because this may back the tip of the tube into the esophagus. The esophagus will not hold 60 mL of food so regurgitation, aspiration, and pneumonia may result. It is also important that the proximal part of the tube be held by the same hand that is holding the syringe barrel to prohibit the tube from detaching as the food is syringed. The first syringe is detached, and the second syringe is attached and emptied. This prevents removal of the tube requiring a second tube passage.
914
• The tube is removed from the cat and washed and disinfected before its next use. • The food that is not fed is refrigerated. It can be stored for up to 5 days. It is important that it be heated before the next feeding. Feeding cold food causes poor syringability and vomiting. If it is overheated, damage to the stomach will occur.
Likely Complications • Passing the tube into the trachea and syringing food into the lungs is fatal. Cats that are fractious or struggle are more likely to be the victim of this unfortunate circumstance. • Cats that have respiratory distress can die due to panic and resulting oxygen deprivation. • Cats with obstructed nasal passages (e.g., rhinitis and trauma) often panic because cats are natural nose breathers. If the nasal passages are not open, they tend to panic easily.
Suggested Readings Norsworthy GD. 1991. Anorexia and force reeding. In GD Norsworthy, ed., Feline Practice, pp. 40–43. Philadelphia: JB Lippincott. Norsworthy GD. 1991. Providing nutritional support for anorectic cats. Vet Med. 86:589–593.
CHAPTER 309
Polymerase Chain Reaction Testing Christian M. Leutenegger
Introduction: Polymerase Chain Reaction Testing for the Practitioner Polymerase chain reaction (PCR) is a tremendously useful diagnostic tool for the practitioner if used in the correct context and for the appropriate application. In this chapter we will review important recent developments in PCR testing, highlight its major applications, and provide guidelines and recommendations for the practitioner, with a focus on infectious disease testing. In general, veterinary molecular diagnostics is used (a) to detect infectious diseases, (b) to detect genetic disorders, or (c) to determine identities of individual animals at the DNA level, which includes identity testing, sex determination (mainly birds), genetic disorder testing (all animals), and breed testing (mainly dogs). Additional applications, such as gene profiling to assess a particular disease state, differentiation between infectious and noninfectious disease conditions, or cancer testing, are close to diagnostic applications but not yet available. Infectious disease diagnostics is by far the most important aspect of PCR testing in companion veterinary medicine, with a wide range of tests and panels available from different university and private laboratories.
What Is Polymerase Chain Reaction? Briefly, PCR detects DNA, and DNA is present in every organism. PCR is a Nobel Prize awarded laboratory method invented in the 1980s, which is revolutionizing the diagnostic landscape. The strength of PCR testing lies in the method by which DNA is detected. PCR is able to amplify minute amounts of DNA to produce a robust and detectable signal. The amplification is achieved with an enzyme called DNA polymerase. To allow the DNA polymerase enzyme to amplify a specific sequence, two synthetic DNA pieces (called PCR primers) function as initiators of the amplification reaction. The primers are specific to a known DNA sequence of an organism, for example feline herpesvirus (FHV-1). The PCR reaction includes, in addition to the two primers and the DNA polymerase, the building blocks to synthesize the DNA copies, the so called nucleotides (i.e., adenosine, thymidine/uracile, guanidine, and cytosine) and an appropriate buffer system. Once these PCR reagents are brought together with the DNA extracted from the diagnostic sample, the primers will find, if present, the FHV-1 DNA, for example, and bind to it at a certain temperature (called annealing temperature), which in turn allows the DNA polymerase to extend the primers and copy the original FHV-1 DNA stretch encompassed by both primers. By repeating this so-called PCR cycle up to 40 times, FHV-1 DNA is copied 240 times (also called exponential amplification) leading to 1 trillion copies of the original FHV-1 DNA. It is easily understandable that such an amount of DNA can be made visible even to the naked eye. See Figure 309-1.
Polymerase Chain Reaction Does Not Equal Polymerase Chain Reaction: Real-Time Polymerase Chain Reaction PCR exists in different forms. The original form of PCR testing includes the visualization of the FHV-1 DNA copies generated during PCR by gel
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
electrophoresis. During this process, the FHV-1 DNA copies are labeled with a fluorescent dye to make them visible under ultraviolet light illumination. Briefly, this process requires each PCR reaction tube to be opened; because of the vast number of PCR products, this step is associated with a substantial risk of contaminating the laboratory environment and subsequent PCR reactions with aerosols. The resulting PCR product carry over is a serious dilemma of traditional PCR and produces falsepositive results. For this and other reasons, real-time PCR has become the gold standard for research and many human and veterinary molecular diagnostics applications. In real-time PCR, detection of the FHV-1 DNA copies accumulated during PCR are detected in each PCR cycle and not, as in traditional PCR, at the end of the PCR process. See Figure 309-2. This simple difference has important implications: (a) it eliminates the need to open the PCR reaction tubes and, therefore, eliminates the risk for PCR product carry over. For this reason real-time PCR is also called a closed-tube detection system. (a) Real-time PCR quantifies the amount of FHV-1 DNA present initially in the PCR reaction. Quantitative PCR can be used to make an interpretation on the state of infection and whether a sample was collected during acute phase of infection (high levels of FHV-1 DNA) or chronic phase (low levels of FHV-1 DNA). Furthermore, DNA quantity can also be used to assess the suitability of a particular diagnostic sample for PCR and reduces the likelihood for false negative PCR results. (c) A third synthetic DNA piece, called a (TaqMan®) probe, labeled with fluorescent dyes at each end is added to the real-time PCR reaction mix allowing the detection of the FHV-1 DNA copies in real time. The addition of a probe in real-time PCR increases analytical specificity and sensitivity and eliminates the need to open PCR reaction tubes. (d) Real-time PCR was introduced in 1996 with a complete set of tools to standardize the PCR process. In particular, the design of primers and probes, the validation of the real-time PCR test itself, amplification conditions, reagent stability, quality controls, disposable requirement, and many other variables were predefined in an industry standard. Because of this standard, real-time PCR tests run in parallel perform nearly identical. This is of great importance for the practitioner ’s evaluation of the use of PCR testing and molecular diagnostics in general and enables the panel approach offered by many molecular diagnostic laboratories, where a number of PCR tests are run in parallel on the same sample. (e) Real-time PCR allows automation of the process to analyze large numbers of samples for many different PCR targets and consequently guarantee a high level of uniformity, precision, accuracy, and reliability.
Polymerase Chain Reaction’s Place in the Diagnostic Work-Up Although antibody testing measures past exposure to infectious agents, PCR detects DNA and, therefore, an infectious agent directly; it is proof of infection (in most instances) rather than proof of exposure. While antibody testing is useful for epidemiological screening, it is not a diagnostic test per se. In turn, PCR testing is a diagnostic test by definition and is most appropriate to be used for the sick animal diagnostic workup to confirm presence of active infection. PCR can be used to confirm a presumptive diagnosis based on clinical signs, positive serology, or other laboratory tests and should always be used in conjunction with these and not as a stand alone result; no one test can reliably dictate a course of action.
915
SECTION 7: Clinical Procedures
First PCR Cycle: Two double stranded DNA molecules consisting of 2 PCR products and 2 original DNA strands
Second PCR Cycle: 4 DNA molecules: 6 PCR products, 2 original DNA strands
Third PCR Cycle: 8 DNA molecules: 14 PCR products, 2 original DNA strands
Fourth PCR Cycle: 16 DNA molecules: 30 PCR products, 2 original DNA strands
Figure 309-1 Polymerase chain reaction amplification. During the process of the polymerase chain reaction, products are accumulated exponentially. Three steps constitute each cycle, as described in the text. After a few cycles of amplification, the population of DNA molecules becomes dominated by a single DNA fragment, called the polymerase chain reaction product. In the example illustrated, four cycles of polymerase chain reaction reaction produce 32 DNA products (16 double-stranded DNA molecules with 30 polymerase chain reaction products and the two original DNA strands). After 40 cycles and with 100% polymerase chain reaction amplification efficiency, the total number of polymerase chain reaction products exceeds 1012 or one trillion with just one original DNA molecular to initiate the polymerase chain reaction reaction.
During the acute phase of infection, nucleic acid is detectable within days while antibody production is still absent. Although maternal or vaccination induced antibody levels almost always interfere with serology, as a rule, PCR does not. In addition, due to its nature to be able to detect single DNA molecules, PCR has exquisite analytical sensitivity, which translates for many applications into excellent diagnostic sensitivity and specificity. Because of its high analytical sensitivity, PCR is able to pick up chronic infections such as feline hemotropic mycoplasma and Ehrlichia canis. For that reason, PCR can play a role in testing healthy animals. Blood donors, in particular, can be tested to exclude healthy but infected animals from donor pools.
A Practitioner’s Guide: Selecting a Polymerase Chain Reaction Diagnostic Laboratory As a practitioner inexperienced with PCR testing, asking the right questions may give you the perspective to start using this diagnostic tool. There are five areas in which a candidate laboratory should be able to give you information about its testing environment.
916
Polymerase Chain Reaction Testing and Nucleic Acid Extraction Platforms As illustrated previously, real-time PCR has many advantages over the more traditional or conventional gel-based PCR methods. The question whether a lab uses real-time PCR versus conventional PCR is, therefore, important because real-time PCR is more likely to be reliable, reproducible, have trustworthy positive and negative results, have faster turnaround time, and be more affordable. Ask whether the nucleic acid extraction is done manually or automated. In general, automated extraction systems provide equal or better quality of nucleic acid, are safer with regard to cross-contamination during the extraction process, provide more consistent results, and largely eliminate human error.
Sample Collection and Submission Guidelines Guidelines for PCR sample collection and submission have to be provided by the diagnostic laboratory. This is essential to guarantee a high
R
(A) 5′ Primer 1
Q
Probe
P
3′
5′
5′
3′ Primer 2
R
(B)
Probe
5′ Primer 1
5′
Q P
3′
5′
5′
3′ Primer 2 R
(C)
cleaved Probe
5″
Q
5′ Primer 1
P
5′
3′
3′
5′ Primer 2 Q
R
(D)
5″
P 5′ Primer 1 3′
5′
5′
3′ 5′
(E)
Fluorescent Signal
POS
NEG 0
5
10
15
20
25
30
35
40
PCR Cycle Number Figure 309-2 An Animation of the real time PCR TaqMan 5′-3′ nuclease assay. A, polymerase chain reaction primers 1 and 2 and a TaqMan probe, labeled with a reporter dye, (R) and a quencher dye, (Q), bind to the DNA template. The 3′ phosphate group (P) prevents extension of the TaqMan probe. B, The presence of the enzyme, Taq DNA polymerase, enables extension of the primer. C, The DNA polymerase displaces the TaqMan probe. The displaced probe is cleaved by Taq DNA polymerase resulting in an increase in relative fluorescence of the reporter. D, Polymerization of the new polymerase chain reaction products is now complete. A through D show the events within one polymerase chain reaction cycle; E, shows the signal generation during real-time polymerase chain reaction over 40 cycles (40–45 is the standard cycle number). During each cycle, fluorescent intensity is measured on a CCD chip and recorded on a computer. If the fluorescent signal increases, a computer-based algorithm determines at what point a signal is considered positive. The positive call is recorded as the polymerase chain reaction cycle at which the signal exceeds a threshold (cycle threshold value).
917
SECTION 7: Clinical Procedures
TABLE 309-1: Possible Quality Controls for Detection of Infectious Agents (DNA and RNA) Quality Control
Purpose
Polymerase chain reaction Negative Control Polymerase chain reaction Positive Control
Show absence of contamination in polymerase chain reaction reagents. Confirm functional performance of a polymerase chain reaction test to generate a positive signal with a specific piece of DNA. Confirm absence of cross-contamination during the extraction process. Preanalytical control confirming that amplifiable DNA was present in the diagnostic sample submitted and that shipping did not negatively affect the quality of the DNA. Pre-nalytical control confirming that amplifiable RNA was present in the diagnostic sample submitted and that shipping did not negatively affect the quality of the DNA. Normally a synthetic piece of DNA with random nature spiked into the extraction lysis solution to confirm absence of polymerase chain reaction inhibition and confirm efficiency of nucleic acid extraction. A swab based control that collects samples from various locations within the Polymerase chain reaction laboratory confirming absence of aerosol-based contamination.
Negative Extraction Control Sample Quality Control DNA Sample Quality Control RNA Internal Positive Control
Environmental Contamination Control
quality of the extracted nucleic acid (DNA and ribonucleic acid [RNA]) from your diagnostic sample material. If the quality of the nucleic acid is low as a consequence of inappropriate sampling or shipping, then the reliability of any molecular test result is in question.
Polymerase Chain Reaction Quality Controls and Quality Assurance PCR quality controls and quality assurance is integral to the reliability of PCR results. They may contain, but are not limited to, the following:
Providing Consulting for Polymerase Chain Reaction Results Ask if there are veterinary specialists able to answer questions regarding laboratory medicine and molecular diagnostics. Interpretation of PCR test results have to be made in conjunction with other laboratory test results and with associated clinical signs to optimize its use for the diagnostic workup. Specialists can help guide you through updated diagnostic workflows with integrated molecular tests.
What Is in It for the Practitioner? Quality Controls It is legitimate to ask which quality controls are run with your diagnostic sample and whether quality control results can be provided by the lab. An overview of quality controls routinely run in molecular diagnostic laboratories is given in Table 309-1.
Use of Standard Operating Procedures in the Laboratory The question whether standard operating procedures (SOPs) are defined and followed in any diagnostic laboratory is of high importance and should be a factor in selecting a diagnostic laboratory for any test.
Proficiency Testing The Veterinary Laboratory Association (VLA) has not yet adopted a proficiency testing module for veterinary molecular diagnostics. However, with the increasing numbers of laboratories adopting real-time PCR, it is foreseeable that this will become available in the near future. Despite the lack of a proficiency testing module, asking this question may provide information about the quality, thoroughness, and knowhow of the diagnostic laboratory to which you intend to send your valuable samples.
Polymerase Chain Reaction Comments and Guide for Interpretation PCR testing results should be provided as positive and negative associated with an interpretative comment relevant for veterinary medicine. In certain cases, quantitative information can add information to a realtime PCR result.
918
Every diagnostic test should provide useful, high quality information within an appropriate time frame and at a reasonable price. This is true for all mainstream diagnostic tests that are available in veterinary medicine. Laboratories offering molecular tests have made significant strides in providing fast turnaround time of high quality results to an affordable price. Because of the significant advancement of real-time PCR, veterinary molecular diagnostics for infectious diseases and genetics applications are on their way to becoming an everyday diagnostic tool implemented into most diagnostic algorithms. Because of the high incidence of infectious diseases, increased knowledge of infectious organisms as stand-alone or coinfectious agents, and vast improvements in sequence information, molecular diagnostics testing will continue to increase in importance. The ease of use, reliability, and safety combined with affordability are the reasons practitioners should desire to use it. It provides useful medical answers and an additional revenue stream for the practitioner in a market place in which multiple competitive forces are reducing market shares for the veterinary profession.
Suggested Readings Csako G. 2006. Present and future of rapid and/or high-throughput methods for nucleic acid testing. Clin Chim Acta. 363(1–2):6–31. Harrus S, Waner T, Aizenberg I, et al. 1998. Amplification of ehrlichial DNA from dogs 34 months after infection with Ehrlichia canis. J Clin Microbiol. 36(1):73–76. Hegarty BC, Vissotto de Paiva Diniz PP, et al. 2009. Clinical relevance of annual screening using a commercial enzyme-linked immunosorbent assay (SNAP 3Dx) for canine ehrlichiosis. J Am Anim Hosp Assoc. 45:118–124.
Polymerase Chain Reaction Testing
Holland PM, Abramson RD, Watson R, et al. 1991. Detection of specific polymerase chain reaction product by utilizing the 5%–3% exonuclease activity of Thermus aquaticus DNA polymerase. Proc Natl Acad Sci 88:7276–7280. Kogan LR, McConnell SL, Schoenfeld-Tacher R. 2005. Response of a veterinary college to career development needs identified in the KPMG LLP study and the executive summary of the Brakke study: a combined MBA/DVM program, business certificate program, and curricular modifications. J Am Vet Med Assoc. 226(7):1070–1076. Leutenegger CM. 2001. The real-time TaqMan PCR and applications in Veterinary Medicine. Vet Sci Tomorrow, Online Journal, Jan 1. Liu YT. 2008. A technological update of molecular diagnostics for infectious diseases. Infect Disord Drug Targets. 8(3):183–188. Mackay IM. 2004. Real-time PCR in the microbiology laboratory. Clin Microbiol Infect. 10(3):190–212.
Mapes S, Leutenegger CM, Pusterla N. 2008. Nucleic acid extraction methods for detection of EHV-1 from blood and nasopharyngeal secretions. Vet Rec. 162(26):857–859. Pusterla N, Wilson WD, Conrad PA, et al. 2006. Cytokine gene signatures in neural tissue of horses with equine protozoal myeloencephalitis or equine herpes-1 myeloencephalopathy. Vet Rec. 159:341–346. Saiki RK, Scharf S, Faloona F, et al. 1985. Enzymatic amplification of beta-globin genomic sequences and restriction site analysis for diagnosis of sickle cell anemia. Science. 230:1350–1354. Sykes JE, Drazenovich NL, Ball LM, et al. 2007. Use of conventional and real-time PCR to determine the epidemiology of hemoplasma infections in anemic and non-anemic cats. J Vet Intern Med. 21(4):685–693. Vögtlin A, Fraefel C, Albini S, et al. 2002. Quantification of feline herpesvirus-1 DNA in ocular fluid samples of clinically diseased cats by real-time TaqMan PCR. J Clin Microbiol. 40(2):519–523.
919
CHAPTER 310
Restraint Techniques and Devices Gary D. Norsworthy
Overview Restraint is a vital part of successful feline practice. Although most feline patients are cooperative and easily handled, some are either difficult or fractious. Difficult cats can generally be handled as long as proper techniques and restraint devices are used. However, they have the potential of accelerating to the fractious category. Fractious cats must be proactively restrained or they will become dangerous to veterinarians, staff, and owners. Generally, anesthesia is needed for most procedures.
The Difficult Cat Definition These cats are manageable but can convert to fractious. They usually hiss but do not spit. When threatened they keep their ears erect and tongues flat. They can usually be handled without sedation. See Figure 231-1A.
Figure 310-1 A cat in a soft carrier can be handled by restraining it in a heavy bath towel through the top opening. The end of the carrier is opened, and an anesthesia mask is used to administer gas anesthetic.
Techniques and Devices • When wrapped in a thick bath towel, they can be examined. • Blood samples can be taken from the medial saphenous vein when they are placed in lateral recumbency while wrapped in a towel. • They can be removed from cages by covering them with a thick bath towel then picking them up. • They can be “poured” from plastic carriers into a bath towel. • Cat bags and cat muzzles can be effective. • Placing Elizabethan collars on them often permits safe handling. • If they try to hide in a litter box, cover the litter box with a towel and lift it from the cage. Once out of the cage, most of these cats are manageable using the techniques and devices above. • Cats in soft carriers can be handled with a large bath towel. The cat’s head must be facing the end of the carrier that unzips. The top of the carrier is unzipped, and the towel is placed over the cat so it cannot move. It is restrained within the towel by one technician. The end of the carrier is unzipped, and an anesthesia mask is placed over the cat’s face so anesthetic gas can be administered. See Figure 310-1.
The Fractious Cat
Figure 310-2 The Wild Child™ is a clear box with a detachable lid that can be secured in several positions to match the size of the cat.
Definition These cats are in attack mode without provocation. They are often either feral cats that have been trapped, cats with dual personalities (cooperative at home; aggressive away from home), or difficult cats that have not been handled well. Handling these cats requires sedation for humane treatment and staff safety.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
920
Techniques and Devices • Cat bags and muzzles are not appropriate because these devices cannot be placed on the fractious cat without serious risk to the veterinarian, staff, or owner. • The Wild Child™ (Veterinary Concepts, Spring Valley, WI) is a clear acrylic box with a detachable lid. See Figure 310-2. I use it in the following situations: • Cats in Plastic Carriers: The lid of the Wild Child is detached. The top half of the carrier is detached. When the latter is lifted from the bottom of the carrier, the Wild Child is lowered over the cat with its top facing downward. See Figure 310-3A. When the Wild Child
Restraint Techniques and Devices
(A)
(B)
(C)
(D)
Figure 310-3 Cats in plastic carriers: A, When the top half of the carrier is lifted from the bottom of the carrier, the Wild Child™with its top facing downward is lowered over the cat. B, C, The carrier, cat, and Wild Child™ are rotated 180 degrees and placed on the table. E, The lid of the Wild Child™ is quickly slid in place as the bottom of the carrier is lifted away.
covers the cat, towels, newspapers, bowls, toys, or other objects are removed from the carrier. Make sure the cat’s tail and feet are all confined within the Wild Child to prevent injury. The carrier, cat, and WC are rotated 180 degrees and placed on the table. See Figures 310-3B and 310-3C. The lid of the Wild Child is quickly slid in place as the bottom of the carrier is lifted away. See Figure 310-3D. Anesthetic gas is pumped into the Wild Child. • Cats in Cages: The lid of the Wild Child is detached. The Wild Child is placed on its side with the opening facing the cat. All but the opening of the Wild Child is covered with a towel. If at all possible, food and water bowls, towels, and litter boxes are removed from the cage. The Wild Child is placed on the cage floor and moved toward the cat. The lid of the Wild Child is used to keep the cat from bolting out of the cage. See Figure 310-4A. The Wild Child is pushed against the back of the cage trapping the cat inside. At this time the towel should be removed. The Wild Child is moved just enough away from the back of the cage to permit its lid to be put in place. See Figure 310-4B. The towel is removed, and the Wild Child is rotated so it is facing upright. The securing pin is put into place. See Figure 310-4C. Anesthetic gas is pumped into the Wild Child. • Cats in Cardboard Carriers: With the lid removed, the Wild Child is held over the cardboard carrier facing downward. The lid of the carrier is opened, and the Wild Child is lowered over the cat. See
Figure 310-5A. The carrier and Wild Child are rotated 180 degrees so the bottom of the Wild Child is resting on the table. See Figure 310-5B. The carrier is removed quickly, and the Wild Child’s lid is secured in place. See Figure 310-5C. Anesthetic gas is pumped into the Wild Child. • Cats in Carriers too Small for the Wild Child: The carrier is placed in a plastic bag, preferably a clear bag. The hose from an anesthetic machine is placed in the open end of the bag and the gas turned on. When the cat relaxes it is removed from the carrier. An anesthesia mask is then applied to reach or maintain the desired anesthesia level. The Catch Net™ (Jorgensen Laboratories, Loveland, CO) is a tightly woven large net attached to a handle. The opening can be closed by pulling on the cable that exits the end of the handle. It is used in the following situations: • Cats in Humane Traps: Oral ketamine plus diazepam is administered first using the formulae in Table 310-1. An open end 3.5 F × 14 cm (5.5 in) tom cat catheter is inserted into the cat’s mouth for drug injection; patience is usually required. The entire amount of ketamine plus diazepam is injected. Because of its taste, the cat may drool. The prescribed dose is enough to induce mild sedation in 5 to 10 minutes. When this occurs the cat is “poured” from the trap into the Catch
921
(A) (A)
(B)
(B)
(C) Figure 310-4 Cats in cages: A,With its lid detached and the opening facing the cat, the Wild Child is placed on the cage floor and moved toward the cat. The lid of the Wild Child is used to keep the cat from bolting out of the cage. A towel covers all but the opening of the Wild Child so the cat sees the Wild Child as a nonthreatening place. B, The Wild Child is pushed against the back of the cage trapping the cat inside, and the towel is removed. The Wild Child is moved just enough away from the back of the cage to permit its lid to be put in place. C, The Wild Child is rotated so it is facing upright. The securing pin is put into place.
922
(C) Figure 310-5 Cats in cardboard carriers: A, The Wild Child’s lid is removed, and it is held over the cardboard carrier facing downward. The lid of the carrier is opened, and the Wild Child is lowered over the cat. B,The carrier and Wild Child are rotated 180 degrees so the bottom of the Wild Child is resting on the table. C,The carrier is removed quickly, and the Wild Child’s lid is secured in place.
Restraint Techniques and Devices
TABLE 310-1: Dosing Ketamine with Diazepam Orally* Small cat Medium cat Large cat
0.15 mL ketamine + 0.3 mL diazepam 0.2 mL ketamine + 0.4 mL diazepam 0.25 mL ketamine + 0.5 mL diazepam
*Ketamine will cause corneal ulceration. It must be injected into the oral cavity without jeopardizing the eyes. Net. It is transported into the Wild Child, and anesthetic gas is pumped into the Wild Child. Note that ketamine will cause corneal ulceration; it must be directed into the mouth in a controlled fashion and not sprayed toward the cat’s open mouth.
Conclusions There are dozens of restraint devices available for safely and humanely handling aggressive cats. The devices described in this chapter are those that my staff and I have found to be consistently reliable. Whatever devices one chooses and techniques one uses, it is important that staff safety and humane treatment of feline patients are the key elements in their use. Cat bites can be painful and expensive to treat. We must weigh the risk of cat bites against being able to help our patients. These devices and techniques help achieve that balance.
Suggested Readings Norsworthy GD. 1993. Dealing with fractious feline patients. Vet Med. 88(11):1053–1060.
923
CHAPTER 311
Testing Procedures Mitchell A. Crystal and Gary D. Norsworthy
Blood Pressure Determination Indications • • • • • •
Cats suspected of having systemic hypertension. See Chapter 107. Cats with hyperthyroidism. See Chapter 109. Cats with renal disease. See Chapters 6, 86, and 189–191. Cats under anesthesia. See Chapter 247. Cats with heart disease. See Chapters 56, 108, 110, and 192. Routine screening of older cats as hypertension is becoming more commonly recognized concurrent with many illnesses and as a primary condition.
Objectives • Determination of systolic blood pressure (minimum). • Determination of systolic, diastolic, and mean blood pressure (preferred).
Equipment • Blood pressure determinations using intra-arterial sensors (direct) are the gold standard. However, direct readings are not practical for clinical practice. • Two types of indirect blood pressure equipment are available: • Doppler: Recommended equipment includes units made by Vmed Technology (1-866-373-9627) and Parks Medical (1-800-547-6427). These units reliably determine systolic pressure only. They are designed for examination room use and work well on awake and anesthetized cats. • Oscillometric: Equipment made specifically for feline patients includes the Cardell® 9401 (Sharn Veterinary; 1-866-447-4276), petMAP™ (Ramsey Medical; 800-231-6370), and the Memo Diagnostic HDO™ (S + B medVet; 1-866-373-9627). These units determine systolic, diastolic, and mean pressure. The Memo Diagnostic HDO™ features high definition oscillometry (HDO) technology that produces a tracing that is displayed on a computer screen during the recording. The tracing allows one to evaluate the quality and reliability of each reading.
• Apply the cuff snugly in one of the following locations. One of the authors (MAC) prefers the forelimb; the other (GDN) prefers the tail. • Just distal to the elbow. • Just proximal to the hock. • At the base of the tail. • The oscillometric units require that a certain part of the cuff (usually marked with an arrow) be over the artery. • Position the cat so the heart and the blood pressure sensor are in the same horizontal plane. • For Doppler machines, apply the sensor distal to the cuff in one of the following locations: • Just proximal to the main carpal pad. • Just proximal to the main tarsal pad. • On the ventral aspect of the tail about 2 cm (0.75 in) distal to the cuff. • Some Doppler equipment requires shaving of the hair where the sensor is applied to the skin; some does not. Applying alcohol then coupling gel may negate the need for shaving. • Take several blood pressure readings. If the first three readings are consistent (within 10% of each other), average them. If not one to four additional readings are taken with the outliers discarded and the remainder averaged. • When using the Memo Diagnostic HDO™, discard readings that do not have a Bell-shaped curve on the computer tracing. These are usually associated with movement during the reading. • Readings should be made 1 minute or more apart. Compressing an artery too frequently in a short period of time results in arterial fatigue and lower blood pressure readings. • If the results are in question, repeat the process on another location. • In general, indirect blood pressure determinations tend to slightly underestimate true pressures.
Reticulocyte Count Indication This test is to assess bone marrow response in the face of anemia.
Objective Technique • Stress greatly affects the blood pressure of cats. The following help obtain a true reading: • A quite room away from the sight or sounds of dogs or other cats. • The presence of the owner. • Gentle handling. • Adequate time to calm and reassure the cat. • Performing the blood pressure determination before other parts of the physical examination or procedures. • Choose a blood pressure cuff whose width is about 30 to 40% of the circumference of the body part encircled.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
924
• To differentiate nonregenerative anemia from regenerative anemia. This has diagnostic, therapeutic, and prognostic implication.
Technique • Mix and incubate ethylenediaminetetra-acetic acid (EDTA) anticoagulated blood with an equal amount of new methylene blue stain for 10 to 20 minutes. • A hematocrit tube or purple top blood tube may be used. • After incubation, place one drop of the stained blood on a microscope slide and make a blood smear. • Examine the cells under oil immersion (1000×). • An aggregate reticulocyte percentage greater than 0.5% likely represents a normal bone marrow response to a mild anemia; a greater aggregate percentage is expected for moderate (2%) or severe (4%) anemias.
Testing Procedures
• Punctate reticulocyte counts are usually ignored except when the anemia is mild; then their presence can suggest a regenerative response.
Formalin-Ether Sedimentation Technique Indication This test is indicated for cats with clinical signs or laboratory evidence of liver disease living in or from locations endemic with liver flukes.
Objective • Detection of liver fluke ova from fecal sample
Technique • • • • • • • • •
Suspend 1 g of feces in 25 mL of saline solution. Shake well. Filter the suspension through a small mesh screen. Centrifuge at 1500 revolutions per minute (rpm) for 5 minutes. Pour off the supernatant. Resuspend the sediment in 7 mL of 10% buffered formalin and incubate at room temperature for 10 minutes. Shake well. Add 3 mL of cold ether to the top of the suspension. Resuspend the sediment at the bottom in a few drops of saline, and shake well. Place the suspension on a slide with a coverslip. Examine at 100 × (low power).
Glucose Curve and Fructosamine Testing Indications • • • • •
Diabetes mellitus monitoring. Diabetes mellitus regulation assessment. Diabetes mellitus dysregulation investigation. To rule out or confirm rebound hyperglycemia. To detect and prevent hypoglycemia in diabetic cats that become noninsulin dependent while receiving insulin.
Objectives Glucose Curve • Determine time of peak insulin effect. • Determine level of peak insulin effect (blood glucose nadir). • Determine duration of insulin action.
Fructosamine • Determine average regulation for prior 1 week.
Technique • Administer insulin and feed as usual; a set insulin dose and feeding schedule should be in effect for at least 1 week prior to testing. • Begin about 12 hours after the last dose of insulin for cats on a twice daily schedule. For cats on a once daily schedule, begin about 24 hours after the last dose of insulin. • The initial blood collection should be of enough volume to perform both glucose determination and serum fructosamine. • Take a glucose reading every 2 hours until you can determine: • The time of peak insulin effect. • The blood glucose nadir.
• If the glucose rises or remains above 20 mmol/L (350 mg/dL) (insulin effectiveness). • If the nadir falls below 5.5 mmol/L (100 mg/dL). • If the nadir falls below 3.3 mmol/L (60 mg/dL), there should be concern for rebound hyperglycemia due to overdosing, although some cats receiving glargine or detemir may have low normal to mildly low blood glucose levels several hours post-insulin as a part of the initial adjustment to these types of insulin and do not require a decrease in insulin dosing. See Chapter 52 and www.uq.edu.au/ ccah/index.html?page=41544 for detailed and informative information about the use of glargine and detemir. • Though rarely necessary, a 24- to 48-hour curve can be performed if duration of insulin action is in question; an 8- to 10-hour curve is usually adequate if the cat is receiving insulin q12h.
Interpretation • Decrease the insulin dose if glucose levels fall below 3.3 mmol/L (60 mg/dL). See comments and reference in Technique. • If concurrent illness or causes of insulin antagonism have been excluded, increase the insulin dose if glucose levels remain above 20 mmol/L (350 mg/dL) on multiple samples of the glucose curve or if the serum fructosamine level indicates poor regulation. • Increase frequency of insulin administration or change type of insulin if duration of action does not provide glycemic control for period between insulin administrations. • Decrease dose of insulin if hypoglycemia followed by rebound hyperglycemia is identified (Somogyi Effect). In cats on glargine or detemir, if the hypoglycemia is mild and not associated with clinical signs, increased or ongoing monitoring without insulin adjustment is appropriate as some cats during the first few weeks of receiving these insulins will demonstrate a dawn phenomenon of moderately high preinsulin glucose levels with good response to insulin.
Notes • Do not tranquilize the cat as many tranquilizers are insulin antagonists. • In newly diagnosed nonketotic diabetics, initial regulation is performed by initiating insulin therapy at 0.25 U/kg, which is a conservative dose. • Following 5 more days of therapy (preferably as an outpatient or, if necessary, as an inpatient), blood glucose curve testing is performed. (Fructosamine testing is not performed unless a baseline for later comparison is desired.) • If the initial blood glucose reading is above 22 mmol/L (400 mg/dL), the insulin dose is increased, and the glucose curve is delayed for 5 to 7 days. This prevents the performance of several meaningless glucose curves and is especially helpful if the client’s finances are limited. • Blood glucose determinations are performed via in-house glucometer. Glucometers with optimum correlation include the AlphaTrak™ (Abbott Laboratories, Abbott Park, IL) and the OneTouch Ultra2™ (LifeScan Inc, Milpitas, CA). It should be noted that most glucometers underestimate the true blood glucose; AlphaTRAK (Abbott) does not. • Blood samples are collected via either marginal ear vein puncture technique (when small samples can be used), or via central venous catheter placement (for prolonged curves or multiple larger samples). • Blood glucose curve testing should always be interpreted with clinical signs (and if appropriate, serum fructosamine) because day-today results can be variable. • Changes in serum fructosamine concentration of less than 33 mmol/L (the fructosamine critical difference) are often due to other factors than changes in glycemic control unless a concurrent blood glucose curve indicates otherwise.
925
SECTION 7: Clinical Procedures
Iohexol Clearance: Renal Function Testing
TRH Response Test
Indications
Indication
• Polyuria or polydipsia of undetermined origin. • Investigate suspect renal insufficiency. • Detailed monitoring of renal function.
• This test is indicated when there are signs of hyperthyroidism (i.e., clinical signs or palpable thyroid lobe) but the TT4 is normal.
Objectives • Determine glomerular filtration rate (renal function).
Technique • Administer thyrotropin-releasing hormone (TRH) at a dose of 0.1 mg/kg IV. • Collect a serum sample 4 hours later for TT4 determination.
Technique • • • •
Give no food for 12 hours; water should always remain available. Record body weight. Place intravenous catheter. Administer 300 mg/kg iohexol as a rapid bolus via catheter; record administration time to the minute. • Collect 2 to 3 mL of blood in red top clot tube at 2, 3, and 4 hours; record time to the minute of each collection; separate serum and place in plastic vials and label (i.e., name and times). • Ship chilled or frozen to lab with request form that documents patient identification, weight, iohexol dose, and times of blood collection.
Interpretation • Values below reference range confirm renal dysfunction.
Notes • Check with the lab to confirm that they perform assay; the test is routinely performed at Michigan State University (phone; 517-3550281; submittal form http://www.animalhealth.msu.edu/Submittal_ Forms/AD.ADM.FORM.017.pdf).
T3 Suppression Test Indication This test is indicated when there are signs of hyperthyroidism (clinical signs, palpable thyroid lobe) but the total T4 (TT4) is normal.
Interpretation • Normal cats and cats with nonthyroidal illness will have a 60% or more rise in serum TT4. • Hyperthyroid cats will have a 50% or less rise in serum TT4. • A 50 to 60% rise is considered borderline (non-diagnostic).
Notes • Transient side effects of salivation, vomiting, tachypnea, and defecation may occur during the 4-hour testing period. • The results are considered extremely accurate. • The advantage of this test over the T3 suppression test is the short testing time and the lack of reliance on owner compliance.
Trichogram Indication • This test is to determine if hair loss is due to chewing, licking, or scratching versus hair loss due to hair falling out.
Technique • Pluck a tuft of hair within the area of alopecia. • Place the hair in a drop of mineral oil on a microscope slide. Attempt to keep the distal ends together. • Cover the mineral oil and hair with a cover slip. • Observe the distal ends of the hair under 100× magnification.
Technique • Collect a serum sample and freeze it. • Administer 25 µg of sodium liothyronine (Cytomel®) every 8 hours for seven doses. • Collect a second serum sample 2 to 4 hours after the last dose. • Submit both serum samples to the laboratory for TT4 and total T3 (TT3) testing.
Interpretation • A normal cat and a cat with nonthyroidal illness will have a post-test TT4 value that suppresses to less than 50% of the pretest TT4 value. • A hyperthyroid cat will have a post-test TT4 value that does not suppress and thus remains greater than 50% of the pretest TT4 value. • The results are considered extremely accurate. • The TT3 values are measured only to confirm owner compliance and tablet absorption. The second TT3 value should be well above baseline. • If the cost of performing this test is prohibitive, the TT3 values can be omitted because they are not involved in the interpretation. However, owner non-compliance or inadequate absorption cannot be determined.
926
Interpretation • Normal distal ends are pointed. • Broken hairs due to chewing, licking, or scratching will be blunt on the end. • The normal rounded proximal end can be confused with broken hairs so be sure you are observing the distal ends.
Zinc Sulfate Fecal Flotation Indication This test is for cats in which giardiasis is suspected. This test identifies about 77% (examination of one fecal sample) to 96% (examination of three fecal samples collected over 3–5 days) of infected cats.
Objective • To find the presence of Giardia cysts. • Nematode parasites (e.g., hookworms, roundworms, whipworms, and Physaloptera) will also be identified by this method.
Testing Procedures
Technique • • • • • •
Mix about 2 g of feces with 15 mL of a 33% zinc sulfate solution. Pour the mixture through a tea strainer or cheesecloth into a tube. Fill the tube with additional zinc sulfate. Centrifuge the tube at 1500 rpm for 5 minutes. Place a cover slip on top of the meniscus of the tube for 4 to 5 minutes. Place the cover slip on a microscope slide and examine for cysts.
Accuracy Note A recent comparison of a rapid enzyme-linked immunosorbent assay (ELISA; i.e., SNAP Giardia Test®, IDEXX Laboratories, Westbrook, ME), laboratory ELISA, and immunofluorescent microscopy showed that the
sensitivity and specificity of the SNAP test was clearly superior to zinc sulfate fecal flotation for detecting Giardia. Polymerase chain reaction (PCR) testing is also available for Giardia; it is also more sensitive and specific compared to zinc sulfate fecal floatation. The advantage of zinc sulfate fecal flotation is its ability to find other parasites.
Suggested Readings Cohen TA, Nelson RW. 2009. Evaluation of six portable blood glucose meters for measuring blood glucose concentration in dogs. J Am Vet Med Assoc. 235(3):276–280. Tilley LP, Smith FWK, eds. 2009. Blackwell’s Five-Minute Veterinary Consult, 4th ed. Ames, IA: Blackwell Publishing.
927
CHAPTER 312
Therapeutic Laser Applications Ronald J. Riegel
Mechanism of Action and Safety Therapeutic lasers accomplish three main objectives: (a) relief of pain, (b) reduction of inflammation, and (c) accelerated healing time. The science of laser therapy is based on photobiostimulation which is dependent on achieving a therapeutic dose of energy. Therapeutic dose is measured in Joules (J) delivered per cm2. The injured cells will elicit a clinical response when a dosage of 5 to 7 Joules/cm2 is received. Effective photobiostimulation depends on the correct combination of power, wavelength, and the amount of time the therapy is administered. Power is the rate of energy delivery measured in Watts. The amount of energy delivered is measured in Joules. By definition one Joule equals one Watt per second. The wavelengths produced by lasers are measured in nanometers. The biological effect on cells is related to the wavelength of light emitted by a laser. Shorter wavelengths are absorbed superficially. Longer wavelengths are less readily absorbed superficially and allow a deeper penetration of photonic energy into the tissues. Therapeutic lasers may have continuous power output, pulsed power output, or both. If the laser emits constantly, the energy delivered is equal to the power in watts multiplied by time in seconds. Pulsing and frequency are used interchangeably to describe the same concept. When lasers pulse photons are emitted for short predetermined periods of time with pauses between each emission. Photobiostimulation is a biochemical cascade of events that occurs at the cellular level. Photons penetrate to the individual target cells and stimulate both the cell membrane and structures within the cell. The mitochondria are the primary photoreceptors. Chromophores are the subcellular organelles, which absorb light. Within the mitochondrial membranes the key photoreceptor is cytochrome c. When photonic energy stimulates this photoreceptor, the reaction time for the formation of cytochrome c to become cytochrome c oxidase is increased resulting in an increase in the cellular respiratory rate. This leads to an increase in the production of adenosine triphosphate (ATP). This increase in cellular energy levels causes a biochemical cascade of events to occur resulting in numerous physiological effects within the tissues. The three main effects are: (a) local and systemic analgesia, (b) a reduction in inflammation, and (c) an acceleration of the feline patients’ own cellular healing processes. The three main photobiochemical cascades of events resulting in analgesia are: (a) increased production and release of nitric oxide, (b) increased β endorphin levels, and (c) decrease in bradykinin levels. The photobiochemical cascade of events resulting in a reduction of inflammation are: (a) increased prostaglandin synthesis, (b) normalization of calcium, sodium, and potassium concentrations over the mitochondrial membrane, (c) stimulation of vasodilation, and (d) reduction of interleukin I. Accelerated tissue repair is a result of photobiostimulation. One of the truly unique characteristics of photobiostimulation by deep penetrating photons is the ability to actually promote and enhance healing. The main physiological events are an increase in leukocytic and macrophage infiltration, and activation of fibroblasts, chondroblasts, and osteoblasts.
Therapeutic laser safety is important because therapeutic lasers used in feline practice pose two main safety concerns. There can be adverse effects on the structures of the eye and the dermis. Always wear the goggles supplied by the manufacturer, and protect the eyes of the patient with thick black felt. Minimize any dermal concerns by using good application technique and ensure that the patient is not on any photosensitive medications.
Operational Guidelines Conditions eliciting chronic pain or conditions involving pathology within anatomical structures deep in the body will require more treatments than those conditions that are superficial and or acute in nature. Laser therapy should be administered aggressively. Laser therapy has a cumulative effect; each therapy session adds to the previous one. A typical treatment regimen consists of treatment every other day for the first week, twice during the second week, and then once or twice per week thereafter until the condition heals. The World Association of Laser Therapy and the current literature have established that 5 to 7 Joules/cm2 are required to stimulate a photobiochemical response at the cellular level. The amount and color of the hair, the pigmentation of the skin, the amount of fat, the density of the tissues, and the amount of circulation and fluids present in the treatment area all result in incidental absorption of the photonic energy before it can reach the target cell. Therefore, dosage administered to target the deeper structures should be increased. For example, photobiostimulation to a 12.9 cm2 (2 in2) area superficially for pain management and accelerated healing of an abdominal incision requires a dosage of 5 J/cm2 = approximately 65 Joules. Photobiostimulation to the same area at a higher dosage for the relief of pain and inflammation involving lower urinary tract disease requires a dosage of 10 J/cm2 = approximately 129 Joules.
Contraindications There are several situations that must be avoided. They include: (a) exposure to the eye, (b) application directly over the abdomen of pregnant felines, (c) application over any lesion that is actively hemorrhaging, (d) any animal receiving photosensitive medications, (e) application over the epiphyseal growth plate in kittens, (f) application directly over the cardiac region in any feline with a cardiac condition, (g) direct application over testicular tissue, and (h) application directly over any primary or secondary neoplastic lesion.
Clinical Disorders Responsive to Photobiostimulation Oral Cavity Stomatitis, gingivitis or peridontitis, postextraction pain, eosinophilic granuloma, indolent, eosinophilic, or rodent ulcer, feline acne, and trauma are the most common conditions receiving treatment.
Nasal Cavity th
The Feline Patient, 4 Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
928
Rhinitis or sinusitis responds with higher dosages used on more congested patients.
Therapeutic Laser Applications
Ear Otitis (therapy of the ear canal from the outside), aural hematomas, and frostbite are the most common applications.
Musculoskeletal System Most conditions are responsive to photobiostimulation except those of neoplastic, metabolic, inherited, congenital, or developmental nature. These include: • Fracture repair or nonunion. • Trauma or Wounds: Stimulate well into the healthy margins of the wound and apply a higher dosage to deep wounds involving tendons and bones. • Degenerative and Inflammatory Arthritis, Degenerative Joint Disease, and Intervertebral Disc Disease: Administer multiple sessions at a dosage of 8 to 10 J/cm2 over a 3-week period. Provide therapy to any secondary anatomical areas that are compensating for the pain originating from the primary area of involvement. Apply while carefully placing the area through a passive range-of-motion exercise. • Neuromuscular Disorders: Traumatic neuropathy, acquired myositis (i.e., result of a bite wound), and peripheral diabetic neuropathies respond well. Photobiostimulation should be provided to the entire anatomical area at a dosage rate of 6 to 8 J/cm2 coupled with an aggressive treatment plan of multiple times per week for several weeks duration. • Laser Assisted Rehabilitation: Photonic therapy allows pain management, improved restoration of mobility and strength, and an accelerated rate of recovery. It is difficult to provide controlled exercise to the feline species; photobiostimulation provides some of the benefits of exercise without leaving the therapy table. Begin laser therapy when the injury is stabilized. For surgical cases apply laser therapy before and immediately after the procedure. When a restoration of mobility is the goal, apply most of the laser therapy while gently placing the limb through passive range of motion exercises. • Dermatological Conditions: Use a superficial dosage of 3 to 5 J/cm2. Responsive disorders include abscesses, cellulitis, burns, allergic dermatitis, miliary dermatitis, and ringworm. Treatment of eosinophilic granuloma complex provides a reduction in pain and inflammation, an increase in the circulation to the area which prohibits a buildup of circulating eosinophils, and an accelerated healing time for the lesions that already exist. • Feline Lower Urinary Tract Disease: Photobiostimulation provides another treatment option in the management of this disorder. Position the patient with the hind legs on the table and the upper portion of the cat held comfortably off the table. The goal is to have the bladder resting on the ventral abdominal wall. Direct the therapy dorsally at a dosage of 10 J/cm2. If diagnosed early, an aggressive protocol of laser application every 48 hours for 2 weeks resolves the disorder;
others may need a maintenance therapy program to manage the issue. • Post-Surgical: A good example is a cystotomy. The indication for the surgery (usually a urolith) has already caused inflammation to the bladder, and surgery will compound the inflammation. Administration before closure will provide an immediate reduction of inflammation, stimulation of regenerative cells, an increase in blood flow, and pain management.
The Economics of Photobiostimulation The addition of laser therapy to a practice has several advantages: (a) laser therapy provides your feline patients with a scientifically based, therapeutic option that initiates accelerated healing at the cellular level, (b) laser therapy provides your practice with a pain management tool, (c) laser therapy is a realistic option for those feline patients with nonsteroidal anti-inflammatory drugs and corticosteroid intolerances, and (d) laser therapy is a noncannibalizing practice builder and an additional income source for the practice using the support staff.
Summary Laser therapy in the feline practice is scientifically based, safe, versatile, effective, and the only modality that enables the body to heal at an accelerated rate, allowing faster recoveries and a higher quality of life for the patient.
Suggested Readings Amat A, Rigau J, Waynant RW, et al. 2005. Modification of the intrinsic fluorescence and biochemical behavior of ATP after irradiation with visible and near-infrared laser light. J Photochem Photobiol. 81: 26–32. Anders JJ, Geuna S, Rochkind S. 2004. Phototherapy promotes regeneration and functional recovery of injured peripheral nerve. Neurol Res. 26:233–239. Baxter GD. 1994. Therapeutic Lasers Theory and Practice. Philadelphia: Churchill Livingstone. Bromiley MW. 1991. Physiotherapy in Veterinary Medicine. London: Blackwell Scientific. Byrnes KR, Barna L, Chenault VM, et al. 2004. Photobiomodulation improves cutaneous wound healing in an animal model of type II diabetes. Photomed Laser Surg. 22:281–290. Chow RT, Barnsley L. 2005. Systemic review of the literature of low-level laser therapy in the management of neck pain. Lasers Surg Med. 37:46–52. Grossweiner LI. 2005. The Science of Phototherapy: An Introduction. Heidelberg: Springer Verlag.
929
SECTION
8 Appendices
CHAPTER 313
Age Approximation Karen M. Lovelace
Overview In addition to constituting a key component of a patient’s signalment, age is a necessary part of the history for guiding many diagnostic and therapeutic recommendations and prognoses. Knowledge of a patient’s age has many implications. Age may help differentiate normal anatomy from an abnormal lesion. It is considered when administering medication and is used to adjust drug dosages and anesthetic protocols. Age also has a strong bearing on the formulation of a list of differential diagnoses. Unfortunately, the feline patient is frequently presented without a known date of birth, and the age of the cat must be approximated. However, there is little information available to help guide the feline practitioner in this endeavor. Although there is some objective data available for determining various stages in a cat’s growth, such as growth plate closure times, dental eruption times, and behavioral development, a lot information is strictly empirical. Studies are still needed to document more precisely when various changes occur in a cat’s development, but until then, the information in this chapter is presented to help take some of the guesswork out of age approximation.
Objective Data Dental Eruption Times Dental eruption times may be useful for differentiating adult cats from kittens and for approximating age during kittenhood. See Table 313-1 and Figure 313-1.
Figure 313-1 Eruption of the first pair of upper adult incisors occurs at 3 1/2 to 4 months of age. This criterion can be used to determine the time for the final vaccines in a kitten series.
Radiographic Changes Growth plate closure times may be used as an ancillary tool to approximate or confirm the age of cats up to 2 years of age. See Tables 313-2 and 313-3.
TABLE 313-2: Approximate Age at Growth Plate Closure Observed on Radiographs TABLE 313-1: Feline Dental Eruption Times Deciduous (weeks) Incisor 1 Incisor 2 Incisor 3 Canines Premolar 2 Premolar 3 Premolar 4 Molar
2–3 3–4 3–4 3–4 8 4–5 4–6 N/A
Permanent (months) 3.5–4 3.5–4 4–4.5 4–5 4.5–5 5–6 5–6 4–5
Adapted from Dental Development. 1998. In The Merck Veterinary Manual, 8th ed., pp. 131–132. Philadelphia: Merck & Co., Inc.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Scapula
Supraglenoid tubercle
3.5–4 months
Humerus
Proximal epiphysis
18–24 months
Distal epiphysis
4 months
Condyles
3.5 months
Medial epicondyle
4 months
Lateral epicondyle
3.5 months
Radius
Proximal epiphysis Distal epiphysis
5–7 months 14–22 months
Ulna
Olecranon tubercle Distal epiphysis
0–13 months 14–25 months
Carpus Metacarpals II–V Phalanges I and II
Accessory carpal epiphysis Distal epiphysis Proximal epiphysis
4 months 7–10 months 4–5.5 months
Adapted from Dyce KM, Sack WO, Wensing CG. 2002. Textbook of Veterinary Anatomy, 3rd ed., pp. 455. Philadelphia: Saunders.
933
SECTION 8: Appendixes
TABLE 313-3: Feline Epiphyseal Plate Closure in Days Bone
Segment
Days
Scapula Humerus
Tuber and coronoid process Proximal epiphysis Medial and lateral condyles Medial epicondyle Proximal Distal Proximal (tuberosity of olecranon) Distal epiphysis Accessory carpal bone epiphysis Distal epiphysis II-V Proximal: Proximal epiphysis II-V Middle: Proximal epiphysis
112 547–730 98 112–126 196 406–616 266–364 406–700 112–126 203–280 126–154 112–140 140 210–280 196–252 238–308 378–532 350–532 350–532 280–364 378–504 280–392 210–364 224–308 126–168 126–154 70–112 70–112 154 112–140
Radius Ulna Carpus Metacarpus Phalanges Sesamoids Femur
Tibia
Fibula Tarsus Metatarsal Phalanx Sesamoid
Femoral head Greater trochanter Lesser trochanter Distal epiphysis Proximal epiphysis Tibial tuberosity Distal epiphysis Proximal epiphysis Distal epiphysis Fibular tarsal Distal epiphysis II–V Proximal II–V Middle II–V Metatarsophalangeal Lateral sesamoid in gastrocnemius muscle Medial sesamoid in gastrocnemius muscle Popliteal sesamoid in muscle
Figure 313-2 Diffuse iris atrophy is present in a 13-year-old cat. This process often starts about 12 years of age and become more prominent with advanced age.
Adapted from CD Newton, DMNunamaker. 1985. Textbook of Small Animal Orthopedics, pp. 1110–1111. Philadelphia: J.B. Lippincott.
Behavioral Development Predictable changes in behavior and their corresponding age ranges are helpful for predicting and confirming age, especially in felines under 12 months of age. See Table 313-4.
Body Weight During the first 6 months of life, body weight can be a useful predictor of age in healthy kittens. When compared with other factors listed in this chapter, age may be approximated within weeks. See Table 313-5.
Ophthalmic Changes • Senile Iris Atrophy: Senile iris atrophy appears as irregular papillary margins and spaces in the iris, which may give it a thready or punched out appearance. Senile iris atrophy is noticeable as early as age 12 years. See Figure 313-2. • Nuclear Sclerosis: Nuclear sclerosis (also called lenticular sclerosis) is a normal consequence of aging. As the lens ages, new lens cells grow at the periphery, packing the older cells towards the center. This increased nuclear density is seen clinically as a grey-blue haziness, which is often mistaken for a cataract and is sometimes incorrectly called a senile cataract. Nuclear sclerosis is first noticeable around age 12 years.
934
Figure 313-3 Pachyonychia (thickening of the claws) is present in a 20-year-old cat. Nails that grow into the pad often result.
Dermatologic Changes • Pachyonychia: Pachyonychia, or thickening of the claws, occurs in cats 10 years of age and older and may be marked in animals over age 16. It has also been associated with hyperthyroidism, a disease commonly found in geriatric cats. See Figure 313-3. • Achromotrichia: Achromotrichia, or leukotrichia, refers to an increase in the number of white hairs on the face and body. This is a normal aging change that is especially noticeable in black cats and usually begins around 12 to 14 years of age. Figure 313-4.
Subjective Data Life stage of a cat can be broadly grouped into kitten (0–1 years), adult (1–6 years), mature/middle aged (7–10 years), senior (11–14 years), and
Age Approximation
TABLE 313-4: Development Periods in Cats Social
Oral
Elimination
Miscellaneous
Birth–2 weeks
Minimal interaction
Drinks only milk
Stimulated by the mother
3–8 weeks
Social play, object play, running, complex learning, climbing, scratching, and predation begins Conflict over status may emerge. Social play peaks Likely to be subordinate to older cats but may challenge them. Sexual maturity if not already neutered Socially mature at age 2–3. Social play declines
Begins to eat solid foods. Milk consumption decreases
Develops fecal and bladder control. Begins to use the litter box
Eats solid food No change
Continues to use the litter box Spraying may occur, but is less likely if the cat is spayed or neutered
Walking begins by day 14, and the eyes open Eye color changes, grooming begins, and the cat can regulate its own body temperature Intense exploration of the environment Outdoor cats may wander farther and for longer periods
Metabolism slows, and weight gain may occur
Urine odor becomes strong in intact males
Decreased physical activity may lead to decreased social interaction
Changes in appetite may occur
Elimination problems may develop due to mental or physical aging (e.g., senility and arthritis)
9–16 weeks 17 weeks–1 year
1–6 years
7 and older
Development of aggression (i.e., intercat, fear, territorial, redirected, or status related) may occur in association with social maturity Altered sleep-wake cycles, cognitive dysfunction, pain, and sensory decline develop and may lead to increased vocalization, phobias, fears, aggression, or wandering
Adapted from Overall KL, Rodan I. 2004. In Feline Behavior Guidelines from the American Association of Feline Practitioners, pp. 10–28.
TABLE 313-5: Approximate Body Weight Gain (lbs) in Cats 0–6 months Age
0–3 weeks
1 months
1.5 months
2 months
2.5 months
3 months
Weight (lbs) Age (months) Weight (lbs)
<1.0 3.5 3.5
1.0 4 4.0
1.5 4.5 4.5
2.0 5 5.0
2.5 5.5 5.5
3.0 6 6.0
Figure 313-4
Marked achromotrichia (leukotrichia) is shown in an 18-year-old cat.
geriatric (15+ years). As more is learned about the unique medical and behavioral needs of the feline species, cats are living longer, higher quality lives. More emphasis has, therefore, been placed on recognizing the special needs of cats based on life stage, especially the aging cat. Cats age rapidly during their first year, up to 18 cat years in human terms, but then maturation slows to approximately 3- to 5-cat years for every actual year of a cat’s life thereafter. For this reason, mature, senior, and geriatric cats should be assessed on a more frequent schedule than their younger counterparts. Whereas an annual examination may be acceptable for young, healthy cats, a general guideline for older cats is every 6 months for physical examination and biochemical evaluation. Examination of a young and otherwise healthy cat may focus on nutrition/obesity, dental care, or behavior, but the examination of an older cat will likely focus more on weight changes, dental disease, behavior-related to cognitive or physical changes, osteoarthritis pain, grooming changes, increased incidence of hypertension, renal disease, neoplasia, endocrinopathy, pain, and quality of life assessment. General knowledge of approximate age and life stage will help to guide veterinarians in making appropriate wellness recommendations to clients of feline patients.
935
SECTION 8: Appendixes
Suggested Readings Dyce KM, Sack WO, Wensing CG. 2002. The forelimb of the carnivores. In KM Dyce, WO Sack, CG Wensing, Textbook of Veterinary Anatomy, 3rd ed., pp. 455. Philadelphia: WB Saunders. Muylle, S. 2005. Dental development. In The Merck Veterinary Manual, 9th ed., pp. 137–140. Whitehouse Station, NJ: Merck & Co., Inc.
936
Newton, CD. 1985. Canine and feline epiphyseal plate closure and appearance of ossification centers. In CD Newton, DM Nunamaker, Textbook of Small Animal Orthopedics, pp. 1110–1111. Philadelphia: JB Lippincott. Pittari J, Rodan I, Beekman G, et al. 2008. American Association of Feline Practitioners Senior Care Guidelines, http://catvets.com/uploads/ PDF/2008SrCareGuidelinesFinal.pdf.
CHAPTER 314
Anatomical Differences in Cats and Dogs Clay Anderson and James E. Smallwood
Overview For many years the cat has been considered a “small dog” in many ways. As feline medicine has evolved over the past 30 years, we are finding multiple examples of the fallacy of that assumption. This chapter contrasts some of the clinically significant anatomical differences in the two species.1
Clinically Significant Anatomical Differences • In general, the long bones of the limbs (both thoracic and pelvic) of the cat are straighter than those of the dog. Also, the bodies of the lumbar vertebrae are relatively longer in the cat than in the dog. Clinical significance: This can be useful in identifying cat versus dog on an unlabeled radiograph. • The clavicle is much better developed and is palpable in the live cat. Clinical significance: The clavicle of the cat must be recognized and appreciated in radiographs of the feline shoulder region. • The feline humerus possesses a supracondylar foramen, through which pass the brachial artery and median nerve. Clinical significance: The artery and nerve may be more vulnerable to injury in distal humeral fractures in the cat. Surgical intervention for repair must take into account the passage of these important structures through the foramen. • Although absent in the dog, cats have a carpal organ, a specialized sensory (tactile) elevation in the skin on the caudal aspect of the forearm. This firm cutaneous nodule is adorned with several stiff vibrissae (whiskers), which are connected to sensitive pressure (tactile) receptors in the skin nodule. Clinical significance: This skin lump is not a tumor or other skin lesion. Clippers can nick it when clipping the caudal aspect of antebrachium. See Chapter 328. • The brachioradialis muscle is much better developed in the cat. Clinical significance: The subcutaneous ridge created by the brachioradialis muscle can be confused with the cephalic vein, which lies medial to the muscle. Insertion of a needle into it is painful. • The cat does not have a nuchal ligament. • The tunica muscularis of the esophagus is composed entirely of skeletal muscle throughout its length in the dog. In the cat there is, however, a transition from skeletal to smooth muscle as one moves caudally from pharynx to cardia. Smooth muscle is the predominant type found in the caudal one-third of the esophagus, which is roughly from the level of the tracheal bifurcation to the stomach. This pattern is apparent on a barium x-ray of the esophagus. See Figure 314-1. • The heart of the cat is located slightly more caudal in the thorax than that of the dog. In the cat its projection onto the thoracic wall is generally considered to be from the fourth intercostal space to the level of the seventh rib. Clinical significance: Cardiac puncture, when necessary, can be performed on the right side of the thoracic cavity at the level of the costochondral junction in the fifth intercostal space of the cat. • Disregarding the “give-me’s” of calico and tortoise-shelled coat colors, which require two X chromosomes to accomplish, sexing of newborn kittens can be challenging for the novice. We recommend
Figure 314-1 A barium swallow shows the cranial esophageal skeletal muscle and the caudal esophageal smooth muscle. Image courtesy Drs. Merrilee Holland and Judith Hudson.
•
•
• • •
•
•
• •
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
the punctuation technique as follows: (a) hold the kitten ventral side up and look directly at the perineum; (b) note the punctuation. If you see a :, you have a male; if you see an ! you have a female; and if you happen to see a ?, it’s too soon to tell. As is obvious, even to the more casual observer, the scrotum of the cat is located in a perineal position rather than inguinal position, as it is in the dog. Clinical significance: Always check under the tail before you attempt to “spay” a supposedly female cat, especially the longhaired variety. More than one “Charlotte,” on closer examination, has turned out to be a “Charles.” This can be really embarrassing. The urinary bladder of the cat has a long, almost tubular neck so that the body and apex of the bladder are located in the caudoventral part of the abdominal cavity, even when the urinary bladder has been emptied. The cats does not have a “pelvic bladder.” In the male cat, just like in other domestic mammals, the body of the prostate is located at the beginning of the pelvic urethra. There is no such thing as a “preprostatic” urethra, as is sometimes alleged in the cat. The prostate of the male cat does not completely surround the pelvic urethra and does not enlarge so much with age as it does in the dog. Clinical significance: Even in intact male cats, prostatitis is rare. The bulbourethral glands of the tomcat are well developed in the sexually mature individual. Clinical significance of bulbourethral glands: They are an important landmark when performing a perineal urethrostomy; however, the glands are usually atrophied in the neutered cat. Except at the glans, the free part of the sexually mature feline penis is covered with numerous highly keratinized, proximally directed penile spines. Like the accessory genital glands, these penile spines are testosterone dependent and will atrophy following castration. This characteristic can be used to determine if a cat is neutered versus unilaterally neutered versus a cryptorchid. See Figure 314-2. The cat does have a small os penis. Clinical significance: Urethroliths do not lodge in bone but rather in the urethral mucosa. The vulva of the cat is small and inconspicuous in the nonpreparturient state. Unlike that of the bitch, the vulva of the queen is covered with hair, its ventral commissure is rounded, and its dorsal commissure is pointed, thus, the (!) configuration when viewed upside down.
937
SECTION 8: Appendixes
(A)
Figure 314-3 The tympanic bulla is divided into a smaller dorsolateral compartment (black arrow) and a larger ventromedial compartment (red arrow) by a prominent septum bullae. Image courtesy Dr. Gary D. Norsworthy.
(B) Figure 314-2 A, Prominent spines are present on the penis of the intact male cat. One testicle produces enough testosterone to maintain their presence. Thus, a bilaterally cryptorchid cat or a cat with one testicle removed and the other present, even in the abdomen, will have spines on the penis. B, Male cats with both testicles removed do not have spines on the penis. Images courtesy Dr. Gary D. Norsworthy. • In agreement with the relatively smaller penis of the male cat versus the dog, the clitoris of the queen is poorly developed. The fossa clitoridis is represented by a small depression just inside the ventral commissure of the vulva. As in the dog, the fossa clitoridis should not be mistaken for the external urethral orifice, which is located at the vaginovestibular junction. Clinical significance: Trying to pass a urinary catheter in a queen by inserting the catheter into the fossa clitoridis, rather than the more deeply located external urethral orifice, will not yield the desired result.
938
• The saphenous vein of the dog is most superficial laterally. The same vein of the cat is most superficial medially and relatively larger than that of the dog. Clinical significance: Venipuncture of the saphenous vein of the cat is performed medially. • In the cat, the tympanic bulla is divided into a smaller dorsolateral compartment and a larger ventromedial compartment by a prominent septum bullae. The two compartments communicate over the septum bullae. Clinical significance: Failure of the surgeon to enter and examine the dorsolateral compartment may cause recurrence of bulla disease (i.e., nasopharyngeal polyp). See Figures 248-7 and 314-3. • The permanent dental formula for the cat is: 2(I3/3, C1/1,P3/2,M1/1) = 30. • The deciduous dental formula for the cat is: 2(I3/3,C1/1,P3/2) = 26. • The only tooth of the cat with three roots is the superior P4 (109 and 209). • The frontal sinus of the cat is not divided into lateral, medial, and rostral parts. • The maxillary recess is extremely small (almost nonexistent) in the cat; however, the cat has a sphenoid sinus, ventral to the cranial cavity, which is absent in the dog. • The constricted pupil of the cat is not circular, but forms a narrow, dorsoventral slit. 1. Gary Norsworthy wishes to thank Dr. James E. Smallwood, one of his anatomy teachers in veterinary school, for allowing his original document, Cats Are Not Small Dogs, to be edited for The Feline Patient, 4th ed.
CHAPTER 315
Body Surface Area Conversion Gary D. Norsworthy
Feline Body Surface Area Conversion Pounds
Kilograms
Meters2
1.1 2.2 4.4 6.6 8.8 11.0 13.2 15.4 17.6 19.8 22.0 24.2
0.5 1.0 2.0 3.0 4.0 5.0 6.0 7.0 8.0 9.0 10.0 11.0
0.063 0.100 0.159 0.208 0.252 0.292 0.330 0.366 0.400 0.433 0.464 0.494
Note: These values are slightly different from those for dogs. They are based on the following formula: BSA in m2 = (10 × W2/3)/104. BSA, body surface area; m2, equal square meters; W, weight (grams).
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
939
CHAPTER 316
Breed-Specific Diseases James K. Olson
Overview The elucidations of congenital diseases in the domestic cat are incomplete and ongoing. Specific studies vary from continent to continent, country to country, state to state, and blood line to blood line. Financial restraints, lack of uniform reporting methods, variations in genetic blood lines around the world, and a limited number of professional researchers pursuing this study have hampered our understanding of feline genetics and development. Congenital defects are usually present at birth and involve abnormal structure, function, and metabolism. The prevalence of congenital disease morbidity and mortality reporting is a mixture of guesstimate, medical research, and statistical analysis. It appears from the few studies that have been done that purebred cats have more congenital disease than the domestic non-purebred cats. Mixing terms such as genetic, congenital, and predisposition are common in reporting. The domestic short hair and domestic longhair cats generally tend to be the healthiest, and only when they are cross-bred to purebreds carrying specific genetic disease are these traits spread to a local population. Underreporting of congenital disease is common because fetal death and miscarriage are usually not reported. In addition, kittens that die young to breeders and family litters are rarely researched and reported. New efforts with specific purebreds, research colonies, and specific diseases are starting to give the veterinary community hard data regarding underreported disease trends and the prevalence of congenital disease in the cat. There are now the beginnings of a worldwide effort to resolve longstanding feline disease issues. Several genetic projects are underway in the United States. See Table 316-1. The following list of breeds (genetic pools) and disease entities are incomplete because our understanding of congenital disease is incomplete. As knowledge grows some diseases will disappear and many more will be added. In addition, better understanding of blood types and their distribution will occur as numbers of “typed” cats grows. Following the breed names are the country and approximate date of origin of the breed. This material is summarized in Table 316-2.
Breed-Specific Diseases • Abyssinian (Asia; around 1860): Congenital hypothyroidism, corneal sequestrum, familial amyloidosis, feline hyperesthesia syndrome, feline infectious peritonitis (predisposition), gingivitis, lysosomal storage disease, myasthenia gravis, patellar luxation, progressive retinal atrophy (late onset), progressive rod/cone degeneration and rod/cone dysplasia (early onset), psychogenic alopecia, pyruvate kinase deficiency, reactive systemic amyloidosis (renal, liver, and gastrointestinal), retinal dystrophy, thromboembolism; Blood Group: United States 86% Type A and 14% Type B. • American Shorthair (United States; around 1904): Hypertrophic cardiomyopathy; polycystic kidney disease; Blood Group: United States 100% Type A. • Balinese (United States; around 1940): Feline acromelanism; Blood Group: United States, approximately 100% Type A. • Bengal (United States; around 1963): Cleft palate, entropion, feline infectious peritonitis (predisposition), flat chest defect (swimmer), pectus excavatum, psychogenic alopecia, retinal atrophy (mid onset),
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
940
TABLE 316-1: Research Sites for Feline Genetic Diseases 1. University of California at Davis, Veterinary Genetics Laboratory (VGL) Primary Investigator/Coordinator: Leslie Lyons, PhD Current Study and Testing: DNA typing, parent verification; Feline blood typing, investigation AB blood groups; Coat color investigation, Agouti, chocolate, cinnamon, and color point dilute; Erythrocyte pyruvate kinas deficiency (PK deficiency); Hypertrophic cardiomyopathy (Maine Coon Cat); GM2 Gangliosidosis, Burmese only, Domestic Longhairs have all four known mutations; Polycystic kidney disease (PKD1); Progressive Retinal Atrophy (PRA), Abyssinian, Somali, and Ocicat; and Karyotyping. 2. Veterinary Genetics Laboratory, One Shields Avenue, Davis, CA 95616-8744, (530) 752-2211 Office, (530) 752-3556 Fax, http:www.vgl.ucdavis.edu/service/cat/index.html. 3. Washington State University, Veterinary Cardiac Genetics Lab Primary Investigator/Coordinator: Kate Meurs, DVM Current Study and Testing: Hypertrophic Cardiomyopathy, Ragdoll, Norwegian Forest Cat, American Shorthair, and Sphinx. Veterinary Cardiac Genetics Lab, Washington State University, College of Veterinary Medicine, PO Box 605, Pullman, WA 99163, (509) 335-6038 Office, e-mail:
[email protected] 4. University of Pennsylvania, PennGen/Section of Medical Genetics Primary Investigator/Coordinator: Urs Giger, DVM Current Study and Testing: Cystinuria; Erythrocyte osmotic fragility test (OF); Erythropoietin concentration; Feline blood typing; Glycogenosis (GSD) Type IV, Norwegian Forest Cat; Karyotyping; Mannosidosis, Persian, domestic shorthair; Metabolic screening, all breeds; Mucopolysaccharidosis VI, Siamese, domestic shorthair; Mucopolysaccharidosis VII, domestic shorthair; Special erythrocyte studies, all breeds; Platelet aggregation studies, all breeds; Polycystic kidney disease (PKD), Persian, all breeds; Pyruvate kinase (PK) deficiency, Abyssinian, Somali, domestic shorthair; Special coagulation studies, all breeds; Special leukocyte studies for immunodeficiencies, all breeds. University of Pennsylvania, School of Veterinary Medicine, Dr. Urs Giger, PennGen, 3900 Delancey Street—Rm 4013, Philadelphia, PA 19104, (215) 898-8894 or (888) PENNGEN, e-mail:
[email protected] 5. DNA Diagnostics and Texas A&M University Primary Investigator/Coordinator: Gus Cothram, PhD & Melba Ketchum, DVM—Director Current Studies and Testing: Albinism, B Blood group; Black coloration, Burmese (gene associated color shading, Chocolate brown, Cinnamon red, Dilute coloration); Hair length; Hypertrophic cardiomyopathy (HCM), Maine Coon Cat and Ragdoll; Identity fingerprint; Mucopolysaccharidosis MPSM; Mucopolysaccharidosis MPSI; Paternity identity; Polycystic kidney disease (PKD); Sex markers; Siamese points. DNA Diagnostics, Inc., PO Box 455, Timpson, Tx 75975, (936) 254-2228, http://www.CatGENES.org or
[email protected].
syndactyly, umbilical hernia; Blood Groups: United States 98% Type A, Type B/AB 1 to 2%. • Birman (Asia; around 1919): Cleft palate, congenital cataract, congenital hypotrichosis, congenital portosystemic shunt, corneal sequestration, distal axonopathy, encephalomyelopathy, feline infec-
Breed-Specific Diseases
TABLE 316-2: Testing and Screening for Feline Diseases Clinical Disease/Syndrome
Predisposition
Test/Screen
Cataracts Eye Diseases (Multiple Diseases) Ganliosidosis (GM1/GM2) Gene Testing, Chromosomal Glycogenosis (GSD) Hip Dysplasia Hypertrophic Cardiomyopathy (HCM) Isoerythrolysis, Neonatal Mannosidosis Mucopolysaccharidosis (MPS) VI Mucopolysaccharidosis (MPS) VII Mucopolysaccharidosis (MPS) Patellar Luxation Phenotypic Diseases Polycystic Kidney Disease (PKD) Progressive Retinal Atrophy (PRA) Pyruvate Kinase (PK) Deficiency Spinal Muscular Atrophy Sphingomyelinosis Transfusion Incompatibility
Himalayans All Breeds, Persian, Siamese Korat, Siamese All breeds Norwegian Forest Cat Maine Coon, Ragdoll, DSH Maine Coon, Ragdoll, all breeds Cross-breeding blood types Persian, Domestic shorthair Siamese, Domestic shorthair Domestic shorthair All breeds All breeds All breeds Persian and related breeds, all breeds All breeds, Persian, Bengal, Somali Abyssinian, Somali, Ocicat Maine Coon Any breed Any breed (A, B, AB)
Eye examination Eye examination DNA testing Karyotyping DNA testing Radiographs DNA testing, NT-proBNP, ultrasound Prebreeding blood typing DNA testing DNA testing DNA testing DNA testing Radiographs Physical examination, lab testing, imaging DNA testing, ultrasound Eye examination DNA testing DNA testing Histochemistry Blood typing
•
•
• •
•
•
tious peritonitis (predisposition), gastroschisis, hemophilia B (factor IX deficiency), neutrophil granulation anomaly, ocular dermoids, renal insufficiency, renal calculi, spongiform degeneration, syndactyly, tail-tip necrosis, thymic aplasia, tremors (“shaking kittens”), umbilical hernia; Blood Groups: United States 84% Type A and 16% Type B, AB rare. British Shorthair (Great Britain; around late 1800s): Hemophilia B (factor IX deficiency), progressive retinal atrophy; Blood Groups: United States 60% Type A and 40% Type B. Burmese (Myanmar [Burma]; Around 16th century/early 1900s): agenesis of nares, congenital deafness, congenital hypotrichosis, congenital vestibular disease, corneal sequestrum, cutaneous asthenia (Ehler-Danlos syndrome),diabetes mellitus (predisposition), endocardial fibroelastosis, feline leukocyte antigen DRB restricted polymorphism, feline acromelanism, flat chest defect (“swimmers”), glaucoma (primary narrow angle glaucoma), hyperesthesia syndrome, hyperoxaluria, hypokalemia myopathy, keratoconjunctivitis sicca, lethal midfacial malformation, meningoencephalocele, ocular dermoids, pectus excavatum, persistent atrial standstill, predisposed to urolithiasis, prolapse of cartilage of third eyelid, urolithiasis, primary endocardial fibroelastosis, psychogenic alopecia, feline orofacial pain syndrome Blood Groups: United States 100% Type A. Chartreux (France; around 14th century): Hip dysplasia, patellar luxation; Blood Groups: United States 100% Type A Cornish Rex (Great Britain; around 1950): Curly coat (“rexing”), dystocia, myopathy, hypothyroidism, hypotrichosis, Malassezia dermatitis, patellar luxation, umbilical hernia, vitamin K-dependent coagulopathy; Blood Groups: United States 66% Type A and 34% Type B, AB rare. Devon Rex (Great Britain; around 1960): Cleft palate, curly coat (“rexing”), dystocia, flat chest defect (“swimmer”), hypotrichosis, Malassezia dermatitis, myopathy, patellar luxation, umbilical hernia, vitamin K dependent multifactor coagulopathy; Blood Groups: United States 59% Type A and 41% Type B, AB rare. Domestic Longhair (Eurasia; in the last hundred years): Basal cell tumor, congenital portosystemic shunt, hypertrophic cardiomyopathy, cutaneous asthenia (Ehler-Danlos syndrome), lysosomal storage disease, polycystic kidney disease; Blood Groups: Blood Groups: United States most 95 to 99% Type A, 1 to 5% B, AB rare.
• Domestic Short Hair (Africa/Eurasia; in the last few thousand years): Coloboma, congenital cataracts, congenital hypothyroidism, congenital portosystemic shunt, corneal sequestrum, deafness (white cats with blue eyes), diabetes mellitus (predisposition), cutaneous asthenia (Ehler-Danlos syndrome), gingivitis/periodontitis (juvenile onset), Hageman (coagulation factor XII) deficiency, hemophilia A, hemophilia B (factor IX deficiency), hypertrophic cardiomyopathy, inguinal hernias, lentigo simplex, lysosomal storage diseases: globoid cell leukodystrophy, mucopolysaccharidosis I, mucopolysaccharidosis VI, GM1 and GM2 gangliosidosis; sphingomyelinosis, alpha mannosidosis, methemoglobin reductase deficiency, myasthenia gravis, neuroaxonal dystrophy, ocular dermoids, Pelger-Huet anomaly, persistent atrial standstill, predisposed to calcium oxalate urolithiasis/ acute renal failure, porphyria, progressive retinal atrophy, psychogenic alopecia, pyruvate kinase deficiency, staphyloma, sebaceous gland tumors, solar dermatitis, upper eyelid agenesis, ventricular septal defect; Blood Groups: United States most (95–99% Type A) unless cross-bred, 1 to 5% Type B, rare AB. • Egyptian Mau (Egypt; around 1953 but maybe related to the prototype domestic cat for thousands of years): Spongiform degeneration; umbilical hernia, Blood Group: United States 100% Type A. • Havana Brown (Great Britain; around 19th century): flat chest defect (“swimmer”), predisposed to blastomycosis; Blood Groups: United States 100% Type A. • Himalayan or Persian (United States around 1930): Basal cell tumor, congenital cataracts, congenital portosystemic shunt, corneal sequestrum, dermatophytosis (predisposition), cutaneous asthenia (EhlerDanlos syndrome), feline acromelanism, feline infectious peritonitis (predisposition), flat chest defect (“swimmer”), hyperesthesia syndrome, idiopathic facial dermatitis, lacrimal punctual aplasia, multiple epitrichial cysts, polycystic kidney disease, predisposed to calcium oxalate urolithiasis, psychogenic alopecia, systemic lupus erythematosis, umbilical hernia; Blood Group: United States 93% Type A and 7% Type B, AB rare. • Korat (Thailand; around 14th century): GM1 (neurological/ocular) and GM2 gangliosidosis; Blood Group: United States >99% Type A. • Maine Coon (United States; around 1860s): Gingivitis/periodontitis juvenile onset, hip dysplasia, familial hypertrophic cardiomyopathy, GM2 and GM3 gangliosidosis, intertrigo, laminin alpha 2 deficiency/
941
SECTION 8: Appendixes
•
•
•
•
• •
•
•
•
•
associated muscular dystrophy (myopathy), patellar luxation, pectus excavatum, polycystic kidney disease (PKD); Blood Groups: United States 95% Type A, 5% Type B, AB rare. Manx (Isle of Man; 1730): Atresia ani, corneal opacity/dystrophy, fecal incontinence, gastroschisis, megacolon/constipation, rectal prolapse, sacrocaudal dysgenesis (urinary incontinence), spina bifida/ spinal dysraphism; Blood Groups: United States 95% Type A, 5% Type B, AB rare, variable depending on outcrosses. Munchkin (United States; around 1953): Cleft palate, gastroschisis, lordosis, pectus excavatum, flat chested “swimmer” kittens, umbilical hernia; Blood Groups: United States Variable depending on which breed the mutation is seen in; mostly Type A. Norwegian Forest Cat (Scandinavia/Norway; around 13th century/1930): Cleft palate, flat chest defect (“swimmer”), type IV glycogen storage disease; Blood Group: United States 100% Type A. Ocicat (United States around 1964): Everted xiphoid process, flat chest defect (“swimmer”), pectus excavatum; Blood Group: United States 100% Type A. Oriental (Thailand/Great Britain; around 19th century): Amyloidosis, psychogenic alopecia; Blood Group: United States 100% Type A. Persian (Persia/Great Britain; around 1530s): Brachycephalic syndrome (i.e., stenotic nares, elongated soft palate, “dirty face syndrome,” and malocclusion), Chediak-Higashi syndrome (blue smoke Persians), chronic degenerative keratitis, coloboma, congenital ankyloblepharon, congenital cataracts, congenital heart defects (e.g., patent ductus arteriosis, aortic stenosis, atrioventricular valve dysplasia, pulmonary stenosis, congenital portosystemic shunts, and congenital epiphora), megacolon/constipation, corneal sequestrum, cryptorchidism, cutaneous basal cell tumors, cutaneous mast cell tumors, dermatophytosis, dystocia, entropion, epitrichial cysts (eyelids), esophageal hypomotility, feline endocrine alopecia, feline hyperesthesia syndrome, feline osteoclastic resorption lesions (predisposition), gangliosidosis, gastrointestinal adenocarcinomas, gingivitis (hyperplastic early onset), glaucoma, hip dysplasia, hydrocephalus, hyperoxaluria, hypertrophic cardiomyopathy, hypotrichosis, idiopathic facial dermatitis/pyoderma, lacrimal punctual aplasia, lysosomal storage disease (mannosidosis), Malassezia (periocular crusting), mammary tumors, mucopolysaccharidosis, nystagmus, patellar luxation, pectus excavatum, peripheral pseudocysts, peritoneopericardial diaphragmatic hernia, polycystic kidney disease, polycystic liver disease, primary endocardial fibroelastosis, primary glaucoma, prognathism, progressive retinal atrophy, pyloric stenosis, sebaceous gland tumors, seborrhea (primary), strabismus, sphingomyelinosis, systemic lupus erythematosus, upper eyelid agenesis; Blood Groups: United States 76% Type A and 24% Type B, AB rare. Ragdoll (United States; around 1960): cleft palate, eyelid coloboma, feline infectious peritonitis (predisposition), hypertrophic cardiomyopathy, thromboembolism; Blood Groups: United States 92% Type A, 8% Type B/AB. Rex or Selkirk (United States; around 1987): Curling coat (“rexing”), feline infectious peritonitis (predisposition), hypotrichosis; Blood Groups: United States 50-70% Type A, 30-50% Type B, AB rare. Scottish Fold (Scotland; around 1961): Arthropathy, osteodystrophy, degenerative joint disease, cartilaginous ear defects, polycystic kidney disease, prognathism, severe vertebral abnormalities; Blood Groups: United States 85% Type A and 15% Type B, rare AB. Siamese (Thailand; first around 14th century, modern 1960): Aguirre syndrome, asthma, ceroid lipofuscinosis, Chediak-Higashi syndrome, cleft palate, congenital hypotrichosis, dilated cardiomyopa-
942
thy, dystocia, endocardial fibroelastosis, familial hyperlipidemia, feline acromelanism, feline pinnal alopecia, food hypersensitivity, gingivitis/periodontitis (juvenile onset), GM1 and GM2 gangliosidosis, hemivertebra causing scoliosis, hydrocephalus, kyphosis or lordosis, kinked tail, hemophilia B (factor IX deficiency), hypotrichosis, mast cell tumors, mucopolysaccharidosis I, mucopolysaccharidosis VI, nystagmus, patent ductus arteriosis, periocular leukotrichia, peritoneopericardial diaphragmatic hernia, persistent atrial standstill, porphyria, psychogenic alopecia, progressive retinal atrophy (PRA), pyloric stenosis, sphingomyelinosis, systemic lupus erythematosus, tail sucking, vitiligo; Blood Group: United States 100% Type A. • Somali (United States/Canada; around 1960): Progressive retinal atrophy, pyruvate kinase deficiency, gingivitis/periodontitis, umbilical hernia; Blood Groups: United States 80 to 90% Type A, 10 to 20% Type B/AB. • Sphinx (Canada; 1966): Alopecia universalis, hypotrichosis, pectus excavatum, seborrhea, spasticity; Blood Groups: United States 80 to 90% Type A, 10 to 20% Type B, AB rare. • Tonkinese (United States /Canada; around 1930s): Cleft palate, predisposition to renal calculi; Blood Group: United States 100% Type A.
Suggested Readings Bell J. 2005. Genetic Counseling and Breeding Management of Hereditary Disorders. Proceedings: Tuffs Canine and Feline Breeding and Genetics Conference, September 30–October 1, 2005, Sturbridge, MA. www.vin.com/proceedings/proceedings.plx?CID=TUFTSBG2005& PID. Bell J. 2009. Ethical Breeding in the Age of Genetic Testing. Proceedings: Tuffs Canine and Feline Breeding and Genetics Conference, September 10–12, 2009, Sturbridge, MA. www.vin.com/proceedings/ proceedings.plx?CID=TUFTSBG2009&PID. Giger U. 2005. How to Recognize and Screen for Hereditary Diseases. Proceedings: Tuffs Canine and Feline Breeding and Genetics Conference, September 30–October 1, 2005, Sturbridge, MA. www.vin.com/proceedings/proceedings.plx?CID=TUFTSBG2005& PID. Little S. 2005. Congenital Defects of Kittens. Proceedings: Tuffs Canine and Feline Breeding and Genetics Conference, September 30– October 1, 2005, Sturbridge, MA. http://www.vin.com/proceedings/ proceedings.plx?CID=TUFTSBG2005&PID. Lyons L. 2005. Feline Genetic Disorders and Genetic Testing Proceedings: Tuffs Canine and Feline Breeding and Genetics Conference, September 30–October 1, 2005, Sturbridge, MA. www.vin.com/proceedings/ proceedings.plx?CID=TUFTSBG2005&PID. Lyons L. 2005. Genetic Relationships of Cat Breeds. Proceedings: Tuffs Canine and Feline Breeding and Genetics Conference, September 30–October 1, 2005, Sturbridge, MA. www.vin.com/proceedings/ proceedings.plx?CID=TUFTSBG2005&PID. Lyons L. 2009. Feline Genomics and Complex Disease Studies Proceedings: Tuffs Canine and Feline Breeding and Genetics Conference, September 10–12, 2009, Sturbridge, MA. www.vin.com/ proceedings/proceedings.plx?CID=TUFTSBG2009&PID. Vella C, Sheldon L, McGonale J, et al., eds. 1999. Robinson’s Genetics for Cat Breeders and Veterinarians, 4th ed., Philadelphia: Elsevier. Willoughby K. 2007. Paediatrics and inherited diseases, In EA Chandler, CJ Gaskell, RM Gaskell, eds., Feline Medicine and Therapeutics, 3rd ed., pp. 355–377. Ames, IA: Blackwell Publishing.
CHAPTER 317
Cattery Hygiene Suvi Pohjola-Stenroos
Overview A group of cats used for breeding purposes is called a cattery. A multicat household with several cats from different sources can sometimes also be called as a cattery. The purpose of keeping cats as a group may vary from boarding to rescuing to breeding. Rescue cattery hygiene is beyond the scope of this chapter. Cats are susceptible to several infectious diseases, and when housed together, there is a potential risk for spread of disease. Disease is produced as a result of changes in the host, the agent (pathogen), or the environment. Population host factors for disease include density, contact among individuals, and the proportion of susceptible individuals. Agents include commensals that coexist with the host and do not cause disease, opportunists that can contribute to disease in a host if there is a defect in the host’s resistance, and primary pathogens that can cause disease in a host not necessarily predisposed. Environmental factors can increase or decrease the risk of disease by the pathogen (e.g., disinfection) or the host (e.g., noise, stress, or overcrowding). The goals of cattery hygiene are to reduce the overall incidence of disease among cats housed together and to advise the cattery owner regarding control and prevention of infectious disease. It is not uncommon for cattery owners to ask, “Where did my cattery get this infectious agent?” Many cattery owners do not understand epidemiology and cannot understand how asymptomatic cats can be the source of infection for others. Professional advice is needed regarding the proper management and care of cats for successful infection control. Cattery hygiene depends on three factors: design of the facilities, management, and care of the cats. Many breeding catteries are in private homes that are not designed to house significant numbers of cats or to be the site of a business. The reader is encouraged to research proper cattery design using the sources in the Suggested Readings section. The goals of cattery hygiene management are to minimize exposure to infectious agents, minimize infectious agent transmission, and minimize infectious agent concentration on surfaces. See Chapters 322 and 329. Population density is the most important factor in minimizing exposure to and transmission of infectious agents in the cattery. When the population density is too great for the available resources, stress and
disease increase. As a general rule one person can properly care for about 10 cats in a home-based cattery. Stress can be manifested in many ways. The most common are overgrooming, inappropriate elimination, and urine marking (spraying). Dividing the feline population into housing groups can minimize stress and disease transmission. The ideal divisions are breeding queens with their kittens, weaned kittens, adult female cats without kittens, adult male cats, newly acquired cats, and cats with clinical signs of disease. Ideally, each division should have its own room and equipment. Daily care for the listed groups should occur in the order presented so diseased cats are handled last. Various aspects of infectious agent transmission in a cattery are presented in Table 317-1. The age of the cat is an important factor in disease susceptibility. In general infectious disease prevalence is lower when there are as few young cats in the cattery as possible because resistance to infectious disease increases with age. Kittens under 12 to 16 weeks of age or those not vaccinated at least twice against panleukopenia and the feline respiratory viruses should be isolated from all cats except their dam. Early weaning of kittens at 4 to 5 weeks of age should be used in a feline infectious peritonitis (FIP) or upper respiratory infection prevention program. Keeping the population as closed as possible is essential. Obviously an outdoor/indoor cat has more potential for spreading disease than the strictly indoor cat. A cattery should not include a cat that is allowed to roam outdoors freely. The term closed population is different from the term indoor population. Closed means no entrance or exit of cats until the entire group is gone. Adult cats may be asymptomatic although they may be carriers of several infectious agents. The most practical method of minimizing the entrance of infectious agents into the cattery is isolation. All incoming cats should be isolated for at least for 4 to 6 weeks. During this time they should have a thorough physical examination. A cat can be released from isolation when it is verified to be free from signs of illness (e.g., upper respiratory infections, diarrhea, and ringworm), tested negative for feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV), tested negative for intestinal parasites, including the protozoans Giardia, Cryptosporidium, and Tritrichomonas. A breeding cat should also be in good body condition, screened free from breed-associated genetic
TABLE 317-1: Aspects of Infectious Agent Transmission in Catteries Type of transmission
Agents
Exposure
Prevention
Direct cat-to-catcontact: touch, sniff Indirect contact: secretions from eyes, nose, saliva, tears urine or feces
Highest risk for viral infections Viable agents in dried secretions
Boarding in the same room, show cages Cleaning utensils, surfaces, food/water bowls, litter boxes, toys, kennel carriers, visitors
Aerosol transmission
Viral agents in sneezed macrodroplets
Boarding when sharing rooms, show cages
Separate cage for each cat, solid barriers between units Provide separate cleaning utensils for each unit; wash hands between cats; wear gloves when possible; follow hygiene protocols; control humidity, ventilation, and temperature; provide enough clean litter boxes Use full height solid barriers or separate rooms; use minimum 120-cm (4 ft) corridors between units; provide adequate ventilation and temperature.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
943
SECTION 8: Appendixes
diseases (e.g., polycystic kidney disease, hip dysplasia, and hypertrophic cardiomyopathy), and blood typed. The isolation unit is a separate room of the cattery in which the cat has no contact with any other cat or access to a communal space. Feeding, sanitation, and housekeeping utensils should not be removed from the isolation unit. It is assumed that a cat in the isolation unit carries infectious disease; therefore, this room is sanitized and disinfected last when cleaning the cattery.
Selected Infectious Agents Requiring Special Attention Feline herpesvirus, feline calicivirus, feline panleukopenia (parvovirus infection), FeLV, immunodeficiency virus infections, FIP and enteric coronavirus infections, rabies, Chlamydophila, and Bordetella bronchiseptica are included in the European Advisory Board on Cat Diseases (ABCD) recommendations. The ABCD was created to provide evidenced-based information on management of feline infectious diseases. Their recommendations include information regarding infectious agents, disease pathogenesis, clinical signs, vaccinations, immunity, diagnosis, and disease management and control in specific situations such as catteries. See Chapters 24, 28, 35, 73, 75, 76, 77, 95, 161, and 185. Dermatophytosis, giardiasis, and cryptosporidiosis require special attention in the cattery environment. These infectious agents are highly contagious between cats, have zoonotic potential, and can easily contaminate the environment for a longer period of time. Time and special effort is required to get rid of these infections. See Chapters 44, 48, and 83.
944
Recent information has revealed that Cryptosporidium is almost exclusively limited to animals under 1 year of age. There is also evidence that cats eliminate more oocysts than dogs suggesting that cats are more likely to be a source of human infection. Infection may result in serious signs in human patients with immunosuppression, such as acquired immune deficiency syndrome (AIDS) or chemotherapy. Giardia transmission from feline to humans may be more common than we have previously believed. In a recent study 6 of 17 cats (35%) excreted the giardial assemblage AI, which is transmissible to humans. The practical applications of this study for the cattery includes proper care of litter boxes, examination of diarrheic stools, and the use of fenbendazole as routine deworming agent. See Chapters 44, 48, and 83.
Suggested Readings American Association of Feline Practitioners. Practice Guideline, Feline Vaccines, www.catvets.com. European Advisory Board on Cat Diseases, www.abcd-vets.org/ quidelines. Bessant C. 2007. Boarding cats suspected or known to be carrying infectious disease. Fel Advis Bureau. Tisbury: Feline Advisory Bureau. 45(1):26–27. Pedersen NC. 1991. Feline Husbandry. Goleta, CA: American Veterinary Publications. Villeneuve Alain. 2009. Giardia and Cryptosporidium as emerging infections in pets. Vet Focus. 19(1):42–45.
CHAPTER 318
Echocardiographic Tables Larry P. Tilley and Francis W. K. Smith, Jr.
TABLE 318-1: Mean ± Standard Deviation, Range, and 95% Confidence Interval Values for M-mode Echocardiographic Parameters and Weight in Nonsedated Healthy Adult Maine Coon Cats and Nonsedated Healthy Adult Domestic Cats Maine Coon cats (n = 105) Parameter
Mean ± SD
LVIDd (cm) LVIDs (cm) LVPWd (cm) LVPWs (cm) IVSd (cm) IVSs (cm) Ao (cm) LADs(cm) LA:Ao %FS Weight (kg)
1.85 0.89 0.43 0.8 0.4 0.75 1.12 1.37 1.23 51.85 5.5
± ± ± ± ± ± ± ± ± ± ±
0.21 0.2 0.06 0.11 0.07 0.13 0.13 0.17 0.16 7.74 1.33
Domestic cats (79)
Range
95% CI
Mean ± SD
1.21– 2.33 0.5–1.45 0.28–0.59 0.54–1.07 0.25–0.57 0.49–1.04 0.81–1.57 1.03–1.76 0.86–1.84 32.08–69.82 2.72–8.39
1.81–1.89 0.85–0.93 0.42–0.44 0.78–0.82 0.39–0.41 0.72–0.78 1.09–1.15 1.34–1.40 1.20–1.26 50.35–53.35 5.24–5.76
1.5 0.72 0.41 0.68 0.42 0.67 0.95 1.17 1.25 52.1 4.7
± ± ± ± ± ± ± ± ± ± ±
0.2 0.15 0.07 0.11 0.07 0.12 0.14 0.17 0.18 7.11 1.2
Range
95% CI
1.08–2.14 0.40–1.12 0.25–0.6 0.43–0.98 0.3–0.6 0.4–0.9 0.6–1.21 0.7–1.7 0.88–1.79 40–66.7 2.7–8.2
1.46–1.54 0.69–0.75 0.39–0.43 0.66–0.70 0.40–0.44 0.64–0.70 0.91–0.98 1.13–1.21 1.21–1.29 50.51–53.69 4.43–4.97
To convert kilograms to pounds, multiply the value by 2.2. Ao, aortic root dimension; CI, confidence interval; %FS, Percentage fractional shortening, IVSd, interventricular septal thickness at end diastole. IVSs, interventricular septal thickness at end systole. LA:Ao = left atrium-to-aortic root ratio; LADs, left atrial dimension at end systole; LVIDd, left ventricular internal dimension at end diastole; LVIDs, left ventricular internal dimension at end systole; LVPWd = left ventricular posterior wall thickness at end diastole; LVPWs = Left ventricular posterior wall thickness at end systole; SD, standard deviation. Table from Droyer L, Lefbon BK, Rosenthal SL, et al. 2005. Measurement of M-mode echocardiographic parameters in healthy adult Maine Coon cats. J Am Vet Med Assoc.226:735–736.
TABLE 318-2: Mean ± Standard Deviation, Range, and 95% Confidence Interval Values for M-mode Echocardiographic Parameters in Male versus Female Adult Maine Coon Cats Male Maine Coon cats (n = 46) Parameter
Mean ± SD
LVIDd (cm) LVIDs (cm) LVPWd (cm) LVPWs (cm) IVSd (cm) IVSs (cm) Ao (cm) LADs(cm) LA:Ao %FS Weight (kg)
1.94 0.95 0.44 0.83 0.42 0.8 1.17 1.44 1.24 51.12 6.47
± ± ± ± ± ± ± ± ± ± ±
0.18 0.18 0.06 0.1 0.06 0.12 0.12 0.14 0.15 7.63 0.92
Female Maine Coon cats (59)
Range
95% CI
Mean ± SD
1.67–2.26 0.61–1.43 0.29–0.59 0.62–1.07 0.28–0.53 0.57–1.04 0.97–1.57 1.15–1.76 0.91–1.55 34.23–67.52 4.08–8.16
1.89–2.0 0.89–1.01 0.42–0.46 0.80–0.86 0.40–0.43 0.76–0.83 1.14–1.21 1.40–1.48 1.19–1.28 48.84–53.39 6.20–6.74
1.79 0.85 0.41 0.77 0.38 0.72 1.08 1.32 1.23 52.43 4.86
± ± ± ± ± ± ± ± ± ± ±
0.22 0.19 0.06 0.11 0.07 0.13 0.11 0.16 0.16 7.84 1.17
Range
95% CI
1.2–2.3 0.5–1.29 0.28–0.54 0.54–1.07 0.25–0.57 0.49–0.98 0.81–1.39 1.03–1.71 0.86–1.84 32.08–69.82 2.72–8.39
1.73–1.85 0.80–0.90 0.39–0.43 0.74–0.80 0.36–0.40 0.69–0.75 1.05–1.11 1.28–1.36 1.19–1.27 50.39–54.47 4.56–5.16
Ao, aortic root dimension; CI, confidence interval; %FS, Percentage fractional shortening, IVSd, interventricular septal thickness at end diastole. IVSs, interventricular septal thickness at end systole. LA:Ao = left atrium-to-aortic root ratio; LADs, left atrial dimension at end systole; LVIDd, left ventricular internal dimension at end diastole; LVIDs, left ventricular internal dimension at end systole; LVPWd = left ventricular posterior wall thickness at end diastole; LVPWs = Left ventricular posterior wall thickness at end systole; SD, standard deviation. Table from Droyer L, Lefbon BK, Rosenthal SL, et al. 2005. Measurement of M-mode echocardiographic parameters in healthy adult Maine Coon cats. J Am Vet Med Assoc.226:735–736.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
945
SECTION 8: Appendixes
TABLE 318-3: Normal Feline Echocardiographic Values Parameter
Range (Unsedated)* (n = 30)
Range (Sedated with Ketamine)† (n = 30)
RVIDd (mm) LVIDd (mm) LVIDs (mm) SF (%) LVPWd (mm) LVPWs (mm) IVSd (mm) IVSs (mm) LA (mm) Ao (mm) LA/Ao EPSS (mm) PEP(s) LVET(s) PEP/LVET Vcf (circumf/s)
2.7–9.4 12.0–19.8 5.2–10.8 39.0–61.0 2.2–4.4 5.4–8.1 2.2–4.0 4.7–7.0 9.3–15.1 7.2–11.9 0.95–1.65 0.17–0.21 — 0.10–0.18 — 2.35–4.95
1.2–7.5 10.7–17.3 4.9–11.6 30–60 2.1–4.5 — 2.2–4.9 — 7.2–13.3 7.1–11.5 0.73–1.64 — 0.024–0.058 0.093–0.176 0.228–0.513 2.27–5.17
Ao, aortic root (end diastole); EPSS, E point to septal separation; IVSd, interventricular septum at end diastole; IVSs, interventricular septum at end systole; LA, left atrium (systole); LVET(s), left ventricular ejection time (seconds); LVIDd, left ventricular internal dimension at end diastole: LVIDs, left ventricular internal dimension at end systole; LVPWd, left ventricular posterior wall at end diastole; LVPWs, left ventricular posterior wall at end systole; PEP(s), pre-ejection period (seconds); RVIDd, right ventricular internal dimension at end diastole; SF, shortening fraction; Vcf(circumf/s), velocity of circumferential fiber shortening. *Data from Jacobs G, Knight DH. 1985. M-mode echocardiographic measurements in nonanesthetized healthy cats: effects of body weight, heart rate, and other variables. Am J Vet Res. 46:1705. †Data from Fox PR, Bond BR, Peterson ME. 1985. Echocardiographic reference values in healthy cats sedated with ketamine hydrochloride. Am J Vet Res. 46:1479.
946
CHAPTER 319
Electrocardiographic Tables Larry P. Tilley and Francis W. K. Smith, Jr.
Normal Feline Electrocardiographic Values Rate • Range: 120 to 240 beats per minute* • Mean: 197 beats per minute
Left Atrial Enlargement • The duration of the P wave is greater than 0.04 sec (two boxes). Notching of the P wave is abnormal when the wave is also wide.
Right Ventricular Enlargement Rhythm • Normal sinus rhythm • Sinus tachycardia (physiologic reaction to excitement)
Measurements (lead II, 50 mm/sec, 1 cm = 1 mv) • P wave • Width: maximum, 0.04 sec (2 boxes wide) • Height: maximum, 0.2 mv (2 boxes tall) • P-R interval • Width: 0.05 to 0.09 sec (2.5–4.5 boxes) • QRS complex • Width: maximum, 0.04 sec (2 boxes) • Height of R wave: maximum, 0.9 mv (9 boxes) • S-T segment • No depression or elevation • T wave • Can be positive, negative, or biphasic; most often positive • Maximum amplitude: 0.3 mv (3 boxes) • Q-T interval • Width: 0.12 to 0.18 sec (6–9 boxes) at normal heart rate (range 0.07 to 0.20 sec, 3.5–10 boxes); varies with heart rate (faster rates, shorter Q-T intervals; and vice versa) • Electrical axis (frontal plane) • 0 to ± 160 degrees (not valid in many cats) • Precordial chest leads • CV6LL (V2): R wave <1.0 mv (10 boxes) • CV6LU (V4): R wave not greater than 1.0 mv (10 boxes) • V10: T wave negative; R/Q <1.0 mv
• The electrocardiographic criteria for right ventricular enlargement in the cat have not been well established. • Severe right ventricular enlargement produces some of the same electrocardiographic features observed in the dog. The most frequently observed electrocardiographic signs include the following: • S wave in leads, I, II, III, and VF (usually 0.5 mv [five boxes] or greater). • Mean electrical axis of the QRS complex in the frontal plane greater than +160 degrees and clockwise, especially when serial electrocardiograms on the same animal are compared. • Prominent S waves in leads CV6LL and CV6LU. • Positive T wave in lead V10.
Left Ventricular Enlargement • The R wave of the QRS complex exceeds 0.9 mv (9 boxes) in lead II. The R wave should not exceed 1.0 mv or 10 boxes in CV6LU or CV6LL. The amplitude of the R wave in V10 exceeds the Q wave amplitude (R/Q > 1.0). • The maximum width of the QRS is 0.04 sec (2 boxes). • Displacement of the S-T segment occurs in a direction opposite the main QRS deflection. This causes the S-T segment to sag into the T wave (S-T coving). • Repolarization changes cause the T wave to be of increased amplitude (usually greater than 0.3 mv or 3 boxes in lead II). • A mean electrical axis deviation in the frontal plane of less than 0 degrees may be present.
Suggested Readings Feline Cardiac Chamber Enlargement—Electrocardiographic Features
Tilley LP, Smith FWK, Jr. 2008. Electrocardiography. In LP Tilley, FWK Smith, Jr., M Oyama, et al., eds., Manual of Canine and Feline Cardiology, 4th ed., pp. 49–77. St. Louis: Elsevier.
Right Atrial Enlargement • The P wave is greater than 0.2 mv (two boxes) and is usually slender and peaked. • The Ta wave is sometimes present. This slight depression of the baseline following the P wave represents atrial repolarization.
* Note that sternal recumbency and left lateral recumbency (versus standard right lateral recumbency) should not be used for recording electrocardiograms if amplitudes and mean electrical axis determinations are to be compared with standard references.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
947
CHAPTER 320
Feral and Free-Roaming Cats Christine L. Wilford
Overview Feral cat trap-neuter-return (TNR) programs are gaining popularity in the United States. Veterinarians are vital to these programs to perform surgical sterilization. This chapter highlights veterinary medical aspects, including protocols for sedation and handling, humane care, considerations of health and lifestyle, preventive health, and treatment. The debate over impact on wildlife and birds, the environment, and other issues is beyond the scope of this chapter.
Cause of Death Free-roaming cats may die from the same causes as other animals living in nature, including disease, trauma, predation, and other natural causes. Opponents of TNR argue that because the cats’ ancestors were domestic that dying from natural causes is inhumane. TNR supporters advocate trapping and euthanizing free-roaming cats that appear severely ill, injured, debilitated, or otherwise suffering.
Temperament Definitions The literal definition of feral is a domestic animal living in a wild state. Specific to domestic cats, feral refers to cats that are unsocialized to people. The term feral describes a specific behavior not a breed or genetic trait. In the same way feral horses are can be trained for riding, feral cats may habituate to people under favorable circumstances; however, this process often requires years. Similarly, a previously tame cat may develop feral behavior if human contact is eliminated.
Feral versus Fractious Feral cats are naturally fearful of potential threats and will flee, hide, climb, hiss, spit, scratch, and bite in self-defense. Without history, feralbehaving free-roaming cats cannot be distinguished from fractiousbehaving pet cats. To illustrate imagine that the most fractious of owned feline patients is presented as a stray. Fractious appears feral. Feralbehaving cats admitted to animal shelters are typically killed because they are not adoptable as pets.
Free-roaming A more accurate term for outdoor cats is free-roaming. Free-roaming describes all outdoor cats without respect to behavior. This category includes owned or not owned; social or unsocial to people; outdoor only and indoor/outdoor. See Figure 320-1.
Myths versus Reality Disease Scientific studies reveal that free-roaming cats are not reservoirs of contagious disease. In fact, infectious disease rates are comparable in pet cats.
Quality of Life and Longevity Free-roaming cats do not typically live short, miserable lives. Subject to natural selection like other animal populations, some kittens die young, whereas others live into their teens.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
948
Healthy feral cats are not vicious and do not attack unprovoked. When approached feral cats flee and hide. If cornered or restrained, they fight for their lives by biting and scratching with continued attempts to flee.
Human Companionship Though people love caring for free-roaming cats, human companionship is not required for the cats’ quality of life. In fact, forcing a feral cat to live indoors with people can be stressful, and arguably, inhumane.
Animal Abandonment Opponents tout the argument that returning feral cats to their colonies constitutes animal abandonment. In reality abandonment refers to leaving individuals in an environment without resources or skills to survive. In colonies of cats that have been subject to TNR, their successful survival has already been established when returned to outdoor homes.
Trap-Neuter-Return TNR programs took place in the United Kingdom decades before becoming popular in the United States. The basics of TNR are the same worldwide. Caretakers trap free-roaming cats in humane live traps, have them altered, and return them home to where they were trapped. When cats cannot return, such as near populations of endangered species or properties slated for demolition, cats may be relocated instead of euthanized. Barns and farms are good alternatives particularly for landowners who desire nontoxic rodent control. Worldwide, compassionate people feed free-roaming cats as well as birds and wildlife. Caretakers are often bonded to the cats despite their inability to touch them. Some caretakers feed one or two cats, whereas others regularly feed numerous large colonies. Instead of feeding, some individuals focus their energies on trapping for other caretakers. Unless the cats are altered, they continue to breed and population increases. TNR provides an acceptable means of population control. Trap and kill programs are unpopular and poorly used by the general public. TNR reduces disease transmission, promotes weight gain, and most importantly, prevents unplanned litters. Kittens overwhelm shelters and rescue groups where lack of space leads to euthanasia of adoptable kittens and cats. One study revealed that 85% of owned cats were altered whereas only 2% of free-roaming cats were altered, leading to a conclusion that most kittens entering shelters originate from freeroaming queens or free-roaming toms that breed with unaltered, owned queens.
Feral and Free-Roaming Cats
Figure 320-1 The dynamic spectrum of a domestic cat in different environments over a lifetime. Sociality toward people may change in response to varying environments. Illustration courtesy of Christine Wilford, DVM, and Mary Ann Davis. Public benefits of TNR include vaccinating free-roaming cats against rabies as well as reducing nuisance behavior. Reducing intake and euthanasia in shelters through reproductive control saves taxpayer dollars.
Special Principles: Working with Feral Cats To reduce stress, reduce risk, and improve efficiency, veterinarians working with feral cats should embrace several principles.
problems, critical triage is necessary to consider cost and practicality issues.
Covered and Quiet Cats must be covered at all times during trapping, transport, and recovery. Under cover, cats feel safer and less stressed, which reduces anesthetic risk and increases safety. Staff should remain quiet and calm toward all cats.
One Cat per Trap High Quality Surgery Although working with feral cats often means working within financial limits, surgery can and should be of highest quality. For other medical
Caretakers should be limited to one cat per trap. Exceptions are queens with young kittens and litters of young kittens that share warmth and security if left together.
949
SECTION 8: Appendixes
Contagious Disease Veterinarians may designate special check in and out times, separate entries, and separate holding and recovery areas for cats with external symptoms of potentially infectious disease, such as upper respiratory infection, ringworm, and diarrhea.
Patient Selection Veterinarians helping free-roaming cats encounter patients of various ages and physical conditions. Some veterinarians limit admission to healthy adults, whereas most veterinarians accept cats of all ages and health conditions. Spay or neuter of free-roaming cats should not be postponed for minor health issues. Many cats become wise to trapping and cannot be retrapped; thus, they may literally have one chance to be altered.
Sedation before Examination To prevent injury and risk of escape, feral cats must not be touched until completely sedated. Intramuscular anesthetic protocols are best because no hands-on restraint is needed. If a cat appears so ill that it may not survive sedation, then a decision is needed whether to risk sedation or sedate with intent to euthanize. Occasionally, trusted and skilled caretakers can successfully treat cats in confinement until they become healthier anesthetic candidates. This approach often works well for cats with severe upper respiratory infections, diarrhea, and other fairly treatable diseases.
Restrain for Sedation Preventing Injury and Escape Safe handling is imperative. Loose cats are terrified and wreak havoc as they scramble to escape. These cats can find small gaps in walls, push through false ceilings, wedge behind appliances, and potentially escape through open doors. Proper equipment and techniques make restraint for sedation safe and straightforward.
Trap Restraint Restraint is easily and safely accomplished using the live trap in which the cat is trapped. Leaving the cat in the trap eliminates risk of escape and prevents human injury unless someone places his or her fingers into the trap.
Capture Net Having a capture net available is advised in case any cat escapes. The ideal capture net, such as the Freeman cage net, allows for safe capture as well as restraint for intramuscular injection. Fishing nets are inappropriate and unsafe.
Intramuscular Injection When approached quietly many cats in traps remain still for intramuscular injection, particularly if the needle is inserted slowly. Delivery should be rapid because the anesthetic stings. Cats in traps that move away from the needle can be fully restrained inside the trap with a trap divider.
Anesthetic complications are most common during induction. Respiratory arrest can develop and usually precedes cardiac arrest by several minutes. If respiratory arrest is identified early, patients are most easily stabilized. If vigorous stimulation does not restore breathing, a few minutes of chest compressions and oxygen via mask are usually effective. In some cases yohimbine is needed.
Anesthesia Caretakers and clinic workers should check each cat for an ear tip before sedation. If ear tipped, the cat is already altered and should not be sedated.
Telazol®-Ketamine-Xylazine Cocktail Hundreds of thousands of free-roaming cats have been safely sedated with Telazol®-Ketamine-Xylazine (TKX). This anesthetic cocktail consists of one bottle of Telazol® reconstituted with 1 mL of xylazine (100 mg/mL) and 4 mL of ketamine instead of sterile water. TKX is relatively inexpensive, quick acting, can be partially reversed, and is well tolerated. Restraint is achieved within 5 to 10 minutes. Atropine or glycopyrrolate may be administered on an individual basis to treat xylazineinduced bradycardia. For additional analgesia, many programs administer buprenorphine as a separate injection after the cat is sedated and weighed.
Anesthesia Dose Most programs simply sort cats into small (<2.3 kg [5 lbs]), medium (2.3–4.5 kg [5–10 lbs]) or large (>4.5 kg [10 lbs]) and use only three doses, respectively, 0.15 mL, 0.25 mL, and 0.30 mL. For shorter anesthetic duration, smaller doses of 0.12 mL, 0.20 mL, and 0.25 mL per cat are used.
Additional Anesthesia Cats that require more anesthetic depth or duration can receive additional intramuscular or intravenous doses of TKX. An alternative is gas anesthesia delivered by mask or endotracheal tube.
Core Services Several services are considered fundamental for free-roaming cats and should always be performed. Keep in mind that the primary goal of TNR is to humanely prevent unplanned kittens. An added benefit is that spaying or neutering improves the health of altered cats.
Scanning for Microchip All cats should be interrogated for microchips of all frequencies. Most programs consider the microchip as proof of pet ownership, although some caretakers microchip feral colonies. In all cases registrants of chipped cats should be contacted immediately. Further elective procedures without owner consent are discouraged.
Physical Examination The physical examination should include body weight, general condition, and gender confirmation as well as noting external parasites and identifying visible abnormalities.
Induction Monitoring and Complications After injection, close monitoring is imperative. Some cats become recumbent with their necks flexed and require repositioning to avoid asphyxiation.
950
Surgical Sterilization Every cat should be surgically sterilized, confirmed as previously sterilized, or if seriously ill, either euthanized or fostered for treatment and
Feral and Free-Roaming Cats
Figure 320-2 Ear tip technique: Placing the clamp to remove a symmetrical 1-cm (3/8-in) tip creates an obvious, intentional ear tip to signify the cat is surgically sterilized. Illustration courtesy of Christine Wilford, DVM, and Mary Ann Davis. returned for surgery. No cat should return to its colony with reproductive capacity.
Ear Tipping, Ear Tattoos, and Ear Notching The ear tip is the international standard designating free-roaming cats as reproductively sterile and does not equate to feral. Ear tipping is for the cat’s safety. If trapped, an ear-tipped cat can be released immediately and avoid transportation, captivity, sedation, and possible exploratory surgery. See Figure 320-2. In some jurisdictions animal control agencies consider all ear-tipped cats as feral and have policies to exterminate the cats upon capture. To protect the cats, caretakers may use ear tattoos or microchips instead of ear tips. In frigid climates frostbite can cause pinnae loss that can be indistinguishable from an intentional ear tip. TNR programs in these areas may elect to perform ear tattoos for clarification. Ear notches are less commonly used because they too closely resemble fight wounds.
of its short duration of action. Nonsteroidal anti-inflammatory drugs are contraindicated because of the cats’ unknown health status.
Optional Services Some caretakers request additional services, while some veterinarians require them. Opponents of these extra services argue that resources should concentrate on spaying and neutering. Proponents feel that each cat should receive every service, even if the benefit is short lived. Extra services include retroviral testing, treating for internal and external parasites, vaccinating for feline panleukopenia and respiratory viruses, declawing ingrown polydactyle nails, treating abscesses, amputating traumatized tails, enucleating ruptured eyes, extracting abscessed teeth, treating lacerations, and administering subcutaneous fluids and iron injections. Only modified-live FVRCP vaccines should be used because they stimulate prompt immunity without need for a booster.
Rabies Vaccination All free-roaming cats should be vaccinated for rabies with a three-year licensed vaccine. Although cats are difficult to trap for booster vaccinations, a single vaccine was demonstrated to protect against virulent challenge for more than 3 years. Veterinarians may determine whether to vaccinate kittens either by using the age estimate of 1 pound per month or by simply vaccinating all kittens being returned to colonies. The canarypox vaccine is licensed for kittens 8 weeks of age and older.
Euthanasia Euthanasia is necessary for any cat apparently suffering when treatment is not appropriate or available. A cat should not return to its colony unless it can humanely live a feral lifestyle (i.e., eat, drink, avoid predators, defend itself, and find shelter).
Ear Tip Technique Sterile surgical prep is not necessary, but the pinnae should be clean. A large clamp should be placed across the entire pinna parallel to the base of the ear leaving a bit more than 1 cm (3/8 in) above the clamp. Remove 1 cm (3/8) of the ear tip from adult cats and proportionally less for juveniles. Sharp, new blades promote bleeding, as will any sharp edge, so scissors are recommended instead. Ear cropping scissors work especially well. Leaving the ear clamped until recovery, ideally 15 minutes or longer, promotes hemostasis. Gauze and cautery are rarely needed to control bleeding. See Figure 320-2.
Ovariohysterectomy Array of Conditions
Additional Analgesia Intramuscular buprenorphine is ideal, because it is effective for 8 to 12 hours and is relatively inexpensive. Butorphanol is not advised because
Free-roaming cats present with a wide variety of reproductive conditions, including each stage of the reproductive cycle and pregnancy, cystic ovaries, pyometra, and deformities.
951
SECTION 8: Appendixes
Ventral Midline Scars Ventral midline abdominal scars on female cats can mimic “spay scars.” Surgical exploration to identify the uterine or ovarian stumps is the only reliable way to determine whether a cat has been spayed. On multiple occasions I have found reproductively intact female cats, often pregnant, with scars that other veterinarians deemed spay scars.
Tattoo on Ventral Midline A tattoo on the ventral midline indicates the cat is altered. Tattoos may be dots, lines, letters or numbers and are usually black, blue or green.
Incision Closure Free-roaming cats typically return to their colonies the day after surgery. To reduce postoperative risks the abdominal wall should be sutured with a simple interrupted pattern. A single cruciate stitch is appropriate for incisions of 1 cm (3/8 in) length or less. Skin should be closed with absorbable suture in a subcuticular pattern. External sutures must always be avoided.
Strive for Small Incisions With proper technique a complete routine ovariohysterectomy (OVH) is easily performed through a small incision to reduce the duration of anesthesia and surgery as well as postoperative pain. Small incisions also lessen the risk of abdominal dehiscence in the event of incisional failure. Strategic placement of the incision, cutting the ovarian suspensory ligament for optimal exposure, self-tying the ovarian stump, and using the Miller ’s knot for uterine stump ligation facilitate high quality surgery via small incisions. Tips for efficient technique can be found by viewing “Cat Spay in Five Minutes” on YouTube.
Flank Approach The flank approach for a routine OVH is more commonly used in the United Kingdom. This approach reduces the risk of catastrophic complications in the event of incisional dehiscence as well as avoids the mammary glands in lactating queens. One drawback is that a ventral abdominal incision may still be required, if surgical complications arise.
rhage. For added security some surgeons prefer the Miller ’s knot circumferentially. The broad ligament can also bleed significantly in full-term cats and should be closely monitored.
Euthanizing Feti The feti of pregnant cats are anesthetized during surgery. Euthanizing more developed feti within the uterus after removal from the abdomen while the feti are still anesthetized is advocated.
Castration Castrations are typically straightforward with a few exceptions.
Large Tom Cats Large tom cats with thicker and more vascular tunics bleed more than younger, smaller males. Ligating the tunics in larger male cats reduces seepage and may prevent dislodgement of large clots from the scrotum during recovery.
Cryptorchidism Approximately 1 to 2% of male cats are unilaterally or bilaterally cryptorchid. Determining whether a sexually mature cat is previously neutered or bilaterally cryptorchid is simple. If spines are present on the penis, the cat is intact. No spines indicate the cat is neutered. See Figure 314-2. In unilateral cryptorchid cats the undescended testicle should be removed first. If the testicle is not located inguinally, then abdominal exploration is required. Following the vas deferens from its origin near the kidney distally through the inguinal canal should always reveal the undescended testicle. Cases of testicular agenesis are exceedingly rare. Inguinal testicles are easily excised. Depending on incision size skin can be closed with surgical glue or subcuticular absorbable suture. If the retained testicle cannot be found, the descended testicle should not be removed! Leaving the descended testicle greatly assists a future surgeon to know which side to explore. Furthermore, the ear tip should not be performed until both testicles have been removed.
Recovery Ovariectomy European veterinarians traditionally perform ovariectomy instead of OVH. The surgery is less involved and more efficient. Evidence does not reveal increased risk associated with leaving the uterus intact in ovariectomized cats.
Pregnant Cats A study of over 100,000 cats from as far south as Hawaii and as far north as Seattle revealed that pregnancy rates are highest during March and April and lowest during November and December, regardless of climate or latitude. For cats in advanced pregnancy, OVHs are more involved and time consuming, yet they can be performed safely with proper technique.
Reversal of xylazine with yohimbine is used routinely in some programs. Other programs reserve yohimbine use for prolonged recoveries or patients with complications. Postoperative recovery of feral cats differs from pet cats. Feral cats should recover in traps or carriers, not in hospital cages. Limiting to one cat per carrier or trap prevents inadvertent suffocation or injury. Plenty of soft, absorbent bedding should line traps and carriers. Partially covering the trap or carrier reduces stimulation and stress while allowing visual access for monitoring. The cat’s head should be placed toward the trap or carrier door to facilitate monitoring. Placing the cat in lateral recumbency with the tipped ear up reduces bleeding. If needed the ear clamp may remain on the ear until the cat begins to awaken.
“R”: Return to Colony Special Attention to Hemostasis The uterus and ligaments are highly vascularized during pregnancy and require extra care to prevent hemorrhage. Individually ligating uterine arteries is advised. Many surgeons avoid transfixing the uterine body because of its increased vascularity and potential to bleed. However, a circumferential ligature must be secure; slippage can lead to fatal hemor-
952
Most feral-behaving cats are stressed in captivity; however, they should not return to their colonies until fully recovered from anesthesia. Some caretakers elect to house cats for as long as a week postoperatively. Although this allows for observation and healing, some cats retain urine, become dehydrated, and do not eat while captive. Each situation must be evaluated for its particular circumstances.
Feral and Free-Roaming Cats
Euthanasia versus Treatment TNR programs support euthanasia when indicated; however, most cats in TNR programs are relatively healthy as demonstrated by a euthanasia rate of less than 0.5% in a large-scale study of six programs. Making the decision to euthanize may not be clear-cut. A basic algorithm to consider is whether the cat can live humanely in a free-roaming lifestyle. Does the cat have sufficient health and ability to find shelter, eat and drink, and defend itself in its particular environment? One must use their best judgment under the circumstances at hand.
Physical Examination and Critical Thinking Euthanasia decisions are based on physical examination, limited history, and critical thinking. Good body condition is a strong indicator that the cat is doing well despite its abnormality. Deformities, wounds, abscesses, dental disease, and healed fractures often affect cats found in otherwise good condition. Some conditions are predictably transient, such as a thin nursing queen that will regain health after weaning and OVH. Euthanasia of a cat in good condition on the basis of a single positive retroviral test is strongly discouraged because multiple factors and individual circumstances affect the accuracy of these tests. The most common indications for euthanasia are emaciation, unhealed fractures, dyspnea from intrathoracc disease (not upper respiratory infections), severe stomatitis, and severe pododermatitis involving more than one foot.
Intravenous Euthanasia Cats should be euthanized IV before recovering from sedation. If the cat is not fully sedated, additional intramuscular anesthesia should be administered before attempting intravenous euthanasia. Intraperitoneal or intracardiac euthanasia should never be performed in a conscious patient.
Treating Captive Feral Cats Performing treatments on conscious, feral-behaving cats can be risky to the cat and the person. If treatment is needed, veterinarians should only consider working with the most seasoned, reliable, and trusted caretakers or none at all. If any aspect of care cannot be guaranteed, then euthanasia may be the better option. Surprisingly many cats eat medications added to food. A squeeze cage or capture net enables administration of topical medications and injections, including subcutaneous fluids. Long-acting medications (i.e., flea control and antibiotics) should be used when appropriate. Housing must allow for cleaning and changing food or water bowls without risking escape or injury. All vital functions should be closely monitored in captivity. Dehydration along with feeding dry cat food may increase the risk of creating new problems, such as crystalluria and urinary obstruction. Canned food is preferable. Treating conditions prior to sedation and spaying or neutering may reduce surgical risk.
Summary People will feed. Cats will breed. Veterinarians can influence the latter and make a huge impact on population control. Working with TNR programs can be rewarding and highly valued. The safety and health of the cats and people involved is paramount to a successful program.
Suggested Readings Association of Shelter Veterinarians Spay-Neuter Task Force. 2008. The Association of Shelter Veterinarians: veterinary medical care guidelines for spay-neuter programs. J Am Vet Med Assoc. 233(1):74–86. Berkeley EP. 2004. TNR: Past, Present, and Future: A History of the TrapNeuter-Return Movement. Washington DC: Alley Cat Allies. Levy JK, Crawford PC. 2004. Humane strategies for controlling feral cat populations. J Am Vet Med Assoc. 225(9):1354–1360. Levy JK, Wilford C. 2010. Feral cat management. In Shelter Medicine for Veterinarians and Staff. In Press. Ames, IA: Blackwell Publishing.
953
CHAPTER 321
Grief Responses by Cat Owners Larry A. Norsworthy, Kacee Junco, Brooke Woodrow
Summary of Previous Research In a 2007–2008 American Pet Products Manufactures Association (APPMA) census, 73% of U.S. households owned at least one pet. Consequently, millions of pet owners deal with pet loss every year in the United States. Many owners experience grief over the loss of their pet, which ranges in duration and severity. Research suggests pet attachment is the best predictor of the level of grief experienced after pet loss. Many aspects of human-pet relationships can be linked with the human attachment criteria identified by Ainsworth (1991) and Hazan and Zeifman (1999). Pets, like people, provide companionship. Also, pets can fill emotional needs when human attachments are lacking. Podberscek and Blackshaw (1994) concluded “high levels of pet ownership, attachment to pets, and replacement of deceased pets indicates how important animals are to humans.” Therefore, there is value in investigating the possibility of pet owners obtaining a new pet in anticipation of the death of their current pet or obtaining a replacement pet following the loss of their pet. In some societies, it is customary to provide an immediate replacement of the loss or to minimizing psychological dependency of the loss by channeling attention to another present member of the family. This is done to lessen the impact of the dysfunction resulting from the missing role the deceased represented. Usually, when a normal bereavement process takes place, a replacement animal can be successful if brought in to the family with sensitivity and delicacy. The home feels less empty, and a familiar routine is once again in place. The length and intensity of mourning appears to be related to investment, experiences prior to the loss, the reaction of peers, and the age of the person involved. If death of the pet is anticipated, getting a new pet before the death appears beneficial. Stewart (1983) found that rapid replacement of the deceased pet was helpful. In contrast, Levinson (1981) specified that replacement of the deceased pet should be postponed. Additionally, presence of another animal tends to alleviate some distress in the bereavement process. For example, if other animals are already present in a household, the bereavement over a deceased pet is usually not felt as intensely, perhaps because there is still an existing feeling of responsibility and routine of taking care of an animal. Replacement of the pet is observed to take place after various periods of time without a sense of betrayal to the original pet being felt, but when bereavement is unresolved, hesitation in getting a new animal may exist. The most common reason for not replacing a pet is the owner ’s fear of another death. It is important to note that a stressful grief period tends to prevent owners from obtaining a new pet too quickly. Additionally, those who were not very attached were less likely than who were very attached to acquire a “replacement pet” should their pet die. Even though the new animal will never be the same as the previous one, a good human-pet bond can develop over time.
Present Study Overview In a 2009 study by the authors, there were seven males and 78 females recruited from six feline veterinary practices across the United States and The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
954
one in Canada totaling seven participating clinics and 85 participants in this research. The participants were contacted within 1 week to 1 month (variability occurred due to extraneous variables and confounding factors) following the death of their cat. Most participants, however, received a packet of questionnaires 2 weeks after the death of their cat. Follow-up packets were mailed to eligible participants 3 and 6 months following the loss of their cat. The following measures were used for the purposes of this study: the revised CENSHARE Pet Attachment Survey (CPAS); Experiences in Close Relationship Scale (ECR); Pet Bereavement Questionnaire (PBQ); Satisfaction With Life Scale (SWLS); and the Center for Epidemiological Studies-Depressed Mood Scale (CES-D).
Findings Findings indicate cat owners who reported higher levels of attachment to their cats reported higher levels of depressed mood 1 to 4 weeks following the death (initial assessment), which was not observed during 3- and 6-month follow-ups. Those who were more intimately attached to their cats also reported lower satisfaction with life, at 1 to 4 weeks and 3 and 6 months following the death of a cat. Higher levels of attachment also indicated higher levels of grief at 1 to 4 weeks and 6-month followups. Increased pet attachment appeared to predict levels of reported grief both initially and 6 months following the cat’s death. Over time, bereaved cat owners reported a decrease in depressed mood and lower levels of grief. However, distress continued even after 6 months. Depression, grief, and guilt levels were higher at the initial assessment among individuals living alone rather than individuals living with others. At both the initial and 3-month follow-up, life satisfaction was higher among those who lived with others compared to those who lived alone. Younger people experienced more guilt at the 3-month period and more anger at the 6-month period relative to older people. Poor adult attachment was associated with stronger pet attachment at the initial period and was not reassessed during either of the follow-up periods. Specifically, anxiety and avoidance of intimacy and anxiety in adult relationships was linked with a higher level of intimacy in a human-pet bond. Poor human attachment was associated with greater reported depressed moods and lower satisfaction with life after losing a cat. In addition, anxiety about abandonment in human attachment relationships was associated with increased grief and guilt after the death of a cat. Further, when cat owners endorsed high levels of grief on the PBQ, higher levels of pet attachment were seen. Also, an increased amount of anger after a cat’s death was related to higher levels of intimacy within the human-pet attachment relationship. Poor human attachment was observed to be associated with greater depression and less satisfaction with life after the loss of a pet. In summary, cat owners with poor human attachments had higher levels of pet attachment. See Tables 321-1, 321-2, and 321-3. Of the 85 participants, 40 indicated they planned to obtain a new pet, whereas 37 reported they did not plan to get a new pet and 8 did not respond. Of the 40, 16 respondents reported plans to obtain a new pet within 1 year following the cat’s death, whereas 4 respondents indicated they planned to obtain a new pet more than 1 year following the cat’s death. Of the 85 participants, 57 reported they were anticipating the death of their pet, whereas 26 reportedly were not anticipating the death, and 2 did not respond. Of the 16 participants who replaced the pet, 10 reported
Grief Responses by Cat Owners
TABLE 321-1: Correlations between CPAS and ECR Subscales ECR-Avoidance CPAS-Intimacy CPAS-Relationship Maintenance
0.248* −0.050
TABLE 321-3: Conclusions based on the Data
ECR-Anxiety †
0.373 0.128
Conclusions: When the CPAS and ECR subscales were correlated avoidance of intimacy in adult relationships indicated more intimacy in a human-pet bond among those who have lost a pet. CPAS, CENSHARE Pet Attachment Survey; Experiences in Close Relationship Scale, ECR. *p < 0.05 †p < 0.01
TABLE 321-2: Correlations between ECR Subscales with CES-D, SWLS, and PBQ Subscales ECR-Avoidance CES-D SWLS PBQ-Grief PBQ-Guilt PBQ-Anger
†
0.403 −0.463† 0.099 0.144 0.084
ECR-Anxiety 0.438† −0.381† 0.252* 0.259* 0.146
Conclusions: Poor human attachments were associated with greater depression and lower life satisfaction after pet loss. Additionally, the more anxiety endorsed in human relationships, the more pet grief and guilt was seen after pet loss. CES-D, Center for Epidemiological Studies-Depressed Mood Scale; ECR, Experiences in Close Relationship Scale; PBQ, Pet Bereavement Questionnaire; SWLS, Satisfaction With Life Scale. *p < 0.05 †p < .01
they were anticipating the death of the initial pet, 4 indicated they were not anticipating the initial pet’s death, and 2 did not respond. Of those receiving follow-up packets, 16 of the eligible participants replaced a pet within 5 months of their cat’s death or in anticipation of their cat’s death. Three participants replaced the pet before their cat’s death, and 4 participants obtained a replacement pet 1 month following the cat’s death. Two months following the cat’s death, four people obtained a new pet, and 3 months following the cat’s death two owners obtained a replacement pet. One owner replaced her cat after 4 months. Finally, 5 months following the cat’s death, one owner obtained a replacement pet. Higher levels of pet attachment were significantly related to replacement of the deceased cat. Levels of bereavement were not significantly related to the likelihood of pet replacement. Owners who replaced a pet were significantly more attached to the deceased pet than the new one. It is predicted this would change over time. Those who were more attached to their deceased pet tended to replace it with a new pet. That is, those who were more attached to their deceased pet tended to replace it with a new pet, and owners who replaced a pet did not have different levels of bereavement than those who did not replace their pet.
Implications Veterinarians may benefit from being informed of owners’ feelings regarding pet loss. Often veterinarians are around pet owners when they find out news regarding the end of their pet’s life. Veterinarians could have screening tools available in their waiting rooms for owners to fill out regarding pet loss. These screening tools could take pet owners’ risks factors into consideration such as: the level at which they are attached to their pet, previous reactions to pet loss, past experience with grief,
Correlations between CPAS Subscales with CES-D, SWLS, and PBQ Subscales The greater the attachment to the pet, the more distress one reported after losing a pet. Higher scores on CPAS-Intimacy indicated lower reported levels of satisfaction with life in those who experienced pet loss. Living Situation Related to CES-D, SWLS, and PBQ Depression was significantly higher in those living alone than those living with others at the initial assessment period. Grief and guilt were higher among those who lived alone. The aforementioned trends were not significant at the follow-up points. Depression and Life Satisfaction Depression was significantly higher among those who lost a pet. However, satisfaction with life was not significantly lower among those who had lost a pet. Pet Attachment and Response to Pet Death over Time Bereaved pet owners who reported higher levels of pet attachment reported higher levels of depression at the initial assessment. These associations were not observed at either follow-up. CES-D, Center for Epidemiological Studies-Depressed Mood Scale; CPAS, CENSHARE Pet Attachment Survey; ECR, Experiences in Close Relationship Scale; PBQ, Pet Bereavement Questionnaire; SWLS, Satisfaction With Life Scale.
owners’ age, whether or not they live with others, number of pets, and available social support. These screening tools could help veterinarians provide appropriate advice and suggestions to give to their clients such as getting a new pet or seeking bereavement therapy. Brochures (e.g., variation of this chapter) could also be developed to give to owners who are about to or have recently lost a pet, highlighting reactions they may experience following the death. These brochures may be able to serve as a means of educating and normalizing the unexpected feelings and stressors following the loss. Veterinarians may suggest pet replacement to clients who have a high level of pet attachment to their deceased pet. However, veterinarians should make it known that replacing the deceased pet does not necessarily reduce the impact of the bereavement experienced in regard to the deceased pet. Not only do professionals involved in pet loss need to be informed of this growing concern, but society as a whole may also aspire to heighten its awareness. Many distressed pet owners indicate dissatisfaction with family and friends due to the lack of support they provide for hurting owners. Society’s increased awareness of the yearly National Pet Memorial Day may be an opportunity for communities to reach out to individuals nearby wishing to grieve, remember, or celebrate that special pet. Family and friends’ support during these difficult times can help them overcome and heal from the loss. There is a need for an overall increase in public education regarding pet loss. Finally, pet owners should be aware of not only the joy their pets provide for them but also the possible challenging experiences following their death. Due to the length of time a pet lives, most pet owners will experience pet loss. As mentioned, veterinarians can help them know what to expect when the time comes and provide them with the necessary resources. Some pet owners may not be aware of the potential reactions to pet loss, owners and potential owners may wish to read and research this area as a means of coping with pet loss. Owners who choose to acquire a replacement pet must be mindful that their attachment level to the new pet may be different than their attachment level to their deceased pet. Based on this study and other research, clients with high levels of attachment to their pet should strongly consider replacing a pet in anticipation of the loss or shortly after the loss.
955
SECTION 8: Appendixes
Suggested Readings Ainsworth MS. 1991. Attachments and other affectional bonds across the lifecycle. In CM Parkes, J Stevenson-Hinde, P Marris, eds., Attachment across the Life Cycle, pp. 334–51. New York: Routledge. Brown BH, Richards HC, Wilson CA. 1996. Pet bonding and pet bereavement among adolescents. J Counsel Develop. 74(5):5054–510.
956
Hazan C, Zeifman D. 1999. Pair bonds as attachments. In J Cassidy, PR Shaver, eds., Handbook of Attachment, pp. 336–354. New York: Guilford Press. Levinson BM. 1981. Acute grief in animals. Arch Found Thanatol. 9(2):paper 11. Podberscek AL, Blackshaw JK. 1994. The attachment of humans to pets and their reactions to death. Canine Pract. 19(5):16–19.
CHAPTER 322
Hospital Hygiene Suvi Pohjola-Stenroos
Overview The goal of hospital hygiene is to prevent the transmission of infections. Cleaning and disinfecting measures are designed to secure a clean, hygienic, and safe environment for both the patient and the veterinary personnel. Besides saving money, prevention of infection outbreaks also strengthens the trust and loyalty of clients to the veterinary healthcare team. A hospital infection, also known as a nosocomial infection, is one a patient acquired while staying in the hospital. The infection may become apparent only after the patient has been released from the hospital. This is possible because most feline patients are treated as outpatients or require only a short stay in the hospital and the incubation period of most feline infections is several days. There are two groups of infections that may affect hospitalized felines. First, infections such as Salmonella spp., Campylobacter jejuni, feline parvovirus, Bordetella bronchiseptica, Chlamydophila felis, feline calicivirus, feline herpesvirus-1, rabies, and plague are contagious and may be passed from patient to patient. They can affect ill patients or healthy, uncompromised felines not protected with vaccines. Second, bacterial organisms that exist either in the environment or belong to the patient′s normal bacterial flora may cause disease in immunocompromised felines or be spread by interventions such as drug therapy, intravenous or urinary catheterization, endotracheal intubation, dental treatment, or surgery. Some of the infections have zoonotic potential. See Chapter 329. Zoonotic diseases are diseases of animals that may be transmitted to humans. Preventative measures, such as feline fecal examinations and proper vaccination programs, will decrease the number of nosocomial infections and benefit the overall health of the patient.
Hospital Hygiene Policy Hospital hygiene policy is a description of good working protocols that have been discussed with the staff, agreed on, and put into action in the hospital. Staff awareness of transmission routes of these infections and meticulous adherence to the written hospital hygienic policy prevent the risk of cross contamination and infection. Table 322-1 presents the risk factors, origin of infection, and hygiene levels that should be addressed when developing hospital hygiene policy. Prerequisite work for developing the hospital hygiene policy begins with a hygiene audit. This includes identification of areas of contamination in the hospital, analysis of working habits, and preferably, the occurrence analysis of methicillin-resistant Staphylococcus aureus (MRSA) in the hospital. The current hygiene protocol after the audit may effectively change in four phases: justification, training, adopting, and measuring. Practice meetings are good opportunity to go deeply into the written statement, which helps staff members to adopt the changes that will occur in the practice. Written protocols should be as short, simple, and as effective as possible and should be clearly posted in several places. Written protocols can be divided into four parts according to the object in question: disinfectants, hand hygiene, surface hygiene, and instrument hygiene. The
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
TABLE 322-1: Risk, Origin of Infection, and Hygiene Level in Hospital Policy Risk
Origin of the Infection
Hygiene Level
Very Small Small
Walls, roof, door, sink Instruments in contact with the feline clean skin: stethoscope, pen light, bandage scissors, clipper blades Instruments in contact with feline mucosal membranes: thermometer, intubation tubes, endoscopes, bronchoscopes. Instruments used on infected patients. Instruments for the immunocompromised patient. Body secretions on surfaces. Instruments in contact with injured mucosal membranes or skin. Instruments that penetrate the skin or mucosal membranes: surgical instruments, needles, catheters.
Cleaning, drying Cleaning and drying
Moderate
Marked
Disinfection or single use
Sterilisation
head technician or practice manager may be the best person for monitoring the policy and carrying out actions needed for better performance.
Disinfectants The optimal disinfectant is effective, nontoxic, easy to dilute, economical, residue free, non-corrosive, odorless, able to penetrate infectious material, and rapid acting. Specific efficacy tests should carefully be studied before selecting a line of products for the hospital. Disinfection does not replace thorough cleaning because most disinfectants work properly only on clean surfaces. Table 322-2 presents a generalized overview of different disinfectant types and their general qualities.
Hand Hygiene The vast majority of the nosocomial infections arise in the hospital from inadequate hand hygiene. Healthcare workers, particularly physicians and likewise probably veterinarians, are notoriously poor at remembering to wash their hands. Studies have shown that hand washing was actually performed less than 50% of the appropriate times. The U.S. National Association of State Public Health Veterinarians has given advice about hand hygiene. “Hands should be washed before and after each patient, after contact with blood, body fluids, secretions, excretions, or articles contaminated with these fluids, before eating, drinking, smoking, after using the toilet, after cleaning animal cages or animal care areas, and whenever hands are visibly soiled. Hand washing can be replaced with alcohol-based gel when there is no visible soiling of the hands. Fingernails should be cut short and be polish-free.” Avoid wearing jewelry because it prevents proper hand washing. Disposable gloves and aprons should be used whenever in contact with high-risk material. Recommendations for effective hand washing include: • Open the water faucet with paper towels. • Wet your hands
957
SECTION 8: Appendixes
TABLE 322-2: Qualities of Various Disinfectants Type
Uses
Effective Against
Comments
Alcohol based
Bacteria, fungi, and lipophilic viruses Viruses, bacteria, and fungi
Quick drying
Oxidants Organic acids Phenolics
Equipment, small surfaces, andhands Buildings, vehicles, equipment, and foot dips Buildings, vehicles, equipment, and surfaces Buildings and water Buildings, foot dips, and water Buildings and equipment
Quaternary ammonium cations
Buildings, equipment, andsurfaces
Glutaraldehyde Iodophors
• Take liquid antiseptic soap from the dispenser. • Wash your hands carefully for at least 30 seconds including the fingernails. • Rinse properly. • Use paper towels to dry. • Close the faucet with paper towels. Damp hands increase the risk for transmitting bacteria; thorough drying is imperative. Warm air dryers or new jet air dryers have been shown to increase bacteria on the hands, whereas paper towels reduced bacteria. Jet dryers also disperse the contamination over a distance of several meters predisposing the staff to inhaled microbes. Whenever possible, including the surgery room, opening and closing the faucet should occur without hand contact by using a touch free faucet.
Methicillin-Resistant Staphylococcus Aureus MRSA is a strain of S. aureus that is resistant to the β-lactams, which include penicillins and cephalosporins. MRSA is responsible for difficultto-treat infections, such as wound infections, urinary tract infections, pneumonia, sepsis, and endocarditis. An unknown proportion of the general public has been exposed to MRSA, and some may be carriers of the bacterium. Healthy individuals may carry MRSA asymptotically for periods ranging from a few weeks to many years. Several studies have shown that the MRSA colonization rate among veterinarians is about 10 to 20%. This is higher than the general public. Thus, a cat catching MRSA from a veterinarian may be more likely than from the owner. Routine MRSA screening of the staff is not practical because transiently contaminated staff will not be recognized. Nurses should not refuse to care for a patient with MRSA but should be familiar with MRSA management. MRSA prevention and infection-control strategies include meticulous hand hygiene. This includes regular hand washings between patients using alcoholic gels; covering all cuts, abrasions or lesions, especially those on hands and forearms, with a waterproof dressing; avoiding invasive procedures when having chronic skin disease; and wearing gloves when in contact with potentially infectious material. Wearing aprons, scrubs, hats, masks, and even eye protection when aerosolization is likely may reduce the risk of cross-contamination. Hospital waste should be properly disposed.
Surface Hygiene The level of cleanliness in various areas of the hospital is determined by the risk of infection, the procedures carried out in that area, and the needs of the individual patients. The goal is to remove contaminants instead of spreading them.
958
Viruses, bacteria, fungi, spores, and Mycoplasma Virus, bacteria, and fungi Virus, bacteria, and fungi Virus, bacteria, fungi, worms, worm eggs, andcoccidia Encapsulated viruses, bacteria, and fungi
Resistant to neutralizing by organic matter, non-corrosive Works at low temperatures, non-corrosive Works at low temperatures Works at low temperatures Very broad spectrum of activity Good bacterial and fungal control
Surface hygiene is achieved by organizing the cleaning process properly. Cleaning should always be directed from ceiling to floor or from the cleanest to the dirtiest. The cleaning interval should fit to the purpose. High-risk areas include the operating room, dental operatory, laboratory, isolation area, and cages. Cleaning should be done either on a terminal, daily, weekly, or monthly basis depending on the use, risk, and patient. Terminal cleaning must be carried out before the ward or cage can be reopened after heavy contamination. Terminal cleaning methods vary but usually include removing all detachable objects in the ward or cage, cleaning lighting and air duct surfaces in the ceiling, and cleaning everything downward to the floor. All items removed from the room are disinfected or sanitized before being returned. Instructions on surface cleaning include: • All cages should be thoroughly cleaned and disinfected between patients. • All surfaces in direct contact with cats should be left in contact with disinfectant for 10 to 15 minutes, if possible, or steam cleaned. • Equipment, such stethoscopes, clipper blades, scissors, and pen lights, should be cleaned with 0.5% chlorhexidine solution after each use if an infectious disease is suspected. Ultrasound probes usually need a special cleaning solution. • Cat carriers, table tops, scales, and such should be immediately disinfected after use. • Cats should not be moved from one cage to another cage during the visit. • Critical touch areas, objects, or surfaces near patients or touched immediately after the patient has been touched should receive special attention. These include faucets, cage doors, computer keyboards, scales, infusion pumps, and door handles. • Infectious material from biological spots should be removed only after being decontaminated using disinfectant-soaked paper towels.
Instrument Hygiene Veterinary practices should also introduce an instrument hygiene policy with established routines. It is important to emphasise to the staff that the correct procedures must be followed every time an instrument is cleaned and sterilized. It is important to stress that it is often impossible to identify infected cats based on their appearance. The only way to avoid the risk of cross-contamination in the hospital is to ensure an optimum hygiene procedure for every cat. Instrument cleaning and sterilization procedures should include: • Handling before Sterilization: Instructions must be given for placement of dirty instruments after use and in the sterilization room. This
Hospital Hygiene
•
• • •
•
will prevent dirty instruments from becoming mixed with clean instruments. Protocol during the Sterilization Process: The instructions must be followed. Remember to validate your autoclave according to regulations in your country and test your autoclaves on a regular basis. Handling after Sterilization: Do not mix sterilized instruments with dirty instruments. Stamp the date of sterilization on the envelopes. Handling during Surgery: Aseptic techniques should be carried out. Employee Information: It is important to ensure that all employees are instructed according to the rules in the hospital. Manuals must be kept updated and accessible. Evaluations: Evaluate each hygiene protocol on a regular basis using proper tests or indicators.
If the aforementioned procedure is not strictly followed, it will be impossible to ensure that instruments are sterilized.
Suggested Readings American Association of Feline Practitioners. 2001. Basic Guidelines for Judicious Therapeutic Use of Antimicrobials in Cats, www.catvets.com/ professionals/guidelines/publications/?Id=179 Lappin MR. 2001. Hospital biosecurity. In MR Lappin, ed., Feline Internal Medicine Secrets, pp. 407–410. Philadephia: Hanley & Belfuss, Inc. Mayne T. 2006. MRSA in veterinary practice: What is your responsibility? Veterinary Management for Today. (6):17–19. Vision Online. Suffolk: AT Veterinary Systems. Polton G, Elwood C. 2006. Wash your hands! Control of nosocomial infections. In Practice. 28:548–550. London: British Veterinary Association. BC Centre for Disease Control. 2003. A Guide to Selection and Use of Disinfectants, www.bccdc.org/downloads/pdf/epid/reports/ CDManual_DisinfectntSelectnGuidelines_sep2003_nov05-03.pdf. www.catvets.com/uploads/PDF/antimicrobials.pdf www.vmd.gov.uk/Publications/Antibiotic/antimicrob120707.pdf.
959
CHAPTER 323
Life Stage Guidelines AAFP/AAHA
Editor’s Note These guidelines are a very important step forward to assure that cats get the proactive health care they deserve. The AAFP/AAHA Feline Life Stage Guidelines were originally published in the Journal of the
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
960
American Animal Hospital Association and are reproduced here with permission of the American Association of Feline Practitioners and the American Animal Hospital Association (aahanet.org). For additional AAHA guidelines, go to aahanet.org.
AAFP–AAHA Feline Life Stage Guidelines
Amy Hoyumpa Vogt, DVM, DABVP (Canine and Feline), Guidelines Co-Chair Ilona Rodan DVM, DABVP (Feline), Guidelines Co-Chair Marcus Brown, DVM Scott Brown, VMD, PhD, DACVIM C A Tony Buffington, DVM, PhD, DACVN M J LaRue Forman, DVM, DACVIM Jacqui Neilson, DVM, DACVB Andrew Sparkes, BVetMed, PhD, DipECVIM, MRCVS Corresponding authors (Co-Chairs): A Hoyumpa Vogt,
[email protected] I Rodan,
[email protected]
Background and Goals Cats have become the most popular pet in the United States, yet statistics about veterinary care for cats remain troubling.1 Although most owners consider their cats to be family members, cats are substantially underserved, compared with dogs. In 2006, owners took their dogs to veterinarians more than twice as often as cats, averaging 2.3 times/year, compared with 1.1 times/year for cats, and significantly more dogs (58%) than cats (28%) were seen by a veterinarian one or more times/year.2 Cat owners often express a belief that cats ‘do not need medical care’. Two reasons for this misconception are that signs of illness are often difficult to detect, and cats are perceived to be self-sufficient.2 One role of the veterinarian is to develop a partnership with cat owners that will pave the way for a lifelong health care plan. These guidelines aim to outline an evidence-based life stage wellness program to aid the veterinary medical team in delivering the best comprehensive care for cats. Specific goals are to provide: • Recommendations for optimal health care for cats throughout the different life stages. • Practical suggestions and tools to facilitate improved veterinary visits and to enhance the client–veterinarian clinical encounter. • A foundation from which to access sources of additional information.
Life Stage Classification Distinct life stages (age groups) in cats are not well defined, in part because individual animals and body systems age at different rates, a process that is influenced by many factors. These guidelines follow one convenient classification (see box on the next page). These age designations help to focus attention on the physical and behavioral changes that occur at different stages (eg, congenital defects in kittens, obesity prevention in the junior cat). It must be recognized, however, that any age groupings are inevitably arbitrary demarcations along a spectrum, and not absolutes.
The AAFP and AAHA welcome endorsement of these guidelines from the European Society of Feline Medicine, and acknowledge the help of the Feline Advisory Bureau’s WellCat for Life programme in helping to formulate the guidance. 70
JOURNAL of the American Animal Hospital Association
961
These guidelines follow a convenient life stage classification developed by the Feline Advisory Bureau and adopted in the recent AAFP Senior Care Guidelines.4,5 Six age groupings are defined, from kitten through to geriatric.
Evidence-based Health Care Supporting references for specific recommendations are supplied where possible, and any previously published guidelines on particular topics are referred to where relevant. Readers should note, however, that the guidelines panel was hampered in its efforts by the relative paucity of disease incidence data by age group that is available, and there is an urgent need for research to guide the future of evidence-based feline health care.3
Getting Started: The Wellness Exam To achieve optimum feline health care, veterinarians must help owners to understand and appreciate the importance of regular preventive care for their cats at all ages. A consistent message from the entire health care team is crucial, beginning with the first kitten visit and reinforced during subsequent visits. Early detection of clinical abnormalities and behavioral changes can improve disease management and quality of life.5,6
How Frequent? The panel supports the recommendations of the American Association of Feline Practitioners (AAFP) and American Animal Hospital Association (AAHA) that a minimum of annual wellness examinations and consultations for all cats 962
is justifiable. More frequent examinations may be recommended for seniors and geriatrics, and cats with medical and behavioral conditions. Semi-annual wellness exams are often recommended for all feline life stages by veterinarians and veterinary organizations. Their reasoning includes the fact that changes in health status may occur in a short period of time; that ill cats often show no signs of disease; and that earlier detection of ill health, body weight changes, dental disease, and so on, allows for earlier intervention. In addition, semi-annual exams allow for more frequent communication with the owner regarding behavioral and attitudinal changes, and education about preventive health care. Further research is needed to identify the optimal examination schedule to maximize the health and longevity of the cat. The panel members concluded that preventive veterinary care can improve quality of life, detect illness earlier and, therefore, reduce the long term expenses associated with a cat’s health care. They believe that cat owners are willing to seek more veterinary care when it improves quality of life and detects illnesses earlier, thereby reducing the long term expenses associated with their cat’s health care. Improved client communication and education of the benefits of regular veterinary care are essential to achieve that goal (Fig. 1).
Identification
Figure 1—The benefits of regular wellness exams often are not immediately apparent to pet owners and need to be well explained. Courtesy of Ilona Rodan.
The reasons pet owners have cited for not seeking care were that they did not know it was necessary, the veterinarian did not recommend it, and the need or benefit was not well explained.7 Other obstacles include the cat’s stress or fear associated with veterinary visits and the practical difficulties of transporting cats to receive veterinary care. Suggestions for overcoming such barriers are provided on page 77.
History-taking It is not the intent of the panel to reiterate the basics of the veterinary visit, but instead to offer a checklist to assist the veterinarian (see Table 1). Where relevant, aspects of feline behavior, nutrition, and various disease prevention and detection strategies are expanded on in the text. History-taking includes the use of open-ended questioning (eg, ‘How has [cat’s name] been doing since the last visit?’).8 This approach is often combined with a template or checklist, such as given in Table 1, to ensure important aspects are not overlooked.
Physical Examination When performing the physical exam, particular attention should be paid to:
According to one study, 41% of people looking for their lost cats considered them to be indoor-only pets.9 American Humane Association records reveal that only about 2% of lost cats ever find their way back from shelters, a major reason being the lack of tag or microchip identification. Assuring the identification of all pet cats, regardless of their lifestyle, is recommended to increase the prospect of lost cats being returned to their owners. The wellness examination is the ideal time to discuss the importance of identification with owners. The benefits of both visible (eg, collar and tag) and permanent (microchip) identification should be explained and compliance with identification recorded in the medical records along with other elements of the history.
Specific recommendations about age and frequency of laboratory testing depend on many factors.5,18,24 One consideration in determining this frequency is that the incidence of many diseases increases as cats age. Guidelines for management of mature, senior and geriatric cats may be found in the AAFP Senior Guidelines.5 Retroviral testing is discussed in detail in the AAFP Retrovirus Testing Guidelines.22 Measurement of blood pressure is discussed in detail in the ACVIM guidelines.25 Although limited incidence studies have been performed to identify the age of onset of hyperthyroidism in cats, the panel recommends that veterinarians strongly consider T4 testing in the apparently healthy mature cat. More robust incidence data is needed to develop firmer recommendations.
Nutrition and Weight Management Diet Basics Energy and nutrient needs vary with life stage, sterilization status and activity, and so general feeding recommendations provide only a starting point. Individual intakes must then be adjusted to maintain the desired weight and body condition score (Fig. 2).
• Observing the cat from a distance to assess breathing patterns, gait, stance, strength, coordination and vision. • Changes in parameters from prior exams (body weight, body condition score [BCS], vital signs). • Other specifics as noted in the discussion/action items in Table 1.
The Minimum Database Although specific data documenting benefits are not available, the panel concluded that regular wellness examinations and collection of the minimum database (MDB; Table 2) can be valuable, allowing early detection of disease or trends in clinical or laboratory parameters that may be of concern. Additionally, it provides a baseline for interpretation of data recorded at subsequent visits.
Figure 2—Regular assessment of weight and body condition score is important in cats of all ages—and this needs to be stressed to owners. Expressing any changes in weight as a percentage, or in terms of an equivalent weight loss/gain in humans, can be helpful. Courtesy of Deb Givin. 963
964
Table 1 Wellness Visit: Discussion and Action Items General discussion/ action items ALL AGES
Specific discussion/action items KITTEN (0-6 m)
General
Educate/discuss: • Recommended frequency of veterinary visits (the panel recommends a minimum of annual exams) • Early and subtle signs of pain or illness; importance of prevention and early detection of disease • Health-care financial planning • Disaster preparedness • Estate planning • Microchipping
Discuss: • Breed health-care predispositions • Claw care and alternatives to declawing • Congenital/ genetic concerns
Behavior and environment
Ask about: • Housing (indoor/outdoor) • Hunting activity • Children and other pets in the home • Environmental enrichment (eg toys, scratching posts) • Behavior • Travel (regional diseases)
• Confirm adequate resource allocation and play with appropriate toys • Teach commands (eg come, sit) • Acclimate to car and veterinary visits
JUNIOR (7 m-2 y)
• Inter-cat interactions and social play may decline or deteriorate with maturity • Provide continued training to allow manipulation of mouth, ears and feet
ADULT (3-6 y)
MATURE (7-10 y)
SENIOR (11-14 y)
GERIATRIC (15+ y)
This age group is often overlooked and would benefit from regular veterinary care
Specific management of mature and older cats is described in the AAFP Senior Care Guidelines5 and AAHA Senior Care Guidelines for Dogs and Cats18
• Review environmental enrichment • Teach techniques to increase the cat’s activity (eg, retrieve) • Encourage object and interactive play as a weight management strategy
Increased importance of good/easy accessibility to litter box, bed, food
• Environmental needs may change (eg, with osteoarthritis): ensure good/easy accessibility to litter box, soft bed, food • Educate clients about subtle behavior changes that are not “just old age”
• Ensure accessibility to litter box, bed, food • Monitor cognitive function (vocalization/ confusion), signs of pain/osteoarthritis • Discuss quality of life issues
(Continued on next page)
Table 1 (continued) Wellness Visit: Discussion and Action Items General discussion/ action items ALL AGES
Specific discussion/action items KITTEN (0-6 m)
JUNIOR (7 m-2 y)
ADULT (3-6 y)
MATURE (7-10 y)
SENIOR (11-14 y)
GERIATRIC (15+ y)
Discuss baseline adult data to assess subsequent changes (weight, BCS, MDB, etc)*
• Monitor for subtle changes such as increased sleeping or decreased activity • Increase focus on mobility, duration and/or progression of any specific signs
Increase focus on mobility, duration and/or progression of any specific signs
Increasing importance for regular review of medications and supplements
Review the size and edge height of litter box to ensure the cat can enter easily as it ages
Adjust litter box size, height and cleaning regimes as necessary
Medical/ surgical history; sterilization
Ask about: • Previous medical/surgical history • Medications • Over-thecounter items (eg supplements, parasiticides, alternative medications)
Discuss sterilization, including pros and cons of surgery at different ages
• Sterilization, if not yet done • Discuss establishing baseline data to assess subsequent changes (weight, BCS, MDB, etc)*
Elimination
Discuss: • Urinary tract health and methods of encouraging healthy litter habits • Elimination habits (frequency, quantity and quality), and litter box management (number, size, location, cleaning, etc)
Litter box set-up, cleaning and normal elimination behaviour10
Confirm that litter box size accommodates growing cat
* See text discussion. m = months, y = years, BCS = body condition score, MDB = minimum database
(Continued on next page)
965
966
Table 1 (continued) Wellness Visit: Discussion and Action Items General discussion/ action items ALL AGES
Specific discussion/action items KITTEN (0-6 m)
JUNIOR (7 m-2 y)
ADULT (3-6 y)
Monitor for weight changes and feed to moderate body condition. (Caloric needs decrease after sterilization and increase in breeding females)
Feed to moderate body condition. Monitor for weight changes and modify food intake accordingly.
Nutrition and weight management*
• Discuss eating behavior, diet(s) and feeding recommendations • Stress importance of regular assessment of weight and BCS
• Feed to moderate body condition • Discuss growth requirements and healthy weight management • Introduce to a variety of food flavors/ textures19
Oral health*
• Discuss dental health and home care • Monitor and discuss dental disease, preventive care, dental prophylaxis and treatment
Educate/ discuss: • Mouth handling, teeth brushing and alternatives • Permanent tooth eruption (timing and signs)
Monitor and discuss
MATURE (7-10 y)
SENIOR (11-14 y)
GERIATRIC (15+ y) Feed to moderate body condition. Monitor food intake and BCS/weight changes
Monitor for oral tumors, and inability to eat and decreased quality of life from painful dental disease
Coordinate: • Any requested deciduous tooth care with sterilization (simultaneous anesthesia)
* See text discussion. m = months, y = years
(Continued on next page)
Table 1 (continued) Wellness Visit: Discussion and Action Items General discussion/ action items ALL AGES
Specific discussion/action items KITTEN (0-6 m)
JUNIOR (7 m-2 y)
ADULT (3-6 y)
MATURE (7-10 y)
SENIOR (11-14 y)
GERIATRIC (15+ y)
Parasite control*
• Tailor laboratory evaluation to lifestyle • Evaluate changing or different risk based on geographic prevalence and travel • Discuss zoonotic risks. Heartworm prevention recommended for all cats in endemic areas.20
Deworming every 2 weeks from 3-9 weeks of age; then monthly until 6 months of age. Fecal exams 2-4 times during the first year of life.
Continue fecal exams 1-4 times/ year depending on health and lifestyle factors
Conduct fecal exams 1-2 times/year, depending on health and lifestyle factors
Vaccination21,22
Core vaccines: • Feline panleukopenia virus • Feline herpesvirus 1 • Feline calicivirus • Rabies virus Tailor: • Vaccine protocols to individuals and state regulations, considering benefits and risks, environment, and referring to current guidelines
FeLV vaccine highly recommended for kittens due to unknown future lifestyle. Review, complete, continue vaccination series
Review, complete, continue vaccination series. Review vaccine history/viral screening
Continue core vaccines as per current guidelines. Evaluate risk assessment and use of non-core vaccines, if indicated, as per current guidelines.
* See text discussion. m = months, y = years, BSC = body condition score, MDB = minimum database
967
Overcoming Barriers to Veterinary Visits The panel recommends that the veterinary team endeavours to make the veterinary encounter comfortable for both cat and client. Integral to this is a better understanding of feline behavior.10,11 Some specific tips to help minimize the challenges associated with bringing a cat to the clinic are given below. Once the client arrives at the veterinary clinic, the health-care team can take steps to reduce stress for both the client and the cat, as is feasible for their situation.12 See below for some ideas for the waiting client and cat, and some tips to facilitate examination and treatment. Reducing the stress of transport • Socialize kittens to the carrier and to travelling: – Keep the transport carrier out and accessible in the home. – Create and maintain a positive association with the transport carrier by making it a comfortable resting, feeding or play location. – When feasible, and if the cat is neutral or favorably inclined to car travel, encourage owners to take the cat on periodic car rides paired with positive experiences. • Withholding food prior to travel may prevent motion sickness, increase interest in treats at the clinic, and is beneficial if blood is to be collected. • Apply a calming synthetic pheromone to, and/or place familiar clothing from a favorite person in, the carrier on a routine basis and just prior to transport.13,14 • Provide cover/hiding options in or over carrier (eg, blanket draped over carrier) during transport. Making the cat and client comfortable at the clinic • Provide a separate waiting room for cats, or ensure their immediate placement into an exam room. • Minimize waiting times. • Provide elevated platforms in the waiting area so owners can place cat carriers out of reach of dogs. • Use calming synthetic pheromones in the environment.14 Facilitating the examination and treatment • Provide a cat-friendly exam room: – Keep the room and table warm, with a non-slip surface for the cat. – Avoid loud noises or ambient sounds that may mimic hissing (eg, whispering). – Distract and reward with tasty treats/catnip/play. • Handle using minimal restraint: – See AAFP Feline Behavior Guidelines for tips on handling cats during the veterinary examination.10 – While gathering historical information, allow the cat time to adjust to the surroundings by removing the top or opening the door of the carrier. The cat should ideally remain in the bottom half of the carrier for as much of the exam as possible; this allows it to adjust to the examiner and the environment.15,16 – Allow the cat to hide partially under a towel; use towels, rather than scruffing, for handling where additional restraint is needed. – Avoid making eye contact with the cat. – Determine the most comfortable position for the cat during the examination, such as the veterinarian’s lap. – Use sedation, anesthesia or analgesics as indicated to reduce stress and/or pain. • Keep hospitalized cats away from dogs and out of visual range of other cats.17 Supplementary Data An AAFP position statement entitled ‘Respectful handling of cats to prevent fear and pain’ is available at www.catvets.com and included in the online version of this article at doi:10.1016/j.jfms.2009.12.006
968
Satisfactory diets for cats contain all the required nutrients in proper balance, are palatable and digestible, and are free of spoilage and contaminants. The specific source of nutrients in feline diets is irrelevant when these criteria are satisfied.26 Both canned and dry food have been found to support health during all life stages.27 The presence of a label guarantee that the food was tested using feeding trials provides the current best initial evidence that a diet is satisfactory. The panel examined published peer-reviewed evidencebased studies in healthy, client-owned cats for any significant health effect of: feeding canned versus dry food (including contribution to dental health); providing a variety of foods versus a consistent diet; feeding high protein, low carbohydrate versus lower calorie and high fiber diets; feeding raw diets; providing dietary supplements, or access to grass or plants. Based on the available data, specific recommendations in favor of any of these practices cannot be made. Despite the concern surrounding the effects of carbohydrate in dry foods, current evidence suggests that housing and activity (which may be a marker of welfare)28 are more significant predictors of health.29–32 Evidence does not support the carbohydrate content of foods as being harmful or an independent risk factor for diseases such as obesity or diabetes.29,33 With regard to home-made foods, the veterinarian should discuss and share evidence about nutritional balance, risks associated with preparation and feeding of foods raw, and advantages of using food formulated for cats, referring clients to additional resources if required (Table 3).
Feeding Regimens A variety of feeding styles can maintain good health in client-owned cats, including free choice or provision of meals. In addition to monitoring intake, considerations include: • Providing water via bowls, dripping faucets and/or fountains, to promote adequate intake. When increased water intake is desirable, feeding of canned foods may help achieve this. • Locating food in a quiet area, especially for nervous or fearful cats (eg, away from other animals or household items that may make noises intermittently).34
Factors to Consider When Changing the Diet • Provide amounts of the new diet equivalent to previous energy (versus volume) intake, adjusting the initial amount as needed to maintain moderate body condition. • Consider offering the new diet as a choice in the presence of the usual diet to enhance acceptability, and make diet changes gradually to minimize the risk of gastrointestinal upset in cats with a history of this response to dietary change. • Warm the food to body temperature; adding fish/clam juice may increase palatability for cats with a depressed appetite.
Table 2 The Minimum Database by Age Group Kitten/junior
Adult
Mature
Senior/Geriatric
CBC Hematocrit, RBC, WBC, differential count, cytology, platelets
+/-
+/-
+
+
CHEM screen As a minimum include: TP, albumin, globulin, ALP, ALT, glucose, BUN, creatinine, K+, phos, Na+, Ca2+
+/-
+/-
+
+
Urinalysis* Specific gradient, sediment, glucose, ketones, bilirubin, protein23
+/-
+/-
+
+
T4*
+/-
+/-
+
Blood pressure*
+/-
+/-
+
Retroviral testing
+
+/-
+/-
+/-
Fecal examination*
+
+
+
+
* See text discussion. CBC = complete blood count, RBC = red blood cells, WBC = white blood cells, CHEM = chemistry, TP = total protein, ALP = alkaline phosphatase, ALT = alanine aminotransferase, BUN = blood urea nitrogen, T4 = thyroxine
969
Table 3 Web Resources for Feline Health Care Veterinarian/ clinic
Clients/ pet owners
General wellness information Feline Advisory Bureau (FAB) WellCat for life downloads: Veterinary Handbook
www.fabcats.org/wellcat/publications/index.php
Wellcat Log
www.fabcats.org/wellcat/owners/index.php
✓
Morris Animal Foundation ‘Happy Healthy Cat Campaign’
www.research4cats.org/
✓
Veterinary Partner
www.veterinarypartner.com
✓
CATalyst Council
www.catalystcouncil.org/
✓
AAHA Compliance Study7
www.aahanet.org
✓
Veterinary Information Network
www.vin.com
✓
Cornell Feline Health Center videos and health information
www.vet.cornell.edu/FHC/
✓
✓
The Ohio State University Indoor Cat Initiative
www.vet.osu.edu/indoorcat.htm
✓
✓
www.hsus.org/pets/pet_care/cat_care/keeping_ your_cat_happy_indoors.html
✓
✓
✓
Behavior, environment and the veterinary encounter
Humane Society of The United States – indoor cats AAFP Feline Behavior Guidelines (also includes feeding tips)
www.catvets.com/professionals/guidelines/ publications/?Id=177
✓
FAB information and Cat Friendly Practice Scheme: The Cat Friendly Home Bringing Your Cat to the Vet Creating a Cat Friendly Practice, Cat Friendly Practice 2
www.fabcats.org/catfriendlypractice/guides.html
Dumb Friends League ‘Play with Your Cat’
www.ddfl.org/behavior/catplay.pdf
✓
Your Cat’s Nutritional Needs – A Science-Based Guide for Pet Owners
http://dels.nas.edu/dels/rpt_briefs/cat_nutrition_final.pdf
✓
American College of Veterinary Nutrition—links to nutrition information websites
www.acvn.org/site/view/58669_Links.pml; jsessionid=20s028q8i1ewt
✓
www.catvets.com/professionals/guidelines/ publications/?Id=176
✓
www.abcd-vets.org
✓
www.fabcats.org/behaviour/cat_friendly_home/info.html www.fabcats.org/catfriendlypractice/leaflets/vets.pdf
✓ ✓ ✓
Nutrition and diet
Medical/dental care AAFP Vaccination Guidelines European Advisory Board on Cat Diseases (ABCD) infectious diseases guidelines
(Continued on next page)
970
Table 3 (continued) Web Resources for Feline Health Care Veterinarian/ clinic
Clients/ pet owners
Medical/dental care (continued) AAFP Zoonoses Guidelines
www.catvets.com/professionals/guidelines/ publications/?Id=181
✓
AAFP Retrovirus Testing Guidelines
www.catvets.com/professionals/guidelines/ publications/?Id=178
✓
AAFP Bartonella Panel Report
www.catvets.com/professionals/guidelines/ publications/?Id=175
✓
AAFP Senior Care Guidelines
www.catvets.com/professionals/guidelines/ publications/?Id=398
✓
AAHA Senior Care Guidelines for Dogs and Cats
http://secure.aahanet.org/eweb/dynamicpage. aspx?site=resources&webcode=SeniorCare Guidelines
✓
AAHA Dental Care Guidelines for Dogs and Cats
http://secure.aahanet.org/eweb/dynamicpage. aspx?site=resources&webcode=DentalCare Guidelines
✓
Veterinary Oral Health Council
www.vohc.org/
✓
AAHA–AAFP Pain Management Guidelines for Dogs & Cats
www.aahanet.org/PublicDocuments/ PainManagementGuidelines.pdf
✓
www.catvets.com/professionals/guidelines/ publications/?Id=174
✓
International Veterinary Academy of Pain Management
www.ivapm.org
✓
Veterinary Anesthesia & Analgesia Support Group
www.vasg.org
✓
Information for veterinary and medical professionals
www.capcvet.org
✓
Information for cat owners
www.petsandparasites.org/cat-owners/
Centers for Disease Control and Prevention (CDC) zoonoses information
www.cdc.gov/ncidod/dpd/animals.htm
✓
American Heartworm Society
www.heartwormsociety.org/
✓
✓
Parasite prevention Companion Animal Parasite Council:
✓
✓
Supplementary Data Table 3, with hyperlinks to the listed web resources, is available at doi:10.1016/j.jfms.2009.12.006
971
• Offering dry foods in foraging devices (eg, food balls or puzzles),35 and in multiple small meals in several widely dispersed bowls to slow intake and increase mental and physical activity.
Weight Management Obesity may occur at any age, but is most commonly encountered in middle age.32,36 The risk of obesity may be reduced by environmental enrichment, increasing opportunities for activity, and individualizing food intake. The energy density of cat foods varies widely, based on the moisture and fat content of the diet. This information should be helpful in determining a guideline of how much to feed. Tips and items for discussion with clients include: • Slowly (<10% increments and decrements) adjust calorie intake to life stage and conditions (eg, sterilization, indoor housing). • Provide environmental enrichment to increase activity.35 • Switch to a diet with lower energy density (reduced fat, increased air, fiber and/or moisture). • Change the feeding strategy. • Switch to meal feeding, with portion control. • Introduce foraging devices (see above). • Introduce barriers to food access (eg, baby gates, elevated feeding stations).
Behavior and Environment An outline of behavior and environmental items for discussion at each life stage is presented in Table 1. The following discussion elaborates on those items, where applicable. For detailed recommendations about normal cat behavior and management refer to the AAFP Feline Behavior Guidelines.10
All Ages • Provide plentiful resources – hiding spots, elevated resting spots, food, water, scratching posts and litter boxes – throughout the home, particularly for cats kept indoors and in multi-cat households (Fig. 3). • Controversy exists over whether cats should be kept indoors-only or in an indoor/outdoor environment (see box on page 82). These debates reflect geographical and cultural differences, as well as individual owner preferences.30,37–41 They underline the importance of providing an appropriate and stimulating environment for the cat.35
Kitten • Play: Kittens have a high play drive; inter-cat social play peaks at about 12 weeks of age,45 then object play becomes prevalent. Toys offer an outlet for normal predatory sequences as part of play, and help prevent play biting.
c Figure 3—Environmental needs change with life stage, although environmental enrichment and adequate resource allocation remain important for all cats. While play and play items are a priority for the kitten and junior (a and b), easy access to a soft bed (c) and a comfortable resting spot, such as a sofa (d), assumes more importance in the senior and geriatric cat. Pictures (a), (b) and (d) courtesy of Deb Givin; (c) courtesy of Ilona Rodan.
a
b
d 972
Lifestyle Choices • Indoor-only: An indoor-only lifestyle may decrease the risks of trauma and certain infectious diseases and increase longevity, but may also increase the risks of compromised welfare and illness due to environmental limitations. Appropriate environmental enrichment is thus essential for maintaining the mental and physical well-being of cats.10,42–44 • Indoor/outdoor: An indoor/outdoor lifestyle may provide a more natural and stimulating environment for cats, but may also increase the risks of infectious disease and trauma, and result in increased predation on wildlife. Supervised or controlled outdoor access, for example via leashed walks or cat-proof enclosures, may reduce some of the risks otherwise associated with access to the outdoors, and has been recommended by the AAFP and others.10,40,44 Photo courtesy of Deb Givin.
• Litter boxes: Litter box set-up and cleaning is critical for box usage. Although individual preferences can vary, most cats prefer clumping litter46 and a clean box in an accessible but not busy location. Initially, kittens can be simultaneously offered a variety of litter box options to permit them to express personal preference through usage. Some cats may find scented litters aversive.47 • Socialization/handling: Kittens should be gradually and positively acclimated as early as possible to any stimuli or handling techniques that owners plan them to encounter during their lifetime (eg, children, dogs, nail trims, tooth and coat brushing, car transport). This can be accomplished with food or other appropriate rewards, avoiding interactive punishment as it may elicit defensive aggression.
Senior and Geriatric • Senior and geriatric cats exhibiting behavioral changes (eg, vocalization, changes in litter box usage) should always be evaluated for an underlying medical problem.5
Parasites Parasite control is important in cats of all ages. Prevention includes both animal and environmental control. The Companion Animal Parasite Council (CAPC) guidelines contain recommendations about prevention of ecto- and endoparasites, fecal testing, and more.20 The United States Centers for Disease Control and Prevention website (see Table 3) also provides information on a variety of zoonoses. Items for discussion are listed in Table 1, and a few specifics are expanded on below.
Junior • Inter-cat relations: The reduction in social play combined with the dispersal effect (when free-living offspring leave the family unit at about 1–2 years of age) means that inter-cat aggression may develop at this stage of life. • Litter boxes and elimination: Litter box rejection can stem from a variety of causes including litter type, box cleaning, box style, and box size. Cats have shown a tendency to prefer larger boxes.48,49 • Urine marking: Most intact cats and about 10% of sterilized cats mark their territory with urine.50 The onset of this behavior can coincide with sexual maturity.
Adult and Mature • Play: Declining play activity increases susceptibility to weight gain. In one study, three 10–15 min exercise sessions per day caused a loss of approximately 1% of body weight in 1 month with no food intake restrictions.51
Heartworm: Key Points • Although the incidence in cats is lower than it is in dogs (10–15% of the rate in dogs), both indoor and outdoor cats are at risk of heartworm infection. • Infection with even a small number of adult worms can cause severe disease. • Signs differ from those in dogs, tending to be nonspecific. • A combination of antigen and antibody testing increases the probability of an accurate diagnosis. • Adulticide treatment is currently not recommended for cats. There is no evidence that it improves survival in infected cats, and the death of adult worms can be life-threatening. • Monthly prophylaxis is both safe and effective. Some heartworm preventives also provide control of other parasites.
973
Kittens • Because prenatal infection does not occur in kittens, roundworm treatment given every 2 weeks can start at 3 weeks of age. Kittens may begin receiving a monthly general endoparasite preventive at 8–9 weeks of age.20
All Life Stages • Feces testing allows monitoring of compliance with preventive medication as well as diagnosis of some endoparasites not treated by broad-spectrum preventives. • Heartworm presents a risk at all life stages in endemic areas.52 Some points of note are listed in the box on page 82; additional details may be found on the websites of the CAPC and American Heartworm Society (see Table 3).
Vaccination
Client Communication and Resources Clients face a potentially overwhelming amount of information at each visit to the veterinarian, so effective communication is essential to allow cats to receive optimum health care. In addition to the literature created by veterinarians for their own clients, a vast number of other resources are available to assist veterinarians and their clients. Websites may be oriented towards pet owners, veterinarians, or both. Table 3 is limited to information about wellness, not disease, and is not intended to be exhaustive. These guidelines (which, at a later date, will be supplemented with additional links and materials to aid client education) are available online at www.catvets.com/ professionals/guidelines/publications/
Table 1 outlines the vaccination priorities to consider when designing a comprehensive, life stage-targeted wellness plan for a cat.
Dental Care common,53
Diseases of the oral cavity are extremely yet most owners are unaware that dental disease can threaten the health and welfare of their cat. The AAHA Dental Care Guidelines for Dogs and Cats provide details of dental care and dental charting.54 Points of note include: • Cats need home and veterinary dental care at all life stages (see Table 1). • Disease affecting the teeth and/or oral cavity can cause pain and may lead to disease elsewhere in the body. • A minimum schedule of annual examinations is recommended for cats with healthy dentition.54 • Client education is fundamental since cats may not show overt signs of pain and discomfort associated with oral disease:4 – Discuss owner-usable interventions that will maintain or improve dental health;55 for example, conditioning at home using treats to allow oral examination by lifting the lips. Although best started with kittens, older cats can be taught to accept brushing using positive interactions and rewards. – Dental diets, treats and chews exist, but do not all have equivalent efficacy and none substitute for veterinary dental care.56,57 The use of dental treats and chews may be a realistic, practical alternative to daily tooth brushing, although data about their comparative efficacy is lacking. The Veterinary Oral Health Council in the USA requires that strict standards are met before certification of food or treats for oral care.58
Evidence-based Wellness Although the panel’s objective to provide evidence-based guidelines for health care related to life stage was not fully realized, the profession could develop more accurate rec974
Key Points • These Life Stage Guidelines aim to enhance the health, welfare and longevity of cats by providing a concise template to help veterinarians, their staff and clients to improve preventive care. • Excellent resources are available to facilitate the design of a comprehensive, life stage-targeted wellness care plan for each cat. • Clear communication among veterinarians, support staff and pet owners should improve adherence to the wellness plan, thus improving the quality of health care delivered to cats. • More robust data about disease incidence by age would assist practitioners in determining the value and desired frequency of routine wellness testing.
ommendations through further research and through cooperation and data sharing. More robust data about disease incidence by age would assist practitioners in determining the value and desired frequency of routine wellness testing. In the meantime, we must rely on the available data, personal knowledge and experience to help owners maintain their cat’s health during its lifetime.
Acknowledgements The AAFP and AAHA would like to thank Boehringer Ingelheim, Merial Ltd, Pfizer Animal Health and IDEXX Laboratories for their sponsorship of these guidelines and their commitment to help the veterinary community develop projects that will improve the lives of cats.
References 1. Flanigan J, Shepherd A, Majchrzak S, Kirkpatrick D, San Filippo M. US pet ownership & demographics sourcebook. Schaumburg, IL: American Veterinary Medical Association, 2007: 1–3.
2. Lue TW, Pantenburg DP, Crawford PM. Impact of the owner–pet and client–veterinarian bond on the care that pets receive. J Am Vet Med Assoc 2008; 232: 531–40. 3. AHRQ. US Preventive Services Task Force grade definitions. Rockville, MD: Agency for Healthcare Research and Quality, 2008. http://www.ahrq. gov/clinic/uspstf/grades.htm (accessed June 1 2009). 4. FAB. WellCat for life veterinary handbook. Tisbury, Wiltshire, UK: Feline Advisory Bureau, 2008: 5. Available at www.fabcats.org/wellcat/ publications/index.php. 5. Pittari, J, Rodan I, Beekman G, et al. American Association of Feline Practitioners’ senior care guidelines. J Feline Med Surg 2009 11: 763–78. www.catvets.com/professionals/guidelines/publications/ ?Id=398 (accessed June 1, 2009). 6. Moffatt KS, Landsbery, GM. An investigation of the prevalence of clinical signs of cognitive dysfunction syndrome (CDS) in cats. J Am Anim Hosp Assoc 2003; 39: 512. 7. American Animal Hospital Association. The path to high-quality care: practical tips for improving compliance. (‘AAHA compliance study’). American Animal Hospital Association, 2003. Compliance follow-up study, American Animal Hospital Association, 2009. 8. Silverman J, Kurtz S, Draper J. Skills for communicating with patients. 2nd edn. Oxford, UK: Radcliffe Publishing, 2005: 43. 9. Lord LK, Wittum TE, Ferketich AK, Funk JA, Rajala-Schultz PJ. Search and identification methods that owners use to find a lost cat. J Am Vet Med Assoc 2007; 230: 217–20. 10. Overall K, Rodan I, Beaver V, et al. Feline behavior guidelines from the American Association of Feline Practitioners, 2004. www.catvets. com/professionals/guidelines/publications/?Id=177 (accessed Aug 17, 2009). 11. Feline Advisory Bureau. Bringing your cat to the vet. Cat Friendly Practice literature. www.fabcats.org/catfriendlypractice/leaflets/vets.pdf (accessed June 15, 2009). 12. McMillan J. Maximizing quality of life in ill animals. J Am Anim Hosp Assoc 2003; 39: 227–35. 13. Griffith CA, Steigerwald ES, Buffington CA. Effects of a synthetic facial pheromone on behavior of cats. J Am Vet Med Assoc 2000; 217: 1154–56. 14. Pageat P, Gaultier E. Current research in canine and feline pheromones. Vet Clin North Am Small Anim Pract 2003; 33: 187–211. 15. Belew AM, Barlett T, Brown SA. Evaluation of the white-coat effect in cats. J Vet Intern Med 1999; 13: 134–42. 16. Sparkes AH, Caney SM, King MC, Gruffydd-Jones TJ. Inter- and intraindividual variation in Doppler ultrasonic indirect blood pressure measurements in healthy cats. J Vet Intern Med 1999; 13: 314–18. 17. McCobb EC, Patronek GJ, Marder A, Dinnage JD, Stone MS. Assessment of stress levels among cats in four animal shelters. J Am Vet Med Assoc 2005; 226: 548–555. 18. Epstein M, Kuehn N, Landsberg G. AAHA senior care guidelines for dogs and cats. J Am Anim Hosp Assoc 2005; 41: 81–91. http://secure. aahanet.org/eweb/dynamicpage.aspx?site=resources&webcode =SeniorCareGuidelines 19. Bradshaw JW. The evolutionary basis for the feeding behavior of domestic dogs (Canis familiaris) and cats (Felis catus). J Nutr 2006; 136 (suppl): 1927S–1931S. 20. Companion Animal Parasite Council. CAPC recommendations: controlling internal and external parasites in US dogs and cats, 2008 general guidelines. www.capcvet.org/recommendations/ guidelines (accessed June 15, 2009). 21. Richards JR, Elston TH, Ford RB, et al. The 2006 American Association of Feline Practitioners Feline Vaccine Advisory Panel report. J Am Vet Med Assoc 2006; 229: 1405–41. www.catvets.com/professionals/guidelines/publications/?Id=176 22. Levy J, Crawford C, Hartmann, K, et al. American Association of Feline Practitioners’ feline retrovirus management guidelines. J Feline Med Surg 2008; 10: 300–16. 23. Lees GE, Brown SA, Elliott J, Grauer GF, Vaden SL. Assessment and management of proteinuria in dogs and cats. J Vet Intern Med 2005; 19: 377–85.
24. Richards J, Rodan I, Beekman G, et al. AAFP senior care guidelines for cats. 1st edn. 1998. www.catvets.com 25. Brown S, Atkins C, Bagley R, et al. American College of Veterinary Internal Medicine. Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats. J Vet Intern Med 2007; 21: 542–58. 26. NRC. Nutrient requirements of dogs and cats. Washington, DC: National Academies Press, 2006. 27. Plantinga EA, Everts H, Kastelein AM, Beynen AC. Retrospective study of the survival of cats with acquired chronic renal insufficiency offered different commercial diets. Vet Rec 2005; 157: 185–87. 28. Yeates JW, Main DCJ. Assessment of positive welfare: a review. Vet J .2008; 175: 293–300. 29. Slingerland LI, Fazilova VV, Plantinga EA, Kooistra HS, Beynen AC. Indoor confinement and physical inactivity rather than the proportion of dry food are risk factors in the development of feline type 2 diabetes mellitus. Vet J 2009; 179: 247–53. 30. Buffington CAT. External and internal influences on disease risk in cats. J Am Vet Med Assoc 2002; 220: 994–1002. 31. Robertson ID. The influence of diet and other factors on owner-perceived obesity in privately owned cats from metropolitan Perth, Western Australia. Prev Vet Med 1999; 40: 75–85. 32. Scarlett JM, Donoghue S, Saidla J, Wills J. Overweight cats: prevalence and risk factors. Int J Obes 1994; 18 (suppl): S22–S28. 33. Backus RC, Cave NJ, Keisler DH. Gonadectomy and high dietary fat but not high dietary carbohydrate induce gains in body weight and fat of domestic cats. B J Nutr 2007; 98: 641–50. 34. Masserman JH. Experimental neuroses. Sci Am 1950; 182: 38–43. 35. Ellis S. Environmental enrichment. Practical strategies for improving feline welfare. J Feline Med Surg 2009; 11: 901–12. 36. Lund EM, Armstrong PJ, Kirk CA, Klausner JS. Prevalence and risk factors for obesity in adult cats from private US veterinary practices. Intern J Appl Res Vet Med 2005; 3: 88–96. 37. Rochlitz I. A review of the housing requirements of domestic cats (Felis silvestris catus) kept in the home. Appl Anim Behav Sci 2005; 93: 97–109. 38. Clancy EA, Moore AS, Bertone ER. Evaluation of cat and owner characteristics and their relationships to outdoor access of owned cats. J Am Vet Med Assoc 2003; 222: 1541–45. 39. Neville PF. An ethical viewpoint: the role of veterinarians and behaviourists in ensuring good husbandry for cats. J Feline Med Surg 2004; 6: 43–48. 40. Toribio JLM, Norris JM, White JD, Dhand NK, Hamilton SA, Malik R. Demographics and husbandry of pet cats living in Sydney, Australia: results of cross-sectional survey of pet ownership. J Feline Med Surg 2009; 11: 449–61. 41. Rochlitz I. The welfare of cats. Dortrecht: Springer, 2005. 42. AAFP. Statement on confinement of owned indoor cats – December 2007. www.catvets.com/professionals/guidelines/position/?Id=293 (accessed June 15 2009). 43. Heidenberger E. Housing conditions and behavioural problems of indoor cats as assessed by their owners. Appl Anim Beh Sci 1997; 52: 345–64. 44. Rochlitz I. Recommendations for the housing of cats in the home, in catteries and animal shelters, in laboratories and in veterinary surgeries. J Feline Med Surg 1999; 3: 181–91. 45. Caro TM. Predatory behaviour and social play in kittens. Behaviour 1981; 76: 1–24. 46. Borchelt PL. Cat elimination behavior problems. Vet Clin North Am Small Anim Pract 1991; 21: 257–64. 47. Nielson J. Thinking outside the box: feline elimination. J Feline Med Surg 2004; 6: 5–11. 48. Neilson, JC. The latest scoop on litter. Vet Med 2009; 104: 140–44. 49. Horwitz DF. Behavioral and environmental factors associated with elimination behavior problems in cats: a retrospective study. Appl Anim Behav Sci 1997; 52: 129–37. 50. Hart BL, Barrett RE. Effects of castration on fighting, roaming and urine spraying in adult male cats. J Am Vet Med Assoc 1973; 163: 290–92.
975
51. Clarke DL, Wrigglesworth D, Holmes K, Hackett R, Michel K. Using environmental enrichment and feeding enrichment to facilitate feline weight loss. J Anim Physiol Anim Nutr (Berl) 2005; 89: 427. 52. Nelson CT, Seward RL, McCall JW. Guidelines for the diagnosis, treatment and prevention of heartworm (Dirofilaria immitis) infection in cats, 2007. www.heartwormsociety.org/veterinary-resources/felineguidelines.html 53. Lommer MJ, Verstraete FJ. Radiographic patterns of periodontitis in cats: 147 cases (1998-1999). J Am Vet Med Assoc 2001; 218: 230–34. 54. Holstrom SE, Bellows J, Colmery B, et al. AAHA dental care guidelines for dogs and cats. J Am Anim Hosp Assoc 2005; 41: 1–7. http://secure.aahanet.org/eweb/dynamicpage.aspx?site=resources& webcode=DentalCareGuidelines
55. Ray JD, Jr, Eubanks DL. Dental homecare: teaching your clients to care for their pet’s teeth. J Vet Dent 2009; 26: 57–60. 56. Logan EI. Dietary influences on periodontal health in dogs and cats. Vet Clin North Am Small Anim Pract 2006; 36: 1385–1401. 57. Harvey CE. Management of periodontal disease: understanding the options. Vet Clin North Am Small Anim Pract 2005; 35: 819–36. 58. Veterinary Oral Health Council. Protocols and submissions. http://www.vohc.org/protocol.htm (accessed Aug 17, 2009).
The need for Feline Life Stage Guidelines was identified by the CATalyst Council, a US initiative comprised of animal health and welfare organizations and corporations to champion the cat in response to statistics that show an increase in the pet cat population coupled with a decline in veterinary visits and increase in shelter population. The guidelines are one part of that effort. Visit www.catalystcouncil.org for more information, or contact:
[email protected] CATalyst Council PO Box 5872 Timonium, MD 21093, USA +1-866-979-0222
976
CHAPTER 324
Normal Laboratory Values Gary D. Norsworthy and Teija Kaarina Viita-aho
This chart is a compilation of normal values from several sources. Note that various laboratories and pieces of laboratory equipment often vary
in their normal values. Therefore, be sure to check with the laboratory or manufacturer when deviations occur.
Test
Normal Value or Normal Range
Units
Normal Value or Normal Range
Units
Serum Chemistry A:G Ratio Albumin Alkaline Phosphatase ALT (SGPT) AST (SGOT) Bicarbonate Bilirubin, Total BUN BUN-to-Creatinine Ratio Calcium Chloride Cholesterol Creatinine CO2, Total CPK GGT Globulin Glucose Magnesium Na:K Ratio Osmolarity, Calculated Phosphorus Potassium Protein, Total Sodium Triglyceride
0.35–1.5 2.5–3.9 6–102 10–100 10–100 17–21 0.1–0.4 14–36 4–33 8.2–10.8 104–128 75–220 0.6–2.4 15–21 56–529 1–10 2.3–5.3 64–170 1.5–2.5 32–41 299–330 2.4–8.2 3.4–5.6 5.2–8.8 145–158 25–160
— g/dL IU/L IU/L IU/L mEq/L mg/dL mg/dL — mg/dL mEq/L mg/dL mg/dL mEq/L IU/L IU/L g/dL mg/dL mEq/L — mOSm/kg mg/dL mEq/L g/dL mEq/L mg/dL
0.35–1.5 25–39 6–102 10–100 10–100 17–21 1.7–6.8 5–13 4–33 2.05–2.69 104–128 1.94–5.68 53–212 15–21 56–529 0.5–5 23–53 3.6–9.4 0.62–1.03 32–41 299–330 0.77–2.65 3.4–5.6 52–88 145–158 0.28–1.81
— g/L U/L U/L U/L mmol/L µmol/L mmol/L — mmol/L mmol/L mmol/L µmol/L mmol/L U/L U/L g/L mmol/L mmol/L — mmol/L mmol/L mmol/L g/L mmol/L mmol/L
Hematology WBC RBC HBG HCT MCV MCH MCHC Neutrophils Absolute Neutrophils Lymphocytes Absolute Lymphocytes Monocytes Absolute Monocytes Eosinophils Absolute Eosinophils
3.5–16 5.92–9.93 9.3–15.9 29–48 37–61 11–21 30–38 35–75 2500–8500 20–45 1200–8000 1–4 0–600 2–12 0–1000
103/mm3 106/mm3 g/dL % µ3 pg g/dL % — % — % — % —
3.5–16 5.92–9.93 93–159 29–48 37–61 11–21 300–380 35–75 2500–8500 20–45 1200–8000 1–4 0–600 2–12 0–1000
109/L 1012/L g/L % fl pg g/L % — % — % — % —
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
977
Test Basophils Absolute Basophils Platelets Reticulocyte Count Reticulocytes, Corrected Reticulocytes, Absolute Miscellaneous Bile acids, pre Bile acids, post Cortisol, resting Cortisol, post–ACTH Cobalamin (Vitamin B12) fTLI fPLI Folate Fructosamine Insulin, Basal Iron, Total Progesterone, anestrus or proestrus Serum or plasma, female Progesterone, diestrus or pregnancy Serum or plasma, female Testosterone Serum or plasma, male T3, Total T4, Total T4, Free
Normal Value or Normal Range
Units
Normal Value or Normal Range
Units
0–1 0–150 200–500 0.0–1.0 0.0–1.0 0–50,000
% — 103/mm3 % % /mm3
0–1 0–150 200–500 0.0–1.0 0.0–1.0 0–50,000
% — 109/L % % 109/L
1.5–5.0 7.5–15.0 1.0–5.0 5.0–12.5 — — — 9.7–21.6 190–400 35–200 68–215 <3.0
µg/L µg/L µg/dL µg/dL — — — µg/dL µmol/L pmol/L µg/dL mmol/L
3.7–12.3 18.4–36.8 27.6–138 138–245 290–1499 12–82 0.0–3.5 9.7–21.6 190–400 35–200 12.5–39.52 <0.3
µmol/L µmol/L nmol/L nmol/L ng/L µg/dL µg/dL µg/ml µmol/L pmol/L µmol/L nmol/L
50–220
mmol/L
5–22
nmol/L
1–20
nmol/L
0.3–6.1
ng/ml
40–150 0.8–4.0 0.9–2.5
mg/dL mg/dL ng/dL
1.2–3.8 12–60 12–33
nmol/L nmol/L pmol/L
Urinalysis Specific Gravity pH Protein Glucose Ketones Bilirubin Occult Blood WBC/HPF RBC/HPF Crystals Casts Squamous Epithe/HPF Bacteria
1.015–1.060 5.5–7.0 Negative Negative Negative Negative Negative 0–3 0–3 None 0–3 Hyaline 0–3 None
Coagulation Tests Prothrombin Time Plasma Protein APTT Fibrinogen Von Willebrand’s
9–12 5.3–7.9 18–22 100–400 70–180
1.015–1.060 5.5–7.0 Negative Negative Negative Negative Negative 0–3 0–3 None 0–3 Hyaline 0–3 None Sec g/dL Sec mg/dL %
9–12 53–79 18–22 2.9–11.6 70–180
Sec g/L Sec µmol/L %
ACTH, adrenocorticotropic hormone; A:G, albumin to globulin; ALT, alanine transaminase; APTT, activated partial thromboplastin time; AST, aspartate aminotransferase; BUN, blood urea nitrogen; CO2, carbon dioxside; CPK, creatine phosphokinase; fTLI, feline trypsin-like immunoreactivity; fPLI, feline pancreatic lipase immunoreactivity; GGT, gamma-glutamyl transpeptidase; HBG, hemoglobin; HCT, hematocrite; HPF, high power field; K, potassium; MCH, mean corpuscular hemoglobin; MCHC, mean corpuscular hemoglobin concentration; MCV, mean corpuscular volume; NA, sodium; RBC, red blood cell; SGOT, Serum glutamic oxaloacetic transaminase; SGPT, erum glutamic-pyruvic transaminase; WBC, white blood cell.
978
CHAPTER 325
Pregnancy, Parturition, and Lactation Teija Kaarina Viita-aho
Pregnancy Overview Queens reach puberty by 4 to 12 months of age. The onset of puberty is most closely linked to growth rate and rarely occurs before the female has reached 2.5 kg (5.5 lbs) of body weight. Oriental cats (i.e., Siamese, Burmese and foreign short hair cats) tend to mature much earlier than other breeds, whereas longhaired and British Shorthairs may not mature until 1 year of age. Queens are seasonally polyestrous, but indoor cats may show signs of estrous throughout the year. Cats have induced ovulation. Copulation causes luteinizing hormone (LH) release from the anterior pituitary, which induces ovulation. Ovulation usually occurs 24 to 48 hours after copulation. A single copulation may not be sufficient to induce ovulation; therefore, multiple copulations should occur in a short period of time to induce sufficient LH-release needed for ovulation. Average gestation length is 63 to 66 days. Pregnancy lasting at least 60 days is required for viable neonates. Surfactant needed for normal lung function of neonates is present around day 62. Increased litter size is associated with a shorter gestation period. Gestation length usually differs between breeds. Persians have a mean gestation length of 65 days, whereas Korats usually have a mean gestation period of 63 days. Some queens may show estrous-like behaviour during pregnancy.
Hormones of Pregnancy Progesterone secretion by corpora lutea begins 1 to 2 days after ovulation. The progesterone concentration increases through days 25 to 30, then it slowly declines throughout the rest of pregnancy and falls to nadir just before parturition. In addition, placental progesterone production starts about day 40. The progesterone level in a pregnant queen should be over 2.5 ng/mL (0.08 nmol/L). The maintenance of feline pregnancy requires serum progesterone levels above 1 to 2 ng/ml (0.03– 0.06 nmol/L). Normally progesterone levels range from 15 to 90 ng/mL (0.48–2.86 mmol/L) during pregnancy. Relaxin production begins around day 20 of gestation and continues throughout the remainder of pregnancy. Relaxin is important for softening the connective tissues that surround the pelvis. It also functions together with progesterone in maintaining the uterus in a quiescent state during pregnancy. Prostaglandin F2-α is produced beginning on about day 30 and reaches peak values at about day 45. A large increase in prostaglandin secretion occurs just before delivery. This increase of secretion plays an important role in initiating parturition. Prolactin levels increase significantly beginning at about day 35 and a sudden increase occurs just prior to parturition. Prolactin is important for development of mammary glands and initiation and maintenance of lactation. Mammary glands enlarge rapidly during the last week before parturition. Milk can usually be expressed from the mammary glands 24 to 48 hours before delivery.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Pregnancy Diagnosis Pregnancy can usually be confirmed by abdominal palpation as early as day 15, when the fetuses are evident as discrete, round, evenly spaced structures. Diagnosis by palpation is most successfully performed 3 to 4 weeks after mating. Individual fetuses become difficult to identify by abdominal palpation after day 35 because the fetuses grow and merge with each other and the placentas within the uterus. Abdominal distension usually becomes evident from about 5 weeks after mating. Hyperemia and swelling of teats occur 3 to 4 weeks after mating. However, that also happens in pseudopregnancy; therefore, it is not a good indicator of pregnancy alone. There are two imaging modalities used by practitioners to diagnose pregnancy, radiography, and ultrasonography. Survey radiographs usually show uterine enlargement at about days 25 to 30. The fetal skeleton is mineralized enough to be first visible at about days 36 to 45. See Figure 325-1. With ultrasonography small embryonic sacs are visualized by days 11 to 17. By days 15 to 23 small embryos attached to uterine wall can be detected. Heartbeat can be visualized from days 20 to 24 onward. See Figure 325-2. Thus, ultrasonography can firmly diagnose pregnancy about 2 weeks prior to radiography. Additionally, using ultrasonography unnecessary radiation to the neonates can be avoided.
Problems during Pregnancy Vaginal Discharge Vaginal discharge is never normal during pregnancy, and it should raise suspicion of an infection, abortion, or other problem in pregnancy.
Uterine Torsion Torsion of uterus occurs rarely in queens, but when it does it usually occurs in the second half of pregnancy. Unilateral torsion is more
Figure 325-1 The fetal skeleton is mineralized enough to be first visible at about days 36 to 45. This pregnancy is near term. Image courtesy Dr. Gary D. Norsworthy.
979
SECTION 8: Appendixes
Parturition Overview Neonatal survival is directly related to the quality of labor. Dystocia is not uncommon among cats; according to one study, approximately 15% of births needed veterinary intervention, and 8% of those resulted in caesarean section. It has been reported that Siamese and Siamese-related cats may have higher risk for dystocia than other breeds. See Chapter 60. Mammary glands enlarge rapidly during the last week before parturition. Milk can usually be expressed from the mammary glands 24 to 48 hours before delivery.
Phases of Parturition
Figure 325-2 Heartbeat can be visualized from days 20 to 24 onward. Color-flow Doppler allows visualization of fetal movement and blood flow (red and blue). Image courtesy Dr. Gary D. Norsworthy.
common; reasons for its occurrence include fetal movements in the uterus or movement of the queen. The uterine horn usually rotates around its long axis. The degree of torsion can vary, and clinical signs are more severe with the higher degree of torsion. Usually the queens are acutely very ill and painful, and there usually is mucoid, serosanguineous, or hemorrhagic vaginal discharge present. The abdomen may be distended, and if torsion happens shortly prior to parturition, it causes dystocia. Prompt surgery is needed.
Pregnancy Loss Midterm Abortion Midterm abortion is not an uncommon event during feline pregnancy. Reasons for pregnancy loss can be infectious or non-infectious. Infectious agents include bacteria, viruses and protozoa. Brucella spp., Salmonella spp., Escherichia coli, Streptococcus spp., and Mycoplasma felis are infectious agents known to cause abortions. However, bacterial infection as a cause of pregnancy loss is rarely reported in cats. Feline leukemia virus (FeLV) infection has been associated with epidemics of abortions in catteries. Feline immunodeficiency virus (FIV) can also be a cause of pregnancy loss in queens. There is some evidence that the feline enteric corona virus (FCoV) may be a reason for reproductive failure, abortion, and dead fetuses at birth. Feline herpesvirus1 infection can cause abortion in addition to upper respiratory disease. Infection or vaccination with a modified-live parvovirus vaccine usually causes either abortion or birth of kittens with cerebellar hypoplasia, depending on the stage of gestation at the time of viral exposure. Toxoplasma gondii is a protozoan parasite that causes neurologic disease and abortion in pregnant queens. Kittens infected transplacentally die soon after birth. Noninfectious causes of feline pregnancy loss include hypoluteoidism, chromosomal errors, improper diet, and administration of embryotoxic drugs or nutrients to the queen. Hypoluteoidism is defined as loss of pregnancy due to decline in serum progesterone concentration caused by dysfunction of corpora lutea. Dietary causes of abortion include severe malnutrition and taurine deficiency. Pregnancy loss may also be idiopathic.
980
Phase I of parturition begins at the first observed contractions and ends at the birth of the first kitten. The median duration of phase I is 30 to 60 minutes, and usually it takes less than 2 hours. Labor starts with mild straining and discomfort for 30 to 60 minutes changing to hard labor involving pronounced straining and discomfort, which usually lasts 5 to 10 minutes. Phase II, the time between the first and the last kittens, can vary greatly. Following the birth of each kitten, the queen may show no obvious signs of labor for periods of 30 to 120 minutes. However, usually the interval between kittens is less than 1 hour. In the majority of labors, phase II takes less than 6 hours, but sometimes it can take more than 24 hours. The placenta may be passed with each kitten or in conjunction with a following delivery. Normal postpartum vaginal discharge is brick red or reddish- to greenish-black in color, non-odorous, and diminishes over several days to 3 weeks. The average litter size is four kittens. Number of matings is not correlated to the litter size. The presence of offspring from more than one sire in the same litter, called super-fecundation, is common in cats. Usually the first litter is smaller than further litters. Litter size may also decrease by age. Burmese, Siamese and related breeds have bigger litter sizes, whereas Persians, Birmans, Abyssinians, and Somalis tend to have the smallest litters. Most non-pedigree kittens have a birth weight about 100 to 120 g (3.5–4.2 oz). Pedigree kittens can vary in birth weight between 80 and 140 g (2.7–5.0 oz) depending on the breed.
Lactation Passive Transfer of Antibodies One of the most important functions of lactation is passive transfer of maternal antibodies to the kittens so they are temporarily protected against infectious diseases. The serum concentration of passively acquired immunoglobulins in kittens is determined by (a) quantity of immunoglobulins in the colostrum, (b) volume of colostrum ingested, and (c) time of ingestion. Absorption of immunoglobulins is completed by 18 hours after birth, and kittens are unable to absorb immunoglobulins after that time. Maternal immunoglobulin G (IgG) is the predominant immunoglobulin acquired by ingestion of colostrum; its duration in the serum is longer than other immunoglobulins. The concentration of passively acquired IgG reaches a nadir at 4 to 6 weeks of age. Failure of passive transfer of immunity (FPTI) predisposes a kitten to infections leading to illness and death. It happens in kittens that fail to ingest adequate amounts of colostrums before cessation of intestinal absorption. Kittens at risk for FPTI include kittens from large litters, small or weak kittens, orphaned or rejected kittens, kittens from queens that fail to lactate on the day of birth, and kittens that must be removed before nursing to avoid neonatal isoerythrolysis (NI). It is suggested that administration of adult cat serum will successfully correct IgG deficiency
Pregnancy, Parturition, and Lactation
in colostrum-deprived kittens, producing serum IgG concentrations comparable to those nursed from birth to 6 weeks of age. The serum is given intraperitoneal or subcutaneouslyat 5 mL per kitten at birth and repeated at 12 and 24 hours postpartum; this is a total of 15 mL for each kitten. Milk ejection, or milk letdown, can be often induced pharmacologically. Oxytocin (0.25–1.0 unit per injection SC, IM, or IV) is given every 2 hours. Alternatively, metoclopramide (0.2 mg/kg PO or SC) can be given q12h as it stimulates prolactin secretion. Therapy is usually rewarding within 24 hours.
Problems Associated with Lactation Agalactia Agalactia is defined as a failure to produce milk. It can be primary (a lack of mammary gland development) or secondary (failure to eject milk). Secondary agalactia is more common than primary. Agalactia may occur secondary to premature parturition, severe stress, malnutrition, concurrent illness, metritis, or mastitis. The use of progesterone compounds late in gestation may also interfere with lactation. Treatment includes providing supplementation to the neonates and encouraging them to suckle to promote milk ejection, providing optimal levels of nutrition and adequate water to the queen, and treating any underlying disease.
Eclampsia Eclampsia is caused by hypocalcemia associated with lactation, and it usually occurs in queens nursing large litters during peak lactation. Nevertheless, it can also occur before parturition. Clinical signs may vary including lethargy, trembling and muscle fasciculations, facial pruritus, anorexia, weakness, and hypothermia. Diagnosis is made by history, physical examination, and demonstration of hypocalcemia. Nevertheless, some queens may have normal serum calcium levels, show clinical signs of hypocalcemia, and respond to treatment. Treatment with intravenous
calcium administration is typically successful. Give 10% calcium gluconate (0.5–1.5 ml/kg slowly IV). If 10% calcium chloride is used the dose is 0.15–0.5 ml/kg. Heart rate should be monitored carefully, and the administration should be stopped if bradycardia develops. See Chapter 60.
Neonatal Isoerythrolysis Cats with blood group B produce large amounts of anti-A-antibodies. Therefore, kittens of blood group A or AB born to B-queen will develop neonatal isoerythrolysis if they are allowed to ingest colostrum. Anti-Aantibodies in colostrum attack kittens’ red blood cells, which leads to intra- and extravascular hemolysis. Kittens are healthy at birth, but they become very ill within hours as they ingest colostrum. Clinical signs include sudden death, failure to suckle, the presence of red-brown urine due to hemoglobinuria, and severe pallor or icterus. Many cases are fatal. If kittens survive, tail or ear-tip necrosis may occur at 7 to 14 days of age. Breeds known to have high incidence of blood type B are Persian, Devon and Cornish Rex, British Shorthair, and Birman. Breeds with relatively low incidence of blood type B are Siamese and Burmese. Neonatal isoerythrolysis is avoided by restricting the access of kittens to colostrum for the first 24 hours. See Chapter 150.
Suggested Readings Root Kustritz MV. 2006. Clinical management of pregnancy in cats. Theriogenology. 66:145–150. Stabenfeldt GH, Pedersen NC. 1991. Reproduction and Reproductive Disorders. In NC Pedersen, ed., Feline Husbandry, pp. 129–162. Goleta, CA: American Veterinary Publications. Levy JK, Crawford PC, Collante WR, et al. 2001. Use of adult cat serum to correct failure of passive transfer in kittens. J Am Vet Med Assoc. 219(10):1401–1405. Sparkes AH, Rogers K, Henley WE, et al. 2006. A questionnaire-based study of gestation, parturition and neonatal mortality in pedigree breeding cats in the UK. J Feline Med Surg. 8:145–157.
981
CHAPTER 326
Purring Sharon Fooshee Grace
Overview Cats, both large and small, are among the most vocal of the carnivorous species. Three major types of vocalization have been identified in cats: sounds made with the mouth closed (purr and trill), sounds made with the mouth open and gradually closing during vocalization (miaows or meows), and sounds made with the mouth held open at a relatively constant position (i.e., growl, snarl, hiss, spit, shriek, and snarl). Purring occurs with the mouth held closed and continues through both inspiration and expiration. Interestingly, cats are able to continue purring when producing other types of vocalizations. Individual cats have unique aspects to their purr relative to tone, loudness, and amount of purring. Not all purring produces an audible sound, but the vibrations generated by the purr can be appreciated while holding the cat. This is a well-known fact among devoted cat owners. While most, if not all, cats can purr, some of the exotic species do not purr in the same manner as the domestic cat. For example, cats in the genus Panthera purr only during expiration instead of through the entirety of respiration, as occurs in small cats. Exotic cats, which are able to roar, lack the purring vocal cords and instead produce a combination roaring/growling sound when they purr. Some large cats, such as cheetahs, are noted for an especially loud purr.
Why Do Cats Purr? Cats purr under a wide range of circumstances, most notably in response to other cats and preferred humans. Because purring requires energy expenditure and is associated with a sustained increase in heart and respiratory rates, there is likely a biologic basis for it, but the specific function of purring and how it may benefit the cat remain unclear. It is likely that the purr represents a form of social or sexual communication between cats. It most often occurs when cats are contented or relaxed, and for this reason, one early researcher suggested that purring is the feline version of a smile. Situations known to elicit purring include recognition of friendly cats, a state of drowsiness, rolling and rubbing on a variety of surfaces, during eating, and when being petted by a human companion. Both the queen and her kittens purr during nursing. Purring may serve to communicate a sense of well-being and to promote bonding. Kittens begin to purr during suckling when only a few days old, and as the kitten matures, the purr can develop new inflections. By the third week of life, the intensity of the purring vocalization increases to a level sufficient for greeting other kittens. Those unfamiliar with cats are often surprised to learn that cats not only purr when content, but also when experiencing distress, pain, and during states of severe debilitation. It is theorized that purring may release endorphins or other substances, which could cause euphoria or soothe the cat during periods of emotional distress or physical discomfort. For example, queens are known to purr during the pain of parturition and terminally ill cats sometimes purr just before death. Purring is also used to communicate with humans. Stroking or petting of cats by humans often elicits a purr, most likely as a result of the cat’s attitude of contentment.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
982
Recent work has identified a unique “solicitation purr,” which contains a somewhat unpleasant high-frequency element embedded in the normal sounding purr. Contained within the normal low-pitched purr is a sound reminiscent of a cry or meow, suggesting a sense of urgency. This distinct type of purr was easily identifiable by humans who participated in the study, regardless of their familiarity with cats as a species. The exact purpose of this unique purr is unknown, but it is speculated that cats may use this vocalization when seeking food, attention, or other favors. Not all cats employ the solicitation purr, but some cats seem to use it to advantage.
How Do Cats Purr? Because the cat lacks a specific anatomical feature, which could create the sound, a definitive explanation for purring has remained elusive, although not for lack of speculation. The historical veterinary literature contains several hypotheses regarding the mechanism of feline purring. Early theories centered on vascular sources of the sound. One researcher suggested that turbulent flow of blood in the aorta might be responsible because cats often purr while arching their backs, thus creating a bend in the vessel where blood could eddy and create sound. Another scientist speculated that blood surging through the caudal vena cava was the source of the purr Present understanding suggests that extremely rapid, regular input from a neural oscillator (likely in the brain) to the intrinsic laryngeal muscles is the driving force behind purring. A rapid (approximately 25–30 times per second) stereotypical rhythmic opening and closing of the glottis produces changes in transglottal pressure which are only milliseconds in length. These fluctuations in airway pressure during steady inspiration and expiration produce air resonance and create sounds which are appreciated as the gentle buzz or rumble associated with purring. Other soft-tissue structures in the neck or thorax (including the intercostal muscles and diaphragm) may contribute to or modify the basic sound. The rapid cycle of events is virtually identical during inspiration and expiration, thus producing a continuous sound and allowing the cat to ventilate while purring. The most consistent frequency across all purring species is approximately 25 Hertz. In domestic cats, purring occurs in the frequency range of 25 to 150 Hertz. The recently documented solicitation purr contains peaks in the 220 to 520 Hertz range.
Therapeutic Effects of Purring? Bioacoustic research (i.e., the study of frequency, pitch, loudness, and duration of animal sounds) suggests that feline purring may have healing properties for both humans and cats. In human medicine, sound frequencies in the range of 20 to 50 Hertz are known to promote healing changes in the body and to relieve pain. Given that cats purr in this frequency range and that having a feline pet is associated with decreased stress, lower blood pressure, and an extended life span for older adults, perhaps purring does indeed have potential health benefits for humans. It is premature to draw such conclusions, but the possible association does warrant further study. Although evidence for it is weak at this time, some have speculated that purring may be associated with the relatively lower incidence of bone, joint, and cardiorespiratory problems in cats as compared to dogs.
Purring
Suggested Readings Beaver BV. 1983. Purr-fect communication. Vet Med Small An Clinic. 78(1):41. Beaver BV. 2003. Feline communicative behavior. In BV Beaver, ed., Feline Behavior: A Guide for Veterinarians, 2nd ed., pp. 100–126. Philadelphia: Saunders. Crowell-Davis SL, Curtis TM, Knowles RJ. 2004. Social organization in the cat: A modern understanding. J Feline Med Surg. 6(1):19–28. Friedmann E, Son H. 2009. The human-companion animal bond: How humans benefit. Vet Clin North Am Small Anim Pract. 39(2):293–326.
LeCouteur RA. 2009. Cats are not small dogs, The neurologist’s perspective. Feline Medicine Symposium Proceedings, University of California–Davis. McComb K, Taylor AM, Wilson C, et al. 2009. The cry embedded within the purr. Curr Bio. 19(13):R507–R508. McCuistion WR. 1966. Feline purring and its dynamics. Vet Med Small Anim Clinic. 61(6):562–566. Remmers JE, Gautier H. 1972. Neural and mechanical mechanisms of feline purring. Respir Physiol. 16(3):351–361.
983
CHAPTER 327
Renal Transplantation Daniel A. Degner
Introduction Chronic renal failure (CRF) in cats is a progressive, irreversible condition, which usually leads to death months to years after initial diagnosis as a result of uremia. Overall, approximately 2% of all cats will be diagnosed with CRF at some point in their life. CRF is a common disease in cats, especially older cats. Recent reports indicate that approximately 10 to 30% of cats 10 to 15 years of age and 32% of cats greater than 15 years of age are diagnosed with CRF. Therefore, this represents a common disease entity in cats. Cats with mild to moderate CRF may be managed medically with dietary and other forms of symptomatic medical management. However, such forms of therapy are largely ineffective in cats with advanced CRF. Renal transplantation has proven to be a successful alternative form of treatment. When treated with immunosuppressive drugs such as cyclosporine and prednisone cats do not have as great a problem with allograft rejection as do dogs. The major histocompatibility complex on feline red cells is similar to those found on endothelial cells of the kidney. As a result, only cross-matching is required for donor recipient compatibility. Using this type of donor recipient matching, hyperacute and acute rejection of renal grafts rarely occurs. Failure of renal grafts in cats usually is due to chronic vascular disease, which results in gradual occlusion of the arterial supply of the graft. This may take a number of years to develop.
Definition of Chronic Renal Failure Cats in CRF have blood urea nitrogen (BUN) and creatinine levels that are above normal range and urine specific gravity less than 1.035. Isosthenuria is common; however, be aware that specific gravity is not always a clear indicator of renal insufficiency in cats as it is in dogs and humans. The presence of clinical signs that suggest chronic renal disease include weight loss, anemia and small to normal kidney size.
Qualifications for Recipients Candidates should be free of underlying diseases. • Cardiomyopathy, if present, should not be severe. Mild to moderate hypertrophic changes may result from increased afterload caused by renal-induced hypertension. • Hypertension is common in cats that have renal failure due to an imbalance of the angiotensin system. Hypertension could lead to seizures, retinal detachment and other significant problems in the postoperative period. Hypertension should be under control with medication prior to surgery. Frequently cats will become normotensive following renal transplantation; if this does not occur, removal of the diseased native kidneys should be considered. • Diabetes mellitus is not an absolute contraindication for renal transplantation; however, it can lead to other complications such as urinary tract infection. • Hyperthyroidism can affect multiple body systems including heart, blood pressure, renal function, and body metabolism; therefore, it should be under control with medication prior to transplantation.
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
984
After transplantation has been completed and the cat is stable, radioiodine therapy should be considered. • Nephrolithiasis is not an absolute contraindication for transplantation; however, it may increase the risk for urinary tract infection or development of stones in the graft, especially if the cause of the stones is extrarenal. In summary, cats should be free of the aforementioned diseases; however, under the care of a diligent owner and internist, other coexisting diseases can be managed in the renal transplant patient.
Candidates Must Be Free of a Number of Diseases • Infections, such as chronic recurrent upper respiratory viral infection, feline leukemia virus (FeLV) infection, feline immunodeficiency virus infection, hemotrophic Mycoplasma, Toxoplasma, and urinary tract infection, to name a few, are contraindications for renal transplantation. • Urinary tract infection (UTI) or previous history of recurrent UTIs is a contraindication for a renal transplant because these cats develop UTI very readily when immunosuppressed with cyclosporine often leading to pyelonephritis and graft dysfunction. • Cats that have inflammatory bowel disease have a high risk of kidney rejection due to hyperimmunity. • No neoplastic or preneoplastic process can be present; cyclosporine immunosuppression will result in rampant cancer growth. • Renal amyloidosis is contraindicated as amyloidosis of the graft will occur. • Glomerulonephritis is a systemic disease that will destroy the graft.
Notes about Coexisting Conditions The presence of coexisting conditions do not necessarily preclude a cat from being a suitable transplant candidate. A cat that has had a previous upper respiratory viral infection or a past history or UTI can be challenged with cyclosporine (with trough blood levels greater than 500 ng/ mL) for 3 weeks; if the cat breaks with an infection, it is a poor candidate for transplantation. Cats that have chronic recurrent UTI are generally not acceptable candidates for transplantation. If a cat develops recurrent UTIs after receiving a renal graft, lifelong antibiotic therapy likely will be needed. Recipients should be in an early decompensated state of renal failure. Recipient cats that have not lost more than 20 to 30% of body weight are better candidates, as loss of a significant amount of weight may coincide with multiorgan disease. However, we have transplanted patients that had lost about 30 to 40% body weight, and they have done well. Anesthetic and surgical risks are increased in these patients.
Recipient Preoperative Workup • The recipient cat should be blood typed as the first step; the recipient should be type A. If the recipient does not have type A blood, transplantation is not advisable as an acceptable donor will be difficult, if not impossible, to identify. • Other tests that should be done include: major and minor red blood cell (RBC) cross-match, complete blood cell count (CBC), chemistry profile, urinalysis, T4, urine culture (collected by cystocentesis only;
Renal Transplantation
do not start antibiotics prior to urine culture), FeLV/FIV tests, hemotrophic Mycoplasma test (by polymerase chain reaction [PCR]), Bartonella by PCR, Toxoplasma titers, echocardiogram, thoracic and abdominal radiographs, renal ultrasound, fundic examination (to evaluate for hypertension), and Doppler blood pressure determination (do repeated evaluations under unstressed conditions). All blood and urine testing should be done by a reputable veterinary laboratory and not by in-house machines.
Recipient Preparation for Surgery Prior to surgery the renal transplant candidate should be in as good nutrition as possible. A good plane of nutrition should be established. Placement of a gastrostomy tube or esophagostomy tube may be important to provide adequate food intake prior to surgery. (We routinely place gastrostomy tubes at the time of transplant surgery, if it is not already in place.) Anemia should be corrected to at least a packed cell volume (PCV) of 30%. Erythropoietin (100 U/kg SC three times per week or 100 U/kg daily for the first 5 days, then a reduced frequency of administration to three times per week) may be administered. It is important to monitor the PCV closely while using this drug. Poor response or worsening of the anemia suggests that the patient is producing antibodies against the erythropoietin, necessitating discontinuation of the medication. Supplementation with vitamin B complex and iron may also help these patients. Blood transfusions, if needed, should be given 2 to 3 days prior to surgery; cross-matching is essential. Fluid therapy should be administered to decrease azotemia. Correction of electrolyte and acidbase balance should be done prior to anesthesia. Immunosuppressive therapy should be started 2 days prior to surgery using cyclosporine (2–5 mg/kg q12h PO; put in gel caps due to bitter taste). The specific cyclosporine product should be approved by the transplant team. Prednisolone (0.25 mg/kg q12h PO) should be started the day of surgery.
be done. Additional testing includes CBC, chemistry profile, urinalysis, urine culture, FeLV/FIV, hemotrophic Mycoplasma test, renal ultrasound, and abdominal radiographs. All blood and urine testing should be done by a reputable veterinary laboratory and not by in-house machines. Owners are to provide a kidney donor. Euthanasia of any kidney donor is strictly in violation of our transplant team’s policy.
Potential Postoperative Complications • • • • • • •
•
•
Complications are frequently related to immunosuppressive therapy. UTIs (most common). Viral upper respiratory infection. Fungal infection. Hypertension can be a side effect of cyclosporine resulting in seizures or blindness in the immediate postoperative period. Hydronephrosis due to ureteral obstruction (usually occurs within 3 weeks after surgery). Rejection of the transplanted kidney. Acute rejection can occur at any time if whole blood cyclosporine levels drop too low (i.e., below 100 ng/mL); hence, the importance of good client compliance and frequent measurement of cyclosporine levels cannot be overemphasized. Hemolytic uremic syndrome is a condition in which progressive anemia and potentially icterus develop due to hemolysis of red blood cells. The cause of this syndrome is believed to be related to cyclosporine, which causes endothelial injury. A CBC shows thrombocytopenia, anemia, and schistocytes; lactic dehydrogenase levels are elevated on a biochemical profile. A definitive diagnosis is based on renal graft biopsy, which demonstrates glomerular microthrombi. The prognosis is grave. Seizures as a result of the blood being cleansed too rapidly by the kidneys. This may be fatal. As mentioned previously hypertension may also cause seizures.
Kidney Donors The blood type of a kidney donor must be same as recipient. A donor must be an adult, healthy, large (4.5+ kg ([10+ lbs]), young cat (1–5 years of age) that is free of FeLV/FIV, UTI, toxoplasmosis, and major organ disease. Renal function must be normal. The donor kidney must have normal architecture on ultrasound imaging. The renal graft must have a single renal artery because the arterial renal blood supply is segmental. If a kidney has two arteries, ligation of one of these vessels will result in necrosis of a portion of the kidney. In addition, the diameter of each renal artery is usually too small to microsurgically anastamose to the aorta; a typical renal artery is 1.5 mm (1/16 in) in diameter. If double renal veins are present, the smaller is ligated and the larger of the two is anastamosed to the cava because the renal venous drainage system is not segmental.
Compatibility of Donor with Recipient The major histocompatibility complex antigens found on feline red blood cells are homologous to those found on the vascular endothelium of the kidneys; therefore, tissue typing has not been traditionally used to identify a suitable donor. To determine compatibility of the donor with the recipient, a major and minor red blood cell cross-match is performed. If the cross-matches are compatible, acute rejection is unlikely. In the rare situation, a cat will not cross-match with any donor due to the presence of idiotypic antibodies. Additional testing, such as the mixed lymphocyte reaction test, can be used to further define compatibility of the donor graft, but it is generally not needed.
Donor Preoperative Workup Blood type and red blood cell cross match with recipient should be done prior to any further testing; if the donor is a match, additional testing can
Postoperative Expectations We have approximately 90% of our patients survive the immediate perioperative period. Our longest survivor was 8 years. If a cat survives beyond the first 6 months, a major hurdle has been overcome. Roughly 40% of patients will die within the first 6-month period. If the transplant patient survives to 1 year and the renal values are still normal at that time, there is a good chance that this patient will survive for a number of years. My impression is that the cats that do the best are owned by clients that are diligent about follow-up evaluations and administering medications. With successful transplantation and function of the graft, the following clinical and biochemical progress of the recipient should be expected. (a) Most grafts begin producing urine within a couple of minutes of being reperfused; within 24 hours after transplantation, the BUN and creatinine are frequently about one-fourth to one-third less than the preoperative levels; BUN, creatinine, and phosphorus return to normal range within 2 to 5 days after surgery. Urine specific gravity may not concentrate to greater than 1.035 during the hospital stay due to diuresis with intravenous fluids. By 2 to 3 weeks after surgery the urine should be concentrated. Resumption of normal appetite and grooming behavior may take place 5 to 7 days after surgery. The quality of life of the patient returns to normal if the patient does not have any other underlying disease processes (i.e. normal activity level, weight, and appetite).
Postoperative Monitoring First 7 Days after Surgery • In addition to a complete physical examination, BUN, creatinine, glucose, PCV, total solids (TS), albumin, and electrolytes should be
985
SECTION 8: Appendixes
measured daily until renal values are normal then every second or third day while in our hospital. • Ultrasound of the kidney with Doppler color flow to evaluate renal perfusion is done during first 3 days then at the time of release from our hospital to evaluate renal perfusion and evaluate for hydroureter. The size of the kidney is measured; a kidney undergoing acute rejection may become enlarged. Ultrasound should be repeated 4 weeks after surgery to check for hydroureter and for renal perfusion. • Whole blood trough cyclosporine levels: Levels are measured on days 0, 3, and at the time of discharge. The levels should be tested more frequently if the levels are well out of expected ranges.
Release from Hospital to 12 Weeks after Transplantation (or until the Cyclosporine Level Is Stable) • Complete physical examination (including Doppler blood pressure, if previously hypertensive, and body weight), chemistry profile, CBC, urinalysis, urine culture, whole blood cyclosporine assays are performed weekly. Abdominal ultrasound is performed monthly. • Cyclosporine levels must be measured weekly for the first 12 weeks after surgery, then monthly for the next 6 months, then gradually wean down to an evaluation every 3 months. Blood levels must be maintained above 500 ng/mL during the first month and around 250 ng/mL thereafter.
• Contact a member of transplant team. • Refer the case back to us or to the nearest specialty referral practice that is capable of managing transplant cases. • Submit blood for stat measurement of at least the following (if you are not located near a referral center): BUN, creatinine, electrolytes, CBC, cyclosporine blood level, urinalysis, and urine culture. • Be prepared to treat cat with the following: cyclosporine (6 mg/kg q12h IV); prednisolone (4 mg/kg IV q24h); Baytril® (2.5 mg/kg q12h IV); ampicillin 20 mg/kg IV q6h; intravenous fluids. Other instructions may be directed by the transplant team. (Note that a Baytril dose of >5 mg/kg q24h may cause retinal problems in cats, especially those with renal compromise.) • Prepare to send the patient to a referral center.
Costs Costs will vary from one transplant site to another. On average, the owner should expect to pay $12,000 to $16,000 to get the donor and recipient through surgery and the postoperative hospitalization. Cyclosporine will cost approximately $100 per month. Follow-up examinations, including the necessary blood tests, may cost $400 to 500 per visit.
Summary • Chronic renal failure in cats usually is progressive and irreversible. • Renal transplantation is a viable option to control renal failure. • Transplantation improves the quality of life of the cat dramatically.
Twelve Weeks after Transplantation • Complete physical examination (including Doppler blood pressure, if previously hypertensive, and body weight), chemistry, CBC, urinalysis, urine culture (by cystocentesis collection), abdominal ultrasound, and whole blood cyclosporine assay is performed. The frequency of this testing is gradually reduced to once every 3 months.
Rejection of Renal Grafts Any signs of illness that the patient exhibits postoperatively may be associated with organ rejection. This could potentially be due to inadequate levels of cyclosporine. It is imperative that continuous communication between the owner, the referring veterinarian, and the transplant team members must occur to assure a successful outcome. If problems arise the following protocol should be used:
986
Suggested Readings Gregory CR. 1992. Renal transplantation for treatment of end-stage renal failure in cats. J Am Vet Med Assoc. 201:285–291. Lulich JP. 1992. Status of renal transplantation in the 1990s. Semin Vet Med and Surg Small Anim. 7:813–186. Gregory CR. 1993. Renal transplantation in cats. Compend Contin Vet Educ. 15:1325–1339. Gregory CR. 1992. Renal transplantation in clinical veterinary medicine: In JD Bonagura, ed., Kirk’s Current Veterinary Therapy XI, pp. 870–875. Philadelphia: WB Saunders Co. Degner DA, Walshaw R, Rosenstein D. 1994. A new rapid technique for renal transplantation in the cat. Proceedings of the Fifth Annual Research Day, Phi Zeta. Katayama M, McAnulty JF. 2002. Renal transplantation in cats: techniques, complications and immunosuppression. Compend Contin Vet Educ. 24(11):874–882.
CHAPTER 328
Vibrissae Sharon Fooshee Grace
Overview Vibrissae (whiskers) serve many important functions. As specialized tactile hairs, they constantly monitor the environment and channel sensory information to the cat’s nervous system. Vibrissae help the cat estimate the size, shape, and presence of objects without seeing or touching them. Because whiskers are freely movable, their position offers an outward indicator of a cat’s emotions and attitude about its immediate environment. Vibrissae are recognized as specialized hairs called “sinus hairs.” They are stiffer and several times thicker than other hairs and taper toward their distal ends. Vibrissae are contained in deeper, wider follicles than other hairs. Each follicle has at least one sebaceous gland and a bit of striated muscle attached to its outer layer, allowing for voluntary movement of the whisker. An endothelial-lined blood sinus is also found in these follicles. The follicular blood sinuses of facial whiskers are abundantly supplied with branches of the trigeminal nerve, although whiskers themselves do not contain nerves.
Locations Four sets of vibrissae are found on the head, and one set is on the forelimbs. See Figure 328-1. The largest and longest vibrissae are the mystacial whiskers found above the upper lips. They are anchored in tubercles or “whisker pads” on either side of the muzzle. Though there is great variation between cats, on average there are about 12 mystacial whiskers set in four rows on each side of the muzzle. The dorsal two rows can move independently of the lower two rows to improve precision when measuring surroundings. Rows two and three are said to contain the strongest whiskers. As the largest, longest, and most numerous of the vibrissae, the mystacial whiskers process and integrate more sensory information than the others. Superciliary vibrissae are located in tufts above each eye. These serve a protective function for the eye and can trigger a blink when stimulated. Small, poorly developed mandibular whiskers are located on the chin (submental organ). Two genal tufts containing a few hairs each are present on the cheeks; genal tuft one is just ventral to the base of each ear and genal tuft two is directly below genal tuft one. Genal tuft two is found along the angle of the mandible. Some cats have only one visible genal tuft. Carpal vibrissae are found on the caudal aspect of the forelimbs just proximal to the carpi. They are structurally identical to other vibrissae. These particular whiskers are sensitive to proximal displacement and are thought to aid in climbing or capturing prey.
Use in Hunting Domestic cats hunt for prey during daylight or dark. A cat with intact mystacial whiskers can make a clean kill regardless of available light. However, a cat without these whiskers misjudges the killing bite during dim light and plunges its teeth into the wrong part of the prey’s body. Cats have a particular dependence on their whiskers because although
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
Figure 328-1 From top to bottom, the arrows point to the superciliary, genal tufts, mystacial, and mandibular vibrissae of this kitten.
they have superior distance vision, they have limited visual accommodation for objects which are close, such as when a small rodent is near the mouth. Thus, the vibrissae are critical to help gauge the distance of close objects and facilitate the killing strike to the nape of the neck at precisely the right moment. Time-stop photography has shown that immediately before attacking, the cat can completely envelop the rodent inside a “basket-like” forward projection of the mystacial vibrissae. The whiskers remain in this position, transmitting information about status of the prey, as long as it is held in the mouth. Thus, during hunting, sensory information obtained via the vibrissae is coordinated with the input of visual information to the brain.
Positioning When a cat is angry or threatened, the mystacial vibrissae are flattened tightly against the sides of the head. During rest or when greeting a friendly cat, whiskers will variably be held in a neutral position out to the side of the face or lightly along the cheeks in a relaxed position. Mystacial whiskers can temporarily move forward for hunting or permanently assume this direction when vision is lost. Cats that lose their vision (including one owned by this author) may have their mystacial vibrissae permanently change direction over time and assume a forwarddirected position. It would be assumed that this permanent change in direction improves the ability of the blind cat to navigate in its environment and avoid bumping into objects.
Breed Variations Some breeds, such as the hairless Sphynx, may have few to no whiskers. Rex-related cats, noted for their curly coats, may also have curly whiskers or sometimes no whiskers. When present, their whiskers are often somewhat brittle and have a tendency to break.
987
SECTION 8: Appendixes
Shortening or Loss Whiskers are periodically shed by healthy cats, just as normal hair is shed. Lost whiskers will regrow and are typically replaced in a matter of a few months. Not uncommonly, the queen will shorten or bite off the whiskers of her kittens as she grooms them. This does not appear to cause any harm, and the whiskers will be replaced in time. Also, cats are sometimes reported to barber or chew off the whiskers of other cats in their household, though the reasons for this are unknown. Chewing off the whiskers of another cat is not a behavior commonly seen with allogrooming, but other than the loss of the whiskers, it is probably a harmless activity. Occasionally, cats are reported to even chew on their own whiskers. Although alopecia is not a common side effect of chemotherapy in cats, it does often result in whisker loss. This is most often associated with antitumor antibiotics, such as mitoxantrone and doxorubicin. See Figure 328-2. Whiskers will usually (but not always) regrow weeks to months after discontinuation of therapy. However, the new vibrissae may be more coarse and of a different color than the original whiskers. Whisker loss may be caused by the self-trauma associated with facial pruritus. Facial dermatoses should not be overlooked as a cause of whisker loss, even if the skin appears relatively normal. Cats are notoriously secretive and will sometimes have relatively normal appearing skin even with intense pruritus. Instead of scratching, some pruritic cats will simply lick themselves to excess. Differential diagnoses for facial pruritus include but are not limited to ear mites, food allergy, atopy, flea allergy, demodicosis, notoedric mange, cheyletiellosis, dermatophytosis, and Malassezia infection. A minimum diagnostic approach should include an otic examination, skin scraping, Wood’s lamp examination, and a dermatophyte culture.
Practical Considerations When a cat is provided food or water from a narrow bowl, the whiskers may come in contact with the sides of the dish and create a nuisance or
988
Figure 328-2 This cat has lost most of the mystacial whiskers as a result of chemotherapy with doxorubicin. irritation for the cat. This can be a special concern for cats reluctant to eat or drink, particularly when hospitalized. It is important to provide a food and water dish wide enough to accommodate the whiskers.
Suggested Readings Friberg C. 2006. Feline facial dermatoses. Vet Clin North Am Small Anim Pract. 36(1):115–140. LeCouteur RA. 2009. Cats are not small dogs. The neurologist’s perspective. Feline Medicine Symposium Proceedings, University of California–Davis. Morris D. 1996. Cat World: A Feline Encyclopedia. London: Ebury Press.
CHAPTER 329
Zoonotic Diseases Suvi Pohjola-Stenroos
Overview Zoonotic diseases are diseases being common to, shared by, or transmitted between humans and other vertebrate animals including cats. Transmission of zoonotic agents from cats to humans can occur by direct contact with the cat, indirect contact with secretions or excretions from the cat, or contact with vehicles like water, food, or fomites that were contaminated by the animal. Infective agents between cats and humans can also be shared by a vector or environmental exposure. Cats bring a lot of joy and happiness to humans. The majority of cats are kept as family members and good companions. However, there are also cat colonies: cattery cats, shelter cats, and the stray cat population. Most zoonotic infections can infect anyone. However, humans are unlikely to acquire infectious diseases from healthy, parasite free, indoor cats. Zoonotic infections in immunocompromized persons can be severe. Risk factors for acquiring a zoonotic disease are presented in Table 329-1. Zoonosis prevention is an important area of veterinary public health, including feline practitioners. Veterinarians and their staff have a significant role in supporting the human-cat interaction. This can be done by increasing knowledge of feline zoonotic agents including how to recognize, manage, and prevent them. Veterinary personnel should also be able to provide information regarding the effects of feline zoonotic dis-
eases on humans and be able to work in cooperation with family physicians regarding disease control. Selected feline zoonotic pathogens, including their occurrence, distribution, transmission, and clinical presentation in cats and humans, are presented in Table 329-2.
Diagnosis Diagnostic measures of selected feline zoonotic infections are listed in Table 329-3. More detailed information of various zoonotic infections is presented in Selected Readings.
Treatment Treatment protocols for feline zoonotic diseases are listed in short in Table 329-4. However, treatment of some infections can be controversial. Questions regarding when to treat, for how long to treat, and should the contact cats also be treated should be investigated in the literature before starting the treatment. Treatment should also include environmental decontamination and riding the affected cat of the pathogen to prevent reinfection. For more detailed information of this subject see Chapters 317 and 322. Recommendations for managing zoonotic diseases for both veterinary personnel and cat owners is given in Tables 329-5 and 329-6.
TABLE 329-1: Risk Factors for Acquiring a Zoonotic Disease Risk factor
Risk population
Risk level
Compromised immune system
Humans with HIV Humans on chemotherapy Humans with neoplasia Humans with inflammatory or immunemediated diseases Humans who have received organ or bone marrow transplants Elderly humans Humans born with congenital immune deficiencies Pregnant women Splenectomized Humans Cats in shelters and catteries Stray animals, cats shelters, and catteries, Humans
high high high high
Animals and humans in crowded environment Animals and humans in unknown environment Veterinary staff, breeders, and volunteers in shelters
varies
Dense animal population Environmental problems Feline behavioral problems, especially aggression Food and water hygiene problems Increased travel activity Occupation
high high high high high increased increased increased
increased relatively low
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
989
TABLE 329-2: Selected Feline Zoonotic Pathogens: Occurrence, Distribution, Transmission, and Clinical Presentation Human aspects related to cats
Geographic distribution
Uncommon in the Western world
Bartonella spp.
Agent
Transmission
Clinical signs in cats and humans
Global
Aerogenic, alimentary,contact infected organs
Relatively common in certain areas with fleas and ticks; risk to humans from fleas
Global
Cat bites, cat scratches, through fleas and ticks
Bordetella bronciseptica
Rare
Global
Aerogenic
Borrelia burgdorferi
Areas where Ixodes is present, shared vector
Global
Through ticks, Ixodes spp.
Campylobacter spp.
Occasionally associated with cat contact
Global
Alimentary
Capnocytophaga canimorsus Francisella tularensis
Extremely rare
Global
Cat bites
Rare in cats; hunters are especially susceptible
Global
Direct contact with infected organs and cat bites
Helicobacter spp
Although common in humans, rare in cats, reverse zoonosis possible Uncommon in Western countries
Global
Alimentary
Cat: subacute to chronic; carbuncular lesions of jowl and tongue; swelling of lips, head and throat Human: Cutaneous ulcer with necrotic center, pneumonia, bloody diarrhea, hematemesis, meningitis Cat: subclinical, uveitis, fever, neurological signs, gingivitis Human: lymphadenopathy, fever, malaise, bacillary angiomatosis, bacillary peliosis, etc. Cat: subclinical, coughing, upper respiratory pneumonia (rare) Human: pneumonia in immunosuppressed patients Cat: subclinical Human: rash, polyarthritis, myocarditis, neurologic disease Cat: subclinical, gastroenteritis Human: subclinical , bacteremia, gastroenteritis, myalgia, arthralgia, polyradiculoneuritis Cat: subclinical Human: bacteremia, keratitis Cat: septicemia, pneumonia Human: ulceroglandular, glandular, oculoglandular, pneumonic, or typhoidal Cat: subclinical, vomiting Human: subclinical, gastric ulcer
Global
Extremely rare, only two cat- associated cases reported Occurs, serious in immunosuppressed person Common, rare from cat contact
Global
Most often (aerogenic) infection from humans to animals (“inverse zoonosis”) Cat bites
Global
Cat bites
Global
Alimentary
Occurs, occasionally associated with cat
Global
Rodent fleas, cat bites, contact with exudates
Uncommon in the Western world, not definitively linked to cat contact
Global
Alimentary
Cat: subclinical Human: Hepatic and pulmonary disease
Common
Global
Contact, direct and indirect
Asymptomatic, skin lesions, pruritus
Occurs
Global
Contact
Occurs
Global
Contact
Cat: Asymptomatic, dandruff, pruritus Human: pruritus Cat: Asymptomatic, otitis externa Human: pruritus
Bacteria Bacillus anthracis
Mycobacterium spp.
Mycoplasma felis
Pasturella multocida Salmonella spp.
Yersinia pestis
Cestodes Echinococcus multilocularis Ectoparasites Ctenocephalides felis, Ctenocephalides canis Cheyletiella spp. Otodectes cynotis
990
Cat: Cutaneous lesions predominant Human: Respiratory disease
Cat: chronic draining tracts, polyarthritis Human: cellulitis, polyarthritis Cat: abscess or cellulitis Human: abscess or cellulitis Cat: subclinical or mixed large bowel diarrhea, bacteremia, abortion Human: subclinical gastroenteritis, abscesses Cat: bubonic, bacteremic, pneumonic Human: bubonic, bacteremic, pneumonic
TABLE 329-2: Continued Human aspects related to cats
Geographic distribution
Transmission
Clinical signs in cats and humans
Occurs
Global
Contact
Cat: Pruritic skin disease Human: Pruritic skin disease
Relatively common
Global
Skin contact
Rare
Most common in warm environment
Skin contact through scratches and bites, environmental pollutant
Cat: subclinical, superficial skin disease Human: superficial dermatologic disease Cat: Chronic draining of cutaneous tracts Human: Chronic draining of cutaneous tracts
Uncommon
Global
Alimentary, skin contact
Dirofilaria immitis
None except as a shared vector
Mosquito bites
Strongyloides stercoralis
Rare
Toxocara cati
Uncommon
Mediterranean, Africa, Asia, South America Global, highest prevalence in tropics and subtropics Global
Protozoan Cryptosporidium spp.
Relatively common
Global
Alimentary
Giardia spp.
Relatively common
Global
Alimentary
Toxoplasma gondii
Uncommon
Global
Alimentary, transplacentally
Rickettsiae and Chlamydiae Chlamydophila psittaci, Occurs Chlamydophila felis
Global
Aerogenic
Coxiella burnetii
Extremely rare
Unknown
Blood sucking arthropods, ingestion of contaminated material, aerosol from infected tissue
Viruses Poxviridae Genus Orthopoxvirus
Uncommon
Contact with infected skin
Cat: circumscribed, ulcerative, pruritic skin lesions, and mild conjunctivitis Human: papulovesicular skin disease
Rhabdoviridae Genus Lyssavirus
Uncommon in Western world
Global, endemic among small rodents in areas of Scandinavia Global, except Australia, Iceland, Sweden, MainlandNorway, United Kingdom
Saliva, usually through bites
Cat: Progressive central nervous system disease Human: Progressive CNS disease
Agent Sarcoptes scabiei var. canis Fungi Microsporum canis, Trichophyton mentagrophytes, Epidermophyton Sporothrix schenkii
Nematodes Ancylostoma spp., Unicinaria stenocephala
Alimentary, skin contact
Alimentary
Cat: subclinical hemorrhagic diarrhea, blood loss anemia Human: pruritic skin disease (cutaneous larva migrans) Cat: Asymptomatic, coughing, vomiting, sudden death Human: subclinical pulmonary mass Cat: subclinical, hemorrhagic diarrhea Human: Pruritic skin disease, disseminated disease in immunosuppressed persons Cat: subclinical, vomiting, failure to thrive Human: subclinical, cough, ocular disease Cat: subclinical or small bowel diarrhea Human: subclinical or small bowel diarrhea Cat: subclinical or small bowel diarrhea Human: subclinical or small bowel diarrhea Cat: subclinical, fever, uveitis, muscle pain, hepatic inflammation, pancreatitis Human: subclinical, lymphadenopathy, abortion, stillbirth, encephalitis Cat: subclinical, conjunctivitis, upper respiratory signs Humans: conjunctivitis Cat: subclinical, abortion, stillbirth Human: fever, pneumonitis, myalgia, lymphadenopathy, arthritis, hepatitis, endocarditis
991
TABLE 329-3: Diagnostic Modalities of Zoonotic Diseases in Cats Agents Bite or Scratch
1. 2. 3. 4. 5. 6. 7.
Enteric Agents
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 1. 2. 3. 4. 5. 6. 7.
Exudate and Skin
Bartonella spp. Capnocytophaga spp. Mycoplasma felis Pasteurella spp. Fransicella tularensis Yersinia pestis Rabies Dipylidium caninum Echinococcus multilocularis Toxocara cati Ancylostoma spp. Ucinaria stenocephala S.stercoralis Cryptosporidum spp. Toxoplasma gondii Giardia spp. Salmonella spp. Campylobacter spp Escherichia coli Helicobacter spp. Microsporum canis Ctenocephalides felis Cheyletiella spp. Sarcoptes scabei Notoedres cati Sporotrix schenkii Yersinia pestis
1. Western blot test, culture 2. Polymerase chain reaction culture 3. Polymerase chain reaction 4. Culture 5. Culture 6. Cytology for bipolar rods, culture, serology inform public health officials 7. Serology, animal inoculation, inform public health officials 1. Segments or egg packets in feces 2. Eggs in feces 3. Eggs in feces 4. Diarrhea, anemia, eggs in feces 5. Anemia, eggs in feces 6. Recover larvae in feces 7. Oocysts in feces or fecal antigen detection 8. Oocysts in feces; serology 9. Cysts in feces or detection of coproantigen 10. Fecal culture 11. Fecal culture 12. Fecal culture 13. Fecal culture 1. Culture, hair microscopy 2. Observation, detection of flea feces, signs of flea allergy 3. Finding mites, eggs on hair shafts, tape test 4. Finding mites in skin scrapings 5. Finding mites in skin scrapings 6. Cytology of the exudate, culture 7. Cytology for bipolar rods, culture, serology, inform public health officials 1. Serology, culture 2. Culture 3. Polymerase chain reaction, culture 4. Culture 5. Tick identification, culture, serology 6. Cytology for bipolar rods, culture, serology, inform public health officials
Respiratory Tract
1. 2. 3. 4. 5. 6.
Urogenital Tract
1. Coxiella burnetii 2. Leptospira interrogans
1. Culture 2. Culture
Vector
1. 2. 3. 4. 5. 6. 7.
1. Clinical signs, detection of microfilariae (rare), or antigen or antibodies detected in blood 2. Microscopy of Giemsa stained blood smear, serology, polymerase chain reaction 3. Host physical examination for fleas, blood culture, polymerase chain reaction, serology 4. Serology, polymerase chain reaction 5. Microscopy of Giemsa stained blood smear, serology, polymerase chain reaction 6. Tick identification, serology 7. Culture, serology
992
Bordetella bronchiseptica Staphylococcus spp. Chlamydophila felis Coxiella burnetii Francisella tularensis Yersinia pestis
Diagnosis
Dirofilaria immitis Anaplasma phagocytophilum Bartonella henselae Borrelia burgdorferi Ehrlichia spp. Rickettsia felis Francisella tularensis
TABLE 329-4: Treatment for Feline Zoonotic Diseases Drug
Dosage
Organism/Parasite
Amoxicillin Amoxicillin- clavulanate
10–22 mg/kg q12h PO 15 mg/kg q12h PO
Ampicillin Azithromycin
22 mg/kg q8h IV 7.5–10 mg/kg q12–72h PO
Clarithromycin Clindamycin Doxycycline
7.5 mg/kg q12–24h PO 10–12 mg/kg q12h PO 5–10 mg/kg q12–24h PO
Enrofloxacin
5 mg/kg q24h PO
Enrofloxacin Erythromycin
5 mg/kg q24h SC or IV 10 mg/kg q8h PO
Fenbendazole
50 mg/kg q24h PO
Fipronil
7.5–15 mg/kg topical 0.25% spray and 10% spot on
Fipronil-methoprene
7.5–15 mg/kg topical spot on
Fluconazole
50 mg/cat q12-24h PO
Griseofulvin (microsize) Griseofulvin (ultramicrosize) Imidacloprid Itraconazole
50 mg/kg q24h PO 5–10 mg/kg q24h PO 10–20 mg/kg topical spot on 5 mg/kg q12h PO for 4 days, then 5 mg/kg q24h PO
Ivermectin
24 µg/kg q30d PO
Ivermectin
200–300 µg/kg q7d PO
Lime sulphur dip Lufenuron
Metronidazole
Dip q5–7d 80–100 mg/kg q14d PO 30 mg/kg q30d PO 10 mg/kg q180d SC 25 mg/kg q12h PO
Streptococcus group A Bartonella spp. Bordetella bronchiseptica Pasteurella multocida Leptospira spp. Cryptosporidium spp. Bartonella spp. Helicobacter spp. Toxoplasma gondii Anaplasma phagocytophilum Bordetella bronchiseptica Bartonella spp. Chlamydophila felis Ehrlichia spp. Mycoplasma felis Bartonella spp. Campylobacter spp. Mycoplasma felis Yersinia pestis Salmonella spp. bacteremia Bartonella spp. Campylobacter spp. Ancylostoma spp. Giardia spp. Strongyloides stercoralis Toxocara cati Tick Fleas Tick Fleas Dermatophytes Sporotrix schenkii Dermatophytes Dermatophytes Fleas Dermatophytes Sporotrix schenkii Dirofilaria immitis Ancylostoma Uncinaria Cheylietella Sarcoptes scabiei Dermatophytes Dermatophytes Fleas
Miconazole and 2% Chlorhexidine Milbecycin
Dip q3–4d 0.5–1.0 mg/kg q30d PO
Paromomycin Praziquantel
150 mg/kg q12h PO for 5 days 5 mg/kg once PO, SC, or IM
Pyrantel
20 mg/kg once PO, repeat in 3 weeks
Pyrantel plus praziquantel
72.6 mg pyrantel and 18.2 praziquantel; 1 tablet/cat PO
Selamectin
6 mg/kg q30d topically
Terbinafine Tylosin
20 mg/kg q24–48h PO 10–15 mg/kg q12h PO
Entamoeba histolytica Giardia spp. Dermatophytes Dirofilaria immitis Ancylostoma spp. Toxocara cati Cryptosporidium spp. Dipylidium caninum Echinococcus multilocularis Ancylostoma spp. Strongyloides stercoralis Toxocara cati Ancylostoma spp. Toxocara cati Cestodes Ancylostoma spp. Toxocara cati Dermatophytes Cryptosporidium spp.
993
TABLE 329-5: Recommendations for Veterinary Personnel for Managing Feline Zoonotic Diseases Education
Familiarize yourself and your staff about zoonotic issues. Discuss the health risks and benefits of cat ownership with your clients; help them decide the management needed. Inform public health authorities if a reportable zoonotic disease is diagnosed.
Clinical actions
Vaccinate all cats against rabies. Routinely administer antihelmintics to kittens at 3, 5, 7, and 9 weeks of age to control nematodes. Routinely administer monthly heartworm preventative in endemic areas. Routinely administer monthly taeniacides to cats allowed outdoor in areas endemic for Echinococcus multilocularis. Test all cats for gastrointestinal parasites at least once yearly. Recommend a diagnostic workup when a disease with zoonotic potential is likely. Offer the following diagnostics for all cats with 1–2 days diarrhea and for cats owned by immunosuppressed individuals: 1. Zinc sulfate centrifugation and microscopic evaluation for oocysts, cyst, and eggs. 2. Fecal wet mount to evaluate trophozoites of Giardia spp. and Tritrichomonas spp. 3. Rectal cytology to look for white blood cells and spirochetes consistent with Campylobacter spp. 4. Cryptosporidium spp. screening by indirect fluorescent antibody (IFA), antigen enzyme-linked immunosorbent assay (ELISA), or acid-fast stain. 5. Fecal culture for Salmonella spp. and Campylobacter spp. Maintain flea and tick control.
Occupational Health
Do not allow clients to restrain cats during procedures. Do not attempt to pull cats from their carriers. Train staff on how to handle cats to avoid bites and scratches. Use feline pheromones at the clinic to calm cats. Provide rabies vaccination for all staff members handling cats in endemic areas. Evaluate rabies antibodies of the staff members handling cats every 2 years. Follow your written hospital hygiene policy.
TABLE 329-6: Recommendations for Cat Owners for Preventing Feline Zoonotic Diseases When adopting a new cat
If you are an immunocompromized person consult your physician and veterinarian before adopting a new cat. Adopt a preferable clinically normal, arthropod-free, adult cat from private family. Do not handle cat with which you are unfamiliar. Quarantine the new cat (owned by immunosuppressed persons) until physical examination and zoonosis risk assessment has been completed by the veterinarian. Consider keeping the cat indoor to reduce the risk for acquiring zoonotic agents.
Diet
Only feed cats cooked or commercially prepared food. Prevent the cat from drinking unpasteurized milk. Prevent the cat from hunting or eating prey. Cook meat for human consumption to 80°C (175°F) for a minimum of 15 minutes. Wear gloves when handling meat, and wash your hands afterwards. Wash garden produce before consumption.
Grooming
Have your cat’s claws clipped frequently. Have your cat bathed as needed. Use a good flea and tick control on a regular basis.
Hygiene
Avoid handling unhealthy cats, particularly those with gastrointestinal, respiratory, skin, neurologic, or reproductive disease. Do not allow cats to drink from the toilet. Wash your hands after handling cats. Remove fecal material from the litter box or environment daily. Avoid, if possible, permitting an immunocompromised person from cleaning the litter box. If you are an immunocompromised person, wear gloves when cleaning litter boxes, and wash your hand afterward. Use litter box liners when possible. Clean the litter box with scalding water and detergent or with steam cleaner. Wear gloves when gardening. Cover children’s sandboxes to avoid fecal contamination of outdoor cats. Filter and boil water from environmental sources before consumption. Do not share food utensils with cats. Avoid being licked on the face by the cats. When bitten, rinse the bite wound or skin scratch immediately with plenty of cool running water before contacting physician.
Veterinary Care
Have your cat seen by a veterinarian at least one times a year, and preferably twice per year. Have all new cats examined by your veterinarian. Seek immediate veterinary care for all unhealthy cats. Keep all vaccinations current. Vaccinate against rabies at appropriate intervals. Have your cat’s feces checked for parasites periodically. Have your (particularly outdoor or new) cat checked for the feline leukemia virus and feline immunodeficiency virus.
994
Zoonotic Diseases
Prognosis The prognosis for feline zoonoses varies between pathogens and is also dependent on the cat’s immunocompetence. For enteric protozoan infections it is not uncommon for infected cats to continue to shed low levels of oocysts in their feces for many months.
Michel R Lappin 2001. Feline Internal Medicine Secrets, Philadelphia: Hanley & Belfuss. Inc. Safe Pet Guidelines. PAWS, Pet Are Wonderful Support, www.pawssf.org Companion Animal Parasite Council, Controlling Internal and External Parasites in U.S. Dogs and Cats, www.capcvet.org
Selected Readings American Association Feline Practitioners, 2003. Report on Feline Zoonosis, www.catvets.com.
995
SECTION
9 Formulary
CHAPTER 330
Drug Formulary Gary D. Norsworthy, Linda Schmeltzer, Sharon Fooshee Grace, and Mitchell A. Crystal
Expanding pharmacologic options have greatly enhanced the practice of feline medicine. We have made every effort to list viable drugs with accurate details. However, the user of this formulary should be aware of some important limitations. Many, if not most, of the drugs and doses listed are not approved for feline use in the United States. Dosing information and indications for unapproved drugs are listed as a guide only. We do not advocate the use of unapproved drugs when equivalent approved veterinary drugs exist. For many of the drugs listed in this formulary, adequate safety and efficacy studies have not been performed in cats. Doses and indications listed in this formulary were derived from a variety of sources of the latest available information at the time of publication; frequently these sources do not agree with each other. We are not responsible for adverse effects or toxicity of drugs used according to the guidelines in this formulary. For drugs listed in this formulary, brand names may be listed as examples only; other brands may exist, and listing of a particular brand name does not constitute advocation of one brand over another. The listed drugs are available in the formulations cited in the United States unless otherwise noted. However, many cats resist oral adminis-
tration of drugs. The use of small tablets is encouraged because large tablets and capsules may be much more difficult to administer. The use of oral liquids made for feline use is generally favored so cats will offer little resistance to administration. Liquids formulated for human use are often flavored with tastes desirable to children and undesirable to cats. When having an oral liquid compounded, aim for a per dose volume of 0.25 mL. Practitioners are encouraged to demonstrate pill administration for two reasons. First and most obvious is for education of the client. Second is to assess whether pill administration is within the capability of the client, given any physical limitations of the client and the resistance level of the patient. When administration of tablets or capsules seems likely to fail, other options should be considered. Many of these drugs may also be formulated in chewable tablets consisting of several flavors that are appealing to cats. However, some cats are resistant even to this approach. Transdermals are topical gels containing medications that are absorbed through the skin in a bioactive state. Although almost all drugs can be put in a transdermal gel, many are not absorbed in a bioactive state. Drugs properly absorbed through human skin may not be properly absorbed through feline skin. Currently, research is ongoing to determine, which drugs are suitable for this dosing route. Pharmacists trained in transdermal preparation should be contacted for specific drug compounding in this form.
Drug
Action
Dose & Route
How Supplied
Acemannan
Immunostimulant. Proposed to stimulate T-cell activity in animals. It has been used to treat tumors. It may stimulate tumor necrois factor and other cytokine release. Phenothiazine tranquilizer. Inhibits action of dopamine as neurotransmitter. Isotonic crystalloid fluid solution for replacement or maintenance. Carbonic anhydrase inhibitor and diuretic to lower intraocular pressure. Decreases viscosity of secretions. Used as a mucolytic agent in eyes and in bronchial nebulizing solutions. As a donator of sulfhydryl groups, antidote for intoxications (e.g., acetaminophen toxicosis). Adsorbent. Used primarily to adsorb drugs and toxins in intestine to prevent their absorption.
Intraperitoneal (1–2 mg/kg) and intralesional injection (2 mg) every week for six treatments
Propriatary preparation: 10–mg vial for injection
Sedation: 0.025–0.05 mg/kg IM, SC, IV, or PO Preanesthesia: 0.05–0.1 mg/kg SC 40–50 mL/kg per day IV, SC, or intraperitoneal 10–25 mg/kg q12h PO
10– and 25–mg tablet; 10 mg/mL injection
Overview
Acepromazine (PromAce, (many generics) Acetated Ringer’s solution (Normosol) Acetazolamide (Diamox)
Acetylcysteine (Mucomyst)
Activated Charcoal (ActaChar, Charcodote, Toxiban, Actidose, generic)
Intravenous solution 250-mg tablet
Antidote: Make 5% solution using 5% dextrose: 140 mg/kg (loading dose) PO or IV, then 70 mg/kg q4–6h PO or IV for five to seven doses. Eyes: 2% solution topically q2h
10% and 20% solution
1–4 g/kg PO (granules; mix as 1 g/ 5 mL slurry); 6–12 mL/kg (suspension) via orogastric tube
47.5% granules; 10.4% oral suspension; 10% suspension with 70% Sorbitol (sodium sulfate) as cathartic continued
The Feline Patient, 4th Edition, Gary D. Norsworthy, © 2011 Blackwell Publishing Ltd.
999
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Acyclovir (Zovirax)
Herpes antiviral ophthalmic agent.
200 mg/cat q6–12h PO May be toxic to liver and bone marrow.
Aglepristone
Progesterone receptor blocker. For mammary hyperplasia; may cause abortion. Nonsurgical treatment of pyometra, use in conjunction with antibiotics if infection is present. Benzimidazole antiparasitic drug. Inhibits glucose uptake in parasites. β2-adrenergic agonist bronchodilator. Stimulates β2 receptors to relax bronchial smooth muscle. May also inhibit release of inflammatory mediators, especially from mast cells. See etidronate disodium. Anesthetic induction agent
15 mg/kg SC on 2 consecutive days or 20 mg/kg q7d SC; pyometra 10 mg/kg on days 1, 2, 7, and 14.
200–mg capsule; 200 mg/5 mL oral suspension (banana flavor); 5% ophthalmic ointment 30 mg/mL injection available in France, Norway, and Sweden (VIRBAC)
Decreases production of uric acid (questionable efficacy). Benzodiazepine for urine spraying, anxiety and intercat aggression. Phosphate binders for hyperphosphatemic renal disease.
10 mg/kg q8h PO for 3 days then reduce to 10 mg/kg q24h PO 0.125–0.25 mg/cat q8–24h PO
Aminoglycoside antibacterial drug. Inhibits protein synthesis. See gentamicin. Antidiarrheal and antiemetic. Anticholinergic. Bronchodilator; Poorly effective for feline asthma.
6.5 mg/kg q8h IV, IM, or SC or 10 mg/kg q12h IV, IM, or SC, or 20 mg/kg q24h IV, IM, or SC 0.1 mg q8–12h IM, SC, or PO
Albendazole (Valbazen)
Albuterol (Proventil, Ventolin)
Alendronate sodium (Fosamax) Alfaxalone (Alfaxan) Allopurinol (Zyloprim) Alprazolam Aluminum carbonate (Basaljel, generic) and aluminum hydroxide (Amphojel, generic)
Amikacin (Amiglyde-V)
Aminopentamide (Centrine) Aminophylline
Amitraz (Mitaban)
Topical anti-parasiticide
Amitriptyline (Elavil)
Tricyclic antidepressant drug. Used to treat a variety of behavioral disorders. Action is via inhibition of uptake of serotonin at presynaptic nerve terminals. Calcium channel blocker. Antihypertensive drug.
Amlodipine (Norvasc)
1000
25–50 mg/kg q24h PO for 21 days. Giardia: 25 mg/kg q12h for 5 days
113.6 mg/mL suspension
8–10 breaths from face mask attached to spacer following two puffs (90 µg/puff) into spacer; used as needed for bronchodilation for acute bronchospasm 5–10 mg q24h PO 1–5 mg/kg IV to effect
90-µg aerosol inhaler
30–90 mg/kg divided daily q12h PO given with meals
4.0–6.6 mg/kg q12h PO or IM; 2–5 mg/kg q12h slow intravenous infusion Dilute to 50% canine concentration = one bottle per 4 gallons of warm water. Pour on after bathing q7–14d; will lower blood glucose; caution with diabetics Behavior: 0.5–1.0 mg/kg PO q12–24h; may take 2–4 weeks for results. Cystitis: 2.5–12.5 mg/kg PO q24h given at night. (mixed results) Ureteral urolith: 1 mg/kg q24h PO. 0.625–1.25 mg/cat q12–24h PO adjusted to effect.
5- and 10-mg tablet Not currently available in the United States 100-mg tablet 0.25- and 0.5-mg tablet Aluminum carbonate not commercially available, but, available via compounding pharmacies; 320-mg aluminum hydroxide gel powder Aluminum hydroxide available as chemical grade powder; 50 mg/kg or 1/4–1 tsp/cat per meal (www.spectrumchemical.com; product code: AL226) 50 and 250 mg/mL injection
0.2-mg tablet; 0.5 mg/mL injection 100-mg tablet; 25 mg/mL injection 10.6-mL bottle containing 19.9% solution for dilution.
10- and 25-mg tablet
2.5-, 5-, and 10-mg tablet Compounded liquid may be necessary to dose properly.
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Ammonium chloride (generic)
Urine acidifier.
200- and 400-mg tablet; 200 and 400 mg per 1/4 teaspoon powder
Amoxicillin (Amoxi-Tabs, other brands)
β-lactam antibiotic. Inhibits bacterial cell wall synthesis. Broad-spectrum activity. β-lactam antibiotic and β-lactamase inhibitor (clavulanic acid) Antifungal drug. Fungicidal for systemic fungi (damages fungal membranes).
20 mg/kg q12h (up to 800 mg; approx. 1/4 to 1/3 tsp) mixed with food daily. Dose to desired urine pH. 10–40 mg/kg q8–12h PO, IM, or SC
Amoxicillin-clavulanic acid (Clavamox) Amphotericin B (Fungizone)
Ampicillin (Polyflex, Omnipen)
β-lactam antibiotic. See amoxicillin.
Ampicillin and Sulbactam (Unasyn) Ampicillin trihydrate (Polyflex)
Same mechanism as amoxicillin-clavulanate. β-lactam antibiotic. Inhibits cell wall synthesis. Antiprotozoal drug. Antagonizes thiamine in parasites. Used for treatment of coccidiosis, especially in kittens.
Amprolium (Amprol, Corid)
Apomorphine
To induce emesis. Questionable efficacy in cats.
Arginine
Arginine deficiency as in hepatic lipidosis Cornel protectant and lubricant
Artificial tears ointment (Celluvisc, I-Drop, Genteal) l-Asparaginase (Elspar)
Aspirin (many generic and brand names [Bufferin, Ascriptin])
Atenolol (Tenormin, generic)
Atovaquone (Mepron)
Anticancer agent for lymphoma protocols. Depletes cancer cells of asparagine and interferes with protein synthesis. Nonsteroidal anti-inflammatory; action is generally considered to be caused by inhibition of prostaglandins. Analgesic, anti-inflammatory, and antiplatelet drug. β-adrenergic blocker. Relatively selective for β1-receptor. For arrhythmias and tachycardia. Anti-protozoal for Cytauxzoon felis
62.5–125 mg q12h PO or 22 mg/kg q12h PO 0.5 mg/kg q48h IV; mix in 5–20 mL 5% dextrose and give over 5–15 minutes; maximum cumulative dose of 4–8 mg/kg, less if azotemia develops. Subcutaneous protocol: Make 5 mg/mL solution of Fungizone. Put calculated dose in 400 mL of 0.45% saline + 2.5% dextrose. Give two to three times per week (3 doses total). Dose: 0.5–0.8 mg/kg. See Table 43-1 for details. 20–40 mg/kg q8h PO; 10–20 mg/kg q6–8h IV, IM, or SC (ampicillin sodium) 10–20 mg/kg q8h IV or IM 10–20 mg/kg q12–24h IM or SC 30 mL of 9.6% amprolium solution to 3.8 L drinking water for 7 days or 110–220 mg/kg q24h PO on food for 7–12 days or 300– 400 mg/kg q24h PO on food for 5 days. 0.04 mg/kg IV or 0.08 mg/kg IM or SC
250 mg/cat q24h PO Apply to cornea q8–12h
50-, 100-, 150-, and 200-mg tablet; 50 mg/mL oral suspension 62.5- and 125-mg tablet; 62.5 mg/mL suspension 50-mg vial for injection
250- or 500-mg capsule; 250 mg/5 mL oral suspension; 250- and 500-mg tablet, 1- and 2-g vials for injection 1.5- and 3-g powder for reconstitution 10- and 25-g vial for injection 9.6% (9.6 g/100 mL) oral solution; 2.5 % crumbles
No longer commercially available. However, available through compounding pharmacies Many formulations available from health food stores Many sizes available
400 U/kg or 10,000 U/m2 weekly IM, SC, or as part of cyclical chemotherapy protocol.
10,000 IU per vial for injection
Anti-inflammatory: 10–20 mg/kg q48–72h PO; antiplatelet: 5, 40, or 81 mg q48–72h PO; few studies to document dose; beware of salicylate toxicity
81-mg tablet Compounded tablet may be necessary to dose properly
6.25–12.5 mg/cat q12–24h
25- and 50-mg tablet
15 mg/kg q8h PO for 10 days
750 mg/5 mL oral suspension (citrus flavor) continued
1001
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Atracurium (Tracurium)
Neuromuscular blocking agent (nondepolarizing). Used during anesthesia or other conditions in which it is necessary to inhibit muscle contractions. Anticholinergic agent (blocks acetylcholine effect at muscarinic receptor), parasympatholytic. Used primarily as adjunct to anesthesia or other procedures to increase heart rate and decrease respiratory and gastrointestinal secretion. Also used as antidote for organophosphate intoxication.
0.2 mg/kg IV initially, then 0.15 mg/ kg every 30 minutes or intravenous infusion at 3–8 µg/kg per minute
10 mg/mL injection
0.02–0.05 mg/kg q6–8h IV, IM, or SC 0.2–0.5 mg/kg SC (as needed, usually q6–8h) for organophos– phate and carbamate toxicosis; 0.2–0.5 mg/kg intratracheally for cardiopulmonary resuscitation. Challenge for dysautonomia: 0.04 mg/kg SC to see if tachycardia occurs. 1–2 drops or 1/4-in ointment q8–48h in eye 0.5–1.0 mg/kg q7d IM until remission then q30d
0.4 and 0.5 mg/mL injection
Atropine (generic)
Atropine ophthalmic ointment and drops (generic) Aurothioglucose (Solganol)
Cycloplegic, mydriatic agent. Used in anterior uveitis to reduce pain For immune-mediated disease and L-P gingivitis/stomatitis.
Azathioprine (Imuran)
Immunosuppressive drug. Inhibits T-cell lymphocyte function. For various immune-mediated diseases. Azalide antibiotic. Similar mechanism of action as macrolides (erythromycin). For gram-positive and gastric spiral bacteria.
0.2–0.3 mg/kg q24–48h PO; use cautiously
Angiotensin-converting enzyme inhibitor. See enalapril for details. Used for vasodilation, treatment of heart failure, systemic and renal hypertension. For feline acne Potent, long-acting corticosteroid. Anti-inflammatory and immunosuppressive effects are 30 times more than those of cortisol. For inflammatory and immunemediated disease. Muscarinic, cholinergic agonist and parasympathomimetic. Stimulates gastric and intestinal motility and urinary bladder. Prostaglandin analog for lowering intraocular pressure; efficacy not proved. Laxative/cathartic. Acts via local stimulation (irritation) of gastrointestinal motility. Antidiarrheal agent and gastrointestinal protectant. Antiprostaglandin action of salicylate component may be beneficial for enteritis. For treating Helicobacter. Source of folic acid (vitamin B9) when long-term sulfa therapy is used. Carbonic anhydrase inhibitor for glaucoma
0.5–1.0 mg/kg q24h PO
100 and 200 mg per 5 mL oral suspension; 1-g powder pack Compounded tablet or liquid may be necessary to dose properly 5- and 10-mg tablet
Apply to chin q12h 0.1–0.2 mg/kg q12–24h PO
5% gel 0.6 mg/mL injectable solution
1.25–7.5 mg q8–12h PO
5- and 10-mg tablet
1 drop q30m topically repeat as needed per intraocular pressure
0.03% ophthalmic solution
5 mg q8–24h PO; one to three10– mg suppositories/day
5-mg enteric coated or delayed release tablet. 10-mg suppository. 262 mg/15 mL and 525 mg/mL oral suspension; 262-mg tablet
Azithromycin (Zithromax)
Benazepril (Lotensin)
Benzoyl peroxide Betamethasone (Betasone, Celestone)
Bethanechol (Urecholine)
Bimataprost (Lumigan)
Bisacodyl (Dulcolax Laxative)
Bismuth subsalicylate (Pepto-Bismol) and Bismuth subcarbonate
Brewer’s yeast
Brinzolamide 1% (Azopt)
1002
5–10 mg/kg q24–48h PO; mixed suspension only good for 10 days.
1–3 mL/kg per day (in divided doses) PO; use with caution over 7 days because of possible salicylate toxicity; do not exceed 10 mL every 3 days
1% ophthalmic ointment and drops No longer commercially available. Must be compounded. 50-mg tablet
100 mg/kg q24h PO
Many over-the-counter formulations available
1 drop q8–12h topically
1% ophthalmic suspension
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Bromocriptine mesylate
Antiprogestin; For severe mammary hyperplasia. A poorly absorbed corticosteroid for certain types of inflammatory bowel disease.
0.25 mg/cat q24h PO for 5–7 days
2.5-mg tablet
1 mg/cat q24h PO
Local anesthetic. Inhibits nerve conduction via sodium channel blockade. Longer acting and more potent than lidocaine or other local anesthetics. Opioid analgesic. Partial µ-receptor agonist, κ-receptor antagonist. More potent than morphine (25–50 times). Absorbed from oral mucosa. Antianxiety agent. Acts to block release of serotonin. Used primarily for stress-induced inappropriate elimination. Anticancer agent. Bifunctional alkylating agent; disrupts DNA of tumor cells. Opioid analgesic. κ-receptor agonist and weak µ–receptor antagonist. For perioperative analgesia, chronic pain, and as antitussive agent. For calcium deficiency and hypocalcemia associated with hypoparathyroidism. Not indicated as vitamin D supplement. Increases calcium absorption in intestine. Phosphate binder for hyperphosphatemic renal disease. Oral calcium supplement for hypocalcemia, antacid to treat gastric hyperacidity and gastrointestinal ulcers; intestinal phosphate binder for hyperphosphatemia. Calcium supplement. Used in acute hypocalcemia, acute hyperkalemia, or as a cardiotonic for electromechanical dissociation.
Dilute to 0.5% solution; give 1 mL/5 kg as an epidural (effective for up to 12 hours)
Available as inhaler in United States. 3-mg tablet available in Canada. 2.5 and 5 mg/mL injection
Budesonide
Bupivacaine (Marcaine)
Buprenorphine (Temgesic, Buprenex)
Buspirone (BuSpar)
Busulfan (Myleran)
Butorphanol (Torbutrol, Torbugesic)
Calcitriol (Rocaltrol, Calcijex)
Calcium acetate (PhosLo) Calcium carbonate (Titralac, Tums, Epakitin, generic)
Calcium chloride (generic 10% solution)
Calcium citrate (Citracal [over the counter]) Calcium gluconate (Kalcinate, generic [10% solution])
Calcium supplement. For hypocalcemia, such as with hypoparathyroidism. Calcium supplement. For acute hypocalcemia and acute hypokalemia.
0.005–0.01 mg/kg q4–8h IV. 0.005–0.4 mg/kg q6–12h IM, SC, or ortransmucosal
0.3 mg/mL injection
0.5–1.0 mg/kg q12h PO; may take 2–4 weeks for desired effect.
5-, 10-, and 15-mg tablet
3–4 mg/m2 q24h PO
2-mg tablet
Analgesia 0.2–0.8 mg/kg q4–12h SC, IM, or IV Antitussive: 0.5 mg/kg q6–12h PO
1-, 5-, 10-mg tablet; 0.5 or 10 mg/mL injection
Renal: 2.5 ng/kg q24h PO or 9 ng/kg q24h PO Hypocalcemia: 15 ng/kg q12h PO for 3 days then 5–15 ng/kg q24h PO
0.25-, 0.5-µg capsule, 1 µg/mL oral solution. For best results, have compounded so calculated dose is in 0.25 mL.
166 mg/cat (1/4 tablet) q12h PO with food Phosphate binder: 90–150 mg/kg per day PO in divided doses Calcium supplement: 0.5–2 g/day in divided doses
667-mg tablet and capsule
0.15–0.5 mL/kg (5–15 mg/kg) IV (slowly); stop if bradycardia develops. Do not give SC. Note: three times more potent than calcium gluconate. 1–2 g/day PO in divided doses
0.2–1.5 mL/kg (5–15 mg/kg) IV (slowly); stop if bradycardia develops 2–4 mEq/day PO
Calcium lactate (generic)
See other oral calcium supplements.
0.5–1 g/day PO (in divided doses)
Captopril (Capoten) Carbenicillin (Geopen, Pyopen)
See enalapril. β-lactam antibiotic. Inhibits bacterial cell wall synthesis. For gramnegative bacteria (Pseudomonas).
3.12–6.25 mg q8h PO 40–50 mg/kg (up to 100 mg/kg) q6–8h IV, IM, SC, or PO
500-, 750-, and 1000-mg chewable tablet; 3.7% powder
10% (100 mg/mL) solution
Citracal regular: 250 mg Calcium + 400 IU Vitamin D per tablet 100 mg/mL (10%) injection; various oral formulations available from health food stores Various formulations available from health food stores 12.5-, 25-, and 50-mg tablet No longer commercially available continued
1003
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Carbenicillin indanyl sodium (Geocillin)
Same as for carbenicillin. For infections of lower urinary tract.
10–20 mg/kg q8h PO
Carbimazole (Neomercazole)
Antithyroid drug metabolized to methimazole.
5 mg q12h PO
Carbimazole, controlled release (Vidalta) Carboplatin (Paraplatin, generic)
Antithyroid drug metabolized to methimazole. Interrupts replication of DNA in tumor cells. Used for various carcinomas. For carnitine deficiency. May help maintain lean muscle mass while improving weight loss. Nonsteroidal anti-inflammatory
15 mg q24h PO
382 mg carbenicillin + 118 mg indanyl sodium ester + 23 mg sodium 5- and 20-mg tablet Not available in the United States. 10-mg tablet
L-Carnitine
Carprofen (Rimadyl) Cascara sagrada (many brands [e.g., Nature’s Remedy]) Castor oil (generic)
225–240 mg/m2 IV every 3–4 weeks; can be used intracavitary.
10 mg/mL injection
250–500 mg/cat q24h PO
Various formulations available from health food stores
2–4 mg/kg q24h IV, SC, or IM Give for 3 days max. 1–2 mg/day
25-, 75-, and 100-mg tablets
Cefaclor (Ceclor)
Stimulant cathartic; stimulates bowel motility. Used as laxative. Stimulant cathartic; stimulates bowel motility. Used as laxative. Second-generation cephalosporin.
Cefadroxil (Duricef)
First-generation cephalosporin.
Cefamandole (Mandol) Cefazolin sodium (Ancef, Kefzol, generic) Cefepime (Maxipime) Cefixime (Suprax)
Cephalosporin antibiotic. First-generation cephalosporin.
Urinary: 22 mg/kg q12–24h PO Pyoderma, stomatitis, orthopedic: 22–35 mg/kg q12h PO 15 mg/kg q4–6h IV or IM 20–33 mg/kg q4–8h IV, IM, or SC
Fourth-generation cephalosporin. Third-generation cephalosporin.
50 mg/kg q8h IV, IM 5–12.5 mg/kg q12h PO
Cefmetazole sodium (Zefazone) Cefotaxime sodium (Claforan)
Seconnd-generation cephalosporin.
20 mg/kg q6–12h IV
Third-generation cephalosporin.
20–80 mg/kg q4–8h IV or IM
Cefotetan (Cefotan) Cefovecin (Convenia) Cefoxitin (Mefoxin)
Second-generation cephalosporin. Third-generation cephalosporin. Second-generation cephalosporin.
30 mg/kg q8h IV, SC 8 mg/kg q14d SC 25–30 mg/kg q6–8h IV, IM, or SC
Cefpodoxime proxetil (Simplicef, Vantin)
Third-generation cephalosporin.
5 mg/kg q12h PO; 10 mg/kg q24h PO
Ceftazidime (Fortaz, Tazicef, Tazidime) Ceftiofur (Naxcel, Excenel)
Third-generation cephalosporin.
15–50 mg/kg q6–12h IV or IM
Third-generation cephalosporin.
2.2–4.4 mg/kg q12–24h SC
Ceftriaxone (Rocephin)
Third-generation cephalosporin.
Cephalexin (Keflex, Ceporex, generic)
First-generation cephalosporin
15–50 mg/kg q12–24h IV, IM Note: max dose, 1 g per administration 22–35 mg/kg q6–8h PO
Cephalothin (Keflin)
Firstst-generation cephalosporin
22–44 mg/kg q4–8h IV or IM
Cephapirin (Cefadyl)
First-generation cephalosporin
10–40 mg/kg q4–8h IV, IM, or SC
1004
4–10 mL/day PO 7–13 mg/kg q8h PO
Various formulations available from health food stores Various formulations available 250- and 500-mg capsule; 125, 187, 250, 375 mg/5 mL oral suspension 50 mg/mL oral suspension
1- and 2-g injection 1- and 10-g injection 500-mg, 1- and 2-g injection 20 and 40 mg/mL oral suspension; 400-mg tablet Not commercially available in the United States 500-mg, 1-, 2- and 10-g vial for injection 1-, 2- and 10-g vial for injection 80 mg/mL injection 1-, 2-, and 10-g vial for injection 100- and 200-mg tablet; 50 and 100 mg/5 mL oral suspension 500-mg, 1-, 2-, and 6-g vial for injection 50-mg, 1-, and 4-g vial for injection 1-g vial for injection
250- and 500-mg tablet; 125 and 250 mg/5 mL oral suspension 1, 2, and 4 g/50 mL vial for injection Not commercially available in the United States 1-g vial for injection Not commercially available in the United States or Canada
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Cephradine (Anspor, Velosef)
First-generation cephalosporin
22 mg/kg q6–8h IV, IM, SC, or PO
Chlorambucil (Leukeran, generic)
Cytotoxic alkylating agent. Acts in similar manner as cyclophosphamide. Used for treatment of various tumors and immunosuppressive therapy.
Chloramphenicol palmitate (Chloromycetin, generic forms)
Antibacterial drug. Mechanism of action is inhibition of protein synthesis via binding to ribosome. Broad spectrum. Injectable form of chloramphenicol. Converted by liver to parent drug.
2–6 mg/m2 or 0.1–0.2 mg/kg q24h PO for 5 days, then q48h or 15 mg/m2 q24h 4 days per week every third week or 1.4 mg/kg PO as a single or intermittent dose or 20 mg/m2 q14d PO or 2 mg/cat q1–3d to avoid splitting tablet Do not split tablets. 12.5–20 mg/kg q12h PO
250- and 500-mg capsule; 125 and 500 mg/5 mL oral suspension 2-mg tablet
Chloramphenicol sodium succinate (Chloromycetin, generic) Chlorhexidine wiping pads (Douxo) Chlorothiazide (Diuril)
Chlorpheniramine maleate (Chlortrimeton, Phenetron, generic) Chlorpromazine (Thorazine)
Chlorpropamide
Chlortetracycline (generic)
Cidoflvir Cimetidine (Tagamet, generic [over the counter and prescription])
Ciprofloxacin (Cipro)
Cisapride (previously Propulsid, now unavailable except via compounding pharmacies; Prepulsid in Canada) Clarithromycin (Biaxin)
Antibacterial Thiazide diuretic. Inhibits sodium reabsorption in distal renal tubules. Used as diuretic and antihypertensive to treat calcium-containing uroliths. Antihistamine (H1 blocker). Blocks action of histamine on receptors and direct anti-inflammatory action. Phenothiazine tranquilizer/ antiemetic. Inhibits action of dopamine as neurotransmitter. Used as antiemetic, for sedation, and as preanesthetic. Potentiates the effects of vasopressin in the renal tubules Tetracycline antibacterial. Inhibits bacterial protein synthesis. Bacteriostatic agent with broad spectrum. Antiviral topical for ophthalmic use Histamine-2 antagonist (H2 blocker). Blocks histamine stimulation of gastric parietal cells to decrease gastric acid secretion. Fluoroquinolone antibacterial. Acts to inhibit DNA gyrase and inhibit cell DNA and RNA synthesis. Broad antimicrobial activity. Prokinetic agent. Stimulates gastric and intestinal motility For gastric reflux, gastroparesis, ileus, esophageal motility disorders, and constipation. Macrolide antibiotic; see erythromycin.
250- and 500-mg and 1-g tablet and capsule
12.5–50 mg q12h IV or IM
100 mg/mL injection
Clean area one to three times per day 10–40 mg/kg q12h PO
3% wiping pad
2–4 mg q8–12h PO
4-mg tablet
0.1–0.5 mg/kg q6–12h IM or SC
10- and 25-mg tablet ; 25 mg/ mL injection
40 mg/cat q24h PO May cause hypoglycemia or hepatotoxity 25 mg/kg q6–8h PO
100- and 250-mg tablets
2 drops to affected eye(s) q2–4h 5–10 mg/kg q6–8h IV, IM, or PO (in renal failure, administer 2.5–5 mg/ kg q12h IV or PO)
5–15 mg/kg q12h PO or IV
2.5–5.0 mg/cat q8–12h PO. (as much as 10 mg/cat q8h has been administered to cats) Give 30 minutes before feeding if being meal fed. 62.5 mg/cat q12–24h PO
250- and 500-mg tablet
102.4 g/lb powder
0.5% ophthalmic solution 200-, 300-, 400-, and 800-mg tablet; 60 mg/mL oral solution; 150 and 300 mg/mL injection in 50 mL sodium chloride 250-, 500-, and 750-mg tablet; 50 and 100 mg/mL oral suspension; 10 mg/mL injection No longer commercially available. However, available through compounding pharmacies 250- and 500-mg tablet; 25 and 50 mg/mL oral suspension continued
1005
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Clemastine (Tavist, Contact 12-Hr Allergy)
Antihistamine. H-1 histamine receptor blocker. Used for allergies. Antibacterial drug of the lincosamide class (similar in action to macrolides). Inhibits bacterial protein synthesis via inhibition of bacterial ribosome. Bacteriostatic with spectrum of activity primarily against gram-positive bacteria and anaerobes. Antimicrobial agent for feline leprosy. Slow bactericidal effect on Mycobacterium leprae.
0.34–0.68 mg q12h PO
1.34- and 2.68-mg tablets, and 0.134 mg/mL syrup
Staphylococcus or Actinomycosis: 5.5 mg/kg q12h PO or 11 mg/kg q24h PO Anaerobes: 11 mg/kg q12h PO or 22 mg/kg q24h PO; toxoplasmosis: 12.5–25 mg/kg q12h PO for 4+ weeks Acne: Apply topical to chin q12h 25–50 mg/cat q24–48h or 8–10 mg/ kg q24h PO for 12+ weeks. Use with rifampin or clarithromycin or both. 2.5 mg/cat q24h PO or 0.25–1 mg/ kg q24h PO
25 mg/mL oral solution; 25-, 75- and 150-mg tablet and capsule; topical: 10 mg/gm
0.5 mg/kg q8–12h PO
0.5-, 1-, and 2-mg tablet
18.75 mg q24h PO
75-mg tablet
2 mg/kg q12h PO
3.75-, 7.5-, 11.25-, and 15-mg tablet
20–40 mg/kg q8h PO
250- and 500-mg capsule Not commercially available in the United States
See vitamin B12
1000, 3000, and 5000 µg/mL
0.01–0.03 mg/kg q24h PO
0.6-mg tablet
2.5 µg/kg q12h SC
300 µg/mL injection
Response test: collect preadrenocorticotropic cortisol sample and inject 0.125 mg IV or IM of aqueous; collect postadrenocorticotropic cortisol samples at 30 and 60 minutes Up to 10 pounds one capsule sprinkled on food daily. Over 10 pounds two capsules sprinkled on food daily.
0.25-mg vial for injection
1 drop q6–12h topically
4% drops
Clindamycin (Antirobe, Cleocin, Cleocin-T)
Clofazimine (Lamprene)
Clomipramine (Clomicalm [veterinary]; Anafranil [human]) Clonazepam (Klonopin)
Clopidogrel (Plavix)
Clorazepate (Tranxene)
Cloxacillin (Cloxapen, Orbenin, Tegopen)
Cobalamin (vitamin B12) (generic) Colchicine (generic)
Colony-stimulating factor (Neupogen, filgrastim)
Corticotropin (adrenocorticotropic hormone) (Cortrosyn)
Cosequin (Cosequin)
Cromolyn (Cromolom)
1006
Tricyclic antidepressant. For variety of behavioral disorders. Action is via inhibition of uptake of serotonin. Benzodiazepine. Anticonvulsant action, sedation, and treatment of some behavioral disorders. Antithrombotic agent for cats with large left atrium or history of thromboembolism Benzodiazepine. Enhances inhibitory effects of γ aminobutyric acid in central nervous system. For seizures, sedation, and some behavioral disorders. β-lactam antibiotic. Inhibits bacterial cell wall synthesis. Spectrum is limited to gram-positive bacteria, especially staphylococci. For vitamin B12 deficiency Anti-inflammatory agent to decrease fibrosis (especially hepatic) and amyloid deposition (especially renal). Stimulates granulocyte development in bone marrow. Used primarily to regenerate blood cells to recover from cancer chemotherapy. Used for diagnostic purposes to evaluate adrenal gland function. Stimulates normal synthesis of cortisol from adrenal gland.
Combination glucosamine hyrdochloride and chondroitin sulfate. Used primarily for degenerative joint disease. Also used for chronic cystitis as a GAG replacer. Ophthalmic antihistamine for allergic conjunctivitis
50-mg capsule
5-, 20-, 40-, and 80-mg tablets (veterinary); 25-, 50-, and 75-mg tablets (human)
Glucosamine Hydrochloride 125 mg + Sodium Chondroiton Sulfate 100 mg + Manganese minimum 1 mg
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Cyclophosphamide (Cytoxan, Neosar, generic)
Cytotoxic agent. Bifunctional alkylating agent. Disrupts base-pairing and inhibits DNA and RNA synthesis. Cytotoxic for tumor cells and other rapidly dividing cells. Used primarily as adjunct for cancer chemotherapy and as immunosuppressive therapy. Immunosuppressive drug. Depresses T lymphocytes.
Antineoplastic therapy: 200–300 mg/ m2 once every 3 weeks; may be used in combination with other agents Immunosuppressive therapy: 6.25–12.5 mg (50 mg/m2) once daily 4 days per week or q48h
25- and 50-mg tablet; 100-, 200-, and 500-mg and 1and 2-g vials for injection
6 mg/kg q12h IV 4–7 mg/kg q24h PO or 5–10 mg/kg q12h PO (Neoral and Atopica are more bioavailable; may allow decreased dosing; assess via blood cyclosporine levels; goal is 200–250 ng/mL) 1 drop q12h topically
10-, 25-, 50-, and 100-mg capsule; 50 mg/mL injection; 100 mg/mL oral solution
Cyclosporine (Atopica, Neoral, Sandimmune)
Cyclosporin Ophthalmic, (Optimmune, compounded forms) Cyproheptadine (Periactin, generic)
Cytosine arabinoside (Cytosar, generic) Dalteparin (Fragmin)
Danazol (Danocrine)
Dantrolene (Dantrium)
Dapsone (generic)
Darbepoetin Alfa (Aranesp)
Dasuquin (Dasuquin)
Used for keratoconjunctivitis sicca and to decrease vascularization and pigmentation in keratitis Phenothiazine with antihistamine and antiserotonin properties. Used as appetite stimulant (probably by altering serotonin activity in appetite center). May be used in resistant asthmatics. Antimetabolite anticancer agent. Inhibits DNA synthesis. Used for lymphoma and leukemia. Low molecular weight heparin; an antithrombotic drug used in cats at high risk for thromboembolism. Gonadotropin inhibitor. Suppresses leutenizing hormone and follicle-stimulating hormone and estrogen synthesis. May reduce destruction of platelets or red blood cell in immune-mediated disease. Muscle relaxant. Also, for malignant hyperthermia and to relax urethral muscle. Antimicrobial drug primarily for mycobacterium. Primarily for dermatologic diseases due to its immunosuppressive properties. Some consider this drug contraindicated in cats. Erythropoietic stimulating protein has a longer half life that epoetin alfa (Epogen)
Glucosamine hydrochloride, chondroitin sulfate, and an avocado extract. Used primarily for degenerative joint disease. Also used for chronic cystitis as a GAG replacer.
Appetite stimulant: 1–2 mg PO 5–20 min prior to feeding; duration of action less than 1 hour. Asthma: 2–4 mg q12h PO; response in 4–7 days; drowsiness possible. 200 mg/m2 SC; repeat per protocol or every 1–3 weeks 100 u/kg q12–24h SC
Optimune: 0.2% ointment. Compounded: up to 2% solution generally used. 4-mg tablet
100- and 500-mg, 1- and 2-g powder for reconstitution
5–10 mg/kg q12h PO
Prefilled syringes: 2,500–10,000 IU/0.2 mL Mulitdose vial: 95,000 IU/3.8 or 9.5 mL 50-, 100-, and 200-mg capsules
0.5–2 mg/kg q12h PO
25-, 50-, and 100-mg capsules
Non-mycobacterial skin conditions: 1.1 mg/kg q8–12h PO Mycobacterial skin conditions: 8 mg/ kg q24h PO for 6 weeks
25- and 100-mg tablet
6.25 µg/cat weekly to start then q2–4w at some future point (remembering to check the hematocrit and make adjustments less frequently than typical for erythropoeitin because darbepoetin has a longer half life). Up to 10 pounds one capsule sprinkled on food daily. Over 10 pounds two capsules sprinkled on food daily.
25 µg per 0.42 mL; 25 µg/mL; 40 µg per 0.4 mL; 40 µg/mL; 60 µg per 0.3 mL vial for injection
Glucosamine hydrochloride 125 mg + sodium chondroitin sulfate 100 mg + Avocado/ soybean Unsaponifiables Powder 25 mg continued
1007
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Deferoxamine (Desferal)
Chelating agent used to treat acute iron toxicosis. Also to chelate aluminum and facilitate removal. Parasympathomimetic to increase aqueous drainage in glaucoma
10 mg/kg q2h IV or IM for two doses, then 10 mg/kg q8h for 24 hours 1 drop q6–12h topically
500-mg and 2-g vial for injection
Synthetic peptide similar to antidiuretic hormone. Replacement therapy for patients with diabetes insipidus. Mineralocorticoid (no glucocorticoid activity) for adrenocortical insufficiency (hypoadrenocorticism). Corticosteroid. Dexamethasone has approximately 30 times the potency of cortisol. Multiple antiinflammatory effects. See betamethasone.
Diabetes insipidus: 2–4 drops (2 µg) q12–24h intranasally or conjunctivally or 2–5 µg/cat q12–24h SC 1.5–2.2 mg/kg IM every 25 days
Demecarium bromide (Humorsol) Desmopressin acetate (DDAVP)
Desoxycorticosterone pivalate (DOCP, Percorten-V)
Dexamethasone (Azium, generic)
Dexamethasone ophthalmic Dexamethasone sodium phosphate (Azium-SP, Decadron, generic) Dextran (Dextran 40, Dextran 70, Dextran 75, generics)
Dextromethorphan (Benylin, others)
Dextrose solution, 5% (D5W)
Dextrose solution, 10% and/or 20% Dextrose solution, 50%
1008
Anti-inflammatory for ophthalmic diseases Corticosteroid. Same as dexamethasone except faster acting. For shock and central nervous system trauma. Synthetic colloid used for volume expansion. High molecular weight fluid replacement. Primarily used for acute hypovolemia, shock, and for fluid therapy in hypoproteinemic patients.
Centrally acting antitussive drug. Similar chemical structure as opioids but does not affect opioid receptors. Appears to directly affect cough receptor. Isotonic solution for hypoglycemia and when low sodium intravenous fluids are needed. For osmotic diuresis. Also for hypoglycemia uncontrollable with dextrose 5% solution For hypoglycemic crisis or hyperkalemia
0.125 and 0.25% aqueous solution; must be compounded 0.01% intranasal solution; 0.1, 500 mg/vial for injection
25 mg/mL injection
Anti-inflammatory: 0.1–0.2 mg/kg q12–24h IV, IM, SC, or PO Shock, spinal injury, asthmatic crisis: 2.2–4.4 mg/kg IV Immunosuppression: 0.2–0.4 mg/kg q12–24h IV, IM, SC, or PO Low Dose Dex Suppression Test (LDDST): 0.1 mg/kg IV, collect cortisol samples at 0, 4, and 8 hours 1 drop q4–12h topically
0.1% solution
2.2–4.4 mg/kg IV
4 mg/mL injection
10–20 mL/kg IV to effect (for shock or hypovolemia, usually over 2–4 hours; for hypoproteinemia patients, usually over 18–24 hours)
500-mL infusion bags. Dextran 40—low molecular weight dextran (LMD®); has an average molecular weight of 40,000 Dextran 75 has an average molecular weight of 75,000. Dextran 70 has an average molecular weight of 70,000 10-mg tablet
0.5–2 mg/kg q6–8h PO (in preparations with guaifenesin, dose based on dextromethorphan fraction)
2 mg/mL injection
25–50 mL/kg over 24h IV or IP For diuresis: 1–5 mL/min over 20 minutes 25–50 mL/kg (10%) over 24 hours or divided slowly q6–12h IV
Intravenous solution
Hypoglycemia: 1–2 mL/kg over 1–2 minutes to effect IV Hyperkalemia: 1 g/kg IV with 0.25–1 u/kg regular insulin
Intravenous solution
Intravenous solution
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Diazepam (Valium, generic)
Benzodiazepine. Central-acting central nervous system depressant. Mechanism of action appears to be via potentiation of γ aminobutyric acid receptormediated effects in central nervous system. For sedation, anesthetic adjunct, anticonvulsant, and behavioral disorders. Diazepam metabolized to desmethyl diazepam (nordiazepam) and oxazepam. Carbonic anhydrase inhibitor. Diuretic. Acts to inhibit enzyme that forms hydrogen and bicarbonate ions. Reduces plasma bicarbonate concentration, producing systemic metabolic acidosis and alkaline diuresis. Primarily for glaucoma. Nonsteroidal anti-inflammatory to reduce vascularization and inflammation in keratitis and uveitis. β-lactam antibiotic. Inhibits bacterial cell wall synthesis. Spectrum is limited to gram-positive bacteria, especially staphylococci. For cardiac glycoside toxicity
Preanesthetic: 0.5 mg/kg IV Status epilepticus: 0.5–1.0 mg/kg IV, 1 mg/kg per rectum, repeat as necessary; can be used as constant rate infusion at 2–5 mg/ hr Appetite stimulant: 0.1–0.2 mg/kg IV Behavior: 0.2–0.5 mg/kg q12–24h PO External urethral sphincter relaxation: 2.5 mg q8–12h PO
2-, 5-, 10-mg tablet; 5 mg/mL injection
1–3 mg/kg q8–12h PO
50-mg tablet Compounding may be necessary to dose properly.
1 drop q8–12h topically
0.1% ophthalmic solution
11–55 mg/kg q8h PO
250- and 500-mg capsule
1.7 mL per mg of digoxin ingested; give slowly over 30 minutes 0.008–0.01 mg/kg (approximately 1/4 of a 0.125-mg tablet) q48–72h PO; monitor and adjust via serum levels; May result in vomiting and anorexia. Not a first-line drug for cats due to side effects. Acute treatment: administer 0.02 mg/kg initially, then 0.01–0.02 mg/kg q24–48h PO thereafter; Time to maximum effect 1–7 days
38 mg/4 mL vial for injecion
Diltiazem: 1.75–2.4 mg/kg q8h PO. Diltiazem sustained release: 10 mg/ kg q12–24h PO (usually 30 mg q12–24h PO)
120-mg capsules
12.5 mg q8h PO
50-mg tablet and chewable (orange flavor) 100 mg/mL injection
Dichlorphenamide (Daranide)
Diclofenac (Voltaren)
Dicloxacillin (Dynapen)
Digoxin immune Fab (Digibind) Digoxin (Lanoxin, Cardoxin)
Dihydrotachysterol (Hytakerol, DHT)
Diltiazem (Cardizem); Diltiazem sustained release (Dilacor XR, Cardiazem CD)
Dimenhydrinate (Dramamine [Gravol in Canada]) Dimercaprol (BAL, BAL in oil)
Dimethyl sulfoxide (DMSO)
Diminazene aceturate (Berenil RTU)
Cardiac glycoside. Used for supraventricular tachyarrhythmias when β-blockers or calcium channel blockers are ineffective or contraindicated. Also used for rare cases of myocardial failure (e.g., dilated cardiomyopathy) Vitamin D analogue. Used as treatment of hypocalcemia, especially that associated with hypoparathyroidism. Vitamin D promotes absorption and utilization of calcium. Calcium channel blocking drug. Blocks calcium entry into cells via blockade of slow channel. Produces vasodilation and negative chronotropic effects. Antihistamine drug. See chlorpheniramine. Chelating agent. For lead, gold, and arsenic toxicity. Used in amyloidosis to solubilize amyloid and decrease tissue inflammation; safety not documented in cats. Aromatic diamidine. Interferes with nuclear metabolism; inhibits DNA, RNA, protein synthesis, and phospholipid synthesis. For Cytauxzoonosis.
4 mg/kg q4h IM for 24 hours, q8h for 24 hours, then q12h for 10 days Dilute 90% solution 1 : 4 with sterile water; give 80 mg/kg SC three times/wk 2 mg/kg IM or SC then repeat in 3–7 days
0.125-mg tablet
0.125-, 0.2-, and 0.4-mg tablet
90% aqueous solution
70 mg/mL injection
continued
1009
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Diphenhydramine hydrochloride (Benadryl, generic)
H1 histamine receptor antagonist.
Diphenoxylate (Lomotil)
50-mg tablet;; 50 mg/mL injection Commercially available: 12.5-mg chewable tablet; 25-mg tablet and capsule; 2.5 mg/mL elixir 2.5-mg tablet
1 drop q6–8h topically
0.1% ophthalmic solution
4–10 mg/kg q24h PO
25-, 50-, 75-mg tablet
Dipyrone
Opioid agonist. Stimulates smooth muscle segmentation in intestine. For nonspecific diarrhea. Sympathomimetic to decrease aqueous production for glaucoma Platelet inhibitor. Mechanism of action is attributed to increased levels of cAMP in platelet, which decreases platelet activation. Indicated primarily to prevent thromboembolism. Antipyretic
Antihistamine: 2–4 mg/kg q6–12h IM, SC, or PO Chronic organophosphate toxicity: 2–4 mg/kg q8h IM for 2 days, then 2–4 mg/kg q8h PO for 21 days 0.05–0.1 mg/kg q12h PO
25 mg/kg q12–24h IM, SC, or IV
dl-methionine
See racemethionine
Dobutamine hydrochloride (Dobutrex)
Adrenergic agonist. Stimulates myocardium via action on cardiac β1-receptors. Increases heart contraction without increase in heart rate. For treatment of acute myocardial failure. Stool softener (surfactant). Acts to decrease surface tension to allow more water to accumulate in the stool. See docusate calcium.
No longer commercially available. However, available through compounding pharmacies 200- and 500-mg tablet; 500-mg chewable tablet 1000 mg/teaspoon powder 12.5 mg/mL injection
Dipivefrin (Dipivalyl HCl, Propine) Dipyridamole (Persantine)
Docusate calcium (Surfak, Dulcolax Stool Softener, generic [available over the counter]) Docusate sodium (Colace, DSS, Dulcolax Stool Softener generic [available over the counter]) Dolasetron mesylate (Anzemet) Domperidone (Motilium)
Dopamine hydrochloride (Intropin)
Doramectin (Dectomax) Dorzolamide (Trusopt) Doxapram (Dopram)
1010
0.5–2.0 mcg/kg/min IV constant rate infusion
50 mg q12–24h PO
Many preparations commercially available
50 mg q12–24h PO
100-mg soft gel capsule by prescription; many preparations commercially available 50- and 100-mg tablet; 20 mg/ mL injection 10-mg tablet Not commercially available in the United States. 40, 80, and 160 mg/mL injection
Serotonin receptor blocker; antiemetic. See ondansetron. Motility modifier (similar to metoclopramide).
0.6–1.0 mg/kg q12–24h PO or 0.3–0.6 mg/kg q12h PO, SC, or IV 2–5 mg q12–24h PO
Adrenergic agonist. To stimulate myocardium via action on cardiac β1–receptors. Not used in acute renal failure because cats lack renal capillary dopamine receptors. Avermectin antiparasitic agent Carbonic anhydrase inhibitor for glaucoma. Respiratory stimulant via action on carotid chemoreceptors and subsequent stimulation of respiratory center. To treat respiratory depression or to stimulate respiration postanesthesia. May also increase cardiac output.
Positive inotropy: 2–10 µg/kg/min IV constant rate infusion Shock and cardiopulmonary resuscitation: 10–20 µg/kg/min IV constant rate infusion 0.6 mg/kg (600 µg/kg) q7d SC 1 drop q6–8h topically
10 mg/mL injectable solution 2% ophthalmic solution
5–10 mg/kg IV; neonate: 1–5 mg SC, sublingual, or via umbilical vein
20 mg/mL injection
Drug Formulary
Drug
Action
Doxorubicin (Adriamycin, generic)
Anticancer agent. Used for treatment of various neoplasms, including lymphoma.
Doxycyline (Vibramycin, generics)
A synthetic antibiotic derived from tetracycline; works by interrupting the production of proteins by bacteria. It is effective against a wide variety of bacteria
Edetate calcium disodium (CaNa2EDTA) (calcium disodium versenate)
Chelating agent. For treatment of lead poisoning. Sometimes used in combination with dimercaprol (BAL). Cholinesterase inhibitor. Short acting and use to test for myasthenia gravis testing). Also used to reverse neuromuscular blockade of nondepolarizing agents (pancuronium). Angiotensin-converting enzyme inhibitor. Inhibits conversion of angiotensin I to angiotensin II. For hypertension, congestive heart failure, and to decrease glomerular protein loss. Inhalant anesthetic
Edrophonium (Tensilon, others)
Enalapril (Enacard, Vasotec)
Enflurane (Ethrane) Enilconazole (Imaverol)
Azole antifungal agent (for topical use only). Like other azoles, inhibits membrane synthesis (ergosterol) in fungus. Highly effective for dermatophytes.
Enoxaparin (Clexane, Lovenox)
Anti-coagulant used for cats predisposed to thromboembolism
Enrofloxacin (Baytril)
Fluoroquinolone antibacterial drug. Bactericidal. Broad-spectrum of activity. Adrenergic agonist. α- and β1-adrenergic receptor (but not β2-receptor) agonist. Used as vasopressor (e.g., during anesthesia), central nervous system stimulant, and to treat urinary incontinence (acts on bladder sphincter muscle). Adrenergic agonist. Nonselectively stimulates α- and β-adrenergic receptors. Used primarily in emergencies for cardiopulmonary arrest and anaphylactic shock.
Ephedrine (many, generic)
Epinephrine (Adrenaline, generic)
Dose & Route
How Supplied 2
1 mg/kg or 25 mg/m IV q21d or per chemotherapy protocol; dilute dose in 30 mL of 0.9% saline; administer over 15–30 minutes. 5–10 mg/kg q24h PO Follow with water to prevent esophageal irritation and stricture.
25 mg/kg q6h SC, IM, or IV for 2–5 days (dilute in 5% dextrose to 10 mg/mL solution)
2, 10, 20, 50, 150, and 200 mg/mL vials for injection
Capsules: 40, 50, 75, and 100 mg. Tablets: 50, 75, 100, and 150 mg. Suspension: 25 mg/teaspoon. Syrup: 50 mg/teaspoon. Powder for injection: 42.5, 100, and 200 mg. 200 mg/mL injection
0.1–0.2 mg/kg IV
10 mg/mL injection
0.5 mg/kg q24h PO
1-, 2.5-, 5-, 10- and 20-mg tablet
Induction: 2–3% Maintenance: 1.5–3% Nasal aspergillosis: 10 mg/kg q12h instilled into nasal sinus for 14 days (10% solution diluted 50 : 50 with water). Dermatophytes: dilute 10% solution to 0.2% and wash lesion with solution four times at 3- to 4-day intervals 1 mg/kg q12–24h SC
Available as solution for inhalation 100 mg/mL concentrated solution Not commercially available in the United States.
2.5 mg/kg q12h PO, IM, or IV (or 5 mg/kg q24h) Do not exceed this dose Urinary incontinence: 2–4 mg/cat q8–12h PO Vasopressor: 0.75 mg/kg IM or SC (repeat as needed)
Cardiac arrest: 0.2 mg/kg IV or 0.4 mg/kg intratracheal (may be diluted in saline before administration). Repeat q3–5min as needed 1 : 1000 solution = 1 mg/mL 1 : 10,000 solution = 0.1 mg/mL
100 mg/mL prefilled and graduated syringes and multidose vials 22.7-mg tablet; 22.7 mg/mL injection 25 and 50 mg/mL injection
1 mg/mL (1 : 1000 solution for injection)
continued
1011
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Epinephrine Ophthalmic, 1% (Epitrate)
Sympathomimetic to decrease aqueous production for glaucoma and to retract prolapsed third eyelid. Anticestodal agent (similar to praziquantel) Vitamin D analogue. Used for vitamin D deficiency and as treatment of hypocalcemia, especially associated with hypoparathyroidism. Vitamin D promotes absorption and utilization of calcium. Macrolide antibiotic. Spectrum of activity limited primarily to gram-positive aerobic bacteria. For skin and respiratory infections. Hematopoietic growth factor that stimulates erythropoiesis. Human recombinant erythropoietin. Used to treat nonregenerative anemia due to renal failure.
1 drop q6–8h topically
Available through compounding pharmacies
2.75 mg/kg PO
12.5- and 25-mg tablet
2,000–6,000 U/kg q24h PO initially; may need to reduce maintenance dose to 1,000–2,000 U/kg q1–7 days PO; time to maximum effect 5–21 days
50,000 IU soft gel capsule Compounding may be necessary to dose properly
10–20 mg/kg q8–12h PO
100- and 250-mg tablet
100 U/kg SC three times per week until packed cell volume = 30%, then 100 U/kg SC two times per week; monitor packed cell volume and adjust dosing interval to keep packed cell volume 30–40%; if >2 months, use with iron supplement. 250 µg IM between 40 hours to 5 days after mating Dilute ethanol to 20% solution in 5% dextrose 5 mL/kg IV q6h three to five treatments, then q8h three to four treatments;
2000 U/mL injection
Epsiprantel (Cestex) Ergocalciferol (vitamin D2) (Calciferol, Drisdol)
Erythromycin (many brands, generic)
Erythropoietin (epoetin alfa, Epogen, Procrit)
Estradiol cypionate (ECP, Depo-Estradiol, generic) Ethanol
Semisynthetic estrogen compound. Used primarily to induce abortion. Inhibits alcohol dehydrogenase to prevent breakdown of ethylene glycol into toxic metabolites. For antifreeze toxicity.
Etidronate disodium (Didronel-EHDP)
Bisphosphonate drug. For osteoporosis and hypercalcemia. Decreases bone turnover, inhibits osteoclast activity, retards bone resorption, and decreases rate of osteoporosis. Anesthetic Induction Agent Used for treatment of idiopathic seborrhea. Normalizes epidermal differentiation. A barbiturate plus phenytoin sodium for rapid euthanasia
Etomidate Etretinate (Tegison)
Euthanasia solution (Beuthanasia, Euthasol)
Famciclovir (Famvir, Valtrex)
Oral antiviral drug; especially for herpesvirus.
Famotidine (Pepcid)
H2 receptor antagonist; antacid. See cimetidine. Immunestimulant
Feline Recombinant Interferon Omega Fenbendazole (Panacur, Safe-Guard)
1012
Benzimidazole antiparasite drug. See albendazole.
10 mg/kg q24h PO
0.5–2 mg/kg IV to effect 2 mg/kg q24h PO
1 mL/ 10 pounds of body weight IV
31.25–125 mg/cat PO; Ave: 62.5 mg/ cat q12h PO; can be doubled if needed for better response 0.5–1.0 mg/kg q12–24h PO, SC, or IV 1 mega unit/kg q48h SC for five doses. 25–50 mg/kg q24h PO for 3–5 days; duration and need for retreatment varies based on parasite treated.
5 mg/mL injection 95% grain alcohol commercially available as Everclear. 20% solution: remove 105 mL from 500-mL bag of saline and replace with 105 mL of Everclear. 200-mg tablet
2 mg/mL vial for injection 10- and 25-mg capsule Not commercially available in the United States or Canada. 390 mg pentobarbital sodium + 50 mg phenytoin sodium/mL solution for injection 125-mg tablet
10- and 20-mg tablet; 10 mg/ mL injection Propriatary product. Not available in United States 100 mg/mL oral suspension
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Fentanyl, transdermal (Duragesic)
Fentanyl patches release sustained levels of fentanyl for 72–108 hours. One 100 mg/hour patch is equivalent to 10 mg/kg of morphine IM every 4 hours.
25 µ/hr patch 0.05 mg/mL intravenous solution in 2-, 5-, 10-, 20-, and 50-mg ampules or vials. CAUTION: Can be fatal if patch is ingested by child. Exercise extreme caution when sending cat home with a patch.
Ferrous sulfate (many over-the counter brands) Filgrastim (Neupogen) Fipronil 9.7%; or (S)methoprene 11.8% (Frontline Plus) Flavoxate
Iron supplement
25-µg patch q72–120h (0.002– 0.004 mg/kg per hour) Intravenous bolus: 0.001–0.005 mg/ kg Constant rate infusion: 0.002– 0.04 mg/kg per hour intraoperatively Constant rate infusion: 0.005– 0.01 mg/kg per hour postoperatively 50–100 mg q24h PO
Florfenicol (Nuflor) Fluconazole (Diflucan)
Flucytosine (Ancobon)
Fludrocortisone (Florinef)
Flumazenil (Romazicon)
Flumethasone (Flucort)
Flunixin meglumine (Banamine)
Fluoxetine hydrochloride (Prozac)
Flurbiprofen (Ocufen)
See colony-stimulating factor. Parasiticide for topical use.
See colony-stimulating factor All weights 8 weeks and older: 0.5 mL vial q1m
Antispasmodic for dysuria.
<10 pounds: 50 mg q12h PO; >10 100 mg q12h PO 22 mg/kg q8h PO 5 mg/kg q12h PO or 30–50 mg q12–24h PO
Chloramphenicol derivative. Azole antifungal drug. Fungistatic. For systemic fungi and dermatophytes. Antifungal drug. Used in combination with other antifungal drugs for treatment of cryptococcosis. Action is to penetrate fungal cells and is converted to fluorouracil, which acts as antimetabolite. Mineralocorticoid. Replacement therapy for adrenal atrophy or adrenocortical insufficiency. Higher mineralocorticoid than glucocorticoid activity. Benzodiazepine receptor antagonist. To reverse benzodiazepines in humans. Not commonly used in cats. Potent glucocorticoid antiinflammatory drug. Potency is approximately 15 times that of cortisol. See dexamethasone. Nonsteroidal anti-inflammatory. Acts to inhibit cyclo-oxygenase enzyme (COX) that synthesizes prostaglandins. Used for short-term treatment of pain and inflammation. Antidepressant drug. Used to treat behavioral disorders. Selective inhibition of serotonin reuptake and down regulation of 5-HT1 receptors. Nonsteroidal anti-inflammatory to reduce vascularization and inflammation in keratitis
Many formulations commercially available 300 µg/mL injection Topical solution
100-mg tablet 300 mg/mL injection 50-mg tablet
25–50 mg/kg q6–8h PO (up to a maximum dose of 100 mg/kg q12h PO). Alternative: 250 mg/cat q4–8h for 1–9 months (small to normal sized cats).
250- and 500-mg capsule
0.05–0.1 mg/kg q12h PO
0.1-mg tablet
0.2 mg IV (total dose) as needed
0.1 mg/mL injection
0.03–0.125 mg q24h IV, IM, SC
0.5 mg/mL injection
1.1 mg/kg once IV, IM, or SC
50 mg/mL injection
0.5–2 mg q24h PO
Chewable tabs: 8, 16, 32, and 64 mg (veterinary) Tablets: 10 and 20 mg Capsules: 10, 20, and 40 mg Oral Solution: 4 mg/ml (mint flavor) 0.03% ophthalmic solution
1 drop q8–12h topically
continued
1013
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Fluticasone propionate (Flovent)
Inhaled steroid primarily for asthma. Full effect takes about 10 days.
44, 110, and 220 µg/actuation aerosol
Folate/Folinic acid/Folic Acid (vitamin B9)
Replacement when long-term sulfa therapy is used.
Fomepizole (4-methylpyrazole) (Antizol-Vet)
For ethylene glycol toxicity
Furazolidone (Furoxone)
Gabapentin (Neurontin)
Antiprotozoal drug, especially for Giardia. Possibly for bacterial infections in intestine; not for systemic therapy. Loop diuretic. Inhibits sodium and water transport in ascending loop of Henle. May increase renal perfusion and decrease preload. Anticonvulsant
110 µg per puff; two puffs twice daily in spacer then allow patient to breathe through face mask for 7–10 breaths. If needed use 220 µg strength Sulfa-induced deficiency: 1–2 mg/cat q24h PO Irritable bowel disease-induced deficiency: 5 mg q24h PO 125 mg/kg within 3 hours postingestion followed by a dose of 31.25 mg/kg at 12, 24, and 36 hours after the initial dose. 8–20 mg/kg q24h PO for 7–10 days
Gemfibrozil (Lopid)
Cholesterol-lowering agent.
7.5 mg/kg q12h PO
Gentamicin (Gentocin)
Aminoglycoside antibiotic. Action is to inhibit bacteria Bactericidal. Broad spectrum of activity (except streptococci and anaerobes). Sulfonylurea oral hypoglycemic agent. For diabetes mellitus. Increases secretion of insulin from pancreas. Sulfonylurea hypoglycemic agent. See glipizide. Osmotic diuretic when given orally. Used for acute glaucoma. Has foul taste, administration through an orogastric tube is preferable. May cause vomiting. Anticholinergic drug. For mechanism, see atropine. Has less effect on central nervous system than atropine. Has longer duration of action than atropine. For autoimmune disease and lymphoplasmacytic gingivitis/ stomatitis.
2–4 mg/kg q8–12h IV, IM, or SC or 9 mg/kg q24h IV, IM, or SC.
Furosemide (Lasix, generic)
Glipizide (Glucotrol)
Glyburide (DiaBeta, Micronase, Glynase) Glycerin USP
Glycopyrrolate (Robinul-V)
Gold sodium thiomalate (Aurolate, Myochrysine)
Gonadorelin (Gn-RH, LH-RH) (Factrel)
Gonadotropin, chorionic (human chorionic gonadotrophin) (Profasi, Pregnyl, generic, APL)
1014
Stimulates synthesis and release of luteinizing hormone and follicle-stimulating hormone. Used to induce luteinization. Action of human chorionic gonadotrophin is identical to that of luteinizing hormone. Used to induce luteinization.
0.5–4 mg/kg q6–24h IV, IM, SC, or PO (low end of dose for maintenance) 5–10 mg/kg q24h PO initially then increased to 5–20 mg/kg q12h PO after 3–5 days
1-mg tablet
1 g/mL injection
100-mg tablet; 50 mg/15mL oral liquid No longer commercially available in the United States 12.5-, 20-, and 40-mg tablets; 10 and 50 mg/mL injection; 8 and 10 mg/mL oral solution (cherry flavor) 100-, 300-, and 400-mg capsules; 600- and 800-mg tablets; solution containing 250 mg per 5 ml. 600-mg tablet Compounding may be necessary to dose properly 5 and 40 mg/mL injection
0.25–0.75 mg/kg q12h PO Usual dose: 2.5 mg initially, then 5 mg q12h
5- and 10-mg tablet
0.2 mg/kg q24h PO
1.25-, 1.5-, and 2.5-mg tablet
50% or 70% solution: 1 gm/kg PO (orogastric tube is preferable) may be repeated once in 30 minutes.
0.6 g/mL solution
0.01 mg/kg IV, IM, or SC
0.2 mg/mL injection
1–5 mg IM first week, 2–10 mg IM second week, then 1 mg/kg q7d IM to remission, then 1 mg/kg q30d IM. 25–50 µg IM once
50 mg/mL injection
50 µg/mL injection
250 U IM once
1,000 U/mL injection
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Griseofulvin (microsize) (Fulvicin U/F)
Antifungal drug. Gets into skin layers and inhibits mitosis of fungi. Only for dermatophytes. Antifungal drug. Gets into skin layers and inhibits mitosis of fungi. Only for dermatophytes. Growth hormone. Used to treat growth hormone deficiencies. Anticoagulant. Potentiates anticoagulant effects of antithrombin III. Used primarily for prevention of thrombosis (efficacy questionable). Anti-coagulant
50 mg/kg q24h PO with high fat meal
500-mg tablet; 125 mg/5 mL oral suspension (orange cream flavor) 125- and 250-mg tablet
Griseofulvin (ultramicrosize) (Fulvicin P/G, Gris-PEG) Growth hormone (HGH) Heparin sodium (Liquaemin [United States], Hepalean [Canada], generics)
Heparin, low molecular weight (daltaperin) (Fragmin) Hydralazine (Apresoline)
Hydrochlorothiazide (HydroDIURIL, generic)
Hydrocortisone acetate (Cortef)
Hydrocortisone sodium succinate (Solu-Cortef) Hydrogen peroxide, 3% Hydroxyamphetamine 1% with tropicamide 0.25% (Paremyd) Hydroxyethyl starch (HES) (HES, Hetastarch, Hespan) Hydroxyurea (Hydrea)
Idarubicin Idoxuridine 0.1% (have compounded) Imidacloprid 9.1% (Advantage) Imidapril Imidocarb dipropionate (Imizol, Forray-65)
Imipenem (Primaxin)
Vasodilator. Antihypertensive. For treatment of congestive heart failure. Onset of action is 1–2 hours and lasts for 12 hours. Thiazide diuretic. Used as diuretic and antihypertensive. Decreases renal excretion of calcium; used to treat calcium containing uroliths. Glucocorticoid anti-inflammatory drug. Weaker anti-inflammatory effects and greater mineralocorticoid effects than prednisolone or dexamethasone. Same as hydrocortisone acetate, except that this is a rapid acting injectable product To induce emesis For determining if Horner’s syndrome is preganglionic or postganglionic Synthetic colloid volume expander (used in same manner as dextran). Antineoplastic agent. For neoplasia, polycythemia vera and polycythemia due to right-to-left cardiac shunts. Oral anthracycline agent for chemotherapy Topical ophthalmic antiviral
Parasiticide for topical use. Angiotensin-converting enzyme inhibitor for hypertension See Diminazene aceturate. For cytauxzoonosis.
β-lactam antibiotic with broadspectrum activity. See amoxicillin. For serious, multiple drugresistant infections.
5–10 mg/kg q24h PO with high fat meal 0.1 U/kg three times per week SC or IM for 4–6 weeks 100–200 U/kg IV loading dose, then 100–300 U/kg q6–8h SC. Low-dose prophylaxis: 70 U/kg q8–12h SC
5 and 10 mg/mL injectable
100 units/kg q12–24h SC
Prefilled syringes: 2,500–10,000 IU/0.2 mL Mulitdose vial: 95,000 IU/3.8 or 9.5 mL 10-, 25-, 50-, and 100-mg tablet
2.5 mg q12–24h PO
1,000 U/mL injection
1–4 mg/kg q12h PO
12.5-, 25-, and 50-mg tablet; 12.5-mg capsule
Replacement therapy: 1–2 mg/kg q12h PO. Anti-inflammatory: 2.5–5 mg/kg q12h PO
5-, 10-, and 20-mg tablet
Shock: 50–150 mg/kg IV Anti-inflammatory: 5 mg/kg q12h IV
100-, 250-, 500-, and 1000-mg/vial for injection
2–5 mL/kg PO not to exceed 15 ml Instill 1 drop into each eye
3% solution Ophthalmic solution
10–20 mL/kg constant rate infusion: over 12–24 hours IV Shock: 5 mL/kg over 15 minutes IV 25 mg/kg 3 days per week PO
6g/100mL + 0.9% NaCL infusion bag
2 mg q24h PO for 3 days, repeated every 21 days 2 drops q2–4h then reduce frequency with response. Treat at least 1 week. Up to 4.1 kg: 0.4 mL vial q1m 4.1–8.2 kg: 0.8 mL vial q1m 0.5 mg/kg q12–24h PO
20-mg vial for reconstitution
2 mg/kg IM, repeat in 3–7 days (pretreat with atropine at 0.05 mg/kg SC to reduce drug reactions) 3–10 mg/kg q6–8h IV or IM
500-mg capsule Compounding may be necessary to dose properly.
Available through compounding pharmacies 9.1% topical solution Not currently available in the United States 120 mg/mL injection
250- or 500-mg vial for injection
continued
1015
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Imipramine (Tofranil)
Tricyclic antidepressant. For behavioral disorders, including obsessive-compulsive disorders. An immune response modifier used for herpes dermatitis. Nonsteroidal anti-inflammatory. Keratitis and uveitis: to reduce vascularization and inflammation. Insulin has multiple effects associated with utilization of glucose. Long-acting insulin for diabetes mellitus.
2– 4 mg/kg q12–24h PO
10-, 25-, and 50-mg tablet
Apply topically three times per week
5% cream
1 drop q8–12h topically
0.5% ophthalmic drops
Initially 0.5 U/kg SC q12h if blood glucose is >360mg/dL, or 0.25U/ kg SC q12h if blood glucose is <360 mg/dL. Adjust insulin dose based on clinical signs, fructosamine levels, and serial blood glucose curves Ketoacidosis: 0.2 U/kg IM initially, then 0.1 U/kg q1h IM until blood glucose is 300 mg/dL then 0.25–0.4 U/kg q6h SC Same as for lente insulin
100 U/mL injection
100 U/mL injection
Same as for lente insulin
40 U/mL injection
Same as for lente insulin
40 U/mL injection
1 Mu/kg q48h SC for five doses followed by 10,000 units orally for 2 months; varies with disease treated. 600–800 mg iodine/kg; MD-76R: 1.6–2.1 ml/kg IV slowly; do not give intrathecally (myelograms)
10 Mu/vial. Available in Europe and Australia. Not available in United States.
Imiquimod (Aldara) Indomethacin, 1%
Insulin glargine (Lantus)
Insulin, regular crystalline
Short-acting insulin; duration of action about 2 hours.
Insulin, NPH isophane
Short-acting insulin; duration of action about 2 hours. Short-acting insulin; duration of action about 2 hours. Short-acting insulin; duration of action about 2 hours. Feline origin interferon. Used to stimulate the immune system.
Insulin, porcine insulin zinc suspension (Vetsulin) Insulin, protamine zinc (PZI) Interferon (feline omega interferon, Virbagen Omega) Iodinated contrast agents (MD-76R)
Contrast agent for intravenous or other use. Not for myelograms
Iohexol
Contrast agent for myelograms, intravenous, or other use. Emetic drug. For emergency treatment of poisoning. Active ingredient is thought to be emetine. Iron supplement; for cats receiving long-term erythropoietin therapy. Inhalant anesthetic. See halothane.
Ipecac syrup (Ipecac)
Iron dextran Isoflurane (AErrane) Isoproterenol (Isuprel)
Isotretinoin (Accutane)
Itraconazole (Sporanox)
1016
Adrenergic agonist. Stimulates both β1- and β2-adrenergic receptors. Used to stimulate heart (inotropic and chronotropic). Also used to relax bronchial smooth muscle for acute treatment of bronchoconstriction. A systemic retinoid for severe acne and other inflammatory skin diseases. Azole (triazole) antifungal drug. For dermatophytes and systemic fungi.
0.45 ml/kg at 240 mg/mL concentraion IV or intrathecal 2–6 mL PO
50 mg/cat q30d IM Induction: 5% Maintenance: 1.5–2.5% Asthmatic crisis: 0.1–0.2 mg q6h IV, IM, or SC or 10 µg/kg q6h IM or SC or dilute 1 mg in 500 mL 5% dextrose or Ringer’s solution and infuse IV 0.5–1 mL/minute (1–2 µg/minute) or to effect
100 U/mL injection
MD-76R: 660 mg Diatrizoate meglumine + 100 mg Diatrizoate sodium /mL (373.65 mg iodine/ml) 180, 240 and 300 mg/mL Oral syrup
50, 100, and 200 mg/mL injection 99.9% liquid inhalant 0.02 and 0.2 mg/mL injection
1–2 mg/kg q24h PO
10-, 20-, 40-mg capsule and softgel capsule
Systemic fungi: 5 mg/kg q12h PO Dermatophytes: 10 mg/kg q24h PO
100-mg capsule and 10 mg/mL oral suspension (cherry or caramel flavor)
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Ivermectin (Heartgard for cats, Ivomec)
Parasiticide. Works by potentiating effects of inhibitory neurotransmitter γ aminobutyric acid. Lungworms: less effective than fenbendazole.
55- and 165-µg chewable tablet; 2.7 and 10 mg/mL injection; 10 mg/mL liquid; 1.87% paste
Ivermectin 0.01% (Acarexx)
Parasiticide for ear mites in cats 4 weeks and older.
Kanamycin (Kantrim)
Aminoglycoside antibiotic. See gentamicin and amikacin for details. Antidiarrheal compound. Kaolin may act as adsorbent for endotoxins and pectin may protect intestinal mucosa. Anesthetic agent. Exact mechanism of action is not known but appears to act as dissociative agent. Ketamine has little analgesic activity. Rapidly metabolized and eliminated in most cats.
Heartworm preventative: 24 µg/kg q30 days PO; Microfilaria: 50 µg/ kg PO or SC; Notoedres and Cheyletiella: 200 µg/kg every week PO for 4 weeks; Lungworms: 400 µg/kg q14d PO for two to four treatments Ear mites: 300–400 µg/kg q7–14d PO, SC for three to five treatments Cuterebra: 0.1 mg/kg q48h SC for three treatments. 1 vial (0.5 mL) in each ear canal; may need to be repeated in 3–4 weeks 10 mg/kg q12h IV, IM, or SC
1–2 mL/kg q2–6h PO
90 g kaolin + 2 g pectin/fl oz
1–5 mg/kg IV or IM (recommend adjunctive sedative or tranquilizer treatment) Constant rate infusion: 0.6 mg/kg per hour for anesthesia Constant rate infusion: 0.12 mg/kg per hour up to 24 hours for postoperative pain 5–10 mg/kg q12–24h PO
10, 50, and 100 mg/mL injection
1–2 mg/kg q24h PO (up to 3 days); 1–2 mg/kg once IV, IM, or SC
50- and 75-mg tablet; 100 mg/ mL injection Available in Canada: 5- and 20-mg tablet Intravenous solution
Kaopectate (kaolin and pectin) (Kaopectate)
Ketamine (Ketalar, Ketavet, Vetalar, generic)
Ketoconazole (Nizoral, generic)
Ketoprofen (Orudis-KT [over-the-counter tablet], Ketofen [injection]) Lactated Ringer’s solution Lactulose (Chronulac, generic)
Lanthanum carbonate (Renalzin) Latanoprost (Xalatan)
Leucovorin (folinic acid) (Wellcovorin, generic)
Azole (imidazole) antifungal drug. Similar mechanism of action as other azole antifungal agents. For dermatophytes and systemic fungi. Nonsteroidal anti-inflammatory. See flunixin meglumine. Not approved in the United States. Isotonic crystalloid fluid solution for replacement or maintenance. Laxative by osmotic effect in colon. Also for hyperammonemia (hepatic encephalopathy) because it decreases blood ammonia concentrations via lowering pH of colon. Phosphate binder
Maintenance: 40–50 mL/kg per day IV, SC, or intraperitoneally Constipation: 0.5–1.0 mL/kg q8–12h PO to effect. Hepatic encephalopathy: 2.5–5 mL q8–12h PO or 20–30 mL/kg of a 30% solution given as a retention enema 200 mg (1 ml/1 pump) q12h in food
Prostaglandin analog for lowering intraocular pressure; efficacy not proved. Reduced to folic acid, which is available for purine and thymidine synthesis. Antidote for folic acid antagonists.
1 drop q30m topically; repeat as needed per IOP With methotrexate administration: 3 mg/m2 IV, IM, or PO Antidote for pyrimethamine toxicosis: 1 mg/kg q24h PO
0.01% Otic suspension
333 mg/mL injection
200-mg tablets
10 g/15 mL solution
Metered pump dispenser; 200 mg/mL Not available in United States. 0.005% ophthalmic solution
5- and 25-mg tablet; 10 and 20 mg/mL injection
continued
1017
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Levamisole (Levasole, Tramisol, Ergamisol)
Antiparasitic drug of the imidazothiazole class. Mechanism of action a result of neuromuscular toxicity to parasites.
Lungworms: 20–40 mg/kg q48h PO for five treatments Stomach worms: 5 mg/kg once PO (2.5% solution)
Levetiracetam (Keppra)
Anticonvulsant to be used as an add-on to phenobarbital. Still under investigation. β-blocker to decrease aqueous production for glaucoma Local anesthetic Converted to dopamine after crossing blood-brain barrier. Stimulates central nervous system dopamine receptors. For treating hepatic encephalopathy. Replacement therapy for treating cats with hypothyroidism. Levothyroxine is T4; converted to the active T3. Local anesthetic. See bupivacaine for mechanism of action. For acute treatment of cardiac arrhythmias. Class I antiarrhythmic. Decreases phase 0 depolarization without affecting conduction. Not useful for supraventricular arrhythmias. Lincosamide antibiotic. Similar in mechanism to clindamycin and erythromycin. Used for pyoderma and other soft-tissue infections. Liothyronine is equivalent to T3. Used for thyroid testing. Cytotoxic alkylating agent; used as chemotherapeutic agent.
20 mg/kg q8h PO
184-mg (sheep) and 2.19-g (cattle) tablet Compounding may be necessary to dose properly Not available in Unites States. In Canada: 50-mg tablet 250-mg tablet; 100 mg/mL oral solution (grape flavor)
Levobunolol (Betoptic) Levo-bupivacaine Levodopa (l-dopa) (Larodopa, l-dopa)
Levothyroxine sodium (Soloxine, Thyro-Tabs, Synthroid) Lidocaine (Xylocaine)
Lincomycin (Lincocin)
Liothyronine (Cytomel) Lomustine (CCNU, CeeNU)
Loperamide (Imodium)
Lorazepam Lufenuron (Program)
L-Lysine (Enisyl, others, generic)
Opioid agonist. Stimulates smooth muscle segmentation. For acute diarrhea. Benzodiazepine for urine spraying, anxiet and intercat aggression. Antiparasitic. Chitin synthesis inhibitor. Used for controlling fleas in animals. Inhibits development in hatching fleas. Amino acid for treatment of herpes infections. Probably not clinically efficacious.
Lyme sulfur dip
Topical anti-parasiticide.
Lymphocyte T-Cell Immunomodulator (Imulan)
Immune stimulant
Lyovac antivenin
Antivenin for black widow spiders (Latrodectus spp.)
Magnesium chloride
Use to treat hypomagnesemia.
1018
1 drop q12h topically Up to 1.5 mg/kg 6.8 mg/kg PO initially, then 1.4 mg/ kg q6h PO
0.25% and 0.5% ophthalmic solution 0.75% solution 100-mg capsule Compounding may be necessary to dose properly
10–20 µg/kg per day PO (adjust dose via monitoring)
0.1-, 0.2-, and 0.3-mg tablet
0.25–0.75 mg/kg IV slowly or 10–40 µg/kg per minute as a constant rate infusion For epidural: 4.4 mg/kg 2% solution Local infiltration: 2–4 mg/kg Topical: up to 0.8 g
20 mg/mL injection EMLA cream 2.5% lidocaine with 2.5% prilocaine
15–25 mg/kg q12h PO Pyoderma: Doses as low as 10 mg/ kg q12h have been used
Injectable: 25, 100, 300 mg/ml; Oral solution: 50 mg/ml; Tablets: 100, 200, 500 mg; 400 mg/g soluble powder 5-, 25-, and 50-µg tablet
For T3 suppression test: see Chapter 311 50–60 mg/m2 PO every 4–6 weeks or 10 mg for average to large size cat PO every 4–6 weeks 0.08–0.16 mg/kg q12h PO
10-, 40-, 100-mg capsule
2-mg capsule and chewable tablet; 1 mg/5 mL oral liquid
0.125–0.25 mg/cat q12–24h PO
0.5-mg tablet
30 mg/kg every 30 days PO or 10 mg/kg every 6 months SC
45-, 90, 204.9-, and 409.8-mg tablet
250–500 mg q12–24h PO
250 mg/1.25mL gel; 250 mg/mL paste; 250 mg/teaspoon powder; 500-mg tablet; 50-mg treat. 97.8% Lime Sulfur Concentrate
Dilute per label directions; dip weekly based on diagnosis. 1 ml (1 µg) q7d SC for 4 weeks then q14d for 2 treatments then as needed Mix one vial with 100 mL of saline and give slowly IV over 30 minutes 0.75–1.0 mEq/kg per day IV constant rate infusion for first day, then 0.3–0.5 mEq/kg per day IV constant rate infusion
Proprietary preparation
One vial; equine origin product
Available over the counter
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Magnesium citrate (Citroma, CitroNesia [Citro-Mag in Canada]) Magnesium hydroxide (Milk of Magnesia)
Saline cathartic. For constipation and bowel evacuation before certain procedures. Same as magnesium citrate. Magnesium hydroxide also is used as oral antacid to neutralize stomach acid. Saline cathartic. For constipation and bowel evacuation before certain procedures. Hyperosmotic diuretic. Increases plasma osmolality, which draws fluid from tissues to plasma. Antiglaucoma agent. Used for treatment of cerebral edema and reducing intraocular pressure. Mannitol also has been used to promote urine production in oliguric renal failure and to facilitate urinary excretion of certain toxins.
2–4 mL/kg q24h PO
160-mg capsule; 200-mg tablet; 58.16 mg/mL oral solution (cherry flavor) 80 and 160 mg/mL oral suspension (various flavors)
Magnesium sulfate (Epsom salts) Mannitol, 20% (Osmitrol, generic)
Marbofloxacin (Zeniquin)
Maropitant (Cerenia)
Meclizine (Antivert, generic) Medetomidine
Medroxyprogesterone acetate (injection [Depo-Provera]) Megestrol acetate (Megace)
Fluoroquinolone antibiotic. Same mechanism as enrofloxacin and ciprofloxacin. Anti-emetic; a neurokinin (NK1) receptor antagonist. Stops vomiting at four points of origin. Antiemetic and antihistamine. Used for treatment of motion sickness. α2-adrenergic agonist. Sedative with some analgesia Progestin hormone. For controlling estrus cycle and some behavioral disorders. See medroxyprogesterone acetate.
Meloxicam (Metacam)
Nonsteroidal anti-inflammatory for pain and inflammation
Melphalan (Alkeran)
Anticancer agent. Alkylating agent, similar in action to cyclophosphamide.
Antacid: 5–10 mL q12–24h PO Cathartic: 15–60 mL q8–12h PO
2–5 g q24h PO
Granules; many generic preparations
To promote /maintain urine flow: 1.25–5.0 mL/kg IV, repeat q4–6h if necessary. Glaucoma or central nervous system edema: 7.5 mL/kg IV over 15–20 minutes, repeat in 6 hours if necessary. Should be administered through an intravenous catheter at a dose of 1.0–1.5 gm/kg once slowly (over 15–20 minutes). If ineffective in 30 minutes, the dose may be repeated once. 2.75–5.55 mg/kg q24h PO
Intravenous 20% Solution
Vomiting: 1 mg/kg q24h SC; 2 mg/ kg q24h PO Motion sickness: 8 mg/kg PO 12.5 mg q24h PO 1–2 µg/kg per hour IV
1.1–2.2 mg/kg q7d SC or IM Behavioral disorders: 10–20 mg/kg q30d SC or IM Urine spraying: 2.5–5 mg q24h PO for 1 week, then reduce to once or twice q7–14d Soft tissue anti-inflammatory: 2.5–5.0 mg q24h PO for 1 week, then reduce to 5 mg q3–7d Suppress estrus: 5 mg/day for 3 days, then 2.5–5 mg weekly for 10 weeks Caution: use may make diabetes mellitus clinical in a borderline diabetic 0.3 mg/kg SC once 0.1 mg/cat per day PO or SC; some dose at 0.05–0.1 mg/kg q24–48h PO. Note: Only approved in cats for one subcutaneous injection for pain in United States. May be nephrotoxic. Use lowest effective dose in well hydrated cat. 1.5 mg/m2 or 0.1–0.2 mg/kg q24h PO for 7–10 days (repeat every 3 weeks or reduce to q48h)
25-, 50-, 100-, and 200-mg tablet 10 mg/mL injection; 16-, 24-, 60-, and 160-mg tablets 12.5-, 25-, and 50-mg tablet 1 mg/mL concentration. Available in a 10 mg/mL strength in Europe 150 and 400 mg/mL injection
5-, 20-, and 40-mg tablet; 40 mg/mL oral suspension 5-mg size not available in the United States. Compounding may be necessary to dose properly
5 mg/mL injection; 1.5 mg/mL oral suspension
2-mg tablet
continued
1019
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Meperidine (Demerol)
Synthetic opioid agonist with activity primarily at the µ-opioid receptor. 75 mg IM or 300 mg PO has similar potency as 10 mg morphine. Local anesthetic. See bupivacaine. Medium potency and duration of action compared to bupivacaine.
3–5 mg/kg IV or IM (as needed or every 2–4 hours)
25, 50, 75 and 100 mg/mL injection
Local infiltration: 2–4 mg/kg Epidural: 10 mg (0.5 mL of a 2% solution) every minute until reflexes are depressed or absent 50 mg/m2 q24h PO to effect, then q48h or as needed
20 mg/mL injection
Mepivacaine (Carbocaine)
6-Mercaptopurine (Purinethol)
Metaflumizone (Promeris for Cats)
Anticancer agent. Antimetabolite agent that inhibits synthesis of purines in cancer cells. For resistant infections. See imipenem. For flea control by blocking gated sodium channels of the insect.
Metaproterenol (Alupent, Metaprel)
β-adrenergic agonist, β2-specific. For bronchodilation. See albuterol.
Methadone (Diskets, Dolophine, Methadose)
Synthetic opioid, used as an analgesic, antitussive, and a maintenance anti-addictive for use in patients on opioids. Carbonic anhydrase inhibitor. Produces less diuresis than others. See acetazolamide. Urinary antiseptic. Converted to formaldehyde in acidic urine. Not effective for systemic infections. Urinary antiseptic. See methenamine hippurate. Antithyroid drug for hyperthyroidism. Action is to serve as substrate for thyroid peroxidase and decrease incorporation of iodide into thyrosine molecules Skeletal muscle relaxant. Depresses polysynaptic reflexes. For skeletal muscle spasms and pyrethrin or pyrethroid toxicosis.
Meropenem (Merrem)
Methazolamide (Neptazane)
Methenamine hippurate (Hiprex, Urex) Methenamine mandelate (Mandelamine) Methimazole (Tapazole, Felimazole, generic)
Methocarbamol (Robaxin-V)
Methohexital (Brevital) Methotrexate (MTX, Mexate, Folex, Rheumatrex, generic)
Methoxamine (Vasoxyl) Methylene blue 0.1% (generic, new methylene blue) Methylprednisolone (Medrol)
Methylprednisolone acetate (Depo-Medrol)
1020
Barbiturate anesthetic. See thiopental for details. Anticancer agent. Used for various carcinomas, leukemia, and lymphomas. Action: antimetabolite. Adrenergic agonist. Used to increase blood pressure For methemoglobinemia. Acts as reducing agent to reduce methemoglobin to hemoglobin. Glucocorticoid antiinflammatory drug. See betamethasone. Depot form of methylprednisolone. Lasts 3–4 weeks.
50-mg tablet
10–20 mg/kg q8–12h IV or SC
500-mg and 1-g injection
Apply one vial q30d. May last 7 weeks. For cats and kittens 8 weeks and older. 0.325–0.65 mg/kg q4–6h PO
2.5–10 mg/kg q12h PO
18.5% topical solution Small: up to 9 pounds Large: 9 pounds or more 10- and 20-mg tablet; 10 mg/5 mL syrup (cherry flavor) 5- and 10-mg tablets 1, 2, and 10 mg/mL oral solution 10 mg/mL for injection 25- and 50-mg tablet
250 mg q12h PO
1-g tablet
10–20 mg/kg q8–12h PO
500-mg and 1-g tablet
2.5–5 mg q12h PO for 1–4 weeks until TT4 is normal, then 2.5–10 mg q12h PO according to TT4 level.
5- and 10-mg tablet
44 mg/kg q8h PO on the first day, then 22–44 mg/kg q8h PO; 50–200 mg/kg IV not to exceed 300 mg/kg per day or 200 mg/min rate. 3–6 mg/kg IV (give slowly to effect)
500- and 750-mg tablet; 100 mg/mL injection
0.05–0.1 mg/kg IV 0.1–0.5 mg/kg IM or SC
2.5–5 mg/m2 q48h PO (dose depends on specific protocol); 0.5–0.8 mg/kg IV every 1–3 weeks. 200–250 µg/kg IM or 40–80 µg/kg IV 1.0–1.5 mg/kg IV slowly once; caution: may cause Heinz body hemolytic anemia See doses for prednisolone; has potency that is 1.25 times prednisolone. 10–20 mg SC or IM every 2–8 weeks Subconjunctival: 4–8 mg
500-mg and 2.5-g vial for injection 2.5-, 5-, 7.5-, 10-, and 15-mg tablets, and 5-, 20-, 50-, 100-, 200-, and 250-mg and 1-g vials for injection 20 mg/mL injection 10 mg/mL injection
2-, 4-, 8-, 16-, 24-, and 32-mg tablet 20 and 40 mg/mL injection
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Methylprednisolone sodium succinate (Solu-Medrol)
Same as methylprednisolone but water soluble; intended for acute therapy when high intravenous doses are needed for rapid effect. For shock and central nervous system trauma.
125-, 500-mg, 1- and 2-g vial for injection
Methyltestosterone (Android, generic)
Anabolic androgenic agent. For testosterone hormone replacement therapy and to stimulate erythropoiesis. Prokinetic drug. Centrally acting antiemetic. Stimulates motility of upper gastrointestinal tract. For gastroparesis and vomiting. For hyperadrenocorticism. Decreases conversion of 11-deoxycortisol to cortisol. Adrenergic blocking agent. β1-adrenergic blocker. For tachyarrhymias and slow heart rate. Antibacterial and antiprotozoal. Disrupts DNA in organism via reaction with intracellular metabolite. Specific for anaerobic bacteria. Resistance is rare. Active against some protozoa, including Giardia. Benzodiazepine. See diazepam. Anesthetic adjunct.
Shock: 30 mg/kg IV over 1–2 minutes, repeat at 15 mg/kg in 2–6 hours if needed Central nervous system trauma: 30 mg/kg IV initially, then 15 mg/ kg IV at 2 hours, then 10 mg/kg q4h IV for 6 doses. 2.5–5 mg q24–48h PO
0.2–0.5 mg/kg q6–12h SC or PO Constant rate infusion: 0.01– 0.02 mg/kg per hour or 1–2 mg/kg per day 65 mg/kg q8–12h PO
5- and 10-mg tablet; 1 mg/mL oral suspension (vanilla flavor); 5 mg/mL injection
2–15 mg q8h PO
50- and 100-mg tablet
Anaerobes: 10–15 mg/kg q12h PO Giardia: 20–25 mg/kg q12h PO for 7 days Irritable bowel disease: 10–20 mg/kg q12h for 2–3 weeks Acne: Apply to chin q12h
250- and 500-mg tablet; compounding recommended. 500-mg vial for injection; 0.75% dermatologic gel
0.1–0.25 mg/kg IV or IM or 0.1–0.3 mg/kg per hour IV constant rate infusion 1 vial (0.5 mL) in each ear canal; may have to be repeated in 3–4 weeks Heartworm prevention: 2 mg/kg q30 days PO
1 and 5 mg/mL injection
Metoclopramide (Reglan, Maxolon [Maxeran in Canada]) Metopirone (Metyrapone)
Metoprolol tartrate (Lopressor)
Metronidazole (Flagyl, generic)
Midazolam (Versed)
Milbemycin 0.1% (MilbeMite)
Parasiticide for ear mites, for cats 4 weeks and older.
Milbemycin oxime (Interceptor)
Antiparasitic. Acts as γ aminobutyric acid agonist in nervous system of parasite Heartworm preventative. Lubricant laxative. Increases water content of stool. Increases passage of feces for treatment of impaction and constipation. Tetracycline antibiotic. Similar to doxycycline. Benzodiazepine. Centrally acting central nervous system depressant. Primarily used as appetite stimulant. Adrenocortical cytotoxic agent. Suppresses adrenal cortex. For adrenal tumors and pituitarydependent hyperadrenocorticism. Cats rarely respond so use is not recommended.
Mineral oil (generic)
Minocycline (Minocin) Mirtazapine (Remeron)
Mitotane (o,p’-DDD; Lysodren)
10–25 mL q12h; must be given by orogastric tube. Inhalation/lipid pneumonia occurs easily if given orally. 5–12.5 mg/kg q12h PO Appetite stimulation: 3.25 mg/cat q2–3d PO. If anxiety occurs, reduce to approximately 1.5 mg q3d PO. Pituitary-dependent hyperadrenocorticism: 50 mg/kg per day PO (in divided doses) for 5–10 days, then 25 mg/kg PO two times per week Adrenal tumor: 50–75 mg/kg per day PO for 10 days, then 25–40 mg/kg two times per week. Note: Assess response and adjust maintenance dosing via adrenocorticotropic hormone stimulation testing.
10-mg tablet
250-mg capsule
0.1% otic solution
2.3-, 5.75-, 11.5-, and 23-mg tablet 100% oil
50-, 75-, and 100-mg tablet; 10 mg/mL oral suspension 7.5- and 15-mg tablet
500-mg tablet
continued
1021
SECTION 9: Formulary
Drug Mitoxantrone (Novantrone)
Montelukast (Singulair)
Morphine (generic)
Mupirocin (Bactroban) Nalbuphine (Nubain)
Nalorphine (Nalline) Naloxone (Narcan)
Naltrexone (Trexan)
Nandrolone decanoate (Deca-Durabolin)
Naphazoline (Naphcon-A) Neomycin (Biosol)
Neostigmine bromide and neostigmine methylsulfate (Prostigmin, Stiglyn)
Nitazoxanide (Alinia)
Nitenpyram (Capstar) Nitrofurantoin (Furadantin, Macrodantin) Nitrofurazone Nitroglycerin (Nitrol, Nitrobid, Nitrostat)
1022
Action Anticancer antibiotic. Similar to doxorubicin in action. For neoplasia. Leukotriene inhibitor. Antiinflammatory for small airway disease. Opioid agonist and analgesic. Binds to µ- and κ-opioid receptors on nerves and inhibit release of neurotransmitters involved with transmission of pain stimuli. For feline acne Antagonist for opioids; Duration may be longer than the agonist so repeat doses may be needed. Opioid antagonist. See naloxone. Opioid antagonist. Used to reverse effects from opioid agonists (such as morphine). Naloxone may be used to reverse sedation, anesthesia, and adverse effects caused by opioids. Opioid antagonist. Similar to naloxone except longer acting and administered PO. For treatment of some obsessive-compulsive behavioral disorders. Anabolic steroid. Derivative of testosterone. Used to reverse catabolic conditions, increase weight gain, increase muscle, and stimulate erythropoiesis. Ophthalmic antihistamine for allergic conjunctivitis. Aminoglycoside antibiotic. See gentamicin and amikacin. Systemic absorption of oral dose is minimal. Anticholinesterase drug. Cholinesterase inhibitor. Inhibits breakdown of acetylcholine at synapse. Antimyasthenic drug. Used primarily for treatment of myasthenia gravis or as an antidote for neuromuscular blockade caused by nondepolarizing neuromuscular blocking drugs. For cryptosporidiosis; may cause vomiting and diarrhea. Short- and rapid-acting (24–36 hour) oral flea adulticide. Antibacterial. Urinary antiseptic. Action is via reactive metabolites that damage DNA. Coccidiostat Nitrate. Nitrovasodilator (venodilator). In congestive heart failure to reduce preload or decrease pulmonary hypertension.
Dose & Route 2
How Supplied
6.5 mg/m q21d IV
2 mg/mL injection
5.0–1.0 mg/kg q24h PO
4- and 5-mg chewable tablet; 10-mg tablet
0.05 mg/mL q1–4h IV 0.1–0.3 mg/kg q4–6 IM
0.5, 1, 2, 5, 8, 10, 15, 20, 25, 30, and 50 mg/mL injection
Apply to skin q12–24h 0.5–1.5 mg/kg IV, SC, or IM
2% ointment 10 mg/mL or 20 mg/mL. Both strengths in 10 mL vials.
0.05–0.2 mg/kg IM or SC 0.01–0.04 mg/kg IV, IM, or SC
5 mg/mL injection 0.02 and 0.4 mg/mL injection
Behavioral disorders: 2.2 mg/kg q12h PO
50-mg tablet
1 mg/kg per week IM
100 and 200 mg/mL injection
1 drop q6–12h topically
0.025% drops
10–20 mg/kg q6–12h PO
25 and 250 mg/mL oral liquid; 500-mg tablet
Antimyasthenic: 2 mg/kg per day PO (in divided doses, to effect). 0.04 mg/kg IM or SC as needed. Antidote for neuromuscular block: 40 µg/kg IV, IM, or SC. Diagnostic aid for myasthenia gravis: 40 µg/ kg IM or 20 µg/kg IV Note: administer atropine if cholinergic side effects occur
Neostigmine bromide: 15-mg tablet Neostigmine methylsulfate: 0.5 and 1 mg/mL injection
25 mg/kg q12h PO for 28 days
500-mg tablet; 100 mg/5 mL oral suspension (strawberry flavor) 11.4- and 57-mg tablet
1 tablet (11.4 mg) per 0.9–11.4 kg PO; can repeat daily. 4 mg/kg q8–12h PO
Add to drinking water (up to 1 gm/2 liters) for 7 days. 2–4 mg (approximately0.5 cm or 1/4 in of ointment) topically q6–8h. Duration about 48h. Wear gloves when applying.
25-, 50-, and 100-mg capsule; 5 mg/mL oral suspension (mint flavor) 4.59% soluble powder Approximately 5 mg/cm (approximately 15 mg/in) transdermal ointment
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Nitroimidazole
Antimicrobial agent for treating Tritrichomonas diarrhea. Nitrate vasodilator for hypertensive crisis. See nitroglycerin. H2 receptor antagonist antacid. See cimetidine. Fluoroquinolone antibacterial drug. Same action as ciprofloxacin; less spectrum. For candidiasis.
30–50 mg/kg q12h PO for 2 weeks
Not commercially available in the United States 25 and 50 mg/mL injection
Nitroprusside (Nitropress) Nizatidine (Axid) Norfloxacin (Noroxin)
Nystatin (Nystatin, Mycostatin) Octreotide acetate (Sandostatin)
Olopatadine (Patanol) Omega-3 fatty acids, (EPA) Omeprazole (Prilosec)
Ondansetron (Zofran)
Orbifloxacin (Orbax) Ormetoprim and sulfadimethoxine (Primor)
Oxacillin (Prostaphlin, generic)
Oxazepam (Serax)
Oxfendazole (Synathic) Oxybutynin (Ditropan)
Oxyglobin (polymerized bovine hemoglobin)
Oxymetazoline HCl (Afrin Pediatric Nasal Drops) Oxymetholone (Anadrol) Oxymorphone (Numorphan)
1–3 µg/kg per minute IV constant rate infusion 2.5–5 mg/kg q24h PO 22 mg/kg q12h PO
100,000 U q6h PO
Somatostatin analogue. For acromegaly and insulinomas and to resolve pleural fluid due to thoracic duct rupture (chylothorax). Ophthalmic antihistamine for allergic conjunctivitis Fatty acid supplement for dermatologic use Proton pump blocker; inhibits gastric acid secretion
10 µg/kg q8h SC for 2–3 weeks; has been used at doses up to 200 µg q8h SC Cylothorax: 3–10 µg/kg SC four times a day for 4 weeks. 1 drop q6–12h topically
Antiemetic drug. Inhibits action of serotonin (blocks 5-HT3 receptors). Used primarily to inhibit vomiting associated with chemotherapy. Fluoroquinolone antibacterial. Antibacterial drug. Bactericidal/ bacteriostatic. Broad antibacterial spectrum and active against some coccidia.
0.5–1.0 mg/kg 30 minutes before administration of cancer drugs IV, IM, SC, or PO Antiemetic: 0.5–1.0 mg/kg q6–12h IV, IM, SC, or PO 2.5–7.5 mg/kg q24h PO 27 mg/kg PO on first day, followed by 13.5 mg/kg q24h
β-lactam antibiotic. Inhibits bacterial cell wall synthesis. Spectrum is limited to gram-positive bacteria, especially staphylococci. Benzodiazepine. Centrally acting central nervous system depressant. For sedation and to stimulate appetite. For treating Ollulanus (stomach worms). Anticholinergic smooth muscle antispasmodic. For detrusor hyperreflexia. Hemoglobin glutamer (bovine) used as an oxygen-carrying fluid for anemia, shock, acetaminophen intoxication, etc. Nasal spray for congestion. Be careful of rebound effect (dependence). Anabolic steroid. See nandrolone. Opioid agonist. Action is similar to that of morphine except that oxymorphone is 10–15 times more potent than morphine.
22–40 mg/kg q8h PO
5–10 mg/kg q24h PO based on eicosapentaenoic acid content 0.7 mg/kg q24h PO
75-mg tablet; 15 mg/mL oral solution (bubble gum flavor) 400-mg tablet
100000 U/mL oral suspension (cherry-mint flavor) 50, 100, 200, and 500 µg and 1-mg injection
0.1% solution Various proprietary products with different concentrations. 10-, 20-, and 40-mg delayed release capsule; 20-mg delayed release tablet 4- and 8-mg tablet; 2 mg/mL injection; 4 mg/5 mL oral solution (strawberry flavor)
5.7-, 22.7-, and 68-mg tablet Primor 120: 100 mg sulfadimethoxine + 20 mg ormetoprim Primor 240: 200 mg sulfadimethoxine + 40 mg ormetoprim. 250 mg/5 mL oral solution
Appetite stimulant: 1.25 mg– 2.5 mg PO Behavior 0.2–1.0 mg/kg q12–24h PO
10-, 15-, and 30-mg tablet
10 mg/kg q12h PO for 5 days
90.6 and 225 mg/mL paste
0.5–1.25 mg q12h PO
5-mg tablet; 5 mg/5 mL syrup (cherry flavor)
5–15 mL/kg IV; infusion rate 0.5–5 mL/kg per hour to prevent pulmonary edema.
Intravenous infusion bag
1 drop q24h in one nostril
0.05% nasal spray
1–5 mg/kg q24h PO 0.05–0.2 mg/kg IV, SC, or IM as needed; redose with 0.05–0.1 mg/ kg q1–2h Preanesthetic: 0.025–0.05 mg/kg IM or SC
50-mg tablet 1 and 1.5 mg/mL injection
continued
1023
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Oxytetracycline (Terramycin)
Tetracycline antibiotic. See tetracycline. Stimulates uterine muscle contraction. Used to induce or maintain normal labor and delivery. Does not increase milk production but will stimulate contraction, leading to milk ejection. A biphosphonate bone resorption inhibitor. Used for hypercalcemia Pancreatic enzyme. Used to treat pancreatic exocrine insufficiency. Provides lipase, amylase, and protease.
7.5–10 mg/kg q12h IV; 20 mg/kg q12h PO 2.5– 5.0 U IM or IV; can be repeated every 20–60 minutes up to three times total Milk ejection: spray intranasally 5–10 minutes prior to nursing
250-mg tablet; 100 and 200 mg/mL injection 10 and 20 USP U/mL
2 mg/kg q24h IV as needed based on serum calcium level Mix 1/2 −1 tsp powder with food per 5 kg body weight. Tabs ineffective unless crushed into powder.
3, 6, and 9 mg/mL injection
Pancuronium bromide (Pavulon)
Nondepolarizing neuromuscular blocker. See atricurium.
Paregoric (corrective mixture)
Paregoric (opium tincture) for diarrhea. Contains 2 mg morphine per 5 mL. Aminoglycoside antibiotic used for various enteric pathogens
0.02–0.1 mg/kg IV or start with 0.01 mg/kg and add 0.01 mg/kg doses q30m 0.05–0.06 mg/kg q12h PO
Oxytocin (Pitocin, Synto-cinon [nasal solution], generic)
Pamidronate sodium (Aredia) Pancrelipase (Viokase, Pancreazyme)
Paromomycin
Paroxetine (Paxil) d-Penicillamine (Cuprimine, Depen) Penicillin G benzathine (Benza-Pen, others) Penicillin G potassium and penicillin G sodium (many) Penicillin G procaine (generic) Penicillin V potassium (Pen-Vee) Pentazocine (Talwin-V) Pentobarbital (Nembutal, generic) Pentosan polysulfate (Elmiron) Pentoxifylline (Trental) Petrolatum Phenobarbital (Luminal, generic)
Phenoxybenzamine (Dibenzyline)
1024
Selective serotonin reuptake inhibitor. For behavioral problems. Chelating agent for lead copper, iron, and mercury. For copper toxicity and cystine calculi. All benzathine penicillin G is combined with procaine penicillin G. β-lactam antibiotic. See amoxicillin. For gram-positive bacteria and anaerobes. Same as other penicillin G except absorbed slowly. Oral penicillin. Otherwise same as other penicillins. Synthetic opioid analgesic. Partial agonist (similar to buprenorphine). Short-acting barbiturate anesthetic and anticonvulsant Duration of action 3–4 hours. For idiopathic cystitis or urethritis. Methylxanthine. Used to promote blood and lymph flow. Lubricant laxative for megacolon or hairballs. Long-acting barbiturate. See thiopental. Major use is as an anticonvulsant; potentiates inhibitory actions of γ aminobutyric acid. α1-adrenergic antagonist. Primarily to relax urethral smooth muscle.
125–165 mg/kg q24h PO; Caution: acute renal failure and deafness reported. 0.25–0.5 mg/kg q24h PO 10–15 mg/kg q12h PO
Each tsp (2.8 g) contains: Lipase 71,400 USP units + Protease 388,000 USP units + Amylase 460,000 USP units + Vitamin A 1,000 IU + Vitamin D3 100 IU + Vitamin E 10 IU 1 and 2 mg/mL injection
2 mg/5 mL elixir
250-mg capsule
10-mg tablet; 2 mg/mL oral suspension (orange flavor) 125- and 250-mg capsule; 250-mg tablet
24,000 U/kg q48h IM Nocardia: 100,000 u/kg q24–48h IM
150000 U/mL injection
20,000–40,000 U/kg q6–8h IV or IM
Numerous strengths available
20,000–40,000 U/kg q12–24h IM
300000 U/mL injection
10 mg/kg q8h PO
2.2–3.3 mg/kg q4–6h IV, IM, or SC
250- and 500-mg tablet; 125 and 250 mg/5 mL oral suspension (fruit flavor) 30 mg/mL injection
10–30 mg/kg IV to effect
50 mg/mL injection
8–10 mg/kg q12h PO 100 mg/cat q8–12h PO
10-mg capsule 400-mg tablet
1–5 mL/day PO
Numerous variations available
2–3 mg/kg q12h PO Status epilepticus: 5–20 mg/kg IV to effect or 2–4 mg/kg per hour as constant rate infusion
15-, 16.2-, 30-, 32.4-, 60-, 65-, and 97.5-mg tablet; 20 mg/5mL elixir; 65 and 130 mg/mL injection
2.5–7.5 mg/cat q12–24h PO or 0.5 mg/kg q12h PO
10-mg capsule Compounding may be necessary to dose properly
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Phentolamine (Regitine [Rogitine in Canada])
Nonselective—αadrenergic blocker. Vasodilator. Primarily for hypertension. Specific adrenergic agonist. Specific for α receptor. Same as methoxamine for determining if Horner’s syndrome is preganglionic or postganglionic Adrenergic agonist. Used to increase tone of urinary sphincter.
0.02–0.1 mg/kg IV
5 mg/mL injection
0.01 mg/kg q15 minutes IV; 0.1 mg/ kg q15 minutes IM or AQ. For Horner’s: use ophthalmic prep or dilute injectable 1 : 10 with saline; place on each eye. 1.5–2 mg/kg q12h PO
10 mg/mL injection 2.5% ophthalmic solution
0.02 mg/kg q12h IV
1 mg/mL injection
1% or 2% solution: 1 drop q6–12h topically
1, 2, and 4% ophthalmic solution
0.1–0.3 mg/kg q12h PO. 1 mL twice in first week then once weekly for 6 weeks SC 44–66 mg/kg PO; repeat in 2–3 weeks
1.25- and 5.0-mg tablets Not currently available in North America 100-mg tablet; numerous formulations commercially available 10- and 20-mg capsule
Phenylephrine (Neo-Synephrine)
Phenylpropanolamine
Phosphate Enema (Fleet) Physostigmine (Antilirium) Pilocarpine
Pimobenden (Vetmedin) PIND-ORF (Baypamune DC)
Contraindicated in cats (leads to critical hypocalcemia) Cholinesterase inhibitor. Antidote for anticholinergic intoxication. Parasympathomimetic to increase aqueous drainage in glaucoma and dysautonomia Positive inotropic agent Immune stimulant.
Piperazine (many)
Antiparasitic compound, primarily for helminthes (ascarids).
Piroxicam (Feldene, generics)
Ponazuril (Marquis)
Nonsteroidal anti-inflammatory. Used for transitional cell carcinomas, nasal adenocarcinomas, polyarthritis with limited response if at all. Anticancer agent. Used to treat carcinomas and hypercalcemia. Saline cathartic. See magnesium citrate. Used for bowel evacuation before surgical or diagnostic procedures. Immune stimulant under investigation for treating feline infectious peritonitis High-molecular-weight compounds similar to normal constituents of healthy joints. Chondroprotective. May be used for chronic cystitis to rebuild GAG layer. Anecdotal treatment for cocidiosis
Posaconazole (Noxafil)
Antifungal
5 mg/kg q24h PO
Potassium bromide
Mechanism uncertain. Believed to hyperpolarize neurons. Used for chronic seizure disorders. Potassium supplement for treatment of hypokalemia. Usually added to fluid solutions.
Contraindicated in cats due to irreversible pneumonitis/ pulmonary fibrosis 0.5 mEq potassium/kg q24h PO Intravenous fluid supplement: 10–40 mEq/500 mL of fluids, depending on serum potassium concentration; do not exceed administration rate of 0.5 mEq/kg per hour 50–100 mg/kg q12h PO to produce urine pH of 7.5.
Plicamycin (mithramycin) (Mithracin) Polyethylene glycol electrolyte solution (GoLYTELY)
Polyprenyl Immunostimulant
Polysulfated glycosaminoglycan (PSGAG) (Adequan)
Potassium chloride (generic)
Potassium citrate (generic, Urocit-K)
Alkalinizes urine to prevent calcium oxalate urolithiasis. Potassium replacement.
0.2–0.3 mg/kg q48h PO
25- and 50-mg chewable tablet; 75-mg time released capsule
Antihypercalcemic: 25 µg/kg q24h IV (slow infusion over 4 hours) 30 mL/kg PO; repeat in 2–6 hours; objectionable taste; give via orogastric tube.
2.5-mg injection
3 mg/kg two to three times per week PO
Propriatary preparatoin
Chronic cystitis: infuse 100 mg + 2 mL saline into empty bladder q7 days for 3 days Chrondroprotection: 2 mg/kg q3–7 days IM 50–60 mg/kg PO once followed by 27.5 mg/kg for 14–21 days.
100 mg/mL injection
Powder for oral suspension
15% oral paste. Compounded product more practical for cats. 40 mg/mL oral suspension (cherry flavor)
8 and 10 mEq extended release tablet; 2 mEq/mL injection
540- and 1080-mg tablet; 300 mg/5 g scoop granules continued
1025
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Potassium gluconate (Kaon, Tumil-K, generic) Potassium phosphate
Same as potassium chloride.
2–4 mEq/day or 0.5–1.5 g/day
2-mEq tablet
For hypophosphatemia due to diabetic ketoacidosis. Acetylcholinesterase reactivator for treatment of organophosphate toxicosis. Antiparasitic. Primarily for tapeworm and liver fluke infections.
0.03–0.12 mmol of phosphate/kg per hour in a calcium-free fluid 10–20 mg/kg q8–12h IV, IM, or SC (initial dose IV slow or IM)
3 mmol P/mL injection
5 mg/kg IM or SC Cats <1.8 kg: 6.3 mg/kg PO Cats >1.8 kg: 5 mg/kg PO Liver flukes: 20 mg/kg q24h SC for 3–5 days Paragonimus: 25 mg/kg q8h PO for 3 days 0.5–1.0 mg q8–12h PO
23-mg tablet; 56.8 mg/mL injection
Anti-inflammatory: 1.0–2.0 mg/kg q12–24h IV, IM, SC, or PO initially then taper to q48h Immunosuppressive: 4.4–8.8 mg/kg q24h IV, IM, SC, or PO initially then taper to q24–48h 1 drop q4–12h topically
5-mg tablet; 15 mg/5mL syrup (cherry flavor); 50 mg/mL injection Injectable form not available in the United States
Shock or acute asthmatic crisis: 15–30 mg/kg IV; repeat in 4–6 hours Central nervous system trauma: 30 mg/kg IV, then 15 mg/kg at 2 hours, then 10 mg/kg q4h for 6 doses
100 and 500 mg/10 mL injection
Same as prednisolone
1-, 2.5-, 5-, 10-, and 20-mg tablet; 1 mg/mL syrup (vanilla flavor) 25-, 50-, 75-, 100-, 200-, and 300-mg capsules 50- and 250-mg tablet
Pralidoxime chloride (2-PAM) (Protopam chloride) Praziquantel (Droncit)
Prazosin (Minipress)
Prednisolone (Delta-cortef, many others)
Prednisolone acetate or sodium phosphate ophthalmic Prednisolone sodium succinate (Solu-Delta-Cortef)
Prednisone (see prednisolone)
Pregabalin (Lyrica) Primidone (Mylepsin, Neurosyn [Mysoline in Canada])
α1-adrenergic blocker. Smooth muscle relaxant for functional urethral obstruction. Glucocorticoid anti-inflammatory drug. Potency is approximately four times that of cortisol.
Anti-inflammatory for ophthalmic diseases Same as prednisolone but water soluble; intended for acute therapy when high intravenous doses are needed for rapid effect. For shock and central nervous system trauma. See also methylpred nisolone sodium succinate. Same as prednisolone, except that after administration, prednisone is converted to prednisolone. A γ aminobutyric acid analog anticonvulsant Anticonvulsant. Primidone is converted to phenylethylmalonamide and phenobarbital, both of which have anticonvulsant activity, but most of activity (85%) is probably a result of phenobarbital. See phenobarbital for more details.
Primor
See ormetoprim and sulfadimethoxine.
Procaine Procalamine
Local anesthetic Partial parenteral nutritional solution. Contains amino acid 3%, glycerin 3%, and electrolytes.
1026
2–4 mg/kg q8–12h PO 8–10 mg/kg q8–12h PO as initial dose, then adjust via monitoring clinical signs and blood phenobarbital levels Note: Cats have a decreased ability to convert primidone to phenobarbital leading to increased risk of neurotoxicity and hepatotoxicity. Many sources say it is contraindicated in cats. Primor 120:Up to 5 pounds: Day 1 = 1/d; thereafter = 2/d 5–10#: Day 1 = 2/d; thereafter = 1/d Up to 15 pounds: Day 1 = 3/d; thereafter = 1.5/d
4–6 mg/kg infiltrated locally 2–3 mL/kg per hour
1-g vial injection
1-, 2-, and 5-mg capsule
1% ophthalmic solution
Primor 120: 100 mg sulfadimethoxine + 20 mg ormetoprim Primor 240: 200 mg sulfadimethoxine + 40 mg ormetoprim Also in 600- and 1200-mg tabs Solution with 5% epinephrine 1000 mL intravenous solution
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Prochlorperazine (Compazine)
Phenothiazine. Central acting dopamine (D2) antagonist. For sedation and vomiting. Phenothiazine with strong antihistamine effects. For allergy and as antiemetic (motion sickness). Anticholinergic used to decrease smooth muscle contraction in gastrointestinal tract and urinary bladder. Immune stimulant
0.1–0.5 mg/kg q6–12h IM, SC, or PO 0.2–0.4 mg/kg q6–8h IV, IM, or PO up to a maximum dose of 1 mg/ kg
5- and 10-mg tablet; 5 mg/mL syrup (fruit flavor); 5 mg/mL injection 12.5-mg tablet; 25 and 50 mg/ mL injection; 6.25 mg/5 mL syrup
5.0–7.5 mg/cat q24–72h PO
7.5- and 15-mg tablet
0.25–0.5 mL twice weekly IV for first week then q14d for 16 weeks.
0.4 mg/mL injection
Phenothiazine sedative. Also antiemetic, antihistaminic. Anesthetic. Used for induction of short-term general anesthesia. Mechanism of action is not well defined but may be barbiturate-like. β-adrenergic blocker. Nonselective for β1-and β2-adrenergic receptors. To decrease heart rate, cardiac conduction, blood pressure and tachyarrhythmias. Antithyroid drug. See methimazole. Inhibits conversion of T4 to T3. Prostaglandin induces luteolysis. Has been used to treat open pyometra in animals. Use for inducing abortion has been questioned.
1.1–4.4 mg/kg q12–24h IM or SC
Must be compounded
2–8 mg/kg IV slowly to effect Constant rate infusion: 0.1–0.6 mg/ kg per hour; taper dose 25% each hour when treating seizures
10 mg/mL injection
0.4–1.2 mg/kg (2.5–5.0 mg) q8–12h PO
10-, 20-, and 40-mg tablet
11 mg/kg q12h PO
50-mg tablet
Pyometra: 0.1 mg/kg q12h SC for 2 days then 0.2 mg/kg q12h SC until uterus is normal in size (approximately 5–7 days total). Abortion: 0.5–1 mg/kg IM q12h for two injections 1 tsp per 5–10 kg BW (added to each meal); use sugar-free Metamucil in diabetic cats.
5-mg vial for injection
1–2 tsps q12–24h PO with food
Sold in grocery stores.
20 mg/kg PO; repeat in 2–3 weeks.
2.27, 4.54, and 50 mg/mL oral suspension; 22.7- and 113.5-mg tablet 60 mg/5 mL syrup (raspberry flavor); 60-mg tablet; 5 mg/ mL injection
Promethazine (Phenergan)
Propantheline bromide (Pro-Banthine)
Propionibacterium acnes (ImmunoRegulin, ImmunoVet) Propionylpromazine (Tranvet, Largon) Propofol (PropoFlo, Rapinovet)
Propranolol (Inderal)
Propylthiouracil (PTU) (generic, Propyl-Thyracil) Prostaglandin F2 α (dinoprost tromethamine) (Lutalyse)
Psyllium (Metamucil, others)
Pumpkin, canned Pyrantel pamoate (Nemex, Strongid) Pyridostigmine bromide (Mestinon, Regonol)
Pyrimethamine (Daraprim)
Racemethionine (dlmethionine) (generic tablets) Ramipril Ranitidine (Zantac)
Bulk-forming laxative. For constipation and bowel evacuation. Absorbs water and expands to provide increased bulk and moisture. Used as a fiber source for cats with constipation. Antiparasitic. Blocks ganglionic neurotransmission via cholinergic action. Anticholinesterase. Same as neostigmine, except that pyridostigmine has longer duration of action. Antibacterial, antiprotozoal. Activity greater against protozoa than bacteria. Urinary acidifier. Lowers urinary pH. Also has been used to protect against acetaminophen overdose. Angiotensin-converting enzyme inhibitor for hypertension H2 antagonist. See cimetadine; 4–10 times more potent and longer acting.
Antimyasthenic: 0.02–0.04 mg/kg q2h IV or 0.5–3 mg/kg q8–12h PO. Antidote (curariform): 0.15–0.3 mg/ kg IM or IV 0.5–1 mg/kg q24h PO for 14–28 days. 1–1.5 g PO
0.25–0.375 mg/kg q24h PO 2.5 mg/kg q12h IV; 1–4 mg/kg q12h PO
Many formulations commercially available
25-mg tablet
200- and 500-mg tablet; 500-mg chewable tablet; 1000 mg/tsp powder 1.25-, 2.5-, 5-, and 10-mg capsules 75-mg tablet; 25 mg/mL injection; 15 mg/mL oral syrup (peppermint flavor) continued
1027
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Rifampin (Rifadin)
Antibacterial. Spectrum of action includes staphylococci, mycobacteria, and streptococci. Isotonic crystalloid fluid solution for replacement or maintenance. Antiprotozoal; used primarily for Tritrichomonas Local anesthetic
10–15 mg/kg q24h PO
150- and 300-mg capsule Compounding may be necessary to dose properly. Intravenous solution
Ringer’s solution (generic) Ronidazole Ropivacaine Rutin (over the counter) S-adenosyl-methionine (SAMe) (Denosyl, Denamarin, generics)
Salicylic acid pads (Stridex, generics) Salmon calcitonin
Up to 1.5 mg/kg
Benzopyrone drug for chylothorax. Intermediate in breakdown of methionine that plays a role in hepatic function, including methylation, antioxidation, and glutathione production. For feline acne
50–100 mg/kg q8–12h PO Up to 5.5 kg: 90 mg q24h PO on empty stomach or 180 mg q24h PO with food; 5.5–11.4 kg: 180 mg q24h on empty stomach or 360 mg q24h PO with food Cleanse chin q12h
For hypercalcemia or vitamin D toxicosis; reduces serum calcium level.
4–6 IU/kg q3–12h SC or IM until serum calcium is normal then 4–20 IU/kg q2–3w as needed SC or IM Up to 2.3 kg: 15-mg vial q1m 2.3–6.8 kg: 45-mg vial q1m (6–12 mg/kg topically q30d for heartworm prevention) 1 mg/kg q24h PO
Selamectin (Revolution)
Topical parasiticide and heartworm prevention.
Selegiline Hydrochloride (Deprenyl, Anipryl), generic Senna (Senokot)
Inhibits monamine oxidase type B.
Sevalamer (Renagel) Sevoflurane
40–50 mL/kg per day IV, SC, or intraperitoneally 30 mg/kg q12h PO
Laxative. Acts via local stimulation or via contact with intestinal mucosa. Phosphate binder Inhalant anesthetic.
5 mL q24h PO (syrup); 1/2 tsp q24h with food (granules) 200 mg/cat q12h Induction: 8% Maintenance: 3–6% to effect Feline Size Tablet: 1 tablet up to 5.5 kg (12 pounds) BW
Have compounded into palatable oral liquid. Solution at 0.2, 0.5, and 0.75% with or without epinephrine 50- and 500-mg tablet Denosyl: 90-mg tablet Denamarin: 90 mg SAMe + 9 mg silybin A + B or 225/24 mg or 425/35 mg 2% salicylic acid 200 IU/mL injection
15-mg and 45-mg per vial topical solution
1.25- and 5-mg tablets 8.8 mg/5 mL syrup (fruit flavor); 15 mg/mL granules 400-mg tablet 100% liquid inhalant Marin: 50 IU Vitamin E + 9 mg silybin A + B Denamarin: 90 mg SAMe + 9 mg silybin A + B 1 mEq/mL injection (8.4% solution)
Silybin/Milk Thistle (Marin, Denamarin)
A nutraceutical useful for treatment of chronic and acute liver disease, cirrhosis, and for hepatotoxicity.
Sodium bicarbonate (generic)
Sodium chloride (0.9%) (generic) Sodium chloride (7.5%) (generic) Sodium iodide (20%) (Iodopen, generic)
Alkalizing agent. Antacid. For systemic acidosis or to alkalize urine. Increases plasma and urinary concentrations of bicarbonate. Decreases serum potassium (reduces extracellular acid causing acid to move from the intracellular to extracellular space in exchange for potassium moving from the extracellular to intracellular space) Isotonic crystalloid fluid solution for replacement or maintenance. For acute hypovolemia/shock.
Acidosis: 0.3 x bicarbonate deficit x weight in kg IV slowly (bicarbonate deficit = desired bicarbonate–patient bicarbonate) or 0.5–1 mEq/kg IV slowly. Hyperkalemia: as for acidosis Renal failure: 10 mg/kg q8–12h PO Alkalization of urine: 50 mg/kg q8–12h PO (Note: 1 tsp powder is approximately 2 g of NaHCO3) 40–50 mL/kg per day IV, SC, or IP 2–8 mL/kg IV over 5 minutes
Intravenous solution
For iodine deficiency. Also used for sporotrichosis
20 mg/kg q12–24h PO
Sodium phosphate (usually 3 mmol/mL)
For hypophosphatemia due to diabetic ketoacidosis.
0.03–0.12 mmol of phosphate/kg per hour in a calcium-free fluid
Somatostatin
See Octreotide
200 mg/mL injectable in 250-mL vials 62.5 mg/mL oral solution in pints and gallons Injectable: each ml contains 3 mmol phosphate (99.1 mg/ dL phosphorus) + 4.4 mEq of potassium in 5, 10-, 15-, 30-, and 50-ml vials 50-, 100-, 200-, and 500-µg and 1-mg injection
1028
Intravenous solution
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Sotalol (Betapace, generic)
Antiarrhythmic. Nonspecific β1- and β2-adrenergic blocker (class II antiarrhythmic). Action is similar to that of propranolol. May also have potassium channel blocking activity, prolonging repolarization thus decreasing automaticity and slowing AV nodal conduction (class III antiarrhythmic). Potassium-sparing diuretic; aldosterone antagonist. For congestive heart failure. Also used for ascites due to liver disease. Discontinue if facial dermatitis occurs. Anabolic steroid. See nandrolone.
1–2 mg/kg q12h PO
80-, 120-, 160-, and 240-mg tablet
0.5–2.0 mg/kg q24h PO
25-mg tablet
1 mg q24h PO; 25 mg/week IM
Staphylococcus protein A (SPA)
Immune stimulant
Succimer (Chemet)
Chelating agent for heavy metal (e.g., lead, mercury, and arsenic) toxicity. Gastric mucosa protectant. Antiulcer agent. Binds to ulcerated tissue in gastrointestinal tract to aid healing of ulcers. Used to treat or prevent ulcers. Opioid agonist. Action of fentanyl derivatives is via µ-receptor. Five to seven times more potent than fentanyl. Competes with para-aminobenzoic acid for enzyme that synthesizes dihydrofolic acid in bacteria. Synergistic with trimethoprim. Bacteriostatic. Competes with para-aminobenzoic acid for enzyme that synthesizes dihydrofolic acid in bacteria. Synergistic with trimethoprim. Bacteriostatic. Competes with para-aminobenzoic acid for enzyme that synthesizes dihydrofolic acid in bacteria. Synergistic with trimethoprim. Bacteriostatic. Competes with para-aminobenzoic acid for enzyme that synthesizes dihydrofolic acid in bacteria. Synergistic with trimethoprim. Bacteriostatic. Sulfonamide and anti-inflammatory drug. For colitis. Sulfonamide has little effect; mesalamine has anti-inflammatory effects. Competes with para-aminobenzoic acid for enzyme that synthesizes dihydrofolic acid in bacteria. Synergistic with trimethoprim. Bacteriostatic.For urinary tract infections.
7.3 µg/kg IP twice weekly for 8 weeks for feline leukemia virus infection 10 mg/kg q8h PO for 2 weeks
2-mg tablet Must be compounded. Propriatary preparation
Spironolactone (Aldactone)
Stanozolol (Winstrol-V)
Sucralfate (Carafate [Sulcrate in Canada])
Sufentanil citrate (Sufenta)
Sulfadiazine (generic)
Sulfadimethoxine (Albon, Bactrovet, generic)
Sulfamethazine (Sulmet, many others)
Sulfamethoxazole (Gantanol)
Sulfasalazine (sulfapyridine and mesalamine) (Azulfidine [Salazopyrin in Canada]) Sulfisoxazole (Gantrisin)
100-mg capsule
0.25–1.0 g q8–12h PO as slurry (tablet crushed in water) Suspension: 100–200 mg/kg q8–12h PO
1-g tablet; 1 g/10 mL oral suspension
2 µg/kg IV up to a maximum dose of 5 µg/kg
50 µg/mL injection
50 mg/kg PO (loading dose), followed by 25 mg/kg q12h PO (see trimethoprim)
500-mg tablet
50–60 mg/kg PO (loading dose), followed by 27.5 mg/kg q12h PO
250- and 500-mg tablet; 50 mg/ mL oral suspension (custard flavor)
100 mg/kg PO (loading dose), followed by 50 mg/kg q12h PO
12.5% solution; 2.5- and 5-g tablet
100 mg/kg PO (loading dose), followed by 50 mg/kg q12h PO
500-mg tablet No longer commercially available in the United States.
10–30 mg/kg q12–24h PO
500-mg tablet
50 mg/kg q8h PO
500 mg/5 mL suspension
continued
1029
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Superoxide dismutase (Oxstrin)
Immunostimulant for feline immunodeficiency virus and feline leukemia virus infected cats Topical nonsteroidal antiinflammatory to reduce vascularization and inflammation in keratitis and uveitis. Decrease vascularization and pigmentation for keratitis and for keratoconjunctivitis sicca. Nutritional supplement for taurine deficiency. Synthetic allylamine antifungal. Used for resistant dermatophytosis.
1 capsule q24h PO
Propriatary preparation
1 drop q8–12h topically
1% ophthalmic solution
1 drop or ribbon q12h topically
0.02–0.03% solution Have compounded to achieve these concentrations. 250-mg tablet
Suprofen (Profenal)
Tacrolimus Ophthalmic
Taurine (generic) Terbinafine (Lamisil)
Terbutaline (Brethine, Bricanyl)
β-adrenergic agonist. β2-Specific. Primarily for bronchodilation. See albuterol for details.
Tetanus antitoxin
Neutralizes unbound tetanus toxin
Testosterone cypionate (Andro-Cyp, Andronate, Depo-Testosterone, others)
Testosterone ester. See methyltestosterone. Testosterone esters are administered IM to avoid first-pass effects. Testosterone injection. See methyltestosterone. Tetracycline antibiotic. Usually bactericidal. Broad spectrum of activity, including bacteria, protozoa, Hemoplasma, and Ehrlichia. Methylxanthine bronchodilator. Poorly effective for feline asthma. Same as theophylline. Also for atrioventricular blocks.
Testosterone propionate (Testex, Malogen) Tetracycline (Panmycin)
Theophylline (many brands, generic) Theophylline, sustained release (Theo-Dur, Slo-Bid Gyrocaps) Thiabendazole (Omnizole, Equizole) Thiamine (vitamin B1) (Bewon and others) Thioguanine (6-TG) (generic) Thiopental sodium (Pentothal)
Thiotepa (generic)
Thyroid-releasing hormone (TRH, Thypinone)
1030
Benzimidazole anthelmintic. See fenbendazole and albendazole. For treatment of thiamine deficiency.
Anticancer agent. Antimetabolite of purine analog type. Inhibits DNA synthesis in cancer cells. Ultrashort-acting barbiturate. Mainly for induction or 10–15 minutes of anesthesia. Anticancer agent. Alkylating agent of the nitrogen mustard type for various tumors, especially malignant effusions. Used to test for hyperthyroidism when TT4 is not elevated.
250–500 mg q12–24h PO to effect. 30–40 mg/kg q24h PO; Note: 3–5 months of therapy may be necessary 0.1–0.2 mg/kg q12h SC or IM or 0.325–0.625 mg q12–24h PO
Human product: 500–1000 IU IM Equine product: 100–1000 IU IM or SC Do 0.1 mL intradermal test dose first to screen for anaphylaxis. See Chapter 208. 1–2 mg/kg IM every 2–4 weeks
250-mg tablet
2.5- and 5-mg tablets; 1 mg/mL injection Dilute 1 : 9 with sterile saline to make 0.1 mg/mL; give 0.5 mL to get dose of 0.01 mg/kg. Human: Immunoglobulin Equine: Antitetanus serum
100 and 200 mg/mL injection
0.5–1 mg/kg IM every 2–4 weeks
100 mg/mL injection
15–20 mg/kg q8h PO; 4.4–11 mg/kg q8h IV or IM
250- and 500-mg tablet; 125 mg/5 mL oral suspension (raspberry flavor)
4 mg/kg q8–12h PO
80 mg/15 mL elixir (mixed fruit flavor) 100-, 200-, and 300-mg tablet and capsule
25 mg/kg q24h PO at night or 10 mg/kg q12h PO Strongyloides: 125 mg/kg q24h PO for 3 days 25–50 mg/cat q24h IM or SC for 3 days. 5–30 mg/cat q24h PO 25 mg/m2 q24h PO for 1–5 days, then repeat q30 days as needed
500-mg chewable tablet 200 and 500 mg/mL injection 20- (enteric coated), 50-, 100-, and 250-mg tablets 40-mg tablet
5–12 mg/kg IV to effect
1-g vial injection
0.2–0.5 mg/m2 weekly or daily for 5–10 days IM, intracavitary, or intratumor
15-mg vial injection
Collect baseline TT4; give 0.1 mg/kg IV; collect post-TRH TT4 sample at 4 hours
0.5 mg/mL injection No longer available in the United States
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Ticarcillin (Ticar, Ticillin)
β-lactam antibiotic. Action similar to amoxicillin. Spectrum similar to carbenicillin. For gram-negative infections, especially Pseudomonas. Same as ticarcillin, except clavulanic acid has been added to inhibit bacterial β-lactamase and increase spectrum. Anesthetic. Combination of tiletamine (dissociative anesthetic agent) and zolazepam (benzodiazepine). Produces short duration (30 minutes) of anesthesia. β-blocker to decrease aqueous production for glaucoma. β-blocker and carbonic anhydrase inhibitor to decrease aqueous production and increase aqueous flow for glaucoma. Aminoglycoside antibacterial drug. Similar mechanism of action and spectrum as amikacin and gentamicin. Anti-parasitic for coccidia
33–60 mg/kg q4–8h IV or IM
3-g vial injection
Same as ticarcillin (dose according to ticarcillin component)
3 g ticarcillin + 0.1 g clavulanic acid vial for injection
5–15 mg/kg IM or 1–5 mg/kg IV to effect
50 mg/mL of each component injection
1 drop q12h topically
0.5–4% ophthalmic solution
1 drop q8h topically
0.5% Timolol + 2% Dorzolamide ophthalmic solution
2–4 mg/kg q8h IV, IM, or SC or 3–6 mg/kg q12h IV, IM, or SC
10 and 40 mg/mL injection
15 mg/kg q24h PO for 3–6 days
Tramadol (Ultram)
Non DEA-controlled monoamine reuptake inhibitor and opioid-like analgesic.
2–4 mg/kg q12h PO or 12.5 mg q12h PO
Travoprost (Travatan)
Prostaglandin analog for lowering intraocular pressure in glaucoma; efficacy in cats not proved. The acid form of Vitamin A for feline acne Glucocorticoid antiinflammatory. See β-methasone for details. Potency approximates that of methylprednisolone (about 5 times cortisol and 1.25 times prednisolone). Same as triamcinolone, but injectable suspension is slowly absorbed from IM, SC, or intralesional injection site.
1 drop q30m topically repeat as needed per intraocular pressure
Oral suspension containing 5% or 10% toltrazuril 50-mg tablet Note: Avoid formulation combined with acetaminophen 0.004% solution
Ticarcillin and clavulanate (Timentin)
Tiletamine and zolazepam (Telezol, Zoletil)
Timolol maleate (Timoptic) Timolol maleate + Dorzolamide Hydrochloride (Cosopt) Tobramycin (Nebcin)
Toltrazuril (Baycox)
Tretinoin Triamcinolone (Aristocort, Genesis Spray, generic)
Triamcinolone acetonide (Vetalog)
Trientine hydrochloride (tetramine tetrahydrochloride) (Syprine) Trifluorothymidine (trifluridine) (Viroptic)
Chelating agent. Used to chelate copper when patient cannot tolerate penicillamine. Topical ophthalmic antiviral
Triflupromazine (Vesprin, Stelazine)
Phenothiazine. Similar action as other phenothiazines (see acepromazine); may have stronger antimuscarinic activity. Antiemetic. See Liothyronine
Triiodothyronine
Apply to chin q12h
0.01–0.25% cream or lotion
Anti-inflammatory: 0.5–1 mg/kg q12–24h PO; taper dose to 0.5–1 mg/kg q48h PO Immune Suppression: 2 mg/kg q12–24h PO
0.5- and 1.5-mg tablet; 0.15% spray
0.1–0.2 mg/kg IM or SC; repeat in 7–30 days as needed Intralesional: 1.2–1.8 mg (or 1 mg for every cm diameter of tumor) every 2w Subconjunctival: 4–8 mg 10–15 mg/kg q12h PO
2 and 6 mg/mL injection
2 drops q2–4h then reduce frequency with response. Use for minimum of 1 week. 0.1–0.3 mg/kg q8–12h IM or PO
250-mg capsule
1% ophthalmic solution
1-, 2-, 5-, and 10-mg tablets. 10 mg/mL oral solution (banana flavored) 2 mg/mL solution in 10-mL vials 5-, 25-, and 50-µg tablet continued
1031
SECTION 9: Formulary
Drug
Action
Dose & Route
How Supplied
Trimeprazine tartrate (Temaril [Panectyl in Canada])
Phenothiazine with antihistamine activity (similar to promethazine). For treating allergies and motion sickness. Combination antibacterial. For action, see sulfadiazine. Together, the combination is synergistic with a broad spectrum of activity.
0.5 mg/kg q12h PO
5-mg tablet
15 mg/kg q12h PO or 30 mg/kg q12–24h PO Toxoplasmosis: 30 mg/kg q12h PO for 28 days Coccidiosis: Under 4 kg 15–30 mg/kg q24h PO for 6 days; Over 4 kg 30–60 mg/kg q24h PO for 6 days 1 mg/kg q12h PO
Trimethoprim/Sulfadiazine: 40/200 mg and 80/400 mg injection; 5/25-, 20/100-, 80/400-, 160/800-mg tablet Trimethoprim/Sulfamethoxazole: 80/400- and 160/800-mg tablet Must be compounded.
1–2 drops on cornea; takes about 1–2 minutes to effect 7–15 mg/kg q8–12h PO
1% ophthalmic solution
Trimethoprim sulfonamides (sulfadiazine or sulfamethoxazole) (Tribrissen, Septra, Bactrim, others)
Tripelennamine (Pelamine, PBZ) Tropicamide Tylosin (Tylan)
Unoprostone (Rescula)
Ursodiol (ursodeoxycholate) (Actigall) Vancomycin (Vancocin, Vancoled) Vasopressin (ADH) (Pitressin)
Verapamil hydrochloride (Calan, Isoptin)
Vinblastine (Velban)
Vincristine (Oncovin, Vincasar, generic)
Vitamin A (retinoids) (Aquasol-A) Vitamin B1 Vitamin B2 (riboflavin) (Riboflavin) Vitamin B12 (cobalamin)
1032
Antihistamine H1-blocker. Similar in action to other antihistamines. See chlorpheniramine. Topical ophthalmic anesthetic Macrolide antibiotic. See erythromycin for action. For chronic diarrhea due to Cryptosporidium parvum and Clostridium perfringens. Prostaglandin analog for lowering intraocular pressure in glaucoma; efficacy not proved. Anticholelithic and increases bile flow. Contraindicated in biliary obstruction. Antibacterial agent primarily for resistant staphylococcus and enterococci. Aqueous antidiuretic hormone for polyuria caused by central diabetes insipidus, not due to renal disease. Calcium channel blocker. Blocks calcium entry into cells via blockade of slow channel. Produces vasodilation and negative chronotropic effects. Similar to vincristine. Do not use to increase platelet numbers (may cause thrombocytopenia). Anticancer agent. Arrests cancer cell division by binding to microtubules and inhibiting mitosis. Used in combination chemotherapy protocols. Also increases numbers of functional circulating platelets; used for thrombocytopenia. For vitamin A deficiency. See thiamine. For vitamin B2 deficiency. For vitamin B12 deficiencies, including anemia, gastronintestinal diseases, pancreatic diseases, and conditions causing chronic anorexia and weight loss.
1 drop q30m topically repeat as needed per intraocular pressure 10–15 mg/kg q24h PO
12–15 mg/kg q8h PO or IV infusion
0.8 U/kg IV may be repeated at 5-minute intervals
2.7 g/tsp powder
0.15% ophthalmic solution No longer commercially available in the United States 250-mg tablet and 300 mg capsule 125- and 250-mg pulvule; 500-mg, 1-, 5-, and 10-g injection 20 U/mL injection
1.1–2.9 mg/kg q8h PO; 0.05– 0.15 mg/kg (up to 2 mg/kg if normal myocardial function) IV over 10–30 min
40-mg tablet; 2.5 mg/mL injection
1.5–2 mg/m2 IV (slow infusion) q7d or per chemotherapy protocol
10-mg vial for injection
Antitumor: 0.5–0.75 mg/m2 IV or 0.05 mg/kg once per week or per chemotherapy protocol Thrombocytopenia: 0.5 mg/m2 or 0.02–.03 mg/kg q7d IV as needed
1 mg/mL injection in 1-, 2-, and 5-mg vials
625–800 U/kg q24h SC
50000 U/mL injection
5–10 mg q24h PO
50- and 100-mg tablet
100–250 mcg q7d SC for 6 weeks then 100–250 µg q14d for 6 weeks then q4 weeks Appetite stim: 1000–2000 µg SC
1000, 3000, and 10,000 µg/mL injection
Drug Formulary
Drug
Action
Dose & Route
How Supplied
Vitamin C (ascorbic acid)
For vitamin C deficiency; not effective as urine acidifier. To reduce methemoglobin (acetaminophen toxicity). See dihydrotachysterol and calcitriol Antioxidant. Supplement and treatment of some immunemediated dermatoses, panniculitis and steatitis. For coagulopathies caused by anticoagulant toxicosis (warfarin, other rodenticides), and for vitamin K malabsorption (i.e., hepatopathies, gastrointestinal disease).
100–500 mg q24h PO Methemoglobinemia: 125 mg/kg q6h PO for six treatments; 30 mg/ kg q6h IV for six treatments
250-, 500-, and 1000-mg tablet 250 mg/ml injectable
200–400 U q12h PO Immune-mediated skin disease: 400–600 U q12h PO
Many formulations commercially available
Short-acting rodenticides: 1 mg/kg q24–48h IM, SC, or PO for 10–14 days. Long-acting rodenticides: Loading: 5 mg/kg SC; then 2.5 mg/kg q12h PO for 3–4 wks Malabsorption: 2.5 mg/kg SC once, then 1 mg/kg q24h SC or PO Preliver biopsy: 1 mg/kg q12h for 2 doses 10 mg/kg q24h PO
2 and 10 mg/mL injection; 5-, 25-, and 50-mg tablet
Vitamin D Vitamin E (α-tocopherol) (Aquasol E, generic)
Vitamin K1 (phytonadione, phytomenadione) (AquaMEPHYTON (injection), Mephyton [tablets], Veta-K1 [capsules])
Voriconazole (Vfend)
Antifungal
Warfarin (Coumadin, generic)
Anticoagulant. Depletes vitamin K, which is responsible for generation of clotting factors. For hypercoagulable disease and to prevent thromboembolism. α2-adrenergic agonist. Primarily for anesthesia and analgesia. α2-adrenergic antagonist. To reverse actions of xylazine or detomidine. Leukotriene inhibitor. Antiinflammatory for small airway disease. Antiviral drug. In humans, used to treat AIDS. In cats, has been experimentally used for treatment of feline leukemia virus and feline immunodeficiency virus infection without impressive results. A carbonic anhydrase inhibitor anticonvulsant
Xylazine (Rompun) Yohimbine (Yobine) Zafirlukast (Accolate)
Zidovudine (AZT) (Retrovir)
Zonisamide (Zonegran)
Thromboembolism: 0.05–0.5 mg q24h PO; adjust dose to clotting time assessment. (Maintain prothrombin time 1.5–2 times normal.) Sedation: 1.1 mg/kg IM; Emesis: 0.4–0.5 mg/kg IV 0.11 mg/kg IV or 0.25–0.5 mg/kg SC or IM 1–2 mg/kg q12h PO
50- and 200-mg tablet; 40 mg/ mL oral suspension (orange flavor) 1-, 2-, 2.5-, 3-, 4-, 5-, 6-, 7.5-, and 10-mg tablet
20 and 100 mg/mL injection 2 mg/mL injection 10- and 20-mg tablet
5–15 mg/kg q12h PO or SC (doses as high as 30 mg/kg per day also have been used) Caution: may cause myelotoxity, Heinz body anemia, and icterus.
100-mg capsule; 10 mg/mL syrup (strawberry flavor); 300-mg tablet
5–10 mg/kg q12h PO
50- and 100-mg capsule
1033
Index
131
I treatment, 258–260 2-PAM: see, Pralidoxine chloride 25-hydroxy vitamin D, 553 4-methylpyrazole, 168, 442 5-fluorocytosine, 98 Abdominal harvest, 285 Abdominocentesis, 25, 28–29, 66, 263, 333, 460 Abducens nerve, 910–911 Ablation, 655–658 Abortion, 225, 382, 435, 470, 975–976 Abscess/abscessation, 10–11, 44–45, 131–133, 356, 470 Abyssinian amyloidiosis, 14 breed-specific diseases, 940 cardiac disease, 129 fungal disease, 131 hyperesthesia, 246 immune mediated hemolytic anemia, 282 litter size, 976 luxating patella, 662 myasthenia gravis, 336 ophthalmic disease, 463 Acantholytic cells, 392–393 ACE-inhibitor, see Angiotensin converting enzyme-inhibitor Acepromazine, 620–621, 625, 682 Acetaldehyde, 330–331 Acetaminophen, 5–6, 682 Acetate tape impression, 484 Acetylcholine receptor antibody titer, 74, 336, 510 Acetylcholinesterase, 364 Acetylcystine, 6 Achromotrichia, see Leukotrichia Acid-fast stain, 338, 356 Acidosis, see Metabolic acidosis Acne, 7, 313 Acromegaly, 8–9 ACTH stimulation test, 239 Actinic keratosis, 489–490 Actinomyces spp., 10–11, 131–133, 356, 721–722, 730 Actinomycosis, 10–11, 131–133 Activated charcoal, 6, 32, 330, 365, 410–411, 439, 442–444, 553, 913 Acupuncture, 684 Acute renal failure, see Renal failure, acute Acyclovir, 94, 551 Addison’s disease, see Hypoadrenocorticism Adenocarcinoma, 12–13 cytology, 728–729 Adipokines, 358 Adiponectin, 358 Adjuvant, see Vaccine, adjuvant Adrenal disease, see Hyperadrenocorticism Adrenal disease, see Hypoadrenocorticism Adrenal tests, 424 ACTH stimulation, 239, 424 endogenous ACTH, 239
1034
high-dose dexamethasone suppression, 239 low-dose dexamethasone suppression, 239, 424 urinary cortisol:creatinine ratio, 424 Adrenalectomy, 240 Aelurostrongylus abstrusus, 96, 306 Age approximation, 933–936 behavioral development, 933–935 body weight, 934–935 dental eruption times, 933 dermatologic changes, 934 ophthalmic changes, 934 radiographic changes, 933 Aggression, 104, 563–565 defensive, 563–565, 583 fearful, 564–565, 582–583 frustration-related, 564–565 intercat, 581–583 irritable, 582 misdirected play-related, 564–565, 583 offensive, 564 petting-related, 564–565 redirected, 564–565, 582–583 social status, 564, 581–583 territorial, 581–582 toward humans, 563–565 Albumin, 267–268 Albuterol, 59–60 Alcohol dehydrogenase, 167 Alcoholization, 40 Aldosterone, 241–242, 265, 272 Alfaxolone, 622–623, 682 Alkalinization therapy, 458 Allergy testing intradermal, 33, 154 serological, 33 Alloantibodies, 879 Allograft rejection, 980–982 Allopurinol, 542 Alopecia, 16 psychogenic, 587–589 Alpha adrenergic agonist, 354–355, 682, 684 Alpha adrenergic antagonist, 354–355 Alpha naphthyl thiouria, 466 Alpha2-agonist, 620–621, 623–625 Alprazolam, 592 Aluminum hydroxide, 456, 458 Alveolar ridge maintenance, 606 Alzheimer’s disease, 14 Amblyomma americanum, 106 American shorthair, 9, 40 Ameroid constrictor, 427 Amitraz, 484, 486 Amitriptyline, 528, 541, 591–592, 684 Amlodipine, 252–255, 258, 456, 458 Ammonia, 426–427 Ammonia toxicity, 340 Ammonium biurate calculus, 426 Ammonium chloride, 74, 542 Amphimerus pseudofelineus, 193, 377, 380
Amphotericin-B, 88, 98–99, 232–233, 452 Amylin, 14 Amyloid, 14, 15 Amyloidosis, 14, 15, 205, 789, 813, 980 Anal glands, 16 Anal reflex, 912 Anal sac disease abscess, 16 impaction, 16 sacculitis, 16–17 Anal sacculectomy, 17 Anal sacculitis, see Anal sac disease Analgesia, 620, 622, 624–625 multimodal, 684 Analgesic, 682–684 Anaphylaxis, 499 Anaplasma spp., 18, 205 Anaplasmosis, 18 Anatomical differences, 937–938 Ancylostoma, 234 Anemia, 5–6, 19–21, 106, 334 hemolytic, 5–6, 19–21, 106, 211–212, 218, 275, 282 hemorrhagic, 466 immune mediated, 106, 282–283 non-regenerative, 19–21, 455–457 regenerative, 19–21, 211–212, 218, 282 Anesthesia general, 620–625 sedation, 620–625 TNR programs, 950 Angiocardiogram, 24, 389, 460, 500 Angiogram, 507–508 Angiography, see Angiogram Angiotensin II, 241 Angiotension converting enzyme inhibitor cardiac, 24, 129–130, 261, 263, 333, 431, 460, 547, 460, 547 hypertension, 252 renal, 458 Anisocoria, 910 Annealing temperature, 915 Anorexia, 22–23, 642, 649 Ant sting, 148–150 Antacid, 557 Antegrade pyelogram, 237 Anterior cruciate ligament, see Cranial cruciate ligament Anterior mediastinal mass, 162 Anti-A-antibodies, 352, 977 Anti-acetylcholine receptor antibody titer, 165 Anticholinergic drug, 354–355 Anticoagulant, 466–467 Anticonvulsant, 160 Antiemetic, 557 Antifreeze, 167 Anti-leukotrienes, 60 Antinuclear antibody titer, 258 Antipyretic, 187, 189 Antithrombin III level, 268
Index
Antivenin arachnids, 145–147 snakes, 151–153 Anuria, 167–168 Anxiety motivated elimination, 578–579 Anxiolytics, 591 Aortic knob, 765 regurgitation, 24, 500 stenosis, 24, 261, 334 thromboembolism, see Thromboembolism undulation, 765, 767 Apexification, 603–604 Apexogenesis, 603–605 Apocrine hidrocystoma, 173 Apoidea spp., 148 Appetite stimulant, 23, 455 Aquamephyton, 467 Aqueocentesis, 545 Aqueous flair, 544 Arachidonic acid, 22 Arachnids, 145–147 Arginine, 22, 71, 226 Arginine vasopressin, 111 Arrhythmia, 26–27, cardiomyopathies, 261, 263, 460 diaphragmatic hernia, 121–122 hyperthyroidism, 257 hypomagnesemia, 274 mitral valve dysplasia, 333 patent ductus arteriosus, 388 Arteriovenous fistula, 250 Arthopod-transmitted disease, 18 Arthropathy, 478–479 Arytenoid lateralization, 301 Ascarids, see Roundworms Ascites cardiac, 15, 28–29, 129, 328, 333, 388, 430, 460 hypoalbuminemia, 267–268 infectious, 181–182 neoplastic, 207, 215, 320 pancreatitis, 377 post-op renal, 395 renal, 453 Ascorbic acid, 6 Aspergillosis, 30–31 Aspergillus spp., 30 Aspiration lung, 96, 904–905 Aspirin, 32, 130, 210, 263, 460, 508 Aspirin toxicosis, 32 Assemblage Giardia, 197 Assisted standing, 689 Asthma, 58–60, 96, 208, 245, 749 Asymmetric septal hypertrophy, 261 Ataxia, 911 Atelectasis, 58–59 Atenolol, 24, 27, 263 Atonic bladder, see Bladder, atonic Atopic dermatitis, see Atopy Atopy, 33, 154, 195, 246, 280, 332 Atresia ani, 447 Atrial fibrillation, 26 Atrial premature complexes, 129, 430 Atrioventricular junction, 26 Atropine, 439, 545 Atropine challenge test, 134 Attachment to pet, 954–955 Attention seeking behavior, 587–589 Atypical bacteria, 131–133, 730–731 Aujeszky disease, 170
Aura, 159 Aural hematoma, 143, 369 Auricle, 369 Auricular cartilage, 369 Aurothioglucose, 200 Auscultation, 26–28, 67, 388 Australian bat Lyssavirus, 441 Autoagglutination, 282 Autoimmune hemolytic anemia, see Immune mediated hemolytic anemia skin disease, 392–393 Autonomic polyneuropathy, 134 AV block, 26 Azathioprine, 385 Azithromycin, 36 Babesia spp., 282–283 Bacillary angiomatosis, 35 Bacterial endocarditis, 861 Bacterial L-forms, 45, 131, Baermann examination, 96, 306, 492 Bain anesthesia system, 623 Balanced anesthesia, 682 Balinese, 940 Balloon catheter dilatation, 164, 430, 448 Barbiturates, 682 Barium burger, 797 impregnated polyethylene spheres, 799 series, 798–799, 913 Bartonella spp., 35–36, 191, 199, 344, 879–880 ophthalmic, 294, 463–464, 543, 545 Bartonellosis, 35, 192 Basal cell tumor, 37, 173, 384, 657 Basal energy requirement, 558–559 Bat, 440 Bat feces, 231 Bates body, 812, 825–826 Bees, 148–149 Bee sting, 148 Beetles, 492 Behavioral pharmaceuticals, 591–593 anxiolytics, 591 benzodiazepines, 592 monoamine oxidase inhibitors, 591 selective serotonin re-uptake inhibitors, 591–592 transdermal administration, 592 tricyclic antidepressants, 591–592 Benazepril, see Angiotensin converting enzyme inhibitors cardiac, 130, 263, 333 renal, 456, 458–459 Bengal, 940–941 Benign characteristics, 723, 725 Bentonite clay, 272 Benzodiazepines, 592, 620, 622, 682 Bereavement of pet loss, 954–955 Besnoitia spp., 89, 513 Beta-adrenergic blocker, see Beta blocker Beta blocker, 27, 263, 430, 508 Bethanechol, 135, 354–355, 533 Biceps reflex, 912 Bicycling, 689 Big kidney-little kidney syndrome, 297, 526 Bile acids, 74, 268, 426, 520 Biliary cyst, 39 Bilirubin, 277–278 Biofilm, 597, 599 Bioterrorism, 400 Birds, 468, 513 Bird feces, 231
Birman, 81, 97, 940, 976 Bite wounds by canine, 41–42 by feline, 44–45 Black snakes, 152 Black widow spider, 145 Bladder atonic, 318, 715 lower motor neuron, 354 marsupialization, 533, 715–716 neurogenic, 354 upper motor neuron, 354 urinary Blalock-Taussig surgery, 500 Blastomyces dermatitidis, 46, 463, 543, 747 Blastomycosis, 46, 737, 747 Blindness, 48–50, 104, 427 adaptation, 48 amaurotic (central), 426 ischemic encephalopathy, 292 retinal, 462–464 temporary, 330 Blood collection, 573 jugular vein, 303 Blood group system, 352, 879 Blood hyperviscosity syndrome, 463 Blood pressure determination, 573, 924 environment, 573 epilepsy, 159, 161 equipment direct, 250 Doppler, 250–251, 924 oscillometric conventional, 251, 924 high definition, 251, 924 hypertension, 250–251, 254–255 hyperthyroidism, 257–258 hypokalemia, 272 murmurs, 334 ophthalmic, 462–465, 545 renal, 453–459 seizures, 480 thromboembolic disease, 507 Blood transfusion, 879–881 acetaminophen toxicosis, 6 amyloidiosis, 15 blood administration, 880–881 blood collection, 879–880 feline leukemia virus disease, 184–185 hemoplasmosis, 219 immune mediated hemolytic anemia, 282–283 neonatal isoerythrolysis, 352 refeeding syndrome, 449 renal failure, 456 Blood types, 352–353, 879 Blood typing kits, 352, 879–880 Blue-tail lizard, 548 Bobcat, 106 Body condition score, 187, 358–359, 558 Body surface area, 939 Bone marrow, 879, 881–884 Bone marrow aspiration, 20, 882–884 Bone matrix implant material, 606–607 Bot fly, 104 Bordetella bronchiseptica, 50, 96, 342, 344, 515, 944, 957 Bordetellosis, 50–51 Bots nasal, 347 Bouginage, 164, 448 Bovine spongiform encephalitis, 14, 170
1035
Index
Bowen’s disease, 489–490 Brachial plexus neuropathy, 52 Brachycephalic cats anesthesia, 624 dystocia, 138 Brachycephalic corneal disease, 53, 93 Brachycephalic syndrome, 53–54 Brachycephalism, see Brachycephalic syndrome Bradycardia, 18, 323, 502 Bradyzoite, 512 Breed-related disease, 940–942 dystocia, 138–139 glomerulonephritis, 205–206 polycystic kidney disease, 418–419 Breed-specific diseases, 940–942 British shorthair, 261, 879, 941, 976 Brodifacoum, 466 Bromadiolone, 466 Bromethalin, 466–467 Bronchial disease, 58, 60, 208 Bronchoalveolar lavage, 59, 96, 137, 306 Bronchodilators inhaled, 60 oral, 59–60 Bronchoscopy, 413 Brown-Brenn stain, 132 Brown mucous membranes, 6 Brown recluse spider, 146 Brown snakes, 152 Brucella spp., 976 Bruxing, 597 Bubble study, 500, 546 Buboes, 400–401 Bubonic plague, see Yersiniosis, bubonic form Budesonide, 285 Buffy coat prep, 321–322 Bufo toad, 193 Bulbourethral glands, 709–711, 937 Bulla osteotomy lateral, 288–289, 350, 704–706 ventral, 288–289, 375, 626–630 Bulldog vascular clamp, 670–671 Bull’s eye lesion, 146 Bumblebees, 164 Bundle branch block, 254, 257, 261, 274 Buphthalmos, 202–204 Bupivacaine, 617–618 Buprenorphine, 200, 620–621, 674–675, 682–684 Burmese, 118, 129, 202, 272, 503, 940–941, 976 Burr cells, 153 Buspirone, 591–592 Butorphanol, 620–621, 682–683 Caffeine, 442–443 Calcipotriol, 553 Calcitonin, 243–244 Calcitriol, 270–271, 456, 458–459, 553 Calcium acetate, 458 carbonate, 456, 458 forms, 243 gluconate, 270–271 Calcium oxalate crystals ethylene glycol toxicity, 167–168 urolith, 526, 707–708 Calcium phosphate urolith, 707 Calculi, see Urolithiasis Calculus, 599, 601 Calculus index, 597, 599, 601 Calicivirus, see Feline calicivirus Call-Exner bodies, 207
1036
Caloric requirements, 558 Campylobacteriosis, 124–125, 284, 957 Cancer associated anorexia-cachexia syndrome, 386 Candidatus Mycoplasma haemominutum, 19, 218–219 Candidatus Mycoplasma turicensis, 218–219 Cannabis sativa, 442–444 Capillaria aerophila, see Eucoleus aerophila Capillary refill time, 28, 67 Capnography, 623–624 Capsulectomy, 395 Carbamate toxicosis, 365–365 Carbimazole, 258 Carbohydrates, 119, 358–359 Carbon dioxide laser, see Laser surgery Carboplatin, 328–329 Carcinoma, 12 pancreatic, 102 Carcinoma in situ, Carcinomatosis, 28, 65 Cardiac arrest, see Cardiopulmonary arrest Cardiac catheterization, 388–389 Cardiac massage, see External cardiac massage Cardiac output, 129 Cardiac tamponade, 328–329 Cardiocentesis, 880 Cardiomyopathy, 83 dilated, 28, 129–130, 334, 460, 852, 857, 863–864 hypertensive, 254–256, 258, 263 hyperthyroidism, 256–258 hypertrophic, 261–264 ascites, 28 as breeding cats, 944 imaging, 850, 852, 856–859 other cardiac diseases, 24, 254, 333–334, 460 intermediate, 460 restrictive, 460–461, 852, 857, 861, 865 right-sided, 849, 861, 868 thyrotoxic, 254, 852 Cardiopulmonary arrest, 67–69 Cardiopulmonary resuscitation, 67–69 Carnitine, see L-carnitine Carpal organ, 937 Carprofen, 683–684 Castration, 493, 952 Cataract, 48, 70–71, 543–545 classification, 70–71 Cat bites to humans, 563 Cat grass, 411 Cat scratch disease, 35–36 Catheter central venous, 885–887, 900 jugular, 885 subcutaneous fluid, 696–697 Catheterization, urethral, see Urethral catheterization Catnip, 411, 566 Cattery, 943–944 housing groups, 943 hygiene, 943 isolation unit, 944 Caudal cruciate ligament, 638 Cauliflower ear, 369–370 CCNU, see Lomustine Celiogram, 121, 136–137, 784, 786 Cellophane banding, 427 Cellulitis, 44–45, 131–133, Central venous catheter, see Catheter, central venous
Central venous pressure, 268, 453, 885 Cerebellar hypoplasia, 382–383, 976 Cerebrospinal fluid, 182, 326, 888–889 Cerebrospinal fluid collection, 888–889 Cerumenolytic, 371–372 Ceruminous gland disease hyperplasia, 72, 372, 655–657 neoplasia, 72, 369, 372–373, 655–657 Cervical line lesion, see Resorptive lesions Cervical ventroflexion, 74–75, 272–273, 336, 364, 449, 502, 509 Cesarean section, 139, Cestodes, 496 Chamber induction, 622 Charting, see Dental, charting Chartreux, 941 Chemoreceptor trigger zone, 555, 557 Chemosis, 295 Chemotherapy intracavitary, 66, 207, 315, 328–329 intravenous, 66 intravesicular, 536 side effects, 76–79 Chemotherapy agent CCNU, CeeNU, lomustine, 77, 321 chlorambucil, 76–78, 310, 393 cyclophosphamide, 76–78 doxorubicin, 76–79 idarubicin, 77 L-asparaginase, 77–78 methotrexate, 78 prednisone, 76–77 vinblastine, 77–79 vincristine, 76–77, 76–79 Chemotherapy protocol chlorambucil/prednisone, 77, 310 CHOP, 76–77 combination, 76–78, 301 COP, 76–77 COPA, 76–77 single agents, 76–77, 310 Cherry eye, 503 Chest tube, see Thoracostomy tube Chewing tobacco, 44 Cheyletiella blakei, 332, 483–485 Cheyletiellosis, 102, 483–485 Cheyne-Stokes respiratory pattern, 145 Chlamydia psittaci, see Chlamydophila felis Chlamydophila felis, 50, 81–82, 294–295, 944, 957 Chlorambucil, 200, 285–286, 310, 385 Chlorpromazine, 557 Chlorpropamide, 112 Chocolate, 442–443 Cholangiohepatitis acute, 39, 220, 222, 277–279, 520 chronic, 39, 222–224, 380, 520 Cholangitis/cholangiohepatitis, 222, 277–279, 519 Cholecalciferol toxicosis, 553 Cholecystocentesis, 193 Cholelith, 222–223 Cholelithiasis, 222 Cholinergic antagonist, 354 Cholinergic drug, 354–355 Cholinesterase activity, 74 Chondrosarcoma, 475–476 Chorioretinitis, 46, 98, 231, 543 Choroiditis, 543 Chromium Chromoproteinuric nephropathy, 352 Chronic pancreatitis, see Pancreatitis, chronic Chronic renal disease
Index
Chronic renal failure, see Renal failure, chronic Chrysotherapy, 200 Chylothorax, 83–84, 96, 698–700 Chylous fluid, 83–84 Cidofovir, 94 Cigars, 444 Cigarettes, 444 Cilia ectopic, 295 Ciliary cyst, 290 Cimetidine, 6 Circling, 292, 326, 548 Cirrhosis hepatic, 222 Cisapride, 325, 522 Clades, FIV, see Subtypes, FIV Clarence River Snake, 152 Clavical, 937 Cleft lip, 676 Cleft palate, 676–677 Clofazimine, 303 Clomipramine, 591–592 Clopidogrel, 130, 263 Closed population, 943 Clostridium botulinum, 134 Clostridium tetani, 125, 498 Coagulation profile, 222–223 Coagulopathy, 216, 277–279, 466–467, 520 Cobalamin, 85–86 anorexia, 22 diarrhea, 125 exocrine pancreatic insufficiency, 169–170 hepatic lipidosis, 220–221 hyperthyroidism, 256–258 inflammatory bowel disease, 284, 286 pancreatitis, 380–381 triad disease, 520 Coccidioides immitis, 87–88, 462–463, 543, 747 Coccidioidomycosis, 87–88, 737, 747 Coccidiosis, 89–90, 125 Cockroaches, 492 Cocoa bean/powder, 443 Cod liver oil, 552 Coenzyme Q10, 201 Coffee, 442–443 Cognitive dysfunction, 14 Cola drinks, 442 Colchicine, 15 Cold therapy, see Cryotherapy Colectomy, 91, 324–325, 631–635 Colloids, 898 natural, 268 synthetic, 268 Colloid osmotic pressure, 267–268 Coloboma, 463–464 Colopexy, 448 Colostrum, 976–977 Colubroidea, 151 Compulsive disorders, 587–588 Congenital diseases, 940 Congestive heart failure, see Heart failure Congo red stain, 14 Conjunctiva, 171–172, 174, bulbar, 294 palpebral, 172, 174, 294 Conjunctival pedical graft, 636 Conjunctivitis, 294–296 Conn’s disease/syndrome, see Hyperaldosteronism Conscious proprioception, 911 Consensual pupillary light reflex, 910 Constipation, 91–92
colectomy, 632, 635 hyperparathyroidism, 632 Manx syndrome, 318–319 megacolon, 323–325 rectal disease, 446–448 refeeding syndrome, 449 tail injury, 495 Contrast antegrade pyelography, 526 Coombs’ test, 20, 218–219, 258, 283, 352 Copper colored iris, 426 Copperhead snake, 152 Cor triatriatum dexter, 28 Coral snake, 151–153 Cornea, 294 Corneal reflex, 911 sequestrum, 53, 225–226, 294–296, 637 surgery, 636–637 ulceration, 53, 93–95, 202, 225–226, 543, 545 Cornish rex, 976 Coronavirus titer, 137, 175, 181–183 Corticosteroids, 682, 684 Cosyntropin, 265 Cottonmouth water moccasin snake, 152 Cough/coughing, 96 ascarids migration, 468 bronchial disease, 58–60, 482, 515–517 chylothorax, 83 heartworm disease, 208 honking, 517 lung parasites, 306 neoplasia, 12, 328, 509 pulmonary fibrosis, 428–429 Coumadin, see Warfarin Counter-conditioning, 588–589 COX-2 inhibitor, 66, 490, 536 Coyotes, 208 Cranial cruciate ligament rupture, 638–639, 662–663 drawer test, 638 nerves, 910–911 trauma, 229 Cranial tibial reflex, 912 Crayfish, 306 Creatine kinase, 74–75, 241 Crickets, 492 Cross-matching, 879, 880, 980–981 Crown amputation, 607 Cryosurgery, 490 Cryotherapy, 688 Cryptococcosis, 97–98, 131–133, 737, 746 Cryptococcus gattii, 97, 99 Cryptococcus neoformans, 46, 97, 99, 131–133, 344, 463, 543, 746 Cryptorchidism, 426, 640–641, 952 Cryptorchidism surgery, 640–641 Cryptosporidiosis, 100, 944 Cryptosporidium spp., 89, 100, 284–285, 943–944 Crystalloids, 268, 898, 900 Ctenocephalides felis, 191, 400 Cushing’s disease, see Hyperadrenocorticism Cutaneous larval migrans, 234 Cutaneous xanthomatosis, 114 Cuterebra spp., 104, 292, 463 Cuterebriasis, 104, 292 Cyanoacrylate tissue glue, 674–675 Cyanocobalamin, 85 Cyanosis, 5, 32, 442, 500, 506–507, 546 Cyclitis, 543 Cyclophosphamide cystitis, 140 inflammatory bowel disease, 285 mammary neoplasia, 666
panniculitis, 385 stomatitis, 200 Cyclosporine, 34, 285, 393, 980–982 Cyproheptadine, 23, 60, 455, 458 Cyst mediastinal, 753, 756 Cystadenoma, 40 Cystectomy partial, 40 Cystocentesis, 531, 533, 573 Cystography, 786, 812, 820–823 Cystoscopy, 532 Cystostomy, see Bladder marsupialization Cystotomy, 541, 715 Cytauxzoon felis, 106, 282–283, 737 Cytauxzoonosis, 106, 282–283 Cytochrome P450 oxidase system, 6 Cytology, 719–752 Daltaparin, 508 Dancing, 690 Dandruff, 484 Dantrolene, 533 Darbepoetin alfa, 456, 458 Dazzle reflex, 48 DDAVP, see Vasopressin Deafness, 548, 940–941 Death Adder snake, 152 Deciduous teeth retained, 606 Declawing, see Onychectomy Defecation reflex, 912 Defibrillation, 68–69 Degenerative joint disease, 366 Degloving injury, 494–495 Dehydration, 558, 898–901 Demodex cati, 143, 172, 483–485 gatoi, 172, 483–484 long species, 483–484 Demodicosis, 143, 172, 483, 489–490 Dendritic ulcer, 93, 95, 225, 295 Dental charting, 597, 600 eruption, 933 examination, 597–598 explorer, see Explorer probe extractions, see Extractions, dental formula, 599–600, 938 fracture, 229 prophylaxis, 599–601 resorption, see Resorptive lesions Deranged stifle, 638 Dermacentor variabilis, 106 Dermatophyte, 108–109 Dermatophyte test media, 108 Dermatophytosis, 10, 102, 108–110, 126, 128, 172, 332, 944 Descemet’s membrane, 294 Desensitization, 588–589 Desflurane, 623, 682 Desmopressin, see vasopressin Desoxycorticosterone pivalate, 265 Detemir insulin, 119 Detrusor atony, 533 Devon Rex, 662, 879, 941, 976 Dexamethasone suppression test, 239, 424 Dexmedetomidine, 684 Dextrans, 268 Diabetes insipidus, 111 nephrogenic, 424 Diabetes mellitus, 8–9, 14, 21, 30 acromegaly, 8–9
1037
Index
amyloidiosis, 14 blindness, 463 cataracts, 113 complications, 102–103, 113–117 demyelination, 113 denervation, 113 dermatitis, 483 foot disease, 114 Heinz bodies, 211 hepatic lipidosis, 220 hyperadrenocorticism, 239 hypertension, 250, 252, 254 hypokalemia, 74 hypomagnesemia, 274 hypophosphatemia, 275–276 ketoacidosis, 115 nephropathy, 113 neuropathy, 113 nonketotic hyperosmolar, 115–117 pancreatitis, 377 plantigrade posture, 113 polyphagic weight loss, 422 polyuria and polydipsia, 424 refeeding syndrome, 449 renal transplant, 980 toe nail overgrowth, 114 weight loss, 558–559 Diabetic cataracts, 113 foot disease, 114 ketoacidosis, 115, 272, 274, 449 neuropathy, 113 nephropathy, 113 Diaphragmatic hernia, 121–123, 136–137, 620, 913 congenital, 121–122 traumatic, 121–122 Diarrhea, 89, 124–125 cobalamin, 85 infectious, 89, 100–101, 124–125, 197–198, 470, 523–524 inflammatory bowel disease, 284–286 large bowel, 124–125, 523–524 small bowel, 124–125 types, 124 Diastema, 599 Diastolic dysfunction, 261 Diazepam, 160, 354, 482, 533, 592 Diet chylothorax, 84 diabetes, 119 glomerulonephritis, 205 hepatic lipidosis, 220 renal, 456, 458–459 urolithiasis, 538, 541–542 Diff-Quik stain, 719–720 Digibind immune fab, 404, 411 Digital disease, 126, 128 Digoxin, 547 Dihydrotachysterol, 271 Dilated cardiomyopathy, see Cardiomyopathy, dilated Diltiazem, 24, 27, 263, 460 Diphacinone, 466 Dipylidium caninum, 191, 496 Direct pupillary light reflex, 910 Dirofilaria immitis, 208, 306, 879 Dirty face syndrome, see Idiopathic facial dermatitis of Persian cats Discoloration of tooth, 602 Discrete cells, 721, 723–724 Disease factors agent, 943–944
1038
environmental, 943 host, 943 population density, 943 stress, 943 Disinfectants, 957 Displacement activities, 587–588 Disseminated intravascular coagulation, 277–278, 328, 330, 352, 400 Distichia, 93, 295 Diuretic, 24 Diverging strabismus, 54–56 Diverticulum esophageal, 165 vesicourachal, 140 DL-methionine, 542 Dobutamine, 130 Dog bites, see Bite wounds, canine Domestic longhair, 118, 394, 941 Domestic shorthair, 314, 328, 394, 509, 662, 879, 940–941 Dopamine, 379, 454 Doppler blood pressure, 250–251, 624, 924 tooth evaluator, 603, 606 Doramectin, 484, 486 Doxorubicin, 666 Doxycycline, 162, 416 Draining tracts and nodules, 131–133 anal sac disease, 16 bacterial, 10, 487–488, 338–339, 356–357 fungal, 46, 87, 97, 302, 487–488 neoplastic, 386 parasitic, 104, Drawer sign, see Cranial drawer test Drooling, see Ptyalism Drug formulary, 995–1028 Dynamic right ventricular obstruction, 334 Dysautonomia, 91, 124, 134–135, 323, 503 Dyscoria, 544 Dysphagia, 162–163, 287, 336, 498 Dysphonia, 298, 300, 336 Dyspnea, 83, 136–137, 287, 428 Dystocia, 138–139, 358 Dystrophic calcification, 553 Dysuria, 138–142, 498 Ear flushing, 371 infection, 370 mites, see Otoacariasis tick, see Spinous ear tick tip necrosis, 977 tipping, 950–952 Ecchymosis, 466 Echinococcus multilocularis, 170 Echocardiogram cardiomyopathies, 261, 263, 460 other heart disease, 24, 27, 333, 388–389, 430, 500, 546 thromboembolic disease, 507 Echocardiographic tables, 945–946 Echocardiography, see Echocardiogram Eclampsia, 977 Ectoparasites, see Skin parasites Ectopic calcification, 243 cilia, 295 thyroid tissue, 256–258 ureter, 297, 813, 820–821 Edema corneal, 202 facial, 5 hypoalbuminemia, 267–268
paws, 5 pulmonary, 8 Edrophonium chloride challenge, 74, 337, 510 Effleurage, 687 Egg basket, 496–497 Egyptian Mau, 941 Ehler-Danlos syndrome, 103 Ehrlichia phagocytophila, see Anaplasma phagocytophilia Ehrlichiosis, see Anaplasmosis Eicosapentanoic acid, 286 Eisenmenger’s physiology, 547 Elapidae, 151 Eld gastrostomy tube device, 649 Electrical stimulation, 688 Electrocardiogram, 26, 129, 261–262, 333, 388–389, 430, 500, 546 left atrial enlargement, 947 left ventricular enlargement, 947 right atrial enlargement, 947 right ventricular enlargement, 947 Electrocardiography, 26, 67, 129, 261–262 Electrocardiographic tables, 947 Electromyography, 74, 337 Electroretinogram, 48, 70, 203, 463–464 Electrotherapy, 687–689 Elongated soft palate, 53, 56–57, Elongated tongue, 55–56 Embolectomy, 508 Emesis, 555–557 Empyema, see Pyothorax Enalapril, 130, 263, 333 Encephalomyelitis, 89–90 Encephalopathy hepatic, 39, 220–221 ischemic, 104, 292–293 Endocarditis, see Bacterial endocarditis Endocrine deficiency alopecia, 587 Endodontics, 602–605 Endometrial hyperplasia, 434 Endoscopy, 96 Endotracheal intubation, 516, 623 Endotracheal tube, 623 Enema, 92 Enilconazole, 100 Enophthalmos, 235 Enrichment broth, 470 Enrofloxacin, 463–464 Enterocolitis, 124 Entropion, 171–172, 174, 294–295 Enucleation, 49, 204, 290–291 Envenomization arachnids, 145 insects, 148–149 snakes, 151–153, 272 Environmental enrichment home, 566, 567–570 hospital, 571–576 Environmental tobacco smoke, 489 Eosinophilia, 245 Eosinophilic granuloma, 154 granuloma complex, 33, 154, 189, 195, 245, 721–723, 737 keratitis, 157–158, 294 panniculitis, 384 plaque, 33, 154–156 ulcer, 154–156 ulcerative facial dermatosis, 225 Ephedrine, 354–355 Epidermal collaret, 392 Epidermal inclusion cysts, 722, 725, 727
Index
Epidural block, see Local anesthetic block, epidural Epilepsy, 159–161, 480–482 Epinephrine, 617, 683 Epinephrine ophthalmic, 503 Epiphora, 53 Episioplasty, 685 Epistaxis, 30, 229 Epithelial cells, 721, 723–725, 727 Epoetin alfa, 456, 458 Epulis, 361 Equine anti-tetanus serum, 499 Ergocalciferol, 271 Erythropoietin, 21, 456–458 Escherichia coli, 976 Esophageal anatomy, 937 diverticulum, 165 esophagitis, 162–163, 165 foreign body, 162–163 hiatal hernia, 163, 165 hypomotility, 162, 165 megaesophagus, 162, 165–166, 336–337 neoplasia, 162–163, 165 stricture, 50, 162–164 vascular ring anomaly, 162, 164 Esophagitis, 162–163, 165 Esophagostomy tube, 22, 43, 220–221, 642–645, 665, 669, 680, 981 Ethanol, 167–168, 442–444 Ethylene glycol, 32, 167–168, 297, 452–454, 463 hypocalcemia, 270–271 Etomidate, 622–623 Eucoleus aerophila, 96, 306 European shorthair, 202 Eustachian tube, 374 Eutectic mixture of lidocaine and prilocaine cream, 619 Euthanasia, 440–441, 893–895, 948–953 agents, 893 client relations, 893 disposition of the body, 894 professional fees, 894 sympathy expression, 894 Euthyroid sick syndrome, 359 Excretory urogram, 237–238, 432–433, 811–813, 817–823 Exenteration, 290–291 Exercise, see Therapeutic exercise Exfoliative dermatitis, 102 Exocrine pancreatic disease acute, see Pancreatitis, acute chronic, see Pancreatitis, chronic insufficiency, 85, 124, 169, 284, 381, 422 Exodontia, see Extractions, dental Explorer probe, 602, 608 Extensor carpi radialis reflex, 912 External acoustic meatus, 369, 704, 706 cardiac massage, 67 ear, 369, 371 ear canal, 369–370, 372, 704 Extracapsular stabilization Stifle, 638–639 Extracellular fluid compartment, 898 Extractions dental, 602–604, 606–609 stomatitis, 199–201 Extrahepatic bile duct obstruction, 277–278 Eye exam, 890–892 Eyelid diseases, 171–174 apocrine hidrocystoma, 173
basal cell tumor, 173 blepharitis, 172 demodicosis, 172 dermatophytosis, 172 drug reactions, 172 ectopic cilia, 172 entropion, 171–172 eyelid agenesis, 171 fibrosarcoma, 173, 732–733 mast cell tumor, 172 reflexes, 910–911 squamous cell carcinoma, 172–173 Facial dermatitis of Persian cats, see Idiopathic facial dermatitis of Persian cats dermatosis calicivirus, 62 herpesvirus, 225 excoriation, 258 fold dermatitis, 313 nerve, 374, 910–911 nerve paralysis/paresis, 374, 706 pruritus, 258, 984 Fading kitten syndrome, 352 False pregnancy, see Pseudopregnancy Famciclovir, 94–95, 226 Famotidine, 455, 458 Fat binder, 84 Fatty liver syndrome, see Hepatic lipidosis FCoV titer, see Coronavirus titer Fecal flotation, 96, 234, 468, 492 Fecal proteolytic activity, 169 radial enzyme diffusion, 169 x-ray film digestion, 169 Feeding tubes, 23, 642, 649 Felicola subrotratus, 332 Feline calicivirus, 50, 62, 81, 176, 199, 342, 344, 667, 957 Feline coronavirus group, 175, 181–183 Feline dental resorption, see Resorptive lesions Feline distemper, see Panleukopenia Feline enteric coronavirus, 175, 181–183, 944, 976 Feline herpesvirus, 225–227 abortion, 976 in cattery, 944 clinical signs, 225–227 corneal disease, 93–94, 157, 294 dermatitis, 550–551 gingivitis-stomatitis-pharyngitis, 199 groups, 225 in hospital, 957 laryngeal rhinitis, 342 tracheal, 50, 515, 517 uveitis, 543 Feline idiopathic cystitis, 140–142, 176–177 Feline immunodeficiency virus, 179–180 abortion, 976 abscess, cellulitis, 44 blood donor collection, 879 in cattery, 943 dermatitis, 483, 550–551 FIP, 179, fungal disease, 231 gingivitis-stomatitis-pharyngitis complex, 179, 199 glomerulonephritis, 205 griseofulvin, 108, 180 otitis externa, 370–371 papillomavirus, 490
phases of infection, 179 pododermatitis, 416 renal transplant, 980 retinitis, 463 salmonellosis, 470 subtypes, 179–180 tests, 179–180 toxoplasmosis, 180 uveitis, 543 vaccine, 180 Feline indolent ulcer, see Eosinophilic ulcer Feline infectious anemia, see Hemoplasmosis Feline infectious enteritis, see Panleukopenia Feline infectious peritonitis, 28, 30, 65–66, 181–183 cattery control, 183, 943 diagnosis, 182–183 as differential, 121 effusive, 181–183 glomerulonephritis, 205 immune mediated hemolytic anemia, 282 non-effusive, 181–183 pancreatitis, 377 renal, 297 Feline infectious peritonitis virus, 175, 181–183 FIV virus, 179 retinitis, 463 uveitis, 543 Feline interferon, 183 Feline ischemic encephalopathy, 292–293 Feline leukemia virus, 184–186 abortion, 976 blood donor testing, 879 in cattery, 943 dermatitis, 550–551 dermatitis, 483 fungal disease, 231 glomerulonephritis, 205 immune mediated hemolytic anemia, 282 latent infection, 184–185 otitis externa, 370–371 outcome of infection, 184–185 regressor, 184–185 renal transplant, 980 retinitis, 463 salmonellosis, 470 stomatitis, 199 subgroups, 184 tests, 184 transient viremia, 184 treatment, 185–186 uveitis, 543 viremia, 184–185 vaccine, 185 Feline lower urinary tract disease, 176 Feline odontoclastic resorptive lesions, see Resorptive lesions Feline oral resorptive lesions, see Resorptive lesions Feline pancreatic lipase immunoreactivity, 102, 193, 285, 377–378, 381, 519, 556 Feline parvovirus, see Parvovirus Feline plasma cell pododermatitis, see Pododermatitis, lymphoplasmacytic Feline sarcoma virus, 475, 477 Feline spongioform encephalopathy, 14 Feline syncytial-forming virus, 176 Feline triad disease, see Triad disease Feline trypsin-like immunoreactivity, 8, 85, 125, 169, 193, 285, 377–381 Fenbendazole, 125, 306, 492 Fentanyl, 200, 620, 622–623, 683
1039
Index
Fenthion, 364, 377 Feral cats, 948–953 Ferguson reflex, 138 Fetal mummification, 382 Fever of unknown origin, 187, 888 Fever, 187–188 Fibrinolytic agent, 508 Fibroadenomatous mammary hyperplasia, see Mammary hyperplasia Fibroepithelial hyperplasia, see Mammary hyperplasia Fibronectin, 65 Fibrosarcoma, 361, 472, 475–477, 723, 725 Fibrosing pleuritis, 83–84 Fiddle back spider, see Brown recluse spider Fight wound infection, see Bite wounds, feline and Bite wounds, canine Filamentous bacteria, 730–731 Fine needle aspirate, 734 Fine needle biopsy, 734, 896–897 Fire ants, 149–150 Fire ant sting, 149–150 Fish bone pattern of esophagus, 797–798 Fish diet, 502 Fish oil supplements, see Omega-3 fatty acids Fistula oroantral, 607 oronasal, 607, 676–681 overlapping sandwich flap, 676–679 silastic nasal septal button, 679–681 sliding bipedical flap, 677–679 split palatal U-flap, 679–680 tongue flap, 679–680 Flame figures, 154 Flea allergy dermatitis, 154, 189, 191, 246, 280, 332, 486 Flea bite hypersensitivity, see Flea allergy dermatitis Flea dirt, 191 Flea hypersensitivity, see Flea allergy dermatitis Fleas, 35, 191, 218, 483, 486, 496 Flexion reflex, 912 Flies, 340–341, 347, 523 Fluconazole, 46–47, 87–88, 98–99, 233, 488 Fluid rate, 900 routes intraosseous, 900 intravenous, 900 subcutaneous, 900 types dextrose 5% in water, 898–899 maintenance, 898–901 replacement, 898–900 therapy, 898–901 fluid choices, 898–899 maintenance, 898–900 rehydration, 899 Flukes biliary, 193 liver, 193 pancreatic, 193 Fluorescein stain, 93, 295, 545, 891 Fluoride, 600, 603 Fluoxetine, 591–592 Fluticasone, 60 Fly larvae, 340 Fly strike, 340 Folate, 284, 380–381 Folded-ear, 478–479 Folic acid, 133, Fomepizole, see 4-methylpyrazole
1040
Food allergy, see Reaction, food elimination diet, 154, 195 hypersensitivity, see Reaction, food intolerance, see Reaction, food reaction, 143, 154, 195, 280, 342–343 trial, 154, 195 Force feeding, 22–23, Foreign body, 555–556 Forelimb fracture, 229 Formalin cytology stains, 719–720 Formalin-ether sedimentation, 193, 925 Formicidae spp., 148 Formulary of drugs, 995–1028 Fox, 440 Fractional shortening, 129, 263, 460 Fractious cats, 920, 948 Fragile skin syndrome, 102–103, 239, 386 Free roaming cats, 948–953 Free T4 test, 257 Friction, 687 Frontal sinus obliteration, 346, 646–648 Fructosamine, 925 Funnel chest, 390 Furcation exposure, 599, 601 Furosemide, 28–29, 129–130, 262–263, 333, 388, 430, 460 Gabapentin, 160, 682, 684 Gallop rhythm, 28, 129, 250, 254, 256, 261, 334, 460 Gamma-aminobutyric acid, 330 Gastritis, 213–214, 555–556 Gastrocnemius reflex, 912 Gastroenteritis, 555–556 Gastroesophageal intussusception, 163 Gastroesophageal reflux, 162–163, 165 Gastrointestinal foreign body, 304, 555–556 Gastrointestinal obstruction, 555–557 Gastropexy, 649 Gastrostomy tube, 22, 43, 220–221, 649–650, 669, 680, 981 Gate control theory, 688 Gecko, 193 Genal tufts, 983 General anesthesia, see Anesthesia, general Genetics, 33, 472 Genetic disease, see Breed specific disease Geriatric, 934–935 Gestation, 975–976 length, 975 Giant cells, 722 Giardiasis, 197–198, 944 testing, 125, 197–198, 926–927 Giardia spp., 124–125, 197–198, 284–285, 523, 943–944 forms, 197 Giemsa stain, 719 Gingival index, 597, 599 Gingivitis periodontal disease, 599–601 Gingivitis (inflammatory), see Gingivitisstomatitis-pharyngitis complex Gingivitis-stomatitis-pharyngitis complex, 199–201 bartonellosis, 35 calicivirus, 62–63 glomerulonephritis, 205 juvenile, 199–200 treatment, 200–201, 567 weight loss, 558 Glands of Moll, 171, 173
Glands of Zeis, 171 Glargine insulin, see Insulin, glargine Glaucoma, 48–49, 70–71, 202–204, 463–464 emergency treatment, 203 intraocular tumors, 290–291 maintenance treatment, 203 surgery blind eye, 204 visual eye, 204 types, 202 Glipizide, 113 Glomerulonephritis, 28, 205–206 chronic renal failure, 205 heartworm disease, 205 insulin, 205 nephrotic syndrome, 205–206 polyarthritis, 205 renal transplant, 980 Glossectomy, 55 Glossopharyngeal nerve, 911 Glucose curve, 925 Glucuronidation, 32 Glutathione, 6 Glyburide, 113 Glycosaminoglycan layer, 176 Gold salts, 200–201 Gomori’s methenamine silver stain, 46, 87, 132, 232, Goniometer, 687 Gonioscopy, 202, 291 Gradual water deprivation test, see Water deprivation test, gradual Gram stain, 338 Granulomatous meningitis, 482 Granulosa cell tumor, 207 Grass gastritis, 556 in nasopharynx, 350–351 Gridding ulcer, 95 Gridley’s stain, 46, 232 Grief response, 954–956 Griseofulvin, 109–110 Grocott-Gomori methenamine silver stain, 87 Growth hormone, 8, 317 Growth hormone assay, 8 Growth plate closure, 933 Guillotine-type nail trimmer, 673 Gutta percha, 605 Gwardar snake, 152 H2 blocker, 455, 458 Haab’s striae, 202 Hair follicle tumor, 725 Hairball, see Trichobezoar Hairlip, see Cleft lip Halitosis, 608 Hammondia hammondi, 89, 513 HARD, see heartworm associated heartworm disease Hard palate, 676–679 Hartmann’s solution, 532 Haws, 503 HDO blood pressure, 251 Head pressing, 250, 254, 426 tilt, 287, 374, 502, 548–549 Heart block, 26 failure, 9, 28, 67, 256, 334, 508, 546–547 biventricular, 388 left-sided, 24, 83, 333, 546–547 right-sided, 65, 267–268, 388, 430 Heart failure cell, 749
Index
Heartworm coughing, 306 disease, 65–67, 96, 136–137, 208–209, 334 encephalopathy, 292 glomerulonephritis, 205 imaging, 850, 862, 876 lung disease, 429 serology, 209 stages adult, 208–210 juvenile/immature adult, 208 tests, 96, 136, 209 vomiting, 555–556 Heartworm associated respiratory disease, see Heartworm disease Heat therapy, 687–688 Heimlich valve, 414, 699 Heinz body, 6, 20, 21, 32, 275, 449, 622 Heinz body hemolytic anemia, 5–6, 20–21, 115, 211–212, 224, 275–278, 449 Helicobacter spp., 213–214, 222, 555–556, 558 Hemangioma, 215, 217, 475 Hemangiopericytoma, 475 Hemangiosarcoma, 40, 173, 215–217, 723 cutaneous, 215–217 visceral, 215–217 Hematoidin crystals, 749–750 Hematoma aural, 369–370 Hemingway cats, 420 Hemistanding, 912 Hemiwalking, 912 Hemoabdomen, 215 Hemobartonellosis, see Hemoplasmosis Hemodialysis, 454 Hemoglobinuria, 352 Hemolysis, 275, 352, 449 Hemolytic anemia, see Anemia, hemolytic Hemolytic uremic syndrome, 981 Hemoperitoneum, 14 Hemoplasmosis, 218–219, 277–278, 282 Hemosiderin, 749–750 Hemosiderophage, 749 Hemothorax, 215, 217 Heparin, 130, 460, 508 Hepatic detoxification, 426 encephalopathy, 39, 85, 159, 220–221, 224, 278–279, 426 lipidosis, 22, 43, 103, 220–221, 275, 277–279, 449 anesthesia, 620 cytology, 734–735 obesity, 358–359 Hepatitis, inflammatory, 222–224 Hepatocutaneous syndrome, 126, 128 Hepatomegaly, 222 Herniorrhaphy, 448 Herpesvirus, see Feline herpesvirus Herpesvirus dermatitis, see Viral dermatitis Herpetic ulcer, 95 Herringbone pattern esophagus, 797–798 Hetastarch, 268 Hiatal hernia, 163, 165, 521, 649 High dose dexamethasone suppression test, 239 High rise syndrome, 228–230, 664, 679 Highland Fold, 478 Himalayan, 37, 39, 53, 256, 294, 418, 426, 941 Hindlimb fracture, 229 Hip dysplasia, 366, 662, 944
Histoplasma capsulatum, 131–133, 231, 463, 543, 746–747 Histoplasmosis, 106, 131–133, 231–233, 277, 344, 543, 737, 746–747 Holter monitor, 27 Honey bees, 148 Hookworms, 234 Hopping gait, 318 Hopping reflex, 912 Horner’s syndrome, 235–236, 289, 374, 503–504, 630, 706 signs, 235, 910 Hornets, 148 Horseshoe kidney, 820 Hospital hygiene, 957–959 disinfectants, 957 hand hygiene, 957 instrument hygiene, 957–958 methicillin-resistant Staphylococcus aureus, 957–958 surface hygiene, 957–958 Hospital infection, see Nosocomial infection Hotz-Celcus, 172, 174 Housesoiling, see Inappropriate elimination Human immunodeficiency virus, 97, 100 Human-pet bond, 954–955 Human tetanus immunoglobulin, 499 Humoral hypercalcemia of malignancy, 243–244, 386 Hydralazine, 252, 255 Hydrocephalus, 426, 480–482, 828, 833 Hydrogen peroxide, 330 Hydromorphone, 620–621, 625, 682 Hydromyelia, 834, 841 Hydronephrosis, 237–238, 297, 526–527, 535 Hydrophiinae, 152 Hydrotherapy, 687 Hydroureter, 526 Hydroxyamphetamine ophthalmic, 504 Hydroxyethyl starches, 268 Hygiene hand, 957–959 hospital, 957–959 instrument, 957–959 surface, 957–958 Hymenoptera, 148 Hyperadrenocorticism, 102–103, 239–240, 386–387, 424 functional adrenal tumor, 239 pituitary-dependent, 239 Hyperaldosteronism, 74, 241–242, 250, 252–253, 272 Hyperbaric oxygen, 385 Hypercalcemia, 243–244 constipation, 632 diabetes insipidus, 111 hypertension, 250 hypoadrenocorticism, 265 idiopathic, 243–244 of malignancy, 243–244, 386–387 pancreatitis, 381 polyuria, 424 renal failure, 452–453 urolithiasis, 542 Hypereosinophilic syndrome, 125, 245, 556 Hyperesthesia syndrome, 246, 444, 564, 587–588 Hyperestrogenism, 207, 640 Hyperglobulinemia FIP, 182 Hyperglycemia, 115, 118–119, 167, 377, 449 Hyperkalemia, 247–249 anesthesia, 624
cardiac, 26–27, 67–69 ethylene glycol toxicity, 167 hypoadrenocorticism, 265 renal, 455–456, 458, 452–453 thromboembolic disease, 508 urinary obstruction, 526, 528, 530, 532 Hypernatremia, 74–75 Hyperparathyroidism, 159, 243–244, 250, 456, 458, 632 Hyperphosphatemia, 92, 114, 167, 272, 452–458, 467, 553 Hypertension, 9 acromegaly, 9 anesthesia, 620, 624 ethylene glycol toxicity, 167 hyperaldosteronism, 242 hyperthyroidism, 250, 252–253, 256–258 hypokalemia, 272 idiopathic/essential, 250 lymphatic, 83 portal, 39 pulmonary, 546–547, 749 renal associated, 452–453, 455–458 renal transplant, 980–981 seizures, 480–481 systemic, 9, 242, 250–258, 261–263, 334, 455–458, 463–464 uveitis, 543–545 Hypertensive cardiomyopathy, see Cardiomyopathy, hypertensive choroidopathy, 250, 463 encephalopathy, 250 heart disease, see Cardiomyopathy, hypertensive hypertrophic cardiomyopathy, see Cardiomyopathy, Hypertensive optic neuropathy, 250 retinopathy, 250, 463 Hyperthermia, 187, 330, 682–683 Hyperthyroidism, 9, 74, 102, 124–125, apathetic form, 256, 559 fever, 187 geriatric cats, 934 Heinz bodies, 21, 211 hypertension, 250, 252–253, 261, 263 hypokalemia, 256, 272–273 murmur, 334 polydipsia and polyuria, 424 polyphagic weight loss, 422–423, 558 renal interaction, 455 renal transplant, 980 vomiting, 555–556 weight loss, 558 Hypertrophic cardiomyopathy, see Cardiomyopathy, hypertrophic Hypertrophic osteopathy, 509 Hyperviscosity syndrome, 501 Hypervitaminosis A, 552 Hypervitaminosis D, 466, 553 Hyphating fungi, 747–748 Hyphema, 464, 543–545 Hypnotics, 620 Hypoadrenocorticism, 247, 265–266 testing ACTH stimulation test, 265 endogenous plasma ACTH, 265 Hypoalbuminemia, 28, 32, 267–269 causes, 267 consequences, 267 Hypocalcemia, 270–271 eclampsia, 977 ethylene glycol toxicosis, 167
1041
Index
hypomagnesemia, 274 megacolon, 325 pancreatitis, 377 portosystemic shunt, 426 renal failure, 452–453 thyroidectomy, 258–259, 701 triad disease, 519 Hypochoremic metabolic alkalosis, 556 Hypocobalaminemia, 256–258 Hypoglossal nerve, 911 Hypoglycemia, 23, 159, 382, 426–427, 442–443 Hypokalemia, 272–273 cervical ventroflexion, 74–75 cytauxzoonosis, 106 diabetes insipidus, 111 diabetes mellitus, 114 hyperaldosteronism, 241–242 hyperthyroidism, 256 hypomagnesemia, 274 obstipation, 91 panleukopenia, 382–383 polydipsia and polyuria, 424 recreational drug toxicosis, 443 refeeding syndrome, 449–450 renal, 452–453, 455 urinary obstruction, 532 Hypokalemic nephropathy, 272 of Burmese, 272 Hypokalemic polymyopathy, 241 Hypoluteoidism, 976 Hypomagnesemia, 274, 449 Hypoparathyroidism, 259 Hypophosphatemia, 115, 221, 275–276, 449–451 causes, 275 Hypopyon, 544 Hypotension, 274, 452–453, 619 Hypothyroidism, 91–92, 259, 359, 703 Hypovitaminosis E, 384–385 Hysterotomy, 435 I131, see 131I treatment Ibuprofen, 682 Icterus, 277–279 hepatic, 220, 222–223, 258, 352, 519 prehepatic (hemolytic), 277–278, 282, 449 posthepatic, 278–279 triad disease, 519 Ictus, 159, 480 Idarubicin, 77 Idiopathic facial dermatitis of Persian cats, 53 Idiopathic megacolon, see Megacolon Idiopathic pulmonary fibrosis, 96, 428–429 Idiopathic ulcerative dermatitis, 280–281 Idiopathic vestibular syndrome, see Vestibular syndrome Idoxuridine, 94 IgG antibodies, 512–513 IgM antibodies, 512–513 Illinois sternal needle, 882 Image receptors, 610 Imaging abdomen adrenal glands, 811–812 aortic thrombosis, 826 ascites, 784–785 Bates bodies, 812, 825–826 biliary sludge, 787, 790–791 bladder calculi, 822 cholecystitis, 790–791 cholelithiasis, 790–791, 797 colon, 794, 798–811, 825 ectopic ureter, 813, 820–821
1042
esophagus, 797–799, 810 free gas, 784–786, 802, 805–806 gall bladder, 786–787, 790–791, 797 gastric dilatation/volvulus, 805, 808 gastrointestinal foreign body, 797–809 gastrointestinal tract, 784–787, 796–810, 816 herniation, 784, 786 hydronephrosis, 813, 815–818, 820–824 ileus, 803, 808–810, 820 inflammatory bowel disease, 809 intussusception, 799, 808, 810 kidneys, 787, 791, 793–794, 796, 800, 811–823 liver, 784796 lymph nodes, 793–796, 799, 806, 809–810, 816, 823, 825 lymphadenopathy, 793–794, 805–806, 823, 825 megacolon, 801, 810 megaesophagus, 797–798 mucocele, 791 obstipation, 810 ovary, 825–826 pancreas, 787, 794–796 pancreatitis, 784, 791, 795–796, 808, 810, 820 pancreatolithiasis, 796 perirenal pseudocyst, 816, 817 polycystic kidney disease, 789, 813, 816 pregnancy, 825 pyelonephritis, 813, 816 pyloric outflow obstruction, 806–807 pyometra, 825–826 renal agenesis, 820 renal ectopia, 813, 819–820 renal failure, 811, 819 ruptured urethra, 820 spleen, 785–796 splenomegaly, 791–792 urachal diverticulum, 823 uterus, 825–826 ureter, 811–824 ureteral calculi, 813, 820 ureteral obstruction, 823–824 ureterocele, 821 urethra, 810, 821–825 urethral stricture, 824 urinary bladder, 785–787, 810, 812–813, 815, 820–826 vascular ring anomaly, 797–798 cardiovascular arrhythmogenic right ventricular cardiomyopathy, 861, 868, 869 bacterial endocarditis, 861 biventricular failure, 850, 852 cardiac enlargement, 849, 852, 870 dilated cardiomyopathy, 852, 857, 863, 864 heartworm disease, 850, 862, 876 hypertrophic cardiomyopathy, 850, 852, 856, 858, 860, 866 left atrial thrombus, 859, 861, 863, 866 patent ductus arteriosus, 862, 873 pericardial effusion, 850–858, 861, 863, 865 pulmonary edema, 850–852, 856–857, 859, 861 restrictive cardiomyopathy, 852, 857, 861, 865 right-sided cardiomyopathy, see Imaging, cardiovascular, arrhythmogenic right ventricular cardiomyopathy thyrotoxic cardiomyopathy, 852
unclassified cardiomyopathy, 861, 867 ventricular septal defect, 862, 871–872 head and spine myelography, 832 nasal disease, 828, 830–832 skull views, 828 spine, 834, 840–842, 846 temporomandibular joints, 828–830, 838 vestibular disease, 830, 832–833, 836 thorax aortic knob/aortic undulation, 765 asthma, 769 caudal thoracic mass, 753, 758, 759 cranial mediastinal mass, 753–759, 772 diaphragmatic hernia, 759, 764–765 heartworm disease, 768–769 hiatal hernia, 765–766 hilar lymphadenopathy, 753, 757, 764 lung patterns, 767–770, 782 peritoneopericardial diaphragmatic hernia, 759, 764–765 pleural effusion, 753, 758–762, 764, 769– 773, 779–780 pneumothorax, 759, 761, 763 tenting of diaphragm, 763, 765, 767, 769 Imiquimod, 490, 550–551 Immune mediated disease, 282–283, 295 hemolytic anemia, 106, 282–283 vaccines, 282 Immune-modulating agent, 185–186 Immunodeficiency virus, see Feline immunodeficiency virus Immunohistochemistry assay FIP, 182 toxoplasmosis, 512 Immunosuppression, 100–101, 179, 184–186, 483 Immunosuppressive drugs, 980–981 Immunotherapy, 33 Impacted teeth, 606 Inappropriate elimination, 176–177, 577–580 litter box/litter aversion, 578 location aversion, 578 location preference, 578 marking elimination behavior, 578–579 stress or anxiety motivated, 578 substrate preference, 577–579 Inappropriate urination, 140, 176–177, 577–580 Incontinence fecal, 318–319, 494–495 urinary, 318–319, 495 Indandione, 466–467 India ink preparation, 98 Indolent ulcer, see Eosinophilic ulcer Induced ovulation, 975 Induced vestibular nystagmus, 910 Infectious tracheobronchitis, 50 Inflammation characteristics, 721–722 eosinophilic, 722–723 lymphocytic, 723, 725 granulomatous, 722–723, 727 pyogranulomatous, 722, 727 suppurative/neutrophilic Inflammatory masses, 287–289 polyps, 287–289 bulla osteotomy, 626, 630 laser surgery, 657 nasopharyngeal, 342–343, 349, 351 otic, 72, 369, 372
Index
Inflammatory bowel disease, 284–286 diarrhea, 124–125 hepatitis, 222–223 hypoalbuminemia, 267 pancreatitis, 380 polyphagic weight loss, 422 renal transplant, 980 triad disease, 519 vomiting, 555–556 weight loss, 558 Inflammatory liver disease, see Hepatitis, inflammatory Infrared tympanic membrane thermometer, 187 Inguinal ring, 640–641 Inhalant anesthetics, 682 Inhaler metered dose, 60 Injection-site sarcoma, 441, 472–474, 722–727, 732–733 Inland Taipan snake, 152 Inner ear, 374–375 Insect ascarids, 468 growth regulator, 191 stings, 148–149 Insecticides, 191 Insulin detemir, 116, 119 glargine, 116–117, 119 glomerulonephritis, 205 lente, 116, 119 protamine zinc, 116, 120 regular, 116–117 resistance, 9, 239 therapy, 115–116, 119 Insulin-Like Growth Factor, 8 Intercat aggression, 581–583, 587–588 fearful/defensive, 582–583 irritable, 582–583 predatory/play-related, 582–583 redirected, 582–583 social status, 581–583 territorial, 581–583 Interferon, 185, 200 Intermandibular space, 304 Intermediate cardiomyopathy, see Cardiomyopathy, intermediate International normalized ratio, 508 Interventricular septal defect, see Ventricular septal defect Intervertertebral disc disease, 834, 840, 844–845 Intestinal lymphangiectasia, see Lymphangiectasia Intestinal parasitism, 124 Intoxication, 442–444 Intracardiac thrombi, 263 Intracavitary chemotherapy, see Chemotherapy, intracavitary Intracellular fluid compartment, 898–899 Intracellular space, 898–899 Intradermal allergy testing, 33, 154 Intralipid, 618 Intraocular lens, 71 Intraocular neoplasia, see Neoplasia, intraocular Intraocular pressure, 202, 545, 891 Schiotz tonometry, 891 Tonopen, 891 Tono-vet, 892 Intraosseous catheter, 620 Intratracheal administration, 69
Intravascular hemolysis, see Hemolysis Intravenous pyelogram, see Excretory urogram Intrinsic factor, 85 Intussusception gastroesophageal, 163 Iodine, 427 Iohexol clearance, 273, 424–425, 926 Ionized calcium, 271 Ipecac, 410–411, 553 Iridiocyclitis, 543 IRIS classification, 455, 457 Iris atrophy, see Senile iris atrophy Iris cyst, 290 melanoma, 291 melanosis, 290 nevus, 290 rubeosis, 543–544 Iritis, 543 Iron deficiency, 282 Irritable bowel syndrome, 124–125, Ischemic encephalopathy, see Feline ischemic encephalopathy Isoflurane, 622–623, 682 Isospora spp., 89 Itraconazole dermatophytosis, 109–110 systemic fungus, 46–47, 87–88, 97–99, 232– 233, 488 Ivermectin, 104–105, 292, 307, 348, 492 Jamshidi needle, 882 Jaundice, see Icterus Jejunostomy tube, 23, 651–654 Jugular blood collection, see Blood collection, jugular Jugular pulse/distention, 129, 388, 430 Jugular vein, 885 Kangaroo posture, 552 Kappa agonist, 620 Kennel cough, 50 Keratectomy, 637 Keratitic precipitates, 544 mutton fat, 544 Keratitis, 294–296 brachycephalic, 53 eosinophilic, 294–295 exposure, 202–204 stromal, 225 Keratoconjunctivitis sicca, 93, 134, 295–296, 505, 911 Ketamine, 620–623, 682, 684 Ketoacidosis, see Diabetic ketoacidosis Ketoconazole, 240 Ketonemia, 115 Ketonuria, 115 Ketoprofen, 683 Key-Gaskell syndrome, 134 Kidney failure, see Renal failure Kidney insufficiency, see Renal insufficiency Kidney transplant, see Renal transplant Kindling phenomenon, 160 Kitten, 934 Korat, 941, 976 Lacrimal duct flush, 891 Lactated Ringer’s solution, 898–901 Lactation, 558, 975–977 agalactia, 977 eclampsia, 977 neonatal isoerthyrolysis, 976–977
Lactulose, 92, 325, 427, 470 Lagophthalmos, 93, 202, 295 Lanthanum carbonate, 456, 458 Larval migration, 96, 463 Laryngeal disease inflammation, 298–301 neoplasia, 298–300 paralysis, 298–301, 703 Laryngeal mask, 623 Laryngopharyngoscopy, 136 Laryngoscopy, 298–299, 301 Laser pointer, 359 surgery, 655–659 glaucoma, 200–201 laryngeal disease, 299–300 onychectomy, 673–675, 575 for neoplasia, 373, 490–491 therapy, 928–930 L-asparaginase, 76–78 Latent infection of FeLV, 184–185 Lateral bulla osteotomy, see Bulla osteotomy, lateral Lateral ear resection, 371 Latrodectus spp., 145–146 L-carnitine, 359 Left anterior fascicular block, 261 Left atrial enlargement, 24, 261, 263, 333, 388, 460 Left ventricular enlargement, 261–263, 333, 388 Left ventricular hypertrophy, 261–263 Left ventricular outflow obstruction, 261, 263 Leiomyoma, 535 Leiomyosarcoma, 475, 535 Lens luxation, 70 Lenticular sclerosis, see Nuclear sclerosis Lentivirus, 179 Leprosy, 10, 302–303 Leptin, 358 Leptospirosis, 453 Leukemia virus, see Feline leukemia virus Leukopenia, 382–383 Leukotrichia, 934 Levetiracetam, 160, 482 L-form bacteria, 131 Lidocaine, 27, 617–619, 683 Life stage guidelines, 960–972 Life stages, 961 Lily/Lilium spp. toxicosis, 167, 452–454 Limbal blush, 202 Lime sulfur dip, 110, 483–485 Linear foreign body, 304–305, 555, 800, 802, 804, 805 Linear granuloma, 154–156 Lingual ulceration, 62 Lip avulsion, 660–661 Lipoma infiltrative, 475 Liposarcoma, 475 Lithrotripsy, 529 Litter aversion, 578–579 Litter box additives, 579 Litter box aversion, 578–579 Litter substrate, 577 Liver aspiration, 734–735 biopsy, 734 dietary, 552 Lizard poisoning, 193 Local anesthetic block brachial plexus, 619 corneal/conjunctival, 619
1043
Index
epidural, 618–619 infraorbital, 681 intercostal, 618 intra-articular, 619 intrapleural, 618–619 laryngeal, 619 major palatine, 681 mandibular, 618–619 mental, 618 splash, 619 Local anesthetics, 617–619, 682–683 Location preference, 578 Lomustine, 76–77, 200, 321 Longevity, 358 Longy, 318 Loss of pet, 954 Low dose dexamethasone suppression test, 239 Low molecular weight heparin, 460 Low profile gastrostomy tube, 649–650 Lower motor neuron, 354 Lower Sonoran life zone, 87 Loxesceles spp., 146 Lufenuron, 110 Lumbosacral disease, 91, 323 Lumpectomy, 666 Lung aspiration, 96, 904–905 Lung digit syndrome, 126, 127 Lung fluke, 306, 429 Lungworms, 96, 306–307 Luteinizing hormone, 975 Luxating patella, 323, 662–663 grading system, 662 Luxating patellar procedures block recession trochleoplasty, 663 capsular imbrication, 662 fabellar-patellar suture, 663 fabellar-tibial anti-rotational suture, 662 releasing incision, 663 retinacular imbrication, 662 sulcoplasty, 663 tibial tuberosity transposition, 663 trochlear wedge recession, 663 trochleoplasty, 663 Lymph node disease, 737 hyperplastic, 736 reactive, 736–737 Lymphadenitis, 736–737 Lymphadenopathy, 736 Lymphangiectasia, 83, 124, 422–423 Lymphangiosarcoma, 475 Lymphoblast, 736, 738–739 Lymphocytic portal hepatitis, 222, 224, 277, 519 Lymphocytic-plasmacytic-gingivitisstomatitis-pharyngitis, see gingivitisstomatitis-pharyngitis complex Lymphoglandular bodies, 738 Lymphoma, 12, 40, 65, 83, 136, 308–312 chemotherapy, 76–80 cutaneous, 102, 131–133, cytology, 723, 736–737 gastrointestinal, 124–125 Heinz bodies, 21, 211 hypercalcemia, 243 hypereosinophilic syndrome, 245 immune mediated hemolytic anemia, 282 inflammatory bowel disease, 284–286 laryngeal, 298–300 nasal, 342–343 nasopharynx, 349–351 ophthalmic, 173, 202, 463–464
1044
polyphagic weight loss, 422–423 renal, 297 seizures, 480–481 thymoma, 509–511 types extranodal, 738–739 histiocytic, 739 intermediate grade, 738 large cell/lymphoblastic, 308, 738 large granular, 739 small cell/lymphocytic, 308, 310, 738–739 urinary bladder, 535–537 vomiting, 555–556 weight loss, 558 Lymphoplasmacytic pododermatitis, see Pododermatitis, lymphoplasmacytic Lymphosarcoma, see Lymphoma Lysine, 94–95, 226, 551 Lysosomal storage disease, 463 Machinery murmur, 388 Macrocyte, 20 Maggot, 340 Magnesium, 274 Maine coon, 118, 172, 199, 261–263, 366, 420, 879, 940–941 Malabsorption, 197, 422 Malassezia dermatitis, 53–54, 313 Malassezia pachydermatis, 313, 369–371 Maldigestion, 422 Malignant criteria, 723, 725 fibrous histiocytoma, 475 histiocytosis, 475–476 lymphoma, see Lymphoma Malnutrition, 28 Malocclusion, 55, 606 Mammae, 666 Mammary fibroepithelial hyperplasia, see Mammary hyperplasia Mammary gland adenocarcinoma, 314, 666 carcinoma, 314 fibroepithelial hyperplasia, 317 hyperplasia, 314–315, 317 neoplasia, 314–316, 666 Mammary hyperplasia, 317 Mandibular fracture, 229 symphyseal separation, 664–665 Mandibulectomy, 362 Mannitol, 454 Manx, 318, 323, 325, 446, 942 Marijuana, 442–444, 566 Marin, 223, 520 Marking behavior, 577–579, 584–586 Maropitant, 557 Marsupialization of bladder, see Bladder marsupialization Mask induction, 622–623 Massage, 687 effleurage, 687 friction, 687 petrissage, 687 Massasauga snake, 152 Mast cell tumor, 321–323 cutaneous form, 131–133, 173, 320–322, 369 cytology, 722–724, 740–741 histiocytic form, 320–321 hypereosinophilic syndrome, 245 mastocytic form, 320–321 visceral form, 124–125, 320–322, 556 Mastectomy, 315, 317, 666
Mature, 934 Maxillectomy, 362 Mayer’s mucicarmine stain, 132 Medetomidine, 620–621, 625, 684 Medial collateral ligament, 638 Mediastinal mass, 74, 753, 756 Medium chain triglycerides, 84 Medullary rim sign, 167–168, 818 Megacolon, 91–92, 318–319, 323–325, 446, 558, 632 Megaesophagus, 74, 134–135, 162, 165–166, 323, 336–337, 509–511 Megestrol acetate, 103, 158, 201 Meibomian gland, 171, 173 Melanoma cutaneous, 72, 131 intraocular, 202, 290–291 oral, 361–363 Melarsomine, 210 Melena, 267–268 Meloxicam, 177, 366, 682–683 Membrana nictitans, 134, 235, 503 Memory loss, 330 Menace response, 48, 910–911 Meningioma, 326–327, 480–482 Meningitis, 470 Meningocele, 318–319 Meow, 978 Meperidine, 620–621 Mepivacaine, 617 Mesenchymal cells, 722–725 Mesothelioma, 65–66, 328–329 biphasic/mixed, 328 epithelioid, 328 fibrosarcomatous/fibrous, 328 Metabolic acidosis, 32, 115, 117, 167–168, 272–273, 453, 508 Metabolic epidermal necrosis, see Hepatocutaneous syndrome Metaldehyde, 330–331 Metered dose inhaler, 60 Methadone, 620–621, 683 Methemoglobinemia, 5–6, 211–212 Methicillin-resistant Staphylococcus aureus, 957–958 Methimazole, 257–258, 260 myasthenia gravis, 336–337 oral, 257 toxicity, 258 transdermal, 257 Methocarbamol, 439, 499 Methotrexate, 78 Methylene blue, 5–6, 211–212 Methylmalonic acid, 85 Methylxanthine, 60, 442–443 Metoclopramide, 557 Metorchus conjunctus, 193 Metronidazole, 286 Metyrapone, 240 Mice, 468 Microchip, 950–951 Microhepatica, 426, 790 Microsporum spp., 108–109 Microvascular angiopathy, see Disseminated intravascular coagulation dysplasia, 427 Micturation, 354 Micturation reflex, 912 Midazolam, 620–621, 623 Middle ear, 374–376 Mik blood group, 352, 879–880 Miliary dermatitis, 33, 191, 195, 332
Index
Milk ejection, 977 Milk letdown, 977 Milk thistle, 220 Mini Lack anesthesia system, 623 Minimum data base for wellness visit, 966 Miosis, 235, 910 Mirtazapine, 23, 455, 458, 592 Mites, 483–486 Mitotane, 240 Mitral regurgitation, 24, 333, 388, 460 Mitral valve dysplasia, 24, 333 Mitral valve leaflet thickening, 263 Mitten cat, 420 Modified Hotz-Celsus, 172, 174 Modified orbital rim tacking technique, 505 Molluscacide, 330 Monoamine oxidase inhibitors, 591 Monorchidism, 640 Monozoic cysts, 89 Morphine, 620–621, 682–683 Morphine mania, 620 Mott cell, 736 Mu antagonist, 620 Mucogingival flap, 607 Mucometra, 434–435 Mulga snake, 152 Multicentric squamous cell carcinoma in situ, see Squamous cell carcinoma in situ Multilobar osteochondrosarcoma, 475 Multimodal anesthesia, 617, 684 environmental modification, 177 Multiple myeloma, 243, 282 Munchkin, 942 Murmur, 28, 129, 334–335 anemia-induced, 19, 106, 282, 334 cardiomyopathies, 261, 263, 460 continuous, 334 continuous left basilar, 388 crescendo-decrescendo, 334 decrescendo, 334 diastolic, 334 ejection, 334, 546 grading, 334 hypertension, 250, 254 location, 334 machinery, 388 mitral valve dysplasia, 333 plateau, 334 pulmonic stenosis, 430 regurgitant, 333–334, 546 systolic, 8, 34 systolic ejection left basilar, 500 Muscle relaxants, 620, 623 Muscle spasm, 498 Muscle weakness, 74, 272–273 Mushy pad disease, 416 Mutation FECV to FIPV, 175, 181 Mutton fat, 544 Myasthenia gravis, 74–75, 151, 241, 336–337, 509–511 clinical presentations, 336 Mycobacteria spp., 131–133, atypical, 131–133, 302–303, 338, 384, 730–731 bite wounds, 44–45 cytology, 730–731 lepraemurium, 302–303 opportunistic, 338 rapidly growing, 338 syndromes, 338
Mycobacteriosis, 10, 131–133, 302–303, 338–339, 356, 722 rapidly growing, 338–339 Mycoplasma felis, 44, 294–295, 342, 344, 976 Mycoplasma haemofelis, 19–20, 106, 205, 218, 282–283, 879, 980–981 Mycoplasma haemominutum, see Candidatus Mycoplasma haemominutum Mycosis fungoides, 102 Mycosis, systemic, see systemic fungal disease Mydriasis, 254, 426, 910 Myelography, 832, 834, 839–841 Myiasis, 104–105, 340–341, 347–348 Myocardial fibrosis, 460 ischemia, 261 Myocarditis, 460 Myosin binding protein C assay, 263 Myringotomy, 375, 657 Myxosarcoma, 475 Nail bed/fold dermatitis, 313 Nail overgrowth, see Toe nail overgrowth Nalbuphine, 682 Naloxone, 682 Naproxen, 682 Nasal aspiration, 906–907 Nasal bot fly, 347 Nasal discharge, 30, 342–343 Nasal disease, see Rhinitis Nasal flushing, 342–344, 906–907 Nasal planectomy, 657, 659 Nasal sampling, 906–907 Nasoesophageal tube, 23, 63 Nasolacrimal duct system, 53 Nasopharyngeal disease, 349–351 bulla osteotomy, 626, 630 foreign body/grass, 350–351 masses, 287–289, 374, 376, 667–669 polyps, 287–289, 342–343, 376, 657, 667–669 radiography, 342–343, 828, 830, 833 stenosis, 349–351 Nasopharyngoscopy, 136, 349 National Animal Poison Control Center, 402 Nausea, 555 Nebulization therapy, 345–346 Neck lesions, see Resorptive lesions Necrolytic migratory erythema, see Hepatocutaneous syndrome Necropsy kittens, 908–909 Nematode, 234, 468, 492 Neonatal isoerythrolysis, 352–353, 879, 976–977 Neoplasia characteristics, 723–727 intraocular, 202, 290–291, 543 Neostigmine, 337, 511 Nepeta cataria, 566 Nepetalactone, 566 Nepetalic acid, 566 Nephrectomy, 238, 297, 419 Nephroblastoma, 297 Nephrolith, 670–672, 707, 980 Nephrostomy tube, 528–529 Nephrotic syndrome, 205–206 Nephrotomy, 433, 541, 670, 672 Nerve injury caudal nerve roots, 494 pelvic, 494 pudendal, 494 Neurofibrosarcoma, 475 Neurogenic bladder, 354–355
detrusor-sphincter dyssynergia, 354 reflex dyssynergia, 354 Neurological examination, 910–912 cranial nerves, 910 spinal cord, 912 Neutering, 493 New methylene blue stain, 20, 98, 888–889, 924 Nicotine, 442–444 Nicotinic post-synaptic acetylcholine receptors, 336 Nictitans prolapse, 91, 235, 270, 323, 503–505 Nictitating membrane, see Membrana nictitans Nitenpyram, 341, 348 Nitroglycerin, 129, 137, 252, 263, 333, 460 Nitrous oxide, 623 Nocardia spp., 131–133, 356–357, 384, 436, 721–722, 730 Nocardiosis, 10, 11, 131–133, 356–357 clinical forms, 356 Nodules, cutaneous, 131–133, Nonaspiration fine-needle biopsy, see Fine needle biopsy Nonketotic hyperosmolar syndrome, 115–117 Non-regenerative anemia, 19 Non-selective angiography, see Angiocardiogram Non-vital tooth, 602–604 Nonsteroidal anti-inflammatory drugs, 366, 452, 682–683 Normal laboratory values, 973–974 coagulation tests, 974 hematology, 973–974 miscellaneous blood tests, 974 serum chemistry, 973 urinalysis, 974 Norwegian Forest Cat, 676, 940–942 Nosectomy, 490 Nosocomial infection, 470, 957 No Sting Barrier Spray, 642, 644 Notoedres cati, 483, 485 Nuchal ligament, 937 Nuclear scintigraphy, see Scintigraphy Nuclear sclerosis, 70, 934 Nucleic acid extraction, 916, 918 Nutritional support indications for, 22 methods of providing, 22 Nystagmus, 374, 548, 910–911 Obesity, 250, 358–360 Obligate carnivore, 358 Obstipation, 91–92, 323, 325, 632 Ocicat, 676, 940–942 Octreotide, 84 Ocular larval migrans, 468 Oculomotor nerve, 910 Odontoclastic lesions, see Resorptive lesions Odontoclastic resorptive lesion, see Resorptive lesions Odontogenic tumor, 361–363 Oestrus ovis, 347 Olfactory nerve, 910 Oliguria, 167–168, Ollulanus tricuspis, 492 Omega-3 fatty acids, 34, 286, 385 Omentalization, 395 Ondansetron, 557 Onychectomy, 673–675 CO2 laser, 655, 673–674 nail trimmers, 673–675 scalpel blade, 673–674
1045
Index
Oocyst, 89, 512–513 Ophthalmic examination, see Eye exam Ophthalmoscopy direct, 70, 982 Panoptic direct, 892 indirect, 892 slit beam, 890 Opioids, 620–621, 624–625, 682–683 Opisthorcus tenuicollis, 193 Optic nerve, 462–464, 910 Oral charting, 597 examination, 597 tumors – neoplasia, 361–362, 657 Orbicularis oculi muscle, 171 Organophosphate toxicosis, 74, 364 Oriental shorthair, 14, 362, 588, 879, 942 Orogastric tube feeding, 63, 913–914 Oronasal fistula, see fistula, oronasal Oscillometric blood pressure, 251, 624, 924 Osmotic fragility, 282 Os penis, 937 Osteoarthritis, 366–367, 577, 682–684, 688–689 Osteochondrodysplasia, see Scottish Fold osteochrondrodysplasia Osteochondrosarcoma, see Multilobar osteochondrosarcoma Osteomyelitis bacterial, 470 fungal, 87, 231–232 Osteopetrosis, 837, 840, 842 Osteosarcoma, 475–477, 723 Otitis externa, 53, 72–72, 143, 369–375 bacterial, 369–372 yeast, 143, 313, 369–371 Otitis interna, 374–375 Otitis media, 374–375, 626–627, 630 Otoacariasis, 143, 483–486 Otobius megnini, 372 Otodectes cyanotis, 143, 332, 483, 486 Ovarectomy, 952 Ovarian tumor, 207 Ovariohysterectomy, 435, 951–952 flank approach, 952 Over-grooming, 587–589 Overlapping “sandwich” flap, 677, 679 Overriding aorta, 500 Ovulation induced, 975 Oxalic acid, 167 Oxazepam, 592 Oxfendazole, 492 Oxidative injury, 211–212 Oxybutynin, 354–355 Oxygen therapy, 129, 263, 333, 388, 460 Oxyglobin, 6, 21 Oxypolygelatin starches, 268 Oxytocin, 138–139 Pachyonychia, 934 Pain, 506–507, 617, 619, 928–929 Pain management, 682–684, 928–929 drugs acetaminophen/paracetamol, 682 amitriptyline, 684 bupivacaine, 683 buprenorphine, 682–684 butorphanol, 682–683 carprofen, 683–684 dexamethasone, 684 dexmedetomidine, 684 fentanyl, 200, 683 gabapentin, 682, 684
1046
hydromorphone, 682 ibuprofen, 682 ketamine, 682, 684 ketoprofen, 683 lidocaine, 683 medetomidine, 684 meloxicam, 682–683 mepivacaine, 683 methadone, 683 morphine, 682–683 naproxen, 682 prednisolone, 684 prednisone, 684 prilocaine, 683 xylazine, 684 Palpebra, see Eyelid Palpebrae superioris muscle, 171 Palpebral reflex, 910–911 Pamidronate, 553 Pancreatic carcinoma, 102, 384, 386 enzyme supplementation, 169–170 insufficiency, see Exocrine pancreatic insufficiency lipase immunoreactivity, see Feline pancreatic lipase immunoreactivity Pancreatitis, 384, 452, 556 acute, 115, 270, 377–379, 512, 519–520, 651 chronic, 220, 222–223, 284–285, 377, 380– 381, 422, 519–520 Pancruonium, 636–637 Panleukopenia, 30, 125, 382–383, 463, 943–944 Panniculitis, 10, 338–339, 384–385 Panniculus reflex, 912 Papillary muscles, 460 Papilledema, 270 Papillomavirus, 489–490, 550–551 Paracetamol, see Acetaminophen Paragonimus kellicotti, 96, 306–307 Paralysis facial, 289 forelimb/thoracic limb, 52 laryngeal, 288 Paramomycin, see Paromomycin Paraneoplastic polycythemia, 12 syndrome, 102, 386–387, 509, 737 alopecia, 313 fever, 386 uveitis, 543 Parasites skin, 483–486 Parathyroid glands, 701–703 hormone, 243–244 hormone-related protein, 243–244, 386 transplant technique, 701 Parenteral nutrition, 22–23 Paresis forelimb, thoracic limb, 52 Paromomycin, 524 Paroxetine, 591–592 Partial mu agonist, 620 Parturition, 975–976 phases, 976 Parvovirus, 382–383, 957 Passive range of motion, 687, 689 transfer of antibodies, 976 Pasturella multocida, 44–45 Patch graft procedure, 430 Patellar luxation, see Luxating patella Patellar reflex, 912
Patent ductus arteriosus, 334, 388–389 Pathfinder, 602, 605 PCR, see Polymerase Chain Reaction Pectus excavatum, 390–391 Pedical flap, see Sliding bipedical flap PEG tube, 649–650 Pelvic bladder, 937 fracture, 229 limb reflexes, 912 Pemphigus foliaceous, 392–393 Penile spines, 937–938 Pentastarch, 268 Pentoxifylline, 385 Pericardectomy, 66, 328–329 Pericardial effusion, 28, 65–66, 83, 263, imaging, 850–858, 861, 863, 865 Pericardiocentesis, 66, 129–130 Perineal dermatitis, 685 hernia, 446, 448 urethrostomy, 446, 531, 533–534, 540–541, 709–712 Perinephric pseudocyst, 238, 297, 394–396 Periodic acid-Schiff reaction stain, 46–47, 87–88 Periodontal disease index, 597–599 pocket depth, 599 pocketing index, 597 Peritoneal dialysis, 168, 454 Peritoneal effusion, see Ascites Peritoneopericardial hernia, 121–122 Peritonitis septic, 304–305, 397–399, 650 Periuria, see Inappropriate urination Perivulvar skin fold surgery, 685–686 Permethrin, 439 Persian brachycephalic syndrome, 53 breed-related diseases, 940–942 cryptorchidism, 640 hepatobiliary, 39 hyperesthesia syndrome, 246 infectious, 30, 313 litter size, 976 neoplasia, 37 ophthalmic, 172–173, 202, 294 osteoarthritis, 366 palate congenital defects, 676 polycystic kidney disease, 418–419, 813 portosystemic shunt, 426 retinal disease, 463 Persian dirty face syndrome, see Idiopathic facial dermatitis of Persian cats Persistent right aortic arch, 164 Persistent viremia, 184–185 Pertechnetate thyroid scan, 257 Pet attachment, 954–955 loss, 954–955 replacement, 954–955 Pethidine, 620–621 Petrissage, 687 Pezzar catheter, 649–650 Phacoemulsification, 71 Phantom limb pain, 619 Pharyngitis (inflammatory), see Gingivitisstomatitis-pharyngitis complex Phenobarbital, 326, 482 Phenol, 32 Phenoxybenzamine, 354–355, 533 Phenylephrine ophthalmic, 504–505
Index
Phenylpropanolamine, 354–355 Pheochromocytoma, 250, 252–253 Phlebotomy, 500, 547 Phosphate binder, 275, 456, 458–459 Phosphate-containing enema, 92, 325 Photobiostimulation, 928–929 Photodynamic therapy, 490 Physaloptera spp., 492 Physical therapy, 687–690 Pica, 19, 85 Pickwickian syndrome, 358 Pigmenturia, 352 Pilocarpine test, 134–135 Pilomaticoma, 725 Pimobendan, 130 Pinna, 369–370, 372–373 abnormal, see Folded ear Piroplasm, 106 Piroxicam, 329, 490, 536–537 Pit vipers, 152 PIVKA, 223 Pixie-Bob, 420 Plague, see Yersiniosis Plant-induced olfactory behavior, 566 Plant toxicities, 402–411, 452 Plaque, 599 Plaque index, 597, 599, 601 Plasma cell, 199–200, 723–724, 736–737 Plasma cell gingivitis-stomatitis-pharyngitis, see Gingivitis-stomatitis-pharyngitis complex Plasmacytoma, 14 Platynosomum concinnum, 193 Plesiotherapy, 490 Pleural effusion, 412–413 anesthesia, 620 cytology, 742–745 forms cardiac, 333, 388, 67, 129, 261, 263, 460, 507 chylous, 83, 742–744 diaphragmatic hernia, 121 hemorrhagic, 742, 744 infectious, 46, 182, 184, 356, 742–743 lymphoma, 744 modified transudate, 742–743 neoplasia, 314–315, 320–321, 328, 509– 511, 744–745 nonseptic exudate, 742–743 septic, 742–743 thymoma, 744 transudate, 742 mechanisms, 412, 742 orogastric tube feeding, 913 thoracostomy tube, 698 Pleural fluid analysis, 83, 412–413, 742 Pleurodesis, 66 Pleuroperitoneal shunt, 84 Pleurovenous shunt, 84 Pneumocolography, 799, 801, 810 Pneumogastrography, 799 Pneumomediastinum, 516 Pneumonitis potassium bromide, 160, 482 Pneumoperitoneum, 398 Pneumothorax, 414–415 anesthesia, 620, 623–624 closed, 414 iatrogenic, 904 open, 414 pain management, 619 tension, 414 thoracostomy tube, 698, 700
Pocket technique, 505 Pododermatitis lymphoplasmacytic, 126, 128, 416–417 Poisoning, see Toxicosis Poisonous plants, 402–404 highly poisonous plants, 404–406 Polioencephalomalacia, 502 Pollakiuria, 140–142 Polyarthritis FIP, 182 glomerulonephritis, 205 Polychromasia, 282 Polycystic kidney disease, 297, 418–419, 455, 479, 944 Polycythemia, 250, 501, 547 Polydactylism, 420–421 Polydipsia/Polyuria, 111, 118, 256, 424–425, 453, 457–458, 577 psychogenic, 424–425 Polymerase Chain Reaction Test, 915–918 feline enteric coronavirus, 175 feline infectious peritonitis virus, 175, 182–183 feline leukemia virus, 184 primer, 915, 917 real-time, 915–918 respiratory pathogens, 63, 342, 344 Toxoplasma gondii, 513 traditional, 915–916 Polymyositis, 74–75, 509–510 Polyneuropathy, 134 Polyphagia, 118, 256, 284 Polyphagic weight loss, 422–423 Polyprenyl immunostimulant, 183 Polyps inflammatory, 287–289 nasopharyngeal, 287–289 otic, 626 respiratory, 287 Portography, 426, 790 Portosystemic shunt, 74, 278, 422–424, 426–427, 480–482, 620 Posterior paralysis, 507 Post-ictal, 159 Postligation seizure syndrome, 427 Post-obstructive diuresis, 272 Postural reflexes, 911 Potassium bromide, 160, 482 citrate, 458, 542 gluconate, 273, 456, 458 supplementation, 74–75 Potts surgery, 500 Prairie dogs, 400 Pralidoxine chloride, 364 Praziquantel, 193, 306 Prazosin, 533 Prebiotics, 125, 286 Prednisone, 76–77, 684 Pregabalin, 160, 482 Pregnancy, 317, 558, 975–976 diagnosis, 975 problems mid-term abortion, 976 uterine torsion975–976 vaginal discharge, 975 Prepubic urethrostomy, 712–714 Primary aldosteronism, see Hyperaldosteronism Primary hyperparathyroidism, see Hyperparathyroidism Prion, 14 Probe, 602
Probing, 597–599 Probiotics, 125, 286 Procaine, 617 Prochlorperazine, 557 Prodome, 159 Progesterone mammary gland, 314, 317, 434 pregnancy, 975 uterus, 434 Progestin, 314–315 Proglottid, 496 Prolactin, 317, 975 Prolapsed gland of the third eyelid, 503, 505 nictitans, see Nictitans prolapse third eyelid, see Nictitans prolapse Proliferative keratoconjunctivitis, 157 Propantheline, 354–355 Proparacaine, 619 Propofol, 160, 622–623, 684 Propranolol, 27, 508 Propylene glycol, 211 Propylthiouracil, 258, 282 Prostaglandin, 435, 975 Prostate, 937 Prostatitis, 140 Protamine zinc insulin, see Insulin, protamine zinc Protein-losing dermapathy, 267 enteropathy, 28, 125, 267 nephropathy, 267, 422–423 Proteins induced by vitamin K antagonism, 223, 467 Pruritic dermatitis of Siamese, see Psychomotor epilepsy Pruritus facial, 258, 984 Prussian blue stain, 750 Pseudochylous fluid, 83 Pseudocoprostasis, 323 Pseudopregnancy, 317 Psychogenic alopecia, 587–590 attention seeking, 587, 589 compulsive disorders, 587–588 displacement activities, 587–588 intercat aggression, 587–588 redirected behavior, 587–588 Psychogenic polydipsia, 424–425 Psychomotor epilepsy, see Hyperesthesia syndrome Psychotropic medications, 591–593 Psyllium, 285–286 Ptosis, 235 Ptyalism dental, 608 esophageal disease, 162 gingivitis-stomatitis-pharyngitis, 199 hepatitis, 224, 278 myasthenia gravis, 336 oral neoplasia, 361 portosystemic shunt, 426 rabies, 440 vomiting, 555 weight loss, 422 PU/PD, see Polydipsia/polyuria Public health significance, see Zoonosis Pulmonary arteries, 208–210 atresia, 500 carcinoma, 126–128 edema, 24, 129–130, 261–263, 333, 460, 507 imaging, 850–852, 856–857, 859, 861
1047
Index
non-cardiac, 8, 453, 913 re-expansion, 415 fibrosis, see Idiopathic pulmonary fibrosis hypertension, see Hypertension, pulmonary interstitial macrophage, 208 thromboembolism, see Thromboembolism, pulmonary Pulmonic stenosis, 334, 430–431, 500 Pulp capping, 603–605 restoration, 602–605 Pulse deficit, 26, 254 Pulse oximeter anesthetic monitor, 623–624 tooth evaluator, 603, 606 Pumpkin, 92, 285, 325 Pupillary light reflex/response, 48, 202, 910 consensual, 890 direct, 890 indirect, 890 Pure mu agonists, 620 Purring, 298, 334, 978–979 solicitation purr, 978 Pustules, 392 P-waves wide, 24 Pyelocentesis, 433 Pyelography, see Contrast antegrade pyelography Pyelolithotomy, 528 Pyelonephritis, 432–433, 452, 670 Pygma snake, 152 Pyloric outflow obstruction, 556 Pyoderma, 685 Pyometra, 207, 434–435 Pyothorax, 356–357, 436–438, 698–699 Pyrethrin toxicosis, 439 Pyrethroid toxicosis, 439 Pyrexia, see Fever Pyridostigmine, 337, 511 Pyrkinje reflex, 70 Pythium spp., 384 Rabbits, 400, 486 Rabbity gait, 318 Rabies, 145, 440–442 cattery control, 944 hospital control, 957 phases, 440 observation period, 440–441 Raccoon, 440 Radioactive iodine, 257–258 Radiographic technique bisecting angle, 610, 612 parallel, 610–611 Radiography dental, 606–607, 610–614 oral, 606–607, 610–614 Radioiodine, see Radioactive iodine Ragdoll, 97, 261, 263, 676, 940–942 Ramipril, 252, 254–255 Range of motion, 687–690 Rapid urease test, 214 Rattlesnake, 152 Reaction food, 246, 332, 483 Reactive amyloidiosis, 14 Real-time PCR, see Polymerase chain reaction, real-time Recreational drugs, 442–445 Rectal diseases, 446–448 atresia ani, 447 perforation, 446–448
1048
prolapse, 446–448 rectovaginal fistula, 446–448 stricture, 446–448 tumors, 446–448 Rectal pull through procedure, 448 Redback spider, 146 Redirected behavior, 587–588 Red imported fire ants, 149 Re-expansion pulmonary edema, 415 Refeeding injury, see Refeeding syndrome Refeeding syndrome, 221, 274, 449–451 Regenerative anemia, 20–21, Regressor, 184–185 Regurgitation, 162–165, 323, 555 Rehabilitation, 687–690 Relaxin, 975 Renal cysts, 418–419 failure acute vs. chronic, 457 acute, 452–454 ethylene glycol, 167 fluid therapy, 899 hypercalcemia, 243 hyperkalemia, 247 nephrolith, 670 phases, 452, 454 polyuria/polydipsia, 424 rodenticides toxicosis, 466–467 urinary obstruction, 530, 534 vomiting, 555 chronic, 297, 455–457 acromegaly, 8–9 amyloidiosis, 14 ethylene glycol toxicosis, 167 fluid therapy, 899 glomerulonephritis, 205 hyperaldosteronism, 241 hypertension, 250–253 hypocalcemia, 270 nephrolith, 670, 672 polycystic kidney disease, 418–419 polyuria/polydipsia, 424 pyelonephritis, 432–433 renal transplant, 980, 982 vomiting, 555 oliguric, 167 function testing, 926 insufficiency, 455, 457–459, 603 hypertension, 250–253 transplant, 168, 454, 456, 980–982 complications, 981 costs, 982 donor, 980–981 post-op monitoring, 981–982 rejection, 980–982 Renin, 241–242 Renin angiotensin aldosterone system, 241, 252, 254 Renolith, 541 Renomegaly, 297 Repetitive nerve stimulation, 337 Replacement of pet, 954–955 Resco nail trimmer, 673 Resistin, 358 Resorptive lesion dental, 22, 602–603, 606–607, 608–609 Respiratory infection calicivirus, see Feline calicivirus Chlamydophila, see Chlamydophila felis herpesvirus, see Feline herpesvirus Respiratory stridor, see Stridorous breathing Restorations, 602–605
Restraint devices Catch Net, 921 Wild Child, 920–923 Restraint techniques bath towel, 573 difficult cats, 920 fractious cats, 920 Restrictive cardiomyopathy, see Cardiomyopathy, restrictive Resuscitation, see Cardiopulmonary resuscitation Retained deciduous teeth, 606 Retention cyst, 39 Reticulocyte count, 19, 282, 924 Reticulocytes aggregate, 20, 282 punctate, 20, 282 Retinal anatomy choroid, 462 posterior segment, 462 sclera, 171, 462 tapetum lucidum, 462 vitreous body/humor, 462 atrophy central, 129 progressive, 463 degeneration, 202 detachment, 462–465, 543–545 bullous, 462 hypertension, 250, 252 rhegmatogenous, 462 trauma, 229 diseases, 462–465 dysplasia, 462–464 hemorrhage, 250 FIP, 463 hypertension, 250, 462–464 thiamine deficiency, 502 Retinoic acid, 359 Retrobulbar palpation, 890 Retrograde hydropropulsion, 541 Retroillumination, 70 Retroviral dermatitis, 550–551 Retrovirus, 184 Rex, 261, 941–941, 976, 983 Rexing, 941–942 Rhabdomyosarcoma, 475–477 Rhinitis, 225, 344–346, 646, 749, 830–832, 906 Rhinosinusitis, 30–31, 225–227, 344–345 Rhinotomy, 342, 691–692 Rhinotracheitis, see Feline herpesvirus infection Rhodococcus equi, 131 Rib spring, 162 Right atrial enlargement, 430, 500 Right sided heart failure, see Heart failure, right sided Right-to-left shunt, 431, 500, 546 Right ventricular enlargement, 500 hypertrophy, 430, 500 outflow obstruction, 500 Ringer’s solution, 899 Ringworm, see Dermatophytosis Ripple back, see Hyperesthesia syndrome Risus sardonicus, 498 Rochalimaea spp., 35 Rodenticide, 243–244, 466–467 Rodents, 400–401, 513, 553 Rodent ulcer, see Eosinophilic ulcer Rolling skin disease, see Hyperesthesia syndrome
Index
Romanowsky-type stains, 719–720 Diff-Quik, 719 Giemsa, 719 Wright’s, 719 Ronidazole, 523–524 Root canal filling, 604–605 obturation, 605 therapy, 603, 605 exposure, 597 exposure length, 599 Ropivacaine, 617 Rosenthal needle, 882 Rouleaux formation, 282 Roundworms, 96, 555 R protein, 85 Rumpy, 318 Rumpyriser, 318 Russian Blue, 118 Rust inhibitors, 167 Rutin, 84 R-wave amplitude increased, 24, 129, 388 Saddle thrombus, 506–507 S-adenosylmethionine, 6, 220, 223, 279, 520 Safety pin rods, 400 Salicylate toxicosis, see Aspirin toxicosis Salmon calcitonin, 244, 553 diet, 502 Salmonella spp., 124, 125, 957, 976 Salmonellosis, 124–125, 284, 470–471, 556 SAM, see Systolic anterior motion SAMe, see S-adenosylmethionine San Joaquin Valley, 8, 87 Saponification of fat, 270 Sarcocystis spp., 89–90 Sarcoma injection site, see Injection-site sarcoma intraocular, 290, 463, 475 Sarcomas, 475–477 Sarna lotion, 150 Savannah, 676 Sawhorse appearance, 498 Scabies, 485, 486 Scale, 483–484, 573 Schiotz tonometry, 890 Schirmer tear test, 93–94, 134, 503, 891 Schwannoma, malignant, 475 Scintigraphy, 426 of thyroid, see Pertechnetate thyroid scan Scissor-type nail trimmer, 673 Sclera, 171 Scooting, 16 Scottish Fold, 478–479 Scottish Fold osteochondrodysplasia, 478–479 Scottish shorthair, 479 Seborrhea olesosa, 313 Sedation, 620–625 Seizure, 159–161, 480–482 focal, 159, 480 generalized, 159, 480 hypercalcemia, 243 hypereosinophilic syndrome, 245 hypertension, 250, 252, 254 hypocalcemia, 270 hypomagnesemia, 274 hypophosphatemia, 275 idiopathic, 159–161 ischemic encephalopathy, 292 meningioma, 326
metaldehyde, 330–331 parasitic, 104, 106 partial, 159 portosystemic shunt, 426–427 probable symptomatic, 159 reactive, 159, 161 recreational drugs, 442–445 stages aura, 159 ictus, 159, 480 post-ictus, 159, 480 prodome/pre-ictus, 159, 480 status epilepticus, 159–161 symptomatic, 159, 161 tetanus, 498 toxicity-induced, 167, 365, 466–467 Selamectin, 210, 348, 486 Selective serotonin re-uptake inhibitors, 591–592 Self antigens, 879 Senile iris atrophy, 934 Senility, 577 Senior, 934 Sepsis, 115, 397–399 Sequestrum, see Corneal sequestrum Serotonin syndrome, 591–592 Sertoli cell tumor, 640–641 Serum bile acids, see Bile acids Serum cholinesterase activity, see Cholinesterase activity Serum cobalamin, see Cobalamin Sevoflurane, 622–623, 682 Sexing kittens, 937 Shake and bake syndrome, 330 Sheather’s sugar solution, 100, 513 Shock, 229 Siamese amyloidiosis, 14 breed-related diseases, 940–942 cardiac disease, 129 esophageal disease, 164–165 fungal disease, 97 gestation length, 976 hyperesthesia, 246 hyperthyroidism, 256 infectious disease, 97, 131, neonatal isoerythrolysis, 352 neoplasia, 37, 314, 320, 328, 489, 666 ophthalmic disease, 202, 463, 910 osteoarthritis, 366 palatine congenital defects, 676 psychogenic alopecia, 588 thymoma, 509 renal, 394 Silastic nasal septal button, 679–681 Silybin, 223, 520 Sino-nasal infection, see Rhinosinusitis Sinus arrhythmia, 26–27 Sinus hairs, 983 Sinus tachycardia, 261 Sinusitis, 225, 344–346, 646–647 Skin flaps, 693–695 advancement, 693–695 axial pattern, 693–694 pedicle advancement, 693–694 rotational, 693 transposition, 694 Skin fold dermatitis, 313 Skin fold pyoderma, 685 Skin fragility, see Fragile skin syndrome Skin grafting, 43, Skin parasites, 486–489 Skin scraping, 483–485
Skink, 193 Skunks, 440 Sliding bipedical flap, 677, 679 skin flaps, see Skin flaps Slit beam, 70, 890–891 Slugs, 306, 330 Small intestinal bacterial overgrowth, 170 Snails, 306, 330 Snake bite, 151–152 Snakes Black, 152 Brown, 152 Copperhead, 152 Coral, 151–153 Cottonmouth water moccasin, 152 Death Adder, 152 Gwardar, 152 Inland Taipan, 152 King Brown, 152 Mulga, 152 Rattlesnake, 152 Taipan, 152 Tiger, 152–153 venomous, 151–152 Snuffling, 225–226 Socialization period, 568–569 Sodium acetate, 193 bicarbonate, 458–459 borate, 234 metabisulfite, 502 nitroprusside, 252, 255 Soft palate, 53, 56–57, 676–678 Soft palate resection, 57 Solar radiation, 489–490 Solenopsis spp., 148 Somali, 282, 336, 940–942, 976 Somatomedin C, 8 Somogyi effect, 925 Spacer, 59–60 Spay scar, 952 Spherocyte, 20, 282 Sphinx, 313, 940, 942, 983 Spiders, 145–146 black widow, 145 brown, 146 funnel web, 146–147 redback, 146 tarantulas, 147 Spider bite, 145–146 Spina bifida, 318–319 Spinal accessory nerve, 911 Spinal cord reflexes, 912 Spinal fracture, 229 Spindle cell sarcoma, 49 Spines, see Penile spines Spinous ear tick, 372 Spiral-shaped bacteria, 213–214 Spirometra spp., 496–497 Spironolactone, 130, 255, 263, 460 Splenomegaly, 282 Split hard palate, 229 palatal U-flap, 679 Spondylosis, 552 Sporothrix schenckii, 131–132, 487–488, 747 Sporotrichosis, 10, 131–133, 487–488 clinical syndromes, 487 cytology, 747 Spraying behavior, 577, 579, 584–586 Squamous cell carcinoma, 12, 243 cutaneous, 131
1049
Index
external ear canal, 72, 369–372 eyelid, 172, 174 intrathoracic, 509 laser surgery, 656–657, 659 oral, 199, 361–362 urinary bladder, 535 Squamous cell carcinoma in situ, 489–491, 550 Squirrels, 400 Staining cytology sample, 719–720 Status epilepticus, 159–161, 482 Stenotic nares, 53, 54, 56, 657 Sternotomy, 510 Stertorous breathing, 298, 349 Stethoscope, 334 Stillbirth, 382, 470 Stimulant appetite, 23, 455 Stomach worms, 492, 555 Stomatitis (inflammatory), see Gingivitisstomatitis-pharyngitis complex Strabismus, 910–911 Stranguria, 140 Streptococcus spp., 976 Streptokinase, 508 Stress motivated elimination, 578–579 Stretching, 687–690 Stridorous breathing, 53, 97 String of pearls sign, 799–800 Strontium 90, 490 Strychnine, 466–467 Stud tail, 493 Stumpy, 318 Subaortic stenosis, 261 ventricular septal defect, 500 Subcutaneous emphysema, 414, 516, 692 fluid catheter, 458, 696–697 complications, 696 nodules, see Nodules Subendocardial fibrosis, 460 Submental organ, 983 Substrate preference, 578–579 Subtotal colectomy, see Colectomy Subtypes, FIV, 179–180 Sulcus bleeding index, 598–599, 601 Sulcus depth, 597 Sulfasalicylic acid turbidometric test, 268 Sulfonylurea, 113 Sulfur granules, 10, 356 Super-fecundation, 976 Superficial necrolytic dermatitis, see Hepatocutaneous syndrome Superoxide dismutase, 180 Supracaudal tail gland, 493 Supracondylar foramen, 937 Surgical monitor, 575 Swimmer, 940–942 Symblephron, 294–296 Synechia, 94, 544–545 Synovial cell sarcoma, 475 Systemic fungal disease, blastomycosis, 46–47 coccidioidomycosis, 87–88, cryptococcosis 97–99, cytology, 746–748 histoplasmosis, 231–233 sporotrichosis, 487–488 Systemic hypertension, see hypertension, systemic Systolic anterior motion of mitral valve, 24, 263
1050
T3 suppression test diagnosis of hyperthyroidism, 256–257 procedure, 926 T3 test, 257 Tachyarrhythmia ventricular, 24 Tachycardia, see Tachyarrhythmia Tachyzoite, 512 Taenia spp., 496–497 Tail injury, see Tail, pull necrosis, 495, 977 pull, 494 classifications, 494 Tailed, 318 Taipan snake, 152 Tape impression, 484 Tapeworms, 191, 486, 496–497, 555 Tarantula, 147 Target organ damage, 250 Tarsal plate, 171, 174 Tarsorrhaphy, 171, 173 Tasmanian and Chappell Island Black Tiber Snake, 152 Tattoo, 951–952 Taurine, 23, 130, 463–464 Tea, 442–444 Technetium pertechnetate, 426 thyroid, see Pertechnetate thyroid scan Temporomandibular joint disease, 828–830, 838 Tenesmus, 16 Tension pneumothorax, 414 Tension relieving procedures, 694–695 Teratoma, 641 Terbinafine, 488 Terbutaline, 59–60 Testing procedures, 924–927 blood pressure determination, 924 formalin-ether sedimentation, 925 glucose curve and fructosamine, 925 iohexol clearance, 926 reticulocyte count, 924 T3 suppression test, 926 TRH response test, 926 trichogram, 926 zinc sulfate fecal flotation, 926 Testosterone, 317 Tetanospasmin toxin, 498 Tetanus, 498–499 Tetany, 270–271, 364, 467, 498–499 Tetracaine, 619 Tetracyclines, 187 Tetralogy of Fallot, 430, 500–501, 546–547 components, 500 Tetramizole, 492 Theobromine, 442–443 Therapeutic exercise, 688–689 assisted standing, 689 bicycling, 689 laser lights, toys, treats, 689 stretching, 688–690 weight shifting, 689 wheelbarrowing-dancing, 690 Therapeutic ultrasound, see Ultrasound, therapeutic Therapy laser, see Laser, therapy Thermometer infrared tympanic membrane, 187 Thermoregulatory set point, 187 Thiamine, 74–75, 450, 502 Thiazide diuretic, 112 Thiopental, 622
Third eyelid diseases, 503–505 Third eyelid prolapse, see Nictitans prolapse Thoracentesis, 137, 413–414, 700 cardiac, 129, 460, 263, 333 chylothorax, 83–84 diaphragmatic hernia, 121 neoplastic, 65–67, 307, 511 pyothorax, 436–438 Thoracic drainage, 700 Thoracic limb reflexes, 911–912 Thoracocentesis, see Thoracentesis Thoracostomy tube, 84, 307, 413, 414, 437–438, 698–700 Thoracotomy, 84, 414, 437–438 Thromboembolic disease, see Thromboembolism Thromboembolism, 506–508 arterial, 126, 128–130, cardiac disease, 460–461 heartworm disease, 208–209, 261, 263–264 hyperkalemia, 247 hypoalbuminemia, 267–268 ischemic encephalopathy, 292 neoplasia, 328 pulmonary, 208–209 renal, 452 Thrombolectomy, see Embolectomy Thrombolytic agent, 508 Thrombus, 506–508 Through-the-needle catheter, 885 Thumb cats, 420 Thymoma, 83, 102, 336–337, 386, 509–511 Thymoma-related dermatitis, 102, 313, 386, 509–510 Thymus, 509 Thyroid adenocarcinoma, 256–257, 259 adenoma, 256–257 adenomatous hyperplasia, 256–257 gland, 256–257, 701 palpation, 256–257 testing free T4, 257 pertechnetate scan, 257 T3 suppression test, 256–257 total T4, 256 TRH response test, 257 Thyroidectomy, 258–260, 701–703 hypocalcemia, 270 techniques, 258, 701 Thyrotoxic cardiomyopathy, see Cardiomyopathy, thyrotoxic Tibial compression test, 638 Tibial plateau leveling osteotomy, 638 Tick-transmitted disease, 18, 106–107 Tiger Snake, 152 Tiletamine, 622 Tincture of Myrrh and Benzoin, 607 Tissue cells, 721–725 discrete (round) cells, 721, 723–724 epithelial cells, 721, 724–725 mesenchymal (spindle) cells, 721, 723–725 Tissue viability, 41 Tobacco products, 442, 444 Tobacco smoke, 308, 444, 489 Toe nail overgrowth, 114, 577 Tomato soup discharge, 356 Tongue flap, 679–680 Tongue protrusion Tonkinese, 352, 879, 942 Tonometry, 202, 545, 891 Tonopen, 891 Tono-vet, 892
Index
Tooth extraction, see Extractions, dental Tooth resorption, see Resorptive lesions Torsion of uterus, see Uterine torsion Torticollis, 502 Total body water, 898 Total ear canal ablation, 350, 371, 373, 704–706 Total T4 test, 256 Toxascaris leonine, 468 Toxicosis acetaminophen, 5–6 aspirin, 32 caffeine, 442–443 carbamate, 365–365 chocolate, 442–443 ethanol, 442–444 ethylene glycol, 167–168 marijuana, 442–444 metaldehyde, 330–331 nicotine, 442–444 organophosphate, 74, 364 phosphate binder, 275 salicylate, 32 theobromine, 442–443 vitamin D, 243–244, 466, 553 Toxocara cati, 468, 543 Toxoplasma gondii, 89, 377, 380, 463, 512–513, 543, 976, 980–982 Toxoplasmosis, 34, 125, 426, 464, 512–514 IgG antibodies, 512–513 IgM antibodies, 512–513 infectious forms, 512 uveitis, 545 T-piece anesthesia system, 623 Tracheal disease collapse, 53, 517 edema, 515, 517–518 foreign bodies, 515–516 hypoplastic, 53 infectious, 515, 517 neoplasia, 518 rupture, 516 stenosis, 516–517 Tracheal wash, see Transtracheal wash Tracheostomy, 299 Traction injury tail, 494 Transdermal administration, 257–258, 592 Transfusion, see Blood transfusion Transient viremia, 184 Transillumination dental, 597, 602 ophthalmic, 70, 93, 290, 543, 545, 890 Transitional cell carcinoma, 12, 535 Transpalatine nasal aspiration, 906–907 Transplant, renal, see Renal transplant Transport stress, 963 Transsphenoidal hypophysectomy, 240 Transthoracic pulmonary aspiration, See Lung aspirate Transtracheal wash, 137, 306, 749–750 Trap-neuter-return program, 948–950 anesthesia, 950 capture net, 950, 953 castration, 952 cryptorchidism, 952 ear notching, 951–952 ear tattoos, 951–952 ear tipping, 951–952 euthanasia, 950–953 microchip, 950 ovarectomy, 952 ovariohysterectomy, 951–952
trap restraint, 950 Tremors, 426, 439–440, 442–444 TRH response test diagnosis of hyperthyroidism, 257 procedure, 926 Triad disease, 222, 380, 519–520 Triadan tooth numbering system, 600–601 Triaditis, see Triad disease Triceps reflex, 912 Trichiasis, 294–295 Trichobezoar, 521–522, 555 Trichoepithelioma, 725 Trichogram, 926 Trichophyton spp., 108–109 Trickle feeding, 379 Tricuspid dysplasia, 28 Tricuspid valve regurgitation, 430 Tricyclic antidepressants, 591–592 Triflorothymidine, 94–95 Trigeminal nerve, 910–911 Triglyceride, 377 Trilostane, 240 Trismus, 498 Tritrichomonas foetus, 124–125, 198, 284, 523, 943 Tritrichomoniasis, 125, 523–525 Trochlear nerve, 910 Trombicula autumalis, 332 Trypsin-like immunoreactivity, see Feline trypsin-like immunoreactivity TSH stimulation test, 257 Tube cystostomy, 715 Tuna diet, 502 Tunica muscularis esophagus, 937 Turbinate bones, 691 Twisty cat, 420 Tympanic bulla, 938 Tympanic membrane, 369, 374–375 Ulcer, cornea, see Corneal ulcer Ultrasound diagnostic, 753–827, 849–878 tables, 574 therapeutic, 687–688 Uncinaria, 234 Unclassified cardiomyopathy, see Cardiomyopathy, unclassified Undercooked eggs, 470 Undercooked meat, 470 Upper motor neuron, 354 Upper respiratory infection, see Respiratory infection Urea breath test, 214 Urease test, see rapid urease test Ureteral obstruction, 526–529, 555, 670 classifications, 526 Ureterolith, 526–529, 707–708 removal, 707–708 Ureterotomy, 238, 528, 541, 707–708 Urethral catheterization, 530–533, 709 obstruction, 530–534, 709, 715 bladder tumor, 535 cardiac, 27 clinical signs, 140–141, 555 hyperkalemia, 247–249 megacolon, 323–324 urethrostomy, 709, 712 sphincter muscle, 354 stricture, 530–533 Urethrogram, 140–141, 824–825 Urethrolith, 709
Urethroscopy, 532 Urethrospasm, 530, 533 Urethrostomy, see Perineal or prepubic urethrostomy Urinary acidifier, 542 bladder tumors, 535–537 calculus, see Urolith creatinine:cortisol ratio, 239, 424 diversion surgery, 709, 712, 715 stone, see Urolith Urine collection, 573 marking, see Marking behavior Uriniferous pseudocyst, 394 Urohydropropulsion, 541 Urokinase, 508 Urolith/urolithiasis, 541–545 bladder, 140–141, 538, 540–542 calcium oxalate, 531–534, 538, 540, 542, 670 calcium phosphate, 538, 542 cystine, 538, 542 magnesium ammonium phosphate, see Urolith, struvite prevention, 541–542 renal, 238, 433, 539, 541, 670–672 struvite, 538, 540–542 triple phosphate, see Urolith, struvite urate, 538, 542 ureteral, 237, 538–541 urethral, 530–534, 538–541 Ursodeoxycholic acid, 223–224, 278, 520 Ursodiol, see Ursodeoxycholic acid Urticating hairs, 147 Uterine torsion, 975 Uveitis, 48, 70–71, 94–95, 543–545 anterior, 70–71, 187, 543–545 FIP, 182, 543–544 fungal, 46, 98, 231, 543–545 glaucoma, 202, 204 intraocular tumor, 290–291 lens induced, 113 phacoclastic, 543 phacolytic, 543 posterior, 543 toxoplasmosis, 512–513, 543, 545 uveitis, 543 viral, 225 weight loss, 558 Vaccination, 472–473 Vaccine adjuvant, 472 Bordetella, 51 calicivirus, 63 Chlamydophila, 82 coronavirus, 175 FeLV, 184, 472 FIP, 175, 183 FIV, 180 herpesvirus, 225–227 immune mediated hemolytic anemia, 282 intranasal, 51, 63 leukemia, 472 rabies for cats, 440–441, 472–473 for humans, 440 sarcoma, see Injection-site sarcoma Vagal stimulation, 26–27 Vagal tone, 26–27 Vaginal discharge, 434–435, 975–976 Vagus nerve, 911 Valuloplasty, 430
1051
Index
Valvulotomy, 430 Vaporization, 655 Vascular ring anomaly, 162, 164 Vasopressin, 111–112 Vasopressin response test, 111 Ventral bulla osteotomy, see Bulla osteotomy, ventral Ventricular hypertrophy, 24, 261, 263 premature complex, 26, 430, 460 septal defect, 333–334, 546–547 imaging, 862, 871–872 nonrestrictive, 546–547 restrictive, 547 tachyarrhythmia, 19, 26–27, 121, 129 tachycardia, see Ventricular tachyarrhythmia Verminous pneumonia, 468 Vesicourachal diverticulum, see Diverticulum, vesicourachal Vespids, 148–149 Vespoidea, 148 Vestibular disease, 371, 830, 832–833, 836 Vestibular syndrome, 548–549 Vestibulocochlear nerve, 911 Vibrissae, 983–984 carpal, 983 loss, 984 mandibular, 983 mystacial, 983–984 superciliary, 983 Vinblastine, 77–79 Vincristine, 76–79 Viral dermatitis, 225–226, 550–551 Viral quiescence, 225 Virulent systemic feline calicivirus, 72 Visceral bacillary peliosis, 35 Visceral larval migrans, 468 Viscoelastic, 636 Visual-evoked potentials, 48 Vital tooth, 602–605 Vitamin A, 22, 359, 552 Vitamin B12, see Cobalamin Vitamin C, see Ascorbic acid Vitamin D, 243–244, 553 Vitamin D rodenticides, 553 Vitamin D2, see Ergocalciferol Vitamin K, 15, 170, 278–279, 466–467 Vitamin K responsive coagulopathy, 170
1052
Vocalization, 250, 254, 978 Vomeronasal organ, 566 Vomiting, 555–557 center, 555, 557 inflammatory bowel disease, 284–286 types Walking dandruff, 484 Warbles, 104 Warfarin, 28, 263, 460, 466–467, 508 Warthin-Starry stain, 213 Wasp sting, 148 Water deprivation test, 111–112, 424–425 gradual, 111 Waterson-Cooley surgery, 500 Wax ball, 371 Wax plug, 369, 371 Weakness, 270, 272–273 Weight loss, 422–423, 558–560, 608 Weight shifting, 689 Wellness visit, 964 Wheal and flare test, 134 Wheelbarrowing, 690, 911 Wheeze, 58–60 Whip Snake, 152 White coat effect/syndrome, 250 Whiskers, see Vibrissae White’s nail trimmer, 673 Withdrawal reflex, 912 Wolbachia, 210 Wolff-Parkinson-White syndrome, 26 Wolves, 104 Wood’s lamp, 108, 167 Wound healing poor, 267–268 stages, 41 Wright’s stain, 719 X-ray table, 574 Xylazine, 410–411, 553, 684 Yeast otitis, see Otitis externa, yeast Yellow jacket sting, 148–149 Yersinia pestis, 400 Yersiniosis, 400–401 bubonic form, 400 hospital control, 957 septic form, 400
pneumonic form, 400 Yohimbine, 442 Ziehl-Neelsen acid fast stain, 10, 100, 302 Zinc phosphide, 466–467 Zinc sulfate fecal flotation, 125, 284, 926 Zolazepam, 622 Zonisamide, 160, 482 Zoonosis, 957, 985–991 Ancylostoma braziliense, 234, 987–989 Ancylostoma tubaeforme, 234, 987–989 Bacillus anthracis, 986 Bartonella spp., 35, 191–192, 986, 988–989 Bordetella bronchiseptica, 50, 986, 988–989 Borrelia burgdorferi, 986, 988 Campylobacter spp., 986, 988–990 Capnocytophaga canimorsus, 986, 988 Cheyletiella blakei, 484, 986, 988–989 Chlamydophila spp., 987–989 Coxiella burnetti, 987–988 Cryptosporidium spp., 100, 987–990 Ctenophalides spp., 986, 988 Dirofilaria immitis, 987–989 Echinococcus multilocularis, 986, 988–990 Epidermophyton, 987 Francisella tularensis, 986, 988 Giardia spp., 197, 987–990 Helicobacter spp., 213, 986, 988–989 herpesvirus-1, 225 Lyssavirus spp., 987 Microsporum canis, 987–988 Mycobacterium lepraemurium Mycobacterium spp., 303, 986 Mycoplasma felis, 986, 988–989 Nocardia spp., 356 Orthopoxvirus spp., 987 Otodectes cyanotis, 143, 986 Pasturella multocida, 986 Rabies, 441, 988, 990 Salmonella spp., 470–471, 986, 988–990 Sarcoptes scabiei, 987–989 Sporothrix schenckii, 487, 747, 987 Strongyloides stercoralis, 987, 989 Toxicara cati, 468 Toxoplasma gondii, 513, 987–989 Trichophyton mentagrophytes, 987 Uncinaria stenocephala, 234, 989 Yersinia pestis, 400–401, 986, 988–989
