Today's Veterinary Practice, September 2017 by davidpsu

IN THIS ISSUE 28 ULTRASONOGRAPHY OF THE ADRENAL GLANDS 38 TOOTH EXTRACTION TIPS 48 COGNITIVE DYSFUNCTION

The Intestinal Microbiota: Its Scope and Significance

SEPTEMBER/OCTOBER 2017 VOLUME 7, NUMBER 5

Advanced Advanced

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SEPTEMBER/OCTOBER 2017

VOLUME 7, NUMBER 5

An Official journal of the

An official journal of the NAVC, Today’s Veterinary Practice is the trusted source for peer-reviewed clinical information in small animal veterinary medicine. Our goal is to enhance knowledge and encourage confidence, inspiring the highest quality of veterinary care. As an NAVC publication, our audience has access to world-class continuing professional development developed for the global veterinary health care community. Subscriptions (only): 630.739.0900, CDS/Today’s Veterinary Practice 440 Quadrangle Drive, Suite E, Bolingbrook, IL 60440. Email subscription form to subscriptions@CDS1976.com or fax to 630.739.9700 Free subscriptions only to qualifying subscribers.* For a new subscription, confirmation, or renewal, please visit tvpjournal.com to fill out an online form. For updates, please include your subscription ID from label. To have a form emailed or faxed to you, please contact us at our 800 number or email above and provide email or fax number. Change Name/Address or Cancel: Please use online form at tvpjournal.com or contact us by phone, fax, or email subscriptions@CDS1976.com. Please provide the ID number (directly above your name on label) for positive identification. If the ID number is not available or legible, provide name and address as it appears on the label to allow identification of the subscription. *Qualifying Subscribers: Veterinarians, members of the veterinary health care team, veterinary school faculty, veterinary students, and other professionals allied to the field. Eastern States Veterinary Association, Inc (NAVC) reserves the right to determine eligibility for a free subscription. WARRANTIES, LIMITATIONS. Except as expressly set forth herein, Eastern States Veterinary Association, Inc (NAVC) makes no warranties whatsoever, express, implied, or statutory. NAVC specifically disclaims any implied warranty of merchantability or fitness for a particular purpose. In no event will NAVC be liable to you or any third party for any indirect, punitive, special, incidental, or consequential damages (including loss of profits, use, data, or other economic advantage), however it arises, even if NAVC has previously been advised of the possibility of such damage. All rights reserved. No part of this publication may be reproduced in any form without written permission from the publisher. Entire contents ©2017 Eastern States Veterinary Association, Inc (NAVC).

Editor in Chief Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN University of Georgia College of Veterinary Medicine SRPlatt@NAVC.com

Chief Executive Officer, NAVC Thomas M. Bohn, MBA, CAE TBohn@NAVC.com

Laura C.S. Walker Senior Vice President of Sales and Publishing LWalker@NAVC.com Chris Kelly, Group Publisher CKelly@NAVC.com Rick Boggess, Vice President of Sales and Marketing, NAVC Publishing RBoggess@NAVC.com Nick Paolo, MS, MBA, Director of Operations and Finance, NAVC Publishing NPaolo@NAVC.com Robin Henry, Executive Editor RHenry@NAVC.com Jackie D’Antonio, Managing Editor JDantonio@NAVC.com Renee Luttrell, Director of Sales RLuttrell@NAVC.com, 610.558.1819

Editorial Advisory Board P. Jane Armstrong, DVM, MS, MBA, DACVIM, (Small Animal Internal Medicine) University of Minnesota, College of Veterinary Medicine

Paige Ellington, Account Executive PEllington@NAVC.com, 404.550.6649 Sondra Reynolds, Director of Audience Development SReynolds@NAVC.com Michelle Taylor, Senior Art Director David Beagin, Art Director Julie Butler, Assistant Editor

Mark Cofone, VMD, DACVS Veterinary Specialty Center, Wilmington, Delaware

Megan Cox, Staff Writer Cheryl Hobbs, Staff Editor Suzanne B. Meyers, Staff Editor Lisa Wirth, VMD, Staff Editor

Sheila Grosdidier, RVT, PHR Veterinary Management Consultation Evergreen, Colorado

Garret Pachtinger, VMD, DACVECC Veterinary Specialty & Emergency Center Levittown, Pennsylvania Michael Schaer, DVM, DACVIM, DACVECC University of Florida College of Veterinary Medicine

NAVC Board of Directors President Gail Gibson, VMD Immediate Past President Melinda D. Merck, DVM President-Elect K. Leann Kuebelbeck, DVM, DACVS Vice President Cheryl Good, DVM Treasurer Laurel Kaddatz, DVM Directors Paige Allen, MS, RVT Harold Davis, Jr, BA, RVT, VTS (Emergency & Critical Care) (Anesthesia & Analgesia) Sally Haddock, DVM Bob Lester, DVM

FEATURES 38

FEATURE

Tips to Avoid Tooth Extraction Complications Brenda L. Mulherin, DVM, DAVDC Even theoretically simple surgical tooth extractions can be difficult. This article presents some factors to consider to make surgical extraction as safe and easy as possible for both surgeon and patient.

FEATURE

Management of Dogs and Cats With Cognitive Dysfunction Lynne Seibert, DVM, MS, PhD, DACVB This article discusses important aspects of behavior changes in older patients, including diagnosis, clinical signs, pathophysiology, and nutritional and pharmacologic treatment.

FEATURE

Intestinal Microbes and Digestive System Disease in Dogs Jan S. Suchodolski, MedVet, DrVetMed, PhD, AGAF, DACVM The complex ecosystem of gut bacteria has a tremendous influence on host health. This article provides an overview of the bacteria in the canine intestine and their role in the etiology of gastrointestinal diseases.

8 TODAY’S VETERINARY NEWS 65 ADVERTISER INDEX Today’s Veterinary Practice does not, by publication of ads, express endorsement or verify the accuracy and effectiveness of the products and claims contained therein. The publisher, Eastern States Veterinary Association, Inc (NAVC), disclaims any liability for any damages resulting from the use of any product advertised herein and suggests that readers fully investigate the products and claims prior to purchasing. The opinions stated in this publication are those of the respective authors and do not necessarily represent the opinions of the NAVC nor its Editorial Advisory Board. NAVC does not guarantee nor make any other representation that the material contained in articles herein is valid, reliable, or accurate; nor does the NAVC assume any responsibility for injury or death arising from any use, or misuse, of same. There is no implication that the material published herein represents the best or only procedure for a particular condition. It is the responsibility of the reader to verify the accuracy and applicability of any information presented and to adapt as new data becomes publicly available. Today’s Veterinary Practice (ISSN 2162-3872 print and ISSN 2162-3929 online) is published bi-monthly (Jan/Feb, Mar/Apr, May/June, Jul/Aug, Sept/ Oct, Nov/Dec; 6x per year) by North American Veterinary Community, NAVC, 622 East Washington St, Ste 300, Orlando, FL 32801. Periodicals postage paid at Orlando, FL 32801 and additional mailing offices. POSTMASTER: Send all UAA to CFS (See DMM 507.1.5.2); NON-POSTAL AND MILITARY FACILITIES: send address corrections to CDS/Today’s Veterinary Practice, 440 Quadrangle Drive, Ste E, Bolingbrook, IL 60440.

TABLE OF CONTENTS

To read this issue online, visit tvpjournal.com

DECHRA’S IV FLUID PORTFOLIO

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Vetivex® Lactated Ringer’s and 5% Dextrose Injection, USP 1000 mL bag

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For current promotion pricing on select fluids or to order, please contact your Dechra or distributor representative or call (866) 683-0660. More Information at www.dechra-us.com 24-hour Veterinary Technical Support available (866) 933-2472. Non-urgent Technical Support available via email at support@dechra.com. CAUTION: Federal law restricts these drugs to use by or on the order of a licensed veterinarian. Dechra is a registered trademark of Dechra Pharmaceuticals PLC. Vetivex is a registered trademark of Dechra Limited. pHyLyte is a registered trademark of Dechra Veterinary Products LLC.

COLUMNS 6 EDITOR’S NOTE

The Foundation for a Cure? Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN

VET REPORT VITALS

How Can We Address Antimicrobial Resistance Head On? Molly McAllister, DVM, MPH

AHS HEARTWORM HOTLINE

Beyond the Map: The State of Heartworm Incidence in the United States Chris Rehm, DVM, and Doug Carithers, DVM

DERMATOLOGY DETAILS

Dermatology Diagnostics: Skin Scrapes, Hair Plucks, and More Chris Reeder, DVM, DACVD

IMAGING ESSENTIALS

Ultrasonography of the Adrenal Glands Elizabeth Huynh, DVM, and Clifford R. Berry, DVM, DACVR

HOW I TREAT…

Pneumothorax An Interview With Dr. Elisa Mazzaferro

TABLE OF CONTENTS

To read this issue online, visit tvpjournal.com

The infl ammation Tamer Help get your patients moving again with Duralactin®. When an active pet becomes less mobile, whether from injury or normal aging, owners trust you to do all you can to get their dogs and cats moving again. While many supplements can strengthen cartilage and connective tissue, only Duralactin® products contain MicroLactin®, to help support joint health and reduce inflammation throughout the body with minimal side effects.

Here’s why Duralactin products should be a key part of your treatment of inflammation and joint conditions. • Ideal for long-term use and high-risk pets • Easy once-a-day dosage • Palatable, with a variety of flavors and dosage types • Multiple formulations for canines and felines • Proven with 14+ years of clinical use SATISFACTION GUARANTEED

DURALACTIN® products come with a risk-free, 100% money-back guarantee if you or your client are not 100% satisfied with results.

To find out more about how Duralactin tames inflammation, speak to your sales representative, or visit our website at duralactin.com.

This product has not been approved by the FDA nor is it intended to diagnose, treat, cure, or prevent any disease. Should only be used through consultation of a veterinarian and in conjunction with an overall wellness program. Microlactin is a registered trademark of Stolle Milk Biologics, Inc. Duralactin is a registered trademark of PRN Pharmacal, Inc. ©2017 PRN Pharmacal, Inc. All rights reserved.

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CE as needed, when needed.

EDITOR’S NOTE

Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN University of Georgia

EDITOR’S NOTE

The Foundation for a Cure?

“ When the number of factors coming into play in a phenomenological complex is too large, scientific method in most cases fails. One need only think of the weather, in which case the prediction even for a few days ahead is impossible.”

— Albert Einstein

Is predicting the success of therapy for a specific veterinary disease impossible? Will we soon be able to know which patients we can actually “cure” based on their genes? Laying the foundation for the answers to these questions has begun now that we have the ability to genetically test our patients. Most medical treatments are designed for the “average patient,” a type of “one-size-fits-all” approach that is not uniformly successful. Precision medicine, sometimes known as personalized medicine, is a novel approach to disease prevention and treatment that takes into account differences in genetics, environment, and lifestyle. Advances in precision medicine in humans have already led to major new discoveries and several new Food and Drug Administration–approved therapies designed to the specific characteristics of individuals. As an example, human patients with a variety of cancers routinely undergo genetic testing, enabling treatment selection that improves their chance of survival and reduces the potential for adverse effects. Although genomic testing is still a relatively new development in drug treatment, this field is expanding. Currently, more than 100 drugs have label information regarding pharmacogenomic

EDITOR’S NOTE

biomarkers (genetic information that can be used to direct the use of a drug). When the genomes of people taking the same drug are compared, people who share a certain genetic variation also seem to share a common treatment characteristic, such as the need for a higher dose to achieve a therapeutic effect or an optimal duration of treatment. This kind of treatment information is currently used to improve the selection and dosage of drugs to treat a wide range of conditions in people, including cardiovascular disease, lung disease, HIV infection, cancer, arthritis, high cholesterol, and depression. Animal DNA testing is now offered by a plethora of companies, confirming breed types, parentage, and predisposition to diseases. We have been aware for many years that we can use such genetic tests to assist in herd health and production performance as well as to confirm disease presence in specific breeds. However, the genetic evaluation of our patients has the potential to revolutionize our practice and improve our treatment outcomes. Molecular characterization of veterinary diseases with similarly characterized human disorders for which precision treatments have been or are being developed will allow us to utilize what is already known. Clinical trials involving human and animal cancer patients are increasingly providing information about shared genetic abnormalities that represent important drug targets. In time, precision veterinary medicine will likely have an impact on treatment not only of cancer but also of diseases such as diabetes, obesity, and infectious disease. The discovery in animals of molecular profiles and biomarkers associated with distinct clinical presentations will provide new insights into veterinary diseases and may lead to the development of new diagnostic criteria, therapeutic targets, and prevention strategies. As such, predicting the future course and treatment of veterinary diseases may become easier than predicting the weather!

TODAY’S VETERINARY NEWS

Recognizing the value of veterinary technicians, the HEARTGARD Plus (ivermectin/pyrantel) team recently conducted a survey to explore the state of the industry. Results showed that almost all veterinarians feel veterinary technicians are knowledgeable about preventive pet health (98%) and capable with regard to patient care (99%). The survey also explored in-clinic heartworm disease discussion and education. Less than 10% of veterinary professionals said dog owners are “very knowledgeable” about heartworm disease, and more than half said the dog owners who visit their clinic do not usually ask about heartworm prevention before the clinicians bring it up. However, according to the survey, once dog owners are educated about heartworm disease and the need for prevention, nearly all of them (98%) are compliant with prevention recommendations.

“

HEARTGARD® (ivermectin); HEARTGARD® Plus (ivermectin/pyrantel)

SURVEY SHOWS: VETERINARY TECHNICIANS FILL NEED FOR HEARTWORM DISEASE EDUCATION The HEARTGARD Plus team recognizes the importance of veterinary technicians. We conducted this proprietary survey to explore the state of the industry and the extent of in-clinic heartworm disease discussion and education.

HOW DO VETERINARIANS FEEL ABOUT VETERINARY TECHNICIANS?

88%

FEEL THEIR CLIENTS VALUE VETERINARY TECHNICIANS’ GUIDANCE AND EDUCATION.

HOW DO VETERINARIANS FEEL ABOUT HEARTWORM DISEASE AND EDUCATION?

RESEARCH NOW SURVEY METHODOLOGY: • 1,002 LICENSED VETERINARIANS • 250 LICENSED VET TECHS • THE SURVEY WAS CONDUCTED MARCH 10 – 28, 2017. ALL RESPONDENTS WERE CURRENTLY EMPLOYED IN A VETERINARY CLINIC.

These results reveal a huge opportunity for veterinarians and veterinary technicians to help keep more dogs healthy and happy by proactively discussing heartworm disease with every pet owner that visits their clinic, says Sarah Cloud, marketing director, HEARTGARD Plus.

“

New Survey Highlights Value of Veterinary Technicians

TOP THREE SKILLS OR ATTRIBUTES VET TECHS BRING: COMMUNICATION EMPATHY TECHNICAL KNOWLEDGE

LESS THAN 10% SAID THAT DOG OWNERS ARE “VERY KNOWLEDGEABLE”

MORE THAN 50% SAID THAT DOG OWNERS DO NOT USUALLY ASK ABOUT IT FIRST

VET TECHS FEEL COMFORTABLE EDUCATING CLIENTS ABOUT:

ONLY 36% DISCUSS HEARTWORM DISEASE WITH DOG OWNERS EVERY VISIT

• ADMINISTRATION OF MEDICATION

STRENGTHEN RELATIONSHIPS WITHIN THE VET TECH COMMUNITY

PROTECT MORE PETS WITH PREVENTIVE MEDICINE

• FLEA AND TICK CONTROL • HEARTWORM PREVENTION

PROVIDE FREE RESOURCES FOR CONTINUING EDUCATION

FIND OUT ABOUT TECH CHAMPIONS AT HEARTGARDCLINIC.COM Tech Champions is a program created by the HEARTGARD Plus team and the National Association of Veterinarian Technicians in America (NAVTA). These selected veterinary technicians serve as advocates for heartworm disease prevention, dental health, and flea and tick control.

IMPORTANT SAFETY INFORMATION: HEARTGARD (ivermectin) and HEARTGARD Plus (ivermectin/pyrantel) are well tolerated. All dogs should be tested for heartworm infection before starting a preventive program. Following the use of HEARTGARD and HEARTGARD Plus, digestive and neurological side effects have rarely been reported. For more information visit www.HEARTGARD.com. Merial is now part of Boehringer Ingelheim. ®HEARTGARD and the Dog & Hand Logo are registered trademarks of Merial. ©2017 Merial, Inc., Duluth, GA. All rights reserved. HGD17VTSURVEYIG (06/17).

■ Learn more at www.HeartgardClinic.com/infographic.

DECHRA LAUNCHES NEW MOUSSES Dechra Veterinary Products has now added its 2 most popular formulas, MiconaHex+Triz and TrizCHLOR 4, in easy-to-use mousses. The mousses are available in 7.1–fluid ounce pump dispensers. MiconaHex+Triz Mousse has 2% chlorhexidine, 2% miconazole, TrizEDTA, and Dechra’s ceramide complex. TrizCHLOR 4 has 4% chlorhexidine and TrizEDTA. Both contain no alcohol, so they are nonirritating to ulcerated or abraded skin. They are labeled for dogs, cats, and horses. ■C ontact your Dechra representative or distributor representative for further details on availability.

GRANT ADVANCES CLINICAL TRIALS AT OSU COLLEGE OF VETERINARY MEDICINE June 2017 marked the first year anniversary of the Blue Buffalo Veterinary Clinical Trials Office (BBVCTO). In 2016, Blue Buffalo announced a $6 million gift to advance clinical trials at the Ohio State University College of Veterinary Medicine. The gift supports initiatives at the BBVCTO to conduct research to enhance medical knowledge and improve patient care for both animals and humans. The research studies focus on the development of new treatments for cancer, heart disease, and arthritis. Pet owners work with veterinary researchers during the trials with the ultimate goal of finding new therapies and diagnostic tests that will improve animal and human health. ■F or more information, visit vet.osu.edu/vmc/cto.

Got news? Submit your press release for consideration for inclusion in Today’s Veterinary News at editor@NAVC.com. Chosen submissions will be edited before publication.

TODAY’S VETERINARY NEWS

Buster’s playmates miss him. It won’t be for long, because you prescribe PREVICOX.® Who isn’t sad when a dog is in too much osteoarthritis pain to play? So trust PREVICOX as your go-to NSAID because PREVICOX: • Provides efficacy both pet owners and veterinarians notice In a field study, after 30 days of use: – 96% of pet owners saw improvement in their dogs1 – Veterinarians saw improvement in 93% of dogs1 • Is rapidly absorbed—detected in plasma levels within 30 minutes2 • Is convenient with once-daily dosing

PUT RELIEF IN MOTION

Important Safety Information As a class, cyclooxygenase inhibitory NSAIDs may be associated with gastrointestinal, kidney or liver side effects. These are usually mild, but may be serious. Pet owners should discontinue therapy and contact their veterinarian immediately if side effects occur. Evaluation for pre-existing conditions and regular monitoring are recommended for pets on any medication, including PREVICOX. Use with other NSAIDs, corticosteroids or nephrotoxic medication should be avoided. Refer to the Prescribing Information for complete details. Merial is now part of Boehringer Ingelheim. REFERENCES: 1. Pollmeier M, Toulemonde C, Fleishman C, Hanson PD. Clinical evaluation of firocoxib and carprofen for the treatment of dogs with osteoarthritis. Vet Rec. 2006;159(17):547-551. 2. Data on file at Merial. ®PREVICOX is a registered trademark of Merial. ©2017 Merial, Inc. Duluth, GA. All rights reserved. PVX15TRADEADA-R (07/17).

TODAY’S VETERINARY NEWS

AAFP ANNOUNCES NEW CLIENT BROCHURES The American Association of Feline Practitioners (AAFP) has just released 2 new client brochures: “How Do I Know if my Cat is in Pain?” and “Degenerative Joint Disease.” These brochures provide valuable and reliable information for cat caregivers on topics that affect the quality of life of their cats. The AAFP had thanked Zoetis and Boehringer Ingleheim for their sponsorship of these brochures and their commitment to improve the lives of cats through client education. The brochures can be downloaded at www.catvets.com/guidelines/client-brochures.

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WSAVA CONGRESS UPDATE The World Small Animal Veterinary Association (WSAVA) Congress will explore healthy breeding and other aspects of small animal practice from September 25 through 28, 2017, in Copenhagen, Denmark. Healthy breeding has been selected as a focus topic by the local host, the Danish Small Animal Veterinary Association, in light of growing concerns about the risks of inherited conditions and the welfare issues they raise for companion animals. A lecture stream covering genetic testing, genetic counseling, and other topics is included in the Scientific Program, and the World Congress will also offer a roundtable discussion on brachycephalic syndrome, hosted jointly by the WSAVA and the Federation of European Companion Animal Veterinary Associations (FECAVA). ■ Learn more at wsava2017.com.

MERITORIOUS SERVICE AWARD ANNOUNCED Professor Bojan Zorko from the University of Ljubljana, Slovenia, will receive the 2017 WSAVA Award for Meritorious Service in recognition of the role he has played in developing the veterinary profession in Slovenia. Zorko is a specialist in canine and feline medicine and professor of veterinary radiology at the University of Ljubljana. He is also Director of the International Veterinary Radiology Association for Central and Eastern Europe. ■L earn more about Zorko and the award at wsava.org/article/recipient-2017-wsavameritorious-service-award-announced.

HEARTWORM REMOVED FROM CAT’S FEMORAL ARTERY Veterinarians from the University of California, Davis recently removed a heartworm from a cat’s femoral artery. After an initial evaluation at a local veterinary emergency room in Berkeley, Stormie, a 4-year-old female Siamese, was brought to specialists at the UC Davis veterinary hospital. Cardiologist Dr. Catherine Gunther-Harrington and Dr. Ingrid Balsa of the Soft Tissue Surgery Service, assisted by cardiology resident Dr. Maureen Oldach, successfully removed a 13-centimeter heartworm from Stormie’s right femoral artery without breaking it. The artery was repaired, and the doctors decided that amputation was not necessary. Removal of a heartworm via the femoral artery is extremely rare in veterinary medicine and has been reported on only a few occasions in dogs, but never in cats. ■ Learn more about the case at vetmed.ucdavis.edu/whatsnew/article.cfm?id=3884.

TODAY’S VETERINARY NEWS

CHEWABLE TABLETS Brief Summary: Before using PREVICOX, please consult the product insert, a summary of which follows: Caution: Federal law restricts this drug to use by or on the order of a licensed veterinarian. Indications: PREVICOX (firocoxib) Chewable Tablets are indicated for the control of pain and inflammation associated with osteoarthritis and for the control of postoperative pain and inflammation associated with soft-tissue and orthopedic surgery in dogs. Contraindications: Dogs with known hypersensitivity to firocoxib should not receive PREVICOX. Warnings: Not for use in humans. Keep this and all medications out of the reach of children. Consult a physician in case of accidental ingestion by humans. For oral use in dogs only. Use of this product at doses above the recommended 2.27 mg/lb (5.0 mg/kg) in puppies less than seven months of age has been associated with serious adverse reactions, including death (see Animal Safety). Due to tablet sizes and scoring, dogs weighing less than 12.5 lb (5.7 kg) cannot be accurately dosed. All dogs should undergo a thorough history and physical examination before the initiation of NSAID therapy. Appropriate laboratory testing to establish hematological and serum baseline data is recommended prior to and periodically during administration of any NSAID. Owners should be advised to observe for signs of potential drug toxicity (see Adverse Reactions and Animal Safety) and be given a Client Information Sheet about PREVICOX Chewable Tablets. For technical assistance or to report suspected adverse events, call 1-877-217-3543. For additional information about adverse drug experience reporting for animal drugs, contact FDA at 1-888-FDAVETS or http://www.fda.gov/ AnimalVeterinary/SafetyHealth Precautions: This product cannot be accurately dosed in dogs less than 12.5 pounds in body weight. Consider appropriate washout times when switching from one NSAID to another or when switching from corticosteroid use to NSAID use. As a class, cyclooxygenase inhibitory NSAIDs may be associated with renal, gastrointestinal and hepatic toxicity. Sensitivity to drug-associated adverse events varies with the individual patient. Dogs that have experienced adverse reactions from one NSAID may experience adverse reactions from another NSAID. Patients at greatest risk for adverse events are those that are dehydrated, on concomitant diuretic therapy, or those with existing renal, cardiovascular, and/ or hepatic dysfunction. Concurrent administration of potentially nephrotoxic drugs should be carefully approached and monitored. NSAIDs may inhibit the prostaglandins that maintain normal homeostatic function. Such anti-prostaglandin effects may result in clinically significant disease in patients with underlying or pre-existing disease that has not been previously diagnosed. Since NSAIDs possess the potential to produce gastrointestinal ulceration and/or gastrointestinal perforation, concomitant use of PREVICOX Chewable Tablets with other anti-inflammatory drugs, such as NSAIDs or corticosteroids, should be avoided. The concomitant use of protein-bound drugs with PREVICOX Chewable Tablets has not been studied in dogs. Commonly used protein-bound drugs include cardiac, anticonvulsant, and behavioral medications. The influence of concomitant drugs that may inhibit the metabolism of PREVICOX Chewable Tablets has not been evaluated. Drug compatibility should be monitored in patients requiring adjunctive therapy. If additional pain medication is needed after the daily dose of PREVICOX, a non-NSAID class of analgesic may be necessary. Appropriate monitoring procedures should be employed during all surgical procedures. Anesthetic drugs may affect renal perfusion, approach concomitant use of anesthetics and NSAIDs cautiously. The use of parenteral fluids during surgery should be considered to decrease potential renal complications when using NSAIDs perioperatively. The safe use of PREVICOX Chewable Tablets in pregnant, lactating or breeding dogs has not been evaluated. Adverse Reactions: Osteoarthritis: In controlled field studies, 128 dogs (ages 11 months to 15 years) were evaluated for safety when given PREVICOX Chewable Tablets at a dose of 2.27mg/lb (5.0 mg/kg) orally once daily for 30 days. The following adverse reactions were observed. Dogs may have experienced more than one of the observed adverse reactions during the study. Adverse Reactions Seen in U. S. Field Studies Adverse Reactions Vomiting Diarrhea Decreased Appetite or Anorexia Lethargy Pain Somnolence Hyperactivity

PREVICOX (n=128) 5 1 3 1 2 1 1

Active Control (n=121) 8 10 3 3 1 1 0

PREVICOX (firocoxib) Chewable Tablets were safely used during field studies concomitantly with other therapies, including vaccines, anthelmintics, and antibiotics. Soft-tissue Surgery: In controlled field studies evaluating soft-tissue postoperative pain and inflammation, 258 dogs (ages 10.5 weeks to 16 years) were evaluated for safety when given PREVICOX Chewable Tablets at a dose of 2.27 mg/ lb (5.0 mg/kg) orally approximately 2 hours prior to surgery and once daily thereafter for up to two days. The following adverse reactions were observed. Dogs may have experienced more than one of the observed reactions during the study. Adverse Reactions Seen in the Soft-tissue Surgery Postoperative Pain Field Studies Adverse Reactions Vomiting Diarrhea Bruising at Surgery Site Respiratory Arrest SQ Crepitus in Rear Leg and Flank Swollen Paw

Firocoxib Group (n=127) 5 1 1 1 1 1

Control Group* (n=131) 6 1 1 0 0 0

*Sham-dosed (pilled) Orthopedic Surgery: In a controlled field study evaluating orthopedic postoperative pain and inflammation, 226 dogs of various breeds, ranging in age from 1 to 11.9 years in the PREVICOX-treated groups and 0.7 to 17 years in the control group were evaluated for safety. Of the 226 dogs, 118 were given PREVICOX Chewable Tablets at a dose of 2.27 mg/lb (5.0 mg/kg) orally approximately 2 hours prior to surgery and once daily thereafter for a total of three days. The following adverse reactions were observed. Dogs may have experienced more than one of the observed reactions during the study. Adverse Reactions Seen in the Orthopedic Surgery Postoperative Pain Field Study Adverse Reactions Vomiting Diarrhea Bruising at Surgery Site Inappetence/ Decreased Appetite Pyrexia Incision Swelling, Redness Oozing Incision

Firocoxib Group (n=118) 1 2** 2 1 0 9 2

A case may be represented in more than one category. *Sham-dosed (pilled). **One dog had hemorrhagic gastroenteritis.

Control Group* (n=108) 0 1 3 2 1 5 0

Post-Approval Experience (Rev. 2009): The following adverse reactions are based on post-approval adverse drug event reporting. The categories are listed in decreasing order of frequency by body system: Gastrointestinal: Vomiting, anorexia, diarrhea, melena, gastrointestinal perforation, hematemesis, hematachezia, weight loss, gastrointestinal ulceration, peritonitis, abdominal pain, hypersalivation, nausea Urinary: Elevated BUN, elevated creatinine, polydypsia, polyuria, hematuria, urinary incontinence, proteinuria, kidney failure, azotemia, urinary tract infection Neurological/Behavioral/Special Sense: Depression/lethargy, ataxia, seizures, nervousness, confusion, weakness, hyperactivity, tremor, paresis, head tilt, nystagmus, mydriasis, aggression, uveitis Hepatic: Elevated ALP, elevated ALT, elevated bilirubin, decreased albumin, elevated AST, icterus, decreased or increased total protein and globulin, pancreatitis, ascites, liver failure, decreased BUN Hematological: Anemia, neutrophilia, thrombocytopenia, neutropenia Cardiovascular/Respiratory: Tachypnea, dyspnea, tachycardia Dermatologic/Immunologic: Pruritis, fever, alopecia, moist dermatitis, autoimmune hemolytic anemia, facial/muzzle edema, urticaria In some situations, death has been reported as an outcome of the adverse events listed above. For a complete listing of adverse reactions for firocoxib reported to the CVM see: http://www.fda.gov/downloads/ AnimalVeterinary/SafetyHealth/ProductSafetyInformation/UCM055407.pdf Information For Dog Owners: PREVICOX, like other drugs of its class, is not free from adverse reactions. Owners should be advised of the potential for adverse reactions and be informed of the clinical signs associated with drug intolerance. Adverse reactions may include vomiting, diarrhea, decreased appetite, dark or tarry stools, increased water consumption, increased urination, pale gums due to anemia, yellowing of gums, skin or white of the eye due to jaundice, lethargy, incoordination, seizure, or behavioral changes. Serious adverse reactions associated with this drug class can occur without warning and in rare situations result in death (see Adverse Reactions). Owners should be advised to discontinue PREVICOX therapy and contact their veterinarian immediately if signs of intolerance are observed. The vast majority of patients with drug-related adverse reactions have recovered when the signs are recognized, the drug is withdrawn, and veterinary care, if appropriate, is initiated. Owners should be advised of the importance of periodic follow up for all dogs during administration of any NSAID. Effectiveness: Two hundred and forty-nine dogs of various breeds, ranging in age from 11 months to 20 years, and weighing 13 to 175 lbs, were randomly administered PREVICOX or an active control drug in two field studies. Dogs were assessed for lameness, pain on manipulation, range of motion, joint swelling, and overall improvement in a non-inferiority evaluation of PREVICOX compared with the active control. At the study’s end, 87% of the owners rated PREVICOX-treated dogs as improved. Eighty-eight percent of dogs treated with PREVICOX were also judged improved by the veterinarians. Dogs treated with PREVICOX showed a level of improvement in veterinarian-assessed lameness, pain on palpation, range of motion, and owner-assessed improvement that was comparable to the active control. The level of improvement in PREVICOX-treated dogs in limb weight bearing on the force plate gait analysis assessment was comparable to the active control. In a separate field study, two hundred fifty-eight client-owned dogs of various breeds, ranging in age from 10.5 weeks to 16 years and weighing from 7 to 168 lbs, were randomly administered PREVICOX or a control (sham-dosed-pilled) for the control of postoperative pain and inflammation associated with soft-tissue surgical procedures such as abdominal surgery (e.g., ovariohysterectomy, abdominal cryptorchidectomy, splenectomy, cystotomy) or major external surgeries (e.g., mastectomy, skin tumor removal ≤8 cm). The study demonstrated that PREVICOXtreated dogs had significantly lower need for rescue medication than the control (sham-dosed-pilled) in controlling postoperative pain and inflammation associated with soft-surgery. A multi-center field study with 226 client-owned dogs of various breeds, and ranging in age from 1 to 11.9 years in the PREVICOX-treated groups and 0.7 to 17 years in the control group was conducted. Dogs were randomly assigned to either the PREVICOX or the control (sham-dosedpilled) group for the control of postoperative pain and inflammation associated with orthopedic surgery. Surgery to repair a ruptured cruciate ligament included the following stabilization procedures: fabellar suture and/or imbrication, fibular head transposition, tibial plateau leveling osteotomy (TPLO), and ‘over the top’ technique. The study (n = 220 for effectiveness) demonstrated that PREVICOX-treated dogs had significantly lower need for rescue medication than the control (sham-dosed-pilled) in controlling postoperative pain and inflammation associated with orthopedic surgery. Animal Safety: In a targeted animal safety study, firocoxib was administered orally to healthy adult Beagle dogs (eight dogs per group) at 5, 15, and 25 mg/kg (1, 3, and 5 times the recommended total daily dose) for 180 days. At the indicated dose of 5 mg/kg, there were no treatment-related adverse events. Decreased appetite, vomiting, and diarrhea were seen in dogs in all dose groups, including unmedicated controls, although vomiting and diarrhea were seen more often in dogs in the 5X dose group. One dog in the 3X dose group was diagnosed with juvenile polyarteritis of unknown etiology after exhibiting recurrent episodes of vomiting and diarrhea, lethargy, pain, anorexia, ataxia, proprioceptive deficits, decreased albumin levels, decreased and then elevated platelet counts, increased bleeding times, and elevated liver enzymes. On histopathologic examination, a mild ileal ulcer was found in one 5X dog. This dog also had a decreased serum albumin which returned to normal by study completion. One control and three 5X dogs had focal areas of inflammation in the pylorus or small intestine. Vacuolization without inflammatory cell infiltrates was noted in the thalamic region of the brain in three control, one 3X, and three 5X dogs. Mean ALP was within the normal range for all groups but was greater in the 3X and 5X dose groups than in the control group. Transient decreases in serum albumin were seen in multiple animals in the 3X and 5X dose groups, and in one control animal. In a separate safety study, firocoxib was administered orally to healthy juvenile (10-13 weeks of age) Beagle dogs at 5, 15, and 25 mg/kg (1, 3, and 5 times the recommended total daily dose) for 180 days. At the indicated (1X) dose of 5 mg/kg, on histopathologic examination, three out of six dogs had minimal periportal hepatic fatty change. On histopathologic examination, one control, one 1X, and two 5X dogs had diffuse slight hepatic fatty change. These animals showed no clinical signs and had no liver enzyme elevations. In the 3X dose group, one dog was euthanized because of poor clinical condition (Day 63). This dog also had a mildly decreased serum albumin. At study completion, out of five surviving and clinically normal 3X dogs, three had minimal periportal hepatic fatty change. Of twelve dogs in the 5X dose group, one died (Day 82) and three moribund dogs were euthanized (Days 38, 78, and 79) because of anorexia, poor weight gain, depression, and in one dog, vomiting. One of the euthanized dogs had ingested a rope toy. Two of these 5X dogs had mildly elevated liver enzymes. At necropsy all five of the dogs that died or were euthanized had moderate periportal or severe panzonal hepatic fatty change; two had duodenal ulceration; and two had pancreatic edema. Of two other clinically normal 5X dogs (out of four euthanized as comparators to the clinically affected dogs), one had slight and one had moderate periportal hepatic fatty change. Drug treatment was discontinued for four dogs in the 5X group. These dogs survived the remaining 14 weeks of the study. On average, the dogs in the 3X and 5X dose groups did not gain as much weight as control dogs. Rate of weight gain was measured (instead of weight loss) because these were young growing dogs. Thalamic vacuolation was seen in three of six dogs in the 3X dose group, five of twelve dogs in the 5X dose group, and to a lesser degree in two unmedicated controls. Diarrhea was seen in all dose groups, including unmedicated controls. In a separate dose tolerance safety study involving a total of six dogs (two control dogs and four treated dogs), firocoxib was administered to four healthy adult Beagle dogs at 50 mg/kg (ten times the recommended daily dose) for twenty-two days. All dogs survived to the end of the study. Three of the four treated dogs developed small intestinal erosion or ulceration. Treated dogs that developed small intestinal erosion or ulceration had a higher incidence of vomiting, diarrhea, and decreased food consumption than control dogs. One of these dogs had severe duodenal ulceration, with hepatic fatty change and associated vomiting, diarrhea, anorexia, weight loss, ketonuria, and mild elevations in AST and ALT. All four treated dogs exhibited progressively decreasing serum albumin that, with the exception of one dog that developed hypoalbuminemia, remained within normal range. Mild weight loss also occurred in the treated group. One of the two control dogs and three of the four treated dogs exhibited transient increases in ALP that remained within normal range. Made in France Marketed by: Merial, Inc., Duluth, GA 30096-4640, U.S.A. 1-877-217-3543 NADA 141-230, Approved by FDA Rev. 09-2015 ®PREVICOX is a registered trademark of Merial. ©2016 Merial, Inc., Duluth, GA. All rights reserved.

VET REPORT VITALS

How Can We Address Antimicrobial Resistance Head On? Molly McAllister, DVM, MPH Banfield Pet Hospital, Portland, Oregon shutterstock.com/Syda Productions

Welcome to VET Report Vitals, a column focused on the results of the groundbreaking Banfield Veterinary Emerging Topics (VET) Report, “Are We Doing Our Part to Prevent Superbugs? Antimicrobial Usage Patterns Among Companion Animal Veterinarians.” This report, a collaboration between the NAVC and Banfield Pet Hospital, focuses on a critical topic: antimicrobial resistance (AMR). It promotes prudent antimicrobial use among companion animal practitioners by contributing a baseline of antimicrobial usage data to the discussion on how to improve concordance with published guidelines. This article examines the issue of AMR within the larger One Health context and proposes a method by which to change behavior among hospital teams and drive quality improvement within the veterinary profession.

THE MODEL FOR IMPROVEMENT Addressing AMR in a veterinary clinic is a quality improvement challenge that can be approached by using structured methods for success. Quality improvement developed as a science in the 1950s. It began as a tool in the manufacturing industry, and its applicability to a variety of other situations, including healthcare, was quickly recognized. The Model for Improvement, developed by Associates in Process Improvement, guides application of key concepts of quality improvement to business challenges of many types.

VET REPORT VITALS

In alignment with the Model for Improvement, a journey of quality improvement begins by asking 3 crucial questions:1 1. AIM: What are we trying to accomplish? To define the aim, the user must explicitly define what is to be accomplished and the timeframe in which it is to be achieved: for example, “Improve concordance with first-line drug recommendations for urinary tract infections [UTIs] by 50% over a 6-month period.” 2. MEASURE: How will we know that a change is an improvement? Objective measures are used to determine the point at which the goal has been reached. This requires data for baseline measurement and results to compare against. Many data sources can be used to measure antimicrobial guideline concordance, but all must be assessed for validity and accuracy to ensure appropriate interpretation. Examples include medical record reviews, logs of antimicrobial dispensing practices, case response logs, doctor surveys, or a combination of data. A sample objective measure is “Track UTI diagnoses and resulting prescriptions on a clipboard in the pharmacy. Assess percentage of cases that received recommended first-line antimicrobial.”

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3. CHANGE: What changes can we make that will result in improvement? Finally, a plan is created by identifying barriers to achieving the desired goal and determining potential strategies to address them. Brainstorming applicable goals, barriers, and strategies should involve all members of the veterinary team and might also include clients, pharmaceutical representatives, and local professional organizations, among other stakeholders. An example is “Relocate first-line antimicrobials in the pharmacy so that they are easier to find. Ensure that pricing of antimicrobial drugs supports use of recommended first-line drugs.”

HUMAN FACTOR ENGINEERING AND NORMALIZATION OF DEVIANCE Not all changes to a system have equal likelihood of driving improvement. Experts in human factors engineering—a discipline that combines engineering and human psychology—have demonstrated that people make mistakes for many reasons: lack of knowledge or experience, misinterpretation or misuse of rules and processes, and lack of necessary skills to accomplish a task.2 Human factors engineering involves identifying and accounting for factors that influence the human ability to perform a function, including environmental conditions (eg, temperature, light level, noise), stress levels, leadership, culture, interruptions, and the need to cut corners or multitask to keep pace with expectations.

Brainstorming applicable goals, barriers, and strategies should involve all members of the veterinary team and might also include clients, pharmaceutical representatives, and local professional organizations, among other stakeholders.

Also important to consider is normalization of deviance: the gradual acceptance of actions that deviate from standards of practice until such actions become the norm.3 For antimicrobial use, this may include straying from the guidelines, ignoring risk factors, or not educating clients about preventive strategies. Any healthcare practitioner can deviate from the norm. In the case of inexperienced

practitioners, it may be due to a lack of knowledge or understanding of why a rule is in place. For experienced practitioners, it may stem from a belief that personal experience is more trustworthy than the standard. Addressing normalization of deviance requires a culture that supports appropriate behaviors and accountability and ensures that communication about standards of practice is consistent and effective. When identifying potential changes for improvement, different strategies have different reliability levels:2 • Most reliable:

• F unctions or physical stops that prevent incorrect actions

• Computerized automation

• Human/machine redundancy

• Somewhat reliable:

• Checklists

• Pauses in a process to recheck details and steps

• Reminders

• Standardization of equipment and supplies

• Self-check or double-check

• Least reliable:

• Education and training

• Rules, policies, and procedures

Fundamental changes that have a higher likelihood of success include those that affect how work is done, produce observable positive differences, and have a lasting impact. Such changes result from design/redesign of a process or system or those that fundamentally change how a system works and what is done to drive it forward. Examples include applying standardization, streamlining choices, and changing the order of tasks; implementing cross-training; and soliciting feedback from customers or employees.1 Any change intended to influence medical prescribing practices requires buy-in from clinicians and team members. As such, large-scale, abrupt changes may not be readily accepted or adopted and are often operationally unfeasible or risky. Small, incremental changes can be more acceptable and allow for better assessment of their true effects in the complex environment of a healthcare facility. The implementation of incremental changes is supported by the “plan, do, study, act” (PDSA) cycle, a tool of the Model for Improvement. The PDSA cycle SEPTEMBER/OCTOBER 2017

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is a recognized method for quality improvement projects that requires thoughtful planning and implementation (“do”) of a step intended to move toward a goal; study of results; and actions to ensure continual progress toward the improvement desired.

PUTTING THE MODEL INTO ACTION Once a clear goal and a model to achieve it are identified, the next step is to identify changes that are believed to lead to meaningful progress. Our goal is to achieve voluntary adjustment of usage patterns among veterinarians to improve concordance with existing guidelines. To begin this process, we must understand the perceived barriers to appropriate antimicrobial use. An American Veterinary Medical Association survey revealed that barriers to antimicrobial use in concordance with guidelines included lack of awareness of guidelines.4 Other surveys indicate that pressure to dispense antimicrobials to satisfy client expectations influences antimicrobial use, as does the cost of culture and susceptibility testing.4,5 Finally, intrinsic factors, such as personal preference, and extrinsic factors, such as perceived compliance by client and willingness/ability of the client to pay, may influence decision-making about antimicrobial use.5 Additional barriers to alignment that might be considered include availability of first-line antimicrobials, dosing regimens, and owner compliance. One proposed change might be to improve visibility to prescriptions and outcomes in a clinic. “Plan” could entail tracking of antimicrobial prescriptions and outcomes across cases. Implementation (the “do”

step) might include a checklist where the drug and outcome are recorded and reviewed weekly. After an appropriate amount of time, results would be evaluated (the “study” step) and potential adjustments to make the process more effective would be assessed. On the basis of that assessment, the “act” step would involve refinement of the goal and planning for subsequent cycles. Another cycle would be started with adjustments for improvement, allowing each subsequent assessment to guide the types of improvements needed to improve guideline concordance. Once potential areas for improvement are identified, it is time to implement a PDSA cycle (Box 1). This method of incremental change allows for operational and behavioral acceptance by minimizing major

BOX 1. Sample “Plan, Do, Study, Act” Cycle PLAN: Consider the goal, what you need to do to get there, and what to measure to ensure it is met. • “ Achieve 80% compliance with first-line antibiotic recommendations for UTIs within 6 months of implementing changes by daily tracking of prescriptions and outcome for each UTI case seen.” DO: Implement the plan. Focus on small, incremental alterations rather than widespread change. • “ Add clipboard to pharmacy and have staff track all UTI diagnoses and associated prescriptions, including client, pet, drug, duration, dose, frequency, and outcome. Review list in weekly team meeting.” STUDY: Work to understand the outcomes of the change. Sometimes unintended results have a larger impact than intended results. By understanding the consequences, you may adjust the plan to better achieve your stated goals.

Banfield has always been dedicated to using its extensive data to provide insights to the profession on topics that can improve veterinary care for pets. The first annual Banfield Veterinary Emerging Topics (VET) Report, supported by the collaborative educational efforts of the NAVC, focuses on a critical topic: antimicrobial resistance. It is titled “Are We Doing Our Part to Prevent Superbugs? Antimicrobial Usage Patterns Among Companion Animal Veterinarians.” “We are proud to team up with the NAVC on the 2017 VET Report to raise awareness about the critical topic of antimicrobial resistance in companion animal practice and how veterinarians can address it in their own practices,” said Dr. Karen Faunt, Vice President of Medical Quality Advancement at Banfield Pet Hospital.

ACT: Finally, make adjustments that were indicated in the “study” phase, and then repeat the cycle. Regularly analyze the results of each new cycle to inform the next step and ensure continual progress toward the goal.1 • “ Based on staff input, outcomes will be recorded after 2 weeks following call back with client and discussing with doctor. Switch from notes to checklist to improve efficiency.” • “Ensure that first-line antimicrobials are always stocked in the hospital by adding them as a standing item to the weekly order list.”

The full report is available at Banfield.com/VETReport or VetFolio.com/VETReport.

• “ Assess process with staff after 3 months for feasibility and efficacy. Assess outcomes after 6 months and review with veterinarians to determine next steps.”

VET REPORT VITALS

Dogs are all

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IMPORTANT SAFETY INFORMATION: PROHEART 6 should be used in healthy dogs. Do not administer to sick, debilitated, underweight dogs or dogs that have a history of weight loss. Prior to administration, PROHEART 6 certified veterinarians should continue to assess patient health through a medical history, physical examination and if deemed appropriate, diagnostic testing. Continue to use caution when administering PROHEART 6 concurrently with vaccinations. Adverse events, including anaphylaxis, have been reported following the concomitant use of PROHEART 6 and vaccines. In some cases, anaphylactic reactions have resulted in death. Use with caution in dogs with pre-existing or uncontrolled allergic disease (food allergy, atopy or flea allergy dermatitis). Dogs receiving PROHEART 6 should be tested for existing heartworms as per the product label. In people, avoid PROHEART 6 contact with eyes. If contact with the eyes occurs, rinse thoroughly with water for 15 minutes and seek medical attention immediately. PROHEART 6 is available only to veterinarians through a restricted distribution program. Only certified veterinarians and staff can administer it. See Brief Summary of full Prescribing Information on page 16. All trademarks are the property of Zoetis Services LLC or a related company or a licensor unless otherwise noted. ©2017 Zoetis Services LLC. All rights reserved. PRO-00206F

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BRIEF SUMMARY:

See package insert for full prescribing information. NADA 141-189, Approved by FDA

ProHeart 6 ÂŽ

Molly McAllister, DVM, MPH

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Dr. Molly McAllister is the Director of Research for the Banfield Applied Research and Knowledge (BARK) team at Banfield Pet Hospital. She is a graduate of Oregon State University College of Veterinary Medicine and subsequently earned her master of public health degree from the University of Minnesota. Dr. McAllister is passionate about the role of preventive and proactive care in the health and quality of life of our pets, as well as the intersection of human, animal, and environmental health. She lives with her family and 4 pets in Vancouver, Washington, where they spend as much time outdoors as possible.

Sustained Release Injectable for Dogs CAUTION Federal (U.S.A.) law restricts this drug to use by or on the order of a licensed veterinarian.

INDICATIONS

ProHeart 6 is indicated for use in dogs six months of age and older for the prevention of heartworm disease caused by Dirofilaria immitis. ProHeart 6 is indicated for the treatment of existing larval and adult hookworm (Ancylostoma caninum and Uncinaria stenocephala) infections.

INFORMATION FOR DOG OWNERS

Always provide Client Information Sheet and review with owners before administering ProHeart 6. Owners should be advised of the potential for adverse reactions, including anaphylaxis, and be informed of the clinical signs associated with drug toxicity (see WARNINGS, PRECAUTIONS and ADVERSE REACTIONS sections.) Owners should be advised to contact their veterinarian immediately if signs of toxicity are observed. The vast majority of patients with drug related adverse reactions have recovered when the signs are recognized and veterinary care, if appropriate, is initiated.

CONTRAINDICATIONS

ProHeart 6 is contraindicated in animals previously found to be hypersensitive to this drug.

HUMAN WARNINGS

Not for human use. Keep this and all drugs out of the reach of children. May be slightly irritating to the eyes. May cause slight irritation to the upper respiratory tract if inhaled. May be harmful if swallowed. If contact with the eyes occurs, rinse thoroughly with water for 15 minutes and seek medical attention immediately. If accidental ingestion occurs, contact a Poison Control Center or a physician immediately. The material safety data sheet (MSDS) contains more detailed occupational safety information.

WARNINGS

ProHeart 6 should be administered with caution in dogs with pre-existing allergic disease, including food allergy, atopy, and flea allergy dermatitis. In some cases, anaphylactic reactions have resulted in liver disease and death. Anaphylactic and anaphylactoid reactions should be treated immediately with the same measures used to treat hypersensitivity reactions to vaccines and other injectable products. Owners should be given the Client Information Sheet for ProHeart 6 to read before the drug is administered and should be advised to observe their dogs for potential drug toxicity described in the sheet. Do not administer ProHeart 6 to dogs who are sick, debilitated, underweight or who have a history of weight loss.

disruption, while measurement and assessment ensure that the right changes are being made. From a healthcare perspective, these safeguards help ensure patient safety and quality of care by confirming that a change has the intended effect before widespread implementation.

PRECAUTIONS

Caution should be used when administering ProHeart 6 concurrently with vaccinations. Adverse reactions, including anaphylaxis, have been reported following the concomitant use of ProHeart 6 and vaccinations (see WARNINGS). Prior to administration of ProHeart 6, the health of the patient should be assessed by a thorough medical history, physical examination and diagnostic testing as indicated (see WARNINGS). ProHeart 6 should not be used more frequently than every 6 months. The safety and effectiveness of ProHeart 6 has not been evaluated in dogs less than 6 months of age. Caution should be used when administering ProHeart 6 to heartworm positive dogs (see ADVERSE REACTIONS). Prior to administration of ProHeart 6, dogs should be tested for existing heartworm infections. Infected dogs should be treated to remove adult heartworms. ProHeart 6 is not effective against adult D. immitis and, while the number of circulating microfilariae may decrease following treatment, ProHeart 6 is not effective for microfilariae clearance.

CLINICAL BOTTOM LINE Addressing an issue such as AMR may seem daunting, but progress can be made if the solution is broken into small, manageable goals to improve medical quality. The science of quality improvement, specifically the Model for Improvement, provides simple yet effective processes and tools for achieving this progress. Through the combined efforts and brainpower of all members of the veterinary team, a clinic can address nearly any problem by following the steps outlined in this article.

ADVERSE REACTIONS

In field studies, the following adverse reactions were observed in dogs treated with ProHeart 6: anaphylaxis, vomiting, diarrhea (with and without blood), listlessness, weight loss, seizures, injection site pruritus, and elevated body temperature. Dogs with clinically significant weight loss (>10%) were more likely to experience a severe adverse reaction. In a laboratory effectiveness study, dogs with 4- and 6-month-old heartworm infections experienced vomiting, lethargy and bloody diarrhea. These signs were more severe in the dogs with 4-month-old heartworm infections, including one dog that was recumbent and required supportive care, than in the dogs with older (6-month-old) infections. Post-Approval Experience (Rev. 2010) The following adverse events are based on post-approval adverse drug experience reporting. Not all adverse reactions are reported to FDA/CVM. It is not always possible to reliably estimate the adverse event frequency or establish a causal relationship to product exposure using these data. The following adverse events are listed in decreasing order of frequency by body system. Immune: anaphylaxis and/or anaphylactoid reactions, urticaria, head/facial edema, pruritus, pale mucous membranes, collapse, cardiovascular shock, erythema, immunemediated hemolytic anemia, immune-mediated thrombocytopenia (signs reflected in other system categories could be related to allergic reactions, i.e., gastrointestinal, dermatologic, and hematologic) Gastrointestinal: vomiting (with or without blood), diarrhea with or without blood, hypersalivation General: depression, lethargy, anorexia, fever, weight loss, weakness Dermatological: injection site pruritus/swelling, erythema multiforme Neurological: seizures, ataxia, trembling, hind limb paresis Hematological: leukocytosis, anemia, thrombocytopenia Respiratory: dyspnea, tachypnea, coughing Hepatic: elevated liver enzymes, hypoproteinemia, hyperbilirubinemia, hepatopathy Urinary: elevated BUN, elevated creatinine, hematuria, polydipsia, polyuria Cardiopulmonary signs such as coughing and dyspnea may occur in heartworm positive dogs treated with ProHeart 6. In some cases, death has been reported as an outcome of the adverse events listed above. To report suspected adverse reactions, to obtain a Material Safety Data Sheet, or for technical assistance, call 1-888-963-8471. For a complete listing of adverse reactions for moxidectin reported to the CVM see: http://www.fda.gov/AnimalVeterinary/SafetyHealth/ProductsSafetyInformation/ ucm055394.htm

References 1.

2. The Joint Commission. Human factors analysis in patient safety systems. The Source 2015;13:1-10. 3. Banja J. The normalization of deviance in healthcare delivery. Bus Horiz 2010;53:139. 4. American Veterinary Medical Association Task Force for Antimicrobial Stewardship in Companion Animal Practice. Understanding companion animal practitionersâ&#x20AC;&#x2122; attitudes toward antimicrobial stewardship. JAVMA 2015;247(8):883-884. 5. Mateus AL, Brodbelt DC, Barber N, et al. Qualitative study of factors associated with antimicrobial usage in seven small animal veterinary practices in the UK. Prev Vet Med 2014;117(1):68-78.

Revised: July 2014

Sterile Vehicle - Made in Spain ProHeart 6 Microspheres - Product of Italy Distributed by: Zoetis Inc., Kalamazoo, MI 49007

Langley GJ, Moen R, Nolan KM, et al. The Improvement Guide: A Practical Approach to Enhancing Organizational Performance. San Francisco: John Wiley & Sons; 2009.

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HEARTWORM HOTLINE

AHS HEARTWORM HOTLINE

Beyond the Map: The State of Heartworm Incidence in the United States Chris Rehm, DVM, President, American Heartworm Society Doug Carithers, DVM, American Heartworm Society Board Member and Symposium Co-Chair shutterstock.com/anetapics

The Heartworm Hotline column is presented in partnership between Todayâ&#x20AC;&#x2122;s Veterinary Practice and the American Heartworm Society (heartwormsociety.org). The goal of the column is to communicate practical and timely information on prevention, diagnosis, and treatment of heartworm disease, as well as highlight current topics related to heartworm research and findings in veterinary medicine.

How many pets in the United States are infected with heartworms? The truth is that no one knows. Because heartworm diagnosis requires one or more blood tests that must be conducted in a veterinary clinic and/or testing laboratory, diagnosis is limited to patients seen in veterinary hospitals and animal shelters. Dogs and cats not seen by veterinarians and/ or not tested for heartworms during annual veterinary visits may be infected but go unrecognized.

has tracked the incidence of heartworm diagnosis in the United States for the past 15 years. The first AHS Incidence Survey was conducted in 2002 and focused on heartworm diagnoses made in veterinary hospitals during the 2001 calendar year, including data from tests conducted both in-clinic and in reference laboratories. The AHS has continued to survey US veterinary practices every 3 years and, since 2007, has added animal shelters to the survey. The survey results are used to create the AHS Heartworm Incidence Map every 3 years. The 2016 map (Figure 1) was unveiled in April 2017. Thousands of veterinary practices and shelters participated in the AHS survey in 2016, and because

BACKGROUND While an exact number of infected pets cannot be pinpointed, the American Heartworm Society (AHS)

FIGURE 1. 2016 AHS Heartworm Incidence Map.

SEPTEMBER/OCTOBER 2017

â&#x2013;

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HEARTWORM HOTLINE

many have reported data survey after survey, the AHS has been able to use the information to track trends in participating practices, as well as the trajectory of heartworm incidence. This is especially important, given that in the past several decades, heartworms have spread from highly endemic regions of the United States, such as the Southeast and Mississippi Delta regions, to states once considered “non-endemic,” including California and Arizona. Because it is not possible to know the exact number of heartworm infections in the United States, the AHS survey focuses on incidence versus prevalence. Nevertheless, the AHS has been able to venture a conservative estimate of heartworm prevalence via the following calculations:

• Of the thousands of veterinary practices that report

testing data to the AHS, a large proportion have reported data from their practice records year after year.

• Using an estimate of client base, and combining

these data with dog numbers from the American Veterinary Medical Association, it is possible to generate a rough estimate of heartworm cases for the United States and, more importantly, to track trends.

• Since 2001, the national estimate has increased from nearly 900,000 heartworm-positive dogs to 1 million in 2010 to 1.2 million in 2016.

KEY FINDINGS OF THE 2016 HEARTWORM INCIDENCE SURVEY Almost 5000 veterinary practices and shelters participated in the AHS survey in early 2017; the incidence numbers reported are based on the 2016 calendar year. Participating veterinarians reported numbers of patients tested for heartworm infection, as well as the number of positive cases from that total. In addition, participants responded to a brief survey designed to provide information on factors behind the data. The following findings were identified:

Of survey respondents, 23.3% reported seeing more heartworm cases in 2016 compared with 2013, while 19.8% reported a decline in their practice area. Veterinarians who reported an upward trend in heartworm diagnoses cited several reasons for the change, according to the AHS opinion survey. Almost half (47.8%) cited failure to give preventives, skipping doses. or failing to give preventives year-round as contributing factors. Other factors believed to contribute to incidence increases in certain regions were weather conditions conducive to heartworm transmission in 2016 (weather may also have been a factor where numbers of heartworm-positive dogs fell; regions such as the Southwest and states such as Alabama suffered from drought in 2016) and the movement of infected dogs into practice areas. Insufficient efficacy of heartworm preventives was viewed as a factor by only 3.3% of respondents who saw incidence rise.

• Heartworm infection was diagnosed nationwide.

No state in the country is heartworm-free. According to the AHS survey, the top 5 states in heartworm incidence were Mississippi, Louisiana, Arkansas, Texas, and Tennessee—all states that have been in the top tier since the AHS began tracking incidence data in 2001. Rounding out the top 10 were South Carolina, Georgia, North Carolina, Alabama, and Florida. Among the top 10 states, only Alabama, Louisiana, and Texas saw decreases in the average number of dogs diagnosed per practice, while increases in the average number of cases were noted in the other 7. In states where few cases have historically been diagnosed (for instance, heartworm-positive dogs in Alaska have, thus far, been non-native), many practitioners reported that the infected dogs originated from out of state. This is an important

• Heartworm incidence is up. The incidence numbers

reported by participants in the 2016 AHS Incidence Survey indicated that the average number of positive cases per veterinary clinic has been climbing, rising by 21.7% over 2013 numbers; this was due to a small increase in both the absolute number of positive cases per reporting clinic and the percent positive per clinic. The average number of heartworm-positive states rose in 26 states, as well as the District of Columbia; stayed the same in 3 states; and dropped in 22 states (Figure 2).

AHS HEARTWORM HOTLINE

FIGURE 2. Heartworm incidence trends: 2013 to 2016.

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point, however, because wherever positive dogs exist, the potential for mosquitoes becoming infected and, in turn, infecting other animals also

Christopher Rehm Chris Rehm, DVM, President of the American Heartworm Society (AHS) board of directors, is a veterinarian and graduate of Auburn College of Veterinary Medicine. He began practicing in Mobile, Alabama, more than 30 years ago. What began as one veterinary clinic, Rehm Animal Hospital, PC, has grown to 4 American Animal Hospital Association–certified hospitals in 2 counties in lower Alabama. He employs 13 veterinarians and more than 70 support staff.

Doug Carithers Doug Carithers, DVM, has held various roles with Merial (now Boehringer Ingelheim) since leaving private mixed-animal practice in 1993. He is responsible for North American postapproval studies and publications, accounting for more than 115 clinical and field studies involving nearly 20,000 animals. In addition, as a committee and board member for the AHS, he conducted the 2001, 2004, 2007, 2010, 2013, and 2016 AHS heartworm incidence surveys. He has authored/co-authored over 20 peer-reviewed papers and 30 scientific articles, and co-authored a best-selling companion animal parasitology atlas. He has edited over 10 book chapters and acted as guest editor of special editions of refereed journals. Dr. Carithers lectures nationally and internationally and has provided over 900 hours of CE. He is known internationally for his interest and expertise in parasitology, currently serving as an officer of the AHS (Symposium Chair) and of the American Association of Veterinary Parasitologists (Secretary Treasurer), as well as a board member of the National Center for Veterinary Parasitology.

exists. Cool or dry weather does not necessarily eliminate transmission; it simply slows the process.

• Compliance is key to reducing heartworm incidence. While it was disappointing to see the average number of heartworm-positive cases per clinic rise between 2013 and 2016, the good news is that the factors involved are controllable. Among veterinarians who reported a drop in heartworm incidence since the 2013 survey, 64% attributed the change to owner behavior, including increased usage of heartworm preventives and improved owner compliance.

• Veterinarians are using AHS resources.

According to the AHS survey, 77% of veterinarians reported that they follow the AHS guidelines on prevention, diagnosis, and treatment of heartworm disease, while roughly half of practitioners use resources on the AHS website. In most cases, the utilization of AHS resources was higher than that reported in the 2013 survey (Table 1).

SUMMARY The results of the AHS Incidence Survey represent a mix of bad and good news. On one hand, heartworm incidence has increased in a number of states, especially those states in the most heartworm-endemic areas of the Southeast, MidSouth, and Delta regions. On the other hand, it is clear that there is a straightforward answer to this: (1) convince more pet owners to use preventives and (2) convince them to protect dogs and cats year-round—with no lapses. The AHS Heartworm Guidelines recommend annual heartworm testing and year-round heartworm prevention for all canine and feline veterinary patients. As the results of this survey suggest, compliance with these guidelines has the potential to dramatically alter the trajectory of heartworm incidence in pets.

TABLE 1 Veterinary Usage of AHS Resources PERCENTAGE OF RESPONDENTS BY SURVEY YEAR RESPONSES

2013

2016

Follow the AHS guidelines on heartworm prevention, diagnosis, and treatment

72.4%

77%

Use the AHS website (heartwormsociety.org)

38.8%

49%

Have used AHS client education tools

32%

39%

Have attended an AHS symposium

4.8%

4.4%

15%

10%

Do not use AHS resources

AHS HEARTWORM HOTLINE

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Dermatology Diagnostics: Skin Scrapes, Hair Plucks, and More Chris Reeder, DVM, DACVD Blue Pearl Veterinary Partners, Franklin, Tennessee

Parasites, such as chiggers and scabies-causing mites, can cause tremendous itching. Fungal organisms, such as dermatophytes, can affect the hair, resulting in fracturing and large areas of crusting, nodules, or excoriations. Not all dermal problems come from external threats; various breed-related issues, such as color-dilution alopecia, pattern baldness, and many autoimmune diseases, can develop over time. Normal inhabitants of the skin (eg, Demodex mites) can also create problems for many dogs. This article looks at how to investigate some dermal conditions in cats and dogs.

Deep Skin Scrapes Deep scrapes are largely used to diagnose dogs with Demodex canis mites and cats with Demodex cati mites; however, more surface-oriented mites, such as scabies mites or Cheyletiella species, may also be found. • Place a few drops of mineral oil on a glass microscope slide. • Hold a #10 scalpel blade firmly in one hand. With the other hand, gently collect a fold of skin on the trunk, or evert a pinna or interdigital space.

SKIN SCRAPES Skin scrapes are typically performed with a #10 scalpel blade and are either deep or superficial (Figure 1). The key to success is to sample multiple sites and evaluate the microscope slide thoroughly in an orderly fashion (eg, scan in a “down, across, then down, across” pattern). Although skin scrapes are helpful in diagnosing external parasites, false-negative results are possible. Chinese sharpeis may require a skin biopsy to determine the presence of Demodex mites.1 Scabies mites on dogs are found only 20% to 50% of the time, depending on the number of sites scraped.2

DERMATOLOGY DETAILS

FIGURE 1. Basic supplies for skin scrapes and hair plucks, clockwise from left: microscope slides, mineral oil, scalpel blade, hemostat. Courtesy of Animal Dermatology South, New Port Richey, Florida.

DERMATOLOGY DETAILS

• Scoop a small amount of mineral oil onto the scalpel blade.

TRICHOGRAPHY (HAIR PLUCKS)

• Squeeze the skin in a fold of tissue between 2 fingers. In a single direction, scrape the skin fold, pinna, or paw with firm and constant pressure over a single site until a small amount of capillary oozing occurs.

This is one of my favorite diagnostic techniques because it is an easy and effective test that can be used for many disease processes, from infectious and parasitic conditions (eg, dermatophytosis, demodicosis) to various forms of alopecia (eg, colordilution alopecia, alopecia areata). A good reference guide for hair shaft evaluation is Muller & Kirk’s Small Animal Dermatology, 7th edition; this topic is discussed in the diagnostic methods section.

• Apply the collected material and exudate to the glass slide containing mineral oil. Repeat 3 to 5 times to cover the slide. • Evaluate under 4× magnification, then move to greater objectives for mite evaluation.

Superficial Skin Scrapes Superficial scrapes are used to detect Demodex gatoi mites in cats, Notoedres cati mites, and occasionally Cheyletiella mites. • Place a drop of mineral oil on a microscope slide. • Apply a drop of mineral oil to a #10 scalpel blade. • In a single, uniform direction, scrape with gentle and light pressure across a broad lesional surface. • Place the debris on the microscope slide with mineral oil and examine on low power (4× and 10×) for mites.

A good hemostat is essential for hair plucks. Many inexpensive hemostats do not grasp the hair well enough to pluck out 10 to 20 hairs at a time, and the hairs can slip through the jaws (Figure 2). • Apply a few drops of mineral oil to a glass microscope slide. • To pluck the hairs, grasp about 10 to 20 hairs at a time at just about the surface of the skin and pull with a quick and deliberate motion in the direction perpendicular to the skin surface (this will help minimize patient discomfort, which is rare). • Place the hairs on the microscope slide with mineral oil. • Evaluate the entire shaft of the hair for such conditions as dermatophytosis or color-dilution alopecia (Figure 3). • Examine the hair bulb region for alopecia areata. • Assess the area just above the bulb region for Demodex mites (Figure 4).

FIGURE 2. Hemostat with solid locking mechanism. When performing hair plucks, grasp the hair shaft close to the skin. Courtesy of Animal Dermatology South.

FIGURE 3. Hair with visible melanin clumping in the shaft, indicating color dilution alopecia, 100× magnification. Courtesy of Animal Dermatology South.

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Dermatophytes can be observed on hairs with spores or hyphae. Some authors recommend digesting the keratin to observe these structures more readily, but this is not always needed. A formula called chlorphenolac has been used to replace KOH preparation solution; this formulation consists of 50 g of chloral hydrate added to 25 mL liquid phenol and 25 mL of liquid lactic acid (note: it may take several days for crystals to go into solution).1

FLEA COMBING

WOOD’S LAMP

• Remove the material from the comb and visually inspect it for fleas and flea debris.

Wood’s lamp evaluation for dermatophytosis is an easy and useful tool. It is a good screening test, although false-positive and false-negative results often occur. Only 30% to 80% of Microsporum canis isolates fluoresce, and Microsporum gypseum and Trichophyton mentagrophytes do not fluoresce under a Wood’s lamp.1 Occasionally, lint, dander, and organic debris can fluoresce and give a falsepositive result. Dermatophytes produce an applegreen color upon fluorescence (Figure 5). Other, less common, species of dermatophytes that fluoresce are Microsporum audouinii, Microsporum distortum, and Trichophyton schoenleinii.

TAPE STRIPPING Clear acetate tape impressions are helpful to identify mites, such as Cheyletiella species, poultry mites, and cat fur mites.

Flea combs are easy to use and allow direct evaluation for mites, such as Cheyletiella species; fleas; and flea excrement. • Place a few drops of mineral oil on a glass microscope slide. • With the comb, use long, broad strokes from cranial to caudal to collect hair and debris. The material is collected on the tines of the comb.

• Place the hair onto the microscope slide containing mineral oil and evaluate it microscopically for mites. • Place suspected flea excrement on a moistened piece of paper towel or gauze; dissolution into a reddish-brown color indicates flea excrement.

FECAL FLOTATION A recent study found that fecal flotation (Sheather’s solution, filtered and centrifuged) from cat stool samples detected various parasitic mites, including D gatoi, N cati, Lynxacarus radovskyi, Cheyletiella species, chigger mites, and Otodectes cynotis.3 This

• Press the tape, sticky side down, directly onto lesional sites. • Place the tape onto a microscope slide for direct evaluation.1

FIGURE 4. Hair with Demodex canis mites at the proximal shaft, 100× magnification. Courtesy of Animal Dermatology South.

DERMATOLOGY DETAILS

FIGURE 5. Feline dermatophytosis (A) in room light and (B) under a Wood’s lamp. Courtesy of Animal Dermatology South.

DERMATOLOGY DETAILS

study used flea combing, acetate tape preps, superficial skin scrapings, and ear swabs to evaluate detection methods in community cats in the Ohio River Valley region of the United States. With the exception of only chigger mites and O cynotis being found on ear swabs, all mites listed above were found with each detection method. Although the numbers of mites found with each detection method varied, fecal flotation detected more free-living mites than parasitic mites. This must be considered a potential false-positive result unless one is well educated in distinguishing parasitic from freeliving mites in stool samples. Many of these cats did not have dermatologic disease upon examination, and fecal flotation may serve as a good surveillance method for mite detection when evaluated at yearly examinations.

PHOTOGRAPHS Photographs of positive findings using any of the diagnostic methods can provide the pet owner a good image of whatever pathogen is found. Photographs can also be uploaded to a pet’s file in many of the currently used patient software systems. A digital camera, iPhone microscope adapter, and specialized cameras that attach to microscopes are all good options. References 1.

Miller WH, Griffin CE, Campbell KL. Diagnostic methods. Canine demodicosis. In: Muller & Kirk’s Small Animal Dermatology. 7th ed. Philadelphia: W.B. Saunders, 2013:78-92.

2. Miller WH, Griffin CE, Campbell KL. Parasitic skin disease. Canine demodicosis. In: Muller & Kirk’s Small Animal Dermatology. 7th ed. Philadelphia: W.B. Saunders, 2013:315-319. 3. Milley C, Dryden M, Rosenkrantz W, et al. Comparison of parasitic mites retrieval methods in a population of community cats. J Feline Med Surg 2016:1-8.

Chris Reeder Chris Reeder, DVM, DACVD, is a graduate of Auburn University’s College of Veterinary Medicine. He practices at Blue Pearl Veterinary Partners in Franklin, Tennessee. Dr. Reeder has published several articles nationally and internationally and enjoys lecturing to local and national audiences on dermatology. He has served on several committees for the American College of Veterinary Dermatology, including the credentials committee and ad hoc exam committee. Dr. Reeder’s special interests include otitis externa, dermatopathology, and immune-mediated skin disease.

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IMAGING ESSENTIALS

Ultrasonography of the Adrenal Glands Elizabeth Huynh, DVM; and Clifford R. Berry, DVM, DACVR University of Florida

Welcome to our series of articles on small animal abdominal ultrasonography. The initial articles provided an overview of basic ultrasonography principles and a discussion about how to perform a systematic scan of the abdomen. The rest of the series discusses ultrasound evaluation of specific abdominal organs/systems. Read the other small animal abdominal ultrasonography articles published in Today’s Veterinary Practice at tvpjournal.com.

• The left phrenicoabdominal vein is the ventral landmark (Figure 1).1 The normal left adrenal gland is in a cranial and medial position relative to the left kidney (Figure 2).1–5 However, the position of the left adrenal gland relative to the left kidney may be altered when the left kidney is displaced by excessive transducer pressure. The significant mobility of that kidney is a result of its being suspended by the renal stalk (vessels and ureter) and bound ventrally by the mesothelial lining of the peritoneum.

LOCALIZATION AND SCANNING TECHNIQUE Left Adrenal Gland The following are anatomic landmarks that help identify the location of the left adrenal gland: • The left kidney is the lateral landmark. • The abdominal aorta is the medial landmark. • The celiac and cranial mesenteric arteries are cranial to the left adrenal gland. • The left renal artery is the caudal landmark. • The left phrenicoabdominal artery is the dorsal landmark.

IMAGING ESSENTIALS

FIGURE 1. Longitudinal axis view of the left adrenal gland including the phrenicoabdominal vein (white arrowhead) on the ventral aspect of the adrenal gland in a dog. Ao, aorta.

IMAGING ESSENTIALS

The left adrenal gland is slightly lateral and ventral to the abdominal aorta and sits adjacent or caudal to the celiac and cranial mesenteric arteries.1,4,5 The caudal pole of the adrenal gland is localized cranial to the “hook” of the left renal artery and its origin from the left lateral margin of the abdominal aorta (Figure 3). The left phrenicoabdominal artery is noted along the dorsal surface of the left adrenal gland. Without color Doppler ultrasound, it may not be visible. The left phrenicoabdominal vein, seen in the near field or ventral aspect of the adrenal gland and transecting it into equal cranial and caudal poles,1 is an inconsistent finding using gray-scale 2D imaging but, when present, helps confirm the localization of the left adrenal gland. In dogs, the transducer motion for finding the left adrenal gland starts lateral in the long axis of the left kidney. Angle medial (nondistance motion) to the level of the aorta and find the celiac, cranial mesenteric, and left renal arteries. Often you will find the caudal pole of the left adrenal gland and 2 of those arteries; all 3 arteries will not necessarily be in the same imaging plane. Once you have the caudal pole of the left adrenal gland, rotate the transducer in a clockwise direction from 12 to 1 o’clock (about 10°) to bring the left adrenal gland into long axis (Figure 1). Identification of the left phrenicoabdominal vein along the ventral (near field) margin of the middle of the left adrenal gland is confirmation that you are evaluating the left adrenal gland.

FIGURE 2. Transverse plane computed tomographic (CT) image at the level of the left adrenal gland (*) of a dog obtained after IV contrast administration. Note the normal lateral and ventral anatomic location of the left adrenal gland relative to the aorta (Ao). CVC, caudal vena cava; LK, left kidney; P, portal vein; RK, right kidney.

FIGURE 3. Dorsal plane reformatted CT image at the level of the left adrenal gland (*) in a dog obtained after IV contrast medium administration. Note the hook of the left renal artery located caudal to the caudal pole of the left adrenal gland. Also, note the phrenicoabdominal vein traversing in between the cranial and caudal poles of the left adrenal gland.

FIGURE 4. Longitudinal axis view of the left adrenal gland of a cat using a linear transducer. Note the left adrenal gland delineated by the 2 calipers. The celiac and cranial mesenteric arteries are not seen in this image.

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In cats, the celiac and cranial mesenteric arteries are used as the target vessels for finding the left adrenal gland. Angle the transducer medial to the left kidney and move ventral to the long axis of the aorta, finding the celiac and cranial mesenteric arteries as two rounded anechoic structures adjacent to each other in the craniocaudal axis (the celiac artery is cranial to the cranial mesenteric artery). The left adrenal gland (hypoechoic) will be in the retroperitoneal fat (hyperechoic), adjacent to and in the near field relative to these vessels. Occasionally the left phrenicoabdominal vein can be seen.

Right Adrenal Gland

It is uncommon to see a distinct cortex and medulla in cats unless using a high-resolution linear transducer (Figure 4).

The right phrenicoabdominal vein is ventral (near field) to the right adrenal gland when it is visualized. It will be seen less frequently than the left phrenicoabdominal vein adjacent to the left adrenal gland.

The right adrenal gland is located ventral and lateral to the caudal vena cava. In dogs, the adrenal gland is in contact with the caudal vena cava (Figure 5).1,4,5 In cats, it can be further away, separated from the caudal vena cava by retroperitoneal fat (Figure 6). The right adrenal gland is located medial to the right kidney in the dog. In the cat, it is craniomedial to the right kidney, located along the caudal vena cava between the cranial pole of the right kidney and the caudate lobe of the liver.

With the right kidney in long axis, angle the transducer medial to the kidney and identify the caudal vena cava. Angle the transducer lateral to the caudal vena cava slowly, and the adrenal gland will be parallel to or at a 30Â° angle relative to the long axis of the caudal vena cava. If at an angle, the caudal pole of the adrenal gland will be further away from the caudal vena cava (Figure 7).

FIGURE 5. Transverse plane CT image at the level of the right adrenal gland (*) of a dog obtained after IV contrast medium administration. Note the normal lateral and slightly dorsal anatomic location of the right adrenal gland relative to the caudal vena cava.

FIGURE 6. Longitudinal axis view of the right adrenal gland (*) of a cat depicting the separation between the right adrenal gland and caudal vena cava due to retroperitoneal fat (white arrowheads).

IMAGING ESSENTIALS

FIGURE 7. Longitudinal axis view (A) without and (B) with color Doppler of the V-shaped right adrenal gland of a dog, adjacent to the caudal vena cava.

IMAGING ESSENTIALS

NORMAL ULTRASONOGRAPHIC FEATURES The left adrenal gland has variable shape in dogs (Figure 8) but is consistently oval or bean shaped in cats (Figure 4).6

The shapes seen in small-breed dogs include a dumbbell or biconcave disc shape (similar to a cross-section of a red blood cell). In medium- and large-breed dogs, the left adrenal gland may have a pancake or lawn-chair shape (Figure 8). All of these shapes are considered normal variants. In dogs, the adrenal gland length and width are variable; however, a caudal pole width of 0.6 to 0.74 cm has been

FIGURE 9. Longitudinal axis view of the right adrenal gland (white arrowheads) of a dog depicting the normal V-shape.

D A

E B

FIGURE 8. Longitudinal axis views of normal variations of the shape of the left adrenal gland in 5 different dogs. (A) “Lawn chair.” (B) Flattened pancake. (C and D) Biconcave discs with more of an indention in the region of the phrenicoabdominal vein. (E) Near perpendicular shape between the cranial and caudal pole of the left adrenal gland.

FIGURE 10. Longitudinal axis views of the (A) right and (B) left adrenal glands of a dog with iatrogenic hypoadrenocorticism. Note the small size of both adrenal glands, measuring approximately 0.3 cm in height.

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shown to be normal.2,3,7,8 Recent literature has suggested that the thickness of the caudal pole of the adrenal gland in the sagittal plane is correlated to the size of the dog: ≤0.54 cm for dogs <10 kg, ≤0.68 cm for dogs 10 to 30 kg, and ≤0.8 cm for dogs >30 kg.9 Adrenal gland length has not been correlated with the age or size of dogs; therefore, the caudal pole measurement is the key to determining enlargement of the adrenal glands in the dog.2,3,7,8 The normal width and/or height of the left adrenal gland in cats is 0.43 ± 0.03 cm.2,3,10 The left adrenal gland in dogs is hypoechoic relative to the surrounding retroperitoneal fat, and often a hyperechoic oval stripe can be visualized in the middle of the gland. This stripe is assumed to be the delineation between the adrenal medulla (hypoechoic) and outer cortex (hypoechoic).2,3

medium- and large-breed dogs. However, the true shape of the right adrenal gland is a V (Figure 9). In cats, the normal shape for the right adrenal gland is an oval or bean shape.

PATHOLOGY OF THE ADRENAL GLAND Small adrenal glands can be seen in dogs and cats with iatrogenic or spontaneous hypoadrenocorticism (Figure 10).2,3,11,12 The adrenal glands of dogs with pituitary-dependent hyperadrenocorticism can be normal sized, be bilaterally enlarged (hypertrophic) with a normal shape and increased caudal pole width/height (Figure 11), or have nodular hyperplasia.2,3,7,13–15 Often there is an accompanying steroid-induced hepatopathy, such as a generalized increase in echogenicity, hypoechoic

The right adrenal shape is typically evaluated in long axis and is oval in small dogs and more of a pancake in

FIGURE 11. Longitudinal axis view of the left adrenal gland of a dog with a mildly enlarged caudal pole (calipers), measuring 0.84 cm in height. Bilateral adrenomegaly (>0.8 cm caudal pole widths) has been seen in dogs with pituitary-dependent Cushing’s disease.

FIGURE 12. Longitudinal axis views of the right division of the liver in a dog diagnosed with vacuolar hepatopathy. Note the diminished portal wall markings that are consistent with a hyperechoic hepatic parenchyma.

IMAGING ESSENTIALS

FIGURE 13. Longitudinal axis view of the left adrenal gland of a dog with an oval, well-defined, hyperechoic nodule in the caudal pole of the adrenal gland. This nodule is presumed to be secondary to hyperplasia or myelolipoma; however, an adenoma cannot be ruled out.

FIGURE 14. Longitudinal axis view of a left adrenal gland pheochromocytoma in a dog. Note the misshapen adrenal gland, distorted architecture, and heterogeneous appearance. This mass measures 7 × 5.5 cm. The caudal vena cava should be evaluated for tumor thrombus invasion.

The power’s in the process ANTINOL’s patented process ensures each dose delivers a concentrated blend of EPA, DHA, ETA, and other beneficial fatty acids with their active properties intact1 Enhances comfort and mobility in dogs: • In a veterinary assessment, up to 90% of dogs showed enhanced mobility2* • In a separate study, dogs showed enhanced mobility within just 2 weeks3 • Safe for long-term daily use Visit www.antinolforpets.com for more information. *90% of dogs in one group showed enhanced mobility; 88% of dogs in a second group showed enhanced mobility References 1. Wolyniak CJ, Brenna JT, Murphy KJ, Sinclair AJ. Gas chromatography-chemical ionization-mass spectrometric fatty acid analysis of a commercial supercritical carbon dioxide lipid extract from New Zealand green-lipped mussel (Perna canaliculus). Lipids. 2005;40(4):355-360. 2. Data on file. 3. Data on file.

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nodules that are ill-defined, hyperattenuation of the ultrasound beam, and biliary debris (Figure 12).2,3,16â&#x20AC;&#x201C;19 Focal enlargement, such as hyperechoic or hypoechoic nodules, can be present in the adrenal glands and can represent benign or malignant lesions (Figure 13).7,13â&#x20AC;&#x201C;15

Marked enlargement >2 cm of the adrenal gland is usually associated with malignant etiologies, such as adenocarcinomas or pheochromocytomas (Figure 14). Adenomas and adenocarcinomas are

Benign adenomas can be unilateral or bilateral and functional (glucocorticoid secreting) or nonfunctional.2,3,20,21

FIGURE 16. (A) Right lateral abdominal radiograph of a 14-year-old cat. Note the poorly circumscribed, mineralopacity structures (white arrowheads) within the cranial retroperitoneal space. These are bilaterally mineralized adrenal glands. Also, within the renal diverticular regions, immediately caudal to the bilaterally mineralized adrenal glands, there are multifocal, faint, linear mineral opaque structures, representing renal diverticular mineralization. (B) Longitudinal axis view of the right adrenal gland of the same cat. Note the hyperechoic right adrenal gland (calipers) with distal acoustic shadowing consistent with mineralization.

FIGURE 15. Images of a dog diagnosed with left adrenal gland pheochromocytoma. (A) Transverse and (B) dorsal plane CT images of a dog at the level of a left adrenal gland mass (*) after IV contrast medium administration. Note the close association between the mass and the caudal vena cava and aorta. (C) Longitudinal axis ultrasonographic image of the same left adrenal gland mass (white arrow); the mass is seen extending into the adjacent phrenicoabdominal vein (white arrowhead).

IMAGING ESSENTIALS

FIGURE 17. Longitudinal axis view of the left adrenal gland of a cat diagnosed with an aldosterone-secreting tumor. Note the enlarged and distorted shape of the caudal pole of the left adrenal gland.

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PEER REVIEWED measurements of adrenal glands in cats with hyperthyroidism. Vet Radiol Ultrasound 2012;53(2):210-216. 7.

Elizabeth Huynh Elizabeth Huynh, DVM, is a diagnostic imaging resident and graduate student at University of Florida College of Veterinary Medicine. Her interests include ultrasonography, cross-sectional imaging, and nuclear medicine. She received her DVM from Ross University, finished her clinical year at Ohio State University, and completed a diagnostic imaging internship at Animal Specialty and Emergency Center in Los Angeles, California.

Clifford R. Berry Clifford R. Berry, DVM, DACVR, is a professor of diagnostic imaging at University of Florida College of Veterinary Medicine. His research interests include cross-sectional imaging of the thorax, nuclear medicine, and biomedical applications of imaging. He received his DVM from University of Florida and completed a radiology residency at University of California–Davis.

Grooters AM, Biller DS, Theisen SK, Miyabayashi T. Ultrasonographic characteristics of the adrenal glands in dogs with pituitary-dependent hyperadrenocorticism: comparison with normal dogs. J Vet Intern Med 1996;10(3):110-115.

8. Choi J, Kim H, Yoon J. Ultrasonographic adrenal gland measurements in clinically normal small breed dogs and comparison with pituitarydependent hyperadrenocorticism. J Vet Med Sci 2011;73(8):985-989. 9. Soulsby S, Holland M, Hudson JA, Behrend EN. Ultrasonographic evaluation of adrenal gland size compared to body weight in normal dogs. Vet Radiol Ultrasound 2015;56(3):317-326. 10. Cartee RL, Finn-Bodner ST, Gray BW. Ultrasonography of the normal feline adrenal gland. J Diagn Med Sonogr 1993;9:327-330. 11. Hoerauf A, Reusch C. Ultrasonographic evaluation of the adrenal glands in six dogs with hypoadrenocorticism. JAAHA 1999;35(3):214-218. 12. Wenger M, Mueller C, Kook PH, Reusch CE. Ultrasonographic evaluation of adrenal glands in dogs with primary hypoadrenocorticism or mimicking diseases. Vet Rec 2010;167(6):207-210. 13. Howell JM, Pickering CM. Calcium deposits in the adrenal glands of dogs and cats. J Comp Pathol 1964;74:280-285. 14. Kantrowitz BM, Nyland TG, Feldman EC. Adrenal ultrasonography in the dog: detection of tumors and hyperplasia in hyperadrenocorticism. Vet Radiol 1986;27:91-96. 15. Gould SM, Baines EA, Mannion PA, et al. Use of endogenous ACTH concentration and adrenal ultrasonography to distinguish the cause of canine hyperadrenocorticism. J Small Anim Pract 2001;42(3):113-121.

more likely to be mineralized,22,23 and malignant tumors often invade the phrenicoabdominal vein and/or caudal vena cava (Figure 15).2,3,20–22,24 Mineralization of the adrenal glands in cats is an age-related change that has not been reported to have clinical significance (Figure 16).13,25 Adrenal tumors are much rarer in cats than in dogs; however, aldosterone-secreting tumors, resulting in Conn’s syndrome, have been reported (Figure 17).2,3,26–32

SUMMARY The vascular anatomy is key to adrenal gland localization. The ability to routinely identify the adrenal glands is a standard part of the complete abdominal ultrasound evaluation. The most common observed abnormality of the adrenal glands is enlargement, which can take the form of hyperplasia, nodules, and masses. In cats, mineralization is seen as an incidental age-related change.

17. O'Brien RT, Zagzebski JA, Lu ZF, Steinberg H. Measurement of acoustic backscatter and attenuation in the liver of dogs with experimentally induced steroid hepatopathy. Am J Vet Res 1996;57(12):1690-1694. 18. Lu ZF, Zagzebski JA, O'Brien RT, Steinberg H. Ultrasound attenuation and backscatter in the liver during prednisone administration. Ultrasound Med Biol 1997;23(1):1-8. 19. Syakalima M, Takiguchi M, Yasuda J, et al. Comparison of attenuation and liver-kidney contrast of liver ultrasonographs with histology and biochemistry in dogs with experimentally induced steroid hepatopathy. Vet Q 1998;20(1):18-22. 20. Gilson SD, Withrow SJ, Wheeler SL, Twedt DC. Pheochromocytoma in 50 dogs. J Vet Intern Med 1994;8(3):228-232. 21. Barthez PY, Marks SL, Woo J, et al. Pheochromocytoma in dogs: 61 cases (1984-1995). J Vet Intern Med 1997;11(5):272-278. 22. Besso JG, Penninck DG, Gliatto JM. Retrospective ultrasonographic evaluation of adrenal lesions in 26 dogs. Vet Radiol Ultrasound 1997;38(6):448-455. 23. Reusch CE, Feldman EC. Canine hyperadrenocorticism due to adrenocortical neoplasia. Pretreatment evaluation of 41 dogs. J Vet Intern Med 1991;5(1):3-10. 24. Davis MK, Schochet RA, Wrigley R. Ultrasonographic identification of vascular invasion by adrenal tumors in dogs. Vet Radiol Ultrasound 2012;53(4):442-445. 25. Herbach N, Wiele K, Konietschke U, Hermanns W. Pathologic alterations of canine and feline adrenal glands. Open J Pathol 2016;6(3):140-153.

References

26. Moore LE, Biller DS, Smith TA. Use of abdominal ultrasonography in the diagnosis of primary hyperaldosteronism in a cat. JAVMA 2000;217(2):213-215, 197.

27. Nelson RW, Feldman EC, Smith MC. Hyperadrenocorticism in cats: seven cases (1978-1987). JAVMA 1988;193(2):245-250.

Evans HE, de Lahunta A. Guide to the Dissection of the Dog. 8th ed. St. Louis: Elsevier; 2017.

2. Mattoon J, Nyland T. Small Animal Diagnostic Ultrasound. 3rd ed. St. Louis: Elsevier Saunders; 2015. 3. Penninck DG, d'Anjou M. Atlas of Small Animal Ultrasonography. 2nd ed. Ames: Wiley Blackwell; 2015. 4. Voorhout G. X-ray-computed tomography, nephrotomography, and ultrasonography of the adrenal glands of healthy dogs. Am J Vet Res 1990;51(4):625-631. 5. Barthez PY, Nyland TG, Feldman EC. Ultrasonographic evaluation of the adrenal glands in dogs. JAVMA 1995;207(9):1180-1183. 6. Combes A, Vandermeulen E, Duchateau L, et al. Ultrasonographic

16. Biller DS, Kantrowitz B, Miyabayashi T. Ultrasonography of diffuse liver disease. A review. J Vet Intern Med 1992;6(2):71-76.

IMAGING ESSENTIALS

28. Immink WF, van Toor AJ, Vos JH, et al. Hyperadrenocorticism in four cats. Vet Q 1992;14(3):81-85. 29. Duesberg C, Peterson ME. Adrenal disorders in cats. Vet Clin North Am Small Anim Pract 1997;27(2):321-347. 30. DeClue AE, Breshears LA, Pardo ID, et al. Hyperaldosteronism and hyperprogesteronism in a cat with an adrenal cortical carcinoma. J Vet Intern Med 2005;19(3):355-358. 31. Ash RA, Harvey AM, Tasker S. Primary hyperaldosteronism in the cat: a series of 13 cases. J Feline Med Surg 2005;7(3):173-182. 32. Ahn A. Hyperaldosteronism in cats. Semin Vet Med Surg (Small Anim) 1994;9(3):153-157.

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TIPS TO AVOID TOOTH EXTRACTION COMPLICATIONS

PEER REVIEWED

Tips to Avoid Tooth Extraction Complications Brenda L. Mulherin, DVM, DAVDC Iowa State University College of Veterinary Medicine

One of the most common procedures performed by general practitioners in the oral cavity is surgical tooth extraction. The procedure is either a closed extraction, in which the tooth is extracted without a mucoperiosteal flap, or an open extraction, in which a mucoperiosteal flap is created to expose and remove alveolar bone and allow a tension-free closure.

• Complicated crown fracture

To a client, tooth extractions may seem routine and commonplace. However, those who have experience with oral surgery are aware that even theoretically simple extractions can be difficult. This article presents some factors to consider to make surgical extractions as safe and easy as possible for both surgeon and patient.

The difficulty of an extraction can be affected by the health of the periodontium surrounding the tooth. If the periodontium is healthy, but the pulp is diseased, the tooth may be difficult to extract. Examples of teeth with healthy periodontium include those extracted to treat a malocclusion, which are healthy teeth in the wrong place. This is common in immature patients with persistent deciduous teeth, or when interceptive orthodontic procedures are performed. Other examples are recently fractured teeth with pulp exposure (Figure 1) for which endodontic therapy is not an option.1

• Endodontic disease • Periodontal disease • Malocclusion • Tooth resorption • Tooth nonvitality

EXTRACTION INDICATIONS AND COMPLICATIONS The decision to extract a tooth stems from a variety of reasons, including1,2:

DENTAL DILEMMA Avoid complications associated with surgical tooth extractions by planning carefully and having a general knowledge of canine and feline dentition and tooth root numbers.

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FIGURE 1. (A) Recent crown fracture of the right maxillary canine tooth with pulp exposure. (B) An endodontic file placed in the pulp chamber of the fractured tooth to confirm pulp exposure. (C) Radiograph of the fractured tooth. The tooth was not mobile and there is no radiographic evidence of periapical lucency.

Planning ahead can help avoid complications relating to surgical tooth extraction. This includes taking intraoral dental radiographs and having the ability to interpret the radiographic findings. Knowledge of dental radiographic interpretation can help avoid some major pitfalls when surgically extracting teeth. This knowledge includes understanding what constitutes normal and abnormal anatomy as well as a general knowledge of the surrounding hard and soft tissue structures.

The permanent (secondary) dentition of the canine oral cavity comprises 42 teeth (Table 1 and Figure 2). There are 3 incisors (I), 1 canine (C) tooth, and 4 premolars (PM) in each of the maxillary and mandibular arcades. Each maxillary arcade has 2 molars (M), and each mandibular arcade has 3 molars: 2 × (I 3/3, C 1/1, PM 4/4, M 2/3) = 42 teeth.3

Feline Dental Formulas

Canine Dental Formulas

The deciduous dentition of the feline oral cavity comprises 26 teeth (Table 1). There are 3 incisors, 1 canine, and 3 premolars in each maxillary arcade. Each mandibular arcade has 3 incisors, 1 canine, and 2 premolars: 2 × (i 3/3, c 1/1, pm 3/2) = 26.3,4

The deciduous (primary) dentition of the canine oral cavity comprises 28 teeth (Table 1). The dentition is multiplied by 2 to include both right and left arcades. There are 3 incisors (i), 1 canine (c) tooth, and 3 premolars (pm) in each of the maxillary and mandibular arcades: 2 × (i 3/3, c 1/1, pm 3/3) = 28 teeth.3

The permanent dentition of the feline oral cavity comprises 30 teeth (Table 1 and Figure 3). There are 3 incisors, 1 canine, 3 premolars, and 1 molar on the right and left maxillary arcades. Each mandibular arcade has 3 incisors, 1 canine, 2 premolars, and 1 molar: 2 × (I 3/3, C 1/1, PM 3/2, M 1/1) = 30.3,4

NORMAL DENTITION AND TOOTH ROOTS

TABLE 1 Canine and Feline Dental Formulas TOTAL TEETH

TEETH IN EACH MAXILLARY ARCADE

TEETH IN EACH MANDIBULAR ARCADE

Deciduous (primary)

i3, c1, pm3

Permanent (secondary)

I3, C1, PM4, M2

I3, C1, PM4, M3

Deciduous (primary)

i3, c1, pm3

i3, c1, pm2

Permanent (secondary)

I3, C1, PM3, M1

I3, C1, PM2, M1

DENTITION CANINE

FELINE

TIPS TO AVOID TOOTH EXTRACTION COMPLICATIONS

PEER REVIEWED

FIGURE 2. Radiographic images of normal canine tooth anatomy. (A) Right maxilla. (B) Central maxilla. (C) Left maxilla. (D through H) Right maxillary teeth. (I through L) Left maxillary teeth. (M) Right mandible. (N) Central mandible. (O) Left mandible. (P through T) Right mandibular teeth. (U through Y) Left mandibular teeth.

Tooth Root Structure A standard number of roots are associated with each tooth (Table 2). The number of roots helps determine the type of extraction necessary; therefore, it is important to know the root structure of the tooth or teeth being treated. However, abnormal tooth and root structures do occur, making presurgical radiographs essential (see Tooth Root Abnormalities). For example, canine maxillary second and third premolars and mandibular second, third, and fourth premolars

each have 2 roots within the normal structure; however, many of these teeth have an accessory root.5 Cats appear to have more variations in normal root structures than dogs. The feline mandibular third and fourth premolars and the mandibular first molar teeth all should have 2 roots.5 One study found that the feline maxillary second premolar is absent in 7.9% of cats, has a single root in 27.7% of cats, has partially fused roots in 55.1% of cats, and has 2 fully formed roots in 9.2% of cats.6 This study also found that the feline maxillary first molar is SEPTEMBER/OCTOBER 2017

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FIGURE 3. Radiographic images of normal feline tooth anatomy. (A) Right maxilla. (B) Central maxilla. (C) Left maxilla. (D and E) Right maxillary teeth. (F and G) Left maxillary teeth. (H) Right mandible. (I) Central mandible. (J) Left mandible.

absent in 2.3% of cats, has a single root in 35% of cats, has partially fused roots in 34.7% of cats, and has 2 fully formed roots in 28% of cats.6

TOOTH ROOT ABNORMALITIES Dental radiography is necessary to assess whether there are root abnormalities that can affect an extraction.

Supernumerary Roots A supernumerary (extra) root can make a seemingly straightforward extraction more difficult, especially if not identified on dental radiography. The feline

maxillary second premolar and first molar can have 1 to 3 roots.6 Dogs can also have supernumerary roots (Figure 4). One study reported that 15.2% of large mesaticephalic-breed dogs have at least 1 supernumerary root within the oral cavity.7

Developmental Abnormalities Some abnormalities can make an extraction easier. These usually involve teeth that normally have 2 roots, but have developed only a single root. These teeth may be affected by fusion, gemination, or concrescence. Identification of these teeth on dental radiographs allows the surgeon to eliminate sectioning during extraction.

TABLE 2 Standard Number of Tooth Roots of Canine and Feline Permanent Teeth ARCADE

INCISOR TEETH

CANINE TEETH

PREMOLAR TEETH

MOLAR TEETH

1 root each

1st: 1 root 2nd: 2 roots 3rd: 2 roots 4th: 3 roots (2 mesial, 1 distal)

1st: 3 roots (2 buccal, 1 palatal) 2nd: 3 roots (2 buccal, 1 palatal)

1 root each

1st: 1 root 2nd: 2 roots 3rd: 2 roots 4th: 2 roots

1st: 2 roots 2nd: 2 roots 3rd: 1 root

Maxillary

1 root each

2nd: 1 or 2 roots 3rd: 2 roots 4th: 3 roots (2 mesial, 1 distal)

1st: 1 or 2 roots

Mandibular

1 root each

3rd: 2 roots 4th: 2 roots

1st: 2 roots

CANINE

Maxillary

Mandibular

1 root each

FELINE

TIPS TO AVOID TOOTH EXTRACTION COMPLICATIONS

PEER REVIEWED

FIGURE 4. (A) Radiographic image of the maxillary third premolar tooth with a supernumerary root (arrows) in a dog. The maxillary fourth premolar has radiographic evidence of a periapical lucency indicative of endodontic disease. (B) Photographic image of the maxillary premolars of the same dog.

FIGURE 5. Crown abnormalities of incisor teeth in a dog.

Fusion is when 2 tooth buds have joined, resulting in a single-rooted tooth with 2 root canals.7,8 Gemination is the incomplete development of 2 teeth from 1 tooth bud, which usually results in a tooth with 2 crowns but only a single root.7,8 Concrescence is the joining of adjacent teeth by the cementum only.7,8 Often, these developmental abnormalities cannot be differentiated without the aid of histopathology (Figures 5 and 6). In many instances, these teeth can remain in the mouth if crowding, periodontal disease associated with the tooth, or radiographic evidence of disease is not present. Regardless of which developmental condition has occurred, if the tooth needs to be extracted, knowing how many roots need to be removed is the most important consideration.

Dilacerated Roots Dilacerated roots are roots that bend at sharp angles, which can make extracting them in their entirety difficult (Figures 7 and 8). Dilacerated roots can curve toward the caudal or rostral aspect of the mouth. In one study, 34.4% of dogs had evidence of tooth root dilacerations.8

FIGURE 6. Radiographic image of root fusion (arrows) that may affect extraction.

Again, presurgical dental radiographs are necessary to identify dilacerated roots and their direction. Without the knowledge of whether dilaceration is present, surgical extraction can fracture dilacerated roots. Of even greater concern is when the dilacerated root is positioned close to the ventral mandibular cortex. If the surgeon is not careful, extraction technique or fractured root tip retrieval can result in a mandibular jaw fracture. SEPTEMBER/OCTOBER 2017

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PLANNING FOR TOOTH EXTRACTIONS

rapid elevation of the mucoperiosteal flap can tear tissue, delay healing, and, if severe enough, reduce flap size.10

Schedule Adequate Time

Adequate bone removal over the tooth roots allows root exposure and visualization of the structures to be extracted and helps reduce the time needed for the extraction. Gentle, consistent pressure applied to the roots during elevation weakens the periodontal ligament. This allows for increased mobility of the root to eventually facilitate removal.

Scheduling the appropriate amount of procedure time alleviates additional stress, allows ideal surgical technique, and permits the procedure to be performed without time constraints. The most important aspect of tooth extraction is patience. When applying pressure to the tooth root, using slow, gentle, consistent pressure to extract the root is better than forceful, jerky, sudden movements. Rushing through an extraction procedure often leads to an audible crack that signifies the fracture of the tooth root or, more seriously, of the surrounding bone. Gently controlling the elevation of the gingiva and mucosa of the tooth to be extracted allows exposure of the underlying alveolar bone and encourages adequate postoperative healing of the extraction site. Traumatic and

Use Proper Equipment Proper equipment ensures smoother surgical extractions. Important items include: • Sharp, appropriately sized elevators for reflecting the soft tissues (Figure 9) and winged elevators or luxators for elevation of the roots in question • Root tip picks, if needed • Extraction forceps (Figure 10) • New, appropriately sized dental burs for tooth sectioning, removing alveolar bone, and smoothing the bone following tooth removal (Figure 11) Having clean and sterile surgical packs made specifically for dental extractions can ensure all of the

FIGURE 9. Sharp periosteal elevator for reflecting soft tissue. FIGURE 7. Dilacerated mandibular tooth roots with evidence of periodontal disease shown by severe horizontal and vertical bone loss.

FIGURE 10. Extraction forceps for tooth root removal.

FIGURE 8. Dilacerated mandibular tooth roots with evidence of periodontal disease shown by vertical bone loss associated with the distal root of the first molar.

TIPS TO AVOID TOOTH EXTRACTION COMPLICATIONS

FIGURE 11. New pear carbide bur for alveolar bone removal.

VETFOLIO WORK Sherri O’Brien, DVM VetFolio User Since 2015

Won her first year of VetFolio

Passion for feline medicine

See how Sherri puts VetFolio to work: Getting Started “We as veterinarians are good at multitasking. I can cook dinner, fold laundry or work out on my exercise bike while I listen to a class. I can even listen to a podcast while I am driving to an alumni event. The education comes to you!” Staying Fresh “Our profession is constantly changing, and VetFolio allows you to engage in this change. If you have recently graduated, there are surgery videos and classes on the subjects you may have not covered deeply in school. If you have been out of school for over five years, VetFolio can help you stay current and academically fresh. We are never too old to learn!” Becoming a Pro “Everyone has their own way that they prefer to learn. There are surgery videos, short podcasts, longer lectures, and articles at your fingers. You can choose how you take your educational adventure.”

Photo credit: Shira Marie Photography

Continuing the Experience “I use the information learned on VetFolio daily. There are a variety of topics that I incorporate into my daily discussions with clients, technicians and rescue groups. Whether it has to deal with the pros and cons of early spay/neuter or the life expectancy of a dog with splenic HSA, the classes offer information that can be used in real-life practice. VetFolio also allows one to stay medically current and have access to the newest products coming out on the market!” Making #Goals I truly try to obtain 100 hours of CE a year. At least 40 are at conferences. I look forward to going to the NAVC Conference every year.

Meet Keenan Smith Loves giving back to the veterinary profession

INDIVIDUAL AND PRACTICE SUBSCRIPTIONS AVAILABLE. SEE HOW VETFOLIO CAN WORK FOR YOU AT VETFOLIO.COM.

PEER REVIEWED

Brenda L. Mulherin Brenda L. Mulherin, DVM, DAVDC, currently practices at Iowa State University College of Veterinary Medicine (CVM). She received her DVM from Iowa State University and later returned to Iowa State to fill a position in primary care. Dr. Mulherin completed a dual appointment with Iowa State University CVM and the University of Wisconsin-Madison School of Veterinary Medicine in a dentistry and oral surgery residency. She is currently developing the dentistry and oral surgery program at Iowa State University CVM.

Consider an appropriate mucoperiosteal flap design with either a single releasing incision or a double releasing incision. The releasing incisions should be divergent to allow exposure of the alveolar bone, but the incision should not be created directly over the area where the bone is removed. This design also helps allow for tension-free closure over the extraction site. An extraction attempted with limited exposure of bone can damage surrounding soft tissue structures, the mucoperiosteal flap, and the bone adjacent to the selected tooth.10 Limited exposure also increases the risk of root fracture during elevation.

SUMMARY hand instruments are ready for use, if needed. Sharpen hand instruments after each use to help maintain their shape, sharpness, and tactile sensitivity (Figure 12). Proper equipment also includes dental radiography. Regardless of whether the dental radiographs are film or digital, radiographic assessment of teeth is the most important diagnostic information needed to make the surgery as straightforward as possible.

Expose the Tooth Extraction Site For a successful extraction, make sure to expose the alveolar bone and tooth root(s). When removing alveolar bone over selected roots, a rule of thumb is to remove onehalf to two-thirds of the bone covering the root surface. Ultimately, the goal is to remove as much bone as necessary to remove the tooth roots without being overly aggressive. Removing too much bone can compromise the surrounding hard and soft tissue structures associated with the tooth. Surgical extraction of the selected tooth can be facilitated by: • Creating a mucoperiosteal flap • Removing an adequate amount of bone • Ensuring appropriate sectioning of the tooth over individual roots, when necessary

Avoid complications associated with surgical tooth extractions by planning carefully and having a general knowledge of canine and feline dentition and tooth root numbers. Using dental radiographs to assess the root structure and surrounding bone is vital to planning an appropriate approach to tooth extraction. With enough time scheduled for the procedure and proper equipment, including sharp instruments and new burs, the surgeon can surgically extract teeth as safely as possible. Carefully preparing the mucoperiosteal flap over the selected tooth provides the visibility needed to remove an appropriate amount of alveolar bone, elevate the tooth roots, extract the roots from the oral cavity, and create a tension-free closure. References 1. Holmstrom SE, Fitch PF, Eisner ER. Exodontics. In: Holmstrom SE, Fitch PF, Eisner ER, eds. Veterinary Dental Techniques for the Small Animal Practitioner. 3rd ed. Philadelphia: Saunders; 2004:291-338. 2. Wiggs RB, Lobprise HB. Oral surgery. In: Wiggs RB, Lobprise HB, eds. Veterinary Dentistry Principles and Practice. Philadelphia: LippincottRaven; 1997:232-258. 3. Wiggs RB, Lobprise HB. Oral anatomy and physiology. In: Wiggs RB, Lobprise HB, eds. Veterinary Dentistry Principles and Practice. Philadelphia: Lippincott-Raven; 1997:55-86. 4. Lewis JR, Reiter AM. Anatomy and physiology. In: Niemiec BA, ed. Small Animal Dental, Oral & Maxillofacial Disease. Boca Raton: Manson; 2013:9-38. 5. Wiggs RB, Lobprise HB. Oral examination and diagnosis. In: Wiggs RB, Lobprise HB, eds. Veterinary Dentistry Principles and Practice. Philadelphia: Lippincott-Raven; 1997:87-103. 6. Verstraete FJ, Terpak CH. Anatomic variations in the dentition of the domestic cat. J Vet Dent 1997;14:137-140. 7. Pavlica Z, Erjavec V, et al. Teeth abnormalities in the dog. Acta Vet Brno 2001;70:65-72. 8. Wiggs RB, Lobprise HB. Dental and oral radiology. In: Wiggs RB, Lobprise HB, eds. Veterinary Dentistry Principles and Practice. Philadelphia: Lippincott-Raven; 1997:140-166.

FIGURE 12. Dull winged elevator; note the rough and irregular surfaces at the edges. At minimum, this instrument needs sharpening, but it may need to be replaced.

TIPS TO AVOID TOOTH EXTRACTION COMPLICATIONS

9. Evans HE. Systemic arteries, aortic arch. In: Evans HE, ed. Miller’s Anatomy of the Dog. 3rd ed. Philadelphia: Saunders; 1993:602-645. 10. Peterson LJ. Prevention and management of surgical complications. In: Peterson LJ, Ellis III E, Hupp HR, Tucker MR, eds. Contemporary Oral and Maxillofacial Surgery. 4th ed. St. Louis: Mosby; 2003:221-235.

PROVEN REDUCTION IN KEY ORAL HEALTH INDICATORS1*

HALITOSIS

PLAQUE

CALCULUS

53% 42% 54%

Block plaque, calculus, and halitosis with the science of prevention OraVet® Dental Hygiene Chews combat plaque, calculus, and halitosis where they start—bacterial biofilms. The mechanism of action is simple but effective: Each daily chew releases delmopinol hydrochloride to create a barrier that prevents bacterial attachment.2,3 When bacteria can’t attach, they can’t produce plaque biofilms or the volatile sulfur compounds of halitosis. And the scrubbing action of the chew works in parallel to effectively remove plaque and calculus.

Science You Can Believe In

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Delmopinol • Delmopinol has been extensively tested in human and animal trials • Proven technology originally developed for a human oral rinse OraVet Dental Hygiene Chews • Efficacy demonstrated in multiple canine trials • Exceptional halitosis control1 • Highly palatable1

*Compared with dry diet alone. References: 1. Data on file. 2. Steinberg D, Beeman D, Bowen W. The effect of delmopinol on glucosyltransferase adsorbed on to saliva-coated hydroxyapatite. Archs Oral Biol. 1992;37:33-38. 3. Vassilakos N, Arnebrant T, Rundegren J. In vitro interactions of delmopinol hydrochloride with salivary films adsorbed at solid/liquid interfaces. Caries Res. 1993;27:176-182.

®ORAVET and SERIOUS ORAL CARE MADE SIMPLE are registered trademarks of Merial. All other trademarks are the property of their respective owners. Merial is now part of Boehringer Ingelheim. ©2017 Merial, Inc. Duluth, GA. All rights reserved. OVC15TRADEAD-R (07/17).

• Available through veterinarians

COGNITIVE DYSFUNCTION

PEER REVIEWED

Management of Dogs and Cats With Cognitive Dysfunction Lynne Seibert, DVM, MS, PhD, DACVB Veterinary Behavior Consultants, Roswell, Georgia

Behavior changes in older patients can indicate underlying medical issues, diminishing sensory capacities, age-related cognitive decline, a primary behavioral disorder, or a combination of these. Behavior problems can cause significant suffering for the patient, may challenge the caregiverâ&#x20AC;&#x2122;s ability to care for the pet, and may prompt the caregiver to relinquish or euthanize the pet. Early diagnosis and treatment are critical.

of CDS in cats was 36% in a population of 11to 21-year-old cats. The incidence of behavior changes increased with advancing age: Fifty percent of cats aged 15 years and older showed behavior changes versus 28% of cats aged 11 to 14 years. The most common behaviors seen in the 11- to 14-year-old age group were alterations in social interactions. In cats aged 15 years and older, the most common signs were aimless activity and excess vocalization.2

Cognitive functions include the mental processes of perception, awareness, learning, and memory, which allow an individual to acquire information about the environment and decide how to act. Cognitive dysfunction syndrome (CDS) is a neurobehavioral disorder affecting geriatric dogs and cats that is characterized by an age-related decline in cognitive abilities sufficient to affect functioning, with behavior changes that are not attributable to other medical conditions. The prevalence of CDS in dogs is extremely high, ranging from 28% in 11- to 12-year-old dogs to 68% in 15- to 16-year-old dogs.1 The prevalence

CDS is underdiagnosed because caregivers may assume behavior changes are a result of normal aging, and veterinarians may not recognize the signs. In a large cross-sectional study of dogs aged 8 to almost 20 years, researchers investigated the prevalence of canine cognitive dysfunction, along with the rate of veterinary diagnosis.3 On the basis of owner questionnaire data, the prevalence rate of CDS was estimated to be 14.2%. However, only 1.9% of cases were diagnosed by a veterinarian. The prevalence of CDS exponentially increased with age but did not differ by breed.3

ELDER CARE Cognitive dysfunction syndrome (CDS) is underdiagnosed because caregivers may assume behavior changes are a result of normal aging, and veterinarians may not recognize the signs.

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DIAGNOSIS

important to exclude other systemic diseases that could account for clinical signs before reaching a diagnosis.

Medical Evaluation CDS is an antemortem diagnosis of exclusion. Caregiver interviews using questionnaires (Table 1) are an important tool for assessing geriatric patients. It is

Aging affects all organ systems, and changes in many systems can present with behavioral signs (Box 1). Human patients with Alzheimerâ&#x20AC;&#x2122;s disease often exhibit movement disorders, including restlessness,

TABLE 1 Senior Pet Checklist BEHAVIOR

DATE

DISORIENTATION Appears lost or confused in familiar environment Decreased ability to recognize familiar people or animals Abnormal response (increased or decreased) to familiar objects Difficulty performing previously learned task Difficulty learning new tasks Getting stuck in corners or behind furniture Staring at walls or into space Difficulty finding the door Difficulty finding the food bowl Does not respond to verbal cues SOCIAL INTERACTIONS Changes in interactions with people, other animals (welcoming, playing, petting) Decreased responsiveness to family members Decreased affection toward, or interaction with, housemates Changes in exploratory behavior Increased irritability Increased aggression (lunging, snapping, biting) Intolerant of being left alone SLEEPâ&#x20AC;&#x201C;WAKE CYCLES Sleeping more overall Sleeping less at night Abnormal night-time behaviors (vocalization, wandering, motor restlessness) HOUSE-TRAINING Elimination in random indoor locations Elimination in sleeping area Decreased signaling to go outside Elimination indoors after a recent walk Elimination at uncommon outdoor locations (concrete) ACTIVITY Aimless wandering, motor restlessness, pacing Decreased activity level Loss of interest in food Slower at obeying commands Repetitive behaviors

COGNITIVE DYSFUNCTION

DATE

PEER REVIEWED

impaired gait, and tremors. Concurrent behavioral and neurologic signs in aging canine patients have also been documented. In a study of 21 dogs older than 7 years, those with CDS were twice as likely to show neurologic deficits as dogs without CDS.4 The medical evaluation should include a thorough physical and neurologic examination, orthopedic examination, pain assessment, and appropriate diagnostic testing, including complete blood profile, biochemistry panel, urinalysis, systemic blood pressure measurement, and additional testing as indicated by the clinical signs (eg, radiography, ultrasonography, endocrine tests). Magnetic resonance imaging and cerebral spinal fluid analysis are useful for assessing the presence of certain intracranial lesions that might mimic CDS, such as inflammatory, infectious, or neoplastic diseases.

Clinical Signs Senior-pet checklists typically include questions about disorientation, social interactions with humans and other animals, sleep–wake cycle changes, house soiling, and changes in activity levels. Locomotor and exploratory behaviors vary as a function of age and cognitive status. One study administered two tests to 85 dogs varying in age and cognitive status to

BOX 1 Organ System Changes That May Affect Behavior Digestive system • Dental disease • Decreased gastrointestinal motility • Obesity Urinary system • Decreased renal function • Urinary bladder disease • Hypertension Musculoskeletal system • Decreased muscle mass • Neuromuscular function deterioration • Degenerative joint disease Other • Endocrinopathies • Sensory decline (loss of vision or hearing) • Central nervous system disorders

explore their locomotor and exploratory behaviors.5 Cognitively impaired older dogs had higher locomotor activity and spent more time in aimless activity than young dogs (younger than 9 years); the more severe the cognitive impairment, the higher both of these measures were. Older dogs also demonstrated an age-dependent decline in exploratory behavior.5 Changes in social interactions with owners and other animals are frequently observed in dogs with CDS. Another pair of tests was administered to assess social responsiveness in dogs of varying ages and cognitive status.6 Social responsiveness was primarily affected by age but was also influenced by severity of cognitive impairment. Young dogs engaged in more physical contact with humans and more vocalizations in response to social isolation, but aged dogs spent more time near a mirror, suggesting a deficit in habituation to the reflection of a dog image.6 To investigate the sleep–wake patterns in aged dogs, radiotelemetry monitoring has been conducted. In elderly dogs, the sleep–wake patterns were dramatically altered.7 The changes were characterized by an increase in the total amount of time spent in slow-wave sleep during the daytime and an increase in time spent awake during the night.

Assessment Tools Rating scales are essential tools for CDS diagnosis and evaluation of the efficacy of therapeutic strategies. An ideal rating scale is simple and quick to administer, statistically validated, and applicable to all stages of the disease. The validity and reliability of scales should be evaluated before use. The Canine Dementia Scale, or CADES, is a statistically validated, highly sensitive rating scale for canine CDS. The scale contains 17 nonredundant items, distributed across 4 relevant domains: (1) spatial orientation, (2) social interactions, (3) sleep–wake cycles, and (4) house soiling. In a study,8 dogs with mild cognitive impairment frequently had impaired social interactions. Most dogs with moderate cognitive dysfunction had abnormal social interactions and sleep–wake cycles. For severe cognitive dysfunction, most dogs displayed impairment in all 4 domains.8

PATHOPHYSIOLOGY The brain consumes 20% of the body’s total oxygen. Its high percentage of polyunsaturated fatty acids and lower levels of endogenous antioxidant activity SEPTEMBER/OCTOBER 2017

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make it very susceptible to oxidative damage. Cellular metabolic processes release reactive oxygen species, which can lead to oxidative damage to proteins, lipids, DNA, and RNA, resulting in neuronal death. Normally, the activity of endogenous antioxidants balances the production of toxic free radicals. However, protective mechanisms begin to fail with age. Oxidative damage is associated with cognitive decline in dogs. An increase in oxidative end products in the brain of aged dogs correlates with more severe behavioral changes.9 The brains of older mammals show several anatomic and physiologic changes. These include a reduction in overall brain mass (including atrophy of cerebral cortex and basal ganglia), a reduction in the number of neurons, generalized gliosis, degeneration of white matter, demyelination, neuroaxonal degeneration, increases in ventricular size, meningeal fibrosis and calcification, and the presence of β-amyloid (Aβ) plaques. Functional changes include depletion of catecholamine neurotransmitters (norepinephrine, serotonin, and dopamine), a decline in the cholinergic system, an increase in monoamine oxidase B (MAO-B) activity, and a reduction of endogenous antioxidants.10 Several histopathologic similarities exist between human brains affected by Alzheimer’s disease and dog brains affected by CDS. The brains of 20 geriatric dogs aged 8 to 18 years were compared with the brains of 10 younger dogs; age-related pathologic changes of the meninges, choroid plexus, neurons, and glial cells were similar to changes seen in human brains.11 In both diseases, the aged brain develops an abnormal Aβ deposition in brain parenchyma and the walls of the cerebral blood vessels. Aβ is a protein produced by the degradation of amyloid precursor protein. The prefrontal cortex is the first area affected, followed by the temporal cortex, the hippocampus, and the occipital cortex. Regardless of position, the amount and extent of Aβ deposits correlate with the severity of cognitive impairment.12

TREATMENT Geriatric patients should receive regular examinations to address nutritional needs, obesity management, pain control, and physical and mental changes. Effective management of CDS may involve environmental and behavioral interventions, dietary modifications and nutritional supplements, pharmaceutical treatments, and complementary therapies.

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Enrichment and Environmental Management The environment may need to be modified to accommodate the aging pet’s needs and improve comfort. Resources need to be easily accessible. Litterboxes may need to be placed in additional locations. Older dogs may require more opportunities for elimination, either outdoors or in an indoor elimination area. If nocturnal waking is a problem, owners should increase the pet’s daytime exercise and reduce disturbances in the evening. Geriatric pets may be less tolerant of children and other household pets and should be provided with protected resting areas. Older pets may also be less tolerant of environmental changes and may require behavioral assistance if changes induce anxiety-related problems. Behavioral modification is similar to approaches used for younger pets, but with some limitations or constraints. Padded surfaces for sitting and traction for movement may help. If the pet is in pain, “stand” or “look” commands may replace frequent “sit” or “down” cues. Owners may need to adjust behavior signals used in training if sensory dysfunction is significant, including tactile cues or hand signals. More powerful motivators for learning may be needed, including the use of high-value food rewards. Maintaining a regular routine can reduce anxiety, and providing regular mental stimulation and enrichment will help maintain cognitive functioning.

Nutritional Intervention Antioxidants Diets containing antioxidants, mitochondrial cofactors, phosphatidylserine, and omega-3 fatty acids have proven beneficial for geriatric patients. Dietary treatment of CDS has focused primarily on reducing the deleterious effects of toxic free radicals. Cognitive improvements have been documented in older dogs fed a therapeutic antioxidant-rich diet containing flaxseed, carrots, spinach, citrus pulp, tomato pomace, grape pomace, α-lipoic acid, vitamin E, vitamin C, vitamin B12, pyridoxine, choline, l-lysine, l-tryptophan, l-carnitine, and β-carotene (Hill’s Prescription Diet b/d Canine; hillspet.com).13 The effects of the fortified diet with and without behavioral enrichment have been evaluated.14,15 Behavioral enrichment consisted of additional training (30 min/d, 5 days/wk), an enriched environment (housing with a kennel mate and weekly rotation

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of play toys), and physical exercise (two 20-minute outdoor walks/wk). The cognitive scores of the dogs fed a fortified diet and receiving behavioral enrichment were superior to those in all the other groups. Neurobiologic studies showed reduced oxidative damage and increased endogenous antioxidant activity in antioxidant-fed dogs, particularly among the dogs that received behavioral enrichment.14,15 Although no equivalent feline diet is available, Hill’s Prescription Diet Feline j/d, which is designed for cats with osteoarthritis, is supplemented with antioxidants and essential fatty acids. This diet may be useful for cats with signs of cognitive decline. Medium-Chain Triglycerides Glucose is the main energy source of neurons. However, glucose metabolism is reduced with aging. Other energy sources, such as ketone bodies, may be needed to maintain neuronal metabolism. Dietary medium-chain triglycerides (MCTs) can increase the levels of ketones in the blood, which can be used as an alternate energy source for cerebral functioning. Fatty acids derived from MCTs could provide up to 20% of the brain’s energy requirements.16 Long-term supplementation with MCTs has improved cognitive function in aged dogs (Purina One Vibrant Maturity 7+ Senior Formula, Purina ProPlan Veterinary Diet NC NeuroCare; purina.com). Dogs given a diet supplemented with 5.5% MCT for 8 months showed significantly better performance on cognitive tasks than control dogs.17 Diets supplemented with this type of lipid also reduce levels of Aβ deposits and improve mitochondrial function.18 Phosphatidylserine

changes in social interactions, and house-soiling behavior within 21 days of starting treatment. A supplement containing 25 mg phosphatidylserine, 50 mg standardized Ginkgo biloba extract, 33.5 mg α-tocopherol, and 20.5 mg pyridoxine per capsule was administered to 8 dogs at 1 capsule per 5 kg body weight in an open-label pilot study (Senilife; ceva.com).21 Dogs treated with this supplement showed marked improvement of CDS-related signs. Apoaequorin Dysregulation of intracellular calcium is associated with increased age and may be linked to CDS in dogs. Apoaequorin is a calcium-buffering protein with neuroprotective effects (Neutricks; quincybioscience.com). Aged beagles given apoaequorin at doses of 2.5 mg or 5 mg were better able to complete discrimination learning and attention tasks than the placebo group.22 Dogs treated with 10 mg apoaequorin showed superior performance on cognitive tasks compared with dogs receiving 1 mg/kg selegiline. S-Adenosyl-l-Methionine S-Adenosyl-l-methionine (SAMe) is an endogenous molecule synthesized by the liver and other cells throughout body and formed from the amino acid methionine. SAMe is essential for the major biochemical pathways and metabolic reactions in the liver. Exogenous SAMe increases endogenous production of the antioxidant glutathione, resulting in increased serotonin turnover and increased dopamine and norepinephrine levels.

Phosphatidylserine is a natural phospholipid in cell membranes and is found at high concentrations in the brain and at synapses. It facilitates membranedependent neuronal processes; enhances acetylcholine release; inhibits loss of muscarinic receptors; activates synthesis and release of dopamine; and may improve memory, learning, and social behavior in dogs and cats.19

Pure SAMe is unstable and highly reactive, so commercially available oral forms of SAMe are salts (Novifit [virbac.com]; Denosyl, Nutramax [nutramaxlabs.com]). Oral bioavailability depends on the salt used. The presence of food in the gut can significantly decrease absorption, so SAMe should be administered on an empty stomach, 1 hour before feeding.

A placebo-controlled trial evaluated a supplement containing essential fatty acids (docosahexaenoic acid and eicosapentaenoic acid), N-acetylcysteine (a primary precursor to glutathione), α-lipoic acid, vitamins C and E, l-carnitine, selenium, coenzyme Q10, and phosphatidylserine.20 The treated group showed significantly more improvement than the placebo group with regard to disorientation,

Oral SAMe tosylate supplementation (Novifit tablets) was evaluated as a dietary aid for the management of age-related cognitive decline in dogs.23 Dogs were administered placebo or 18 mg/kg SAMe tosylate for 2 months, with no associated behavior modification. SAMe-treated dogs showed significantly greater improvement in activity and awareness at 4 weeks and 8 weeks compared with placebo-treated dogs.23

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Data on file at Merial.

IMPORTANT SAFETY INFORMATION: NexGard® is for use in dogs only. The most frequently reported adverse reactions included pruritus, vomiting, dry/flaky skin, diarrhea, lethargy, and lack of appetite. The safe use of NexGard in pregnant, breeding, or lactating dogs has not been evaluated. Use with caution in dogs with a history of seizures. For more information, see full prescribing information or visit www.NexGardForDogs.com.

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Pharmacologic Intervention

CAUTION: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian. Description: NexGard® (afoxolaner) is available in four sizes of beef-flavored, soft chewables for oral administration to dogs and puppies according to their weight. Each chewable is formulated to provide a minimum afoxolaner dosage of 1.14 mg/lb (2.5 mg/ kg). Afoxolaner has the chemical composition 1-Naphthalenecarboxamide, 4-[5- [3-chloro-5-(trifluoromethyl)-phenyl]-4, 5-dihydro-5-(trifluoromethyl)-3-isoxazolyl]-N-[2-oxo-2-[(2,2,2-trifluoroethyl)amino]ethyl. Indications: NexGard kills adult fleas and is indicated for the treatment and prevention of flea infestations (Ctenocephalides felis), and the treatment and control of Black-legged tick (Ixodes scapularis), American Dog tick (Dermacentor variabilis), Lone Star tick (Amblyomma americanum), and Brown dog tick (Rhipicephalus sanguineus) infestations in dogs and puppies 8 weeks of age and older, weighing 4 pounds of body weight or greater, for one month. Dosage and Administration: NexGard is given orally once a month, at the minimum dosage of 1.14 mg/lb (2.5 mg/kg). Dosing Schedule: Body Weight 4.0 to 10.0 lbs. 10.1 to 24.0 lbs. 24.1 to 60.0 lbs. 60.1 to 121.0 lbs. Over 121.0 lbs.

Selegiline Hydrochloride Selegiline hydrochloride (Anipryl; zoetis.com) is approved for the control of clinical signs associated with canine CDS. Selegiline is a selective and irreversible inhibitor of the enzyme MAO-B. In the central nervous system, MAO-B is responsible for catabolism of catecholamines, dopamine, and, to a lesser extent, norepinephrine and serotonin. Inhibition of MAO-B results in increased levels of phenylethylamine, increased dopamine release, decreased uptake of dopamine and other monoamine neurotransmitters, antioxidant activity, and decreased free radical formation.

Afoxolaner Per Chewables Chewable (mg) Administered 11.3 One 28.3 One 68 One 136 One Administer the appropriate combination of chewables

NexGard can be administered with or without food. Care should be taken that the dog consumes the complete dose, and treated animals should be observed for a few minutes to ensure that part of the dose is not lost or refused. If it is suspected that any of the dose has been lost or if vomiting occurs within two hours of administration, redose with another full dose. If a dose is missed, administer NexGard and resume a monthly dosing schedule. Flea Treatment and Prevention: Treatment with NexGard may begin at any time of the year. In areas where fleas are common year-round, monthly treatment with NexGard should continue the entire year without interruption. To minimize the likelihood of flea reinfestation, it is important to treat all animals within a household with an approved flea control product. Tick Treatment and Control: Treatment with NexGard may begin at any time of the year (see Effectiveness). Contraindications: There are no known contraindications for the use of NexGard. Warnings: Not for use in humans. Keep this and all drugs out of the reach of children. In case of accidental ingestion, contact a physician immediately. Precautions: The safe use of NexGard in breeding, pregnant or lactating dogs has not been evaluated. Use with caution in dogs with a history of seizures (see Adverse Reactions). Adverse Reactions: In a well-controlled US field study, which included a total of 333 households and 615 treated dogs (415 administered afoxolaner; 200 administered active control), no serious adverse reactions were observed with NexGard. Over the 90-day study period, all observations of potential adverse reactions were recorded. The most frequent reactions reported at an incidence of > 1% within any of the three months of observations are presented in the following table. The most frequently reported adverse reaction was vomiting. The occurrence of vomiting was generally self-limiting and of short duration and tended to decrease with subsequent doses in both groups. Five treated dogs experienced anorexia during the study, and two of those dogs experienced anorexia with the first dose but not subsequent doses. Table 1: Dogs With Adverse Reactions. Treatment Group Afoxolaner

Vomiting (with and without blood) Dry/Flaky Skin Diarrhea (with and without blood) Lethargy Anorexia

N1 17 13 13 7 5

% (n=415) 4.1 3.1 3.1 1.7 1.2

Clinical trials showed selegiline hydrochloride to be effective in controlling clinical signs associated with CDS after 4 weeks of treatment.24 Dogs receiving selegiline hydrochloride showed significant improvement when compared with placebo-treated controls in sleeping patterns, housetraining, and activity level.

Oral active control

N2 25 2 7 4 9

% (n=200) 12.5 1.0 3.5 2.0 4.5

The approved dose of selegiline hydrochloride for dogs is 0.5 to 1.0 mg/kg q24h, to be given in the morning, dosed to the nearest whole tablet, with adjustments based on response and tolerance. The onset of action varies (4 to 12 weeks), and improvement may increase with extended use. Selegiline hydrochloride has been used off-label in cats with cognitive dysfunction at 0.25 to 0.5 mg/kg q24h.

Number of dogs in the afoxolaner treatment group with the identified abnormality. 2 Number of dogs in the control group with the identified abnormality. In the US field study, one dog with a history of seizures experienced a seizure on the same day after receiving the first dose and on the same day after receiving the second dose of NexGard. This dog experienced a third seizure one week after receiving the third dose. The dog remained enrolled and completed the study. Another dog with a history of seizures had a seizure 19 days after the third dose of NexGard. The dog remained enrolled and completed the study. A third dog with a history of seizures received NexGard and experienced no seizures throughout the study. To report suspected adverse events, for technical assistance or to obtain a copy of the MSDS, contact Merial at 1-888-6374251 or www.merial.com/NexGard. For additional information about adverse drug experience reporting for animal drugs, contact FDA at 1-888-FDA-VETS or online at http://www.fda.gov/AnimalVeterinary/SafetyHealth. Mode of Action: Afoxolaner is a member of the isoxazoline family, shown to bind at a binding site to inhibit insect and acarine ligand-gated chloride channels, in particular those gated by the neurotransmitter gamma-aminobutyric acid (GABA), thereby blocking preand post-synaptic transfer of chloride ions across cell membranes. Prolonged afoxolaner-induced hyperexcitation results in uncontrolled activity of the central nervous system and death of insects and acarines. The selective toxicity of afoxolaner between insects and acarines and mammals may be inferred by the differential sensitivity of the insects and acarines’ GABA receptors versus mammalian GABA receptors. Effectiveness: In a well-controlled laboratory study, NexGard began to kill fleas four hours after initial administration and demonstrated >99% effectiveness at eight hours. In a separate well-controlled laboratory study, NexGard demonstrated 100% effectiveness against adult fleas 24 hours post-infestation for 35 days, and was ≥ 93% effective at 12 hours post-infestation through Day 21, and on Day 35. On Day 28, NexGard was 81.1% effective 12 hours post-infestation. Dogs in both the treated and control groups that were infested with fleas on Day -1 generated flea eggs at 12- and 24-hours post-treatment (0-11 eggs and 1-17 eggs in the NexGard treated dogs, and 4-90 eggs and 0-118 eggs in the control dogs, at 12- and 24-hours, respectively). At subsequent evaluations post-infestation, fleas from dogs in the treated group were essentially unable to produce any eggs (0-1 eggs) while fleas from dogs in the control group continued to produce eggs (1-141 eggs). In a 90-day US field study conducted in households with existing flea infestations of varying severity, the effectiveness of NexGard against fleas on the Day 30, 60 and 90 visits compared with baseline was 98.0%, 99.7%, and 99.9%, respectively. Collectively, the data from the three studies (two laboratory and one field) demonstrate that NexGard kills fleas before they can lay eggs, thus preventing subsequent flea infestations after the start of treatment of existing flea infestations. In well-controlled laboratory studies, NexGard demonstrated >97% effectiveness against Dermacentor variabilis, >94% effectiveness against Ixodes scapularis, and >93% effectiveness against Rhipicephalus sanguineus, 48 hours post-infestation for 30 days. At 72 hours post-infestation, NexGard demonstrated >97% effectiveness against Amblyomma americanum for 30 days. Animal Safety: In a margin of safety study, NexGard was administered orally to 8 to 9-week-old Beagle puppies at 1, 3, and 5 times the maximum exposure dose (6.3 mg/kg) for three treatments every 28 days, followed by three treatments every 14 days, for a total of six treatments. Dogs in the control group were sham-dosed. There were no clinically-relevant effects related to treatment on physical examination, body weight, food consumption, clinical pathology (hematology, clinical chemistries, or coagulation tests), gross pathology, histopathology or organ weights. Vomiting occurred throughout the study, with a similar incidence in the treated and control groups, including one dog in the 5x group that vomited four hours after treatment. In a well-controlled field study, NexGard was used concomitantly with other medications, such as vaccines, anthelmintics, antibiotics (including topicals), steroids, NSAIDS, anesthetics, and antihistamines. No adverse reactions were observed from the concomitant use of NexGard with other medications. Storage Information: Store at or below 30°C (86°F) with excursions permitted up to 40°C (104°F). How Supplied: NexGard is available in four sizes of beef-flavored soft chewables: 11.3, 28.3, 68 or 136 mg afoxolaner. Each chewable size is available in color-coded packages of 1, 3 or 6 beef-flavored chewables. 1

Possible side effects include restlessness or agitation, vomiting, disorientation, or diarrhea. Selegiline should not be used in combination with other MAO inhibitors, including amitraz, opioids, α2 agonists, phenylpropanolamine, tricyclic antidepressants, selective serotonin reuptake inhibitors, or any other serotonergic agents (including trazodone, tramadol, and buspirone). At least 14 days should elapse between discontinuation of selegiline and initiation of treatment with a tricyclic antidepressant or selective serotonin reuptake inhibitor. Because of the long half-life of fluoxetine and its active metabolites, at least 6 weeks should elapse between discontinuation of fluoxetine and initiation of treatment with selegiline. N-Methyl-d-Aspartate Receptor Antagonists

NADA 141-406, Approved by FDA Marketed by: Frontline Vet Labs™, a Division of Merial, Inc. Duluth, GA 30096-4640 USA

Memantine binds to N-methyl-d-aspartate receptors in the brain and blocks the activity of glutamate. Excessive

COGNITIVE DYSFUNCTION

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glutaminergic activity resulting in neurotoxicity is suspected in the pathology of dementia. Memantine is used in the treatment of moderate to severe Alzheimer’s disease. It has been used in dogs to treat compulsive behaviors, at a dose of 0.3 to 1.0 mg/kg q12h.25

Complementary Therapies Older pets often have anxiety-related conditions. Therefore, anxiolytic agents may also be indicated, including selective serotonin reuptake inhibitors, tricyclic antidepressants, azapirones, γ-aminobutyric acid agonists, or benzodiazepines, with attention to potential drug interactions. Complementary therapies may include compression garments (Thundershirt [thundershirt.com], Anxiety Wrap [anxietywrap.com]), pheromones, aromatherapy, herbal supplements, acupuncture, acupressure, massage, or physical therapy.

CONCLUSION Senior dogs and cats should be evaluated for signs of cognitive impairment by using the diagnostic tools available, and treatment should be initiated as early as possible. Treatment options include pharmaceutical agents, dietary therapy, nutritional supplements, and behavioral enrichment. With thorough senior pet evaluations and clear client communication, veterinarians can help older pets live happier, healthier, more comfortable lives. References 1. Neilson JC, Hart BL, Cliff KD, Ruehl WW. Prevalence of behavioral changes associated with age-related cognitive impairment in dogs. JAVMA 2001;218(11):1787-1791. 2. Moffat KS, Landsberg GM. An investigation of the prevalence of clinical signs of cognitive dysfunction syndrome (CDS) in cats. JAAHA 2003;39(5):512. 3. Salvin HE, McGreevy PD, Sachdev PS, Valenzuela MJ. Under diagnosis of canine cognitive dysfunction: a cross-sectional survey of older companion dogs. Vet J 2010;184(3):277-281. 4. Golini L, Colangeli R, Tranquillo V, Mariscoli M. Association between neurologic and cognitive dysfunction signs in a sample of aging dogs. J Vet Behav 2009;4(1):25-30. 5. Rosado B, González-Martínez A, Pesini P, et al. Effect of age and severity of cognitive dysfunction on spontaneous activity in pet dogs— part 1: locomotor and exploratory behavior. Vet J 2012;194(2):189-195. 6. Rosado B, González-Martínez A, Pesini P, et al. Effect of age and severity of cognitive dysfunction on spontaneous activity in pet dogs—part 2: social responsiveness. Vet J 2012;194(2):196-201. 7. Takeuchi T, Harada E. Age-related changes in sleep-wake rhythm in dog. Behav Brain Res 2002;136(1):193-199. 8. Madaria A, Farbakova J, Katina S, et al. Assessment of severity and progression of canine cognitive dysfunction syndrome using the Canine Dementia Scale (CADES). Appl Anim Behav Sci 2015;171:138145. 9. Skoumalova A, Rofina J, Schwippelova Z, et al. The role of free radicals in canine counterpart of senile dementia of the Alzheimer type. Exp

Lynne Seibert Dr. Seibert owns a behavior referral practice in Roswell, Georgia. She received her DVM degree from the University of Tennessee and completed her master’s and PhD degrees in psychology at the University of Georgia. After her conforming residency, she became board-certified with the American College of Veterinary Behaviorists (ACVB). She has taught behavior courses at 6 veterinary colleges. She is a past president of the American Veterinary Society of Animal Behavior and served 2 terms as secretary– treasurer on the ACVB Board of Regents. She has presented over 2000 hours of behavior education.

Gerontol 2003;38(6):711-719. 10. Landsberg GL, Araujo JA. Behavior problems in geriatric pets. Vet Clin North Am Small Anim Pract 2005;35(3):675-698. 11. Borras D, Ferrer I, Pumarola M. Age related changes in the brain of the dog. Vet Pathol 1999;36(3):202-211. 12. Schmidt F, Boltze J, Jager C, et al. Detection and quantification of β-amyloid, pyroglutamil Aβ, and tau in aged canines. J Neuropathol Exp Neurol 2015;74(9):912-923. 13. Cotman CW, Head E, Muggenburg BA, et al. Brain aging in the canine: a diet enriched in antioxidants reduces cognitive dysfunction. Neurobiol Aging 2002;23(5):809-818. 14. Milgram NW, Head E, Zicker SC, et al. Learning ability in aged beagle dogs is preserved by behavioral enrichment and dietary fortification: a two-year longitudinal study. Neurobiol Aging 2005;26(1):77-90. 15. Opii WO, Joshi G, Head E, et al. Proteomic identification of brain proteins in the canine model of human aging following a long-term treatment with antioxidants and a program of behavioral enrichment: relevance to Alzheimer's disease. Neurobiol Aging 2008;29(1):51-70. 16. Pan Y. Enhancing brain function in senior dogs: a new nutritional approach. Topics Compan Anim Med 2011;26(1):10-16. 17. Pan Y, Larson, B, Araujo JA, et al. Dietary supplementation with medium-chain TAG has long-lasting cognition-enhancing effects in aged dogs. Br J Nutrition 2010;103:1746-1754. 18. Taha AY, Henderson ST, Burnham WM. Dietary enrichment with medium chain triglycerides (AC-1203) elevates polyunsaturated fatty acids in the parietal cortex of aged dogs; implications for treating agerelated cognitive decline. Neurochem Res 2009;34(9):1619-1625. 19. Osella MC, Re G, Badino P, et al. Phosphatidylserine (PS) as a potential nutraceutical for canine brain aging: a review. J Vet Behav Clin Appl Res 2008;3(2):41-51. 20. Heath SE, Barabas S, Craze PG. Nutritional supplementation in cases of canine cognitive dysfunction—a clinical trial. Appl Anim Behav Sci 2007;105(4):274-283. 21. Osella MC, Re G, Odore R, et al. Canine cognitive dysfunction syndrome: prevalence, clinical signs and treatment with a neuroprotective nutraceutical. Appl Anim Behav Sci 2007;105(4):297310. 22. Milgram NW, Landsberg G, Merrick D, Underwood MY. A novel mechanism for cognitive enhancement in aged dogs with the use of a calcium-buffering protein. J Vet Behav 2015;10(3):217-222. 23. Rème CA, Dramard V, Kern L, et al. Effect of S-adenosylmethionine tablets on the reduction of age-related mental decline in dogs: a double-blinded, placebo-controlled trial. Vet Therap Res Appl Vet Med 2008;9(2):69-82. 24. Milgram NW, Ivy GO, Head E, et al. The effect of L-deprenyl on behavior, cognitive function, and biogenic amines in the dog. Neurochem Res 1993;18(12):1211-1219. 25. Schneider BM, Dodman NH, Maranda L. Use of memantine in treatment of canine compulsive disorders. J Vet Behav 2009;4(3):118-126.

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INTESTINAL MICROBES AND DISEASE IN DOGS

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Intestinal Microbes and Digestive System Disease in Dogs Jan S. Suchodolski, MedVet, DrVetMed, PhD, AGAF, DACVM Texas A&M University

The intestinal microbiota comprises viruses, bacteria, fungi, and protozoa. In the past, the word microflora has been used to describe this complex ecosystem, but microbiota (from –bios, “living organisms”) is the more appropriate term. The microbiome is the collective genome of all these microbes. Most studies to date have focused on the bacterial microbiota, which is estimated to make up the vast majority of the intestinal microbiota. An estimated 100 trillion microbial cells are present within the intestine, up to 10 times the number of mammalian cells in the whole body. Combined, microbial genes outnumber host genes by an estimated factor of 10. This complex ecosystem of gut bacteria has a tremendous influence on host health. The interactions between bacteria and host are mediated through direct contact between

microbes and the immune system and through various microbiota-derived metabolites. A physiologic microbiome modulates the immune system, protects against enteropathogens, and provides nutritional benefits to the host. Conversely, changes in the intricate relationship between gut bacteria and host cells affect the host’s immune responses and metabolic status and may result in disease (Figure 1). Recent studies have described intestinal dysbiosis (ie, changes in intestinal microbiota composition and/or diversity) in various acute and chronic gastrointestinal (GI) disorders.1 Additionally, initial data in human and animal models have linked chronic dysbiosis, such as that caused by antibiotic exposure, to extraintestinal disorders such as diabetes and obesity.2,3 These findings highlight the importance of gut microbiota and dysbiosis in regulating host metabolism, with effects reaching far beyond the GI tract.

RARE BREED Every dog harbors a unique microbial community, with distinct differences in the proportions of these bacterial groups. Yet the bacterial gene content is conserved across individuals, suggesting that functional aspects of the microbiome are similar across animals. Individual differences in microbial species may cause individualized responses to different diets, fiber sources, and probiotics.

shutterstock.com/Elena Glezerova

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FIGURE 1. The interplay between the intestinal microbiota and the host immune system and metabolism. (A) In a healthy intestine, proper spatial arrangements exist between the highly abundant luminal microbiota, the epithelium, and immune cells (dendritic cells, lymphocytes, macrophages, neutrophils) that are present in low numbers. The microbiota provides immunomodulatory stimuli to the immune system and metabolizes and ferments complex carbohydrates into beneficial short-chain fatty acids (SCFA). These SCFA provide energy for endothelial cells, are anti-inflammatory, and regulate intestinal motility. The normal microbiota also converts primary bile acids to secondary bile acids, which are also anti-inflammatory, induce glucagon-like peptide 1 (which in turn increases insulin), and decrease, for example, sporulation of Clostridium difficile. (B) In a diseased state, regardless of the initiating cause, the decreased production of antimicrobial peptides and mucus leads to increased intestinal permeability and translocation of bacteria. Innate immune receptors, such as Toll-like receptors on macrophages and other immune cells, recognize specific pathogen-associated molecular patterns due to dysbiosis (eg, lipopolysaccharides in bacterial cell walls) and trigger inflammatory reactions. Macrophages phagocytize microbes, also triggering immune responses that can lead to oxidative stress. Oxidative stress, in turn, can cause intestinal dysbiosis.

The dysbiosis patterns and metabolic signatures observed in acute and chronic GI diseases and the metabolic syndrome are only beginning to be described. Dysbiosis signatures and metabolic alterations are being evaluated for their diagnostic and therapeutic potential. This article provides an overview of the bacteria in the canine intestine and the role of dysbiosis in the etiology of GI diseases.

THE INTESTINAL MICROBIOTA IN HEALTH Identification and Components Until recently, identification of intestinal bacteria was almost exclusively achieved using traditional bacterial culture. Fecal culture may still be useful for the detection of specific enteropathogens such as Salmonella or Campylobacter jejuni, as this approach allows for antibiotic susceptibility testing of clinical specimens, but the vast majority of intestinal bacteria are strict anaerobes and undetectable using standard cultivation methods. Therefore, routine bacterial culture does not allow in-depth characterization of complex intestinal bacterial communities (Figure 2). A number of molecular-based methods are now used for the characterization of the intestinal microbiota.4

INTESTINAL MICROBES AND DISEASE IN DOGS

Traditional bacterial culture as well molecular approaches have revealed differences in the type and amount of bacteria along the GI tract. Bacterial numbers in the duodenum of healthy dogs range from 102 to 109 colony-forming units (cfu)/g.5 The colon harbors much higher numbers, with up to 1011 cfu/g.6 Molecular tools have allowed identification of previously uncultivable, and hence unknown, bacteria. While the duodenum harbors a mixture of aerobic and facultative anaerobic bacteria, the colon is colonized almost exclusively by strict anaerobes.7 The bacterial groups Clostridiaceae, Bacteroidaceae, Prevotellaceae, and Fusobacteriaceae predominate in the large intestine (Figure 2). Of note is that every dog harbors a unique microbial community, with distinct differences in the proportions of these bacterial groups. Yet the bacterial gene content is conserved across individuals, suggesting that functional aspects of the microbiomes are similar across animals.8 Nevertheless, individual differences in microbial species may cause individualized responses to different diets, fiber sources, and probiotics. The GI tract is also home to a diverse population of viruses and fungi. One study described up to 40 fungal species in canine fecal samples; most were various Candida spp.9 Based on these findings, it is expected that fungal organisms would be observed on routine

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fecal smears. Their exact contribution to health and disease remains unclear, as no significant differences in the types of fungi were reported when healthy dogs were compared with dogs with acute diarrhea.

Roles A balanced microbiome is crucial for maintaining host health. The normal microbiota performs the following functions: • Modulates the immune system • Keeps invading enteropathogens in check • Provides nutrients to the host by metabolizing and fermenting various dietary components Intestinal bacteria also contribute to the development of gut physiology. This has been demonstrated in studies with germ-free raised mice, which show altered epithelial architecture (eg, decreased number of lymphoid follicles) compared with mice that have been exposed to bacteria at birth. Consistent crosstalk between the intestinal microbiota and host immune cells is mediated through a combination of microbial-derived metabolites (eg, short-chain fatty acids [SCFA], indole, secondary bile acids) as well as molecules on the surface of bacteria that activate receptors of the host innate immune system (eg, Toll-like receptors, dendritic cells).

Commensal bacteria, which prevent mucosal invasion of transient pathogens through competition for nutrients and epithelial adhesion sites, are an important part of the intestinal barrier. Furthermore, they establish a physiologically restrictive environment for nonresident bacterial species through secretion of antimicrobial compounds and modulation of luminal pH. The major bacterial groups in the gut are strict or facultative anaerobes. The predominant bacterial families in the large intestine (Figure 2) ferment dietary carbohydrates (eg, starch, cellulose, pectin, inulin), resulting in the production of SCFA (eg, acetate, propionate, butyrate) and other metabolites. SCFA are an important source of energy and growth factors for intestinal epithelial cells and have a modulating effect on intestinal motility. Furthermore, SCFA are immunomodulatory. For example, butyrate induces immunoregulatory T cells and acetate beneficially modulates intestinal permeability. An emerging area of research aims to better characterize the biologic functions of additional bacterial-derived metabolites that have been recently recognized as regulators of host health, such as indole and secondary bile acids. For example, dietary tryptophan is metabolized by bacteria into indole, which has been shown to decrease interleukin-8 expression, strengthen intestinal barrier function, and ameliorate nonsteroidal anti-inflammatory

FIGURE 2. Predominant bacterial taxa in fecal samples of healthy dogs. Each bar represents one healthy dog. Note that the bacterial families present vary widely, anaerobic bacteria predominate, and the ratios of these bacterial groups differ in each healthy dog. Routine bacterial culture misses these anaerobic bacteria. Fecal smears that evaluate ratios of gram-positive to gram-negative bacteria are also not useful to assess dysbiosis, as each dog harbors a unique ratio of these groups.

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drug–induced enteropathy in mice.10 Some bacterial species in the colon convert primary bile acids into secondary bile acids (eg, lithocholic and deoxycholic acids). Therefore, secondary bile acids are present at much higher concentrations in the colon than primary bile acids. This high concentration of secondary bile acids in the colon is beneficial, as these acids are an important regulator of host homeostasis through activation of various receptors throughout the body. For example, the bile acid–specific membrane receptor TGR5 is expressed in the gallbladder, in bile duct epithelium, on monocytes and macrophages, and in muscle, kidney, pancreatic, and intestinal cells. The activation of these receptors, for which secondary bile acids have the highest affinity, downregulates the expression of proinflammatory cytokines and modulates insulin and glucose metabolism through activation of glucagon-like peptide 1.11 Secondary bile acids also inhibit germination of Clostridium difficile spores, whereas an increase in primary bile acids (an effect of dysbiosis) promotes the germination of bacterial spores. Intestinal dysbiosis leads to a decrease in bile-acid converting bacterial species and, therefore, is associated with bile acid dysmetabolism (decrease in secondary and increase in primary bile acids) and potentially systemic effects on host metabolism.12,13 Furthermore, an abnormal increase in primary bile acids may cause secretory diarrhea.

DYSBIOSIS Intestinal dysbiosis is defined as differences in ratios of bacterial groups compared with those found in healthy dogs and is often accompanied by a reduction in species diversity. Intestinal dysbiosis has been reported in various acute and chronic GI disorders, but it can also be induced through use of broad-spectrum antibiotics.1 The importance of the gut microbiota in host immune regulation and metabolism (Figure 1) means that a dysbiotic microbiome may have negative consequences for the host. However, the extent of clinical signs varies between individuals. For example, administration of metronidazole to healthy dogs induced major changes in the gut microbiota, with reductions in commensal anaerobic bacteria and a concurrent increase in Escherichia coli; these changes were accompanied by extensive changes in metabolomic pathways in the gut lumen (eg, increase in oxidative stress, reductions in secondary bile acids).14 Nine of 16 dogs developed loose stools while on antibiotics, but the remaining dogs exhibited no clinical signs despite having similar microbial and biochemical

INTESTINAL MICROBES AND DISEASE IN DOGS

changes. This suggests that clinical signs depend on the interplay of multiple microbial and host factors, some of which (eg, underlying genetic susceptibility of the host, dietary and environmental triggers) remain to be elucidated. Nevertheless, antibiotic-induced dysbiosis is an example of how changes in microbial composition and metabolism can affect host health, as antibiotic-induced dysbiosis in early childhood or repeated pulse therapy has been recognized as a risk factor for development of allergies, obesity, and inflammatory bowel disease in humans.3,15 The emerging epidemiologic data in humans and our evolving understanding of the immunomodulatory and metabolic properties of the gut microbiota suggest that proper diagnosis and correction of dysbiosis will be important goals in various diseases. A dysbiotic microbiome may cause harm through several mechanisms (Box 1), which are likely to be concurrent. Diarrhea can be due to bacterial enterotoxins that stimulate mucosal fluid secretions. Another recently recognized mechanism for diarrhea in humans is bile acid malabsorption due to the inability of the dysbiotic microbiota to convert primary to secondary bile acids.13 Initial studies suggest that such a mechanism may also occur in dogs and warrants further study.12,16

Assessment of Dysbiosis Because of the importance of the commensal microbiota to host homeostasis, it is important to diagnose dysbiosis. As noted, fecal bacterial culture cannot characterize the many anaerobes in the GI tract. It is estimated that only a very small percentage of intestinal bacteria are cultivable with standard laboratory techniques. The best way to fully

BOX 1 Effects of Dysbiosis •O verproduction and translocation of bacterial toxins • Inflammatory stimulation of the immune system •R eductions in anti-inflammatory metabolites (eg, SCFA, indoles, secondary bile acids) • Alterations in brush border enzymes • Damage to mucosal receptors • Competition for nutrients (eg, vitamin B12) • Increased intestinal permeability

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characterize the microbiota is by high-throughput sequencing platforms that can provide an overview of the proportions of all bacterial groups within a sample; however, cost and long turnaround times limit the use of this method to research studies. Use of polymerase chain reaction (PCR) assays to target specific bacterial taxa that are consistently altered in dogs with chronic enteropathies (CE) can provide more rapid results.1

signs. In the remaining 2 dogs, a partial improvement in clinical signs was observed, and their DI stayed below 0 for most of the 8-week follow-up period. This initial small dataset suggests a potential for monitoring the microbiota over time in patients with CE and after fecal microbial transplantation, but more studies are needed to determine the accuracy and clinical utility of microbiota analysis.

The results of these multiple PCR assays can be combined and expressed as a mathematical ratio, the Dysbiosis Index (DI; Figure 3). A negative DI (<0) indicates a normal microbiota, whereas a positive DI (>0) indicates dysbiosis associated with CE.17 The DI can then be used to monitor the microbiotaâ&#x20AC;&#x2122;s response to therapy for CE. Initial long-term follow-up studies in dogs with CE suggest that the microbiome requires several months to normalize, even when dogs respond within a few weeks with a decrease in clinical activity scores.18

Analysis of fecal samples provides information only about changes in the luminal microbiota. The use of fluorescence in-situ hybridization (FISH) of intestinal biopsy specimens allows visualization of whether bacteria have translocated into the mucosal epithelium, as is observed in dogs with granulomatous colitis.20 A positive result indicates the need for antimicrobial therapy to clear the translocated bacteria. FISH requires special analysis and is only available in a few reference laboratories.

A recent small study evaluating 3 dogs with CE used the DI to monitor fecal microbial changes in response to fecal microbial transplantation.19 All 3 dogs initially showed an immediate reduction in the DI, but after 3 weeks dysbiosis returned in 1 dog (increase in DI above 2), which showed no improvement in clinical

Although assessing the fecal microbiota is useful for recognizing dysbiosis in the large intestine, fecal samples probably do not accurately reflect the situation in the small intestine. Although the fecal samples of many dogs with small intestinal disease show dysbiosis, a subset of dogs may have exclusively small intestinal dysbiosis. Measurements of serum cobalamin and folate concentrations remain the most useful markers of small intestinal dysbiosis. Serum cobalamin may be decreased and serum folate concentrations may be increased in dogs with small intestinal dysbiosis; alteration of both parameters is highly suggestive of the condition. Recent studies have evaluated links between dysbiosis and changes in various biochemical pathways (eg, abnormal metabolism of bile acids, amino acids, and tryptophan) that affect the host immune system and metabolism.18,21 Many novel metabolic biomarkers, such as concentrations of fecal bile acids, are being investigated for better assessment of the etiology and treatment of GI diseases, and these may soon become useful for routine practice.

Therapeutic Considerations for Correction of Dysbiosis FIGURE 3. The Dysbiosis Index (DI) is increased in dogs with chronic enteropathies (CE). The DI is a mathematical ratio that summarizes the abundances of various bacterial groups (eg, E coli, Faecalibacterium, Blautia, Fusobacterium) into a single number. A DI below 0 indicates a normal microbiota, and a DI above 0 indicates dysbiosis in the large intestine. The DI assay is commercially available through the Gastrointestinal Laboratory at Texas A&M University.

The microbiota is an important player in host metabolism. Recent metabolomic studies have clearly linked dysbiosis with various diseases within and outside the GI tract. However, more work is needed to determine how to modulate the microbiome for best therapeutic success and to predict response to a specific therapy.

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Jan S. Suchodolski Jan S. Suchodolski, MedVet, DrVetMed, PhD, AGAF, DACVM, earned his veterinary degree from the University of Veterinary Medicine in Vienna, Austria, and his PhD in veterinary microbiology from Texas A&M University. He is board certified in immunology by the American College of Veterinary Microbiologists (ACVM) and currently serves as associate professor and associate director for research at the Gastrointestinal Laboratory at Texas A&M. His research is focused on gastrointestinal function testing and intestinal microbial ecology, with an emphasis on probiotic and dietary interventions as therapeutic applications in animals with inflammatory bowel disease, obesity, and diabetes mellitus.

Diet and Antimicrobial Therapy Dysbiosis is present in many dogs with CE and may be the cause of diarrhea in some patients, but dysbiosis may also be the consequence of GI inflammation in other patients. A gradient of various disease patterns across patients is likely, with host immune system and microbiome contributing to various degrees. Therefore, the presence of dysbiosis does not equate to an immediate need for antimicrobial therapy, as dogs with diet-responsive CE may also have a dysbiosis. Some animals with diarrhea respond favorably to antimicrobials, but antibiotics may induce diarrhea in others. Long-term antibiotic administration may induce dysbiosis patterns that could create a risk factor for various metabolic diseases, such as through induction of bile acid dysmetabolism.3 At this time, the best therapeutic approach to chronic GI disease remains empiric, with a sequential protocol of food trials, anti-inflammatory drugs, and/or antimicrobials. Probiotics and Prebiotics Because the microbiota is implicated in the pathophysiology of chronic GI disease, the addition of probiotic and prebiotic therapy may be appropriate. Probiotics are live microorganisms that, when administered in sufficient quantities, confer a health benefit to the host. Few studies have evaluated the benefits of probiotics in acute and chronic GI disease. Data suggest that probiotics have only a minor effect on the intestinal microbiota, but their beneficial effect in dogs with inflammatory bowel disease may be due in part to immune stimulation and/or enhancement of intestinal barrier function.22

INTESTINAL MICROBES AND DISEASE IN DOGS

Also, it appears that administration of higher doses and multiple strains leads to a higher probability that probiotic bacteria will be able to colonize the gut. Prebiotics are fermentable and nonfermentable fibers that, after reaching the large intestine, are metabolized by intestinal bacteria to produce SCFA and other metabolites that may be immunomodulatory. Most commercial intestinal diets contain prebiotics. Fecal Microbial Transplantation Fecal microbial transplantation has garnered a lot of interest. Although it is a highly successful therapeutic approach in humans with recurrent C difficile, its use in CE of dogs requires further study because the pathophysiology between these diseases differs. Anecdotal evidence and small-scale studies suggest that fecal microbial transplantation may be promising in a subset of dogs with CE,19 but at this time proper patient selection is purely empiric and more studies are required. References 1. Honneffer JB, Minamoto Y, Suchodolski JS. Microbiota alterations in acute and chronic gastrointestinal inflammation of cats and dogs. World J Gastroenterol 2014;20:16489-16497. 2. Saari A, Virta LJ, Sankilampi U, et al. Antibiotic exposure in infancy and risk of being overweight in the first 24 months of life. Pediatrics 2015;135:617-626. 3. Vrieze A, Out C, Fuentes S, et al. Impact of oral vancomycin on gut microbiota, bile acid metabolism, and insulin sensitivity. J Hepatol 2014;60:824-831. 4. Suchodolski JS. Diagnosis and interpretation of intestinal dysbiosis in dogs and cats. Vet J 2016; doi: 10.1016/j.tvjl.2016.04.011 5. German AJ, Day MJ, Ruaux CG, et al. Comparison of direct and indirect tests for small intestinal bacterial overgrowth and antibioticresponsive diarrhea in dogs. J Vet Intern Med 2003;17:33-43. 6. Mentula S, Harmoinen J, HeikkilĂ¤ M, et al. Comparison between cultured small-intestinal and fecal microbiotas in beagle dogs. Appl Environ Microbiol 2005;71:4169-4175. 7. Suchodolski JS, Camacho J, Steiner JM. Analysis of bacterial diversity in the canine duodenum, jejunum, ileum, and colon by comparative 16S rRNA gene analysis. FEMS Microbiology Ecology 2008;66:567-578. 8. Guard BC, Suchodolski JS. Horse Species Symposiumâ&#x20AC;&#x201D;Canine intestinal microbiology and metagenomics: From phylogeny to function. J Anim Sci 2016;94:2247-2261. 9. Foster ML, Dowd SE, Stephenson C, et al. Characterization of the fungal microbiome (mycobiome) in fecal samples from dogs. Vet Med Int 2013;2013:658373. 10. Whitfield-Cargile CM, Cohen ND, Chapkin RS, et al. The microbiotaderived metabolite indole decreases mucosal inflammation and injury in a murine model of NSAID enteropathy. Gut Microbes 2016;7:246-261. 11. Pavlidis P, Powell N, Vincent RP, et al. Systematic review: bile acids and intestinal inflammation-luminal aggressors or regulators of mucosal defence? Aliment Pharmacol Ther 2015;42:802-817. 12. Honneffer J, Guard B, Steiner JM, et al. Mo1805 Untargeted metabolomics reveals disruption within bile acid, cholesterol, and tryptophan metabolic pathways in dogs with idiopathic inflammatory bowel disease. Gastroenterology 2015;148:S-715 (abstract). 13. Duboc H, Rajca S, Rainteau D, et al. Connecting dysbiosis, bile-acid dysmetabolism and gut inflammation in inflammatory bowel diseases. Gut 2013;62:531-539.

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PEER REVIEWED 14. Suchodolski JS, Olson E, Honneffer J, et al. Effects of a hydrolyzed protein diet and metronidazole on the fecal microbiome andmetabolome in healthy dogs. J Vet Intern Med 2016;30:1455 (abstract). 15. Cox LM, Blaser MJ. Antibiotics in early life and obesity. Nat Rev Endocrinol 2015;11:182-190.

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HOW I TREAT

How I Treat… Pneumothorax AN INTERVIEW WITH DR. ELISA MAZZAFERRO

Today’s Veterinary Practice “How I Treat” column is based on the popular How I Treat sessions presented at the annual NAVC Conference (now VMX) in Orlando, Florida (navc.com/conference). This column features interviews with leading veterinary specialists on pertinent clinical topics, with the goal of bringing practitioners essential information on therapeutic approaches.

In this “How I Treat” column, Elisa Mazzaferro, DVM, PhD, DACVECC, answers our questions on diagnosing and treating pneumothorax. Q. What are the most common causes and clinical signs of pneumothorax? A. The most common cause of pneumothorax is trauma, either from interaction with a moving vehicle, a kick by a large animal, or penetrating injuries into the thorax, including bite wounds or impalement. A less common cause of pneumothorax is spontaneous pneumothorax, which I have seen months after thoracic trauma and pulmonary contusions. This can result from migration of foreign bodies, such as grass awns and porcupine quills, or from rupture of diseased lung tissue (bullae,

Elisa Mazzaferro, DVM, PhD, DACVECC Staff Criticalist, Cornell University Veterinary Specialists, Adjunct Associate Clinical Professor of Emergency-Critical Care, Cornell University College of Veterinary Medicine

blebs, pneumonic lesions, or neoplasia). Most cases of spontaneous pneumothorax are idiopathic. Clinical signs of pneumothorax include a rapid and shallow restrictive respiratory pattern, cyanotic or muddy mucus membranes, increased respiratory effort/ orthopnea, inappetence, and weakness. In some cases, a pet may breathe with its head and neck extended and with elbows abducted away from the body wall. Q. What are the most appropriate diagnostic steps in a suspected case, and what test results would you expect? A. When an animal presents with a history of trauma and there is an index of suspicion for pneumothorax, careful observation and a physical examination SEPTEMBER/OCTOBER 2017

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with an eye to the clinical signs mentioned above are the best initial diagnostic tests. Auscultation of the thorax will reveal muffled lung sounds. Although air usually rises to the dorsal portion of the thorax and fluid is ventral, auscultation of all areas bilaterally is necessary. Thoracocentesis (Box 1) can be both diagnostic and therapeutic.

In animals that are hypovolemic secondary to trauma or hemorrhage from some other cause, the heart can appear elevated away from the sternum on the lateral view, but the caudal vena cava will be small. With pneumothorax

If auscultation of the thorax is equivocal, lateral and dorsoventral thoracic radiographs can be obtained to look for free air within the pleural space. Radiography should only be performed if it does not cause undue stress for the patient. A lateral thoracic radiograph of an animal with pneumothorax (Figure 1) will show that the heart is elevated away from the sternum, and the lungs will appear retracted away from the spine, ventral body wall, and diaphragm. On the dorsoventral radiograph, lung(s) will appear retracted from the lateral body wall.

FIGURE 1. Lateral thoracic radiograph of a dog with pneumothorax.

BOX 1. Step by Step: Thoracocentesis Step 1. Envision the ribcage as a box, then clip a square in the center of the box. Most texts say to tap air dorsally and to tap fluid ventrally; however, I’ve seen instances where needles are inserted too high on the thoracic wall and hit the epaxial muscles, resulting in an unsuccessful attempt at withdrawing air. Step 2. Aseptically scrub the clipped area with chlorhexidine and sterile water or isopropyl alcohol (Figure A). While the patient is being clipped and scrubbed, prepare the extension set, 3-way stopcock, and syringe (Figure B).

FIGURE B Supplies needed to perform thoracocentesis.

Supplies Required • Clipper with clean blades •C hlorhexidine scrub/sterile water or isopropyl alcohol • 2 2-gauge ¾- to 1 ½-inch needle (size to be determined by size of animal) or 22- to 20-gauge over-the-needle IV catheter • 3 -way stopcock FIGURE A Scrub the clipped area with chlorhexidine and sterile water or isopropyl alcohol.

HOW I TREAT

• Length of IV extension tubing • 3 0- to 60-mL syringe

HOW I TREAT

alone, the caudal vena cava will appear normal in size. On the dorsoventral view, with hypovolemia, small pulmonary vessels can be traced to the level of the diaphragm.

2. Place sterile lubricant or triple antibiotic ointment around the penetrating injury (Figure 2). 3. Wearing sterile gloves and using sterile instruments,

Q. What short and long-term treatment options exist for this condition? A. The treatment for pneumothorax typically involves performing thoracocentesis (Box 1). In some cases, placement of a thoracostomy tube may be necessary (Box 2). If there is an obvious penetrating wound into the thorax, you must first create a seal from the external environment and the pleural space to prevent ongoing suction of air into the thorax. 1. First, clip and aseptically scrub the lateral thoracic wall as indicated for placement of a thoracostomy tube (Box 2).

Step 3. Wearing nonsterile gloves, visualize the bevel (open portion) of the needle and point the bevel ventrally. Insert the needle into the center of the box, perpendicular through the skin into the pleural space. If there is doubt about whether the pleural space has been entered, a drop of sterile saline can be placed in the hub of the needle. The fluid will be drawn into the needle once the needle penetrates the pleural space (Figure C). Step 4. Connect the hub of the needle to the length of IV extension tubing and have an assistant withdraw air. The hub of the needle should be pushed down, such that the needle is directed parallel with the thoracic wall,

FIGURE C The fluid is drawn into the needle once the needle penetrates the pleural space.

FIGURE 2. Place sterile lubricant or triple antibiotic ointment around the penetrating injury.

to avoid iatrogenic puncture or laceration of the lung (Figure D). The air should be evacuated until negative pressure is obtained. In some instances, sweeping the hub of the catheter and the needle around like the hands of a clock can help in hitting various air pockets without the need for reinsertion of the needle. Step 5. Once negative pressure has been obtained, repeat the process on the contralateral side, in the event that the mediastinum does not communicate. If negative pressure cannot be obtained, or if air reaccumulates more than twice, a thoracostomy tube can be inserted.

FIGURE D The hub of the needle should be pushed down to avoid iatrogenic puncture or lung laceration.

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BOX 2. Step by Step: Thoracostomy Tube Placement Step 1. Clip the entire lateral thorax from dorsal to ventral, and caudally from the last rib cranial to the third rib. Step 2. Aseptically scrub the clipped area using chlorhexidine and sterile water or isopropyl alcohol (Figure A). Step 3. Wearing sterile gloves, drape the clipped area with sterile field towels and secure with towel clamps. Step 4. Make a small stab incision in the dorsal thoracic wall at the 10th intercostal space (Figure B). Step 5. Have an assistant pull the skin cranially and ventrally toward the elbow to help create a tunnel of skin. Step 6. When the hole is over the 7th or 8th intercostal space, insert a hemostat forceps through the hole and through the subcutaneous tissues. Using blunt dissection, make a stab through the intercostal muscles into the thorax. Avoid the caudal aspect of each rib, where the intercostal vessels are located (Figure C). Step 7. Insert a rigid, sterile polypropylene urinary catheter through the red rubber catheter to make it more rigid (Figure D). Keep the hemostat open and push the red rubber catheter through the hemostat into the thorax, directing the tube cranioventrally, such that the tip sits at the 3rd to 5th intercostal space (Figure E).

FIGURE A Use chlorhexidine and sterile water or isopropyl alcohol to scrub clipped area.

Step 8. Attach the Christmas tree adapter, 3-way stopcock, IV extension tubing, and 60-mL syringe. Have an assistant withdraw air from the pleural space. Step 9. Suture the tube in place using first a horizontal mattress suture, then a purse-string suture around the tube. Once the purse-string is attached, secure with a finger-trap suture (Figure F). Step 10. Secure the tube and Christmas tree adapter to the extension tubing and a 3-way stopcock using the 22-gauge orthopedic wire. Step 11. Bandage the thoracostomy tube. The tube can be used for intermittent suction as needed or connected to a continuous suction device for constant evacuation of air from the thorax.

Supplies Required • Clippers with clean blades • Chlorhexidine scrub with sterile water or isopropyl alcohol • Sterile gloves • Sterile drape material • Towel clamps • Scalpel handle and number 11 scalpel blade • Needle holders • Thumb forceps • Kelly hemostat forceps • Red rubber catheter or trocarized thoracic drainage catheter • Christmas tree adapter • 3 -way stopcock • IV extension tubing • 60-mL syringe • 2 2-gauge orthopedic wire

HOW I TREAT

FIGURE B Make a small stab incision in the dorsal thoracic wall at the 10th intercostal space.

FIGURE C Using blunt dissection, make a stab through the intercostal muscles into the thorax.

HOW I TREAT

cut a sterile glove and place it over the wound and sterile lubricant (Figure 3). 4. Place a thoracostomy tube, then bandage as described in Box 2. The penetrating wound can be surgically repaired once the patient’s hemodynamic status has been stabilized. Most cases of traumatic pneumothorax seal themselves within several days without surgical intervention.

FIGURE D Insert a rigid, sterile polypropylene urinary catheter through the red rubber catheter to make it more rigid.

FIGURE E Push the red rubber catheter through the hemostat into the thorax, directing the tube cranioventrally, such that the tip sits at the 3rd to 5th intercostal space.

Cases of spontaneous pneumothorax are more challenging. It is often unknown if one isolated area of abnormal pulmonary parenchyma is leaking air, or if multiple blebs or bullae (essentially, air bubbles) have leaked to cause the pneumothorax. Performing a computed tomography scan can sometimes determine whether there is isolated versus diffuse disease; however, the most sensitive method of evaluating the lungs for abnormalities is a diagnostic and therapeutic thoracotomy. During the thoracotomy, abnormal areas of lung can be removed to prevent further leakage of air. Prognosis in cases of spontaneous pneumothorax is more guarded, as some animals, particularly Siberian Huskies, can develop progressive recurrent disease for unknown reasons. If surgical thoracotomy is not financially possible, blood patch pleurodesis can be performed instead. Blood patch pleurodesis involves obtaining fresh blood from the patient’s jugular vein in aliquots of 20–50 mL, for a total volume of 5–10 mL/kg. The blood is then inserted directly into the patient’s thorax using a 22-gauge needle or over-the-needle catheter. A retrospective study using this technique was successful in more than 50% of patients treated.

FIGURE F Once the purse-string is attached, secure with a finger-trap suture. FIGURE 3. Cut a sterile glove and place it over the wound and sterile lubricant.

SEPTEMBER/OCTOBER 2017

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TVPJOURNAL.COM

HOW I TREAT

Q. What are the most important prognostic factors to consider in cases with pneumothorax?

Elisa Mazzaferro Dr. Mazzaferro is a graduate of Michigan State University College of Veterinary Medicine and completed an internship at the Veterinary Institute of Trauma in Wisconsin. She then completed a residency and earned a PhD in emergency–critical care at Colorado State University. She is currently is a staff criticalist at Cornell University Veterinary Specialists in Stamford, Connecticut, and an Adjunct Associate Clinical Professor of Emergency and Critical Care at Cornell University College of Veterinary Medicine. She is President of the American College of Veterinary Emergency & Critical Care and has authored/ edited 4 books and numerous manuscripts related to fluid therapy, emergency procedures, emergency and critical care, and other related topics. She lectures extensively nationally and internationally, speaking in more than 21 states and 9 countries.

crx1_7-17_Spark_TVB_July_Half.pdf

7/17/17

A. Most animals with traumatic pneumothorax have a generally good prognosis with appropriate care. However, they often have concurrent traumarelated injuries that can adversely affect outcome. This includes the degree of hypovolemic shock and the patient’s response to therapy, as well as the presence of traumatic brain injury and orthopedic injuries. These sometimes lead to euthanasia if the prognosis for return to function is poor.

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