Today's Veterinary Practice, November 2016 by davidpsu

NOVEMBER/DECEMBER 2015 2016

Volume Volume 6,5, Number Number 63

6 EDITOR’S NOTE Life Without Hope 8 NAVC PERSPECTIVES From Conference to Community 10 TODAY’S VETERINARY NEWS What’s New & Noteworthy 24 FELINE ORAL SQUAMOUS CELL CARCINOMA A Review 36 PAIN MANAGEMENT IN DOGS & CATS Practitioners’ Top Questions

DIAGNOSING ACUTE BLINDNESS IN DOGS

45 ACVN NUTRITION NOTES Nutrition for Pancreatitis 52 PRACTICE STEP BY STEP Jackson-Pratt Drains 60 PRACTICAL ONCOLOGY Canine Insulinomas 67 PRACTICE BUILDING Adding Exotic Pets 72 THE BACK PAGE Suicide in Veterinary Medicine

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November/December 2016

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volume 6, Number 6

November/December 2016

Table of Contents : FEATURES DIAGNOSING ACUTE BLINDNESS IN DOGS..........................18 Caryn E. Plummer, DVM, Diplomate ACVO

Acute vision loss in dogs is generally considered an emergency and warrants prompt evaluation by a veterinarian to confirm vision loss, localize the causative lesion, and institute therapy. This article describes the diagnostic approach to blindness, including history, vision tests, and ophthalmic examination.

RACE-AppRoVEd CE CREdIT ARTIClE

A REVIEW OF FELINE ORAL SQUAMOUS CELL CARCINOMA ...................................................................24 MacKenzie Pellin, DVM, Diplomate ACVIM (Oncology), and Michelle Turek, DVM, Diplomate ACVIM (Oncology) & ACVR (Radiation Oncology)

Feline oral squamous cell carcinoma is the most common oral tumor in cats. This article discusses the risk factors, clinical presentation, diagnosis, staging, surgical and medical management—including the merits of definitive versus palliative management—and prognosis of this disease.

CE TEST.....................................................................................32 A Review of Feline Oral Squamous Cell Carcinoma

CANINE & FELINE PAIN MANAGEMENT ................................36

expert Insight into Practitioners’ Top Questions B. Duncan X. Lascelles, BSc, BVSc, PhD, MRCVS, CertVA, Diplomate SAS(ST), ECVS, & ACVS, and Mark E. Epstein, DVM, Diplomate ABVP (Canine/Feline), CVPP

This topic was originally presented at the first annual Today’s Veterinary Practice symposium—expert Insights— which took place at the 2016 NAvc conference. This article reviews the information provided by Dr. Lascelles and Dr. epstein in the session Pain Management: Top Questions from Practitioners.

NOVEMBER/DECEMBER 2015 2016

Volume Volume 6,5, Number Number 63

DIAGNOSING ACUTE BLINDNESS IN DOGS

45 ACVN NUTRITION NOTES Nutrition for Pancreatitis 52 PRACTICE STEP BY STEP Jackson-Pratt Drains

Cover photo courtesy of Lyon Duong, University of Florida | UF Photography.

60 ELEMENTS OF ONCOLOGY Canine Insulinomas 67 PRACTICE BUILDING Adding Exotic Pets 72 THE BACK PAGE Suicide in Veterinary Medicine

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Dr. Caryn Plummer performs slit lamp biomicroscopy of the anterior segment of a patient’s eye. Learn more by reading Diagnosing Acute Blindness in Dogs on page 18 of this issue.

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 Conference, 37 Paul Lane, Glen Mills, PA 19342. Periodicals postage paid at Glen Mills, PA 19342 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.

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Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

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Table of Contents : COLUMNS EDITOR’S NOTE ...................... 6 LETTER TO THE EDITOR......... 7 NAVC PERSPECTIVES.............. 8 2016 VETERINARY GUIDELINES ............................ 9 TODAY’S VETERINARY NEWS ..................................... 10 USPS OWNERSHIP STATEMENT ........................... 44

PRACTICE STEP BY STEP ...... 52 Placement & Management: Jackson-Pratt Closed Active Suction Drain

Bonnie Grambow Campbell, DVM, PhD, Diplomate ACVS

Dr. campbell describes the benefits of the Jackson-Pratt drain and provides stepby-step instructions for drain placement, management, and removal. Advice is also provided on how to troubleshoot problems with drains and whether patients with drains should be managed as inpatients or outpatients.

ADVERTISER INDEx .............. 69 PRACTICAL ONCOLOGY......60

ACVN NUTRITION NOTES.... 45 To Feed or Not to Feed? Controversies in the Nutritional Management of Pancreatitis

Justin Shmalberg, DVM, Diplomate ACVN & ACVSMR

Pancreatitis is a common clinical condition of both dogs and cats. Due to lack of controlled clinical trials, however, nutritional management of pancreatitis continues to be guided primarily by the human literature and clinical experience. This article discusses nutritional approaches to acute and chronic pancreatitis in dogs and cats.

Canine Insulinoma: Diagnosis, Treatment, & Staging

Eliza Reiss Grant, DVM, and Kristine E. Burgess, DVM, Diplomate ACVIM (Oncology)

Insulinoma in the dog is a malignant tumor that inappropriately secretes excessive insulin, resulting in profound hypoglycemia. This article discusses diagnostic testing options, classification, and management of insulinomas.

PRACTICE BUILDING ............ 67 Are Exotics a Fit for Me? Part 2: Day-to-Day Logistics of Exotics Practice

Angela M. Lennox, DVM, Diplomate ABVP (Avian & Exotic Companion Mammal) & ECZM (Small Mammal)

Visit Today’s Veterinary Practice at tvpjournal.com to search past issues or to download resources for your practice.

This article is the second in a 2-part series that discusses the many factors that should be considered before adding care for exotic pets to a practice’s offerings, including what questions practice owners should ask themselves and what supplies and staff training may be needed.

THE BACK PAGE: VETERINARY VIEWPOINTS.......................... 72 Suicide in the Veterinary Profession

An Interview with Dr. Aaron Werbel

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4 Today’s VeTerinary PracTice ToDAy’s veTerINAry | an official Journal PrAcTIce of the naVc | November/December | november/december2016 2016||tvpjournal.com tvpjournal.com

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Life Without Hope Simon R. Platt, BVM&S, MRCVS, Diplomate ACVIM (Neurology) & ECVN

Life without hope is hopelessly difficult but, at the end, hope can so easily make fools of us all. —Henry Marsh, Do No Harm: Stories of Life, Death, and Brain Surgery No matter how scientifically trained we believe ourselves to be, we are ultimately human—and we use hope in our approach to work each day: • We hope a patient will improve, even when the odds are stacked against recovery. • We hope we do a better job today than we did last week. We hope pet owners understand that we do our best even when things do not go as planned. • We hope we are not alone in our struggle to face each unpredictable day of challenges brought to us by our chosen profession of veterinary medicine. If we lose hope in any of these areas, the personal toll can be immense. Emotional WEll-bEing We are all aware that our scientific knowledge and training are worthless if they are not balanced by our own emotional well-being. This well-being impacts our relationships with colleagues and clients, and our ability to survive the trials and tribulations encountered in practice. Those of us in this profession have become acutely aware that the rigors and demands of the job impact our mental health. The facts are not pretty: Up to 11% of the veterinary profession has a serious mental illness/psychiatric disorder or feelings of hopelessness and worthlessness (compared with < 5% of the general population).1 Nearly 20%—3 times the U.S. national average—has considered suicide since leaving veterinary school.1 The three trigger factors most frequently identified as contributing to veterinary suicide are: 1. Demands of veterinary practice 2. Veterinary practice management responsibilities 3. Professional mistakes and client complaints. Ultimately, we need to take responsibility for the health of the profession ourselves, and sooner rather than later.

read Prevalence of Risk Factors for Suicide Among Veterinarians— United States, 2014 at cdc.gov/ mmwr/preview/ mmwrhtml/ mm6405a6.htm.

HoW Early to bEgin So how do we learn to care for our mental wellbeing as we go throughout our day, interacting with 6

patients, clients, and veterinary staff? Should this be a self-learned art form, or does discussion begin at an early point in veterinary training? “Coping skills” classes are now taught at many undergraduate colleges across the country and “success over stress” courses are even available online. While it may be suggested that the already over-burdened curriculum at veterinary schools should contain stress management training, this may be difficult to implement and does not help those of us who have completed our schooling. Thankfully, several schools have added resources to address students’ emotional needs: University of Tennessee College of Veterinary Medicine offers mental health education to students through its SAVE program (www.vet.utk.edu/save), Auburn University and Washington State University’s Colleges of Veterinary Medicine have full-time psychologists on staff, and the Ohio State University College of Veterinary Medicine provides extensive emotional support services. We still, though, must ask why this type of training does not have more prominence in veterinary education? Even the level of awareness in our profession about such education is most likely lower than it should be. SourcES for Support However, resources for veterinarians who are looking for emotional support are becoming more available, and developing greater reach through the efforts of veterinary organizations. The American Veterinary Medical Association has a webpage dedicated to emotional well-being (avma.org > Professional Development > Personal Development > Wellness & Peer Assistance), which includes a self-assessment tool to evaluate your mental health; resources for handling compassion fatigue, work stress, and work–life balance; and instructions about initiating a workplace wellness program. The Veterinary Social Work website, vetsocialwork. utk.edu, provided by the University of Tennessee—

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

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Knoxville, focuses on social work in veterinary medicine and provides access to veterinary social workers, education (and certificate programs) in veterinary social work, and resources that address critical topics, such as veterinary suicide and compassion fatigue. Additional emotional wellness resources can be found on the UK-based website vetlife.org.uk. In addition, since the CDC article was published, other associations and publications have tackled this difficult topic in their own articles (see Resources). Finally, while the routine routes of counseling and therapy may be expensive and difficult for us to accept as necessary, they are a critical resource— whether you or a colleague needs help handling the stress of our profession. rESponSibility for EacH otHEr Many of us look to spread hope in our practice of veterinary medicine, and we also need to be responsible for spreading awareness. We need to recognize who around us—our colleagues—may need our help. We are the ones with the inside knowledge about how difficult our jobs can be, and it’s our role, and our time, to step up. Of course, it is harder to recognize that we may need help ourselves. But, just as we are proactive in caring for our patients, we must also be proactive in caring for ourselves. nEitHEr WEak nor fooliSH It is important to realize that these struggles do not mean we are weak; we have to be strong to pursue the work we do each day and even stronger to admit how emotionally tough that work can be. At some point in our careers, we can all benefit from emotional and mental support. The recent surge in acknowledgment and acceptance of the emotional challenges the veterinary profession faces is a step in the right direction but much work still needs to be done. It is time for us to give hope to ourselves and our colleagues, just like we give hope to owners who fear the worst for their pets. None of us is foolish for acknowledging that we need help to keep hope in our lives.

LeTTer To eDiTOr’s THe ediTor NOTe

Words of comfort Dear Dr. Platt,

I enjoyed your comments in the September/ October 2016 issue of Today’s Veterinary Practice (Editor’s Note: The Written Word—Spreading Ideas & Changing Lives, page 11). I especially appreciated your thought on bringing comfort to the pet. This reminds me of a comment in Abraham Verghese’s book Cutting for Stone in which the young doctor is reminded not to forget the medicine that is poured directly in the patient’s ear: words of comfort. I know that I have been professionally remiss on this. Every day, I am presented with fearful animals going to surgery and in my “let’s get ‘er done” mentality, I fail to address that fear. It takes only a moment to give a kind word and a calming touch. This topic also speaks to me personally. My cat recently died of heart failure and, while I was there with him in the ER, I had neither the presence of mind nor the strength to give him any words of comfort before he died. —Robin Hughes, DVM Sarasota, Florida

read The Back Page interview with suicidologist Dr. aaron Werbel, page 72.

attend the NAVC Conference Health & Wellness track, offering sessions, such as the Vet confessionals project, the Dynamics of the Struggle, and finding the path to resiliency, on Wednesday, February 8, 2017.

Dear Dr. Hughes,

Thank you for sharing your poignant thoughts. Don’t be too hard on yourself—when caught up in the everyday challenges we face in the practice of veterinary medicine, it is all too easy to forget the importance of “words of comfort.” And, in the final moments you spent with your own cat, the presence of a familiar face meant as much as any words that may have been spoken. —Simon R. Platt, BVM&S, MRCVS, Diplomate ACVIM (Neurology) & ECVN Editor in Chief, Today’s Veterinary Practice

—Simon Platt, Editor in Chief Reference

Readers can send letters to the editor to

Nett RJ, Witte TK, Holzbauer SM, et al. Notes from the field: Prevalence of risk factors for suicide among veterinarians— United States, 2014. MMWR 2015; 64(5):131-132.

Dr. Simon Platt, Editor in Chief, at SRPlatt@

Resources

Director, at KSoldavin@navc.com. Reader

Larkin M. Study: 1 in 6 veterinarians have considered suicide. JAVMA 2015; 246(7):707-709. Nett RJ, Witte TK, Holzbauer SM, et al. Risk factors for suicide, attitudes toward mental health, and practice-related stressors among US veterinarians. JAVMA 2015; 247(8):945-955. Stoewen DL. Suicide in veterinary medicine: Let’s talk about it. Can Vet J 2015; 56(1):89-92.

navc.com or Kelly Soldavin, Editorial

feedback and testimonials can be submitted through our website (tvpjournal.com); select About Us and click on Feedback.

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NAVC PersPeCtiVes

Bringing services to Conferences and Communities Peter R. Scott, CAE, APR NAVC, Orlando, Florida

It has now been almost five years since the NAVC became the North American Veterinary Community—changing the “C” in NAVC from Conference to Community. This change was a deliberate effort to not only recognize and embrace the entire profession, but to bolster the NAVC’s evolution from one of the largest and most respected conferences in the world to the profession’s most dynamic and engaging community. A key to fostering this community is recognizing that the NAVC is both a community of individuals and a community of organizations—a place where members of the veterinary health care team can learn, develop, and grow their passions. A great deal of change has occurred since we became a Community: The NAVC launched the profession’s leading digital platform for “continuous education,” VetFolio. Quickly thereafter, this tremendous journal was acquired and Today’s Veterinary Technician was launched. Earlier this year, the NAVC brought the Veterinary Innovation Council (VIC) to the profession—a natural outcome of this continuing evolution. The VIC is headed by Meghan Golden, MBA, the NAVC’s Vice President of Industry Services and International Relations. Since 2003, Meghan has established herself as a trusted advisor to thousands of people, providing strategic counsel and operations support to the NAVC’s rapidly growing list of clients and partners. This approach led to the development of NAVC Industry Services (navc. com/industry-services), which provides customized association and conference management to the veterinary profession. Why Industry servIces? The NAVC has the unique opportunity to interact with many fantastic volunteer-led associations that are ready to grow beyond their current means. The Industry Services division has been carefully positioned as one of the world’s only non-profit association management groups exclusively for the veterinary profession. This means that we continue 8

to find new ways to give back to the community by growing membership, driving attendance, and improving the financial health of its many members. This division offers full-service association and conference management—but it is not a one-sizefits-all approach. We tailor every engagement to the specific needs of every organization. Some organizations simply need help developing their strategic and operating plans, while others need assistance in branding, marketing, and membership growth. NAVC Industry Services is focusing on four primary areas—credentialing, exotic animals, nutrition, and awards/recognition—and we intend to quickly expand from there. credentIalIng Elevating your professional credentials to the highest level is not only a personal achievement, but one that demonstrates—to your peers and clients—your commitment to being the absolute best. Many NAVC team members hold multiple credentials within their respective professions and understand the value they bring to everyday performance. Together—with the American Board of Veterinary Practitioners (abvp.com), International Veterinary Academy of Pain Management (ivapm.org), and American College of Veterinary Behaviorists (dacvb.org)—we are dedicated to encouraging the pursuit of diplomate status, which demonstrates your commitment to be the absolute best in your area of specialization. exotIc anImals With such a broad spectrum of animals represented, we are excited to be the management company for the Association of Reptilian and Amphibian Veterinarians (arav.org), and we are also assisting with management of ExoticsCon (exoticscon.org), a conference that recently welcomed over 850 members of the veterinary team to Portland, Oregon. This successful event brings together “the best of the best” in exotics veterinary medicine.

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

NAVC PersPeCtiVes NAVC PersPeCtiVes

nutrItIon The NAVC shares the same belief as many of our colleagues—that nutrition should be the fifth vital assessment in every examination. We are committed to helping this happen by partnering with the Pet Nutrition Alliance (PNA), which is led by Doug Aspros, DVM, the PNA Board President and Past President of the AVMA. Together, with other member and sponsoring organizations, we are working to provide the veterinary team with the tools and resources to educate pet owners on the importance of proper nutrition. aWards & recognItIon While there has never been a great explanation for this, veterinarians are not the best at recognizing greatness from within the profession, but the NAVC believes that time has come. Through the VIC, the NAVC is launching the Veterinary Innovation Awards in early 2017. This crowdsourced program will honor and recognize those in our profession who have made a significant difference in their areas of specialization, whether technology, scientific advancements, practice management, education, or a technique that has been perfected over years and become common practice. We are also going to have fun and recognize the world of veterinary marketing and advertising with The Vetty Awards. Designed primarily for those who develop creative and inspiring campaigns for the veterinary health care team, this program will recognize designers, copywriters, photographers, website designers, and others who pour their hearts and souls into making advertising that stops you in your tracks. While this has been quite an exciting time, there is more to be done. We see so much opportunity in helping the profession inspire more members of health care teams to pursue their passions, provide better care for their patients, and build a truly world-class Community. We are all truly humbled to be a part of it. —Pete Scott, NAVC Chief Operating Officer

Veterinary Guidelines Released in 2016 guidelines for the management of Feline hyperthyroidism American Association of Feline Practitioners (catvets.com) Available at www.catvets.com/guidelines/practice-guidelines guidelines for the vaccination of dogs and cats World Small Animal Veterinary Association (wsava.org) Available at www.wsava.org/guidelines/vaccination-guidelines oncology guidelines for dogs and cats American Animal Hospital Association (aaha.org) Available at www.aaha.org/professional/resources/oncology.aspx veterinary guidelines for Infrared thermagraphy American Academy of Thermology (aathermology.org) Available at www.aathermology.org/organization/guidelines

For the treatment of skin infections (wounds and abscesses) in cats. Do not use in dogs. BRIEF SUMMARY: Before using Veraflox Oral Suspension for Cats, 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. Federal law prohibits the extra-label use of this drug in food-producing animals. PRODUCT DESCRIPTION: Pradofloxacin is a fluoroquinolone antibiotic and belongs to the class of quinolone carboxylic acid derivatives. Each mL of Veraflox Oral Suspension provides 25 mg of pradofloxacin. INDICATIONS: Veraflox is indicated for the treatment of skin infections (wound and abscesses) in cats caused by susceptible strains of Pasteurella multocida, Streptococcus canis, Staphylococcus aureus, Staphylococcus felis, and Staphylococcus pseudintermedius. CONTRAINDICATIONS: DO NOT USE IN DOGS. Pradofloxacin has been shown to cause bone marrow suppression in dogs. Dogs may be particularly sensitive to this effect, potentially resulting in severe thrombocytopenia and neutropenia. Quinolone-class drugs have been shown to cause arthropathy in immature animals of most species tested, the dog being particularly sensitive to this side effect. Pradofloxacin is contraindicated in cats with a known hypersensitivity to quinolones. HUMAN WARNINGS: Not for human use. Keep out of reach of children. Individuals with a history of quinolone hypersensitivity should avoid this product. Avoid contact with eyes and skin. In case of ocular contact, immediately flush eyes with copious amounts of water. In case of dermal contact, wash skin with soap and water for at least 20 seconds. Consult a physician if irritation persists following ocular or dermal exposure or in case of accidental ingestion. In humans, there is a risk of photosensitization within a few hours after exposure to quinolones. If excessive accidental exposure occurs, avoid direct sunlight. Do not eat, drink or smoke while handling this product. For customer service or to obtain product information, including a Material Safety Data Sheet, call 1-800633-3796. For medical emergencies or to report adverse reactions, call 1-800-422-9874. ANIMAL WARNINGS: For use in cats only. The administration of pradofloxacin for longer than 7 days induced reversible leukocyte, neutrophil, and lymphocyte decreases in healthy, 12-week-old kittens. PRECAUTIONS: The use of fluoroquinolones in cats has been associated with the development of retinopathy and/or blindness. Such products should be used with caution in cats. Quinolones have been shown to produce erosions of cartilage of weight-bearing joints and other signs of arthropathy in immature animals of various species. The safety of pradofloxacin in cats younger than 12 weeks of age has not been evaluated. The safety of pradofloxacin in immune-compromised cats (i.e., cats infected with feline leukemia virus and/or feline immunedeficiency virus) has not been evaluated. Quinolones should be used with caution in animals with known or suspected central nervous system (CNS) disorders. In such animals, quinolones have, in rare instances, been associated with CNS stimulation that may lead to convulsive seizures. The safety of pradofloxacin in cats that are used for breeding or that are pregnant and/or lactating has not been evaluated. ADVERSE REACTIONS: In a multi-site field study, the most common adverse reactions seen in cats treated with Veraflox were diarrhea/loose stools, leukocytosis with neutrophilia, elevated CPK levels, and sneezing. ANIMAL SAFETY: In a target animal safety study in 32, 12-week-old kittens dosed at 0, 1, 3, and 5 times the recommended dose for 21 consecutive days. One 3X cat and three 5X cats had absolute neutrophil counts below the reference range. The most frequent abnormal clinical finding was soft feces. While this was seen in both treatment and control groups, it was observed more frequently in the 3X and 5X kittens. U.S Patent No. 6,323,213 May, 2012 84364593/84364607, R.0 NADA141-344, Approved by FDA Made in Germany Bayer, the Bayer Cross and Veraflox are registered trademarks of Bayer. 17928 Bayer HealthCare LLC BAY022614 Animal Health Division Shawnee Mission, Kansas 66201, U.S.A.

veterinary medical care guidelines for spay–neuter Programs Association of Shelter Veterinarians (sheltervet.org) Available at www.sheltervet.org/veterinary-medical-care-guidelinesfor-spay-neuter-programs Noteworthy news can be emailed to tvpnews@navc.com.

tvpjournal.com | November/December 2016

Veraﬂox (pradoﬂoxacin) Oral Suspension for Cats 25 mg/mL

Today’s VeTerinary news

The Latest news in Veterinary Medicine

For more veterinary news, go to Facebook.com/ TodaysVeterinary Practice

NEW DIETS FOR DOGS & CATS WITH KIDNEY DISEASE Blue Buffalo Company has announced the launch of KS Kidney Support for Dogs and KM Kidney + Mobility Support for Cats. Formulated by veterinarians and PhD animal nutritionists to help manage kidney disease, both new products feature controlled levels of proteins, phosphorus, and sodium. In addition, both KS and KM formulas are clinically proven to produce a calcium oxalate relative supersaturation of < 3, and clinically proven to produce an average urine pH of 6.5 to 7.5. For more information, visit bluevetdiets.com. NEW JERSEY VETERINARIAN TO RECEIVE MERITORIOUS SERVICE AWARD Jorge Guerrero, DVM, MSc, PhD, Diplomate ACVM & EVPC (ret), is the recipient of the 2016 Meritorious Service Award from the World Small Animal Veterinary Association (WSAVA). Passionate about veterinary education, Dr. Guerrero was the visionary behind the development of the Latin American Veterinary Conference and is a past board member of the Southern European Veterinary Conference. A Peruvian veterinarian residing in Pennington, New Jersey, Dr. Guerrero was awarded the Distinguished Veterinary Parasitologist Award from the American Association of Veterinary Parasitologists and, in 2007, he became the first Latin American president of the North American Veterinary Community. NEW BITE-RESISTANT DIGITAL SENSOR FOR DENTAL IMAGING Midmark Animal Health has introduced the new VetPro OptiMax Digital Sensor System, which offers resistance to bite damage—4 times more than the standard sensor. The new sensor is available in 2 sizes to best accommodate patient needs and examination requirements. The patented complementary metal-oxide semiconductor (CMOS) technology is designed to deliver enhanced image quality, including soft tissue visualization and crown and root definition, while its rounded corners provide easier positioning in tight spaces for better capture of roots. For more information, call 1-800-MIDMARK or visit midmarkanimalhealth.com.

LAUNCH OF RAWHIDE CHEWS, ANTIBIOTIC TABLETS

Dechra Veterinary Products recently announced the launch of PhycoDent Rawhide Chews for canine patients. PhycoDent Chews are designed not only for pet dental health, but also to support joint health. The chewing action helps reduce plaque buildup, while sodium hexametaphosphate, a sequestering agent, helps reduce tartar (calculus). Also, Dechra Veterinary Products has received FDA-CVM approval for amoxicillin trihydrate and clavulanate potassium tablets, which will join the existing Dechra anti-infective portfolio. Please contact your Dechra representative or distributor representative for further details on availability. NEW SUPPORT FOR CHANGING HEARTWORM PROTOCOL A new study addresses the fight against the rising incidence of heartworm infection in dogs. New data from Phase 2 of a CEVA Animal Health sponsored investigation, led by John McCall, MS, PhD, shows that blocking transmission from dogs to mosquitoes, and from mosquitoes to dogs, using repellents/insecticides and macrocyclic lactone preventives is part of a multi-modal approach. Ceva Animal Health will continue its extensive campaign to educate the veterinarian community on this groundbreaking research. See more details at fightheartwormnow.com.

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

HELP SUPPORT BEST FRIENDS ANIMAL SOCIETY For over 30 years, Best Friends has been running the nation’s largest no-kill sanctuary for companion animals and building effective programs that reduce the number of animals entering shelters. bestfriends.org

HELP YOUR CAT’S HEALTH & HELP BEST FRIENDS BY USING ENISYL-F CHEWS! ®

Vetoquinol USA will donate $1.00* to Best Friends Animal Society for every bag of Enisyl-F Chews purchased through veterinarians nationwide from 9/1/16–12/31/16

SUPPORT FELINE HEALTH WITH ENISYL-F CHEWS Enisyl-F – the most trusted name in L-Lysine therapy Convenient size Cats love the taste DID YOU KNOW? Current recommended L-Lysine administration is 500mg twice per day

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Today’s VeTerinary news

NEW EDITION OF THE MERCK VETERINARY MANUAL Merck and Co, Inc has introduced the 11th edition of the Merck Veterinary Manual for animal health reference. Utilized by veterinarians, veterinary students, veterinary technicians, and other animal health professionals since 1955, the comprehensive reference has been updated and covers all species and disorders of veterinary interest worldwide. Nearly 400 veterinary experts from academia, government, research organizations, and specialty practices, from more than 20 countries, contributed to this edition. Published as a not-for-profit service for the animal health profession, the 11th edition costs $65.00 and can be purchased at leading book retailers or ordered by calling 1-877-762-2974 or by visiting merckbooks.com.

NEW LOW FAT GI DIET FOR DOGS Dogs with compromised fat absorption have 2 new dietary options: Purina Pro Plan Veterinary Diets EN Gastroenteric Low Fat Canine dry and canned formulas. The new EN Low Fat Dry Formula is the lowest fat (g/100 kcal) GI therapeutic canine diet available, yet it maintains a moderate caloric density of 327 kcal/cup and a high total digestibility of 87.8% to promote nutrient absorption. In addition, both new EN diets contain the prebiotic soluble fiber inulin, which nourishes beneficial bacteria in the GI tract, and antioxidant vitamins A and E to support a healthy immune system, including a high level of vitamin E to help reduce oxidative stress. More information about Purina Pro Plan Veterinary Diets can be found at PurinaProPlanVets.com.

HEARTWORM PREVENTION, DIAGNOSIS, AND TREATMENT DETAILED AT 15TH TRIENNIAL SYMPOSIUM Changes in climate, heartworm vectors, diagnostic challenges, prevention practices, and treatment protocols all were cited during the 2016 American Heartworm Society (AHS) Triennial Symposium as reasons the persistence of heartworm disease continues to confound veterinarians, researchers, and pharmaceutical companies. During the symposium, which took place in New Orleans in September, 2013–2016 AHS president Dr. Stephen Jones of Moncks Corner, South Carolina, turned over leadership of the AHS board to new president Dr. Christopher Rehm of Mobile, Alabama (see the Today’s Veterinary Practice interview with Dr. Rehm in the September/ October 2016 issue). For more information visit heartwormsociety.org. Keep up to date with industry news on

the Today’s Veterinary Practice Facebook page or @tvpjournal on Twitter.

VIDEO SERIES ILLUSTRATES BOND BETWEEN SERVICE DOGS, OWNERS

Elanco Animal Health has launched its Celebrate the Bond video series that lets viewers share the experience of two individuals embarking on lifechanging relationships. The documentary series, which can be viewed at celebratethebond.com, chronicles the growing connection between two Canine Assistants dogs—Spirit and Ringer—and their recipients, Sean and Tim. The video series was developed collaboratively by Elanco and Canine Assistants, a nonprofit organization that provides service dogs to people with physical disabilities and special needs. RESOURCE FOR NEUTERING PROTOCOLS Veterinarians can now reference newly updated and expanded professional guidelines that encompass all aspects of the spay–neuter process. The Association of Shelter Veterinarians 2016 Veterinary Medical Care Guidelines for Spay–Neuter Programs were recently published, thanks to the work of a 20-member task force of veterinarians with expertise in spay–neuter practices, anesthesiology, surgery, and small animal internal medicine. These guidelines are available at avmajournals.avma.org/doi/pdf/10.2460/ javma.249.2.165.

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

Scarlet is why

SDMA

matters

The IDEXX SDMA Test is a more reliable indicator of kidney function than creatinine Name

Gender

Breed

Scarlet

Spayed female

Golden retriever

Scarlet's story

Scarlet presented for her annual preventive care visit. Her creatinine result was normal, but an increased SDMA prompted her veterinarian to investigate further, discovering stage 2 chronic kidney disease. Result

Because Scarlet’s veterinarian acted on the IDEXX SDMA™ Test, Scarlet is on a kidney therapeutic diet, and she's alive and happy today.

The IDEXX SDMA Test identifies chronic kidney disease up to 27 months earlier in dogs than creatinine* and up to 48 months earlier in cats.* The IDEXX SDMA Test is more reliable than creatinine in assessing kidney function as it can identify the disease earlier and is not affected by muscle mass and extrarenal factors that impact creatinine.* In fact, the IDEXX SDMA Test has been included in the International Renal Interest Society (IRIS) Chronic Kidney Disease (CKD) Staging and Treatment Guidelines as a useful adjunct for diagnosing CKD and to help determine treatment for the appropriate stage of CKD. With the IDEXX SDMA Test, you can diagnose CKD earlier in cats and dogs, giving you more time for effective treatment options, so you can improve and possibly extend the lives of your patients. The IDEXX SDMA Test is the new standard of care for veterinary medicine and your patients.

To see the full chemistry report, idexx.com/SDMAGuide

Get the 5-Minute Guide to the IDEXX SDMA Test Visit idexx.com/SDMAGuide

Strengthen the bonds. *To see the proof and a complete list of references, visit idexx.com/5minutes. © 2016 IDEXX Laboratories, Inc. All rights reserved. • 110448-00 All ®/TM marks are owned by IDEXX Laboratories, Inc. or its affiliates in the United States and/or other countries. The IDEXX Privacy Policy is available at idexx.com.

Today’s VeTerinary news

NEW HERO VETERINARIAN AND HERO VETERINARY TECHNICIAN NAMED Zoetis once again sponsored the Hero Veterinarian and Hero Veterinary Technician Awards at the American Humane Hero Dog Awards’ 6th annual gala in Beverly Hills, California. Zoetis helped establish the awards in 2014 to honor the exceptional people behind the animals we all love. The recipient of the American Humane Hero Veterinarian Award was Dr. Natalie Isaza of the University of Florida College of Veterinary Medicine, and the recipient of the Hero Veterinary Technician Award was Kim Knap of the University of Illinois Veterinary Teaching Hospital. Learn more at herovetawards.org.

13TH VET TECH SPECIALTY RECOGNIZED BY NAVTA The National Association of Veterinary Technicians in America (NAVTA) announced the 13th veterinary technician specialty academy of the veterinary technology profession. The Academy of Veterinary Ophthalmic Technicians (AVOT) has been recognized as an official specialty by NAVTA. The AVOT joins the existing 12 NAVTA recognized veterinary technician specialties. For more information about NAVTA and the veterinary technician specialties, visit navta.net.

ANTECH

Pre-Op Diagnostics ANTECH Diagnostics provides you the peace-of-mind you need when your patients require anesthesia, surgerical procedures and general dentistry. At ANTECH, it is not just a blood test, it is our patient too!

West: 800.745.4725 East: 800.872.1001 Test Express: 8 88.397.8378 www.ANTECHDiagnostics.com

NEW TREATS FOR CATS & DOGS ON THERAPEUTIC DIETS Cats and dogs on therapeutic diets deserve a treat, says Royal Canin, who has unveiled Royal Canin Treats, a veterinaryexclusive line of treats designed to support special dietary needs. Many pet owners don’t realize treats may compromise the benefit of certain diets prescribed by their veterinarian, so Royal Canin created this line of treats to provide new options to reward pets. The new line of treats are also safe and effective, backed by science that pet owners can trust. Additional information is available online at royalcanin.com/treats.

NAVC CONFERENCE 2017

WE’VE

GOAT IT ALL IN ONE

NEW LOCATION

Orange County Convention Center • West Concourse Orlando, Florida • February 4-8, 2017 (Exhibits 5-8) Attending the NAVC Conference 2017 at the Orange County Convention Center will feel like your homecoming. Our new fully-inclusive venue features all of your conference excitement in one spot. Get ready for a bigger, better and more exhilarating experience than ever before.

WELCOME

HOME REGISTER NOW AT NAVC.COM

Before prices increase on December 15 /TheNAVC

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MONOCLONAL ANTIBODIES:

A New Treatment Option For Canine Atopic Dermatitis

Monoclonal antibody therapy is the fastest growing therapeutic area in human medicine. In recent years, research has focused on how these therapies can be translated to animal health. Speciﬁcally, Zoetis has invested in bringing an innovative biological therapy to the treatment of canine atopic dermatitis. While many therapeutic options are available for canine atopic dermatitis, there is room for improvement. Dog owners are seeking treatments that allow greater flexibility to suit their needs and lifestyles—and with few side effects. Treatment protocols may need to be customized for dogs suffering from an acute condition compared to dogs with seasonal allergies or those affected year-round. Special consideration may need to be given to dogs with atopic dermatitis that are under 12 months of age, those already on medications (such as NSAIDs) that limit additional therapies or those with co-existing diseases (such as neoplasia or serious infections) that may impact therapeutic options.

Harnessing the power of the immune system Monoclonal antibodies (mAbs) are developed in a laboratory from a single cell line and, when administered to patients, target and neutralize specific antigens. Unlike some biological therapies such as vaccines, mAbs mimic the activity of the animal’s own naturally produced antibodies without provoking an immune response from the host. Stopping the itch cycle before it starts To create an effective mAb therapy, you first have to determine the specific target(s) of most relevance to the disease process. Research over the past decade has shown that cytokines play an important role in the cycle of itch and inflammation in canine atopic dermatitis. Cytokines are proteins produced by cells

that act as messengers between cells to promote and drive allergic inflammation. Research at Zoetis has focused on the pruritogenic cytokine interleukin (IL)-31. A key function of IL-31 is to stimulate the neuronal itch pathway by activating peripheral sensory nerves in areas of allergic dermatitis. Additionally, the most recent research would suggest that IL-31 may have effects on the immune functions and its possible role in other inflammatory diseases.1 A study has shown that IL-31 can be identified in the serum of dogs with atopic dermatitis, but not in healthy dogs; and when IL-31 is injected into laboratory dogs, pruritic behaviors are induced.2 Through this research, Zoetis has discovered and manufactured an anti-IL-31 monoclonal antibody that will target and neutralize only this cytokine to rapidly and effectively help reduce clinical signs of canine atopic dermatitis. Because of the exquisite specificity in the targeting of IL-31, other cellular functions and immune responses are not adversely affected.

Introducing Canine Atopic Dermatitis Immunotherapeutic* A conditional license from the USDA was granted to Zoetis in August 2015 for Canine Atopic Dermatitis Immunotherapeutic*, a new treatment for canine atopic dermatitis. Veterinary dermatologists across the United States have since been using this product—an injectable monoclonal antibody that aids in the reduction of clinical signs associated with atopic dermatitis in dogs. “This is a ﬁrst-of-its-kind antibody therapy in veterinary medicine to help break the itch cycle and provide relief for dogs that suffer from atopic dermatitis. It also helps pet owners enjoy their pets and avoid daily medications for itch relief,” said Andrew Hiller, BVSc, MANZCVS, Dipl ACVD, Veterinary Specialty Operations and Medical Lead Allergy, Dermatology at Zoetis. This anti-IL-31 mAb was initially developed in the mouse. However, mouse

TREATMENT SUCCESS3

PERCENT OF DOGS ACHIEVING TREATMENT SUCCESS

(>20 mm reduction of owner-assessed pruritus VAS)

PERCENT OF DOGS ACHIEVING TREATMENT SUCCESS inis ter e

DAY OF STUDY Canine Atopic Dermatitis Immunotherapeutic* 2mg/kg

d inis ter e

DAY OF STUDY Canine Atopic Dermatitis Immunotherapeutic* 2mg/kg

Placebo

Signiﬁcantly different compared to placebo (p<0.05)

Along with itch relief, the mAb also leads to improvement in skin condition, giving the skin a chance to heal.

Canine Atopic Dermatitis Immunotherapeutic* is safe for dogs of all ages. Since the mAb mimics the dog’s own antibodies, it is eliminated via normal protein degradation pathways that do not involve the kidneys or liver, thus avoiding potential side effects associated with traditional pharmacotherapy.

Want to learn more? Visit canineantibodytherapy.com/tvp for more information about how Canine Atopic Dermatitis Immunotherapeutic* can help relieve the clinical signs of atopic dermatitis and improve the quality of life for dogs with atopic dermatitis as well as for their owners.

*This product license is conditional. Efficacy and potency test studies are in progress. 1

Placebo

Signiﬁcantly different compared to placebo (p<0.05)

There are no known drug interactions or contraindications, thus the mAb can be administered with other common medications, including parasiticides, antibiotics, antifungals, corticosteroids, vaccines, allergen-specific immunotherapy, antihistamines and other antipruritics, such as oclacitinib and cyclosporine.

Ad m se Do

Ad m

Once injected in the patient during an office visit, Canine Atopic Dermatitis Immunotherapeutic* begins to reduce clinical signs of atopic dermatitis within one day. On average, patients will experience 30 days of relief of itch and the clinical signs of atopic dermatitis. Dogs may receive additional monthly treatments, as needed, for continued relief.

Fast, safe and long-lasting relief for canine patients

TREATMENT SUCCESS3

(veterinarian-assessed 50% CADESI-03 reduction vs. baseline)

antibodies are recognized as “foreign” proteins by dogs and will be rapidly eliminated by the immune system, thus losing efficacy. This anti-IL-31 mAb has been engineered to mimic dog antibodies, a process referred to as “caninization.” As a result, the mAb is not seen as “foreign” and is accepted by the dog’s immune system, thus maintaining efficacy even when used repeatedly over the long term.

Cornelissen C, Lüscher-Firzlaff J, Baron JM, Lüscher B. Signaling by IL-31 and functional consequences. Eur J Cell Biol. 2012;91(6-7):552-566.

Gonzales AJ, Fleck TJ, Humphrey WR, et. al. IL-31-induced pruritus in dogs: a novel experimental model to evaluate anti-pruritic effects of canine therapeutics. Vet Dermatol. 2016;27(1):34-e10.

Data on file, Study Report No. C863R-US-12-018, Zoetis Services LLC.

Peer Reviewed

Diagnosing acute BlinDness in Dogs

Diagnosing Acute Blindness in Dogs Caryn E. Plummer, DVM, Diplomate ACVO University of Florida

An Eye Toward Anxiety When a dog is presented for acute blindness, or what is perceived as acute blindness, it is important to proceed with patience and care because the patient is likely anxious and upset, while its owner is often distraught. Slow movements, accompanied by a calm voice, facilitate the examination, may soothe or allay some anxiety, and make the clinician’s presence known to the dog at all times.

Vision loss can occur gradually or manifest acutely in dogs, but acute and complete blindness can be particularly devastating. The abrupt nature of this blindness is very disconcerting for all involved and pet owners may make hasty conclusions and decisions. The diagnostic approach to these patients should include: 1. Ophthalmic history identifying the onset and duration of blindness, degree of blindness (as perceived by the owner), other signs of disease, and medication regimen 2. Vision assessments, including menace response, visual placing, and “maze” tests, that confirm whether the patient is blind 3. Causative lesion localization by pupillary light reflex examination of the eye, potentially with ocular ultrasound, blood pressure measurement, electrophysiologic testing, specifically electroretinogram. HISTORY A thorough general and ophthalmic history is crucially important to the investigation of blindness because differential diagnoses can be

VISION ASSESSMENT As the history is being gathered, confirmation of vision—or the lack thereof—should be performed. Note that some patients—those with neurologic disease and aged animals with cognitive dysfunction—may behave as if they are visually impaired even though their visual systems are functional.

FigurE 1. Complete resting mydriasis in a young Chihuahua with bilateral optic neuritis. Both direct and consensual PLrs were absent. 18

quite different depending upon the onset and duration of the deficits. The history should determine: • Whether vision loss is partial or complete. • Whether vision loss is acute or has been developing gradually: Did the dog have functional vision yesterday, but blindness today or has it been gradually losing vision and now is completely blind? • When signs of vision loss developed: Did signs of vision loss manifest yesterday or 2 months ago? • Whether the appearance of the eye has changed. If so, when was this change noted? This information is important because, in many instances, the physical appearance of the eye may change over time. • Systemic signs of disease are present, or whether a systemic problem has been previously diagnosed. Note that many systemic diseases (eg, infectious disease, lymphoma, hypertension) may initially be recognized by their ophthalmic manifestations.1,2 • What medications the patient receives/has received, both chronically and more recently, including inadvertent administration/ingestion. For example, has the dog recently received or ingested ivermectin?

Menace Response Vision requires functioning central and peripheral ophthalmic systems, and may be roughly assessed with a menace response. The menace response test is performed by making

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

Diagnosing acute BlinDness in Dogs

a menacing gesture with the hand toward the patient’s eye. Take care not to touch the vibrissae or cause excessive air currents, both of which stimulate the sensation of touch rather than sight, potentially inducing a false-positive result.2 If the animal can see, it should blink or move its head away from the stimulus.

LESION LOCALIZATION The next step in the evaluation of the blind patient is to determine where the causative lesion is located. Is the patient blind because something is obscuring the visual axis, such as pigmentary keratitis, corneal edema, or a cataract? Or is the patient blind because the retina or central nervous system is at fault?

Cotton Ball Test The patient’s vision can be further evaluated by noting its response to cotton balls (or some such noiseless, scentless object) tossed into the visual field or observing the visual placing reaction.

Pupillary Light Reflex The size of the pupils and the direct and consensual (response in the fellow, non-stimulated eye) pupillary light reflexes (PLRs) are very important for lesion localization (Figure 1).2 These assessments should be performed with a bright light in a dimly lit room. The PLR evaluates: • Rapidity of pupillary light response • Extent of miosis • Ability to maintain miosis to constant light stimulation. The consensual pupillary reflex is normally equal to the direct. The PLRs require integrity of retinal neural cells, optic nerves, optic chiasm, optic tracts, midbrain (Edinger-Westphal nucleus), and parasympathetic fibers via the oculomotor nerve, ciliary ganglia, and the iridal sphincter musculature, but integrity of the cerebral cortex is not required (Figure 2). The reflex is,

Visual Placing Reaction Visual placing is assessed most easily in small patients that are able to be held. For this test, the patient is held in the examiner’s arms so that the forelimbs dangle freely. The dog is moved slowly toward a table or other elevated flat surface. As the limbs approach the edge of the table/ flat surface, if visual and able to respond, the dog will raise its limbs in order to step onto the table.2 If the dog does not see the table, it will not raise its limbs, allowing them to bump into the edge.

Maze Test In patients with suspected blindness, an obstacle course or “maze test” may be used to determine whether vision is present. Traffic cones, foam cylinders, or even examination room furniture, such as chairs and waste cans, suffice, although elaborate mazes may be constructed for standardized testing. The dog should be placed at the opposite end of the maze from its human companion, who is asked to call the dog’s name only once, which keeps the dog from following voice cues in order to maneuver. Vision should be evaluated in normal light and then dim light (after dark adaption) and obstacles should be adjusted between tests to avoid memorization and mapping. To assess night vision, dim the ambient illumination until you can barely distinguish the room furniture and maze course obstacles. Normally sighted dogs have better developed night vision than humans; therefore, the patient should be able to see the maze obstacles better than FigurE 2. The pathway of the pupillary light reflex. the examiner.3

tvpjournal.com | November/December 2016 | An Official Journal of the NAVC | TODAy’s VeTeriNAry PrACTiCe

Peer Reviewed

Eye Evaluation For the menace response, cotton ball test, and visual placing reaction, each eye should be evaluated separately by covering each in turn and testing the exposed eye.

Dark adaption is the adjustment of the eye to low light intensities, involving reflex dilation of the pupil and activation of the rod cells in preference to the cone cells.

Peer Reviewed

Diagnosing acute BlinDness in Dogs

Table 1. Acute Blindness & Pupillary Light Reflexes VISION

PLR RESULTS

LESION LOCALIZATION

Visual

Normal

No lesion

Visual

Abnormal

Lesion in efferent pathway dictating pupillary constriction (iris sphincter muscle atrophy, lesion in oculomotor cranial nerve III)

Avisual

Normal

Lesion obscuring visual axis (corneal pigment or edema, cataract) or interfering with cortical processing of visual information (brain or central nervous system disease)

Avisual

Abnormal

Lesion in retina or optic nerve of affected eye

therefore, subcortical and should be considered an evaluation of the integrity of the retina and optic tracts, not of vision.2 In general, in dogs with vision impairment, when PLRs are (Table 1): • Absent or diminished: The lesion is likely located in the retina or optic nerve. • Intact: The lesion often obscures the visual axis or interferes with the cortical processing of visual information. Examination of the Eye Because the eye can often be visualized to the level of the posterior segment (in its normal state), a complete ophthalmic examination can provide a rapid and accurate diagnosis for many ophthalmic diseases (Table 2). During the ophthalmic examination, keep in mind the general causes of vision loss: • Lesions that prevent light from reaching the retina

Keep in Mind During PLr

Remember, PLRs are affected by the psychological state of the animal, room illumination, age, many topical and systemic drugs, and the intensity of the light stimulus. If an animal is highly nervous or frightened, the pupils may be dilated and respond poorly to low-intensity light. However, with acclimation or a strong light source, this effect is minimized. Older animals may exhibit slow and incomplete PLRs resulting from atrophy of the iris sphincter muscle. This response is common in small dogs, especially poodles. The pupil margin may have an irregular or scalloped appearance or an irregular pupil shape, referred to as dyscoria (Figure 3).

in a focused (non-scattered) manner • Lack of response by the retina to light stimulation • Inability of the optic nerve and tracts to transmit the electrical response of the retina • Inability of the occipital cortex to process the information supplied by the eyes and optic pathways. Lesions obscuring the visual axis are often relatively easy to diagnose and may develop slowly or rapidly. Table 3, page 22, provides a list of ocular lesions that may present as an acute onset of vision loss. Because vision can potentially be restored with appropriate management, rapidly developing cataracts, corneal ulcers, severe uveitis, intraocular hemorrhage, and anterior lens luxation should be considered urgent or emergent depending on severity. Acute glaucoma should always be considered an emergency. A thorough fundic examination is the next step if the: • Anterior segment (ie, cornea, anterior chamber, and lens) appears normal • Anterior segment abnormalities found are not severe enough to account for the degree of vision loss noted. Often, if the retina or optic nerve is affected, the pupil is dilated, making pharmacologic mydriasis unnecessary. Optic Nerve The optic nerve should be thoroughly examined for evidence of disease or inflammation.

FigurE 3. iris atrophy in a Yorkshire terrier has resulted in mydriasis and an incomplete pupillary light reflex. Note the scalloping of the pupil margin and the holes in the temporal iris stroma. This aged individual also has an immature cataract.

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

Diagnosing acute BlinDness in Dogs

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Table 2. Acute Blindness: Diagnostic Approach DIAGNOSIS

VISION LOSS PLR

VISUAL AXIS

FUNDUS

OTHER DIAGNOSTICS

Anterior lens luxation

Acute or chronic

Impaired, depending on position of lens and IOP

Obscured

Visualization of fundus may be limited

Measure IOP; consider ocular ultrasound

Chorioretinal inflammation

Acute or chronic

Normal or abnormal, depending on degree of involvement and severity

Variably affected, anterior uveitis may be present concurrently

Tapetal hyporeflectivity

Pursue systemic inflammatory/ neoplastic disease workup

Cortical disease

Acute or chronic

Normal

Pursue electrophysiologic testing, MRI/ CT, CSF analysis, systemic inflammatory/neoplastic disease workup

Corneal ulcers/ perforation

Acute

Normal or abnormal, depending on position of iris and degree of anterior uveitis present

Obscured

Visualization of fundus may be limited

Consider corneal culture and cytology; evaluate for concurrent anterior uveitis

Diabetic cataracts

Acute or chronic

Normal

Obscured

Visualization of fundus may be limited

Measure IOP; evaluate for lens-induced anterior uveitis

Glaucoma (acute)

Acute

Abnormal (mydriatic)

Obscured

Visualization of fundus may be limited

Evaluate for concurrent ocular conditions (eg, uveitis, lens luxation) that would indicate that glaucoma is secondary

Glaucoma (chronic)

Acute or chronic

Abnormal (mydriatic)

Variably affected

Optic nerve recessed or atrophic

Evaluate for concurrent ocular conditions (eg, uveitis, lens luxation) that would indicate that glaucoma is secondary

Intraocular hemorrhage

Acute or chronic

Normal or abnormal, depending on etiology

Obscured

Visualization of fundus may be limited

Consider systemic blood pressure and ocular ultrasound

Ocular neoplasia

Acute or chronic

Normal or abnormal

Variably affected

Visualization of fundus may be limited

Consider ocular ultrasound and measure IOP

Optic neuritis (acute)

Acute

Abnormal

Usually normal, unless there is concurrent anterior uveitis

Optic nerve raised, swollen, or hemorrhagic (optic disc); may be unremarkable if retrobulbar optic nerve is solely affected

Pursue MRI/CT, CSF analysis, systemic inflammatory/neoplastic disease workup + neurologic examination

Optic neuritis (chronic)

Acute or chronic

Abnormal

Usually normal

Optic nerve recessed or atrophic

Pursue electrophysiologic testing, MRI/ CT, CSF analysis, systemic inflammatory/neoplastic disease workup

Progressive retinal atrophy

Gradual onset

Normal or abnormal

Usually normal; cataracts often develop over time

Tapetal hyperreflectivity

Consider genetic testing in purebred dogs

Retinal degeneration

Gradual onset (usually)

Abnormal

Usually normal

Tapetal hyperreflectivity, retinal vascular attenuation

Complete ophthalmic examination and history (Toxins? Antibiotics? Medications? Historical ophthalmic disease?)

Retinal detachment

Acute

Abnormal

Usually normal, unless there is hemorrhage or anterior segment involvement

Retina edematous, displaced anteriorly; hemorrhage may be present; visualization of fundus may be limited

Consider ocular ultrasound; measure systemic blood pressure; consider systemic/vascular/inflammatory/ neoplastic disease workup

Retinitis

Acute

Abnormal

Usually normal

Normal

Pursue electrophysiologic testing

SARDS

Acute

Normal or abnormal

Normal

Initially normal; tapetal hyperreflectivity and vascular attenuation develop over time

Pursue electrophysiologic testing

Uveitis (severe)

Acute

Abnormal (miotic)

Obscured

Visualization of fundus may be limited

Evaluate for presence of concurrent ophthalmic disease (cataract); measure IOP; consider systemic inflammatory/ neoplastic disease workup

CSF = cerebrospinal fluid; CT = computed tomography; IOP = intraocular pressure; MRI = magnetic resonance imaging; PLR = pupillary light reflex; SARDS = sudden acquired retinal degeneration syndrome

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Diagnosing acute BlinDness in Dogs

Table 3. Lesions Obscuring the Visual Axis & Resulting in Acute Blindness Anterior lens luxation Corneal ulcers or perforation Diabetic cataracts Glaucomaa Intraocular hemorrhage Severe uveitisb a. Generally manifests with episcleral injection, corneal edema, and mydriasis b. Recognized by presence of episcleral injection, corneal edema, aqueous flare, fibrin, and miosis

If the optic nerve is raised, swollen, or hemorrhagic, optic neuritis is a likely diagnosis. A variety of infectious or inflammatory diseases and neoplastic processes may result in optic neuritis, which usually manifests with an acute onset of marked vision loss. Once diagnosed, neurologic evaluation should be pursued as other neurologic deficits often are present concurrently. Conversely, if the optic nerve is recessed or atrophic, the changes present are chronic. This condition can occur due to damage from chronic glaucoma, retinal degeneration, or chronic optic neuritis. Optic nerve disease carries a guarded to poor prognosis for vision return. Retina Examination of the retina should include both the tapetal and non-tapetal regions and the retinal vasculature. The appearance of the tapetal fundus should be carefully evaluated, particularly its reflectivity. Generalized tapetal hyperreflectivity (excessively shiny tapetal appearance) indicates retinal thinning and degeneration, which can be associated with: • Gradual onset of vision loss, as found with progressive retinal atrophy (PRA) • Acute onset of vision loss, as found with sudden acquired retinal degeneration syndrome (SARDS). Dogs with PRA generally lose night vision

CARyn E. PlummER Caryn E. Plummer, DVM, Diplomate ACVO, is an associate professor in comparative ophthalmology at University of Florida College of Veterinary Medicine, where she also serves as chief of the comparative ophthalmology service. Her research interests include corneal wound healing and glaucoma, and she has lectured extensively— both nationally and internationally—on many topics associated with clinical veterinary ophthalmology and animal models of ophthalmic disease, especially glaucoma. Dr. Plummer received her DVM from University of Florida; then she completed an internship in small animal medicine and surgery at Michigan State University and a residency in comparative ophthalmology at University of Florida.

first, followed by decreasing day vision and then complete blindness. In both advanced PRA and SARDS, vascular attenuation and diffuse tapetal hypereflectivity develop; a dog with SARDS, though, has a normal fundus initially and becomes acutely blind. Physical evidence of retinal degeneration (tapetal hyperreflectivity and vascular attenuation) develops over time in SARDS patients. Tapetal hyporeflectivity (dull tapetal appearance) is seen with chorioretinal inflammation. Since much of the retina must be inflamed for obvious vision loss to be present, diagnosis is often easily made by fundus examination. Ocular Ultrasound If the fundus cannot be visualized due to vitreal hemorrhage or inflammation, an ocular ultrasound should be performed to assess for conditions that result in ocular hemorrhage: retinal detachment and ocular neoplasia. Blood Pressure Measurement If retinal detachment is identified—either by fundus examination or by ultrasound—or if posterior segment hemorrhage is present, systemic blood pressure should be measured. As a result of increased hydrostatic pressure in the vasculature, systemic hypertension can cause fluid accumulation in the subretinal space, which displaces the retina into the vitreal chamber, resulting in retinal detachment.1,4 Retinal detachments can also occur: • With congenital or developmental disorders (eg, collie eye anomaly) • Secondary to inflammatory disease (eg, chorioretinal inflammation), vitreal degeneration, cataracts, or lens luxation • As a complication of intraocular surgery (eg, following cataract surgery). Electrophysiologic Testing If the fundus appears normal and the animal is avisual, especially if vision loss was acute, consider the following retinal conditions: • SARDS (as hyperreflectivity occurs over time) • Retinitis (typically immune-mediated) • Cortical disease • Retrobulbar optic neuritis (optic disc appears normal but retrobulbar optic nerve is affected). These conditions can usually be differentiated with PLRs and electrophysiologic testing. Abnormal PLRs are typically associated with retinal or optic nerve disease and normal PLRs with cerebral cortical disease.

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DIAGNOSING ACuTE BLINDNESS IN DOGS

Electroretinogram Sometimes a normal PLR is present with retina and optic nerve disease, even if the animal is avisual. An electroretinogram (ERG) can be used to differentiate vision loss due to retinal disease (abnormal ERG result) from vision loss due to disease of the optic nerve or cerebral cortex (normal ERG result).3 Further Diagnostic Testing Animals with cortical or optic nerve blindness should be evaluated with: • Magnetic resonance imaging or computed tomography • Cerebrospinal fluid analysis • Generalized workup for systemic inflammatory or neoplastic diseases. In addition, a normal ophthalmic examination should prompt consideration of the central nervous system as the primary site of disease, especially when the PLRs are normal. IN SUMMARY Acute vision loss in the dog is generally considered an emergency and warrants prompt evaluation by a veterinarian to confirm vision loss, localize the causative lesion, and institute therapy. In some cases, prompt medical treatment will result in return of vision. Delayed care carries a poor prognosis for sight and may delay diagnosis of a significant systemic condition. ERG = electroretinogram; PLR = pupillary light reflex; PRA = progressive retinal atrophy; SARDS = sudden acquired retinal degeneration syndrome References 1. Webb AA, Cullen CL. Neuro-ophthalmology. In Gelatt KN (ed): Veterinary Ophthalmology, 5th ed. Ames, IA: Wiley-Blackwell, 2013, pp 1820-1896. 2. Webb AA, Cullen CL. Ocular manifestations of systemic disease: The dog. In Gelatt KN (ed): Veterinary Ophthalmology, 5th ed. Ames, IA: WileyBlackwell, 2013, pp 1897-1977. 3. Ekesten B. Ophthalmic examination and diagnostics: Electrodiagnostic evaluation of vision. In Gelatt KN (ed): Veterinary Ophthalmology, 5th ed. Ames, IA: Wiley-Blackwell, 2013, pp 684-702. 4. Ofri R. Retina. In Maggs DJ, Miller PE, Ofri R (eds): Slatter’s Fundamentals of Veterinary Ophthalmology, 4th ed. St. Louis: Saunders, 2008, pp 285-317. tvpjournal.com | November/December 2016

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A Review of feline oRAl SquAmouS Cell CARCinomA

A Review of Feline Oral Squamous Cell Carcinoma MacKenzie Pellin, DVM, Diplomate ACVIM (Oncology) Michelle Turek, DVM, Diplomate ACVIM (Oncology) & ACVR (Radiation Oncology) University of Wisconsin

Feline oral squamous cell carcinoma (FOSCC) is the most common oral tumor in cats, accounting for 70% to 80% of all oral tumors.1 Squamous cell carcinoma (SCC) arises from the normal squamous epithelium of the oral cavity. RISK FACTORS The underlying cause of carcinogenesis is unknown, but potential risk factors include: • Feeding of canned foods, particularly canned tuna • Use of flea collars • Cigarette smoke exposure. In a study2 evaluating these risk factors, cats that consumed canned food had a 3.6× increased risk for

oral SCC, while those that consumed canned tuna had a 4.7× increased risk. The proposed mechanism for this association has been an increased rate of dental disease or differences in food content, but further studies are needed. Use of flea collars was associated with a 5.3× increased risk for oral SCC, possibly due to oral carcinogen exposure during grooming.2 A common genetic cause may be the loss or mutation of the p53 tumor suppressor gene, which helps regulate the cell cycle in the presence of DNA damage. Exposure to environmental tobacco smoke has been associated with a 4.5× increased risk for p53 mutation on FOSCC biopsy results.3 Human papillomavirus is a risk factor for head and neck SCC in humans, but no association has been made with FOSCC.4 CLINICAL PRESENTATION Clinical Signs Common clinical signs of FOSCC may include inappetence or dysphagia, halitosis, increased drool or oral discharge, or blood present in the food or water dish. Signs, such as weight loss, decreased grooming, or increased hiding, may be subtle and nonspecific.

Figure 1. right mandibular lip lesion (A and B); histologically confirmed as squamous cell carcinoma. Courtesy Dr. Chris Snyder, Department of Surgical Sciences, University of Wisconsin

ArTIClE

Figure 2. Sublingual squamous cell carcinoma. Courtesy Dr. Chris Snyder, Department of Surgical Sciences, University of Wisconsin

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A Review of feline oRAl SquAmouS Cell CARCinomA

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Figure 3. Large maxillary lesions (A and B); histologically confirmed as squamous cell carcinomas.

Figure 4. Smaller, more subtle (compared to Figure 3 lesions) right mandibular lesion; histologically confirmed as squamous cell carcinoma. Courtesy Dr. Marilia Ferreira, SĂŁo Paulo State University

Figure 5. Subtle left mandibular lesion (white arrows) confirmed as squamous cell carcinoma (A and B). extensive lysis of the mandible (black arrow) is visible on the dental radiograph (C). This patient was presented for ptyalism, difficulty prehending food, and weight loss. Courtesy Dr. Chris Snyder, Department of Surgical Sciences, University of Wisconsin

Physical Examination FOSCC can arise in the sublingual area, lips, maxilla, or mandible (Figures 1 to 3) and behaves in a locally aggressive fashion, with extensive tissue invasion, including invasion of adjacent bone. Masses may be incidentally found during dental examination and cleaning (Figures 4 and 5). Underlying neoplasia should be suspected during dental evaluation when focal areas of

extreme dental disease or tooth mobility are present or when nonhealing lesions remain after dental biopsy. 5 rostrally located tumors may be more readily noticed by an owner, leading to earlier detection and potentially more effective treatment. Tumors located within the caudal oral cavity may pose an increased risk for metastasis because of increased density of lymphatic and vascular channels.6

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A Review of feline oRAl SquAmouS Cell CARCinomA

• Obtain the best estimates of size and location of the mass • Assess for bone invasion and possible extension into the lymphatics, including the tonsils.

Figure 6. Cytologic features of squamous cell carcinoma. Note the inflammatory cells and blood vessels in the background. The inset provides a closer view of malignant squamous cells. (Wright-Giemsa stain; magnification, 600×). Courtesy Dr. Kristen Friedrichs, Department of Pathobiological Sciences, University of Wisconsin

Metastasis Metastasis is generally considered rare;1 however, a recent study of 49 cats assessed via 3-view thoracic radiography and mandibular lymph node aspiration found metastasis in 10% and 31% of patients, respectively.7 DIAGNOSIS A cat with an oral mass or a suspected oral mass requires examination under sedation to:

Staging Feline Oral Squamous Cell Carcinoma

Biopsy A punch or wedge biopsy may be completed under the same sedation as the oral examination, although complications, including jaw fractures, delayed wound healing, or secondary infection, may result from the often friable and necrotic nature of this tumor. Samples should not be taken from the center of a lesion, where necrosis is most likely to be present, due to the potential for obscured histopathologic results. In addition, ideally the biopsy should be completed in such a way that the biopsy tract can be removed or treated with local therapy; for example, a biopsy should not be taken through the lip if that area is not otherwise involved. Owners should be counseled about the risk for an increase in oral discharge or hemorrhage as a result of the biopsy procedure. Occasionally, fine-needle aspiration is sufficient for diagnosis and can be attempted before biopsy. Cytologic Assessment Cytologically, SCC typically appears as round to irregularly shaped squamous cells that occur individually or in small clusters (Figure 6). The

Staging tests to evaluate for metastasis can be readily performed during biopsy of the primary mass and include: ` Fine-needle aspiration of the mandibular lymph nodes (ideally both ipsilateral and contralateral lymph nodes because lymphatic drainage for the oral cavity is not strictly one-sided9) ` Thoracic radiography. Even if the lymph nodes appear normal on palpation or computed tomography (CT), aspirates should be obtained because studies of other head and neck cancers have shown discrepancies between lymph node size and presence of metastatic disease.10 In older patients, a minimum database for general health screening—complete

blood count, serum biochemistry profile, and urinalysis—is advisable. Rarely, cats with FOSCC can present with hypercalcemia.11,12 Skull radiography can be performed but is limited by superimposition of tissues and the need for heavy sedation or anesthesia. CT proves more informative, if available, because it can show the extent of disease for treatment planning (surgery or radiation) (Figure 7). Including the thorax in the CT examination is recommended to evaluate for possible pulmonary metastatic disease. Most important, if radiation therapy is a treatment consideration, the CT scan should be obtained at the same facility where treatment will be administered because CT may be required for radiation planning and set-up.

Figure 7. Computed tomographic scan in a cat with a proliferative right maxillary mass, histologically confirmed as feline oral squamous cell carcinoma. This cat was treated with hypofractionated palliative radiation therapy.

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

A Review of feline oRAl SquAmouS Cell CARCinomA

Figure 8. gross photo of a feline mandible with squamous cell carcinoma after mandibulectomy (A); the canine tooth is to the left. Histopathologic features of squamous cell carcinoma (B). Courtesy Dr. Cindy Bell, Center for Comparative Oral and Maxillofacial Pathology, University of Wisconsin

cytoplasm is usually pale to deep blue, with a “ground glass” appearance.8 Malignant squamous cells can be distinguished from normal squamous epithelium by the retention of nuclei and more pronounced anisocytosis and anisokaryosis. Inflammatory cells may or may not be present. In the case of severe inflammation, normal squamous cells can undergo dysplastic changes that may mimic neoplastic changes, which is one of the reasons biopsy is recommended. SURGICAL THERAPY Surgery is considered first-line therapy for most local cancers, including FOSCC. Surgical Challenges Surgical management of FOSCC faces many challenges, including the commonly occurring sublingual location, invasion of bone, late detection, and advanced tumor stage. Surgical excision to achieve adequate surgical margins, or even to resect

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Figure 9. Postoperative images taken after left mandibulectomy in a cat (A and B); note the mandibular drift in B. Courtesy Dr. Chris Snyder, Department of Surgical Sciences, University of Wisconsin

gross disease, is usually limited given the small stature and anatomy of the cat skull. Furthermore, unlike dogs, cats do not tend to tolerate aggressive oral surgery without significant morbidity. In the Literature A study13 evaluated 42 cats that underwent mandibulectomy for management of oral neoplasia, 21 of which were diagnosed with SCC: • 72% experienced dysphagia or inappetence postoperatively • 12% never regained the ability to eat • 41% required placement of enteral (esophageal) feeding tubes. The overall complication rate in the acute setting was 98%, while 78% of cats had long-term side effects; complications included tongue protrusion, ptyalism, mandibular drift, and difficulty grooming, in addition to the previously mentioned dysphagia and inappetence (Figures 8 and 9). Despite these risks, 83% of owners were pleased with the outcome and stated that they would pursue mandibulectomy again. In this study, cats

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A Review of feline oRAl SquAmouS Cell CARCinomA

with FOSCC had a decreased median survival time compared with cats that had other tumor types (217 days versus median not reached in cats with fibrosarcoma or odontogenic tumors). Other studies have reported similar outcomes and complication rates.14,15 Median survival in these reports has ranged from 1 to 10 months in cats treated with surgery alone. The longest reported survival, 14 months, occurred in a study evaluating the combination of surgery and definitive radiation therapy.11 Postoperative Radiation Therapy The role of postoperative radiation therapy is to sterilize or slow the growth of residual microscopic disease that often remains after surgical resection of even the smallest tumors. Unfortunately, FOSCC is often locally advanced at time of diagnosis; as a result, surgery is not a viable option for most affected cats. Client Education Owners should be adequately counseled about the risk for postoperative complications when surgery is being considered. CT and consultation with a soft tissue or oral surgeon are useful to help determine whether surgery is feasible in a particular patient. RADIATION THERAPY When surgery is not pursued due to anatomic limitations or owner preference, radiation therapy can usually be considered. Definitive versus Palliative In general, radiation therapy can be used to treat cancer with definitive (curative) or palliative intent: â&#x20AC;˘ Definitive protocols involve daily radiation treatments for 2 to 4 weeks â&#x20AC;˘ Palliative courses are shorter with less frequent treatments. Palliative-intent radiation therapy has the primary goal of alleviating pain and clinical signs associated with the tumor rather than sterilizing a maximum number of cancer cells. Disease regression or extending patient survival is not necessarily expected, although alleviation of clinical signs and discomfort can inherently lead to increased survival times. Side Effects With definitive-intent radiotherapy, early radiation side effects, such as mucositis and moist desquamation, are more prevalent, while late side effects, such as fibrosis, bone necrosis (osteoradionecrosis), and cataracts, are rare. 28

With palliative-intent radiotherapy, the incidence of early side effects is low, which is in line with the palliative goal of the treatment. While the risk for late-term side effects may be increased in this setting, these complications are generally expected to occur beyond the anticipated survival of the patient. Interestingly, in our clinical experience, cats generally appear to have a higher tolerance for radiation than dogs. Given similar radiation treatments, the risk for early or late effects in cats is lower than that in canine patients. Definitive Therapy Results Due to the combination of hypoxia and necrosis in most tumors, SCC is considered relatively radioresistant, with decreased responsiveness to radiation.7,16 In addition, rapid cell proliferation/regrowth has been noted between radiation treatments, contributing to poor long-term tumor control. Various definitive protocols have been investigated, including accelerated radiation delivery, but despite attempts to optimize radiation schedules, definitive radiation has failed to achieve a significant survival benefit.16-22 Given the aggressive nature of FOSCC and poor responsiveness to definitive radiation, the focus of radiotherapy often centers on palliation in most cats. Palliative Therapy Protocols Several different palliative or hypofractionated radiation protocols have been evaluated in the veterinary literature. Most reports suggest a median survival time of 2 to 4 months, with approximately 50% of cats experiencing palliation.16-21 At our institution, the typical palliative protocol involves 4 fractions of 8 Gray given once weekly to a total radiation dose of 32 Gray. The 1-week interval between fractions allows the mucosal lining of the oral cavity and external skin to heal, minimizing early side effects. In a study17 evaluating 54 cats treated with similar hypofractionated protocols, the overall median survival time was 113 days. The addition of chemotherapy did not improve clinical outcomes.16,19 Another palliative protocol of 5 fractions of 4 Gray given over the course of 1 week (Monday through Friday to a total of 20 Gray) has been evaluated, and cats with FOSCC had an overall response rate of 54.5%. The median progression-free survival time and median survival time were brief for this protocol (1.8 months and 3 months, respectively).21 In smaller, nonresectable SCC lesions (size < 2 cm), a more aggressive radiation protocol of 10

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A Review of feline oRAl SquAmouS Cell CARCinomA

fractions of 4.8 Gray (48 Gray total) given Monday through Friday for 2 weeks has been associated with the best reported clinical outcome after radiotherapy.22 In a small study of 21 cats:22 • The overall median survival time for this protocol was 174 days. • Cats with T1 lesions (n = 4) had a favorable median survival time of 590 days. • All cats experienced grade 2 oral mucositis secondary to radiation therapy (defined as patchy mucositis with patient seemingly pain free23), which was effectively managed with oral antibiotics and pain medications. • All patients prophylactically received esophageal feeding tubes for management of early radiation side effects. For most cats with FOSCC, palliative radiotherapy is a logistically feasible treatment approach associated with minimal side effects. Unfortunately, clinical benefit is achieved in only about half of patients and is short-lived in most animals that respond favorably. CHEMOTHERAPY FOSCC is considered resistant to traditional cytotoxic chemotherapy agents. High levels of necrosis within these tumors limit chemotherapy delivery to cancer cells and lead to increased chemotherapy resistance.1 Because chemotherapy kills a fraction of actively dividing cancer cells with each dose, the presence of large, bulky tumors in most patients means that chemotherapy will likely have only minimal effect, if any.1 Various IV or locally administered chemotherapy agents, including bleomycin, carboplatin, doxorubicin, gemcitabine, and mitoxantrone, have been used, with minimal to no benefit.1,7 TYROSINE KINASE INHIBITOR Toceranib phosphate (Palladia, zoetisus.com) is a small-molecule inhibitor that targets receptor tyrosine kinases, including C-kit, vascular endothelial growth factor receptor, platelet-derived growth factor receptor, and Flt-3. Tyrosine kinase receptors are transmembrane receptors that control downstream cellular functions, such as replication, growth, differentiation, and angiogenesis. Although the drug was originally marketed and licensed for the treatment of canine mast cell tumors, activity against a variety of canine and feline solid tumors, including oral SCC, has been demonstrated with off-label use.24 A study25 of cats with oral SCC compared toceranib phosphate treatment with no treatment:

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• Those that received toceranib phosphate had a longer median survival time (145 days versus 45 days). • Of those that responded to toceranib phosphate (with response defined as stable disease or better), median survival time was 201 days. • Anorexia was the most common adverse event, occurring in 70% of cats. Most anorectic episodes were transient and mild, and no cats required medical intervention. • Other reported adverse events included afebrile, low-grade neutropenia; elevation of liver enzymes; and progressive azotemia. A major limitation and potential confounding factor of this study was the allowance of nonsteroidal anti-inflammatory drugs (NSAIDs) in both the treatment and control groups. Progressive azotemia was seen only in patients receiving concurrent toceranib phosphate and NSAIDs; therefore, the contribution of each medication is difficult to elucidate. Overall, toceranib phosphate appears to be well tolerated in cats. Among various studies, reported adverse events have included anorexia, other gastrointestinal signs (such as vomiting and diarrhea), lethargy, anemia, and liver enzyme elevation; most of these side effects were considered mild.25-27 Further studies are needed to determine whether toceranib phosphate, alone or in combination with chemotherapy or radiotherapy, has a role in the treatment of FOSCC. MEDICAL MANAGEMENT NSAIDs Cyclooxygenase-1 and -2 (COX-1 and -2) have been demonstrated to be upregulated in FOSCC.28 In neoplasia, upregulation of COX can lead to increased cellular proliferation, growth, invasion, and angiogenesis. Therefore, use of COX-inhibiting antiinflammatory medications may have several beneficial effects in cats with SCC, including: • Pain relief • reduction of neoplasia-associated inflammation and edema • Potentially, anticancer effects, such as disease response or stabilization. No studies have assessed the response of FOSCC to NSAIDs alone, although in one study NSAID use was associated with a 2-fold reduction in the hazard ratio for death.29 Clinical experience suggests that, while NSAID use may have a short-lived palliative effect in some cats with FOSCC, significant tumor responses are not observed.

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A Review of feline oRAl SquAmouS Cell CARCinomA

Currently, meloxicam is the only NSAID licensed for use in cats in the United States, and only as a 1-time injection for perioperative pain (0.3 mg/ kg). A “black box” notice warns against repeated use of meloxicam given the risk for acute kidney injury. However, in Australia and Europe, low-dose meloxicam (0.01–0.03 mg/kg Q 24 H) has been evaluated for use in cats with osteoarthritis.30 This and many other studies have assessed the safety and efficacy of this dosing and have found no progression of azotemia, even in cats with pre-existing renal disease.30,31 Another study showed no increased risk for death in cats with pre-existing renal disease that received meloxicam versus those without pre-existing renal disease.32 In our opinion, cats with FOSCC are good candidates for meloxicam. As previously stated, using this medication has many potential benefits, especially increase in patient comfort. These patients are more likely to die of FOSCC progression than of renal disease. Of course, the risks and benefits of every medication should be assessed on an individual patient basis and thoroughly discussed with the pet owner. Other Medications Other oral medications can be used to increase patient comfort and control clinical signs of disease. The most commonly used and effective oral pain medication in cats is buprenorphine. This synthetic opioid acts as a partial mu agonist. It is especially beneficial in cats given its ability to be administered and fully absorbed across mucous membranes. recommended dosing is 0.01 to 0.03 mg/kg Q 8 H.33 Oral antibiotics may help treat infections of tumor tissue secondary to normal oral flora, which can cause increased clinical signs and often be mistaken for disease progression. In general, antibiotics that penetrate bone and/or have anaerobic spectrum activity, such as doxycycline, amoxicillin trihydrate/clavulanate potassium, and clindamycin, are recommended. Nutritional Support As tumors progress and grow in size, cats may have progressive anorexia and dysphagia due to difficulty with prehension, discomfort, or both. As previously discussed, mucositis secondary to radiation therapy can also contribute to these side effects. Feeding tubes are sometimes considered to support cats with FOSCC. A complete discussion of parenteral feeding options is beyond the scope of this text, but esophageal feeding tubes are generally the most commonly used given the relative ease of placement and client use. 30

In our opinion, feeding tubes should be considered only for transient use to manage treatment side effects. Difficulty eating due to the oral tumor itself indicates that the disease is negatively affecting the patient’s quality of life. Given the overall poor prognosis and the lack of effective treatment options, humane euthanasia should be considered at this point. PROGNOSIS Despite the availability of therapeutic options, including radiotherapy, chemotherapy, and toceranib phosphate, the prognosis for FOSCC remains poor. Most cats present with advanced (T2 or greater), nonresectable local disease, and treatment is generally ineffective or associated with a short-lived tumor response. Median survival times range from 2 to 5 months. Cats with small tumors, especially those located in the rostral mandible that are amenable to surgical resection, may have improved outcomes. Adjuvant definitive radiotherapy may delay tumor recurrence in that setting. As new treatments become available, multimodal therapy, including combinations of local therapy, chemotherapy, and medical therapy, may prove beneficial for this uniformly aggressive disease and should be evaluated in future studies. COX = cyclooxygenase; CT = computed tomography; FOSCC = feline oral squamous cell carcinoma; NSAID = nonsteroidal anti-inflammatory drug; SCC = squamous cell carcinoma References 1.

6. 7.

Withrow SJ, Vail DM, Page rl. Withrow & MacEwen’s Small Animal Clinical Oncology, 5th ed. Philadelphia: Elsevier Saunders, 2013, pp 389-395. Bertone Er, Snyder lA, Moore AS. Environmental and lifestyle risk factors for oral squamous cell carcinoma in domestic cats. J Vet Intern Med 2003; 17(4):557-562. Snyder lA, Bertone Er, Jakowski rM, et al. p53 expression and environmental tobacco smoke exposure in feline oral squamous cell carcinoma. Vet Pathol 2004; 41(3):209-214. Munday JS, Howe l, French A, et al. Detection of papillomaviral DNA sequences in a feline oral squamous cell carcinoma. Res Vet Sci 2009; 86(20):359-361. Bilgic O, Duda l, Sánchez MD, lewis Jr. Feline oral squamous cell carcinoma: Clinical manifestations and literature review. J Vet Dent 2015; 32(1):20-40. Vogel DWT, Zbaeren P, Thoeny HC. Cancer of the oral cavity and oropharynx. Cancer Imaging 2010; 10(1):62-72. Soltero-rivera MM, Krick El, reiter AM, et al. Prevalence of regional and distant metastasis in cats with advanced oral squamous cell carcinoma: 49 cases (2005–2011). J Fel Med Surg 2014; 16(2):164-169. Cowell rK, Tyler rD, et al. Diagnostic Cytology and Hematology of the Dog and Cat, 3rd ed. St. louis: Mosby Elsevier, 2008, pp 140-143. Skinner OT, Boston SE, Souza CH. Patterns of lymph node metastasis identified following bilateral mandibular and medial retropharyngeal lymphadenectomy in 31 dogs with malignancies

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

A rEVIEW OF FElINE OrAl SQUAMOUS CEll CArCINOMA

of the head. Vet Comp Oncol May 2016 [epub ahead of print]. 10. Williams lE, Packer rA. Association between lymph node size and metastasis in dogs with oral malignant melanoma: 100 cases (1987–2001). JAVMA 2003; 222(9):1234-1236. 11. Savary KC, Price GS, Vaden Sl. Hypercalcemia in cats: A retrospective study of 71 cases (1991–1997). J Vet Intern Med 2000; 14(2):184-189. 12. Hutson CA, Willauer CC, Walder EJ, et al. Treatment of mandibular squamous cell carcinoma in cats by use of mandibulectomy and radiography: Seven cases (1987–1989). JAVMA 1992; 201(5):777-781. 13. Northrup NC, Selting KA, rassnick KM, et al. Outcomes of cats with oral tumors treated with mandibulectomy: 42 cases. JAAHA 2006; 42(5):350-360. 14. Fiani N, Arzi B, Johnson EG, et al. Osteoma of the oral and maxillofacial regions in cats: 7 cases (1999-2009). JAVMA 2011; 238(11):1470-1475. 15. lascelles BD, Henderson rA, Sequin B, et al. Bilateral rostral maxillectomy and nasal planectomy for large rostral maxillofacial neoplasms in six dogs and one cat. JAAHA 2004; 40(2):137-146. 16. Evans SM, laCreta F, Helfand S, et al. Technique, pharmacokinetics, toxicity, and efficacy of intratumoral etanidazole and radiotherapy for the treatment of spontaneous feline oral squamous cell carcinoma. Int J Rad Onc Bio Phys 1991; 20(4):703-708. 17. Sabhlok A, Ayl r. Palliative radiation therapy outcomes for cats with oral squamous cell carcinoma (1999-2005). Vet Radiol Ultrasound 2014; 55(5):565-570. 18. Fidel Jl, Sellon rK, Houston rK, Wheeler BA. A nine-day accelerated radiation protocol for feline squamous cell carcinoma. Vet Radiol Ultrasound 2007; 48(5):482-485. 19. Fidel J, lyons J, Tripp C, et al. Treatment of oral squamous cell carcinoma with accelerated radiation therapy and concomitant carboplatin in cats. J Vet Intern Med 2011; 25(3):504-510. 20. Bregazzi VS, larue SM, Powers BE, et al. response of feline oral squamous cell carcinoma to palliative radiation therapy. Vet Radiol Ultrasound 2011; 42(1):77-79. 21. McDonald C, looper J, Greene S. response rate and duration associated with a 4Gy 5 fraction palliative radiation protocol. Vet Radiol Ultrasound 2012; 53(3):358-364. 22. Poirier VJ, Kaser-Hotz B, Vail DM, Straw rC. Efficacy and toxicity of an accelerated hypofractionated radiation therapy protocol in cats with oral squamous cell carcinoma. Vet Radiol Ultrasound 2012; 54(1):81-88. 23. laDue T, Klein MK. Toxicity criteria of the veterinary radiation therapy oncology group. Vet Radiol Ultrasound 2001; 42(5):475476. 24. london C, Mathie T, Stingle N, et al. Preliminary evidence for biologic activity of toceranib phosphate (Palladia) in solid tumors. Vet Radiol Ultrasound 2012; 10(30):194-205. 25. Wiles V, Hohenhaus A, lamb K, et al. retrospective evaluation of toceranib phosphate (Palladia) in cats with oral squamous cell carcinoma. J Fel Med Surg 2016 [epub ahead of print]. 26. Olmsted GA, Farrelly J, Post GS, Smith J. Tolerability of toceranib phosphate (Palladia) when used in conjunction with other therapies in 35 cats with feline oral squamous cell carcinoma: 2009-2013. J Fel Med Surg 2016 [epub ahead of print]. 27. Harper A, Blackwood l. Toxicity and response in cats with neoplasia treated with toceranib phosphate. J Fel Med Surg 2016 [epub ahead of print]. 28. Hayes A, Scase T, Miller J, et al. COX-1 and COX-2 expression in feline oral squamous cell carcinoma. J Comp Pathol 2006; 135(23):93-99. 29. Hayes AM, Adams VJ, Scase TJ, Murphy S. Survival of 54 cats with oral squamous cell carcinoma in United Kingdom general practice. J Small Anim Pract 2007; 48(7):394-399. 30. Gunew MN, Menrath VH, Marshall rD. long-term safety, efficacy and palatability of oral meloxicam at 0.01-0.03 mg/kg for treatment of osteoarthritic pain in cats. J Fel Med Surg 2008; 10(3):235-241. 31. Gowan rA, lingard AE, Johnston l, et al. retrospective casecontrol study of the effects of long-term dosing with meloxicam

tvpjournal.com | November/December 2016

Peer reviewed

MACkenzie Pellin

MacKenzie Pellin, DVM, Diplomate ACVIM (Oncology), is currently a radiation oncology resident at University of Wisconsin School of Veterinary Medicine. She previously completed a medical oncology residency at University of Wisconsin and a small animal rotating internship at Wheat Ridge Animal Hospital, Wheat Ridge, Colorado.

MiChelle Turek

Michelle Turek, DVM, Diplomate ACVIM (Oncology) & ACVR (Radiation Oncology), is an assistant professor of radiation oncology at University of Wisconsin School of Veterinary Medicine. She received her DVM from University of Montreal and completed residencies in medical and radiation oncology at University of Wisconsin. Michelle practiced at Angell Animal Medical Center in Boston and University of Georgia before returning to University of Wisconsin, where she works as a radiation oncologist, researcher, and instructor of oncology and communication.

on renal function in aged cats with degenerative joint disease. J Fel Med Surg 2011; 13(10):752-761. 32. Gowan rA, Baral rM, lingard AE, et al. A retrospective analysis of the effects of meloxicam on the longevity of aged cat with and without over chronic kidney disease. J Fel Med Surg 2012; 14(12):876-881. 33. Plumb DC. Plumb’s Veterinary Drug Handbook, 6th ed. Hoboken, NJ: Blackwell Publishing, 2008, pp 150-152.

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A Review of feline oRAl SquAmouS Cell CARCinomA

CE TEsT. A REvIEW oF FElInE oRAl sqUAmoUs CEll CARCInomA This article is RACE-approved for 1 hour of continuing education credit. To receive credit, take the approved test online at vetmedteam.com/tvp.aspx (CE fee of $5/article).

Learning Objectives

After reading this article, the practitioner should be able to recognize, diagnose, and stage feline oral squamous cell carcinoma; discuss treatment options and adverse events; and recommend specific treatment and management options to clients. The practitioner should also understand and be able to counsel pet owners regarding the prognosis.

Article Overview

Feline oral squamous cell carcinoma is the most common oral tumor in cats. This article presents a basic overview for the general practitioner, including diagnosis, treatment options, and prognosis.

Note Questions online may differ from those here; answers are available once the CE test is taken at vetmedteam. com/tvp.aspx. Tests are valid for 2 years from date of approval.

1. Which of the following risk factors has nOT been associated with feline oral squamous cell carcinoma (FOSCC)? a. Use of flea collars b. Canned foods, specifically canned tuna c. Environmental tobacco smoke d. Papilloma viruses

4. Which of the following is the least ideal method to obtain a diagnosis of FOSCC? a. Fine-needle aspiration b. Biopsy of an oral mass through the external skin/lip c. Punch biopsy d. Wedge biopsy

2. Which of the following clinical presentations should increase suspicion for FOSCC? a. Cat with a visible oral mass and hypercalcemia b. Cat with oral discharge, halitosis, and weight loss c. Cat with a focal area of tooth laxity and gingivitis on dental examination d. All of these scenarios could represent FOSCC

5. Which of the following cats would be the best candidate for surgical resection of FOSCC? a. Cat with a sublingual tumor b. Cat with a small (< 2 cm) mandibular tumor and bilateral lymph node metastases c. Cat with a small (< 2 cm) rostrally located maxillary tumor d. Cat with a small (< 2 cm) rostrally located mandibular tumor

3. Which of the following are the most appropriate staging tests for a cat with FOSCC? a. Blood analysis (complete blood count, serum biochemistry profile) and skull radiography b. Abdominal ultrasound and thoracic radiography c. Blood analysis (complete blood count, serum biochemistry profile), thoracic radiography, and aspiration of both mandibular lymph nodes d. Full-body computed tomography and aspiration of regional ipsilateral lymph nodes only if enlarged

6. Which of the following is FAlSe regarding complications of surgical resection of FOSCC? a. In one study, 12% of cats never regained the ability to eat on their own and 17 of 42 required esophagostomy tubes. b. It is uncommon to have incomplete margins when a tumor is resected. c. Common complications include mandibular drift, dysphagia, ptyalism, and difficulty grooming. d. Complications after surgery are common, with one study reporting an acute complication rate of 98%.

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A Review of feline oRAl SquAmouS Cell CARCinomA

7. Which of the following is True regarding radiation therapy? a. Definitive intent radiation therapy protocols are associated with a high risk for early side effects and a low risk for late side effects. b. Palliative-intent radiation therapy protocols for FosCC have resulted in survival times of 300+ days. c. Prolonged survival can be achieved with a 10-fraction radiation protocol regardless of tumor size. d. Cats are more sensitive to early radiation side effects compared with dogs.

9. Which of the following is FAlSe regarding the use of nonsteroidal anti-inflammatory drugs for FOSCC? a. Cyclooxygenase (CoX)-1 and CoX-2 are upregulated in FosCC. b. Upregulation of CoX receptors has been associated with increased cellular growth, proliferation, and angiogenesis. c. low-dose meloxicam has been evaluated in Europe and is associated with a high risk for progression of renal disease. d. standard-dose meloxicam is associated with a “black-box” warning due to risk for renal toxicity.

8. Which of the following is True regarding chemotherapy for FOSCC? a. Chemotherapy is effective in FosCC, with high response rates and improved survival. b. Toceranib phosphate should be used only for mast cell disease. c. A possible reason for FosCC chemotherapy resistance is tumor necrosis leading to decreased chemotherapy delivery. d. Toceranib phosphate is not well tolerated in cats, with neutropenia reported as a common adverse event.

10. Which of the following is True? a. oral masses can frequently become secondarily infected, and treatment with antibiotics should be considered. b. All patients with FosCC should have a feeding tube placed for nutritional support. c. Buprenorphine must be injected via sC or Iv route to be effective in cats with FOSCC. d. nasogastric tubes are considered the best feeding tube option for FosCC given the ease of placement, ease of use, and permanence of placement.

The Smith’s dog just ate ______ and she’s ______.

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Canine & Feline Pain ManageMent

Canine & Feline Pain ManageMent:

Expert Insight into Practitioners’ Top Questions B. Duncan X. Lascelles, BSc, BVSc, PhD, MRCVS, CertVA, Diplomate SAS(ST), ECVS, & ACVS North Carolina State University Mark E. Epstein, DVM, Diplomate ABVP (Canine/Feline), CVPP Carolinas Animal Pain Management & TotalBond Veterinary Hospitals, Gastonia & Charlotte, North Carolina

The first annual Today’s Veterinary Practice symposium—Insights from Experts—took place at the 2016 NAVC Conference in Orlando, Florida. This article reviews the information provided by Dr. Duncan Lascelles and Dr. Mark Epstein in the session Pain Management: Top Questions from Practitioners. The second annual Today’s Veterinary Practice symposium—Diagnosis & Management of the Acute Abdomen—takes place on Sunday, February 5, at the 2017 NAVC Conference. For more information, visit navc.com/conference.

Pain management in dogs and cats can be challenging because clinicians often have to rely on the observations of owners to determine whether a prescribed analgesic is having a positive effect on the pet. In addition, patients with concurrent major organ disease present unique challenges for pain management. Following are some of the most common questions from practitioners about pain management. Q: IS TRAMADOL EFFECTIVE IN DOGS & CATS? Tramadol Use in Dogs Clinical evidence of oral tramadol as an analgesic in dogs is scant—to the point of being almost nonexistent. There is a parenteral version of tramadol in Europe for which the clinical evidence demonstrating a pain-modifying effect is good, especially in the surgical environment.1-5

Pharmacodynamics Tramadol—predominantly through its negative enantiomer metabolite—modulates the serotonergic and noradrenergic pathways, which underpin the most powerful endogenous analgesic system in mammals. Using various inhibitory neurotransmitters, especially serotonin and 36

norepinephrine, these pathways descend from the higher centers down to the rostroventral medulla and, from there, feed to the spinal cord. Basically, tramadol is a drug that may modulate, enhance, or “pep up” the endogenous inhibitory analgesic system. In some, but not all species (eg, human and cat but not dog), tramadol’s M1 metabolite is opioidergic.

Pharmacokinetics The pharmacokinetic profile of oral tramadol in dogs is poor. After oral administration, very low plasma levels of the parent compound and metabolites exist, and the plasma half-lives are very short compared with humans and cats. If tramadol is administered orally to dogs over a period of days to weeks, those low plasma levels decrease to negligible and, sometimes, undetectable levels.6,7 There is no reason—from a pharmacokinetic profile perspective—to expect that oral tramadol has a really robust pain-modifying effect in dogs. If it does—perhaps if it has been administered parenterally—the pain-modifying effect is presumptively from inhibition of reuptake of serotonin and norepinephrine, which enhances the effect of these neurotransmitters, rather than due to any opioid activity.

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

Canine & Feline Pain ManageMent

In the Literature Literature describes tramadol as a synthetic mu-receptor opioid-like agonist compound. One metabolite is O-desmethyltramadol, an M1 metabolite, which humans make in abundance. In contrast, dogs make very little—in some cases, undetectable amounts—of the M1 metabolite, and what they do make has an extremely short half-life. Any hearsay that tramadol has any significant opioid or opioid-like activity in the dog, for all intents and purposes, is not true. Insofar as current research has shown, tramadol has negligible to no opioid activity in the dog. In humans, tramadol’s opioid activity provides much, if not most, of its analgesic effect. It is also worth noting that the caregiver placebo effect (aka client feedback) can be very strong. Studies in the literature that are performed in a blinded manner are trying to answer the question: Is this therapeutic better than giving nothing or something that is ineffective? In clinical practice, there is not enough time to try to understand whether feedback is the caregiver placebo effect or a real effect. The published studies of oral tramadol administration in dogs include a total of less than 30 dogs, and the results are mixed. A number of entities have tried to develop a veterinary formulation of oral tramadol as an analgesic for dogs, but they have failed because a beneficial effect could not be measured. While that doesn’t negate the fact that tramadol may have a beneficial effect, it is very difficult to measure it. Use in Practice I (D.L.) occasionally prescribe tramadol for dogs (5–10 mg/kg Q 8–12 H), but do not use it as a first-line analgesic—it is a second- or thirdtier therapy that can be added to therapies that have been proven to work. The higher doses, while required in some patients, may also result in more adverse effects related to serotonin and norepinephrine. While clients have reported a perceived benefit of tramadol administration in their dogs, the feedback does not reflect significant relief. Furthermore, the caregiver placebo effect in dogs is about 40% to 50%; therefore, it could very well be that anything perceived in terms of a pain-modifying effect is a placebo effect. From a pharmacokinetic perspective, and due to the lack of clinical evidence, we are skeptical that

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tramadol has any significant pain-modifying effect in the dog. Tramadol Use in Cats Tramadol has much more potential when administered to cats.

Pharmacokinetics With regard to pharmacokinetics, studies have demonstrated that, when cats metabolize tramadol, they make enough of the M1 metabolite to produce an opioid pain-modifying effect, with a plasma half-life similar to that in humans.8-11 Analgesic effects have been observed in cats in experimental situations at relatively low doses of approximately 2 to 3 mg/kg. Use in Practice The biggest challenge is administering tramadol to cats—tramadol is bitter. Cats tend to drool terribly when they taste it, and obtaining a palatable formulation is very difficult. Even when tramadol is compounded into gelatin capsules, a little tramadol dust on the outside of the capsule can put cats off of the medication and their food, upsetting owners and the animal–owner bond. A very appealing route for cats is transdermal medication. However, while compounding pharmacies will compound tramadol into a transdermal formulation, there should not be an expectation that it will achieve significant plasma levels. For example, fentanyl moves through the skin easily in a transdermal fentanyl patch, but, in cats, fentanyl compounded in pluronic lecithin organogel (PLO) transdermal cream does not move through the skin. Much more needs to be understood about the bases in which these various drugs are combined, as well as the assumptions made about transdermal delivery. Tramadol Safety & Toxicity Currently there is no information on dose titration, safety, or toxicity of tramadol in either dogs or cats. However, there are case reports of dogs and cats experiencing toxic effects, particularly at higher doses.12 Clinical signs commonly associated with these effects include anorexia, vomiting, behavioral or mentation changes (eg, agitation), and tremors. Tramadol enhances serotonin, and if it is administered concurrently with fluoxetine or any other serotonergic drug, the likelihood of adverse effects increases. Clinical signs associated

tvpjournal.com | November/December 2016 | An Official Journal of the NAVC | TODAy’s VeTeriNAry PrACTiCe

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Canine & Feline Pain ManageMent

with serotonin toxicity are similar to those for tramadol toxicity. In rodent models, there is conflicting evidence that tramadol may worsen the gastrointestinal (GI) toxicity of nonsteroidal anti-inflammatory drugs (NSAIDs) due to increased serotonin levels affecting platelet aggregation and regulation of vasoconstriction.

Learn More For further information on diagnosis of CKD, read Early Diagnosis of Chronic Kidney Disease in Dogs & Cats: Use of Serum Creatinine & Symmetric Dimethylarginine (March/april 2016), available at tvpjournal.com.

Q: CAN NSAIDS BE USED FOR LONGTERM PAIN CONTROL IN CATS WITH CHRONIC KIDNEY DISEASE? NSAIDs in Cats with CKD Historically, NSAIDs have been contraindicated in cats with chronic kidney disease (CKD). However, to treat chronic pain effectively in a cat population, it is likely that NSAIDs will need to be used in conjunction with CKD—approximately 70% of cats with painful degenerative joint disease (DJD) have concurrent CKD.13 It has been recognized that many cats—even young cats—have DJD. In one study, just over 90% of all cats (between 6 months and 20 years of age) had radiographic changes consistent with DJD.14 In order to properly manage the inflammatory component of the disease, which, at its core, causes pain, the prospect of using NSAIDs chronically needs to be cautiously considered.

In the Literature In cats with stable International Renal Interest Society (IRIS) Stage 1 and 2 CKD, clinical data have shown that CKD is not necessarily worsened by NSAIDs.15-17 This includes patients that have been treated with the NSAIDs meloxicam (Metacam, metacam.com) or robenacoxib (Onsior, us.onsior.com). In the studies that demonstrated meloxicam did not hasten the severity of CKD in cats, meloxicam was administered for 6 months at a dose of 0.02 mg/kg PO Q 24 H, which is almost half of the lowest dose that has been shown to be effective.16 That low dose did not hasten CKD, but it has not been confirmed whether meloxicam is effective at that dose. The lowest dose of meloxicam that has demonstrated efficacy is 0.035 mg/kg Q 24 H.18 In a retrospective study of cats with DJD-related pain and CKD, one group of cats was administered meloxicam and one group was not.16 However: • The groups were not blinded or randomized. • CKD cats that appeared relatively healthy with reasonable body condition scores were administered meloxicam, while CKD cats that appeared slightly unthrifty or had poor body 38

condition scores did not receive meloxicam. Therefore, the cats that may have done poorly on the drug did not receive meloxicam. • Cats were withdrawn from meloxicam as soon as their appetites started to decrease or if they demonstrated any other negative clinical signs. • The survival time of the IRIS Stage 1 and 2 CKD cats that received low-dose meloxicam was not shortened in comparison to the cats that did not receive meloxicam. In another clinical study, robenacoxib was administered at the label dose of 1 to 2 mg/kg PO Q 24 H for 30 days in cats with IRIS Stage 1 and 2 CKD.17 Results demonstrated that robenacoxib did not worsen CKD in that time period; some cats improved and some worsened in both the placebo and treatment groups. Similar to the meloxicam study, in the robenacoxib clinical study the drug was administered to CKD cats that were, in general, fairly healthy.

Use in Practice If cats have GI upset, they are more likely to have decreased appetites rather than vomiting and/ or diarrhea and then, by extension, they may not drink well, which may push them, especially those with IRIS Stage 1 and 2 CKD, into a renal crisis. Appetite is probably the most sensitive indicator as to whether or not a cat is doing well while receiving an NSAID. Clinically, NSAIDs can be used to control pain in cats that have CKD, but we are most comfortable using NSAIDs in CKD cats that look relatively healthy with relatively good body condition scores. Once patients begin to lose their appetites, lose weight, and/or look unthrifty, we recommend exercising more caution. Meloxicam versus Robenacoxib We have gravitated from meloxicam to robenacoxib; however, robenacoxib tablets are more expensive than the oral meloxicam suspension, which may make robenacoxib cost prohibitive for some owners. Robenacoxib is generally palatable; about threequarters of cats will eat it. In practice, we prescribe oral robenacoxib for chronic use either Q 24 H, Q 48 H, or sometimes owners will titrate it down to an “as needed” basis. Owners do report a positive analgesic effect but, in cats, the caregiver placebo effect is about 80% (unpublished data). Robenacoxib remains at the site of inflammation for 24 hours, which is similar to many NSAIDs,

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

Canine & Feline Pain ManageMent

including meloxicam, as most NSAIDs are very highly protein bound, following the protein to the site of inflammation. The main difference between robenacoxib and meloxicam is plasma half-life: Robenacoxib’s plasma half-life when administered orally is about 1.7 hours, while meloxicam’s plasma half-life is significantly longer at approximately 15 to 20 hours. Therefore, if meloxicam is administered every day, it remains in the plasma on a sustained basis, bathing renal tubules, GI tissue, and other nontarget tissues, which may increase the chances of adverse effects. Other Long-Term Pain Control Options for Cats When deciding whether or not to use an NSAID in a CKD cat, we consider the patient’s: • Blood analysis • Severity/IRIS stage of CKD • Physical condition. For example, if the cat has IRIS Stage 2 CKD and is in poor physical condition, we consider administering steroids—in some cases, methylprednisolone acetate injectable (Depomedrol, zoetisus.com)—instead of NSAIDs.

Use of Steroids Cats with DJD often have a positive response to steroids. Of course, there are adverse effects associated with chronic use of steroids, including ligament deterioration, muscle mass deterioration, and development of diabetes mellitus. If there is concern regarding these adverse side effects, we recommend administering steroids intermittently. Neuropathic Pain Many cats with longstanding pain are hyperaesthetic: They do not want to be touched and, if someone tries to touch them, they may walk away, yowl, or try to bite. It is likely that these cats—“grumpy” cats—have neuropathic pain. One of our first-line in north america, with the label warnings on meloxicam and robenacoxib, there are concerns about using nSaiDs in cats beyond any label claim, which is a single dose of meloxicam or 3 doses of robenacoxib. the main concern is that, if something “goes wrong” with a patient prescribed off-label use of an nSaiD, the owner has legal recourse due to the “black box” label warning on meloxicam or the standard label on robenacoxib.

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drugs for these patients is gabapentin; however, there is no evidence in the current literature regarding the efficacy of gabapentin in cats.

Other Adjunctive Therapies In a blinded, placebo-controlled study, a prescription joint diet was shown to have measurable benefit in cats with DJD.19 Many other adjunctive therapies may be tried (eg, amantadine, polysulfated glycosaminoglycans, amitryptiline) but none has been tested for efficacy in cats with DJD. One injectable polysulfated glycosaminoglycan product has demonstrated high bioavailability and distribution to joints when administered subcutaneously.20 New Therapies Recently, an anti-nerve growth factor antibody was shown to produce significantly improved activity in cats with DJD for up to 6 weeks after a single injection.21

The animal– owner relationship must be considered when deciding which therapies are possible to administer to a particular cat. generally, our goal is to get one drug in the cat, maybe twice a day, and then use adjunctive therapies.

Q: WHAT MEDICATIONS SHOULD BE USED IN DOGS WITH ELEVATED LIVER ENZYMES AND CHRONIC KIDNEY DISEASE? Elevated Liver Enzymes It has been shown that, in the absence of liver dysfunction, elevated liver enzymes—serum alkaline phosphatase (ALP) and/or alanine aminotransferase (ALT)—are not necessarily a contraindication to the administration of NSAIDs in dogs.22 NSAIDs do not cause hepatotoxicity—in the classic sense—because toxicosis is dose-dependent. Acute hepatocellular necrosis that sometimes occurs due to NSAIDs is an exceedingly rare intrinsic reaction of a dog to the NSAID molecule; this reaction cannot be prevented or predicted as liver enzymes may be elevated or normal. It is always a good approach to perform baseline blood analysis before initiating NSAID therapy; then perform blood analysis 2 to 4 weeks later. We do not have owners sign a consent form when prescribing nSaiDs for cats, but we do make sure to clearly inform owners that long-term administration of nSaiDs in cats is off-label. We also inform owners that in Europe there is an infinite label for chronic use of meloxicam at 0.05 mg/kg PO Q 24 H in cats, which is over twice the dose being used here for musculoskeletal pain.

tvpjournal.com | November/December 2016 | An Official Journal of the NAVC | TODAy’s VeTeriNAry PrACTiCe

Off-Label Use of NSAIDs in Cats

Peer Reviewed

Canine & Feline Pain ManageMent

If there is a rise in liver enzymes, it is very often related to NSAID administration. Under those circumstances, discontinue the NSAID, perform blood analysis a few weeks later, and then consider administering a different NSAID. It is always prudent to assess liver function (serum bile acids) any time liver enzymes are raised. We do not use NSAIDs in the face of liver dysfunction (eg, elevated serum bile acids). Many older dogs have elevated ALP; however, if ALT is elevated and at least twice the high end of the normal range, we recommend checking serum bile acids to evaluate liver function. If there is decreased liver function, there is an increased risk of GI irritation. Additionally, metabolism of the NSAID will be decreased, which translates to essentially higher than normal levels of the NSAID in circulation and a greater risk of GI irritation and ulceration. We feel comfortable using NSAIDs in dogs with normal liver function, even if ALP and/ or ALT are elevated, as long as liver function is normal and careful monitoring (including client communication) is pursued. Chronic Kidney Disease NSAIDs can be nephrotoxic and, in general, the renal damage is dose-dependent. When managing chronic pain in dogs with CKD, we have transitioned from use of classic NSAIDs to administration of non-acidic NSAIDs, such as acetaminophen. While we do not believe the efficacy of acetaminophen is as good as that of other NSAIDs, our clinical experience has shown us that acetaminophen appears to have a much lower risk of worsening CKD. However, there is a point at which quality of life becomes a concern, and classic NSAIDs may be more appropriate because acetaminophen does not have significant antiinflammatory activity.

B. DUnCAn X. LASCELLES

B. Duncan X. Lascelles, BSc, BVSC, PhD, MRCVS, CertVA, Diplomate SAS(ST), ECVS, & ACVS, is professor in small animal surgery and pain management at North Carolina State University College of Veterinary Medicine. He manages the Comparative Pain Research Program, is associate director of the Comparative Medicine Institute, and directs the clinical studies core. Dr. Lascelles’ research is focused on developing algometry methods in spontaneous disease animal models and probing tissues from well-phenotyped animals with spontaneous disease in order to improve pain control in companion animals.

Serum creatinine can be used as a rough benchmark of glomerular filtration rate (GFR). For example, if serum creatinine is 3 mg/dL in a dog with CKD (reference range, about 1 mg/dL), NSAID administration can be decreased from once a day to once every 3 days. This administration interval provides more time for the kidneys to clear the drug. We may also lower the dose of the NSAID. Gastrointestinal Surgery We do not administer preoperative NSAIDs to patients undergoing GI surgery; instead, we assess the GI tract during surgery and determine whether compromised GI mucosa is present at the end of surgery. If compromised GI mucosa remains postoperatively, we do not administer NSAIDs because they can potentially inhibit, decrease, or retard the healing process of that mucosa. We would, instead, consider a local anesthetic or wound catheters for analgesia. If only healthy GI mucosa remains, we administer an NSAID, but only in the first 24 hours. Our choice is one of the more “balanced” NSAIDs, which are less cyclooxygenase (COX)-2 selective (eg, meloxicam or carprofen) rather than more COX-2 selective (eg, deracoxib or firocoxib). This rationale is based on the concern that the natural healing process will be slowed if COX-2 is inhibited, as COX-2 induces vasodilation, which in turn promotes healing. IN SUMMARY Options for pain control in patients with concurrent disease are not as limited as previously assumed. When used cautiously, often with decreased doses and careful monitoring, NSAIDs can be administered to dogs and cats with CKD or elevated liver enzymes. Tramadol is not likely to be very effective in dogs; however, its use as an analgesic is more promising

MArK E. EPSTEIn

Mark E. Epstein, DVM, Diplomate ABVP (Canine/ Feline), CVPP, is the senior partner and medical director of Carolinas Animal Pain Management & TotalBond Animal Hospitals, a group of AAHA-accredited practices in the Charlotte and Gastonia, North Carolina, areas. He is a member of the American Academy of Pain Management and International Veterinary Academy of Pain Management; a past president of the IVAPM and ABVP; and an author and lecturer on the recognition, prevention, and treatment of pain. Dr. Epstein received his DVM from University of Georgia.

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

if your patient clucks or oinks

YOU MAY NEED A VFD Whether you're working with production animals, backyard food animals, or even certain pets, you may need a Veterinary Feed Directive (VFD) order to comply with federal regulations.

Visit www.avma.org/VFDtvp for VFD step by step instructions and to download the fillable VFD form.

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Canine & Feline Pain ManageMent

in cats. When addressing perioperative analgesia, we recommend using an opioid, NSAID, and local anesthetic in combination for the best perioperative pain management of animals. ALP = alkaline phosphatase; ALT = alanine aminotransferase; CKD = chronic kidney disease; COX = cyclooxygenase; DJD = degenerative joint disease; GFR = glomerular filtration rate; GI = gastrointestinal; IRIS = International Renal Interest Society; NSAID = nonsteroidal anti-inflammatory drug; PLO = pluronic lecithin organogel References 1.

Martins TL, Kahvegian MA, Noel-Morgan J, et al. Comparison of the effects of tramadol, codeine, and ketoprofen alone or in combination on postoperative pain and on concentrations of blood glucose, serum cortisol, and serum interleukin-6 in dogs undergoing maxillectomy or mandibulectomy. Am J Vet Res 2010; 71(9):1019-1026. Vettorato E, Zonca A, Isola M, et al. Pharmacokinetics and efficacy of intravenous and extradural tramadol in dogs. Vet J 2010; 183(3):310-315. Kongara K, Chambers JP, Johnson CB. Effects of tramadol, morphine or their combination in dogs undergoing ovariohysterectomy on peri-operative electroencephalographic responses and post-operative pain. N Z Vet J 2012; 60(2):129-135.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

Kongara K, Chambers JP, Johnson CB, Dukkipati VS. Effects of tramadol or morphine in dogs undergoing castration on intraoperative electroencephalogram responses and post-operative pain. N Z Vet J 2013; 61(6):349-353. Morgaz J, Navarrete R, Muñoz-Rascón P, et al. Postoperative analgesic effects of dexketoprofen, buprenorphine and tramadol in dogs undergoing ovariohysterectomy. Res Vet Sci 2013; 95(1):278-282. Matthiesen, Wöhrmann T, Coogan TP, Uragg H. The experimental toxicology of tramadol: An overview. Toxicol Lett 1998; 95(1):63-71. Malek S, Sample SJ, Schwarz Z, et al. Effect of analgesic therapy on clinical outcome measures in a randomized controlled trial using client-owned dogs with hip osteoarthritis. BMC Vet Res 2012; 8:185. Pypendop BH, Siao KT, Ilkiw JE. Effects of tramadol hydrochloride on the thermal threshold in cats. Am J Vet Res 2009; 70(12):1465-1470. Pypendop BH, Ilkiw JE. Pharmacokinetics of tramadol, and its metabolite O-desmethyl-tramadol, in cats. J Vet Pharmacol Ther 2008; 31(1):52-59. Brondani JI, Loureiro Luna SP, Beier SL, et al. Analgesic efficacy of perioperative use of vedaprofen, tramadol or their combination in cats undergoing ovariohysterectomy. J Feline Med Surg 2009; 11(6):420-429. Evangelista MC, Silva RA, Cardozo LB, et al. Comparison of preoperative tramadol and pethidine on postoperative pain in cats undergoing ovariohysterectomy. BMC Vet Res 2014; 10:252. Indrawirawan Y, McAlees T. Tramadol toxicity in a cat: Case report and literature review of serotonin syndrome. J Feline Med Surg 2014; 16(7):572-578. Marino C, Lascelles BD, Vaden S, et al. The prevalence and classification of chronic kidney disease in a randomly selected group of cats and in cats with degenerative joint disease. J Feline Med Surg 2014; 16(6):465-472. Lascelles BDX, Thomson Sumrell A, Henry III JB, et al. Cross-sectional study evaluating the prevalence of radiographic degenerative joint disease in domesticated cats. Vet Surg 2010; 39:535-544. Gowan RA, Lingard AE, Johnston L, et al. Retrospective casecontrol study of the effects of long-term dosing with meloxicam on renal function in aged cats with degenerative joint disease. J Feline Med Surg 2011; 13(10):752-761. Gowan RA, Baral RM, Lingard AE, et al. A retrospective analysis of the effects of meloxicam on the longevity of aged cats with and without overt chronic kidney disease. J Feline Med Surg 2012; 14(12):876-881. King JN, King S, Budsberg SC, et al. Clinical safety of robenacoxib in feline osteoarthritis: Results of a randomized, blinded, placebo controlled clinical trial. J Fel Med Surg 2016; 18(8):632-642. Gruen ME, Griffith EH, Thomson AE, et al. Criterion validation testing of Clinical Metrology Instruments for measuring degenerative joint disease associated mobility impairment in cats. PLoS One 2015; 10(7):e0131839. Lascelles BDX, DePuy V, Thomson Summrell A, et al. Pain relieving and activity-enhancing properties of a putative therapeutic diet for feline degenerative joint disease associated pain. J Vet Intern Med 2010; 24(3):487-495. Heidrich JE, Fox SM, Royer R, et al. Fluorescein-labeled polysulfated glycosaminoglycan in a feline acute traumatic knee model. Vet Ortho Soc Proc 2008. Gruen ME, Thomson AE, Griffith EH, et al. A feline-specific anti-nerve growth factor antibody improves mobility in cats with degenerative joint disease-associated pain: A pilot proof of concept study. J Vet Intern Med 2016; 30(4):1138-1148. Monteiro-Steagall BP, Steagall PV, Lascelles BD. Systematic review of nonsteroidal anti-inflammatory drug-induced adverse effects in dogs. J Vet Intern Med 2013; 27(5):1011-1019. Erratum in: J Vet Intern Med 2014; 28(2):745.

Today’s VeTerinary PracTice | an official Journal 42 of the naVc November/December | november/december 2016 | tvpjournal.com 2016 | tvpjournal.com

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ACVN NutritioN Notes

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to Feed or Not to Feed?

Controversies in the nutritional ManageMent of PanCreatitis Justin Shmalberg, DVM, Diplomate ACVN & ACVSMR University of Florida The american College of veterinary nutrition (acvn.org) and Today’s Veterinary Practice are delighted to bring you the nutrition notes column, which provides the highest quality, cutting edge information on companion animal nutrition, provided by the ACVN’s foremost nutrition specialists. The primary objectives of the ACVN are to: • Advance the specialty area of veterinary nutrition • Increase the competence of those practicing in this field • Establish requirements for certification in

Pancreatitis is a common clinical condition of both dogs and cats (Figure 1), and significant research has been devoted to improved diagnostic identification of the disease.1-3 However, nutritional management of pancreatitis continues to be guided primarily by the human literature and clinical experience due to lack of controlled clinical trials. Any nutritional intervention in the treatment of pancreatitis is predicated on the practitioner distinguishing acute or chronic pancreatitis from other causes of gastrointestinal signs.

veterinary nutrition • Encourage continuing education for both specialists and general practitioners • Promote evidence-based research • Enhance dissemination of the latest veterinary nutrition knowledge. The ACVN achieves these objectives in many ways, including designating specialists in animal nutrition, providing continuing education through several media, supporting veterinary nutrition residency programs, and offering a wide array of resources related to veterinary nutrition, such as this column.

RISK FACTORS in most patients, the definitive cause of pancreatitis is unknown. Published risk factors for pancreatitis are extensive and include endocrine disease, obesity, breed, and others.1-6 the nutritional factors that are anecdotally reported to precede episodes in dogs include dietary indiscretion and consumption of more dietary fat than normal for a particular dog. in a single retrospective study that interviewed owners of dogs affected by pancreatitis and those

Learn More For more information on acute pancreatitis in dogs and cats, read the following articles from Today’s Veterinary Practice, available at tvpjournal.com: a Case of Canine acute Pancreatitis: from Diagnosis to treatment (September/October 2016)

Figure 1. ultrasound images of pancreatitis demonstrating (a) heterogeneous echogenicity in the pancreas of a dog affected by chronic pancreatitis and (B) significant pancreatic enlargement, hypoechoic regions in the pancreas, and adjacent hyperechoic peripancreatic fat in a dog with acute pancreatitis.

tvpjournal.com | November/December 2016 | An Official Journal of the NAVC | TODAy’s VeTeriNAry PrACTiCe

feline Pancreatitis: Current Concepts in Diagnosis & therapy (January/February 2015)

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ACVN NutritioN Notes

presenting with renal disease, factors that were more prevalent in the pancreatitis group included:5 • Dietary indiscretion of items in the trash, which conferred greatest risk (13× more likely) • unusual food items consumed prior to presentation (4×–6× more likely) • table scraps given in the preceding week or generally (2× more likely) • obesity (2.6× more likely). CLINICAL SIGNS Cranial abdominal pain and nausea are thought to be characteristic of acute pancreatitis in dogs.1-3 Dogs with chronic pancreatitis may display vague signs of anorexia, hyporexia, lethargy, or behavioral changes, and an acute trigger may not be immediately identified in these patients. Cats commonly present with nonspecific signs of anorexia and lethargy for both acute and chronic disease, which makes detection more challenging.4 CANINE ACUTE PANCREATITIS To feed or not to feed? No objective information is available to determine whether fasting is associated with beneficial or poor outcomes in dogs with pancreatitis. • Fasting was, and continues to be, a mainstay of acute pancreatitis treatment by many veterinarians.2 • the premise for this approach is to avoid both pancreatic stimulation and premature activation of zymogens, but these effects have not been demonstrated in clinical patients receiving nutritional support. • Many veterinarians relate personal observations that early feeding is associated with increased nausea or morbidity, especially in the presence of abdominal pain or severe gastrointestinal signs prior to feeding. some practitioners, nutritionists, and internists advocate early enteral nutrition in dogs with acute episodes of pancreatitis because: 1. A large body of evidence from human critical care medicine supports decreased morbidity and mortality associated with early enteral nutrition 2. While evidence for early enteral nutrition in dogs is comparatively sparse: • early enteral nutrition accelerated recovery in dogs with parvoviral enteritis, with food administered by nasogastric tube irrespective of whether dogs were vomiting or regurgitating;7 however, the significance to older dogs and those with pancreatitis remains unclear. 46

• enteral nutrition by jejenostomy tube maintained intestinal villous height and mucosal thickness better than parenteral nutrition in dogs with experimentally induced pancreatitis.8,9 However, this information may not be relevant to most practitioners, who will choose between fasting or enteral support, rather than intravenous nutrition. 3. Feeding during illness helps provide essential nutrients that affect cellular function. However, • Many of these nutrients are present in reserve, and dogs are more resistant to starvation than humans, with higher rates of fat oxidation at rest.10 • Protein catabolism may occur in critical illness despite the presence of adequate caloric intake due to increased protein requirements.11 this increased interest in early enteral nutrition is challenged by some who routinely fast animals with acute pancreatitis. these clinicians argue that there is no evidence—in naturally occurring pancreatitis in companion animals—that shows a favorable effect of nutrition and that assistive enteral feeding, when necessary, adds risk and cost to treatment of a patient with pancreatitis. it is important to consider, however, that: • if enteral tubes are placed inappropriately, aspiration may be a risk, but aspiration due to placement errors is rare and risk is mitigated by documenting negative pressure in a feeding KeY Point: Short-term fasting has not been associated with poorer outcome in dogs with pancreatitis, and the benefits of feeding require additional validation in dogs with naturally-occurring pancreatitis.

Figure 2. Radiographs should confirm placement of nasoenteral tubes; this lateral radiograph shows a nasogastric tube placed in a cat with the distal tip clearly evident in the stomach.

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

ACVN NutritioN Notes

tube, absence of a cough when sterile saline is given via the tube, radiographic confirmation (Figure 2) of correct placement, or even capnography.12 • the expense of feeding dogs with severe acute pancreatitis amounts to a small fraction of the overall care (< 5%), but these costs could be significant if the owner’s budget is limited. in the absence of evidence specific to canine pancreatitis, practitioners should evaluate the risks of enteral feeding in the context of the patient’s overall clinical picture. Dogs with intractable vomiting or regurgitation, in normal body condition, or those with owners who have financial limitations may tolerate a period of fasting without any clinically relevant adverse effects. KeY Point: Maintenance of enteral nutrition appears beneficial in humans with critical illness and is likely worth the time and effort of intervention—when risks of feeding the patient are low—until additional studies are performed.

Enteral or parenteral feeding? enteral nutrition in humans with pancreatitis may prevent bacterial translocation, metabolic and electrolyte complications of parenteral feeding, immune system impairment, villous atrophy, and reduced mortality.13 However, human guidelines also suggest that parenteral nutrition should be considered: • if nutrition is indicated due to prolonged or anticipated anorexia • When enteral nutrition is either contraindicated or not well tolerated.14 the optimal route of enteral nutrition has not been defined in humans or animals.15 While veterinary guidelines for parenteral nutrition have been extrapolated from human guidelines, the pathophysiology of small animal pancreatitis cases may be quite different, as well as prognosis and response to parenteral nutrition.16 KeY Point: Enteral nutrition is generally associated with more favorable outcomes in humans and possibly in dogs when compared with parenteral nutrition.

How much is too much? Dogs with pancreatitis should eventually achieve their estimated resting energy expenditure when feeding is appropriate and elected.

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resting energy requirement (rer) can be estimated in 2 ways: 1. 70 × (BWkg)0.75 = rer (kcal/day) 2. [30 × (BWkg)] + 70 = rer (kcal/day) the first formula is the more accurate of the 2 equations, while the second is an approximation of rer for dogs weighing 5 to 25 kg. Body weight should always be entered in kg. if partial intolerance to enteral nutrition is present, it is likely that a lesser amount provides some benefit in maintaining absorptive surface area of the intestines. illness factors, which increase calculated rer, should not be used as the available literature suggests that such values overestimate calories needed in hospitalized patients.17 Animals may require assistive enteral feeding. • syringe feeding is not recommended due to the practical inability to deliver full nutrient requirements with this method and the risk of food aversion and aspiration. • Nasoesophageal and nasogastric tubes are often used in management of canine and feline pancreatitis. • esophagostomy tubes are generally reserved for severe chronic pancreatitis in dogs, or in cats with concurrent morbidities that make the need for continued supportive feeding likely. What should the patient be fed? Commercially available low fat enteral diets (Table 1) may best be reserved for patients that have been discharged from the hospital or those that are severely hyperlipidemic. TabLe 1. fat Content (g/1000 kcal) of veterinary therapeutic Diets labeled for Management of Pancreatitis Diet

DrY

CanneD

low fat Kangaroo Maintenance 22 (raynenutrition.com)

Prescription Diet i/d low fat (hillspet.com)

veterinary Diet gastrointestinal low fat (royalcanin.com)

veterinary Diets en gastroenteric (proplanveterinarydiets.com)

veterinary Diets ha hydrolyzed (Vegetarian/Chicken) (proplanveterinarydiets.com)

26/32

n/a

veterinary formula intestinal Plus low-residue (iams.com)

tvpjournal.com | November/December 2016 | An Official Journal of the NAVC | TODAy’s VeTeriNAry PrACTiCe

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ACVN NutritioN Notes

TabLe 2. fat Content & energy Density of selected liquid Diets Diet

fat Protein KCal/Ml (g/1000 kcal) (g/1000 kcal)

CliniCare liquid Diet (abbottnutrition.com)

≥ 50a

≥ 80a

ensure Plus (abbottnutrition.com)

1.5

intensive Care hDn (emeraid.com)

rebound liquid Diet (virbacvet.com)

≥ 60

sustain hDn (emeraid.com) vivonex elemental formula (nestlehealthscience.us)

≤ 1.36

≥ 60

0.84

≤ 1.34

a. Estimated from guaranteed analysis b. Manufacturer does not recommend for constant rate infusion

• similar outcomes have been reported in dogs receiving parenteral nutrition for acute pancreatitis and in those receiving early enteral nutrition, but dogs fed parenterally had increased catheter complications.18 • the provision of complete parenteral nutrition solutions is often difficult in practices not equipped with a fully staffed emergency and/ or critical care unit or in those without previous experience with these formulations.

Long-term Nutritional Assessment & Recommendations Dogs with acute pancreatitis may fully recover, and may not display any histologic features or clinical signs of chronic disease. in such cases, a diet otherwise optimal for the pet’s age and health can eventually be fed. once the patient is discharged: • if the patient received a low fat diet during hospitalization, slowly transition the animal to the previous or intended maintenance diet. • Do not make this transition until the owner has verified the patient is eating well and clinically stable after discharge. there are often no contraindications to extended administration of a low fat diet. • Discontinue food transition and reevaluate recommendations if there is any evidence of lethargy, hyporexia, or abdominal pain. • owners should be counseled to avoid the risk factors highlighted at the beginning of this article (eg, significant abrupt food changes, ingestion of trash, table scraps, obesity).

• initiation of therapeutic diets during acute illness has been hypothesized to risk food aversion to the diet offered, and only a limited number of fatrestricted diets are available on the market. • Dogs fed a fraction of normal maintenance energy requirements tolerate a moderate fat “sacrificial” maintenance diet during hospitalization, in my experience. Liquid veterinary-specific enteral diets are available (Table 2): • Veterinary-specific diets are usually higher in fat than human formulas but are complete and balanced. • Human enteral diets may be used for short-term feeding as they are lower in fat but are generally also lower in protein and essential nutrients, making them inappropriate for long-term use without detailed analysis. CANINE CHRONIC PANCREATITIS • Liquid diets are generally required for Low fat, no fat, or normal fat? nasoenteral tubes. the evidence for dietary fat restriction in chronic elemental diets are liquid diets designed for canine pancreatitis is based on clinical impression humans. the name “elemental” refers to a basic and the published management of relatively few mixture of simple nutrients, such as free amino cases. the lack of prospective controlled clinical acids or small peptides, simple sugars, and low trials assessing fat tolerances in dogs with acute amounts of dietary fat. these diets tend to be more or chronic pancreatitis has resulted in a range of expensive per calorie than all other common diets, recommendations. and are not complete and balanced for long-term feeding. However, TabLe 3. they may be beneficial if an animal Published Maximal Dietary fat Concentrations suggested has concurrent food hypersensitivity. for use in Dogs with Pancreatitis standard parenteral nutrition villaverde C 201220 All dogs: 24 grams fat per 1000 kcal solutions can be given in the event hand M et al Obese dogs: 25 grams fat per 1000 kcala,b of severe acute pancreatitis. 21 2011 Non-obese dogs: 38 grams of fat per 1000 kcala • there is no evidence parenteral All dogs: 25 grams fats per 1000 kcala lipid emulsions increase pancreatic Xenoulis Pg et al2 release of proteases or worsen a. As estimated from dry matter percentage given b. Obese dogs = BCS ≥ 7/9 prognosis. 48

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

ACVN NutritioN Notes

some specialists generically advise that a low fat diet be given,1,19 while others provide specific empirical maxima (Table 3). None of the values has a primary basis in scientific experimentation and as such should be interpreted cautiously. Moreover, the diets marketed and labeled for management of pancreatitis vary widely in nutrient composition (Table 1). the precise fat content tolerated is likely patientspecific. Human patients with chronic pancreatitis eating high fat diets had increased abdominal pain but fat intake was not associated with increased disease severity or complications.22 KeY Point: Based on available evidence, it is prudent to feed lower fat diets (< 30 grams per 1000 kcal) in order to assess an individual dog’s response. Diets with higher fat contents may be tolerated by some dogs as precise data are unavailable.

Nutritionally responsive hyperlipidemic dogs should consume no more fat than necessary to maintain serum triglycerides in a normal range. these dogs should, however, minimally receive their recommended allowance of 14 grams of fat per 1000 calories, assuming a normal intake of food.10 Fat free diets are not appropriate because minimum intake of dietary fat is needed for absorption of fat-soluble vitamins and provision of essential fatty acids. What type of fat? the type of fat consumed may influence a dog’s response to a particular diet. Dietary fat may be saturated or unsaturated and have different lengths of fatty acid chains. For a further discussion on dietary fat, read Role of Dietary Fatty Acids in Dogs & Cats (september/october 2016), available at tvpjournal.com. In vitro studies have suggested that acinar cells are differentially sensitive to the types of dietary fat to which they are exposed, with saturated fats the most lipotoxic, polyunsaturated fats less so, and monounsaturated fats protective.23 such studies have not been performed in veterinary patients or cell lines. oral or parenteral omega-3 fatty acids (eg, docosahexaenoic acid [DHA], alpha-linolenic acid [ALA], eicosapentaenoic acid [ePA]) may reduce pancreatic inflammation and prevent apoptosis of acinar cells.23-25 • efficacy and dosing in dogs has not been established; however, other omega-3

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responsive conditions typically require 1 to 3 mg of combined ePA and DHA per kcal, or approximately 1 to 3 standard fish oil capsules (containing 300 mg ePA and DHA) per 10 pounds of body weight.26 • each capsule adds 1 gram of fat to a dog’s intake; therefore, omega-3 fatty acids should be used judiciously while monitoring clinical signs. • extended administration is required and, therefore, is only likely to be beneficial in patients with chronic pancreatitis. oxidized or rancid fats should be avoided. While avoiding improper food storage is important for all dogs, it is especially important for those predisposed to pancreatitis because: • oxidative stress may be a component of the pathophysiology of pancreatitis • oxidized lipids may activate inflammatory cells.27,28 A protein problem? Published anecdotal recommendations have suggested restriction of dietary protein to less than 75 grams per 1000 kcal for dogs based on the stimulation of pancreatic enzyme secretion in response to amino acids and protein.2,21 However, there is no evidence that such a maximum is beneficial or necessary. Critically ill dogs may have increased protein requirements, as in humans, due to the systemic inflammatory response; changes in plasma amino acids of dogs with pancreatitis have been documented.29 KeY Point: In the absence of definitive data regarding dietary protein, nutritional plans for dogs with pancreatitis should ensure that patients receive at least the recommended daily allowance of protein (3.3 grams per [BWkg]0.75).10

FELINE PANCREATITIS in most cats, the underlying inciting cause of pancreatitis is not identified. it commonly occurs as a co-morbidity with other conditions, including those affecting the small intestine and liver. this so-called triaditis may occur in a majority of cats diagnosed with pancreatitis. Feline pancreatitis is histologically consistent with the chronic form in 2⁄3 of affected cats.30 Cats with suspected acute or chronic pancreatitis should be carefully screened for cholangiohepatitis, inflammatory hepatic disease, inflammatory bowel disease, and bacterial infections of the pancreas.4,30

tvpjournal.com | November/December 2016 | An Official Journal of the NAVC | TODAy’s VeTeriNAry PrACTiCe

Peer reviewed

ACVN NutritioN Notes

KeY Point: Feline pancreatitis is not the same as pancreatitis in a small dog, and dietary fat restriction is generally not required in cats.

the nutritional treatment of feline pancreatitis and associated conditions is centered on provision of adequate caloric intake for both short- and longterm feeding. Most cats require between 200 to 250 kcal daily during hospitalization and in their home environment. there is no evidence that dietary fat restriction is warranted in feline pancreatitis, whether acute or chronic. therefore, higher fat recovery diets can be fed if palatable and available.4,16 Anecdotally cats require increased time and treatment to begin eating compared with dogs. if a patient has a history of significant weight loss or a protracted period of anorexia, feeding tubes should be considered. • esophagostomy tubes (Figure 3) should be placed in cats with hepatic lipidosis or other co-morbidities and when a protracted recovery is expected. • short-term enteral feeding is typically best achieved by nasoesophageal tube placement; cats should not be given human enteral formulas during hospitalization as most formulas do not meet the unique nutritional requirements of cats.16 • Appetite stimulant drugs are unreliable in many cases.

Decoding the label: assessing Commercial Diets for fat Content Dietary nutrient comparisons are best performed on a caloric basis (see Beyond the guaranteed analysis: Comparing Pet foods, available at tvpjournal.com under Clinical Resources). Ideally, the amount of fat in grams per 1000 calories would be obtained directly from the manufacturer. In the absence of such information, the dietary fat content can be estimated: 1. Add 1% to the guaranteed analysis fat minimum on the label to estimate the actual or typical content.33 2. Divide the as-fed caloric density (kcal/kg) on the label by 10,000. 3. Divide the number from Step 1 by the number from Step 2. If evaluating a dry diet with a caloric density of 4000 kcal/kg and fat content of 15%, the equation would be:

Figure 3. esophagostomy tubes help facilitate nutritional management of acute and chronic pancreatitis characterized by hyporexia.

Cats may benefit from parenteral vitamin B12 (cobalamin) supplementation given that the absorptive cofactor necessary for B12 absorption, known as the intrinsic factor, is produced only in the pancreas of cats (as opposed to the pancreas and stomach in dogs).31 SECONDARY EFFECTS OF PANCREATITIS severe pancreatitis may be associated with diabetes mellitus and exocrine pancreatic insufficiency (ePi). these occur more frequently in dogs than in cats, but have been reported in both species.2,32 • ePi can be managed with a variety of different dietary strategies but relies on exogenous pancreatic enzyme powders to aid in normal digestion. • Pancreatitis is documented in a number of diabetic dogs (> 1⁄3), and may have a causal role.32 • the relationship between pancreatitis and diabetes in cats is less clear, with insulin resistance secondary to increased adiposity being the primary risk factor. Cats with diabetes mellitus benefit from weight loss and, possibly, a low carbohydrate, high protein diet; neither would be detrimental to managing concurrent pancreatitis based on available knowledge.

(15+1) / (4000/10,000) = 40 grams of fat (estimated) for every 1000 kcal fed The National Research Council’s recommended allowance for fat content (g/1000 kcal) in canine diets is 13.8; less than 30 is considered low fat, 30 to 50 is considered moderate fat, and greater than 50 is considered high fat by the author.

IN SUMMARY small animals with pancreatitis should receive an assessment of their dietary history and nutritional status. unfortunately, current knowledge is inadequate to provide a strong evidence-based

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

ACVN NutritioN Notes

recommendation on when and how to feed many patients. Dietary fat restriction appears to be a critical part of successful management of chronic disease in dogs, but its role in acute pancreatitis is less clear, and is generally unnecessary in cats. the definition of a low fat diet for patients with pancreatitis is not well established but may be less than 30 grams per 1000 kcal. Hyperlipidemic animals may benefit from restricted intake of fat to achieve lower serum triglycerides and cholesterol, but all animals require sufficient fat intake to ensure fat soluble vitamin absorption and to meet essential fatty acid requirements. When nutrition is elected for acute or severely affected patients, assistive feeding may be required. Current evidence suggests that enteral nutrition is preferred over parenteral nutrition unless there is a contraindication to luminal nutrition. ALA = alpha-linolenic acid; BWkg = body weight in kilograms; DHA = docosahexaenoic acid; ePA = eicosapentaenoic acid; ePi = exocrine pancreatic insufficiency; kcal = kilocalorie; rer = resting energy requirement References 1. Watson P. Pancreatitis in dogs and cats: Definitions and pathophysiology. J Small Anim Pract 2015; 56:3-12. 2. Xenoulis PG, suchodolski Js, steiner JM. Chronic pancreatitis in dogs and cats. Compend Cont Ed Pract Vet 2008; 30(3):166-180. 3. Xenoulis P. Diagnosis of pancreatitis in dogs and cats. J Small Anim Pract 2015; 56:13-26. 4. Armstrong PJ, Williams DA. Pancreatitis in cats. Top Comp Anim Med 2012; 27:140-147. 5. Lem KY, Fosgate Gt, Norby B, et al. Associations between dietary factors and pancreatitis in dogs. JAVMA 2008; 233:14251431. 6. Watson P, Archer J, roulois A, et al. observational study of 14 cases of chronic pancreatitis in dogs. Vet Rec 2013; 1:ec4912. 7. Mohr AJ, Leisewitz AL, Jacobson Ls, et al. effect of early enteral nutrition on intestinal permeability, intestinal protein loss, and outcome in dogs with severe parvoviral enteritis. J Vet Intern Med 2003; 17:791-798. 8. Qin H-L, su Z-D, Gao Q, et al. early intrajejunal nutrition: Bacterial translocation and gut barrier function of severe acute pancreatitis in dogs. Hepatobiliary Pancreat Dis Int 2002; 1:150154. 9. Qin H-L, su Z-D, Hu L-G, et al. effect of parenteral and early intrajejunal nutrition on pancreatic digestive enzyme synthesis, storage and discharge in dog models of acute pancreatitis. World J Gastroenterol 2007;13:1123. 10. National research Council. Nutrient Requirements of Dogs and Cats. Washington DC: National Academies Press, 2006. 11. Hoffer LJ. Human protein and amino acid requirements. JPEN J Parenter Enteral Nutr 2016; 40(4):460-474. 12. Johnson PA, Mann F, Dodam J, et al. Capnographic documentation of nasoesophageal and nasogastric feeding tube placement in dogs. J Vet Emerg Crit Care 2002; 12:227-233. 13. Marik Pe. What is the best way to feed patients with pancreatitis? Current Opinion Critic Care 2009; 15:131-138. 14. Mirtallo JM, Forbes A, McClave sA, et al. international consensus guidelines for nutrition therapy in pancreatitis. JPEN

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J Parenter Enteral Nutr 2012; 36(3):284-291. 15. Lodewijkx PJ, Besselink MG, Witteman BJ, et al. Nutrition in acute pancreatitis: A critical review. Expert Rev Gastroenterol Hepatol 2016; 10(5):1-10. 16. Jensen KB, Chan DL. Nutritional management of acute pancreatitis in dogs and cats. J Vet Emer Crit Care 2014; 24:240-250. 17. o’toole e, Miller CW, Wilson BA, et al. Comparison of the standard predictive equation for calculation of resting energy expenditure with indirect calorimetry in hospitalized and healthy dogs. JAVMA 2004; 225:58-64. 18. Mansfield C, James F, steiner J, et al. A pilot study to assess tolerability of early enteral nutrition via esophagostomy tube feeding in dogs with severe acute pancreatitis. J Vet Intern Med 2011; 25:419-425. 19. Williams DA, steiner JM. Canine exocrine pancreatic disease. in ettinger sJ,Feldman eC (eds): Textbook of Veterinary Internal Medicine. 6th ed. st. Louis: elsevier, 2005, pp 1482-1488. 20. Villaverde C. Nutritional management of exocrine pancreatic diseases. in Fascetti AJ, Delaney sJ (eds): Applied Veterinary Clinical Nutrition. somerset, NJ: John Wiley & sons, 2012, pp 221-234. 21. Hand M, Zicker sC, Novotny BJ. Acute and chronic pancreatitis in Hand M, Zicker sC, Novotny BJ (eds): Small Animal Clinical Nutrition Quick Consult. topeka, Ks: Mark Morris institute, 2011, pp 208-212. 22. Castiñeira-Alvariño M, Lindkvist B, Luaces-regueira M, et al. the role of high fat diet in the development of complications of chronic pancreatitis. Clin Nutr 2013; 32:830-836. 23. Danino H, Ben-Dror K, Birk r. exocrine pancreas er stress is differentially induced by different fatty acids. Exp Cell Res 2015; 339:397-406. 24. Park Ks, Lim JW, Kim H. inhibitory mechanism of omega-3 fatty acids in pancreatic inflammation and apoptosis. Ann NY Acad Sci 2009; 1171:421-427. 25. Lei QC, Wang XY, Xia XF, et al. the role of omega-3 fatty acids in acute pancreatitis: A meta-analysis of randomized controlled trials. Nutrients 2015; 7:2261-2273. 26. Bauer Je. therapeutic use of fish oils in companion animals. JAVMA 2011; 239:1441-1451. 27. McClave sA. Drivers of oxidative stress in acute pancreatitis: the role of nutrition therapy. J Parenter Enteral Nutr 2012; 36:24-35. 28. schoenberg MH, Birk D, Beger HG. oxidative stress in acute and chronic pancreatitis. Am J Clin Nutr 1995; 62:1306s-1314s. 29. Chan DL, rozanski eA, Freeman LM. relationship among plasma amino acids, c-reactive protein, illness severity, and outcome in critically ill dogs. J Vet Intern Med 2009; 23:559-563. 30. simpson KW. Pancreatitis and triaditis in cats: Causes and treatment. J Small Anim Pract 2015; 56:40-49. 31. simpson KW, Fyfe J, Cornetta A, et al. subnormal concentrations of serum cobalamin (vitamin B12) in cats with gastrointestinal disease. J Vet Intern Med 2001; 15:26-32. 32. Davison L. Diabetes mellitus and pancreatitis–cause or effect? J Small Anim Pract 2015; 56:50-59. 33. Choate CJ, Hill rC, scott KC, et al. Comparison of the guaranteed analysis with the measured nutrient composition of commercial pet foods. J Anim Physiol Anim Nut 2009; 93:141-141.

Justin shMalBerg

Justin Shmalberg, DVM, Diplomate ACVN & ACVSMR, is a clinical associate professor, service chief of integrative medicine, and a small animal hospital medical director at the University of Florida College of Veterinary Medicine. He received his DVM from University of Wisconsin–Madison and completed an internship in veterinary acupuncture and a residency in small animal clinical nutrition at University of Florida.

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Placement & Management:

Jackson-Pratt closed active suction drain Bonnie Grambow Campbell, DVM, PhD, Diplomate ACVS Washington State University

Learn More Read Moist Wound Healing: The New Standard of Care in the September/ October 2015 issue of Today’s Veterinary Practice, available at tvpjournal.com.

Drains are placed in wounds to evacuate fluid that would otherwise accumulate due to dead space, inflammation, infection, and/or necrosis. Fluid accumulation in a wound can be detrimental because it: • acts as a medium for bacteria • Separates tissues that need to heal together • creates pressure that can cause pain and decrease local blood flow.1 CONSIDERATIONS Drains do not replace debridement and lavage, and wounds that contain bacteria, foreign material, or tissues that might necrose are preferably left open and bandaged with moisture retentive dressings rather than being prematurely closed over a drain.2 Drains should be used sparingly in neoplastic sites due to the potential of tumor cell tracking along the drain. if a drain must be placed after

Troubleshooting

if the JPd will not hold suction, make sure: • The grenade is securely attached to the tube • The evacuation port is closed • There are no holes in the external tubing (eg, from patient chewing or from the needle used for the pursestring suture). If the incision itself is not airtight, add sutures or staples or cover it with a dressing +/- sterile ointment. The incision should become more airtight as the fibrin clot in the wound edge becomes more organized. a JPd can become obstructed with blood clots, fibrin, pus, or tissue, although due to the large number of holes, this is 52

tumor resection, it should be exited close to the wound edge at a site that could be readily resected or radiated if clean margins were not obtained.1,3 JACKSON-PRATT DRAINS a Jackson-Pratt drain (JPD) is an active suction drain consisting of a fenestrated, flexible, silicone tube connected by a nonfenestrated tube to a compressible reservoir (called a grenade due to its shape) (Figure 1, page 54). the fenestrated end of a JPD (which is placed in the wound bed) is available in a range of widths and may be flat or round. the fenestrations direct fluid into the nonfenestrated portion of the tubing and then into the grenade. the grenade has a oneway valve to prevent retrograde movement of the fluid. common grenade sizes range from 100 mL to 400 mL.

unusual. If there is an obstruction: • Make sure the bulldog clamp is open and the tube is not kinked. • Empty and then reactivate the grenade to maximize the amount of suction and determine if the improved suction dislodges the obstruction. A tube that remains obstructed may be flushed with sterile saline using sterile technique. This should only be done after carefully considering whether keeping the drain functional is more important than the potential risk for introducing contaminants into the wound when flushing. Drains that are not functioning should be removed, as their presence may increase the amount of wound fluid and risk for infection.4,5

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Practice SteP By SteP

STEP BY STEP: PLACING THE DRAIN as with any drain placement, aseptic technique is essential when placing and handling a JPD.8 Disposable or sterile gloves should be worn when handling the drain and grenade, and when removing the drain.

FIGURE 1. Anatomy of a Jackson-Pratt closed active suction drain.

Benefits of a closed, active suction drain, such as the JPD, over an open, passive drain, such as the Penrose drain, are many (Table) and include the: • Use of suction to actively remove exudate and close down dead space • Flexibility of being able to exit the active drain in a nondependent location • collection of exudate in a closed system. in addition, a closed system: • Lowers the risk for ascending infection6,7 • is cleaner to manage • Protects skin • allows easy quantitative and qualitative assessment of exudate.

Step 1. Choosing Drain Exit Site after wound debridement and lavage, choose a drain exit site in healthy skin, where it is: • easy to cover the exit site • easy to manage the grenade • comfortable for the patient. For example, a good exit site for a wound over the caudolateral abdomen is a location where the JPD exits dorsally, which allows the clinician easy access to the tubing and grenade (rather than working under the dog or next to the hindlimb, if the drain exited ventrally or on the side, respectively) and allows the dog to lie in lateral or sternal recumbency without lying on the drain or getting the exit site dirty. Do not exit the tube through the incision itself, as this may: • Prevent an airtight seal • interfere with healing • increase the risk for wound infection.

TABlE. comparison of closed, active suction drains versus open, Passive drains

closed, active suction drain (Jackson-Pratt drain)

oPen, Passive drain (Penrose drain)

Path of drainage

Interior of tubing

Exterior of drain

Fluid collection site

Collection device (eg, grenade)

Bandage material

Mechanism of action

Negative pressure generated by collection device

Gravity

exit site

Exit where most convenient for drain management and patient comfort

Ventral, dependent site

Monitoring fluid quantity

Easy to quantify

Difficult to quantify

Monitoring fluid character

Easy to monitor fluid color and consistency and collect relatively pure sample for cytology or culture

Difficult because fluid is absorbed in dressing, dehydrated, and contaminated by skin flora

relative risk for ascending infection6,9

Lower, since closed system

Higher, since open system

Need fully closed wound?

Yes

Ability to collapse dead space, hold tissues in contact

Good; achieved via active suction and fluid removal

Fair; achieved only via fluid removal

irritation of skin

Minimal, since fluid is contained inside drain

Risk for maceration and excoriation of skin by wound fluid

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

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Step 2. Placing the Drain to place the drain, tunnel a pair of forceps from inside the wound to the planned exit site (A). Push the forceps tips against the deep surface of the skin and incise the skin immediately over the tips with a scalpel blade, making a hole no larger than the JPD tube. (Some JPDs have a trocar; push the trocar through the skin from the wound-side out, then cut the trocar off). Open the forceps enough to interlock with a second pair of forceps (B) and pull the latter into the wound (C). Grasp the nonfenestrated end of

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the JPD tube with the second forceps and pull it from inside to outside the wound (D). Protect the fenestrated end of the drain during this process so it does not rub along the skin where it might pick up contaminants (E). Place the JPDâ&#x20AC;&#x2122;s fenestrated end into the most dependent part of the wound where fluid will accumulate (F). the entire fenestrated area must be underneath the skin and, therefore, inside the wound when it is closed; the end can be cut shorter as needed.

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Step 3. Closing the Wound Place a purse-string suture (eg, 2-0 nylon) in the skin around the exit site to help hold the tube and create a seal. it is important to: • Locate the knot where the tube naturally lies against the body to avoid kinking when the tube is pulled in the direction of the knot (A) • Leave both ends of the purse-string suture

A Step 4. Placing the Grenade trim the external tubing to a length that allows convenient manipulation of the grenade; then place a bulldog clamp on the tube, which allows it to be readily closed off if the grenade is dislodged. Securely attach the nonfenestrated end of the tube to the port with the one-way valve on the grenade (A). to activate the grenade, compress it to push air out the evacuation port, close the evacuation port with the built-in plug or an iV catheter adapter cap (PrN), and release the compression (B). as the

A 56

equally long to use them for a fingertrap pattern on the tube (B). • additional security can be achieved by placing a butterfly of surgical tape on the tube and stapling it to the skin (see Step 7 Figure, page 58). close the wound in multiple layers as appropriate. Do not catch the drain in the sutures.

grenade tries to resume its original shape, negative pressure is exerted through the tubing and into the wound. Higher suction can be generated by rolling up the grenade from its apex to base on a table top to push out the air rather than squeezing it by hand.10 residual fluid from lavage, and/or residual air after surgery, may cause the grenade to fill up right away. if this occurs, simply empty the grenade (see Step 6) and repeat the activation process until negative pressure is achieved.

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Step 5. Protecting the Drain cover the JPD’s exit site with an adhesive dressing to prevent bacteria entry around the tube. Put a shirt, stockinette, or bandage on the patient to protect the external tubing and grenade from being stepped on, caught in a kennel door, or soiled. if the patient can reach the drain with its mouth, the patient should wear an elizabethan collar when not under direct observation. Step 6. Maintaining the Drain

Monitor the quantity and quality of fluid in the grenade, starting with checks every 1 to 2 hours to get a sense of the production rate for the wound; then every 4 to 6 hours as appropriate. empty and reactivate the grenade at least once a day or whenever it is half full (whichever is shorter), since the strength of suction decreases as the grenade fills.11 to empty the grenade: • close the bulldog clamp • clean the secondary port with alcohol • Open and attach a syringe to the secondary port

• evacuate the grenade with the syringe. alternatively, if a PrN was placed in the secondary port, clean the PrN with alcohol and aspirate the fluid with a needle and syringe (as seen in the Figure). reactivate the drain as described in Step 4. Daily cytology can be performed on a sample of fluid to monitor the state of inflammation or infection. Step 7. Removing the Drain

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it is difficult to establish rules on when to remove a drain because fluid production varies with the wound’s etiology, dimensions, location, and degree of inflammation or infection.1,10 Because the drain itself stimulates some fluid production, the amount of drainage is not expected to reach zero. When a wound is healing, the: • Fluid becomes serosanguineous • Volume decreases to a steady state • cytology shows resolving inflammation and improved cell health. all these signs indicate that it is time to remove the drain. the risk for seroma formation was higher in human and canine patients that were still producing relatively large amounts of wound fluid when the JPD was removed compared with patients in which the wound fluid production had steadily decreased.8,9 to remove the drain: • close the bulldog clamp on the tube • cut the purse-string suture • apply steady, gentle traction to remove the JPD (shown in the Figure) • cover the hole in the skin with a sterile dressing; allow it to heal by second intention. INPATIENT OR OUTPATIENT

MANAGEMENT there are several important reasons to keep patients with a JPD in the hospital, which is my preference: • Drains need to be handled with aseptic technique.1,8 • Patients must be closely supervised to prevent damage or dislodgment of the drain. • Fluid quantity and quality need to be observed multiple times a day to assess the healing process, recognize problems with drain function, and determine when the drain can be removed. if a patient is sent home with a JPD, i advise clinicians to: • Spend time training the client in aseptic drain management (such as wearing gloves), which includes watching the client empty and reactivate the drain • check the patient and drain daily. JPD = Jackson-Pratt drain References 58

Discomfort with Drains? Human patients report: • discomfort when the reservoir is

activated if the wound has little fluid or dead space, likely because the suction is directly against the healing tissues. • More pain with abrupt removal of

closed suction drains than during removal over a 15-second interval, with the most discomfort occurring as the fenestrated portion of the drain emerged.2 In my experience, JPDs are well tolerated by dogs, and removal can be done in a fully awake patient. Just as for vaccine administration, distracting the patient with petting and talking is typically all that is needed.

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Bonnie GraMBow caMPBell

Bonnie Grambow Campbell, DVM, PhD, Diplomate ACVS, is a clinical associate professor of small animal surgery at Washington State University. Dr. Campbell received her DVM and PhD from Cornell University and completed a small animal surgical residency at University of Wisconsin. She has received a number of teaching awards and speaks at continuing education programs nationally and internationally. Her special clinical interests include wound management and oncologic and reconstructive surgery.

1. campbell BG. Bandages and drains. in tobias M, Johnson Sa (eds): Veterinary Surgery Small Animal, 1st ed. St. Louis: elsevier Saunders, 2012, pp 221-230. 2. campbell BG. Moist wound healing: the new standard of care. Today’s Vet Pract 2015; 5(4):32-42. 3. Lascelles BDX. Strategic planning in oncological surgery. British Small Animal Veterinary Congress Proc, 2007, Belfast, ireland. 4. isik O, Kaya e, Dundar HZ, Sarkut P. Surgical site infection: re-assessment of the risk factors. Chirurgia 2015; 110(5):457-461. 5. Bristow Pc, Halfacree ZJ, Baines SJ. a retrospective study of the use of active suction wound drains in dogs and cats. J Sm Anim Prac 2015; 56(5):325-330. 6. raves JJ, Slifkin M, Diamond DL. a bacteriologic study comparing closed suction and simple conduit drainage. Am J Surg 1984; 148(5):618-620. 7. reiffel aJ, Barie PS, Spector Ja. a multi-disciplinary review of the potential association between closed-suction drains and surgical site infection. Surg Infect 2013; 14(3):244269. 8. chim JH, Borsting ea, thaller Sr. Urban myths in plastic surgery: Postoperative management of surgical drains. Wounds 2016; 28(2):35-39. 9. Shaver SL, Hunt GB, Kidd SW. evaluation of fluid production and seroma formation after placement of closed suction drains in clean subcutaneous surgical wounds of dogs: 77 cases (2005-2012). JAVMA 2014; 245(2):211-215. 10.Halfacree ZJ, Wilson aM, Baines SJ. evaluation of in vitro performance of suction drains. Am J Vet Res 2009; 70(2):283-289. 11.Williams J, toews D, Prince M. Survey of the use of suction drains in head and neck surgery and analysis of their biomechanical properties. J Otolaryngol 2003; 32(1):16-22.

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Canine insulinoma: Diagnosis, TreaTmenT, & sTaging Eliza Reiss Grant, DVM, and Kristine E. Burgess, DVM, Diplomate ACVIM (Oncology) Tufts University

an insulinoma is a malignant pancreatic tumor that inappropriately secretes excessive insulin, resulting in profound hypoglycemia.1 Pancreatic tumors are classified as: • Exocrine, which includes adenocarcinomas of ductular or acinar origin • Endocrine, which arise from the islets of langerhans. insulinomas are functional neuroendocrine tumors that originate in the beta cells of the islets of langerhans.1 PRESENTATION Signalment any breed of dog can be affected, but large breeds tend to be overrepresented.1 While, in humans, insulinomas affect females far more frequently than males, there is no apparent sex predilection in dogs.1-3 Dogs also commonly present with a malignant variant, while humans often have a benign adenoma (80%).1 insulinoma is rare in cats.4 Clinical Signs Most affected dogs do not have abnormalities on physical examination, and early clinical signs related to the disease can be sporadic and vague. classically, dogs present with signs attributable to hypoglycemia, such as weakness, ataxia, extreme fatigue after exercise, and collapsing episodes. Seizures can occur later in the disease process and increase progressively in frequency and intensity over time.1 Hypoglycemic episodes are often precipitated by exercise or fasting (increased glucose utilization) as well as by the ingestion of food (stimulation of insulin release). intravenous or oral administration of glucose alleviates clinical signs. if prolonged seizure activity occurs, cerebral laminar necrosis can ensue. 60

DIAGNOSIS aside from a histologic confirmation of insulinoma, no currently available diagnostic test provides a definitive diagnosis of insulinoma. Existing techniques may help increase suspicion for an insulin-secreting tumor but, with most diagnostic testing, it is imperative to interpret all results in the context of the coexisting clinical signs. Differential Diagnosis a complete work-up, including careful patient history, physical examination, bloodwork, and diagnostic imaging tests, should be performed to rule out other causes of hypoglycemia, such as sepsis, hepatic failure, adrenal cortical insufficiency, toxin ingestion, and other forms of neoplasia. Laboratory Tests Blood glucose a simple fasting blood glucose level of less than 40 mg/dl can suggest hyperinsulinemia, although careful monitoring of a fasted dog with suspected insulinoma is strongly recommended due to high risk for seizure activity. Insulin-to-Glucose Ratio additional blood analysis evaluating the amended insulin-to-glucose ratio (aigr) may be warranted. • this assay capitalizes on the lack of response to physiologic negative feedback inhibitory loops that decrease insulin secretion in the face of hypoglycemia in dogs with an insulinoma. • a positive insulin-to-glucose ratio demonstrates an inappropriately elevated insulin level in the setting of hypoglycemia.1 • nevertheless, an elevated aigr is neither sensitive nor specific for the diagnosis of insulinoma. the aigr can be elevated from insulin-producing tumors other than insulinoma or normal in dogs with insulinoma.

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• this test can be performed on serum samples and submitted to most large commercial laboratories. Serum Fructomsamine Serum fructosamine can indicate insulinoma as it may be low in dogs with chronic or episodic hypoglycemia. However, this assay is not specific and should never be considered a confirmatory test. Imaging Radiography & Ultrasound thoracic radiography and abdominal ultrasound are recommended to assess for the presence of a possible pancreatic mass and associated metastatic disease (eg, lymph nodes, liver, lungs). although abdominal ultrasound is considered a relatively insensitive and nonspecific assessment for insuli-

Figure 1. ultrasound image of mass lesion within the left wing of the pancreas. Approximately 50% of insulinomas are not visualized by this technique.

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noma, it is recommended to rule out other causes of hypoglycemia. in addition, some insulinomas are large enough to be detected on ultrasound (Figure 1). Advanced Imaging conventional computed tomography (ct) with contrast has an improved sensitivity of 71% for pancreatic lesions.5 Most recently, dual-phase ct angiography has been reported to successfully localize pancreatic lesions and stage patients before surgery (Figure 2).6 Further Diagnostics Some insulinomas are challenging to localize even on advanced imaging, and a lack of definitive identification of the tumor on preoperative imaging should not discredit a working diagnosis of insulinoma. in some instances, an exploratory laparotomy may be recommended when there is a strong clinical suspicion for insulinoma in the absence of visible disease. TREATMENT Surgical Management in patients with hypoglycemia and inappropriate insulin production, exploratory abdominal surgery is the recommended treatment. Surgical removal of the tumor: • Provides the best chance for relief of clinical signs and the best survival times1,2,7 • allows complete staging via biopsy of regional lymph nodes and liver to determine the extent of suspected metastatic disease. Metastatic Disease Because dogs commonly have a malignant form of insulinoma, approximately half will have metastatic disease detected before or at the time of surgery. nevertheless, surgery is still indicated in patients with suspected or confirmed metastatic disease because removal of metastatic disease reduces the extent of aberrant insulin secretion and may improve clinical signs.1,3



Figure 2. Arterial phase dorsal oblique computed tomography (CT) reconstruction (soft tissue algorithm) of a pancreatic mass (arrow). CT angiography is a more sensitive imaging modality for insulinoma.

Surgical Approach Most insulinomas are solitary masses that can be detected intraoperatively with gentle palpation of the pancreas. intraoperative ultrasound with iV 1% methylene blue has been used for additional visualization of the pancreatic lesion but is of questionable value.

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Partial pancreatectomy is the preferred procedure, with pancreatitis as a possible postoperative complication. Other complications include ongoing hypoglycemia, diabetes mellitus causing hyperglycemia, and neurologic complications from historic neuroglycopenia. those with persistent hyperglycemia after surgery should be treated as diabetic until they are no longer insulin dependent. Stabilization Hypoglycemic patients should be stabilized with iV dextrose supplementation. in a crisis situation, iV dextrose should be given slowly so that further insulin release is not stimulated. glucagon, a peptide hormone produced by the pancreas, opposes the effects of insulin by raising blood glucose. it has been used to stabilize hypoglycemia in a crisis setting when given as a constant rate infusion at approximately 10 to 15 ng/kg per minute.8 Medical Management Medical management of insulinoma is possible in patients: • that are not good surgical candidates • Whose owners are not interested in pursuing surgery

• that have persistent hypoglycemia after surgery. this approach includes dietary management as well as medications, such as prednisone, diazoxide, and octreotide.1,2,7 Dietary Management the goal of dietary management is to maintain appropriate blood glucose levels throughout the day and avoid foods that may incite a spike in insulin release. this is achieved by feeding multiple small meals throughout the day and using foods that are high in protein, fat, and complex carbohydrates. Oral prednisone can be used as an adjunctive therapy because glucocorticoids decrease insulin sensitivity and increase endogenous (hepatic) glucose production. Prednisone can be dosed to effect in the range of 0.5 to 4 mg/kg Q 24 H.1,2 Diazoxide Diazoxide is used in the medical management of hypoglycemia to inhibit the intracellular release of ionized calcium, thereby preventing the exocytosis release of insulin by the beta cells. it also contributes to hyperglycemia through its ability to stimulate the release of epinephrine. Diazoxide is commonly instituted in patients that do not respond to dietary management and prednisone.

insulinoma: staging & Prognosis Insulinoma is classified as: • stage i: Insulinoma confined to pancreas • stage ii: Insulinoma with regional lymph node metastasis • stage iii: Insulinoma with distant metastasis. Reported insulinoma survival times are listed in the Table.

TAble. insulinoma survival Times reported in the literature: 1993 – 2013 oVerall

meDiCal managemenT

surgiCal managemenT

Polton et al (2007)2 MST: Stage I: 785 d Stage II: 547 d Stage III: 217 d

Polton et al (2007)2

Tobin et al (1999)7

Trifonidou et al (1998)3 MST: 258 d MDFI: 244 d

MST: 196 d MST: 74 d

MST: 785 d MST: 381 d

Dunn et al (1993)

MST: 14 mo

aDJuVanT THeraPY (sTrePTozoToCin) northrup et al (2013)12

(all stages): MPFS: 196 d MST: 308 d

moore et al (2002)11

(stage II or III) MTN: 163 d

MDFI = median disease free interval; MPFS = median progression free survival; MST = median survival time; MTN = median time of normoglycemia

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

Practical OncOlOgy

the dose of diazoxide for dogs with insulinoma and refractory hypoglycemia has been reported to be 5 to 10 mg/kg PO Q 12 H.1,7 the ideal dose for a clinical patient can be determined on the basis of successful management of clinical signs. Octreotide Octreotide is also used to manage hypoglycemia in both humans and dogs with insulinoma. this somatostatin analog can be given as an Sc, iM, or iV injection. inhibition of insulin release is one of somatostatin’s many physiologic actions, and scattered reports of efficacy in dogs exist in the veterinary literature.9 One study of 10 dogs with insulinoma demonstrated an increase in plasma glucose and decrease in plasma insulin after Sc administration of octreotide, with successful binding of the canine somatostatin receptor.10 However, in a controlled study of 3 dogs that received octreotide and a placebo (physiologic saline), no significant difference in insulin or glucose concentrations was noted.9 One dog in the group did experience an improved blood glucose compared with placebo at 8 hours after administration of octreotide, suggesting that some patients may have a clinical benefit.9 Management of Metastatic Disease Streptozotocin the veterinary oncology literature has reported on streptozotocin as the adjuvant therapy for recurrent or metastatic insulinoma. Streptozotocin is an alkylating agent that is structurally similar to glucose and is selectively taken up by the glUt2 transporter. this transporter is found in high levels on pancreatic beta cells, causing cytotoxicity. While streptozotocin has not provided a statistically significant longer survival in canine patients, objective responses have been documented; in 2 patients with paraneoplastic peripheral neuropathy, neurologic signs resolved with this treatment.11

eliza reiss granT

Eliza Reiss Grant, DVM, is a medical oncology resident at Tufts Cummings School of Veterinary Medicine. She received her veterinary degree from Tufts University and completed an internship at Angell Animal Medicine Center. Her interests include canine lymphoma and tumor genomics.

Peer reviewed

Streptozotocin can be given to dogs at a dosage of 500 mg/m2 every 2 to 3 weeks. Due to an elevated risk for renal tubular necrosis, saline diureses for 7 hours (3 hours before administering the drug and 2 hours after discontinuation of the drug) is recommended. Other adverse effects of streptozotocin reported in the veterinary literature include vomiting, reversible elevations in alanine aminotransferase (with discontinuation of the drug), and diabetes mellitus. in a recent study of biweekly streptozotocin, 6 of 19 dogs developed diabetes mellitus, resulting in death or euthanasia.12 Tyrosine Kinase Inhibitors recently, there has been interest in evaluating the efficacy of tyrosine kinase inhibitors, such as toceranib phosphate (Palladia, pfizer.com), for dogs with insulinoma. this interest is based on studies evaluating sunitinib, a human multitargeted tyrosine kinase inhibitor, which has proven efficacy in phase ii trials of humans with pancreatic neuroendocrine tumors.13,14 anecdotally, we have experienced antitumor activity with toceranib phosphate in dogs with insulinomas in the measurable disease setting. toceranib phosphate is well tolerated at a dose of 2.75 mg/kg PO Q 48 H. the most common adverse effects are gastrointestinal (diarrhea, decreased appetite, nausea), with myelosuppression and proteinuria15 being less common but welldocumented adverse effects. IN SUMMARY insulinoma is an uncommon malignant neoplasia in dogs that can result in significant illness, seizures, and death. • Patients often present with clinical signs attributable to hypoglycemia. • Diagnostics should include baseline bloodwork and imaging tests to rule out other causes of hypoglycemia.

KrisTine e. Burgess

Kristine E. Burgess, DVM, Diplomate ACVIM (Oncology), is an assistant professor in oncology at Tufts University Cummings School of Veterinary Medicine. She received her veterinary degree from Tufts University, and completed an internship at VCA West Los Angeles Animal Hospital and residency in oncology at University of Wisconsin—Madison. Dr. Burgess’ interests include comparative oncology with a special interest in canine lymphoma.

tvpjournal.com | November/December 2016 | An Official Journal of the NAVC | TODAy’s VeTeriNAry PrACTiCe

Practical OncOlOgy

• thoracic radiography and abdominal ultrasound are recommended but are frequently unrewarding. • Dual-phase ct angiography may be the best imaging study to diagnose insulinoma. • Surgery is recommended and provides the best reported survival times. • Medical management with dietary change, prednisone, diazoxide, and octreotide is possible. • Streptozotocin is a reasonable adjuvant chemotherapy for patients with metastatic or recurrent insulinoma but is nephrotoxic, causes diabetes mellitus in some patients, and should be used with caution. • toceranib phosphate has not been formally studied in dogs with insulinoma but, on the basis of data in human studies, it may be an effective and well-tolerated treatment option. aigr = amended insulin-to-glucose ratio; ct = computed tomography References 1. 2.

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goutal cM, Brugmann Bl, ryan Ka. insulinoma in dogs: a review. JAAHA 2012; 48:151-163. Polton ga, White rn, Brearley MJ, Eastwood JM. improved survival in a retrospective cohort of 28 dogs with insulinoma. J Sm Anim Prac 2007; 48(3):151-156. trifonidou Ma, Kirpensteijn J, robben JH. a retrospective evaluation of 51 dogs with insulinoma. Vet Q 1998; 20(1):S114-S115. Elie MS, Zerbe ca. insulinoma in dogs, cats and ferrets. Comp Cont Edu Pract Vet 1995; 17(1):5159. robben JH, Pollak yW, Kirpensteijn J, et al. comparison of ultrasonography, computed tomography, and single-photon emission computed tomography for the detection and localization of canine insulinoma. J Vet Intern Med 2005; 19:15-22. Mai W, caceres aV. Dual-phase computed tomographic angiography in three dogs with pancreatic insulinoma. Vet Rad US 2008; 49(2):141-148. tobin rl, nelson rW, lucroy MD, et al. Outcome of surgical versus medical treatment of dogs with beta cell neoplasia: 39 cases (1990-1997). JAVMA 1999; 215(2):226-230. Fischer Jr, Smith Sa, Harkin Kr. glucagon constant-rate infusion: a novel strategy for the management of hyperinsulinemic-hypoglycemic crisis in the dog. JAAHA 2000; 36(1):27-32. Simpson KW, Stepien rl, Elwood cM, et al. Evaluation of the long-acting somatostatin analogue ocretotide in the management of insulinoma in three dogs. J Sm Anim Prac 1995; 36:161-165. robben JH, Visser-Wisselaar Ha, rutterman gr, et al. In vitro and in vivo detection of functional somatostatin receptors in canine insulinomas. J Nuc Med 1997; 38(7):1036-1042. Moore aS, nelson rW, Henry cJ, et al. Streptozocin for treatment of pancreatic islet cell tumors in dogs: 17 cases (1989-1999). JAVMA 2002; 221(6):811-818. northrup nc, rassnick KM, gieger tl, et al. Prospective evaluation of biweekly streptozotocin in 19 dogs with insulinoma. J Vet Intern Med 2013; 27(3):483-490. Fjallskog MlH, lejonklou MH, Oberg KE, et al. Expression of molecular targets for tyrosine kinase receptor antagonists in malignant endocrine pancreatic tumors. Clin Canc Res 2003; 9:14691473. Papaetis gS, Syrigos Kn. Sunitinib: a multitargeted receptor tyrosine kinase inhibitor in the era of molecular cancer therapies. BioDrugs 2009; 23(6):377-389. tjostheim SS, Stepien rl, Markovic lE, et al. Effects of toceranib phosphate on systolic blood pressure and proteinuria in dogs. J Vet Intern Med 2016 [epub ahead of print]. Dunn JK, Bostock DE, Herrtage ME, et al. insulin-secreting tumours of the canine pancreas: clinical and pathological features of 11 cases. J Sm Anim Prac 1993; 34:325-331.

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Summer 2001. 238-246. 2Based on dollar and unit sales of Purina® Pro Plan® Veterinary Diets DM Dietetic Management formulas as a percentage of total diabetes therapeutic diet sales as reported by GfK Retail and Technology US LLC, Vet Panel Market Database, 52 w/e 8/13/16.

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PRACTICE BUILDING

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Are Exotics a Fit for Me?

Part 2: Day-to-Day Logistics of Exotics PracticE Angela M. Lennox, DVM, Diplomate ABVP (Avian & Exotic Companion Mammal) & ECZM (Small Mammal) Avian and Exotic Animal Clinic, Indianapolis, Indiana To see (exotics) or not to see… that is a very good question. The quality of exotic pet medicine has increased dramatically over the last decade, which is illustrated by the appearance of board-certified specialists for exotic animals and increasing numbers of high-quality articles in the peerreviewed veterinary literature. However, the decision whether to incorporate exotic pets into a practice should be made carefully. The first part of this article (Development of the Exotics Practice, July/August 2016) discussed: • Whether to add exotics medicine to your practice • Training existing staff • Acquisition of equipment and resources • Developing relationships with mentors and experts. This article discusses the day-to-day logistics of operating an exotic pet practice. LEGALITIES OF EXOTIC PET OWNERSHIP Exotic pet ownership regulations vary from state to state, and certain municipalities may also have laws regarding such ownership. Practitioners must have a working knowledge of how the law affects each species. Keeping up-to-date on certain legal aspects is particularly difficult as laws frequently change, and often without warning. For example, ferrets are illegal to own as pets in certain states and, in some areas, ownership of native wildlife, such as raccoons, is prohibited. In Indiana (my state), laws regarding ownership of wildlife have changed dramatically, with permits required then not required then required again. There are also laws regarding vaccination of exotic pets (ie, most states require annual

rabies vaccination of pet ferrets). The American Veterinary Medical Association website provides a regularly updated, state-by-state list of laws regarding rabies vaccination that includes, in particular, information on such animals as ferrets: avma.org/Advocacy/StateAndLocal/Pages/ rabies-vaccination.aspx. Liability insurance policies may not cover claims involving illegally owned animals. Each practice should check with their liability insurance carrier for clarification.

Learn More Read are Exotics a fit for Me? Part 1: Development of the Exotics Practice (July/August 2016) at tvpjournal.com.

ONGOING TRAINING & EDUCATION Suggestions for acquiring basic skills for exotic pet handling and medical care—for both practitioners and the veterinary team—were provided in Part 1. Regular continuing education is important, as well as in-house training. For instance, in my clinic, the veterinary team receives 2 to 3 hours of mandatory training once weekly.

Exotic terminology The term exotic pets traditionally refers to any pet that is not a dog, cat, or

large farm animal, such as pet goats and chickens, parrots, reptiles, rabbits, and rodents. Some practices elect to add exotic companion mammals first, as mammal medicine is generally more familiar than avian and reptile medicine.

Exotic Pet Laws

The website bornfreeusa.org provides helpful information on laws governing ownership of exotic animals, including: • Color-coded U.S. map of state laws governing private possession of exotic animals • Summary of laws relating to the keeping of wild and exotic animals as pets • Partial summary of which cities and counties have prohibited the keeping of these animals. Visit bornfreeusa.org/b4a2_exotic_animals.php to access this information.

tvpjournal.com | November/December 2016 | An Official Journal of the NAVC | TODAy’s VeTeriNAry PrACTiCe

Peer Reviewed

PRACTICE BUILDING

It is important that team members who work in reception also receive this education and training. Reception staff need to develop the skills that help them identify emergencies on the phone and also allow intelligent communication with exotic pet owners. Some signs described by owners are often indications of severe disease in certain exotics. For example, clients with anorexic rabbits should be encouraged to come in immediately, whereas a snake that is anorexic but otherwise appears normal may not require immediate emergency intervention. Because of these discrepancies, in some mixed practices, queries regarding exotic pets are only handled by designated support staff with special training. THE RECEPTION AREA A practice that exclusively cares for exotic animals does not need to worry about dogs barking or straining against leashes. In these practices, it should be a requirement that all pets, regardless of size, enter the clinic in a secure carrier, no matter their demeanor or the pet ownerâ&#x20AC;&#x2122;s preferences. This prevents injuries to pets and owners while in the waiting room. For clinics that see both exotic and traditional pet species, a separate entrance or waiting area for exotic pets is ideal to prevent stress, especially for prey species, such as rabbits. Another option is to escort the exotic pet owner and pet directly into a designated (and quiet) examination room. SCHEDULING APPOINTMENTS Many exotic pets have complicated husbandry needs, which necessitates more time for the initial examination. For this reason, appointments for exotic pets are often lengthier. In my clinic, the average wellness examination for a new bird is scheduled for 1 hour. In addition to the discussion of care and feeding, practitioners who are new to exotic pets need more time to research disease conditions and treatment options. Because of the wide variety of husbandry requirements and the overwhelming information (and misinformation) from various sources, it is often useful to ask owners to bring a picture of their housing set-up as well as all foods offered to the pet (in the original packaging). Reptile owners should also be asked to bring in any supplements offered and UV bulbs, which can be tested with a meter to confirm that adequate UV light for the species in question is being produced. 68

BASIC SERVICES Wellness Examination Practices serving exotic pets should be capable of offering wellness examinations, which require a thorough understanding of the most up-to-date diet, husbandry, and enrichment recommendations for each species. To complicate matters, recommendations change as new research and information emerge. Vaccination Certain exotic species can be vaccinated. As mentioned earlier, rabies vaccination of a ferret is required in most states. Currently there is only a single product licensed for use in ferrets. It is important to note that it is not appropriate to substitute another product when a licensed product for the species in question is readily available. Use of unapproved rabies vaccines in ferrets may not protect those patients from rabies testing and euthanasia in cases of human bite exposure. Vaccines are recommended for a number of other species as well, including exotic pet carnivores, such as foxes and raccoons, as well as miniature pigs. Vaccines are also available for pet birds, but these have limited application. Practitioners must understand and be able to explain the risks and benefits of each vaccine for each patient. Gonadectomy Basic services can also include elective neutering for certain exotic species. For some, gonadectomy is an important preventive health measure (eg, spaying female rabbits to prevent uterine neoplasia). Neutering may also be selected to improve pet behavior or prevent reproduction. It is important to understand the indications for spay/ castration in each exotic species in order to help clients make informed decisions for each pet. Euthanasia Practitoners must be aware of current standards for euthanasia of exotic pets, which require modifications of techniques typically used in traditional pet practice. The 2013 edition of the AVMA Guidelines for the Euthanasia of Animals (avma.org/KB/Policies/Documents/euthanasia. pdf) contains a wealth of information for avian, exotic mammal, and reptile species and also includes information on fish and handling of viable eggs.

Todayâ&#x20AC;&#x2122;s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

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ADVANCED SERVICES Practices that accept exotic patients must be able to provide advanced medical and surgical care or have the ability to refer patients to a specialist or a colleague with more experience. This care includes diagnostic testing, diagnostic imaging, and surgical services. Of these, imaging and surgery often require referral to a clinician and facility that can provide this specialized care. Laboratory Analysis Many large veterinary reference laboratories accept exotic animal samples. However, the ability to handle certain important tests, such as evaluation of a complete blood count, requires experience and training. Before choosing a reference laboratory, be certain the laboratory has significant experience with exotic animal samples. A few private and university-based reference laboratories have an exotics focus, while a number of specific pathogen tests are only offered by limited facilities. While it may be more economical to send samples directly to these laboratories rather than through a larger reference laboratory, the larger laboratories, such as Antech Diagnostics (antechdiagnostics.com) and IDEXX (idexx.com), can direct samples to the appropriate laboratory quickly and easily. Diagnostic Equipment The size of the patient often severely limits diagnostic capabilities. Many exotics practitioners rely on in-house biochemistry analyzers capable of producing results from a very small but highquality whole blood sample. The Abaxis VetScan (abaxis.com) offers a biochemistry panel that can be run on as little as 0.13-mL whole blood, which makes analysis feasible even in small rodents, birds, and lizards. SETTING FEES In principle, fees for services for any exotic animal should be similar to those for traditional pet species.

angELa M. LEnnox

Angela M. Lennox, DVM, Diplomate ABVP (Avian & Exotic Companion Mammal) & ECZM (Small Mammal), owns Avian and Exotic Animal Clinic in Indianapolis, Indiana, and is an adjunct professor at Purdue University College of Veterinary Medicine. She has exclusively practiced exotic animal medicine since 1991 and is a past president of the Association of Exotic Mammal Veterinarians. Dr. Lennox lectures extensively throughout the U.S. and internationally, and has authored and edited many books, book chapters, and scientific articles. She received her DVM from Purdue University.

There is a temptation to reduce fees for exotic pets based on the incorrect perception that some pets are less valuable than a dog or cat and, in some cases, fees are reduced because the clinician feels less competent in evaluating exotic pets. In actuality, veterinarians often spend more time during exotic pet consultations than during those for dogs and cats. This may be because of husbandry needs that are often unfamiliar and complex and, in many cases, clinicians further invest in the patient by searching the literature and exotic animal databases for information on diagnostic and treatment options. In some cases, significant effort and resources are spent on continuing education and specialized equipment. For these reasons, some advocate that exotic pet examination fees should actually be higher than those for traditional pet species. AFTER HOURS & EMERGENCY CARE Any practice that accepts exotic pets needs a plan for clients who experience after-hours emergencies. If local emergency clinics will not evaluate exotic patients, then the regular practice must be willing to do so, or have an arrangement with another clinic that will. My clinic’s on-call staff frequently receive calls from owners whose primary veterinarian is unavailable, and the practice’s after-hours message recommends referral to emergency clinics that do not accept exotic pets. This situation often causes anxiety and resentment. The great majority of clients who present to us for emergencies (especially postsurgical complications) elect not to return to the primary veterinarian. ADDING A BOARD-CERTIFIED SPECIALIST Practitioners wishing to offer the highest level of care for exotic patients should strongly consider either adding a board-certified specialist to the practice or becoming one. Boarded specialists are listed on the American Board of Veterinary Practitioners (abvp.com) and American College of Zoological Medicine (aczm.org) websites. IN SUMMARY Exotic animal medicine and surgery are exciting and interesting components to any practice. The increasing demand for high quality of care provides incentive to take the time and effort to learn more about these special pets.

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

The Back Page: VeTeRINaRY VIeWPOINTS

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:

Continued from page 72 Signs of compassion fatigue include: Appearance of exhaustion (“worn out”) Cynicism about the job or relationships Less efficiency in normally easy tasks Questioning deeply held moral or existential beliefs. Without signs of acute risk or obvious fatigue, I would recommend paying attention to significant changes—a colleague is drinking more than usual, seems more withdrawn or purposeless than normal, or is acting more angry or irritable than you would expect. Another sign is recklessness—taking big risks and/or acting as if negative consequences are of little concern. • • • •

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.

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

What should a person do if they notice these signs in a colleague? The most important thing to do is ask your colleague the most difficult question: Have you been having thoughts of killing yourself? This is going to sound strange, but I would recommend practicing it. You can talk about this column with colleagues, family, or friends and ask each other the question in a completely innocuous, safe setting when you aren’t concerned about anyone’s risk. Yes, it will feel awkward, but you’re a professional, so you know how this works. If you practice asking someone in a relaxed environment with no risk, it will be much easier to verbalize this critical question when someone’s life is on the line. And you must ask it then. Rest assured, you cannot put the thought of suicide into someone’s mind if the person is not already thinking about it. It will most likely be a relief to a colleague that you noticed and cared enough to ask. Be prepared to set everything else aside and listen. If your colleague does disclose thoughts of self-harm, don’t leave them alone. You can even call the national suicide prevention hotline (1-800-2738255) together to figure out what to do next. If it’s depression without any suicide-related thoughts, you might recommend a few visits with a mental health provider to see if treatment is necessary. Please use the Resources below for more information.

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

Oral active control

N2 25 2 7 4 9

% (n=200) 12.5 1.0 3.5 2.0 4.5

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.

ResouRces Suicide Hotline: 1-800-273-TALK (8255) Websites: suicidepreventionlifeline.org, suicidology.org, afsp.org

tvpjournal.com | November/December 2016

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

NADA 141-406, Approved by FDA Marketed by: Frontline Vet Labs™, a Division of Merial, Inc. Duluth, GA 30096-4640 USA Made in Brazil. ®NexGard is a registered trademark, and TMFRONTLINE VET LABS is a trademark, of Merial. ©2015 Merial. All rights reserved. 1050-4493-03 Rev. 1/2015

The Back Page: VeTeRINaRY VIeWPOINTS

Suicide in the Veterinary Profession

an Interview with Dr. aaron Werbel Captain Aaron D. Werbel, PhD—Chief of Staff for Healthcare Operations, U.S. Navy Bureau of Medicine and Surgery—is a suicidologist and clinical psychologist. He leads a staff of 270 in policy development that guides 63,000 providers in their care of over 2.7 million beneficiaries. Captain Werbel has extensive experience with suicide: He was the chair (and founder) of the International Task Force on Defense and Police Force Suicide Prevention and chair of the Federal Executive Partners Working Group on Suicide Prevention. He is a member of the American Association of Suicidology (suicidology.org) and International Association for Suicide Prevention (iasp.info) and speaks frequently at both national and international conferences. In light of rising concerns regarding suicide risk in the veterinary profession, Today’s Veterinary Practice reached out to Dr. Werbel to discuss this distressing trend.

Read Dr. simon Platt’s editor’s Note, Life Without Hope, on page 6.

Attend The NAVC Conference Health & Wellness track, offering sessions, such as The Vet confessionals Project, The Dynamics of the struggle, and Finding the Path to Resiliency, on Wednesday, February 8, 2017.

Tell us about your background with regard to medical practitioners and their emotional well-being. I’ve been a suicidologist almost as long as I’ve been a practicing clinical psychologist—about 20 years. I have always been drawn to helping people in crisis, and there is no larger crisis in mental health care than when people feel that life is not worth living and they would be better off dying by suicide. As Chief of Staff for Navy Healthcare Operations, I pay close attention to provider well-being and work to ensure resilience through a program called Caregiver Operational Stress Control, which is designed to educate providers to identify and respond to compassion fatigue. What types of experiences lead medical practitioners, particularly veterinary personnel, to make the decision to end their lives? The high risk of suicide among veterinarians is a perfect storm of two factors—compassion fatigue and an acquired capability for self-harm— further compounded by the unique professional experiences of veterinarians. Compassion fatigue (also known as secondary traumatic stress) develops when a veterinarian is consistently exposed to the trauma of animals and their owners. While a veterinarian can speak directly to the owners, compassion fatigue is uniquely compounded by the inability to verbally process the relationship between surgeon and patient. The prolonged chronic empathy a veterinary practitioner experiences at work can lead not only to emotional and physical exhaustion, but also to cynicism,

questioning deeply held beliefs, and decreased efficiency in their work. The second factor that increases the risk for veterinarians is the acquired capability to kill oneself. People are hard-wired for survival, and many individuals who have suicide-related thoughts or even a “desire to die” may not have the ability to kill themselves. Suicide is actually a fairly herculean act that goes against our nature, but it becomes easier for clinicians—who see trauma and abuse daily and repeatedly incise patients during surgery. Not surprisingly, studies have found that suicides by overdose with medication (think of the easy availability) and cutting/piercing (acquired capability) are more common methods for physicians than the general population. While surgeons have higher suicide rates than other health professionals, the experience of euthanizing animals is a unique risk factor for veterinarians that further compounds the equation. What signs demonstrate that a colleague may be struggling with depression or thoughts of suicide? The most important signs of acute risk are also the most obvious: • Talking about wanting to die or threatening to harm oneself • Searching for ways to kill oneself, like buying a gun or collecting pills • Talking or writing more than usual, or in a concerning way, about death, dying, or suicide.

Continued on page 71

Today’s VeTerinary PracTice | an official Journal of the naVc | november/december 2016 | tvpjournal.com

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IMPORTANT SAFETY INFORMATION: NexGard is for use in dogs only. The most frequently reported adverse reactions included 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.