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CompendiumCONTINUING EDUCATION FOR VETERINARIANS®

CompendiumVet.com | Peer Reviewed | Listed in MEDLINE Vol 31(3) March 2009

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6 CE Contact Hours

VomitingTreatment Options

Stress-Induced Hypersensitivity in Cats

Squamous Cell Carcinoma

Understanding Behavior

ProMeris is a registered trademark of Wyeth. ©2008 Fort Dodge Animal Health, a division of Wyeth.

Available from the following authorized veterinary distributors: DVM Resources • Great Western Animal Health Supply • Henry Schein Animal Health • IVESCO • Midwest Vet Supply • NLS Animal Health

Nelson Laboratories • Penn Vet Supply • PCI Animal Health • VetSource • Vet Pharm • Victor Medical Company • Webster Vet Supply

ProMeris:• Metaflumizone – no other flea control product utilizes this active ingredient

• Metaflumizone kills fleas by targeting voltage-dependent sodium channels along presynaptic and postsynaptic nerves resulting in paralysis and death

• Convenient topical application

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Dosing Convenience:• Five sizes for dogs and two sizes for cats with three- or six-dose packs for monthly application

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Discover the difference ProMeris offers you and your patients. Contact your ProMeris distributor, visit www.ProMeris.com or call 1-888-PROMERIS today.

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to four weeks on dogs. Controls fleas for up to seven weeks on cats. Fits easily into a monthly regimen.

FLEA & TICKPROTECTION

Kills fleas and ticks on dogs.Kills fleas on cats.

EASY TO USENon-drip applicator designmakes treatment a snap.

GENTLEFormulated for dogs and puppies 8 weeks and older and cats and

kittens 8 weeks and older.

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CompendiumVet.com 97

Published monthly by Veteri-nary Learning Systems, a division of MediMedia, 780 Township Line Road, Yardley, PA 19067. Copy right © 2009 Veterinary Learn ing Systems. All rights reserved. Printed in the USA. No part of this issue may be reproduced in any form by any means without prior written permis-sion of the publisher.

Printed on acid-free paper, effec tive with volume 29, issue 5, 2007.

Periodicals postage paid at Morris ville, PA, and at addi-tional mailing offices.

Postmaster: Send address changes to Compendium: Continuing Education for Veteri narians®, 780 Township Line Road, Yardley, PA 19067. Canada Post international publications mail product (Canadian distribution) sales agreement no. 40014103. Return undeliverable Canadian addresses to MediMedia, PO Box 7224, Windsor, ON N9A 0B1. Printed in USA.

March 2009 Vol 31(3)

CompendiumVet.com | Peer Reviewed | Listed in MEDLINE

EXECUTIVE EDITORTracey L. Giannouris, MA

800-426-9119, ext 52447 | [email protected]

MANAGING EDITORKirk McKay


SENIOR EDITORRobin A. Henry


ASSOCIATE EDITORChris Reilly


EDITORIAL ASSISTANTBenjamin Hollis


VETERINARY ADVISERDorothy Normile, VMD, Chief Medical Officer


SENIOR ART DIRECTORMichelle Taylor

267-685-2474 | [email protected]

ART DIRECTORDavid Beagin

267-685-2461 | [email protected]

OPERATIONSMarissa DiCindio, Director of Operations267-685-2405 | [email protected]

Elizabeth Ward, Associate Production Manager–Journals267-685-2458 | [email protected]

SALES & MARKETINGJoanne Carson, National Account Manager

267-685-2410 | Cell 609-238-6147 | [email protected]

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Lisa Siebert, Account Manager913-422-3974 | Cell 215-589-9457 | [email protected]

CLASSIFIED ADVERTISINGLiese Dixon, Classified Advertising Specialist

800-920-1695 | [email protected] | www.vetclassifieds.com

EXECUTIVE OFFICERDerrick Kraemer, President

CUSTOMER SERVICE800-426-9119, option 2 | [email protected]

Subscription inquiries:800-426-9119, option 2. Subscription rate: $79 for 1 year; $143 for 2 years; $217 for 3 years. Canadian and Mexican subscriptions (sur-face mail): $95 for 1 year; $169 for 2 years; $270 for 3 years. Foreign subscriptions (surface mail): $175 for 1 year; $275 for 2 years; $425for 3 years. Payments by check must be in U.S. funds drawn on a U.S. branch of a U.S. bank only; credit cards are also accepted. Change of Address: Please notify the Cir cu lation Department 45 days before the change is to be effective. Send your new address and enclose an address label from a recent issue. Selected back issues are available for $15 (United States and Canada) and $17 (foreign) each (plus postage).

Indexing: Compendium: Con-tinuing Education for Veteri-narians® is included in the international indexing cover-age of Cur rent Contents/Agriculture, Biol ogy and Environ mental Sciences (ISI); SciSearch (ISI); Research Alert (ISI); Focus On: Veteri-nary Science and Medicine(ISI); Index Veterinar ius (CAB International, CAB Ab stracts, CAB Health); and Agricola (Library of Congress).Article re trieval systems include The Genuine Article (ISI), The Copyright Clear-ance Center, Inc., University Microfilms International, and Source One (Knight-Ridder Information, Inc.). Yearly author and subject indexes for Compendium are pub-lished each December.

Compendium: Continuing Education for Veterinarians®

(ISSN 1940-8307)

PUBLISHED BY

98 CompendiumVet.comm


AnesthesiaNora S. Matthews, DVM, DACVATexas A&M University

CardiologyBruce Keene, DVM, MSc, DACVIMNorth Carolina State University

Clinical Chemistry, Hematology, and UrinalysisBetsy Welles, DVM, PhD, DACVPAuburn University

DentistryGary B. Beard, DVM, DAVDCAuburn University

R. Michael Peak, DVM, DAVDCThe Pet Dentist—Tampa Bay Veterinary

DentistryLargo, Florida

Emergency/Critical Care and Respiratory MedicineLesley King, MVB, MRCVS, DACVECC, DACVIMUniversity of Pennsylvania

Endocrinology and Metabolic DisordersMarie E. Kerl, DVM, ACVIM, ACVECCUniversity of Missouri-Columbia

EpidemiologyPhilip H. Kass, DVM, MPVM, MS, PhD, DACVPMUniversity of California, Davis

Exotics AvianThomas N. Tully, Jr, DVM, MS, DABVP (Avian), ECAMSLouisiana State University

ReptilesDouglas R. Mader, MS, DVM, DABVP (DC)Marathon Veterinary HospitalMarathon, Florida

Small MammalsKaren Rosenthal, DVM, MS, DABVP (Avian)University of Pennsylvania

Feline MedicineMichael R. Lappin, DVM, PhD, DACVIM (Internal Medicine)Colorado State University

Margie Scherk, DVM, DABVP (Feline Medicine)Cats Only Veterinary ClinicVancouver, British Columbia

GastroenterologyDebra L. Zoran, DVM, MS, PhD, DACVIM (Internal Medicine)Texas A&M University

Infectious DiseaseDerek P. Burney, PhD, DVMGulf Coast Veterinary SpecialistsHouston, Texas

Internal MedicineDana G. Allen, DVM, MSc, DACVIMOntario Veterinary College

Internal Medicine and Emergency/Critical CareAlison R. Gaynor, DVM, DACVIM (Internal Medicine), DACVECCNorth Grafton, Massachusetts

NephrologyCatherine E. Langston, DVM, ACVIMAnimal Medical CenterNew York, New York

NeurologyCurtis W. Dewey, DVM, MS, DACVIM (Neurology), DACVSCornell University Hospital for Animals

OncologyAnn E. Hohenhaus, DVM, DACVIM (Oncology and Internal Medicine)Animal Medical CenterNew York, New York

Gregory K. Ogilvie, DVM, DACVIM (Internal Medicine and Oncology)CVS Angel Care Cancer Center and Special

Care Foundation for Companion AnimalsSan Marcos, California

OphthalmologyDavid A. Wilkie, DVM, MS, DACVOThe Ohio State University

ParasitologyByron L. Blagburn, MS, PhD Auburn University

David S. Lindsay, PhDVirginia Polytechnic Institute

and State University

PharmacologyKatrina L. Mealey, DVM, PhD, DACVIM, DACVCPWashington State University

Rehabilitation and Physical TherapyDarryl Millis, MS, DVM, DACVS University of Tennessee

SurgeryPhilipp Mayhew, BVM&S, MRCVS, DACVSColumbia River Veterinary SpecialistsVancouver, Washington

C. Thomas Nelson, DVMAnimal Medical CenterAnniston, Alabama

Surgery and OrthopedicsRon Montgomery, DVM, MS, DACVSAuburn University

ToxicologyTina Wismer, DVM, DABVT, DABTASPCA National Animal Poison Control

CenterUrbana, Illinois

EDITORIAL BOARD

Any statements, claims, or product endorsements made in Compendiumare solely the opinions of our authors and advertisers and do not necessarily refl ect the views of the Publisher or Editorial Board.

EDITOR IN CHIEF

Douglass K. Macintire, DVM, MS, DACVIM, DACVECC

Department of Clinical SciencesCollege of Veterinary MedicineAuburn University, AL 36849


EXECUTIVE ADVISORY BOARD MEMBERS

BehaviorSharon L. Crowell-Davis, DVM, PhD, DACVBThe University of Georgia

DermatologyCraig E. Griffi n, DVM, DACVDAnimal Dermatology ClinicSan Diego, California

Wayne S. Rosenkrantz, DVM, DACVDAnimal Dermatology ClinicTustin, California

NutritionKathryn E. Michel, DVM, MS, DACVNUniversity of Pennsylvania

SurgeryElizabeth M. Hardie, DVM, PhD, DACVSNorth Carolina State University

Compendium is a refereed journal. Articles published herein have been reviewed by at least two academic experts on the respective topic and by an ABVP practitioner.

AMERICAN BOARD OF VETERINARY PRACTITIONERS (ABVP) REVIEW BOARD

Kurt Blaicher, DVM, DABVP (Canine/Feline)Plainfi eld Animal HospitalPlainfi eld, New JerseyCanine and Feline Medicine

Eric Chafetz, DVM, DABVP (Canine/Feline)Vienna Animal HospitalVienna, VirginiaCanine and Feline Medicine

Henry E. Childers, DVM, DABVP (Canine/Feline)Cranston Animal HospitalCranston, Rhode IslandCanine and Feline Medicine

David E. Harling, DVM, DABVP (Canine/Feline), DACVOReidsville Veterinary HospitalReidsville, North CarolinaCanine and Feline Medi cine,

Ophthalmology

Jeffrey Katuna, DVM, DABVPWellesley-Natick Veterinary

HospitalNatick, MassachusettsCanine and Feline Medicine

Robert J. Neunzig, DVM, DABVP (Canine/Feline)The Pet HospitalBessemer City, North CarolinaCanine and Feline Medicine

Understanding Behavior116 Feline Hyperesthesia Syndrome ❯❯ John Ciribassi The etiology of feline hyperesthesia

syndrome can be diffi cult to determine. Behavior modifi cation and medications may help in treatment.

Each CE article is accredited for 3 contact hours by Auburn University College of Veterinary Medicine.

Features

Departments100 CompendiumVet.com

102 The Editor’s Desk: Meet Our New Online CE “Sister”❯❯ Tracey L. Giannouris

104 Clinical Snapshot Pruritus in a Great Dane

❯❯ Karen A. Moriello

113 Letters

132 Product Forum

143 Index to Advertisers

143 Market Showcase

143 Classifi ed Advertising

Cover image © 2009 Michael Woodruff/Shutterstock.com

105 Disclosing Medical Errors: Restoring Client Trust

❯❯ Kathleen A. Bonvicini, Daniel O’Connell, and Karen K. Cornell

Discussing medical errors with affected clients can ultimately benefi t your practice. This article provides tips on creating a protocol for resolving medical errors.

122 Vomiting ❯❯ Héctor J. Encarnación, Joshua Parra,

Erick Mears, and Valerie Sadler

Antiemetic drugs act by affecting neurotrans-mitter–receptor interactions in many areas of the body. Learn why different drugs are used for different causes of vomiting.

133 Squamous Cell Carcinoma ❯❯ Julie L. Webb, Rachel E. Burns,

Holly M. Brown, Bruce E. LeRoy, and Carrie E. Kosarek

The authors review the causes, diagnosis, and treatment of this tumor type.

Clinical Snapshot PAGE 104



FREE

CE

d C i E K

FREE

CE

EACE

Compendium: Continuing Education for Veterinarians® 99

CE ARTICLES

❯❯ Canine Thoracolumbar Intervertebral Disk Disease: Pathophysiology, Neurologic Examination, and Emergency Medical Therapy

❯❯ John F. Griffi n IV, Jonathan M. Levine, and Sharon C. Kerwin

Thoracolumbar intervertebral disk disease (IVDD) is a common, important cause of paraspinal hyperesthesia, pelvic limb ataxia, paraparesis, paraplegia, and urinary and fecal incontinence in dogs. Recent research offers new insights into the pathophysiology, diagnosis, prognosis, and treatment of this disorder. The comparative effi cacy of many familiar therapies remains unknown and controversial. This article reviews the pathophysi-ology and epidemiology of this condition and the examination and emergency medical therapy of dogs with suspected thoracolumbar IVDD.

❯❯ Canine Thoracolumbar Intervertebral Disk Disease: Diagnosis, Prognosis, and Treatment

❯❯ John F. Griffi n IV, Jonathan M. Levine, Sharon C. Kerwin, and Robert C. Cole

Thoracolumbar intervertebral disk disease (IVDD) is a common, important cause of paraspinal hyperesthesia, pelvic limb ataxia, paraparesis, paraplegia, and urinary and fecal incontinence in dogs. This article addresses the diagnosis, prognosis, and treatment of dogs with thoracolumbar IVDD.

CLINICAL SNAPSHOT

❯❯ Pekinese With Acute Onset of Collapse

NEWS BITES

❯❯ Vet Study Finds Aggressive Owners Have Aggressive Dogs

A University of Pennsylvania study has found that most aggressive dogs will remain aggressive when dog owners use confrontational or aversive methods to try to train their pets.

❯❯ Economy Means Slowdown for Some Vet Practices

A number of small animal practices have reported a drop in client visits.

❯❯ New SPCA Vet Hospital a San Francisco Treat

The $29-million Leanne B. Roberts Animal Care Center is the new home of the San Francisco SPCA’s nonprofi t veterinary hospital, spay/neuter clinic, and shelter medicine program.

❯❯ Beware of Cocoa MulchA popular option for landscaping, cocoa mulch can be deadly to pets.

❯❯ COMPENDIUM EXTRA Our monthly e-newsletter provides Web Exclusive articles and news, as well as a preview of this month’s journal. Sign up at CompendiumVet.com.

❯❯ Email your questions, suggestions, corrections, or letters to the editor:[email protected]

E-NEWSLETTER

CONTACT US

100 CompendiumVet.com

❯❯ Laparoscopic Gastropexy

Three videos show some aspects of the techniques described in the February 2009 Surgical Views column, “Laparoscopic-Assisted and Laparoscopic Prophylactic Gastropexy: Indications and Techniques.”

WEB EXCLUSIVEVIDEOS

March 2009 Vol 31(3) WEB EXCLUSIVES

Visit www.aspca.org/freemagnet for your free ASPCA Animal Poison Control Center magnet − an easy way to keep our emergency number handy.

*American Board of Veterinary Toxicology www.abvt.orgFor information on our online Toxicology CE courses, visit www.apcc.aspca.org. No animals were harmed during the production of this ad.

ORDER A FREE MAGNET

Vet Tech | Trim: 8 x 10 3/4 | Live: 7 x 9 3/4 | Bleed: 8 1/4 x 11

A pill bottle accidently knocked off a sink. Everyday things can quickly become a poison emergency for a pet. It’s the reason the ASPCA® Animal Poison Control Center is here 24/7/365 to support you with critical recommendations. As the only center in North America dedicated solely to animals, we have an experienced team of board certifi ed veterinary toxicologists* on staff with the special expertise needed to save a pet’s life. Our exclusive AnTox™database of more than one million cases of animal poisonings also gives us immediate access to crucial case information. When potential danger turns into a real emergency, don’t hesitate. Call us.

T h e p o t e n t i a l f o r a n a n i m a l p o i s o n e m e r g e n c y i s a l w a y s t h e r e , s o w e a r e t o o .

ASPCA_Beagle_8.75x10.indd 1 12/7/07 6:25:23 PM

102 Compendium: Continuing Education for Veterinarians® | March 2009 | CompendiumVet.com

The Editor’s Desk

For more than 30 years, Compendium has been your trusted source for continuing education (CE), both in print and, more

recently, on the Internet. Now, all of us here at Compendium are pleased to announce the expansion of our CE efforts with the launch of a new Web site: CECenter.com. CECenter.com, a companion site to VetLearn.com (which comprises CompendiumVet.com, CompendiumEquine.com, SOCNewsletter.com, VetTechJournal.com, VeterinaryTherapeutics.com, and ForumVet.com), is devoted exclusively to provid-ing interactive online CE to veterinarians and veteri-nary technicians. The mission behind the site is to provide veterinary practitioners with new, timely information that can be immediately incorporated into practice. To achieve this goal, we have gathered in one central location a wide array of CE activities, from peer-reviewed CE content from Compendium, Compendium Equine, and Veterinary Technician to presentations given by recognized experts. Our realization of the need for a dedicated veterinary CE portal crystallized with our rec-ognition of the increasing number of veterinary practitioners who are using the VetLearn.com and CompendiumVet.com sites to meet CE require-ments. In an average month, approximately

145,000 registered users (43.3% of whom are practicing veterinarians; 47.7%, veterinary tech-nicians; 3%, veterinary technician students; and 1.2%, veterinary students) visit VetLearn.com. While there, they investigate a total of 200,000 pages (40,000 of which are clinical CE review articles) and obtain a total of 2,000 CE credits. Based on these numbers, we saw a clear need to expand our CE offerings by creating a compan-ion portal dedicated to “all things CE.” CECenter.com gives both veterinarians and veterinary technicians the ability to search for and participate in CE activities. In addition to the archive of our own peer-reviewed arti-cles, CECenter.com offers exclusive, interactive, sponsored courses accredited by the Registry of Approved Continuing Education, as well as a complete list of CE requirements by state and links to CE programs from other respected sources such as the AVMA, the American Animal Hospital Association, and accredited universities and institutions. Other features of CECenter.com include a preview of upcoming courses and activ-ities. Users get individual accounts that contain a permanent online record of their CE history and allow them to reprint any CE certifi cate at any time. And our plans call for more CE offerings—and more CE-related features and content—as CECenter.com grows throughout 2009. CECenter.com is accessible to everyone regis-tered on VetLearn.com or CompendiumVet.com, and registration is free. If you haven’t already registered, we invite you to sign up now so that you can explore CECenter—and our other sites—for yourself. We are confi dent that, along with CompendiumVet.com, CECenter.com will become the preferred online CE source for you and your technician staff.

❯❯ Tracey L. Giannouris, MA, Executive Editor

Meet Our New Online CE “Sister”

As always, we welcome your feedback, comments, and suggestions for both VetLearn.com and CECenter.com. Please feel free to email me at [email protected].

Tracey with her son, Michael Francis

LET YOUR CONSCIENCE GUIDE YOU.

LETLETYOURSCIENCESCIENCE

GUIDE GUIDE YOU. YOU.

1Milbemycin oxime. Parasiticide Usage Study, June 2005. Data on fi le. Novartis Animal Health US, Inc. 2Data on fi le. Novartis Animal Health US, Inc.©2009 Novartis Animal Health US, Inc. INTERCEPTOR and Flavor Tabs are registered trademarks of Novartis AG. Heartgard is a registered trademark of Merial Ltd.

Dogs and Cats should be tested for heartworm prior to use. In a small percentage of treated dogs, digestive and neurologic side effects may occur. In cats, safety studies at up to 10 times the label dose did not detect any adverse drug reactions. Please see brief summary on page 104 for more information.

Dogs and Cats should be tested for heartworm prior to use. In a small percentage of treated dogs, digestive and neurologic side effects may occur. In cats, safety studies at up to 10 times the label dose did not detect any adverse drug reactions. Please see brief summary on page XX for more information.

Milbemycin oxime is trusted #1 by veterinarians for use on their own dogs.1

Veterinarians also believe that INTERCEPTOR® (milbemycin oxime) Flavor Tabs® provide better science and value for the money than Heartgard.2

L:7”L

:9.75”

T:8”T:10.75”

B:8.25”B

:11”

43955_Interceptor_Ad_I2.indd 1 2/12/09 2:45:59 PM

Clinical Snapshot


Particularly intriguing or diffi cult cases

This Great Dane (A) was one of 12 dogs in a kennel, all of which had had intense pruritus for 1 year. The owners reported that the other dogs looked similar and that all the dogs were los-ing weight and were irritable with the owners and each other. Close examina-tion of the skin revealed a generalized papular eruption without evidence of pustules or epidermal collarettes. Any manipulation of the skin triggered an intense episode of self-mutilation. All the dogs were currently vaccinated and received monthly heartworm medica-tion and monthly spot-on fl ea control. The owners reported no lesions or dis-comfort after handling the dogs. Flea combings were negative. Skin scrap-ings revealed the organism shown (B).1. What is the diagnosis?2. The owners of the kennel have three

border collies and seven cats in addi-tion to these dogs. What are the treat-ment options for this kennel of dogs?

3. A similarly named condition occurs in cats. What is the cause, and what treatment can be used for this condition?SEE PAGE 114 FOR ANSWERS AND EXPLANATIONS.

Case Presentation #1 ❯❯ Karen A. Moriello, DVM, DACVD, University of Wisconsin-Madison

TO LEARN MORE

For more information or to obtain any of the

books in the series, call 800-862-6657

or visit BlackwellProfessional.com

Clinical Snapshot presents illustrated

case histories and challenges you to

answer the questions posed. This case

is part of the series of Self-Assessment Colour Review books on multiple topics

from Manson Publishing Ltd., London,

available from Blackwell Publishing

Professional.

NADA 140-915, Approved by FDAINTERCEPTOR® (milbemycin oxime) Flavor Tabs® for Dogs and CatsBrief Summary—For full product information see product insert.

Caution: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian.

Indications and Usage: INTERCEPTOR Flavor Tabs for dogs are indicated for use in the prevention of heartworm disease caused by Dirofilaria immitis, the control of adult Ancylostoma caninum (hookworm), and the removal and control of adult Toxocara canis and Toxascaris leonina (roundworms) and Trichuris vulpis (whipworm) infections in dogs and in puppies four weeks of age or greater and two pounds body weight or greater. INTERCEPTOR Flavor Tabs are indicated for use in the prevention of heartworm disease caused by Dirofilaria immitis, and the removal of adult Ancylostoma tubaeforme (hookworm) and Toxocara cati (roundworm) in cats and kittens six weeks of age or greater and 1.5 lbs. body weight or greater.

Dosage and Administration: Dogs: INTERCEPTOR Flavor Tabs for Dogs are given orally, once a month, at the recommended minimum dosage rate of 0.23 mg milbemycin oxime per pound of body weight (0.5 mg/kg).

Recommended Dosage Schedule for Dogs Body Weight INTERCEPTOR Flavor Tabs

2–10 lbs. One tablet (2.3 mg) 11–25 lbs. One tablet (5.75 mg) 26–50 lbs. One tablet (11.5 mg) 51–100 lbs. One tablet (23.0 mg)

Dogs over 100 lbs. are provided the appropriate combination of tablets.

Cats: INTERCEPTOR Flavor Tabs for Cats are given orally, once a month, at the recommended minimum dosage rate of 0.9 mg milbemycin oxime per pound of body weight (2.0 mg/kg).

Recommended Dosage Schedule for Cats Body Weight INTERCEPTOR Flavor Tabs

1.5–6 lbs. One tablet (5.75 mg) 6.1–12 lbs. One tablet (11.5 mg) 12.1–25 lbs. One tablet (23.0 mg)

Cats over 25 lbs. are provided the appropriate combination of tablets.

INTERCEPTOR Flavor Tabs are palatable and most often will be consumed by the dog or cat when offered by the owner. As an alternative, the dual-purpose tablet may be offered in food or administered as other tablet medications. Watch the dog or cat closely following dosing to be sure the entire dose has been consumed. If it is not entirely consumed, redose once with the full recommended dose as soon as possible.

INTERCEPTOR Flavor Tabs must be administered monthly, preferably on the same date each month. The first dose should be administered within one month of the dog or cat’s first exposure to mosquitoes and monthly thereafter until the end of the mosquito season. If a dose is missed and a 30-day interval between dosing is exceeded, administer INTERCEPTOR Flavor Tabs immediately and resume the monthly dosing schedule.

If INTERCEPTOR Flavor Tabs replace diethylcarbamazine (DEC) for heartworm prevention in dogs, the first dose must be given within 30 days after the last dose of DEC.

Warnings: Not for human use. Keep this and all drugs out of the reach of children.

Precautions:Dogs: Do not use in puppies less than four weeks of age and less than two pounds of body weight. Prior to initiation of the INTERCEPTOR Flavor Tabs treatment program, dogs should be tested for existing heartworm infections. Infected dogs should be treated to remove adult heartworms and microfilariae prior to initiating treatment with INTERCEPTOR Flavor Tabs. Mild, transient hypersensitivity reactions manifested as labored respiration, vomiting, salivation, and lethargy may occur after treatment of dogs carrying a high number of circulating microfilariae.

Cats: Do not use in kittens less than six weeks of age or less than 1.5 lbs. body weight. Safety in heartworm positive cats has not been established. Safety in breeding, pregnant, and lactating queens and breeding toms has not been established.

Adverse Reactions: The following adverse reactions have been reported following the use of INTERCEPTOR in dogs: depression/lethargy, vomiting, ataxia, anorexia, diarrhea, convulsions, weakness, and hypersalivation.

Efficacy:Dogs: INTERCEPTOR Flavor Tabs eliminate the tissue stage of heartworm larvae and the adult stage of hookworm (Ancylostoma caninum), roundworms (Toxocara canis, Toxascaris leonina), and whipworm (Trichuris vulpis) infestations when administered orally according to the recommended dosage schedule.

Cats: INTERCEPTOR Flavor Tabs for Cats eliminate the tissue stage of heartworm larvae and hookworm (Ancylostoma tubaeforme) and roundworm (Toxocara cati) infections when administered orally according to the recommended dosage schedule.

For technical assistance or to report suspected adverse events, call 1-800-332-2761.

Manufactured for: Novartis Animal Health US, Inc. Greensboro, NC 27408, USA

©2008 Novartis Animal Health US, Inc.

INTERCEPTOR and Flavor Tabs are registered trademarks of Novartis AG.

NAH/INT-FT/BS/5 06/08

A

B

CompendiumVet.com | March 2009 | Compendium: Continuing Education for Veterinarians® 105

Disclosing Medical Errors:Restoring Client Trust*

The purpose of this article is to help veterinarians reach a mutually satis-fying resolution with clients when

individual, team, or system errors result in an adverse outcome. It offers a model that integrates the ethics of veterinary medi-cine with specifi c skills and attitudes that have been shown to promote psychologic and practical resolution of these situations for clients and veterinary practices.

Case ScenarioConsider the following1:

Your nephew, a recent veterinary school graduate who is newly employed at a pri-vate small animal hospital, calls you for advice. Four days ago, he admitted a dog to the hospital for vaccinations and board-ing. During the admission process, he administered a Bordetella bronchisepticavaccine to the dog. The dog died this morn-ing. In retrospect, your nephew realizes that he picked up a syringe of intranasal B. bronchiseptica vaccine that still had a needle on it from being drawn from the vial, then gave the vaccine subcutaneously. This inappropriate route of administration resulted in the development of liver failure while the dog was boarded at the hospital.

Your nephew says, “I feel terrible—what should I tell my clients?”

How would you respond? What one piece of advice would you give to your nephew?

Ethics, Values, and Moral CompassIn examining this scenario and consid-ering your own opinions, you are likely relying on the values that guide the way you practice veterinary medicine. Still, this will be a very tough conversation to have. Many clinicians report feelings of shame, heartbreak, and vulnerability in situations like this one. Our natural instinct for self-preservation, coupled with advice we may have received previously, can tempt us to be very guarded when talking with clients about adverse outcomes and to use cal-culated omissions and rationalizations to conceal evidence of an error. In the above scenario, one might argue that vaccination has inherent risks. A frightened young vet-erinarian might be attracted to such seduc-tive reasoning as, “Disclosing the actual cause of death will increase the clients’ dis-tress and certainly will not bring back the animal. What good could come from tell-ing the clients what really happened?”

Rationale for OpennessThe ethical positions of organizations such as the American Medical Association,2 the American College of Physicians,3 and the

❯❯ Kathleen A. Bonvicini, EdD, MPHa

Institute for Healthcare Communication New Haven, Connecticut

❯❯ Daniel O’Connell, PhDa

Institute for Healthcare Communication Seattle, Washington

❯❯ Karen K. Cornell, DVM, PhD, DACVS

The University of Georgia Athens, Georgia

Case Scenario Page 105

Ethics, Values, and Moral Compass

Page 105

Disclosure and Resolution: A Protocol

Page 106

What to Do When an Error Occurs

Page 108

Guidelines for Disclosure 0

Establish Practice Protocol Page 112

At a Glance

*Adapted with permission from Compendium Equine 2008;3(1):14-22.aDrs. Bonvicini and O’Connell disclose that their nonprofi t foundation receives funding from Bayer Animal Health.

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Disclosing Medical Errors: Restoring Client Trust


Joint Commission4 have clear statements that require accurate disclosure of adverse medi-cal outcomes in human medicine. Similar ethi-cal positions exist in veterinary medicine.5 Research in human medicine and other pro-fessions6–10 has described the potential advan-tages of a more open approach with patients, families, and “customers” in these situations. When applied to veterinary medicine, these benefi ts include the following:

More situations can be worked out directly between the veterinarian, the client, and the insurance carrier without stimulating legal action or formal complaints to licensing boards. The AVMA Professional Liability Insurance Trust (PLIT) recommends that veterinarians call the PLIT offi ce as soon as possible after an event that could give rise to a claim.b

Rebuilding rapport and trust and resolving disagreements can turn initial client disap-pointment into an even stronger relationship.

When the practice and the insurance carrier are willing to initiate discussion of fair settlements with clients who have been legitimately affected by errors in practice, the dollar amounts tend to be easier to negotiate and more reasonable than those obtained through legal action7,8,11 because client bitterness is minimized and dol-lar amounts are focused on reasonable com-pensation rather than punishment.

Adverse Outcomes and Medical ErrorsAdverse outcome is the term used in veterinary and human medicine to indicate unanticipated harm that results from a medical treatment rather than from a disease or condition itself.12 An ethical approach to disclosure of harm hinges on the veterinarian’s commitment to determining and then sharing the most accurate conclusions about how the harm was caused. While sometimes fairly clear, many situations require the veterinarian to draw a bright line through a gray situation to determine whether a breach of the standard of care caused the harm (and, therefore, the harm was prevent-able) or whether the harm occurred in the con-text of care that most veterinarians would judge as reasonable in a similar instance.13,14 Practically and emotionally, this can be diffi cult to do, yet who is in a better position to investigate, con-

clude, and explain than the practice where the adverse event took place? Most client disappointments with veterinary outcomes are not the result of negligent care. For instance, clients may have unreasonable expectations that were not adequately addressed or corrected. They may not appreciate the vari-ability between animals or that diagnostic and treatment plans are based on probabilities rather than certainties. The clinical picture may change as additional signs emerge and the response to treatment is assessed.15 Almost every effective treatment brings with it the potential for untow-ard side effects and complications. Unless clients are apprised of these risks, they may mistakenly believe that similarly trained clinicians would have been able to solve the problem more quickly, with less suffering, and at a lower cost. Each of the above factors is a reminder of the importance of obtaining true owner consent, recognizing and correcting unreasonable expectations, and offering adequate explanations when diagnosis and treatment are unsuccessful, even when the standard of care is met.16

Errors and Harm in Veterinary MedicineWhile research into the incidence, type, and impact of errors in veterinary medicine is limited, it is clear that adverse events related to errors do occur. For instance, one small UK study17 found that 78% of recent practicing veterinary gradu-ates surveyed reported they had made a mistake that resulted in a less-than-optimal or potentially adverse outcome for a patient. Most mistakes involved failure to conduct appropriate diagnostic tests, surgical mistakes during procedures other than neutering, and administration of inappro-priate drugs or medical treatment. Forty percent reported that they had not discussed the error with the client. These mistakes caused many of the respondents considerable distress.

Disclosure and Resolution: A ProtocolResearch has consistently indicated that, in human medicine, patients and families typically want to hear the following from the care provider when an adverse event or outcome occurs10,18–21:

What happened How it happened What the immediate medical consequences are, and what impact they will have on quality of lifebEllis LJ. Personal communication, AVMA PLIT, 2007.

Most client disap-pointments with veterinary outcomes are not the result of negligent care.

QuickNotes

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What can be done now How the problem will be prevented in the future (i.e., the promise that something good will come from the adverse event)An apology if appropriate (if errors led to the harm)

The following protocol (summarized in BOX 1) provides specifi c approaches to assist you in organizing a thorough, appropriate, construc-tive response that meets the needs of the patient and the expectations of clients and that restores clients’ trust, regardless of the severity of the adverse event.

Tend to the patient’s immediate clinical care.In the event of an adverse outcome, the pri-mary responsibility of the veterinarian is to address the needs of the patient and, if appro-priate, obtain medical consultation or arrange for necessary follow-up. Consider that charges for services in these circumstances may not be billable if they are addressing conditions caused by errors (including equipment fail-ures and system or procedural mistakes that caused harm).

Address your own emotions and needs.Emotional self-awareness is key to adopting the most constructive attitude and behavior. A clinician who is fl ooded with worries about potential complaints and possible malpractice suits may be unconsciously pushed to mini-mize or even distort the facts and explana-tion offered to the client. On the other hand, the clinician who is overwhelmed with guilt

and heartbreak for the patient’s and client’s situation may leap to self-blame too quickly, only to have the investigation determine that no deviation from the standard of care was implicated in the outcome. There is usually enough time to consult with a trusted col-league to clarify your thinking and reestablish your emotional equilibrium before needing to make a full explanation to a client about how an adverse outcome arose.

Investigate the details of the event.Develop clarity about what happened. The client is entitled to the most accurate under-standing of what happened, which may take some time and investigation to clarify. You can ask for the client’s patience while you investigate. Make—and keep—a clear prom-ise to discuss the conclusions when they are reached. In many cases, the cause of the harm is never fully determined; however, it remains the veterinarian’s responsibility to disclose the most likely causal pathway. Determining whether error was the cause of harm should be guided by asking,22 “What would have been expected of a similarly trained individual in that situation?”

Prepare for discussion with the client.Start by trying to imagine and anticipate what the client may be thinking and feeling when hearing the news. O’Connell and Reifsteck23 suggest asking yourself the following self-refl ection questions to help guide you in your discussion with the client:

What is the most accurate explanation for the adverse event?

How would I want the situation to be han-dled if I were in the client’s position? How would I feel if I suspected or later learned that the provider had not been forthright with me about the injury and its causes?

It is helpful to rehearse the actual words you will use in explaining the adverse event because hearing them will help you determine whether they are likely to be adequate to address the cli-ent’s expected thoughts and feelings. Consider carefully who should attend the disclosure conversation. The veterinarian who is primarily responsible for the care of the animal should be there and take the lead in

Emotional self-awareness is key to adopting the most constructive attitude and behavior.

QuickNotes

BOX 1

1. Care for the patient.2. Compose yourself and investigate the

details of the event.3. Disclose to the client what occurred and

apologize, if appropriate.4. Discuss with the client the

plan of care for the animal.5. Be accountable and discuss

methods of reparation.6. Share how you plan to

keep this from happening in the future.

What to Do When an Error Occurs

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the discussion, even if the adverse event was primarily caused by another staff member’s actions. The presence of a person who was not directly involved with the adverse event and who has credibility, maturity, and strong communication skills, such as the practice manager, can help facilitate and mediate what can be a diffi cult conversation. Plan when and how to begin the discussion. An initial discus-sion with the client should take place as soon as possible after the adverse event.

Disclose to the client what occurred and apologize. Disclose what you know, but guard against premature conjecture until you are as certain as you can be about causes and consequences. When possible, make an initial phone call to set up an in-person meeting rather than have the discussion over the phone. If a phone dis-closure cannot be prevented, start the discus-sion by acknowledging how sorry you are to have to be sharing the news over the phone. In person, start the discussion by offering a frame for the information to follow:

“I have some difficult news to share with you. I’m very sorry to have to tell you…”

Then explain the situation by addressing each of the issues listed above. BOX 2 offers some additional guidelines to approaching the disclosure conversation.

Elicit and acknowledge client reactions.Frequently throughout the discussion, you should solicit the client’s perspective through questions and statements such as, “What thoughts or questions do you have about what I have explained so far?” and “I imag-ine you have many emotions and questions, and I want to hear from you fi rst before going on.” Eliciting reactions serves to validate the client’s perspective on the medical error and adverse outcome and sets the stage for effec-tive interaction. Voice tone and body language are as important as actual words in conveying empa-thy for the client’s experience. Showing your

“human side” through genuine expressions of empathy can strengthen the bond and trust between you and your client. An empathetic veterinarian is not defensive, even when a cli-ent expresses anger and makes accusations. Acknowledging the client’s reaction as a legiti-mate one by making a statement such as, “It is normal to feel shocked and angry to learn that something like this has happened,” does not indicate that you agree with the conclusions that prompted it.

Apologize appropriately.After an adverse event or outcome, the proper type of apology can have a powerful effect on the client, making him or her less angry and suspicious. There are two types of apol-ogy: an apology of sympathy and an apology of responsibility. An apology of sympathy is:

“I’m sorry this happened to you and your pet.”

An apology of responsibility is:

“I am terribly sorry for this error we made that has caused more problems for your pet.”

Mazor and colleagues6,24 demonstrated that in situations in which a breach of the standard of care caused harm, respondents reported more trust and satisfaction and less likelihood of changing doctors when they received full disclosure with an apology of responsibility. In instances in which an adverse event is not the result of medical error, an apology of sym-pathy is appropriate.

Disclose what you know, but guard against premature conjecture until you are as certain as you can be about causes and consequences.

QuickNotes

Guidelines for Disclosure

1. Choose a quiet place.2. Ensure that there will be no distractions

(e.g., turn cell phones and pagers off).3. Provide a warning (e.g., “ I have diffi cult

news to share.”).4. Be attentive to your own and your client’s

nonverbal messages. ❯ Make eye contact. ❯ Sit at the client’s level. ❯ Respond appropriately to client nonverbal

cues (e.g., “I see that this is shocking to you. Should I go on or do you need a moment?”).

5. Facilitate discussion and encourage questions.6. Finish with a plan for the next contact.

BOX 2



Discuss the plan for care of the animal. In many instances, by the time the disclosure conversation takes place, steps have already been taken to care for the animal, and the veterinarian is thinking about other poten-tial consequences of the error. However, it is important to remember that the client has just received the news. Discuss the recommended plan for continuing care of the animal, includ-ing the potential short- and long-term out-comes. Often, clients are unclear about what lasting effect the error will have on their pet and may not comprehend the gravity or—in some cases—the limited impact of the error. It is critical that immediate concerns as well as the potential long-term impact be discussed in a manner the client understands.

Be accountable and offer reparation.Finally, the practice must acknowledge respon-sibility to help the client recover as much as possible from the harm that has been caused. Appropriate fees for the animal’s care should be waived. The veterinarian should anticipate discussion of who will pay for follow-up care before the disclosure conversation. Again, the AVMA PLIT recommends that it be contacted early on to discuss how best to approach this situation. Being accountable and willing to make rep-arations is crucial in the disclosure process; however, it does not mean immediately offer-ing money. Rather, it means opening up the conversation: “Can we do more to resolve this with you? We stand ready to do what we can to help you recover from this as much as possible.” According to the Sorry Works! Coalition,25 a leading advocacy organization for disclosure after adverse medical events, paying for errors is the ethical thing to do. However, there may be a fear that it will appear as if you are “buy-ing” clients off. This is an understandable con-cern. In veterinary medicine, all of the steps of disclosure—admission of error, explanation, apology—can still be delivered sincerely, and PLIT or your liability carrier can be consulted on how to offer reparation.

Describe plans to fi x the behavior or sys-tem that contributed to the harm.Consumers who are affected by a medical error want to know that something good has

come from the harm they have experienced. It is unacceptable to clients to think that a veterinarian’s failure to change or refl ect on the incident means that others are likely to suffer similarly.23 These sentiments become expressed as complaints to licensing boards as well as malpractice suits. Therefore, the vet-erinarian’s goal is to convey to the client that he or she has learned everything that can be learned from the adverse event:

“I can promise you that we’ll all be meeting later today to review every step of our proce-dures. We want to immediately change any-thing that makes it more likely that this could happen again to any other animal in our care.”

Don’t rush.Keep in mind that all these elements of dis-closure may take more than one meeting or conversation to deliver effectively to the client. Discussion of reparation may take the longest to resolve in cases in which the impact of the harm on the surviving animal and the extent of needed ongoing treatment are uncertain. However, if a client has suffered serious loss or even fi nancial harm (e.g., economic impact on a breeding kennel), he or she is going to want to promptly hear that you (with your liability carrier’s guidance) intend to offer fair compensation. The heart of all effective and ethical disclo-sure is to provide the client with an accurate understanding of what has happened. The form an apology takes and the offers made to help a client recover from an injury caused by medical error should fl ow naturally from the veterinarian’s own understanding of his or her degree of responsibility for the injury.

SummaryConsider your recommendations to your nephew in the scenario at the start of this col-umn. Ask yourself the following questions: Are my recommendations based on ethical stan-dards of openness, transparency, and integ-rity? Would I be satisfi ed if I were the client? Despite our best efforts, animals will occasion-ally be harmed by problems that occur while they are in our or our staff’s care. Having a standard approach to disclosure and resolu-tion that is consistent with our values, despite

The heart of all effective and ethical disclosure is to provide the client with an accurate understanding of what has happened.

QuickNotes



the fears and vulnerabilities we are likely to feel at these times, can help us earn our cli-ents’ forgiveness and enable us to forgive our-selves. BOX 3 lists some questions to ask when developing a disclosure protocol. We believe in using ethical standards and values of openness and honesty as a spring-board for conversations about medical errors. However, many veterinary practices may hesi-

tate to embrace such openness for fear that it may increase malpractice risk. Acknowledging errors has been evaluated positively, leading to increased trust and lessening the possibility of negative impact7; however, clinicians may still worry about the potential costs of openness and transparency. Although disclosure discus-sions are diffi cult and may still result in formal complaints and malpractice suits, evidence8

tells us that acknowledging errors can signifi -cantly reduce litigation costs, reduce bitterness and mistrust, and avoid unnecessarily lengthy legal proceedings with the accompanying emo-tional pain for consumers and clinicians alike. We encourage all veterinarians, whether joining a practice or established in one, to engage in conversations with their colleagues about the practice’s approach to and protocol for disclosure discussions in the event of a medical error. In addition, it is crucial to con-sult your malpractice liability insurance carrier to establish its position on the management of disclosure and resolution.

References1. Greene CE, Schulz RD. Immunoprophylaxis. In: Greene CE, ed. Infectious Diseases of the Dog and Cat. St. Louis: Elsevier Saun-ders; 2006:1097.2. Council on Ethical and Judicial Affairs. Code of Medical Eth-ics—Current Opinions, 2006–2007 Edition. Chicago: American Medical Association; 2006.3. American College of Physicians. Ethics Manual. 5th ed. Ann Intern Med 2005;142:560-582. Accessed January 2009 at www.acponline.org/ethics/ethicman5th.htm.4. Joint Commission on Accreditation of Healthcare Organiza-tions. 2006 Comprehensive Accreditation Manual for Hospitals: The Offi cial Handbook. Oakbrook Terrace, IL: Joint Commission Resources; 2005.5. American Veterinary Medical Association. Principles of Veteri-nary Medical Ethics. 2003. Accessed January 2009 at www.avma.org/issues/policy/ethics.asp.6. Mazor KM, Simon SR, Yood RA, et al. Health plan members’ views about disclosure of medical errors. Ann Intern Med 2004;140(6):409-418.7. Kraman S, Hamm G. Risk management: extreme honesty may be the best policy. Arch Intern Med 1999;131:963-967.8. Boothman R. Apologies and a strong defense at the University of Michigan Health System. Physician Exec 2006;32(7):7-10.9. American Society for Healthcare Risk Management. Disclosure of Unanticipated Events: The Next Step in Better Communication with Patients. Chicago: American Society for Healthcare Risk Man-agement; 2003.10. Schneider B, Bowen DE. Understanding customer delight and outrage. Sloan Manage Rev 1999;41(1):35-45.11. COPIC Insurance Company. A success story. COPIC’s 3Rs Program Newsletter 2007;4(2). Accessed January 2009 at www.callcopic.com/resources/custom/PDF/3rs-newsletter/vol-4-iss-2-oct-2007.pdf.12. Halbach JL, Sullivan L. Medical Errors and Patient Safety: A Curricu-lum Guide for Teaching Medical Students and Family Practice Residents.New York Medical College, Department of Family Medicine; 2003. Ac-

cessed January 2009 at www.nymc.edu/fammed/medicalerrors.pdf.13. Nunalee MM, Weedon GR. Modern trends in veterinary mal-practice: how our evolving attitudes toward non-human animals will change veterinary medicine. Animal Law 2004;10:125-161. Accessed January 2009 at www.animallaw.info/journals/jo_pdf/vol10_p125.pdf.14. Wilson JF. Limited legal liability in zoonotic cases. NAVC Clin Brief May 2005. Accessed January 2009 at www.cliniciansbrief.com/?p=articles&newsid=678. 15. O’Connell D, Bonvicini KA. Addressing disappointment in veterinary practice. Vet Clin North Am Small Anim Pract 2007;37(1):135-149.16. Bonvicini KA. Are clients truly informed? Communication tools and risk reduction. Compend Equine 2007;2(2):74-80.17. Mellanby RJ, Herrtage ME. Survey of mistakes made by recent veterinary graduates. Vet Rec 2004;155:761-765.18. Liebman CB, Hyman CS. A mediation skills model to man-age disclosure of errors and adverse events to patient. Health Aff 2004;23:22-32.19. Witman AB, Park DM, Hardin SB. How do patients want physi-cians to handle mistakes? A survey of internal medicine patients in an academic setting. Arch Intern Med 1996;156:2565-2569.20. Lazare A. Apology in medical practice: an emerging clinical skill. JAMA 2006;296(11):1401-1404.21. Blendon RJ, DesRoches CM, Brodie M, et al. Views of prac-ticing physicians and the public on medical errors. N Engl J Med2002;347(24):1933-1940.22. Reason J. Human Error. New York: Cambridge University Press; 1990.23. O’Connell D, Reifsteck SW. Disclosing unexpected outcomes and medical error. J Med Pract Manage 2004;19(6):317-323.24. Mazor KM, Simon SR, Gurwitz JH. Communicating with pa-tients about medical errors: a review of the literature. Arch Intern Med 2004;164:1690-1697.25. Question and answer. Sorry Works! Coalition Newsletter; De-cember 4, 2006. Accessed January 2009 at www.sorryworks.net/newsletter20061204.phtml.

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Establish Practice Protocol

How will the practice handle an error? Who will discuss it with the client? Who will be present during the discussion? Will individuals involved be identifi ed? What time frame do we recommend? Where is the contact information for our liability carrier? When and how will we discuss this with staff members?

BOX 3

l

n???

Letters


Five Common Toxins and Activated CharcoalI have a question for the author about his re-search for the November 2008 Pharm Profi le article, “Activated Charcoal.” The article states that charcoal is contraindicated for metalde-hyde ingestion. Yet it is widely accepted that it is proper protocol to give activated charcoal in these cases. In fact, in the article “Five Com-mon Toxins Ingested by Dogs and Cats” in the same issue, charcoal is recommended as an antidote to help eliminate metaldehyde. I am curious about the discrepancy. Also, I was wondering if there is any research on UAA gel, which is mentioned in the Pharm Profi le article.

Angela LeBrun, CVT

Puget Sound Veterinary Referral Center & Animal Emergency Clinic, Tacoma, Washington

I have just fi nished reading the November

2008 journal and am puzzled by the

contradiction between the paper by Drs.

Luiz and Heseltine and that by Dr. El

Bahri in reference to the effectiveness

of activated charcoal in the treatment of

ethylene glycol and metaldehyde poison-

ings. The former says to use it; the latter

says it’s ineffective. Is there an explana-

tion as to the correct information?

Philip T. Durfee, DVM, MPH, MVSc

The Authors’ RepliesThe administration of activated charcoal

in the treatment of metaldehyde intoxi-

cation is controversial. Several references

I consulted do not either include1,2 or

recommend3,4 the administration of acti-

vated charcoal in the treatment of met-

aldehyde intoxication. The Handbook

of Poisoning in Dogs and Cats, which

is considered a veterinary toxicology

reference, states, “Metaldehyde report-

edly does not bind to activated charcoal

and therefore use of adsorbents is not

indicated.”4 On the other hand, activated

charcoal has been shown to help inhibi-

tion of metaldehyde absorption in rats.5

Universal Animal Antidote (UAA) gel

(Vedco, Inc. St. Joseph, Missouri) con-

tains activated hardwood charcoal and

thermally activated attapulgite clay in

an aqueous gel suspension. The recom-

mended oral dosage is 1 to 3 mL/kg in

dogs, cats, and large animals. The manu-

facturer states that the product should

be shaken well before use and protected

from freezing.

Lotfi El Bahri, DVM, MSc, PhD

References1. Buck WB, Osweiler GD. Metaldehyde. In: Van Gelder GA, ed. Clinical and Diagnostic Veterinary Toxicology. 2nd ed. Dubuque, IA: Kendall/Hunt Publishing Compa-ny; 1976:227-228.2. Andreasen JR Jr. Metaldehyde toxicosis in duck-lings. J Vet Diagn Invest 1993;5:500-501.3. Booth NH, McDonald LE, eds. Veterinary Pharma-cology and Therapeutics. 5th ed. Ames: The Iowa State University Press; 1982:1013-1014.4. Campbell A. Metaldehyde. In: Campbell A, Chap-man M, eds. Handbook of Poisoning in Dogs and Cats. Oxford: Blackwell Science; 2000:181-185.5. Shintani S, Goto K, Endo Y, et al. Adsorption effects of activated charcoal on metaldehyde toxicity in rats. Vet Hum Toxicol 1999;41(1):15-18.

I double-checked our sources about the

use of activated charcoal in ethylene gly-

col and metaldehyde toxicoses. For eth-

ylene glycol, we wrote, “Early diagnosis

and treatment are critical for a successful

outcome. Emetics should be adminis-

tered if no signs are observed and the

exposure occurred less than 4 hours pre-

viously. Activated charcoal and a saline

cathartic may be given, although [ethyl-

ene glycol] is not signifi cantly adsorbed

by charcoal.” I verifi ed this information

with the sources cited in the article.1,2

I also gathered information from the

sixth edition of Ettinger’s Textbook of

Veterinary Internal Medicine,3 which

states to administer activated charcoal

for recent exposure (≤2 hr). The recom-

mendation we stated is conditional on

the duration of exposure.

For metaldehyde, we wrote, “If the

patient presents acutely, is alert, and

does not have excessive muscle tremors

or seizures, an emetic should be given,

followed by activated charcoal and a

cathartic.” Again, I verifi ed this statement

with the sources cited in the article4,5 as

well as The 5-Minute Veterinary Consult

by Tilley,6 which recommends emetics

or gastric lavage followed by adminis-

tration of activated charcoal to prevent

further absorption in animals with no

clinical signs.

Julie Ann Luiz, DVM

References1. Osweiler GD. Common household products. In: Nie-ginski EA, ed. The National Veterinary Medical Series:

COMPENDIUM 596 November 2008

Activated charcoal—also known as active carbon, activated carbon, adsorbent charcoal,medicinal charcoal, or carbo medicinalis1—is a carbon residue derived from vegetablematerial (e.g., wood pulp). It is produced by exposing the original material to an oxi-dizing gas compound of steam, oxygen, and acids at high temperatures (900°C). Thisactivation process creates a network of fine pores (10 to 20 nm in size) in the result-ing charcoal.2 The result is a highly porous material with an enormous surface arearelative to its weight.3 The adsorptive capacity of activated charcoal is a function ofits binding surface area. In commercial products, the surface area varies from 1000 to2000 m2 per gram.3,4

PHARMACOKINETICSActivated charcoal comes as a very fine, porous, black powder or granules measuringless than 1.0 mm in diameter. It does not contain any gritty material.2 It is insoluble inwater and all usual solvents.1 Activated charcoal is not absorbed in the gastrointestinaltract, and all ingested activated charcoal is excreted in the feces.1 It is a stool marker,indicating that the toxin has passed through the gastrointestinal tract and no furthersignificant toxin absorption from the original ingestion will occur.

PHARMACOLOGYOwing to its large surface area, activated charcoal can adsorb many drugs and toxins(e.g., acetaminophen, salicylates, digoxin, organophosphate and carbamate insecticides,pyrethrins and pyrethroids, anticoagulant rodenticides, strychnine) in the upper gas-trointestinal tract.1–3 It thereby facilitates the excretion of the adsorbed toxicant in thefeces and reduces the amount of free agent available for absorption into the blood-stream. Activated charcoal maintains its attachment to toxins through covalent bindingand van der Waals forces.5

Adsorption of substances onto charcoal is a reversible process, with rapid adsorptionand slow desorption. Optimal adsorption occurs when the ratio of charcoal to toxin is10:1 or higher.6 Administration of activated charcoal can lead to a 30% to 40% drop indigoxin levels within 12 to 18 hours.7 In one canine study, oral administration of acti-vated charcoal solution (2.5 g/kg) 30 minutes after a single oral dose of carprofen (16mg/kg) effectively decreased the maximum plasma carprofen concentration (85.9 ±11.9 mg/L to 58.1 ± 17.6 mg/L) by decreasing carprofen absorption in the gastroin-testinal tract.8 Elimination of substances that undergo enterohepatic recirculation (e.g.,NSAIDs, theobromine, cholecalciferol, tetrahydrocannabinol) may be enhanced byrepeated oral doses of activated charcoal.1,3

Activated Charcoal

Lotfi El Bahri, DVM, MSc, PhD

École Nationale de Médecine Vétérinaire

Sidi Thabet, Tunisia

Pharm Profile

Indication: Emergency treatment of acute poisoning after ingestion of a largeamount of toxin or drug.

Send comments/questions via email [email protected] fax 800-556-3288.

Visit CompendiumVet.com for full-text articles, CE testing, and CE test answers.

Pharm Profile focuses on

new drugs or indications in the

veterinary market as well as

pharmacologic products of high

interest to practitioners.

CONTINUES ON PAGE 114

Clinical Snapshot


SEE PAGE 104 FOR CASE PRESENTATION.

1. Scabies infestation. The organism is a Sarcoptes egg. One mite or egg is diagnostic for scabies. Defi nitive evidence of a scabies infestation (eggs or mites) is not always found, even in “classic cases.” Most dogs with scabies are diagnosed based on response to treatment; therefore, if scabies is suspected, it should be treated accordingly.

2. Scabies mites can live for a short period of time off the host. The kennel facilities should be thor-oughly cleaned with high-pressure water, scrubbed with detergent, and sprayed with an environmental par-asiticidal agent. All dogs in contact with these Great Danes should be treated for scabies. Lime sulfur dips once weekly for 6 weeks or amitraz dips every 2 weeks for 6 weeks are effective topical therapies. Lime sul-fur can be combined with ivermec-tin therapy. Ivermectin (200 μg/kg PO or SC) every 2 weeks for 6 weeks is also an effective treatment. I use a test dose of 100 μg/kg PO in all dogs. If there are no adverse effects consistent with ivermectin sensitiv-

ity (e.g., tremors, salivation) within 24 hours, I administer a full treatment dose of 200 μg/kg PO the next day.

Herding breeds of dogs, especially collies, are known to be sensitive to ivermectin. Thus, this drug is best avoided in collies. Dogs sensitive to ivermectin can often tolerate milbemycin oxime at 3 mg/kg PO weekly for 3 to 6 weeks. Lime sulfur dips are also an effective therapy. Doramectin at 0.2 mg/kg SC or IM has also been reported to be effective. Finally, two applications of selamectin or fi pronil at 30-day intervals may be effective. Selamectin is licensed for the treatment of scabies, and the manufacturer reported it to be effective in 70% of cases. Fipronil is not licensed for scabies treat-ment but has been found to be effective. It is important to remem-ber that no treatment is 100% effi -cacious in all patients. If scabies is suspected and the patient does not respond, retreatment with a differ-ent therapy should be performed before scabies is ruled out.

3. Canine scabies is not considered con-tagious to cats. However, Sarcoptes mites have been reported in a small number of cats with severe debilita-tion and in pruritic cats in England. There may be some geographic varia-tion with respect to contagion to cats. These cats do not need to be treated. True “feline scabies” is caused by Notoedres cati, a contagious mange mite. In contrast to canine scabies mites, N. cati is easily found in large numbers on skin scrapings. Lesions occur on the head, feet, and perineum. This infestation can cause large amounts of crust; cats should be sedated, the haircoat clipped, and the cats bathed to remove the contaminated crusts before treatment. Because cats are extremely sensitive to parasiticidal agents, lime sulfur and ivermectin are the most commonly used treatments. Affected cats, and all animals in con-tact with them, should be treated for at least 6 weeks.

Answers and Explanations Case Presentation #1 A B

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Letters

Toxicology. Philadelphia: Williams and Wilkins; 1996:317-328.2. Gaynor AR, Dhupa N. Acute ethyl-ene glycol intoxication. Part II. Compend Contin Educ Pract Vet 1999;21(12):1124-1133.3. Dorman DC, Dye JA. Chemical tox-icities. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. 6th ed. St. Louis: Elsevier Saunders; 2005:257-258.4. Richardson JA, Welch SL, Gwaltney-Brant SM, et al. Metaldehyde toxicoses in dogs. Compend Contin Educ Pract Vet 2003;25(5):376-380.5. Mull RL. Metaldehyde poisoning. In: Kirk RW, ed. Current Veterinary Therapy: Small Animal Practice VIII. London: WB Saunders; 1983:106-107.6. Tilley LP, Smith FWK Jr. The 5-Min-ute Veterinary Consult: Canine and Feline. 2nd ed. Philadelphia: Lippincott Williams & Wilkins;2000:958-959.

Editor’s note: Thank you to

the attentive readers who

pointed out the difference

between these articles and to

the authors for their clarifi ca-

tion. As in many aspects of

veterinary medicine, differ-

ent recommendations exist

based on clinical experience

and patient presentation ver-

sus laboratory chemistry, and

different references refl ect

these variations. Awareness

of both laboratory and clini-

cal data is useful when deter-

mining the most appropriate

treatment for an individual

patient.

CONTINUED FROM PAGE 113

It’s not just therapeutics!

This information has not been peer reviewed and does not necessarily reflect the opinionsof, nor constitute or imply endorsement or recommendation by, the Publisher or EditorialBoard. The Publisher is not responsible for any data, opinions, or statements provided herein.

C A S E i n B R I E F

Sponsored by

Probiotic Therapy Improves Chronic Feline DiarrheaChristy Evans Cutting, DVMCompanion Animal ClinicRoseburg, Oregon

Patient: Calliope, an 11-year-old domestic short-haired cat

History: In January 2004, Calliope presented with constipation. We administered twoenemas and prescribed 1 mL lactulose once every 12 to 24 hours. She did reason-ably well on lactulose for approximately 1 year, but the constipation returned. At thispoint, we increased the dose of lactulose to 1 mL every 8 hours, which worked untilJanuary 2006.

This time, the constipation didn’t respond to enemas, so we sedated Calliope formanual removal of the impacted feces. Unfortunately, she didn’t tolerate sedation well.She became hypothermic and almost comatose; intensive care, including intravenousfluids with corticosteroids, was needed to help pull her through. She slowly improvedover the next 3 days and began eating on the fourth day.

She was sent home but returned the next day with diarrhea and vomiting. I referredher owner to the nearest specialist for more involved diagnostics and treatment. Luck-ily they obliged—Calliope was diagnosed with an abnormal colon that required a partial colectomy 2 days later.

Calliope has had no more problems with constipation, but she developed diarrheafor 6 months following surgery.

Therapy Plan: After her surgery, I expected Calliope to have some loose stools, butwhen she presented with persistent diarrhea, I felt that her digestive system needed alittle help to restore its normal microflora balance. I recommended that we try Purina Veterinary Diets® FortiFlora® Feline Nutritional Supplement. I started sprinkling FortiFloraon her food each day. FortiFlora was definitely what she needed. Within the first week,she started eating more and her diarrhea resolved.

Eating has always been a challenge for Calliope; she’s very particular and will be-come anorectic if she doesn’t like a particular food. She’s small to begin with (6 lb),so we’re constantly watchful for any weight loss. Because Calliope’s digestive systemwas so delicate after surgery, maintaining her appetite was a priority for us and herowner. In addition, Calliope had lost a significantamount of weight, so we offered her a variety ofcommercial foods to encourage her to eat.

Outcome: Calliope really didn’t seem “better” untilwe started FortiFlora. Until recently, her owner wasgiving her the nutritional supplement daily because ifshe missed one dose, the diarrhea would return. Af-ter 2 years, her owner was able to discontinue FortiFlora, and Calliope is now eating well and doinggreat without any gastrointestinal problems!

Calliope

©Jeannine C

ook

Veterinarian’s CommentsI have been recommending Purina Veteri-nary Diets® FortiFlora® as a nutritionalsupplement for more than 2 years. I likeFortiFlora for several reasons: It’s conven-ient to dispense and administer, it’s easyon the GI tract, cats love the taste, and itworks! Calliope’s owner really feels that FortiFlora made the difference for her cat.

I commonly use the nutritional supple-ment in dogs and cats that develop milddiarrhea when receiving antibiotics. It’snice to have something to offer ownerswhen they call with this problem, withouthaving to change antibiotics or bring thepet back in for a recheck. I also com-monly use FortiFlora for pets with stressdiarrhea—It seems to work very well forthese cases.

I recommend that my veterinary col-leagues try FortiFlora. It’s easy to admin-ister; you just sprinkle the nutritional sup-plement on the pet’s food. It works fastand is so simple and effective!

Nestle_CaseinBrief-0309_PV.qxp:Masthead-Oct VT 05 2/27/09 11:20 AM Page 1

Understanding

Behavior Feline Hyperesthesia Syndrome*

About This ColumnBehavior problems are a signifi -cant cause of death (euthanasia) in companion animals. While most veterinary practices are necessarily geared toward the medical aspect of care, there are many opportuni-ties to bring behavior awareness into the clinic for the benefi t of the pet, the owner, and ourselves. This column acknowledges the importance of behavior as part of veterinary medicine and speaks practically about using it effectively in daily practice.

❯❯ John Ciribassi, DVM, DACVB Chicagoland Veterinary Behavior ConsultantsCarol Stream, Illinois

*Adapted with permission from John Ciribassi, DVM, and the Veterinary Information Network (VIN).

116 CompendiumVet.com | March 2009

Feline hyperesthesia syndrome (FHS) is known by several names, including rolling skin disease, neurodermatitis, neuritis, psychomotor epilepsy, and pru-

ritic dermatitis of Siamese.1,2 As evidenced by these names and by the use of the term syndrome, FHS is not characterized as having a single etiology. In fact, it is often a diagnosis of exclusion. The differential diagnosis for FHS includes diseases related to the fi elds of dermatology, neurology, and behavior. Only after conditions relating to skin and the nervous system have been ruled out can this condition be labeled a behavior disorder.

SignalmentFHS can occur in cats of any age, but it is commonly seen in cats aged 1 to 5 years. Males and females are equally affected. While all breeds can be affected, Siamese, Burmese, Persian, and Abyssinian cats are more commonly affl icted.3

Clinical SignsAs indicated by the name rolling skin disease, affected cats often show rippling or rolling skin along the lum-bar spine. Palpation of the lumbar musculature may elicit signs of pain. Mydriasis is common during bouts of FHS. Affected cats commonly stare at their tail, then attack the tail and/or fl anks. Biting of the tail base, forelegs, and paws is common. These cats often run wildly around the home, vocalizing at the same time. Normally calm cats may display aggression toward people or other cats in the household, while aggressive cats may display increased affection. The behavior may be induced by pet-ting or stroking the cat’s fur and most commonly occurs in the morning or later in the evening.2

DiagnosisThe differential diagnosis for FHS can be categorized by the type of clinical signs displayed:

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FHS can occur in cats of any age, but it is commonly seen in cats aged 1 to 5 years.

QuickNotes

Raising the level of care

Anna Worth, VMD 2008-2009 AAHA PresidentWest Mountain Veterinary HospitalBennington, VT

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Dermatologic: Flea allergy dermatitis, food allergy, atopy, infectious dermatitisNeurologic: Epilepsy, brain tumors, spinal disease (disk disease, neoplasia, infectious myelitis)

Musculoskeletal: Myositis, myopathyBehavioral: Compulsive disorder, displace-ment behavior

A minimum database to aid in diagnos-ing FHS should include a physical exami-nation, neurologic examination, complete blood count, serum chemistry profi le (espe-cially hepatic and renal function), urinalysis, and spinal radiography. Depending on these results, further diagnostics might include skin scraping, fungal culture, skin and/or muscle biopsy, spinal or cranial imaging (computed tomography or magnetic resonance imaging), electromyography, food trials, and pharma-ceutical trials (fl ea control, corticosteroids, antiseizure medication). The decision of which tests to run and in what order depends on the patience and fi nancial situation of the owner and the severity of the clinical signs. While running the gamut of tests is ideal, it may be more practical to use pharmaceuti-cal trials once the baseline database has been collected. I typically suggest a trial of fl ea control medication and, if there is no change, treatment with corticosteroids at antiinfl am-matory doses. If the patient does not respond to steroid treatment, treatment with an anti-seizure medication is indicated. Phenobarbital is my initial antiseizure drug of choice; some practitioners also use gabapentin. If none of the above approaches results in an improvement in the cat’s condition, then a presumed diagnosis of behavioral FHS can be made.

PathophysiologyFHS is commonly considered to be a com-pulsive disorder resulting in self-injurious behavior. One proposed trigger of FHS is displacement behavior. Displacement behav-ior occurs as an alternative to two other con-fl icting behaviors. An example might be a cat that wants to eat but is being prevented from doing so by an aggressive cat in the house-hold. The competing motivations, hunger and fear, cause the affected cat to want to simulta-neously perform the confl icting behaviors of eating and escaping. As a consequence, the cat might perform a species-appropriate, but

unrelated, behavior such as grooming. If this confl icting situation persists over a prolonged period, the cat may engage in the displace-ment behavior even when the competing motivations are no longer present. This is then defi ned as a compulsive behavior. The environmental factors that trigger compulsive behaviors exert their infl uence by stimulating the hypothalamus and the limbic system, which in turn activate motor activity through the basal ganglia. Three types of neu-rotransmitters are reported to be involved:

Dopamine. Increased dopamine levels can result in increased frequency of compulsive behaviors.Opiates. One theory is that when animals engage in compulsive behaviors, levels of opiates in the brain are elevated, and the pleasurable effects that opiates promote reinforce the behaviors. Another theory is that opiates initiate stereotypic behavior. This theory is based on the observation that administration of opioids enhances the dis-play of amphetamine-induced stereotypic behaviors, but these behaviors are blocked when narcotic antagonists (such as nalox-one) are administered.4

Serotonin. Serotonin is produced in the dor-sal raphe nucleus, and its infl uence on the basal ganglia and frontal cortex affects behav-iors such as compulsive disorders. Higher levels of serotonin reduce the incidence of compulsive disorders, which is the rationale for the use of selective serotonin reuptake inhibitors (SSRIs) to treat these disorders.

TreatmentSuccessful therapy is based on reasonable owner expectations and the ability to moni-tor the degree of improvement. This can be accomplished by recording the frequency and severity of signs of FHS during the treatment period.

Behavior Modifi cationAs with many behavior problems in compan-ion animals, the treatment of FHS combines behavior modifi cation protocols and the use of psychoactive pharmaceuticals. Behaviorally, the goal is to create a stable and consistent environment for the cat. This can be accom-plished in the following ways: Institute a regular feeding schedule to pro-vide a more predictable source of food.

Successful therapy is based on reasonable owner expectations and the ability to monitor the degree of improvement.

QuickNotes

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Behavior

SEVO-210

February 2009

©2009 Abbott Laboratories

• SevoFlo is only a few dollars more per procedure and with your normal

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from others.

• SevoFlo doesn’t irritate airways1 and is less of a respiratory depressant

than isoflurane2.

• SevoFlo has low blood:gas solubility and a greater range of vaporizer settings

to give veterinarians rapid, precise control over the depth of anesthesia.

For only a few dollars more* you get all of the benefits of SevoFlo.

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1 T Mutoh, A Kanamura, H Suzuki, H Tsubone, R Nishimura, N Sasaki. AJVR 2001:62:311-319

2 DS Galloway JCH Ko, HF Reaugh, RE Mandsager, ME Payton, T Inoue, E Portillo. JAVMA (2004) Vol 255, No 5, 700-704 * Per procedure.

Important Information: How Supplied: SevoFlo is packaged in amber colored bottles containing 250 mL sevoflurane. Indications:

SevoFlo is indicated for induction and maintenance of general anesthesia in dogs. Warnings, Precautions, and Contraindications:

Like other inhalation anesthetics, sevoflurane is a profound respiratory depressant. Respiration must be monitored closely in the dog

and supported when necessary with supplemental oxygen and/or assisted ventilation. Due to sevoflurane’s low solubility in blood,

increasing concentration may result in rapid hemodynamic changes compared to other volatile anesthetics. SevoFlo is contraindicated

in dogs with a known sensitivity to sevoflurane or other halogenated agents. Adverse Reactions: The most frequently reported adverse

reactions during maintenance anesthesia were hypotension, followed by tachypnea, muscle tenseness, excitation, apnea, muscle

fasciculations and emesis. See package insert for full prescribing information.

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Abbott_USE.qxp:1 2/18/09 9:30 AM Page 1

SevoFlo® 5458

(sevoflurane) Inhalation Anesthetic For Use in Dogs Caution: Federal law restricts this drug to use by or on the order of a licensed veterinarian. DESCRIPTION: SevoFlo (sevoflurane), a volatile liquid, is a halogenated general inhalation anesthetic drug. Its chemical name is fluoromethyl 2,2,2-trifluoro-l- (trifluoromethyl) ethyl ether, and its structural formula is:

Sevoflurane Physical Constants are: Molecular weight 200.05 Boiling point at 760 mm Hg 58.6°C Specific gravity at 20°C 1.520-1.525 g/mL Vapor pressure in mm Hg at 20°C 157 at 25°C 197 at 36°C 317 Distribution Partition Coefficients at 37°C: Blood/Gas 0.63-0.69 Water/Gas 0.36 Olive Oil/Gas 47-54 Brain/Gas 1.15 Mean Component/Gas Partition Coefficients at 25°C for Polymers Used Commonly in Medical Applications: Conductive rubber 14.0 Butyl rubber 7.7 Polyvinyl chloride 17.4 Polyethylene 1.3

Sevoflurane is nonflammable and nonexplosive as defined by the requirements of International Electrotechnical Commission 601-2-13. Sevoflurane is a clear, colorless, stable liquid containing no additives or chemical stabilizers. Sevoflurane is nonpungent. It is miscible with ethanol, ether, chloroform and petroleum benzene, and it is slightly soluble in water. Sevoflurane is stable when stored under normal room lighting condition according to instructions. INDICATIONS: SevoFlo is indicated for induction and maintenance of general anesthesia in dogs. DOSAGE AND ADMINISTRATION: Inspired Concentration: The delivered concentration of SevoFlo should be known. Since the depth of anesthesia may be altered easily and rapidly, only vaporizers producing predictable percentage concentrations of sevoflurane should be used. Sevoflurane should be vaporized using a precision vaporizer specifically calibrated for sevoflurane. Sevoflurane contains no stabilizer. Nothing in the drug product alters calibration or operation of these vaporizers. The administration of general anesthesia must be individualized based on the patient’s response. WHEN USING SEVOFLURANE, PATIENTS SHOULD BE CONTINUOUSLY MONITORED AND FACILITIES FOR MAINTENANCE OF PATENT AIRWAY, ARTIFICIAL VENTILATION, AND OXYGEN SUPPLEMENTATION MUST BE IMMEDIATELY AVAILABLE.Replacement of Desiccated CO2 Absorbents: When a clinician suspects that the CO2 absorbent may be desiccated, it should be replaced. An exothermic reaction occurs when sevoflurane is exposed to CO2 absorbents. This reaction is increased when the CO2 absorbent becomes desiccated (see PRECAUTIONS). Premedication: No specific premedication is either indicated or contraindicated with sevoflurane. The necessity for and choice of premedication is left to the discretion of the veterinarian. Preanesthetic doses for premedicants may be lower than the label directions for their use as a single medication.1Induction: For mask induction using sevoflurane alone, inspired concentrations up to 7% sevoflurane with oxygen are employed to induce surgical anesthesia in the healthy dog. These concentrations can be expected to produce surgical anesthesia in 3 to 14 minutes. Due to the rapid and dose dependent changes in anesthetic depth, care should be taken to prevent overdosing. Respiration must be monitored closely in the dog and supported when necessary with supplemental oxygen and/or assisted ventilation.Maintenance: SevoFlo may be used for maintenance anesthesia following mask induction using sevoflurane or following injectable induction agents. The concentration of vapor necessary to maintain anesthesia is much less than that required to induce it. Surgical levels of anesthesia in the healthy dog may be maintained with inhaled concentrations of 3.7-4.0% sevoflurane in oxygen in the absence of premedication and 3.3-3.6% in the presence of premedication. The use of injectable induction agents without premedication has little effect on the concentrations of sevoflurane required for maintenance. Anesthetic regimens that include opioid, alpha2-agonist, benzodiazepine or phenothiazine premedication will allow the use of lower sevoflurane maintenance concentrations. CONTRAINDICATIONS: SevoFlo is contraindicated in dogs with a known sensitivity to sevoflurane or other halogenated agents. WARNINGS: Sevoflurane is a profound respiratory depressant. DUE TO THE RAPID AND DOSE DEPENDENT CHANGES IN ANESTHETIC DEPTH, RESPIRATION MUST BE MONITORED CLOSELY IN THE DOG AND SUPPORTED WHEN NECESSARY WITH SUPPLEMENTAL OXYGEN AND/OR ASSISTED VENTILATION. In cases of severe cardiopulmonary depression, discontinue drug administration, ensure the existence of a patent airway and initiate assisted or controlled ventilation with pure oxygen. Cardiovascular depression should be treated with plasma expanders, pressor agents, antiarrhythmic agents or other techniques as appropriate for the observed abnormality. Due to sevoflurane’s low solubility in blood, increasing the concentration may result in rapid changes in anesthetic depth and hemodynamic changes (dose dependent decreases in respiratory rate and blood pressure) compared to other volatile anesthetics. Excessive decreases in blood pressure or respiratory depression may be corrected by decreasing or discontinuing the inspired concentration of sevoflurane. Potassium hydroxide containing CO2 absorbents (e.g. BARALYME®) are not recommended for use with sevoflurane. ADVERSE REACTIONS: The most frequently reported adverse reactions during maintenance anesthesia were hypotension, followed by tachypnea, muscle tenseness, excitation, apnea, muscle fasciculations and emesis. Infrequent adverse reactions include paddling, retching, salivation, cyanosis, premature ventricular contractions and excessive cardiopulmonary depression. Transient elevations in liver function tests and white blood cell count may occur with sevoflurane, as with the use of other halogenated anesthetic agents.

PRECAUTIONS: Halogenated volatile anesthetics can react with desiccated carbon dioxide (CO2) absorbents to produce carbon monoxide (CO) that may result in elevated carboxyhemoglobin levels in some patients. To prevent this reaction, sevoflurane should not be passed through desiccated soda lime or barium hydroxide lime. Replacement of Desiccated CO2 Absorbents: When a clinician suspects that the CO2 absorbent may be desiccated, it should be replaced before administration of sevoflurane. The exothermic reaction that occurs with sevoflurane and CO2 absorbents is increased when the CO2 absorbent becomes desiccated, such as after an extended period of dry gas flow through the CO2 absorbent canisters. Extremely rare cases of spontaneous fire in the respiratory circuit of the anesthesia machine have been reported during sevoflurane use in conjunction with the use of a desiccated CO2 absorbent, specifically those containing potassium hydroxide (e.g. BARALYME). Potassium hydroxide containing CO2 absorbents are not recommended for use with sevoflurane. An unusually delayed rise in the inspired gas concentration (decreased delivery) of sevoflurane compared with the vaporizer setting may indicate excessive heating of the CO2 absorbent canister and chemical breakdown of sevoflurane. The color indicator of most CO2 absorbent may not change upon desiccation. Therefore, the lack of significant color change should not be taken as an assurance of adequate hydration. CO2 absorbents should be replaced routinely regardless of the state of the color indicator.

The use of some anesthetic regimens that include sevoflurane may result in bradycardia that is reversible with anticholinergics. Studies using sevoflurane anesthetic regimens that included atropine or glycopyrrolate as premedicants showed these anticholinergics to be compatible with sevoflurane in dogs. During the induction and maintenance of anesthesia, increasing the concentration of sevoflurane produces dose dependent decreases in blood pressure and respiratory rate. Due to sevoflurane’s low solubility in blood, these changes may occur more rapidly than with other volatile anesthetics. Excessive decreases in blood pressure or respiratory depression may be related to depth of anesthesia and may be corrected by decreasing the inspired concentration of sevoflurane. RESPIRATION MUST BE MONITORED CLOSELY IN THE DOG AND SUPPORTED WHEN NECESSARY WITH SUPPLEMENTAL OXYGEN AND/OR ASSISTED VENTILATION. The low solubility of sevoflurane also facilitates rapid elimination by the lungs. The use of sevoflurane in humans increases both the intensity and duration of neuromuscular blockade induced by nondepolarizing muscle relaxants. The use of sevoflurane with nondepolarizing muscle relaxants has not been evaluated in dogs. Compromised or debilitated dogs: Doses may need adjustment for geriatric or debilitated dogs. Because clinical experience in administering sevoflurane to dogs with renal, hepatic and cardiovascular insufficiency is limited, its safety in these dogs has not been established. Breeding dogs: The safety of sevoflurane in dogs used for breeding purposes, during pregnancy, or in lactating bitches, has not been evaluated. Neonates: The safety of sevoflurane in young dogs (less than 12 weeks of age) has not been evaluated. HUMAN SAFETY: Not for human use. Keep out of reach of children. Operating rooms and animal recovery areas should be provided with adequate ventilation to prevent the accumulation of anesthetic vapors. There is no specific work exposure limit established for sevoflurane. However, the National Institute for Occupational Safety and Health has recommended an 8 hour time-weighted average limit of 2 ppm for halogenated anesthetic agents in general. Direct exposure to eyes may result in mild irritation. If eye exposure occurs, flush with plenty of water for 15 minutes. Seek medical attention if irritation persists. Symptoms of human overexposure (inhalation) to sevoflurane vapors include respiratory depression, hypotension, bradycardia, shivering, nausea and headache. If these symptoms occur, remove the individual from the source of exposure and seek medical attention. The material safety data sheet (MSDS) contains more detailed occupational safety information. For customer service, adverse effects reporting, and/or a copy of the MSDS, call (888) 299-7416. CLINICAL PHARMACOLOGY: Sevoflurane is an inhalational anesthetic agent for induction and maintenance of general anesthesia. The Minimum Alveolar Concentration (MAC) of sevoflurane as determined in 18 dogs is 2.36%.2 MAC is defined as that alveolar concentration at which 50% of healthy patients fail to respond to noxious stimuli. Multiples of MAC are used as a guide for surgical levels of anesthesia, which are typically 1.3 to 1.5 times the MAC value. Because of the low solubility of sevoflurane in blood (blood/gas partition coefficient at 37°C = 0.63-0.69), a minimal amount of sevoflurane is required to be dissolved in the blood before the alveolar partial pressure is in equilibrium with the arterial partial pressure. During sevoflurane induction, there is a rapid increase in alveolar concentration toward the inspired concentration. Sevoflurane produces only modest increases in cerebral blood flow and metabolic rate, and has little or no ability to potentiate seizures.3Sevoflurane has a variable effect on heart rate, producing increases or decreases depending on experimental conditions.4,5 Sevoflurane produces dose-dependent decreases in mean arterial pressure, cardiac output and myocardial contraction.6 Among inhalation anesthetics, sevoflurane has low arrhythmogenic potential.7 Sevoflurane is chemically stable. No discernible degradation occurs in the presence of strong acids or heat. Sevoflurane reacts through direct contact with CO2 absorbents (soda lime and barium hydroxide lime) producing pentafluoroisopropenyl fluoromethyl ether (PIFE, C4H2F6O),also known as Compound A, and trace amounts of pentafluoromethoxy isopropyl fluoromethyl ether (PMFE, C5H6F6O), also known as Compound B. Compound A: The production of degradants in the anesthesia circuit results from the extraction of the acidic proton in the presence of a strong base (potassium hydroxide and/or NaOH) forming an alkene (Compound A) from sevoflurane. Compound A is produced when sevoflurane interacts with soda lime or barium hydroxide lime. Reaction with barium hydroxide lime results in a greater production of Compound A than does reaction with soda lime. Its concentration in a circle absorber system increases with increasing sevoflurane concentrations and with decreasing fresh gas flow rates. Sevoflurane degradation in soda lime has been shown to increase with temperature. Since the reaction of carbon dioxide with absorbents is exothermic, this temperature increase will be determined by the quantities of CO2 absorbed, which in turn will depend on fresh gas flow in the anesthetic circle system, metabolic status of the patient and ventilation. Although Compound A is a dose-dependent nephrotoxin in rats, the mechanism of this renal toxicity is unknown. Two spontaneously breathing dogs under sevoflurane anesthesia showed increases in concentrations of Compound A as the oxygen flow rate was

decreased at hourly intervals, from 500 mL/min (36 and 18 ppm Compound A) to 250 mL/min (43 and 31 ppm) to 50 mL/min (61 and 48 ppm).8Fluoride ion metabolite: Sevoflurane is metabolized to hexafluoroisopropanol (HFIP) with release of inorganic fluoride and CO2. Fluoride ion concentrations are influenced by the duration of anesthesia and the concentration of sevoflurane. Once formed, HFIP is rapidly conjugated with glucuronic acid and eliminated as a urinary metabolite. No other metabolic pathways for sevoflurane have been identified. In humans, the fluoride ion half-life was prolonged in patients with renal impairment, but human clinical trials contained no reports of toxicity associated with elevated fluoride ion levels. In a study in which 4 dogs were exposed to 4% sevoflurane for 3 hours, maximum serum fluoride concentrations of 17.0-27.0 mcmole/L were observed after 3 hours of anesthesia. Serum fluoride fell quickly after anesthesia ended, and had returned to baseline by 24 hours post-anesthesia. In a safety study, eight healthy dogs were exposed to sevoflurane for 3 hours/day, 5 days/week for 2 weeks (total 30 hours exposure) at a flow rate of 500 mL/min in a semi-closed, rebreathing system with soda lime. Renal toxicity was not observed in the study evaluation of clinical signs, hematology, serum chemistry, urinalysis, or gross or microscopic pathology. DRUG INTERACTIONS: In the clinical trial, sevoflurane was used safely in dogs that received frequently used veterinary products including steroids and heartworm and flea preventative products. Intravenous Anesthetics: Sevoflurane administration is compatible with barbiturates, propofol and other commonly used intravenous anesthetics. Benzodiazepines and Opioids: Benzodiazepines and opioids would be expected to decrease the MAC of sevoflurane in the same manner as other inhalational anesthetics. Sevoflurane is compatible with benzodiazepines and opioids as commonly used in surgical practice. Phenothiazines and Alpha2-Agonists: Sevoflurane is compatible with phenothiazines and alpha2- agonists as commonly used in surgical practice. In a laboratory study, the use of the acepromazine/oxymorphone/ thiopental/sevoflurane anesthetic regimen resulted in prolonged recoveries in eight (of 8) dogs compared to recoveries from sevoflurane alone. CLINICAL EFFECTIVENESS: The effectiveness of sevoflurane was investigated in a clinical study involving 196 dogs. Thirty dogs were mask-induced with sevoflurane using anesthetic regimens that included various premedicants. During the clinical study, one hundred sixty-six dogs received sevoflurane maintenance anesthesia as part of several anesthetic regimens that used injectable induction agents and various premedicants. The duration of anesthesia and the choice of anesthetic regimens were dependent upon the procedures that were performed. Duration of anesthesia ranged from 16 to 424 minutes among the individual dogs. Sevoflurane vaporizer concentrations during the first 30 minutes of maintenance anesthesia were similar among the various anesthetic regimens. The quality of maintenance anesthesia was considered good or excellent in 169 out of 196 dogs. The table shows the average vaporizer concentrations and oxygen flow rates during the first 30 minutes for all sevoflurane maintenance anesthesia regimens:

Average Vaporizer

Concentrationsamong

Anesthetic Regimens

Average Vaporizer

Concentrationsamong

IndividualDogs

Average Oxygen

Flow Ratesamong

Anesthetic Regimens

Average Oxygen

Flow Ratesamong

IndividualDogs

3.31 - 3.63% 1.6 - 5.1% 0.97 - 1.31 L/minute

0.5 - 3.0 L/minute

During the clinical trial, when a barbiturate was used for induction, the times to extubation, sternal recumbency and standing recovery were longer for dogs that received anesthetic regimens containing two preanesthetics compared to regimens containing one preanesthetic. Recovery times were shorter when anesthetic regimens used sevoflurane or propofol for induction. The quality of recovery was considered good or excellent in 184 out of 196 dogs. Anesthetic regimen drug dosages, physiological responses, and the quality of induction, maintenance and recovery were comparable between 10 sighthounds and other breeds evaluated in the study. During the clinical study there was no indication of prolonged recovery times in the sighthounds. HOW SUPPLIED: SevoFlo (sevoflurane) is packaged in amber colored bottles containing 250 mL sevoflurane, List 5458. STORAGE CONDITIONS: Store at controlled room temperature 15°-30°C (59°-86°F). REFERENCES:1. Plumb, D.C. ed., Veterinary Drug Handbook, Second Edition, University of Iowa Press, Ames, IA: p. 424 (1995). 2. Kazama, T. and Ikeda, K., Comparison of MAC and the rate of rise of alveolar concentration of sevoflurane with halothane and isoflurane in the dog. Anesthesiology. 68: 435-437 (1988). 3. Scheller, M.S., Nakakimura, K., Fleischer, J.E. and Zornow, M.H., Cerebral effects of sevoflurane in the dog: Comparison with isoflurane and enflurane. Brit. J. Anesthesia 65: 388-392 (1990). 4. Frink, E.J., Morgan, S.E., Coetzee, A., Conzen, P.F. and Brown, B.R., Effects of sevoflurane, halothane, enflurane and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs. Anesthesiology 76: 85-90 (1992). 5. Kazama, T. and Ikeda, K., The comparative cardiovascular effects of sevoflurane with halothane and isoflurane. J. Anesthesiology 2: 63-8 (1988). 6. Bernard, J. M., Wouters, P.F., Doursout, M.F., Florence, B., Chelly, J.E. and Merin, R.G., Effects of sevoflurane on cardiac and coronary dynamics in chronically instrumented dogs. Anesthesiology 72: 659-662 (1990). 7. Hayaski, Y., Sumikawa, K., Tashiro, C., Yamatodani, A. and Yoshiya, I., Arrhythmogenic threshold of epinephrine during sevoflurane, enflurane and isoflurane anesthesia in dogs. Anesthesiology 69: 145-147 (1988). 8. Muir, W.W. and Gadawski, J., Cardiorespiratory effects of low-flow and closed circuit inhalation anesthesia, using sevoflurane delivered with an in-circuit vaporizer and concentrations of compound A. Amer. J. Vet. Res. 59 (5): 603-608 (1998).

NADA 141-103, Approved by FDA SevoFlo® is a registered trademark of Abbott Laboratories.

Manufactured by Abbott Laboratories, North Chicago, IL 60064, USA Product of Japan

Under license from Maruishi Pharmaceutical Co., LTD 2-3-5, Fushimi-Machi, Chuo-Ku, Osaka, Japan

For customer service call (888) 299-7416.

©Abbott 8/2006 Taken from Commodity Number 03-5474/R6, SevoFlo, sevoflurane, package insert, January 11, 2007

SEVO-152 January 2007 page 1 of 1 ©2007 Abbott Laboratories

Abbott_USE.qxp:1 2/18/09 9:31 AM Page 2


Maintain consistency in interactions with the cat. When managing dogs with a compulsive disorder, one common recommendation is for the owners to use a command–response–reward technique for all interactions. For example, the owner asks the dog to sit and, after the dog obeys, gives it a treat. The same technique can be used with cats. Provide regular play sessions using target-type toys (e.g., feather toys). Anticipate situations that trigger the behavior. When the behavior is likely to occur, redirect the cat’s activity to more appropriate behav-iors, such as training exercises or play.3,5

FHS behaviors should not be punished be cause punishment will increase the cat’s con-fl ict and stress, resulting in a likely increase in the problem behaviors.

Pharmaceutical InterventionThere are no US Food and Drug Administration–approved medications for treating FHS or any other compulsive disorder in pets. Con-sequently, owners should be informed of the potential risks as well as the possible benefi ts of the use of behavior medications. It is always wise to conduct appropriate laboratory testing to confi rm normal hepatic and renal function before prescribing these medications, which are metabolized and eliminated by the liver and kidneys. It is also helpful to repeat test-ing approximately 4 weeks after instituting therapy to evaluate the medication’s effect on organ (particularly hepatic) function. The three main classes of med ications used to treat FHS are SSRIs, tricyclic antidepressants (TCAs), and benzodiazepines. When using any of these medications in cats, it is best to begin at the lower end of the dose range, then titrate upward as needed to achieve the desired response. This approach minimizes the poten-tial for serious side effects such as prolonged anorexia or excessive sedation. Once the frequency of the behavior reaches an acceptable level, treatment should be maintained for 4 to 6 months. The dose can then be gradually reduced (25% reduction every 1 to 2 weeks) until the patient has been weaned off the drug. If the behavior recurs or increases in frequency during the weaning process, the previously effective dose should be reinstituted. Another reduction may be attempted after another 4 to 6 months of ther-apy; however, some patients require lifelong

administration of the medication. If the patient is receiving combination therapy (an SSRI or TCA with a benzodiazepine), the medications should be weaned one at a time to determine which drug is responsible if signs return as the dose is reduced.

Selective Serotonin Reuptake Inhibitors The following dosages are recommended for cats with FHS6:

Fluoxetine: 0.5 to 2.0 mg/kg PO q24hParoxetine: 0.5 to 1.0 mg/kg PO q12–24h

The adverse effects of SSRIs include seda-tion, anorexia, irritability, vomiting, and diar-rhea. In addition, SSRIs inhibit the function of the liver cytochrome P450 enzymes CYP2C9, CYP2D6, CYP2C19, and CYP3A4. As a conse-quence, care should be taken when prescrib-ing concurrent medications that rely on these enzymes for their metabolism (e.g., pheno-barbital, carbamazepine, benzodiazepines, TCAs). SSRIs should not be used in combina-tion with each other or with other drugs that increase serotonin levels, such as monoam-ine oxidase inhibitors (e.g., selegiline), other SSRIs (e.g., paroxetine, sertraline), or TCAs (e.g., amitriptyline, imipramine, doxepin).

Tricyclic AntidepressantsOf the TCAs, clomipramine (0.5 to 1.0 mg/kg PO q24h)7 can be used to treat FHS. Adverse effects associated with this drug include sedation, anticholinergic effects, potentiation of arrhythmias in predisposed patients, and lowering of the seizure threshold in patients with seizure disorders.

BenzodiazepinesThe following dosages8 are recom-mended for cats with FHS. These benzodiazepines are recommended in cats because they do not have active metabolites. Diazepam has been impli-cated in cases of hepatic necrosis in cats.Lorazepam: 0.125 to 0.50 mg PO q8–24h Oxazepam: 0.20 to 0.50 mg/kg PO q12–24h

The potential adverse effects of these drugs include sedation, ataxia, and temperament changes. Combination therapy with an SSRI or a TCA is acceptable with either of these drugs if no agent alone provides suffi cient response.

Understanding

Behavior

FHS behaviors should not be punished because punishment will increase the cat’s confl ict and stress, resulting in a likely increase in the problem behaviors.

QuickNotes

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CE Article 1

Vomiting

Emesis, or vomiting, is one of the most common reasons dogs and cats present for medical evalua-

tion.1 Vomiting is often associated with mild, self-limiting diseases that resolve with minimal diagnostic tests and therapy. However, it can be related to debilitating conditions that have life-threatening con-sequences. The history obtained from the client should be as detailed as possible because historical details are often helpful in selecting the appropriate treatment and diagnostic plan. Questions to ask during the history should include onset of vomit-ing, duration of clinical signs, type and frequency of vomiting, relation to food ingestion, characteristics of the vomited contents, diet history, and environment. Questions about known medical condi-tions and current therapies are also per-tinent because these factors may play an active role in the inciting cause.

The Vomiting Refl exPathophysiologyVomiting is a refl ex act that is mediated neurologically by the activation of the bilateral nucleus tractus solitarii, or emetic center, situated in the parvicellular reticu-lar formation in the lateral region of the medulla oblongata. This is the area that initiates, controls, regulates, and orga-nizes the vomiting refl ex.2–5

Vomiting can be triggered by both neural and humoral pathways.2 The neu-ral pathway comprises six fundamental

components. The emetic center (1)2,6–12 receives input from (2) the gastrointestinal tract (afferent neurons),2,7–11,13 (3) the higher centers of the brain,2,7–9,13 (4) the vestibu-lar apparatus,2,6–13 and (5) the CRTZ.2,6–13 Finally, to coordinate the vomiting refl ex, the vomiting center sends signals through (6) the efferent motor neurons.7,8,10 The vagal and sympathetic afferent neurons originate from the gastrointestinal tract, particularly the duodenum, as well as other areas, including the urinary and reproductive system, liver, pancreas, peri-toneum, and cardiac vessels. Stimulation of these neurons initiates the impulse that travels directly to the emetic center. The higher centers of the brain, including the cerebral cortex and the limbic system, can trigger emesis through three mechanisms: direct stimulation of the vomiting center by infl ammatory diseases, hydrocephalus, or neoplasia; psychogenic stimulation caused by fear, stress, excitement, or pain; and trau-matic stimulation related to head injuries and increased intracranial pressure.7,9 The CRTZ is a bilateral set of centers in the brainstem, located on the fl oor of the fourth ventricle. It possesses free nerve end-ings that maintain direct contact with the cerebrospinal fl uid via ependymal pores or the sheath surrounding fenestrated capil-laries.9,14 These free nerve endings are acti-vated by the vestibular system or through the humoral pathway by conditions affect-ing the blood or cerebrospinal fl uid (e.g., drug administration, infection, osmolar

❯❯ Héctor J. Encarnación, DVMGulf Coast Veterinary SpecialistsHouston, Texas

❯❯ Joshua Parra, DVMFlorida Veterinary Referral Center and 24-Hour Emergency and Critical Care HospitalEstero, Florida

❯❯ Erick Mears, DVM, DACVIMValerie Sadler, DVM, DACVRFlorida Veterinary Specialists and Cancer Treatment CenterTampa, Florida

3 CECREDITS

The Vomiting Refl ex Page 122

Antiemetics Page 124

Vomiting Refl ex Components, Receptors, and Controlling Neurotransmitters and Medications

Page 125

Most Common Antiemetics Used in Small Animal Medicine

Page 127

Treatment of Common Vomiting Conditions

Page 128

Most Common Causes of Vomiting in Dogs and Cats

Page 129

At a Glance


Abstract: Vomiting is the forceful expulsion of stomach contents through the mouth, caused by humoral stimulation of the chemoreceptor trigger zone (CRTZ) or neural stimulation of the emetic center. The CRTZ is activated and controlled by neurotransmitter manipulation at the receptor level. Clinical signs preceding vomiting may include ptyalism, tachycardia, depression, hiding, and yawning. Gastritis, gastrointestinal ulceration, pancreatitis, motion sickness, uremia, chemo-therapy, and drug administration are common initiating causes of vomiting. This article reviews the anatomic and physiologic aspects of the vomiting refl ex and its neurotransmitters, associated receptors, and rational management.

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VomitingFREE

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and acid–base disorders, electrolyte derangements, metabolic diseases).15 Finally, to initiate the vomiting refl ex, efferent motor signals must be transmitted to the upper gastro-intestinal tract through the sensory aspect of cranial nerves V, VII, IX, X, and XII and to the diaphragm and abdominal muscles via the spi-nal nerves.8

AnatomyThe act of vomiting is composed of three phases: nausea, retching, and expulsion of proximal duodenal and gastric contents.6,7,16 Nausea is the conscious recognition of sub-conscious excitation in an area of the medulla that is closely associ-ated with the vomiting center. This excitation is caused by irritative impulses coming from the gastroin-testinal tract, lower brain, or cerebral cortex.15,17–19 Ptyalism, tachycardia, nervousness, hiding or seeking attention, shivering, and yawning are all characteristic signs of nau-sea triggered by general activation of the sympathetic and parasympa-thetic branches of the autonomic nervous system. Hypersalivation stimulates swallowing, which stimu-lates relaxation of the gastroesopha-geal sphincter. The bicarbonate-rich saliva secreted by the salivary glands in the mouth lubricates the esopha-gus and helps neutralize the stom-ach’s acidic environment before vomiting.8,13 Before retching, abo-ral gastric and esophageal motility diminishes and the lower esopha-geal and pyloric sphincters relax. Retching is the second phase of vomiting and begins with the onset of a retrograde giant contraction.20,21

This contraction is a single-phase, ret-rograde, peristaltic motion that emp-ties the proximal duodenal contents into the stomach.20–22 It is followed by deep inspiratory movements, force-ful contractions of the abdominal muscles and diaphragm, and closure of the glottis. These actions produce

negative intrathoracic pressure and positive intraabdominal pressure, facilitating the movement of gastric contents into the esophagus. Before expulsion, the respiratory center is inhibited and the nasopharynx and glottis close to prevent pulmonary aspiration and nasal regurgitation of the gastric contents. The third and last phase of vomiting is the expul-sion of stomach contents through the mouth.

AntiemeticsAntiemetics are drugs that block the vomiting refl ex9,23,24 by impeding neurotransmission at central (CRTZ, emetic center) and peripheral (gas-trointestinal epithelium) recep-tor sites. These drugs are classifi ed based on the type of receptor they block (TABLE 1). However, antiemet-ics have the potential to prolong gas-trointestinal infections, predispose patients to such infections, and pre-vent toxin elimination by decreas-ing gastrointestinal motility. The use of most of these drugs in animals is off-label, and some dosages are extrapolated from the human medi-cal literature (TABLE 2).

PhenothiazinesPhenothiazines are broad-spec-trum antiemetics that have antido-paminergic and antihistaminergic properties at low doses in the CRTZ and anticholinergic effects at higher doses at other central sites, including the emetic center.9 These drugs also block norepinephrine at peripheral α-adrenergic recep-tors. Drugs in this group include chlorpromazine, prochlor perazine, and acetylpromazine. Common adverse effects in small animals, especially dogs, include ataxia, hypotension, and excessive seda-tion. Generalized central nervous system (CNS) stimulation, aggres-siveness, violent behavior, extrapy-ramidal effects, and seizures are rare. Fluid therapy is indicated in

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Vomiting is a neuro-logically mediated refl ex that depends on neural or humoral activation of the emetic center.

QuickNotes

TABLE 1 Vomiting Refl ex Components, Receptors, and Controlling Neurotransmitters and Medications

Receptor Receptor Agonists Receptor Antagonists

Chemoreceptor trigger zone

D2-Dopaminergic Dopamine Metoclopramide Prochlorperazine Haloperidol Trimethobenzamide Acetylpromazine Droperidol Chlorpromazine

M1-Cholinergic Acetylcholine Propantheline Chlorpromazine Methscopolamine Isopropamide Scopolamine Acetylpromazine Prochlorperazine

H1-Histaminergic Histamine Diphenhydramine Prochlorperazine Acetylpromazine Dimenhydrinate Chlorpromazine Promethazine Meclizine

α2-Adrenergic Norepinephrine Prochlorperazine Yohimbine Chlorpromazine Acetylpromazine

5-HT3-Serotonergic Serotonin Ondansetron Mirtazapine Metoclopramide Dolasetron Propofol Granisetron

ENKμ,δ-Enkephalinergic Met-enkephalin Leu-enkephalin

Butorphanol

Neurokinin-1 antagonist Substance P Maropitant

Emetic center

5-HT1A-Serotonergic Serotonin Diphenhydramine Dimenhydrinate Meclizine

α2-Adrenergic Norepinephrine Prochlorperazine Chlorpromazine Yohimbine

Glucocorticoid receptors Dexamethasone Cyproterone Mifepristone


Vestibular apparatus


H1-Histaminergic Histamine Diphenhydramine Prochlorperazine Cyclizine Dimenhydrinate Chlorpromazine Promethazine Meclizine Diazepam

Vagal afferents

5-HT3-Serotonergic Serotonin Ondansetron Mirtazapine Granisetron Dolasetron Metoclopramide


Vagal efferents

D2-Dopaminergic Dopamine Metoclopramide Prochlorperazine Haloperidol Trimethobenzamide Acetylpromazine Droperidol Chlorpromazine

5-HT4-Serotonergic CisaprideMetoclopramideSerotonin

Piboserod


Motilin ErythromycinMotilin

—

patients undergoing phenothiazine therapy because of the vasodilatory properties of these drugs.

Anticholinergics Anticholinergic drugs block cholinergic afferent pathway transmission from the gastrointesti-nal tract (peripheral action) and the vestibular system to the emetic center (central action).9

Scopolamine and isopropamide are centrally act-ing anticholinergics that cross the blood–brain

barrier. They have a short duration of action and can cause excitement in cats. Peripherally acting anticholinergics include propantheline and methscopolamine. Isopropamide and pro-pantheline are the drugs in this group that are most commonly used in small animals for vom-iting related to motion sickness.25 Side effects reported in humans and small animals include xerostomia (dry mouth), sedation, visual distur-bances, drowsiness, dysphoria, confusion, gas-trointestinal ileus, and disorientation.9,26

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AntihistaminesAntihistamines can intercept cholinergic and histaminic nerve transmission responsible for vestibular stimulation of the vomiting center.25 Drugs in this classifi cation include diphen-hydramine, dimenhydrinate, and meclizine. These drugs display H

1-antihistaminergic

properties and are mainly used to control the clinical signs of motion sickness. Mild seda-tion, xerostomia, and drowsiness are some of the adverse effects. Meclizine can be terato-genic if administered at high doses.25 Cats do not have histamine receptors in the CRTZ, and antihistaminic drugs do not control their vomiting.27

Serotonin AntagonistsSerotonin antagonists are specifi c inhibitors of 5-HT-serotonergic receptors. They control vomiting by acting on receptors located on the periphery of vagal nerve terminals and centrally on the CRTZ.25,26 These receptors are normally stimulated by serotonin released from the enterochromaffi n cells of the small intestine in response to damage to the gastro-intestinal mucosa. Ondansetron, a member of this class of antiemetic drugs, has been shown to control vomiting in dogs28,29 and is used in dogs receiving radiation and chemotherapy when metoclopramide and other antiemet-ics fail to control vomiting.28,29 Dolasetron, another member of this group, acts on recep-tors in the CRTZ.25 Both of these drugs are used extensively in human medicine, and they seem to be safe antiemetic alternatives in veterinary medicine.30,31 However, they are not effective in controlling vomiting caused by motion sickness.25,26

Side effects of these drugs that have been reported in people include electrocardiographic changes, including PR and QT prolongation and QRS widening, that are believed to be caused by sodium channel blockage by dolasetron metabolites. Diarrhea, headache, dizziness, and musculoskeletal pain have been reported as well. These medications can be expensive.

Substituted BenzamidesSubstituted benzamides exert antiemetic effects through different mechanisms. Some, such as metoclopramide and trimethobenzamide, antag-onize dopamine receptors in the CNS and block 5-HT

3-serotonergic receptors when administered

at high concentrations.9,25 Metoclopramide is known for its potent dopaminergic antagonism, but trimethobenzamide, which is also a weak antihistamine, has not been a very effective anti-dopaminergic agent clinically. Metoclopramide has more action on D

2-dopaminergic recep-

tors than trimethobenzamide and is 20 times more potent than phenothiazines.7 As a result, metoclopramide should not be used in patients receiving dopamine.12 Cisapride, another substituted benzamide, activates neuronal 5-HT

4 receptors, which

facilitates gastric emptying. Metoclopramide also activates neuronal 5-HT

4 receptors

and blocks 5-HT3-serotonergic receptors,

increases the lower esophageal sphincter tone, and enhances aboral gastrointestinal motility; therefore, these drugs are classi-fi ed as prokinetics as well.9 Adverse effects of these drugs include CNS excitement and behavioral changes, especially during rapid intravenous administration or if given at high doses. Metoclopramide controls peripherally induced and humorally mediated vomiting due to numerous conditions, but it should be avoided if gastrointestinal obstruction is suspected because its prokinetic properties could predispose these patients to gastric or intestinal perforation. This contraindication also applies to cisapride.

Butyrophenone and Benzimidazole Derivatives

Butyrophenone derivatives (e.g., haloperidol, droperidol) are potent dopamine antagonists in the CRTZ and are used as tranquilizers.9 Their side effects are very similar to those of phenothiazines. The benzimidazole deriva-tives antagonize dopamine receptors in the gastrointestinal smooth muscle and display prokinetic properties like those of metoclo-pramide,32 but their use in veterinary medicine is minimal if any.

OpioidsEnkephalins—endogenous opiates belong-ing to the endorphin family—are believed to have antiemetic properties. Neurons containing enkephalins have been identifi ed near the CRTZ and the emetic center.33 Evidence suggests that opioid κ and/or μ receptors are present in the vomiting center and are involved in inhibition of emesis in dogs and cats.34 Butorphanol, a pri-

Antiemetics are drugs that block specifi c superfi cial cell receptor sites, consequently dis-rupting the vomiting refl ex.

QuickNotes

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TABLE 2 Most Common Antiemetics Used in Small Animal Medicine

Drugs Site of Action Dosage Side Effects

α2-Adrenergic antagonists

Prochlorperazinea,13 CRTZ and emetic center Dogs and cats: 0.1–0.5 mg/kg SC or IM q6–8h Hypotension, sedation

Chlorpromazinea,2,13 CRTZ and emetic center Dogs: 0.1–0.5 mg/kg SC, IM, or IV q6–8hCats: 0.2–0.5 mg/kg SC, IM, or IV q6–8h

Hypotension, sedation

Yohimbinea,2 CRTZ and emetic center Dogs: 0.25–0.5 mg/kg SC or IM q12h Hypotension, sedation

D2-Dopaminergic antagonists

Metoclopramidea,2,13 CRTZ, GI smooth muscle Dogs: 0.1–0.4 mg/kg PO, SC, or IM q6hCats: 0.2–0.4 mg/kg PO, or SC q6–8h CRI: 1–2 mg/kg/day

Extrapyramidal signs, constipation

Trimethobenzamide2,13 CRTZ Dogs: 3 mg/kg IM q8–12h Allergic reactions

H1-Histaminergic antagonists

Diphenhydraminea,2,13 CRTZ Dogs and cats: 2–4 mg/kg PO or IM q8h Sedation, GI effects

Dimenhydrinatea,2,13 CRTZ Dogs and cats: 4–8 mg/kg PO q8h Sedation, GI effects

Meclizinea CRTZ Dogs and cats: 4 mg/kg PO q24h Sedation, xerostomia, tachycardia

M1-Cholinergic antagonists

Propanthelinea Parasympathetic nervous system Dogs and cats: 0.25 mg/kg PO q8h Gastric retention, ileus, tachycardia

Isopropamideb Parasympathetic nervous system Dogs and cats: 0.2–0.4 mg/kg PO q8–12h Gastric retention, ileus, tachycardia

5-HT3-Serotonergic antagonists

Ondansetrona,2 CRTZ and vagal afferent neurons Dogs: 0.11–0.176 mg/kg slow IV push q24hCats: 0.1–0.15 mg/kg slow IV push q24h

Sedation

Dolasetrona CRTZ Dogs: 0.6 mg/kg IV q24h or 0.5 mg/kg PO, SC, or IV q24hCats: 0.6 mg/kg IV q12h or 0.6–1 mg/kg PO q12h

Electrocardiogram changes

Mirtazapinea CRTZ and vagal afferent neurons Dogs: 0.6 mg/kg PO q24h, not to exceed 30 mg/dayCats: 3–4 mg/cat PO q72h

Sedation, ataxia, depression, vocalization

NK1-Neurokinin antagonist

Maropitant40 CRTZ and emetic center Dogs: 1 mg/kg SC q24h up to 5 days or 2 mg/kg PO q24h up to 5 days

Injection site soreness, ataxia, anorexia, diarrhea

5-HT4-Serotonergic antagonist

Cisapridea,2 Myenteric neurons Dogs: 0.1–0.5 mg/kg PO q8hCats: 0.1–1.0 mg/kg or 5 mg (total dose) PO q8–12h

None

Motilin agonist

Erythromycina,2 GI smooth muscle Dogs and cats: 0.5–1.0 mg/kg IV q8h, up to 5.0 mg/kg PO q8h Vomiting at antimicrobial doses (15 mg/kg tid)

Opioid

Butorphanola,13 Emetic center Dogs: 0.2–0.4 mg/kg IM 30 min before cisplatin infusion Sedation, ataxia, anorexia, diarrhea

Others

Propofola CRTZ None reported in veterinary medicine Apnea, hypotension, seizurelike signs

Dexamethasone13 Emetic center, medulla Dogs: 0.1 mg/kg SC or IV before chemotherapy GI ulceration

Diazepama Vestibular system suppression 0.1–0.2 mg/kg PO q6h Sedation

a Plumb DC. Veterinarian Drug Handbook. 6th ed. Ames, IA: Wiley-Blackwell; 2008.b Richter KP. Treating acute vomiting in dogs and cats. Vet Med 1992;87(8):814-818.

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marily κ and σ agonist, is used to prevent vomit-ing related to cisplatin therapy in dogs.35,36

Neurokinin AntagonistsNeurokinin (NK

1) antagonists are a new group

of antiemetics that includes maropitant, an agent developed for dogs that acts as a ligand for the substance P receptors located in many areas of the brain, including the emetic center and CRTZ.37 It is believed that the substance P–NK

1

receptor complex is in the fi nal common path-way of the neural and humoral pathways of the vomiting refl ex.38 Studies in dogs have showed that maropitant prevents vomiting caused by peripheral and central emetogens, including apomorphine, cisplatin, and syrup of ipecac,39 and clinical conditions such as pancreatitis and gastroenteritis.39 Maropitant is also effec-tive against vomiting caused by motion sick-ness.39 Adverse effects reported with this drug include ataxia, anorexia, diarrhea, and injection site soreness.40 This drug should not be used in dogs younger than 16 weeks because bone mar-row hypoplasia has been reported.40

Other DrugsOther drugs used to control vomiting centrally include yohimbine, diazepam, dexamethasone, propofol, and mirtazapine. Yohimbine, a pure α

2-adrenergic antagonist, is a very potent antiemetic

used in dogs and cats. It may cause CNS excitement, excessive sedation, muscle tremors, tachypnea, pty-alism, and hyperemic mucous membranes.36

Diazepam relieves nausea and vomiting in people.41 Studies with animal models and clin-ical trials in human medicine suggest that this drug suppresses the vestibular system.41–43

The antiemetic properties of corticosteroids are incompletely understood, but their mecha-nism involves the activation of glucocorticoid receptors in the medulla, especially the emetic center in cats.44 Dexamethasone has been shown to be useful in controlling chemother-apy-associated nausea and vomiting in human patients45 and dogs.45,46

Propofol, an alkylphenol derivative, is used as an antiemetic in people with chemotherapy-asso-ciated nausea and vomiting that is unresponsive to serotonin antagonists or dexamethasone.47,48 It has been proposed that its antiemetic mechanism involves reduction of the serotonin concentration in the CRTZ via γ-aminobutyric acid activity and 5-HT

3 serotonin receptor antagonism.49

Mirtazapine is a piperazinoazepine drug used as an antidepressant in people. It antagonizes central presynaptic α

2-receptors and blocks

serotonin receptors.50 It is a weak 5-HT1 sero-

tonin receptor antagonist, a potent 5-HT2 and

5-HT3 sero tonin receptor antagonist, and an

H1-histamine antagonist.50 It is used to control

chemotherapy-associated nausea and vomiting in humans50,51 and, more recently, in small animals.

Treatment of Common Vomiting Conditions BOX 1 lists several conditions and diseases that commonly cause vomiting.

Gastritis or Gastric UlcerationTreatment to manage vomiting caused by gas-tritis or gastric ulceration must include proper fl uid therapy and gastric mucosal protection. Many clinicians use broad-spectrum antiemetics because they cover local and peripheral recep-tors. Chlorpromazine, serotonin antagonists, and metoclopramide are good options. Maropitant seems to work extremely well in dogs. If vomit-ing is associated with gastrointestinal ulceration due to NSAID administration, therapy with misoprostol, a prostaglandin E

1 (PGE) analog,

may be effective in controlling both the ulcer-ative lesion and vomiting as a secondary prob-lem.52 Proton pump inhibitors and H

2-histamine

antagonists provide more complete inhibition of gastric acid secretion in severe cases of ulcer-ation.12,25,53 If Helicobacter spp are the underly-ing cause of ulceration, appropriate antibiotic therapy and antacids should relieve the clinical signs of the infection. Patients with neoplastic diseases often have gastrointestinal ulceration. Mast cell tumors of any stage, grade, and size can cause vomit-ing in dogs by increasing the plasma hista-mine concentration.16,54 Histamine acts on the CRTZ and the gastric mucosa. Mast cell tumor ulceration and its effects are treated with H

2-histamine antagonists. Tumor size and his-

tamine release in dogs are controlled with the administration of corticosteroids.12,55

PancreatitisPancreatitis causes ileus due to intestinal infl ammation, resulting in direct afferent input to the vomiting center.12 Metoclopramide is the most common antiemetic used in these patients because it acts centrally and peripherally. In dogs, phenothiazines, 5-HT

3-serotonergic

Phenothiazines are broad-spectrum antiemetics that have antidopamin-ergic and antihista-minergic properties in the CRTZ and anticholinergic effects in the emetic center.

QuickNotes

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antagonists, and maropitant can be useful if metoclopramide fails to control vomiting.

Chemotherapy and Other DrugsEmesis caused by cancer chemotherapy and other drugs (e.g., digitalis) is mediated by 5-HT

3-serotonergic receptors.2,12,25 In humans,

the chemotherapeutic drugs most commonly associated with vomiting include cisplatin, cyclophosphamide, dacarbazine, and doxorubi-cin.56 Drugs with 5-HT

3-serotonergic antagonist

properties, especially the serotonin antago-nists ondansetron, granisetron, dolasetron, block these receptors in the CRTZ in cats and in the vagal afferent neurons in dogs.25,26,28,29,57

Metoclopramide is widely used to control chemotherapy-induced vomiting.6,58 The new agent maropitant is also effective in controlling cisplatin-induced vomiting in dogs, and even though there is coexpression of substance P with 5-HT receptors in the primate brain,37 this has not been documented in dogs or cats.

Motion SicknessMotion sickness, or kinetosis, is generated from the vestibular apparatus.2,9,11 Studies in humans have revealed that motion sickness is caused by three mechanisms: (1) confl icting inputs from the visual and vestibular systems; (2) confl ict-

ing inputs from the two vestibular systems (the semicircular canals and the otolith organs); or (3) comparison of input from these systems with the individual’s expectations derived from previous experiences.59 Vomiting caused by motion sickness involves M

1-cholinergic

and H1-histaminergic receptors,2,11 and treat-

ment should antagonize both receptors. Phenothiazines like chlorpromazine and prochlorperazine can antagonize both receptors at the same time, but diphenhydramine, dimen-hydrinate, cyclizine, meclizine, and promethaz-ine are H

1-histamine blocking agents only, and

they should be combined with a M1-cholinergic

receptor blocker for effective control of emetic signals originating from the vestibular appara-tus. Maropitant prevents kinetosis in dogs by blocking the fi nal common pathways of the vomiting refl ex, including signals from the ves-tibular system.40 Scopolamine is a muscarinic M

1-cholinergic antagonist used to treat motion

sickness, but results are not consistent.

UremiaUremic toxins cause decreased gastrin clear-ance and irritate the gastrointestinal mucosa, resulting in ulcerative lesions and gastritis. When these toxins cross the blood–brain barrier, they stimulate central and peripheral receptors and activate D

2-dopaminergic recep-

tors in the CRTZ.2,11 Dopamine antagonists like metoclopramide and chlorpromazine effectively block these receptors. Diuresis with appropriate fl uid therapy and a proton pump inhibitor or H

2-histaminergic

antagonist helps relieve uremia by diminish-ing the secretion of hydrogen ions into the stomach, providing protection and promoting mucosal healing.

Gastrointestinal Motility DisordersProkinetics—cisapride, metoclopramide, and erythromycin—should be used to control vom-iting due to nonobstructive delayed gastric emptying. These drugs exert their effects on different receptors. Cisapride, the most effective prokinetic agent available,11 lacks direct anti-emetic effects but stimulates 5-HT

4-serotonergic

receptors.60 Metoclopramide’s antagonism of D

2-dopaminergic receptors enables it to stimu-

late motility in areas where these receptors are present (the higher gastrointestinal tract, lower esophageal sphincter, stomach, and duode-

Vomiting caused by motion sick-ness involves M1-cholinergic and H1-histaminergic receptors, and treat-ment should antago-nize both receptors.

QuickNotes

Most Common Causes of Vomiting in Dogs and Cats

Abdominal disorders Dietary factors Disorders of the small and large intestines Disorders of the stomach Drugsa Endocrine disorders

❯ Hypoadrenocorticism ❯ Hypoparathyroidism Neurologic disorders Parasitism

❯ Ollulanus tricuspis in cats ❯ Physaloptera ❯ Salmon poisoning (Neorickettsia helminthoeca) Systemic diseases Toxins, chemicals, and poisons

BOX 1

aAlmost any drug can cause vomiting, especially if given orally.

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num).2,11 Erythromycin, a macrolide used for its antimicrobial properties, is useful as a prokinetic at low doses.2,11 In dogs, it stimulates the release of motilin, which initiates phase III of the migrat-ing myoelectric complex,61,62 the sequence of motor activity during the interdigestive period in the small bowel.63 This cyclic pattern originates in the gastric antrum and extends over the entire length of the small intestine.62,63 The third and fi nal phase of this pattern is generally associated with the propulsion of ingesta.64,65 It is unknown whether cats can benefi t from this effect. Dogs that vomit bile in the morning before eating may have bilious vomiting syndrome. This is a condition characterized by grass inges-tion, vomiting, and lack of other defi nitive clin-ical signs. It mostly occurs in the morning and is believed to be commonly associated with gastritis, infl ammatory bowel disease, and bile and gastroesophageal refl ux. Affected patients usually respond to a single evening dose of cisapride, metoclopramide, or erythromycin.

Undetermined EtiologyPatients with vomiting of undetermined etiology must be treated with the safest approach pos-sible once systemic diseases (e.g., liver disease, renal disease, endocrine disease) have been ruled out. Patients that are uncomfortable from excessive vomiting or are at high risk for aspira-tion pneumonia and have not been exposed to a toxic agent should be treated with antiemetics when available. α

2-Adrenergic antagonists and

D2-dopaminergic receptors are fi rst-line anti-

emetics. Maropitant is a good alternative not only because it seems to block impulses in the fi nal common pathways of the vomiting refl ex but also because it is administered once daily, dogs seem to tolerate it fairly well, and, so far, adverse effects are minimal. 5-HT

3-serotonergic

antagonists have become very popular over the past few years and have good results. The addi-tion of other drugs to antiemetic therapy should be considered if vomiting becomes refractory in these patients.

Patients with vomit-ing of undetermined etiology must be treated with the safest approach possible once sys-temic diseases have been ruled out.

QuickNotes

References1. Tams TT. A diagnostic approach to vomiting in dogs and cats. Vet Med1992;87(8):785-792.2. Washabau RJ, Elie S. Antiemetic therapy. In: Kirk RW, Bonagura JD, eds. Kirk’s Current Veterinary Therapy XII Small Animal Practice. Philadel-phia: WB Saunders; 1995:679-684.3. Andrews PLR, Rapeport WG, Sanger GJ. Neuropharmacology of em-esis induced by anti-cancer therapy. Trends Pharmacol Sci 1988;9:334-341.4. Johnson SE. Clinical pharmacology of antiemetics and antidiarrheals. Proc of the Kal Kan Waltham Symp Treat Small Anim Dis 1984;8:7-15.5. Merrifi eld KR, Chaffee BJ. Recent advances in the management of nausea and vomiting caused by antineoplastic agents. Clin Pharm 1989;8:187-199.6. Leib MS. Acute vomiting: a diagnostic approach and symptomatic management. In: Kirk RW, Bonagura JD, eds. Kirk’s Current Veterinary Therapy XI Small Animal Practice. Philadelphia: WB Saunders; 1995:583-587. 7. Burrows CF. Vomiting and Regurgitation in the Dog: A Clinical Perspec-tive. Lehigh, Pennsylvania. ALPO Pet Center; 1990:18-38. Viewpoints in Veterinary Medicine.8. Guyton AC, Hall JE. Textbook of Medical Physiology. 9th ed. Philadel-phia: WB Saunders; 1996.9. Adams HR. Veterinary Pharmacology and Therapeutics. 8th ed. Ames: Iowa State University Press; 2001.10. Cunningham JG. Textbook of Veterinary Physiology. 3rd ed. Philadel-phia: WB Saunders; 1997.11. Richter K. Approach to acute vomiting. Proc WVC 2004. Accessed January 2009 at vin.com/Members/Proceedings/Proceedings.plx?CID=wvc2004&PID=pr05345&O=VIN.12. Simpson KW. Managing persistent vomiting. Proc ACVIM 2003. Ac-cessed January 2009 at vin.com/Members/Proceedings/Proceedings.plx?CID=acvim2003&PID=pr03873&O=VIN.13. Strombeck DA, Guilford WG. Vomiting: pathophysiology and phar-macology control. In: Strombeck DA, Guilford WG, Center SA, et al, eds. Strombeck’s Small Animal Gastroenterology. 3rd ed. Philadelphia: WB Saunders; 1996:256-260.14. Willard MD. Some new approaches to the treatment of vomiting. JAV-MA 1984;184:590.15. Miller AD, Leslie RA. The area postrema and vomiting. Front Neuroen-docrinol 1994;15(4):301-320. 16. Twedt DC. Vomiting. In: Ettinger SJ, Feldman EC, eds. Textbook of Vet-erinary Internal Medicine. 6th ed. Philadelphia: WB Saunders; 2005:132-136.

17. Miller AD. Central mechanisms of vomiting. Dig Dis Sci 1999; 44(8 suppl):31S-43S.18. Miller AD, Nonaka S, Jakus J, et al. Modulation of vomiting by the medullary midline. Brain Res 1996;737(1-2):51-58.19. Miller AD, Nonaka S, Jakus J. Brain areas essential or non-essential for emesis. Brain Res 1994;647(2):255-264.20. Lang IM, Dana N, Medda BK, et al. Mechanisms of airway protection during retching, vomiting, and swallowing. Am J Physiol Gastrointest Liver Physiol 2002;283(3):G529-G536.21. Sarna SK, Otterson MF. Small intestinal physiology and pathophysiology. Gastroenterol Clin North Am 1989;18(2):375-404.22. Furukawa N, Hatano M. An acute experiment on retrograde intesti-nal peristalsis with emesis using decerebrated dogs. J Auton Nerv Syst 1998;70(1-2):56-65.23. Peroutka SJ, Snyder SH. Antiemetics: neurotransmitter receptor bind-ing predicts therapeutic actions. Lancet 1982;1(8273):658-659.24. Costall B, Naylor RJ. Neuropharmacology of emesis in relation to clini-cal response. Br J Cancer Suppl 1992;19:S2-S8.25. Dowling PM. GI therapy: when what goes in won’t stay down. Proc WVC 2003. Accessed January 2009 at vin.com/Members/Proceedings/Proceedings.plx?CID=wvc2003&PID=pr03480&O=VIN.26. Flake ZA, Scalley RD, Bailey AG. Practical selection of antiemetics. Am Fam Phys 2004;69:1169-1174,1176.27. King GL. Animal models in the study of vomiting. Can J Physiol Phar-macol 1990;68:260.28. Martirosov KS, Grigor’ev IuG, Borovkov MV, Zorin VV. Experimental study of the role of blocking 5-HT3-receptors of serotonin and D2-recep-tors of dopamine in the mechanism of early radiation vomiting in dogs. Radiats Biol Radioecol 2002;42(1):75-79.29. Martirosov KS, Grigor’ev IuG, Borovkov MV, Zorin VV. Comparative experimental study of antiemetic action of lantranum in radiation-induced vomiting and vomiting caused by apomorphine. Radiats Biol Radioecol 2003;43(1):60-64.30. Product information: Zofran. Research Triangle Park, NC: GlaxoSmith-Kline; 2006. 31. Andrews PLR, Naylor RJ, Joss RA. Neuropharmacology of emesis and its relevance to anti-emetic therapy: consensus and controversies. Support Care Cancer 1998;6:197-203.32. Takahashi T, Kurosawa S, Wiley JW, et al. Mechanism for the gastrokinetic actions of domperidone. Gastroenterology 1991;101:703-710.33. Kolh RL, MacDonald S. New pharmacologic approaches to the preven-tion of space/motion sickness. J Clin Pharmacol 1991; 31(10):934-946.

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1. Emesis is initiated, controlled, regulated, and organized by the

a. higher centers of the brain. b. CRTZ. c. vestibular apparatus. d. emetic center.

2. The vomiting pathways are controlled by a. neurotransmitter–receptor interactions. b. the higher centers of the brain. c. the peripheral nervous system. d. vestibular neurons.

3. ___________ are considered broad-spectrum antiemetics because of their effect on multiple receptors.

a. Anticholinergics b. Phenothiazines c. Serotonin antagonists d. Opioids

4. Emesis caused by cancer chemotherapy and other drugs is mediated by ___________ receptors.

a. D2-dopaminergic

b. M1-cholinergic c. H2-histaminergic d. 5-HT3-serotonergic

5. Which antiemetic is also classifi ed as a prokinetic?

a. ranitidine b maropitant c. metoclopramide d. propofol

6. Which condition or pathogen is the least likely to cause gastric ulceration?a. Helicobacter spp

b. mast cell tumor c. gastrinoma d. kinetosis

7. Mirtazapine does not antagonize ___________ receptors.

a. H1-histaminergic b. 5-HT3-serotonergic c. central presynaptic α2- d. D2-dopaminergic

8. ___________ can be used for chemother-apy-associated nausea and/or vomiting, especially when patients do not respond to the newer serotonin antagonists and when multiple medication therapy fails.

a. Propofol b. Diazepam c. Mirtazapine d. Dexamethasone

9. Which antiemetic antagonizes neuroki-nin receptors in many areas of the brain?

a. mirtazapine b. maropitant c. dolasetron d. prochlorperazine

10. Select the correct antiemetic–adverse effect pair.

a. ondansetron; renal toxicity b. chlorpromazine; hypotension c. metoclopramide; sedation d. meclizine; gastrointestinal perforation

3 CECREDITS CE TEST 1 This article qualifi es for 3 contact hours of continuing education credit from the Auburn University College of

Veterinary Medicine. Subscribers may take individual CE tests online and get real-time scores at CompendiumVet.com. Those who wish to apply this credit to fulfi ll state relicensure requirements should consult their respective state authorities regarding the applicability of this program.

34. Kobrinsky NL. Regulation of nausea and vomiting in cancer chemotherapy. A review with emphasis on opiate mediators. Am J Pediatr Hematol Oncol 1988;10(3):209-213.35. Schurig JE, Florczyk AP, Rose WC, et al. Antiemetic activity of butorphanol against cisplatin-induced emesis in ferrets and dogs. Cancer Treat Rep 1982;66(10):1831-1835.36. Plumb DC. Veterinary Drug Handbook. 4th ed. Ames: Iowa State Press-Blackwell; 2002.37. Davis KL, Charney D, Coyle JT, Nemeroff C. Neuropsychopharmacology: The Fifth Genera-tion of Progress. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2002;169-177.38. Hornby PJ. Central neurocircuitry associated with emesis. Am J Med 2001;111(suppl 8A):106S-112S.39. Benchaoui HA, Cox SR, Schneider RP, et al. The pharmacokinetics of maropitant, a novel neu-rokinin type-1 receptor antagonist in dogs. J Vet Pharmacol Ther 2007;30(4):336-344.40. Product information: Cerenia. New York: Pfi zer Animal Health: 2006.41. McClure JA, Lycett P, Baskerville JC. Diazepam as an anti-motion sickness drug. J Otolar-yngol 1982;11(4):253-259.42. Sekitani T, McCabe BF, Ryu JH. Drug effects on the medical vestibular nucleus. Arch Otolaryngol 1971;93:581-589.43. Zanjoc TP, Roland PS. Vertigo and motion sickness. Part II: pharmacologic treatment. Ear Nose Throat J 2006;85(1):25-35.44. Ho GM, Ho ST, Wang JJ, et al. Dexamethasone has a central antiemetic mechanism in decer-ebrated cats. Anesth Analg 2004;99(3):734-739.45. Dexamethasone alone or in combination with ondansetron for the prevention of delayed nausea and vomiting induced by chemotherapy. The Italian Group for Antiemetic Research. N Engl J Med 2000;342(21):1554-1559.46. Fukui H, Yamamoto M. Methotrexate produces delayed emesis in dog: a potential model of delayed emesis induced by chemotherapy. Eur J Pharmacol 1999;372:261-267.47. Borgeat A, Wilder-Smith OH, Saiah M, et al. Subhypnotic doses of propofol possess direct antiemetic properties. Anesth Analg 1992;74:539-541.48. Gan TJ, El-Molem H, Ray J, et al. Patient-controlled antiemesis: a randomized, double-blind comparison of two doses of propofol versus placebo. Anesthesiology 1999;90:1564-1570.49. Cechetto DF, Daib T, Gibson CJ, Gelb AW. The effect of propofol in the area postrema in rats. Anesth Analg 2001;92:934-942.50. Pae C. Low-dose mirtazapine may be successful treatment option for severe nausea vomit-ing. Prog Neuropsychopharmacol Biol Psychiatry 2006;30:1143-1145.

51. Kang H, Kim S, Kim J, et al. Mirtazapine for severe gastroparesis unresponsive to conven-tional prokinetic treatment. Psychosomatics 2006;47:5.52. Murtaugh RJ, Matz ME, Labata MA, et al. Use of synthetic prostaglandin E1 (misoprostol) for prevention of aspirin-induced gastroduodenal ulceration in arthritic dogs. JAVMA 1993;202(2):251-256. 53. Bersenas AME, Mathews KA, Allen DG, et al. Effects of ranitidine, famotidine, pantoprazole, and omeprazole on intragastric pH in dogs. Am J Vet Res 2005;66(3):425-431.54. Fox LE, Rosenthal RC, Twedt DC, et al. Plasma histamine and gastrin concentrations in 17 dogs with mast cell tumors. J Vet Intern Med 1990;4:242.55. Ogilvie GK. Mast cell tumors: hot new diagnostics and treatment! Proc WSAVA 2002. Ac-cessed January 2009 at vin.com/Members/Proceedings/Proceedings.plx?CID=wsava2002&PID=pr02637&O=VIN.56. American Cancer Society. Nausea and vomiting. Accessed January 2009 at cancer.org/do-croot/MBC/content/MBC_2X_Nausea_and_Vomiting.asp?sitearea=MBC.57. Tucker ML, Jackson MR, Scales MDC, et al. Ondansetron: pre-clinical safety evaluation. Eur J Cancer Clin Oncol 1989;25:S79.58. Ogilvie GK, Moore AS, Curtis CR. Evaluation of cisplatin-induced emesis in dogs with ma-lignant neoplasia: 115 cases (1984-1987). JAVMA 1989;195:1399.59. Eyeson-Annan M, Peterken C, Brown B, et al. Visual and vestibular components of motion sickness. Aviat Space Environ Med 1996;67(10):955-962.60. Gullikson GW, Loeffl er RF, Viriña AM. Relationship of serotonin-3 receptor antagonist activ-ity to gastric emptying and motor-stimulating actions of prokinetic drugs in dogs. J Pharmacol Exp Ther 1991;258:103.61. Itoh Z. Erythromycin mimics exogenous motilin in gastrointestinal contractile activity in the dog. Am J Physiol 1984;247:G688.62. Granger DN, Barrowman JA, Kvietys PR. Clinical Gastrointestinal Physiology: A Saunders Monograph in Physiology. Philadelphia: WB Saunders; 1985.63. Thomas EA, Sjovall H, Borstein JC. Computational model of the migrating motor complex of the small intestine. Am J Physiol Gastrointest Liver Physiol 2004;286(4):G564-G572.64. Kruis W, Azpiroz F, Phillips SF. Contractile patterns and transit of fl uid in canine terminal ileum. Am J Physiol 1985;249(2 Pt 1):G264-G270.65. v Schönfeld J, Evans DF, Goebell H, et al. Comparison of the small bowel motor response to solid and liquid meals in man. Digestion 1997;58(4):402-406.


effective in the treatment of Cushing’s syndrome in dogs. The product will be indicated for use in pituitary-dependent hyperadrenocorticism, which causes most cases of Cushing’s syndrome in dogs. It is the fi rst drug to receive a Minor Use designation for the treatment of hyperad-renocorticism caused by adrenal tumors in dogs.Dechra Veterinary Products | 866-933-2472 | www.dechra-us.com

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ConclusionFHS has multiple possible etiologies. It requires patience and close communication with the pet’s owner in order to arrive at the correct diagnosis. As with most behavior disorders,

FHS can be controlled but is not likely to be cured. By developing a clear diagnostic plan and following it closely, veterinarians can avoid confusion for the owner and foster a sense of cooperation between the owner and themselves. Overall, this is the true measure of success.

References1. Fears, anxieties and stereotypes. In: Overall K. Clinical Behav-ioral Medicine for Small Animals. St. Louis: Mosby; 1997:227.2. Lundgren B. Feline hyperesthesia syndrome. Accessed January 2009 at VeterinaryPartner.com. 3. Psychogenic alopecia/overgrooming: feline. In: Horwitz D, Neilson J. Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Canine and Feline Behavior. Ames: Blackwell Publishing; 2007:425-431.4. Opioids and opioid antagonists. In: Crowell-Davis S, Murray T. Veteri-nary Psychopharmacology. Ames: Blackwell Publishing; 2006:212.

5. Tail chasing and spinning: canine and feline. In: Horwitz D, Neilson J. Blackwell’s Five-Minute Veterinary Consult Clinical Companion: Canine and Feline Behavior. Ames: Blackwell Publishing; 2007:475-483.6. Selective serotonin reuptake inhibitors. In: Crowell-Davis S, Murray T. Veterinary Psychopharmacology. Ames: Blackwell Pub-lishing; 2006:80-110.7. Tricyclic antidepressants. In: Crowell-Davis S, Murray T. Veterinary Psychopharmacology. Ames: Blackwell Publishing; 2006:179-206.8. Benzodiazepines. In: Crowell-Davis S, Murray T. Veterinary Psy-chopharmacology. Ames: Blackwell Publishing; 2006:34-71.

CONTINUED FROM PAGE 121Understanding

Behavior



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Squamous cell carcinoma (SCC) is a malignant neoplasm arising from squamous epithelium. The skin, oral

cavity, and digits are the most common sites of SCC in dogs and cats.1 SCCs account for 15% of skin tumors in cats.2 Most cutaneous SCCs in cats occur on the head (FIGURE 1), often involving the pinna, eyelid, and nasal planum.2 In dogs, less than 5% of cutane-ous neoplasms are SCC, and common sites include the legs, scrotum, perineum, nasal planum, and various lightly pigmented areas.1,3 SCCs account for 70% of feline and 25% of canine oral neoplasms and may arise from virtually any surface in the oral cavity, including the gingiva (FIGURE 2), tongue, ton-sils, pharynx, lips, and buccal mucosa.1 In a retrospective series evaluating lingual lesions in dogs, more than one-half of the lesions were neoplastic, and 17% of those neo-plasms were SCC.4 Of digital tumors in dogs (FIGURE 3), 38% to 50% are SCC, and multi-ple digits may be involved.5,6 Digital SCC was previously reported to be rare in cats, but a recent study diagnosed SCC in 24% of ampu-tated feline digits.7 Other locations reported to develop SCC in dogs and cats include the

conjunctiva, cornea, nasal passages, larynx, lung, esophagus, bladder, prostate, penis, cervix, vagina, and anal sac.1,8,9 Most SCCs are locally invasive and, in certain areas of the body, exhibit bone inva-sion and osteolysis. Tumor spread to local lymph nodes may occur, but distant metas-tases are rare and usually do not occur until late in the disease process. However, cer-tain anatomic locations have a higher rate of metastasis. TABLE 1 lists some common sites of SCC and the biologic behavior asso-ciated with those sites.1

A premalignant form of SCC, composed of dysplastic cells that do not cross the epi-thelial basement membrane, is called SCCin situ.10 Complete excision of an SCC in situ is curative for that lesion, but new lesions may develop in other areas. Two forms of SCC in situ have been reported in dogs and cats: solar keratosis and multicentric SCC in situ (MSCC). The lesions of solar kerato-sis are usually singular and range from an erythematous, scaly thickening of the skin to shallow, crusting lesions. They occur on lightly haired, nonpigmented skin and are associated with ultraviolet (UV) light expo-

❯❯ Julie L. Webb, DVM, DACVP❯❯ Rachel E. Burns, DVM❯❯ Holly M. Brown, DVM❯❯ Bruce E. LeRoy, DVM, PhD,

DACVPa

❯❯ Carrie E. Kosarek, DVM, MS, DACVIM (Oncology)

The University of Georgia

3 CECREDITS

Risk Factors and Etiology Page 134

Common Locations and Associated Biologic Behavior of SCC

Page 134

Gross Description and Clinical Signs

Page 135

Diagnosis Page 136

Distinguishing Features of Cytologic Samples That Contain Squamous Cells

Page 137

Treatment Options and Prognosis

Page 137

At a Glance

Abstract: Squamous cell carcinoma (SCC) is a relatively common, malignant neoplasm of dogs and cats that can arise in a variety of locations. The gross appearance of SCC can be variable and nonspecifi c, so defi nitive diagnosis requires microscopic examination of the tissue (cytology or histology). Several treatment modalities exist, but surgical excision, if possible, is regarded as the best treatment option. Early diagnosis and treatment of SCC are key because small, early-stage tumors are the most amenable to treatment and carry the best prognosis.

Periocular SCC in a cat.

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FIGURE 1

Maxillary gingival SCC in a dog.

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FIGURE 2

aDr. LeRoy discloses that he has received fi nancial support from Novartis Animal Health and Pfi z-er Animal Health.



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sure.3 With time and continued exposure to UV light, most solar keratosis lesions can progress to SCC. MSCC, similar to Bowen’s disease in humans, presents as multiple plaque-like or papillary lesions on pigmented, haired skin and is not related to UV light exposure. MSCC is rare in cats and very rare in dogs.1,10 Its progression to SCC seems to be slow, if it occurs at all.

Risk Factors and EtiologyOlder animals are at greater risk for developing SCC, with the average age at presentation being 8 to 10 years for dogs and 10 to 12 years for cats.2,3,10 Prolonged

exposure to UV light, lack of skin pigment, and a sparse haircoat all contribute to the develop-ment of cutaneous SCC.1 Siamese cats, with their pigmented extremities, may be less likely to develop cutaneous SCC.2 Cats with long hair-coats, such as Himalayans and Persians, also have a decreased risk, whereas domestic short-haired cats are overrepresented.1 Dogs with white haircoats are more susceptible to cuta-neous SCC, whereas dogs with dark haircoats appear to be overrepresented in cases of digi-tal tumors.1,6 Rarely has a sex predilection been reported; in one study, female dogs appeared to be at increased risk for development of lingual SCC4, while tonsillar SCC may be more common in male dogs.11,12

The mechanism frequently proposed for cutaneous SCC and its association with UV light involves the tumor suppressor gene p53.13 This gene encodes a protein (p53) that arrests the cell cycle when DNA damage is present, giving the cell time to repair the damage before continu-ing mitosis. If the damage cannot be repaired, p53 will induce apoptosis of the cell. UV light is a common carcinogen that can mutate the p53gene. Cells in which the p53 gene is mutated continue replication even if DNA damage is pres-ent, leading to the accumulation of other muta-tions and a greater chance of neoplasia.13 The mutant form of p53 has been detected in 82% of feline pinna SCCs, emphasizing the importance of p53 in preventing solar-induced SCC.13

Few studies investigating carcinogens that may contribute to the development of SCC in cats and dogs have been conducted. Reported risk factors for oral SCC in cats include wearing fl ea collars and eating canned food (especially tuna-based food).14 Small but statistically insig-nifi cant correlations have been found between environmental tobacco smoke and feline oral SCC.14,15 Urban pollutants may increase the risk for tonsillar SCC.3

Another potential contributor to the devel-opment of SCC in dogs and cats is chronic infl ammation. Chronic dermatosis is a reported risk factor for cutaneous SCC,16 and, although extremely rare, bilateral aural SCC was reported in two dogs that had a history of chronic aural infl ammation.17 In addition, multiple corneal SCCs developed in a dog with keratoconjunc-tivitis sicca.18

TABLE 1 Common Locations and Associated Biologic Behavior of SCCTumor Location Local

InvasionRegional Lymph Node Spread

Distant Metastasis

Comments

Skin Frequent Rare Rare Lymph node spread mostly occurs in poorly differentiated tumors or those present for longer periods

Gingiva Frequent Rare Rare Frequent bone invasion and destruction

Tongue Frequent Common Rare Local recurrence common after surgical removal

Tonsil Frequent Frequent Common Lungs, liver, and spleen are the most common metastatic sites

Cheek/Lip Common Rare Rare —

Nasal passages Frequent Rare Rare Bone invasion common

Lung Frequent Common Common Solitary or multiple masses; metastases to one or multiple digits reported in cats

Digit Frequent Common Common Bone invasion and destruction common; lungs are the most common metastatic site

Digital SCC in a dog.

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Viral etiologies have been linked to certain SCCs in people. Papillomavirus type 16 infection is associated with a signifi cant number of SCCs of the head and neck in humans, particularly in the oropharynx and in patients lacking the risk factors of tobacco and alcohol consumption.19

Papillomavirus DNA has been detected within approximately 20% of canine and feline cutane-ous and mucosal SCCs, but the signifi cance of this association has yet to be determined.20,21

Radiation-induced carcinogenesis is well doc-umented in people and animals, as reviewed by Suit and colleagues in 2007.22 In one study23 evaluating orthovoltage radiotherapy for the treatment of acanthomatous epulides (now called acanthomatous ameloblastomas), seven of 39 dogs (18%) developed second tumors within the radiation fi eld; 71% of the tumors were SCC. However, a more recent study24 found that the risk of developing a second tumor was less than 4%. In this study, only two of 57 dogs that underwent defi nitive radiation therapy (RT) for acanthomatous epulides developed second tumors, both of which were sarcomas. The authors of the more recent study suggest that the earlier paper may have included patients whose original tumors were SCC, misdiagnosed as acanthomatous epulides.

Gross Description and Clinical SignsIn many cases of SCC, the animal presents with a visible mass. The mass may appear as any of the following3:Shallow crusting lesion (often SCC in situ)

Deeply ulcerated lesion Proliferative, raised, red plaque Caulifl ower-shaped growth

The appearance of the lesion may change over time, often progressing from a shallow or ulcerated lesion to a more proliferative, raised tumor. The time from lesion occurrence to diag-nosis also varies but is generally prolonged. In two studies of cats with SCC of the nasal pla-num or pinnae, lesions were reportedly present for a median duration of 3 to 5 months before diagnosis.25,26 Often, the tumor is initially misdi-agnosed as an infl ammatory or traumatic lesion, and therapies such as antibiotics and corticos-teroids may have been used before diagnosis.25

Clinical signs of SCC depend on the tumor’s location. Digital tumors often cause lameness and ulceration of the digit.5 Nasal tumors can cause facial deformity, nasal discharge, and sneezing. Signs of oral tumors include excess salivation, oral bleeding, anorexia, loose teeth, dysphagia, weight loss, and halitosis.27 Numerous other clini-cal signs have been reported: coughing and dys-pnea with pulmonary tumors, regurgitation with esophageal masses, voice change with laryngeal SCC, and ocular discharge with periocular and ocular tumors.1 Hypertrophic osteopathy is a rare complication with pulmonary SCC.28

There are no consistent abnormal labora-tory fi ndings in animals with SCC. One study found that 32% of cats with oral SCC had a neutrophilic leukocytosis, likely refl ecting sec-ondary infection of ulcerated masses.27 One

The most common locations for cats and dogs to develop SCC are the skin, digits, and oral cav-ity, but tumors may also arise at other sites, including the cornea, lungs, esophagus, and bladder.

QuickNotes

Asynchronous maturation in a neoplastic squamous cell. The mature, fully keratinized cell

has retained a large nucleus (arrow; Wright’s stain,

1000×).

Fine-needle aspirate from a cutaneous SCC. A small cluster of cells displays anisocytosis, aniso-

karyosis, multinucleation, prominent nucleoli (thin

arrow), keratohyaline granules (thick arrow), and

emperipolesis (arrowhead; Wright’s stain, 1000×).

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case of paraneoplastic neutrophilic leukocyto-sis has been reported with pulmonary SCC,29

and several cases of paraneoplastic hypercal-cemia have been documented.30

DiagnosisEarly diagnosis of SCC is paramount for early therapeutic intervention, which may result in long-term control or cure for affected patients. SCC may be suspected based on the gross appearance of a lesion and its location, but defi nitive diagnosis requires microscopic exam-ination of the affected tissue. Cytology is a rapid, easy, noninvasive method that may provide the diagnosis of SCC and is often attempted as the fi rst diagnostic technique, especially for cutane-ous lesions. Biopsy with histopathology may be required to obtain a defi nitive diagnosis if cytol-ogy is nondiagnostic or equivocal.

CytologySeveral methods may be used to obtain a spec-imen for cytologic analysis. The best method depends on the lesion location and gross appearance. Fine-needle aspiration is used to obtain material from nodular lesions, whereas surface imprints and scrapings are often used to collect material from shallow or plaquelike lesions. Unfortunately, many SCCs are ulcer-ated and infl amed, so superfi cial sampling may retrieve only the infl ammation and not the deeper neoplastic cells. Impression smears from biopsy samples also provide material for cytologic examination.

As with other epithelial neoplasms, SCCs tend to exfoliate readily, leading to highly cellular samples. The cells may be in closely adherent sheets or clusters, although numerous individual cells are often present. Squamous cells undergo several stages of maturation; thus, a pleomorphic population of cells may be observed. Immature (basal-type) squamous cells are small, round to cuboidal cells with a scant amount of glassy, basophilic cytoplasm and a high nuclear–cyto-plasmic ratio. Mature (superfi cial) squamous cells are large, angular cells with a large amount of lightly basophilic cytoplasm and pyknotic or absent nuclei.31 Keratinized cells have deeply basophilic cytoplasm with angular borders. Poorly differentiated SCCs consist predominantly of immature cells, and well-differentiated tumors contain more mature cells. Asynchronous nuclear and cytoplasmic maturation, in which large, fully keratinized cells retain large nuclei, is commonly seen with SCC (FIGURE 4). Other criteria of malig-nancy found in SCC include prominent aniso-cytosis and anisokaryosis, multinucleated cells, and variable numbers and sizes of nucleoli. Keratohyaline granules are frequently present as small, round, cytoplasmic vacuoles concen-trated around the nucleus. SCC cells may also display emperipolesis, in which other cells are able to passively penetrate the neoplastic squamous cell and are found within its cyto-plasm31 (FIGURE 5). Cells with a long cytoplas-mic process resembling a tail, called tadpole cells, are occasionally observed (FIGURE 6).

Tadpole cells in a cutaneous SCC aspirate (Wright’s stain, 500×).

Septic purulent infl ammation with squamous cell hyperplasia. A small cluster of dysplastic

squamous cells is surrounded by degenerate neutro-

phils and numerous bacteria. The squamous cells dis-

play cytoplasmic basophilia and mild anisocytosis. A

binucleated cell is also present (Wright’s stain, 1000×).

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FIGURE 6 FIGURE 7

On initial presenta-tion, many SCCs are misdiagnosed as infl ammatory or traumatic lesions.

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The cytologic diagnosis of SCC is often com-plicated by concurrent infl ammation. Secondary infl ammation, often present when the tumor is ulcerated, may mask the neoplastic cell popula-tion. Additionally, primary infl ammatory condi-tions can induce epithelial hyperplasia, creating dysplastic changes, such as increased cytoplas-mic basophilia, anisocytosis, and anisokaryo-sis, that mimic neoplasia (FIGURE 7). Therefore, extreme caution should be used when attempt-ing to diagnose SCC on cytology in a highly infl amed area. Histologic examination of the lesion may be necessary for a defi nitive diagno-sis in these situations. Other samples containing squamous cells, such as contaminated slides, papillomas, and keratin-producing cysts or tumors (FIGURE 8), must be differentiated from SCC on cytology. TABLE 2 details features that can help distin-guish these lesions from SCC.31

HistologyBiopsy of the lesion and histologic analy-sis are often needed to defi nitively diagnose SCC, especially if the tumor is poorly differ-entiated or highly infl amed. If not excisional, the biopsy should always contain the junction of grossly normal and abnormal epithelium, as this is usually the most diagnostic region. A typical well-differentiated SCC maintains a loose epithelial maturation sequence from basal layer to stratum corneum, but instead of growing toward the skin surface, the neoplas-tic cells form irregular whorls and cords within the tumor (FIGURE 9). Nests of neoplastic cells surrounded by stroma may have the equiva-lent of the basal cell layer at the outer edge of the nest and the keratin-producing layer in the center, creating the classic appearance of intensely eosinophilic, densely packed rings of keratin (a keratin pearl, FIGURE 10). In less dif-ferentiated tumors, epithelial layering is indis-tinct, cells are smaller, and keratinization is less likely to be seen. Highly anaplastic SCCs may require special immunohistochemical stains, such as cytokeratin, to positively identify the cell of origin.1

StagingSCC is typically a locally aggressive neoplasm with a variable potential for distant metastasis. Diagnostic staging tests that may be advised include routine hematologic and biochemical

analysis, urinalysis, local lymph node evalu-ation, three-view thoracic radiography, and abdominal imaging (radiography and ultra-sonography). The extent of staging that is under-taken is often dictated by the primary tumor location. Advanced imaging techniques, such as computed tomography, may be required to further defi ne the location and extent of the primary tumor, especially for tumors involving the ear canal, oral, and sinonasal cavities.32–34 Imaging is also useful for surgical and radia-tion treatment planning.

Treatment Options and PrognosisEarly diagnosis and implementation of therapy is advised for all patients with SCC, especially because small tumors are more amenable to

TABLE 2 Distinguishing Features of Cytologic Samples That Contain Squamous Cells

Lesion Cytologic Description

SCCa Pleomorphic population of nucleated squamous cells with numerous features of malignancy

Papillomaa Mature squamous cells lacking features of malignancy

Keratin-producing cyst or tumorb (FIGURE 8)

Numerous anucleate squamous cells and keratin debris ± cholesterol crystals

Contaminated sample (often due to handling)

A few anucleate squamous cells and a small amount of keratin debris

aIt may be diffi cult to differentiate between a well-differentiated SCC and a papilloma on cytology.bIncludes epidermal inclusion cysts, follicular cysts, pilomatrixomas, and trichoepitheliomas.

An aspirated sample from a follicular cyst (keratin-producing lesion) containing abundant, anucleate, keratinized

squamous cells and keratin debris (Wright’s stain, 200×). Grossly,

these lesions contain caseous white material.

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local control. Local treatment options for dogs and cats with SCC include surgery, cryother-apy, RT, plesiotherapy, photodynamic therapy (PDT), and intratumoral chemotherapy. Systemic therapy, such as chemotherapy and cyclooxy-genase-2 (COX-2) inhibitors, may be advised for patients with SCCs that are inoperable, are poorly differentiated, have metastasized at the time of diagnosis, or are in a location with a report-edly aggressive biologic behavior (TABLE 1). It is important to note that, with certain forms of SCC (i.e., those induced by UV light), cellular damage may already be present at other sites. Therefore, new lesions may develop even with excellent local control of the primary lesion.

Surgical ExcisionSurgical excision is the primary treatment option for most patients with SCC. The ability to completely excise the tumor depends on fac-tors such as the size and location of the tumor. In a retrospective study25 evaluating response to therapy (surgery, RT, or cryotherapy) in 61 cats with nasal planum or pinna SCC, sur-gery provided the longest disease-free inter-val, with a median of 594 days. Early surgical intervention is also advised for digital tumors. Digital amputation resulted in complete tumor control for all but one of 21 dogs with subun-gual SCC.35 If complete surgical excision is not possible, adjuvant therapies may be pursued.

CryotherapyCryotherapy may be considered for local con-trol of small, superfi cial tumors or tumors that

are incompletely excised. It is inexpensive and readily available and provides excellent cos-metic results. Studies have reported that cryo-therapy provides good local control for 1 year or longer for SCCs of the cornea.18,36 For the pinna and nasal planum, cryotherapy provided a median disease-free interval of 254 days in 11 cats.25 In a larger study37 of cats with nasal pla-num SCC treated with cryotherapy, the median remission time was 26.7 months.

Radiation TherapyDefi nitive RT is a local treatment modality that is generally recommended as an adjuvant treat-ment for incompletely excised tumors or as a primary treatment for inoperable tumors. In the case of SCC, RT is most commonly employed for tumors of the nasal planum, nasal cavity, and oral cavity. The response to defi nitive RT for dogs with oral SCC varies with the size of the tumor: small, early-stage tumors had the best response and the longest progression-free intervals38 (FIGURE 11). In cats with nasal planum SCC treated with defi nitive RT, the 1- and 5-year survival rates were 60% and 10%, respectively.39

In dogs, nasal planum tumors treated with RT recurred in an average of 2 to 3 months, and the median survival time was 6 months.40,41 The median survival time of eight dogs with tonsillar SCC treated with surgery plus defi nitive RT was 110 days.11 Protocols vary among institutions; however, most protocols involve low-dose frac-tions (3 to 4 Gy) given daily to every other day over a 3- to 4-week period. The side effects of these protocols are generally mild and limited to acute reactions such as mucosal infl amma-tion. No radiation-induced tumors have been specifi cally reported with these protocols, but any RT has the potential to induce neoplasia. Palliative RT typically involves a total of three to four treatments given at a higher dose per fraction than defi nitive RT. The goals of pallia-tive RT are to provide pain relief, stabilize tumor growth, or improve dysfunction associated with the tumor. Palliative RT may be recommended for patients for which a cure is not possible due to advanced local or metastatic disease or other severe illness. Unfortunately, reports evaluating the effi cacy of palliative RT in dogs and cats with SCC are limited, and the few that exist are not encouraging. A 2001 study evaluating pal-liative RT in seven cats with nonresectable oral SCC found that 87% of the cats had tumor pro-

Nests of neoplastic squamous epithelium in a moderately differen-

tiated SCC (hematoxylin–eosin stain, 400×).

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FIGURE 9

Many SCCs are ulcerated and infl amed. Superfi cial sam-pling (impression smears, scrapings, or swabs) may retrieve only the infl ammation and miss the underlying neoplastic cells.

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gression or acute radiation side effects, with a mean survival time of only 60 days.42

PlesiotherapyPlesiotherapy involves the topical applica-tion of a radiation source to the target lesion. Topical radiation doses drop off signifi cantly after a depth of 2 mm; therefore, the use of plesiotherapy is limited to superfi cial or incom-pletely excised tumors, particularly those of the nasal planum or ocular region. In a recent retrospective study26 evaluating the effi cacy of strontium-90 plesiotherapy for cats with nasal planum SCC, 13 of 15 cats achieved a complete response with a median disease-free interval of 692 days. Excellent cosmetic results were also obtained. Strontium-90 plesiotherapy has also been used to treat SCC in dogs.43

Photodynamic Therapy PDT is yet another local treatment modality that has been used for treatment of SCC. The process involves the topical administration or intravenous injection of a photosensitizer that preferentially accumulates in neoplastic cells. Once activated by light of a specifi c wavelength, the photosensitizer causes cytotoxicity and tis-sue necrosis. Studies of intravenous PDT44,45 in dogs and cats with oral and cutaneous SCC have shown moderate to good response rates (62% to 73% of patients experience a cure or good local control) that last 1 year or longer. In a more recent study46 evaluating topical PDT in cats with facial SCC, 85% achieved a complete response. Unfortunately, 63% of these cats developed recurrence in a median time of 21 weeks. The results of these studies suggest that PDT may be an effective local treatment modality, but PDT is not readily available in private practice.

ChemotherapySCCs generally are not considered chemore-sponsive tumors; however, chemotherapy may be considered under certain circumstances. For example, chemotherapy may be advised for tumors that are inoperable, anaplastic, or metastatic at the time of diagnosis. Single-agent or combination therapy protocols containing bleomycin, cisplatin, carboplatin, cyclophos-phamide, doxorubicin, and 5-fl uorouracil have been evaluated.12,47 In 16 dogs with tonsillar SCC treated with multidrug chemotherapy, there was no appreciable reduction in tumor

volume, and 62% of the dogs were euthanized because of progressive disease.12 There are few reports of the use of intra-tumoral chemotherapy for cats and dogs with SCC.48–50 Intratumoral therapy with a cisplatin analog was ineffective in cats with oral SCC, many of which experienced signs of toxicity ranging from lethargy and inappetence to acute anaphylactoid reactions.49 In comparison, intra-tumoral treatment with carboplatin appeared safe and effective for cats with nasal planum SCC.48 In a study of 13 dogs with cutaneous SCC treated with intratumoral sustained-release chemotherapy (5-fl uorouracil or cisplatin), all the dogs had a 50% or greater re sponse, and 54% achieved a complete re sponse.50 The mean disease-free interval was 153 weeks. The use of chemotherapeutics as sensitizers before RT has also been evaluated in dogs and cats with SCC. Cisplatin combined with RT has shown some promise in dogs with nasal SCC,51 while results of combining gemcitabine with RT are less encouraging.52,53

COX-2 InhibitorsCOX-2 is an inducible enzyme responsible for the production of infl ammatory prostaglandins. Overexpression of COX-2 has been implicated in the progression of certain cancers, specifi -cally carcinomas. Several studies in dogs and cats have reported increased expression of COX-2 in SCCs in various locations.54–58 In light of these fi ndings, the role of COX-2 inhibitors in the management of SCC needs to be further explored.

Surgical excision is the treatment of choice for SCC, but a variety of local and systemic treat-ment modalities are available to treat tumors that can-not be completely excised.

QuickNotes

A single nest of neoplastic squamous epithelial cells sur-

rounded by fi brous stroma (keratin pearl; hematoxylin–eosin stain,

400×). This is a common fi nding in well-differentiated SCCs.

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CE In addition to their antiin-fl ammatory effects, COX-2 inhibitors may have anti-tumor properties. The use of piroxicam, a nonspecifi c COX inhibitor, given alone or in combination with other therapies has been evalu-ated in dogs with SCC.59–62 Schmidt and colleagues60

prospectively evaluated the effi cacy of daily oral piroxi-cam in 17 dogs with mea-surable oral SCC. Three dogs obtained partial or complete remission for a median of 180 days; fi ve other dogs had stable disease for a median of 102 days. A recent pharma-cokinetic study evaluat-ing piroxicam in cats with carcinoma suggested that a dose of 0.3 mg/kg/day PO would be appropri-ate for clinical trial use in cats with COX-2–positive oral SCC.58 Although these studies have shown only minimal toxicity (mild vomiting or diarrhea in a few animals), it should be noted that, as a nonspe-cifi c COX inhibitor, piroxi-

cam can induce serious side effects, including gastrointestinal ulceration and renal failure. COX-2–selective inhibitors have a lower inci-dence of these side effects, but, as yet, there are no studies evaluating their effect on SCC.

Novel and Multimodality TherapiesImmunotherapy, the stimulation of the immune system to “reject” a tumor, has been employed in human medicine for treating a variety of cancers, including SCC. Experience with this therapy in small animal medicine is limited. Imiquimod is a topical immunomodulator that induces cytokine production and may induce tumor apoptosis.63 In a small retrospective study64 evaluating the effi cacy and toxicity of topical imiquimod in cats with MSCC, treatment appeared effective in all 12 cats and was associ-ated with mild toxicity (local erythema in three cats, partial anorexia in one cat, and increased

liver enzymes and neutropenia in one cat). Retinoids (vitamin A derivatives) have been evaluated for the treatment of solar-induced SCC and its associated preneoplastic lesions (solar keratosis). In a study assessing the effi -cacy of etretinate for dogs with solar-induced preneoplastic lesions, fi ve of 10 dogs showed a partial or complete response.65 However, thera-peutic effi cacy of 13-cis-retinoic acid was not evident in 10 cats with preneoplastic lesions or SCC of the head.66 A multimodal approach to treating dogs and cats with SCC may provide the most therapeutic benefi t when surgery cannot be curative. The effi cacy of a combination of surgery, carboplatin, and RT was reported in fi ve dogs with tonsil-lar SCC: the mean survival time was 211 days.67 In an earlier study, fi ve of six dogs with tonsil-lar SCC treated with a combination of surgery, doxorubicin, cisplatin, and RT had a complete response with a median disease-free interval of 240 days.12 Carboplatin combined with RT has also been employed for treatment of nasal pla-num SCC in cats with a good response (six of six cats had a complete response and no recurrence for up to 268 days).68 Further prospective studies evaluating multimodal therapy are warranted.

ConclusionSCCs are common tumors of dogs and cats. They vary in appearance, location, and biologic behavior; however, they are typically locally aggressive, with a reported low to moderate metastatic potential. Early recognition, diagnosis, and treatment are essential. Diagnosis of SCC relies on cytologic or histologic examination of the tumor. Many treatment modalities are avail-able, with surgical excision being the mainstay of therapy. The prognosis for patients with SCC varies. A favorable prognosis exists for patients with well-differentiated tumors that can be com-pletely excised and without evidence of vascu-lar or lymphatic invasion or distant metastases. Conversely, the prognosis is poor for patients with inoperable or poorly differentiated tumors or with metastatic disease. Further investiga-tion into the tumorigenesis of SCC is warranted. The fi ndings of these studies may lead to addi-tional preventive measures and novel treatment modalities that improve outcomes for dogs and cats with this type of cancer.

Acknowledgment: The authors thank Dr. C. G. Couto for his editing assistance.

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Mandibular gingival SCC in a dog.

FIGURE 11

(A) Before radiation therapy. (B) Two

months after radiation therapy.

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Prognostic factors associated with radio-therapy of squamous cell carcinoma of the nasal plane in cats. JAVMA 1995;206(7):991-996.40. Thrall DE, Adams WM. Radiotherapy of squamous cell carcinomas of the canine nasal plane. Vet Radiol Ultrasound 1982;23(5):193-195.41. Lascelles BD, Parry AT, Stidworthy MF, et al. Squamous cell carcinoma of the nasal planum in 17 dogs. Vet Rec 2000;147:473-476.42. Bregazzi VS, LaRue SM, Powers BE, et al. Response of feline oral squamous cell car-cinoma to palliative radiation therapy. Vet Radiol Ultrasound 2001;42(1):77-79.43. Andrade AL, Fernandes MAR, Biazzona L, et al. Clinical trial with strontium-90 low ra-diation for treatment of third eyelid neoplasms in dogs. Proc Genes Dogs Cancer 3rd Annu Canine Cancer Conf 2003.44. McCaw DL, Pope ER, Payne JT, et al. Treatment of canine oral squamous cell carci-noma with photodynamic therapy. Br J Cancer 2000;82(7):1297-1299.45. Chang CJ, Lai YL, Wong CJ. Photodynamic therapy for facial squamous cell carci-noma in cats using Photofrin. Changgeng Yi Xue Za Zhi 1998;21(1):13-19.46. Stell AJ, Dobson JM, Langmack K. Photodynamic therapy of feline superfi cial squamous cell carcinoma using topical 5-aminolaevulinic acid. J Small Anim Pract2001;42(4):164-169.47. Buhles WC, Theilen GH. Preliminary evaluation of bleomycin in feline and canine squamous cell carcinoma. Am J Vet Res 1973;34(2):289-291. 48. Theon AP, VanVechten MK, Madewell BR. Intratumoral administration of carbopla-tin for treatment of squamous cell carcinomas of the nasal plane in cats. Am J Vet Res1996;57(2):205-210. 49. Fox LE, Rosenthal RC, King RR, et al. Use of cis-bis-neodecanoato-trans-R,R-1, 2-diaminocyclohexane platinum (II), a liposomal cisplatin analogue, in cats with oral squamous cell carcinoma. Am J Vet Res 2000;61(7):791-795. 50. Kitchell BK, Orenberg EK, Brown DM, et al. Intralesional sustained-release chemo-therapy with therapeutic implants for treatment of canine sun-induced squamous cell car-cinoma. Eur J Cancer 195;31A(12):2093-2098. 51. Lana SE, Dernell WS, Lafferty MH, et al. Use of radiation and a slow-release cisplatin formulation for treatment of canine nasal tumors. Vet Radiol Ultrasound 2004;45(6):577-581.52. Jones PD, de Lorimier LP, Kitchel BE, et al. Gemcitabine as a radiosensitizer for non-resectable feline oral squamous cell carcinoma. JAAHA 2003;39:463-467.53. LeBlanc AK, LaDue TA, Turrel JM, et al. Unexpected toxicity following use of gem-citabine as a radiosensitizer in head and neck carcinomas: a veterinary radiation therapy oncology group pilot study. Vet Radiol Ultrasound 2005;45(5):466-470.54. De Almeida EMP, Piche C, Sirois J, et al. Expression of cyclo-oxygenase-2 in naturally occurring squamous cell carcinomas in dogs. J Histochem Cytochem 2001;49:867-876.55. Beam SL, Rassnick KM, Moore AS, et al. An immunohistochemical study of cyclooxy-genase-2 expression in various feline neoplasms. Vet Pathol 2003;40:496-500.56. Mohammed SI, Khan KN, Sellers RS, et al. Expression of cyclooxygenase-1 and 2 in naturally-occurring canine cancer. Prostaglandins Leukot Essent Fatty Acids2004;70(5):479-483.57. Hayes A, Scase T, Miller J, et al. COX-1 and COX-2 expression in feline oral squamous cell carcinoma. J Comp Pathol 2006;135(2-3):93-99.58. DiBernardi L, Dore M, Davis JA, et al. Study of feline oral squamous cell carcinoma: potential target for cyclooxygenase inhibitor treatment. Prostaglandins Leukot Essent Fatty Acids 2007;76:245-250.59. Knapp DW, Richardson RC, Bottoms GD, et al. Phase I trial of piroxicam in 62 dogs bearing naturally occurring tumors. Cancer Chemother Pharmacol 1992;29(3):214-218.60. Schmidt BR, Glickman NW, DeNicola DB, et al. Evaluation of piroxicam for the treat-ment of oral squamous cell carcinoma in dogs. JAVMA 2001;218(11):1783-1786.61. Boria PA, Murray DJ, Bennett PF, et al. Evaluation of cisplatin combined with piroxicam for the treatment of oral malignant melanoma and oral squamous cell carcinoma in dogs. JAVMA 2004;224(3):388-394.62. Langova V, Mutsaers AJ, Phillips B, et al. Treatment of eight dogs with nasal tumors with alternating doses of doxorubicin and carboplatin in conjunction with oral piroxicam. Aust Vet J 2004;82(11):676-680.



FREE

CE

1. The most common sites of SCC in dogs and cats are

a. the reproductive and gastrointestinal tracts.

b. within the abdominal and thoracic cavities. c. the skin, oral cavity, and digits. d. the urinary bladder and prostate gland.

2. Most cutaneous SCCs in cats occur a. on the head, often involving the pinna,

eyelids, and nasal planum. b. on the torso, often along the dorsal

midline and at the tail base. c. on the digits. d. in the perianal region.

3. Which statement regarding the growth and spread of SCC is true?

a. Most tumors are well circumscribed and encapsulated, with no risk of local spread or distant metastasis.

b. Most tumors are locally invasive, and spread to local lymph nodes may occur.

c. Most tumors are accompanied by paraneoplastic leukocytosis or hyper-trophic osteopathy.

d. Most tumors develop rapidly, with dis-tant metastases present upon initial examination.

4. SCC in situ is a. a large, caulifl ower-like SCC, often

present on the digit of an affected cat. b. a large, intrathoracic SCC resulting

from metastasis. c. the scar that remains within the der-

mis of cats affl icted with an SCC that has spontaneously resolved.

d. a premalignant form of SCC in which the dysplastic cells do not cross the epithelial basement membrane.

5. Which statement regarding solar kera-tosis is false?

a. Solar keratosis always results in wide-spread, multiple skin lesions in dogs and cats.

b. The lesions of solar keratosis range from an erythematous, scaly thicken-ing of the skin to shallow, crusting lesions.

c. The lesions of solar keratosis occur on lightly haired, nonpigmented skin and are associated with UV light exposure.

d. With time and continued exposure to UV light, solar keratosis lesions may progress to SCC.

6. Which statement regarding the develop-ment of cutaneous SCC is false?

a. Prolonged exposure to UV light, lack of skin pigment, and a sparse haircoat all contribute to the development of cutaneous SCC.

b. The mechanism frequently proposed for cutaneous SCC and its association with UV light involves the tumor sup-pressor gene p53.

c. In SCC, the p53 gene is activated by UV light, and the protein product signals increased cell cycling and uncontrolled proliferation of neoplas-tic squamous cells.

d. Cells in which the p53 gene is mutated continue replication even if DNA dam-age is present, leading to mutation accumulation and a greater chance of neoplasia.

7. Asynchronous nuclear and cytoplasmic maturation, which is a common cyto-logic fi nding with SCC, is typifi ed by

a. large, anucleate cells that are fully keratinized.

b. large, fully keratinized cells with retained large nuclei.

c. small, eosinophilic cells with multiple, irregular nuclei.

d. small, anucleate cells with granular, eosinophilic cytoplasm and vacuoles.

8. Which statement regarding the appear-ance of SCC is false?

a. Many SCCs are ulcerative lesions. b. Secondary infl ammation is often pres-

ent when an SCC lesion is ulcerated. c. An infl amed SCC can always be eas-

ily differentiated from nonneoplastic infl ammatory lesions by cytologic examination.

d. Histologic examination may be neces-sary to differentiate infl ammatory from neoplastic cutaneous lesions.

9. Which statement regarding treatment of SCC is true?

a. The size of the tumor does not affect treatment decisions.

b. Surgery is only necessary if primary treatment modalities fail.

c. Tumors respond rapidly and com-pletely to chemotherapy.

d. RT is most commonly applied to tumors of the nasal planum, nasal cavity, and oral cavity.

10. The prognosis for animals with SCC depends on the

a. size of the tumor. b. location of the tumor. c. treatment modalities employed. d. all of the above

3 CECREDITS CE TEST 2 This article qualifi es for 3 contact hours of continuing education credit from the Auburn University College of

Veterinary Medicine. Subscribers may take individual CE tests online and get real-time scores at CompendiumVet.com. Those who wish to apply this credit to fulfi ll state relicensure requirements should consult their respective state authorities regarding the applicability of this program.

63. Shon M, Schon MP. The antitumoral mode of action of imiquimod and other imidazoquinolones. Curr Med Chem 2007;14(6):681-687.64. Gill V, Bergman P, Baer K, et al. Evaluation of imiquimod 5% (Al-dara) in cats with multicentric squamous cell carcinoma in situ (MSC-CIS). Proc 26th Vet Cancer Soc 2006:18.65. Marks SL, Song MD, Stannard AA, et al. Clinical evaluation of etret-inate for the treatment of canine solar-induced squamous cell carcino-ma and preneoplastic lesions. J Am Acad Dermatol 1992;27(1):11-16. 66. Evans AG, Madewell BR, Stannard AL. A trial of 13-cis-retinoic

acid for the treatment of squamous cell carcinoma and preneoplastic lesions of the head in cats. Am J Vet Res 1985;46(12):2553-2557.67. Murphy S, Hayes A, Adams V, et al. Role of carboplatin in multi-modality treatment of canine tonsillar squamous cell carcinoma—a case series of fi ve dogs. J Small Anim Pract 2006;47(4):216-220.68. De Vos JP, Burm AGO, Focker BP. Results from the treatment of advanced stage squamous cell carcinoma of the nasal planum in cats, using a combination of intralesional carboplatin and superfi cial radio-therapy: a pilot study. Vet Comp Oncol 2004;2(2):75-81.

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Index to Advertisers For free information about products advertised in this issue, email the product names to [email protected].

Company Product PageAbbott Animal Health SevoFlo 119, 120ASPCA Animal Poison Control Free magnet 101 (US only)

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DER090042A

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