Today's Veterinary Practice, November 2017

IN THIS ISSUE 10 THE ROLE OF WOLBACHIA IN HEARTWORM DISEASE 46 CHRONIC VOMITING IN CATS 68 CANINE HOUSE SOILING

Diabetic Diets: Assessing the Evidence

NOVEMBER/DECEMBER 2017 VOLUME 7, NUMBER 6

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VOLUME 7, NUMBER 6

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

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

FEATURES 46 CE ARTICLE

Chronic Vomiting in Cats: When to Recommend Endoscopy Kyle Restle, DVM, and Jacqueline Whittemore, DVM, PhD, DACVIM This article provides an overview of common diseases and valuable diagnostic tests to differentiate among causes of chronic vomiting in cats. Additionally, it discusses when advanced diagnostic testing, such as endoscopy, is warranted.

60

FEATURE

Advances in Feline Cardiac Diagnostics Brent Aona, DVM, and Darcy Adin, DVM, DACVIM This article presents a patient with and a patient without clinical signs of heart disease to highlight the use of tailored diagnostics to diagnose cardiac disease in cats.

68

FEATURE

Canine House Soiling: Back to Basics Kelly C. Ballantyne, DVM, DACVB This article reviews steps to take to identify the causes of, diagnose, and treat canine house soiling.

28 ADVERTISER INDEX Today’s Veterinary Practice does not, by publication of ads, express endorsement or verify the accuracy and effectiveness of the products and claims contained therein. The publisher, Eastern States Veterinary Association, Inc (NAVC), disclaims any liability for any damages resulting from the use of any product advertised herein and suggests that readers fully investigate the products and claims prior to purchasing. The opinions stated in this publication are those of the respective authors and do not necessarily represent the opinions of the NAVC nor its Editorial Advisory Board. NAVC does not guarantee nor make any other representation that the material contained in articles herein is valid, reliable, or accurate; nor does the NAVC assume any responsibility for injury or death arising from any use, or misuse, of same. There is no implication that the material published herein represents the best or only procedure for a particular condition. It is the responsibility of the reader to verify the accuracy and applicability of any information presented and to adapt as new data becomes publicly available.

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TABLE OF CONTENTS

To read this issue online, visit tvpjournal.com

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EDITOR’S NOTE

BRIEF SUMMARY (For Full Prescribing Information, see package insert.)

Global Problems, Personal Fulfillment

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

DESCRIPTION: VETORYL Capsules are an orally active synthetic steroid analogue that blocks production of hormones produced in the adrenal cortex of dogs.

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

INDICATION: VETORYL Capsules are indicated for the treatment of pituitary- and adrenal-dependent hyperadrenocorticism in dogs.

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CONTRAINDICATIONS: The use of VETORYL Capsules is contraindicated in dogs that have demonstrated hypersensitivity to trilostane. Do not use VETORYL Capsules in animals with primary hepatic disease or renal insufficiency. Do not use in pregnant dogs. Studies conducted with trilostane in laboratory animals have shown teratogenic effects and early pregnancy loss.

FROM THE FIELD

Focus on Overweight and Obesity in Dogs Kirk Breuninger, VMD, MPH, DACVPM

WARNINGS: In case of overdosage, symptomatic treatment of hypoadrenocorticism with corticosteroids, mineralocorticoids and intravenous fluids may be required. Angiotensin converting enzyme (ACE) inhibitors should be used with caution with VETORYL Capsules, as both drugs have aldosterone-lowering effects which may be additive, impairing the patient’s ability to maintain normal electrolytes, blood volume and renal perfusion.

Potassium sparing diuretics (e.g. spironolactone) should not be used with VETORYL Capsules as both drugs have the potential to inhibit aldosterone, increasing the likelihood of hyperkalemia.

AHS HEARTWORM HOTLINE

10

Wolbachia and Heartworm: Why Doxycycline Is Needed in Heartworm Treatment Andy Moorhead, DVM, MS, PhD

HUMAN WARNINGS: Keep out of reach of children.

Not for human use. Wash hands after use. Do not empty capsule contents and do not attempt to divide the capsules. Do not handle the capsules if pregnant or if trying to conceive. Trilostane is associated with teratogenic effects and early pregnancy loss in laboratory animals. In the event of accidental ingestion/overdose, seek medical advice immediately and take the labeled container with you.

17

PRACTICAL TOXICOLOGY

Christmas Plants: Hazards, History, and Holiday Dangers

PRECAUTIONS: Hypoadrenocorticism can develop at any dose of VETORYL Capsules. A small percentage of dogs may develop corticosteroid withdrawal syndrome within 10 days of starting treatment. Mitotane (o,p’-DDD) treatment will reduce adrenal function. Experience in foreign markets suggests that when mitotane therapy is stopped, an interval of at least one month should elapse before the introduction of VETORYL Capsules. The use of VETORYL Capsules will not affect the adrenal tumor itself. Adrenalectomy should be considered as an option for cases that are good surgical candidates.

The safe use of this drug has not been evaluated in lactating dogs and males intended for breeding.

Charlotte Means, DVM, MLIS, DABVT, DABT

24

ACVN NUTRITION NOTES

Diabetic Diets for Dogs and Cats: Assessing the Evidence Deborah E. Linder, DVM, MS, DACVN

ADVERSE REACTIONS: The most common adverse reactions reported are poor/reduced appetite, vomiting, lethargy/dullness, diarrhea, elevated liver enzymes, elevated potassium with or without elevated sodium, elevated BUN, decreased Na/K ratio, weakness, elevated creatinine, shaking, and renal insufficiency. Occasionally, more serious reactions, including severe depression, hemorrhagic diarrhea, collapse, hypoadrenocortical crisis or adrenal necrosis/rupture may occur, and may result in death.

31 IMAGING ESSENTIALS

Ultrasonography of the Urinary Tract: Kidneys and Ureters Elizabeth Huynh, DVM, and Clifford R. Berry, DVM, DACVR

Distributed by: Dechra Veterinary Products 7015 College Boulevard, Suite 525 Overland Park, KS 66211 VETORYL is a trademark of Dechra Ltd. © 2015, Dechra Ltd. NADA 141-291, Approved by FDA

4

CONTENTS

To read this issue online, visit tvpjournal.com

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

EDITOR’S NOTE

Global Problems, Personal Fulfillment “ An understanding of the natural world and what’s in it is a source of not only a great curiosity but great fulfillment.”

— Sir David Attenborough

In September 2017, The World Small Animal Veterinary Association (WSAVA) gathered veterinarians from around the globe to attend a meeting in Copenhagen, Denmark, which included an educational bonanza with sessions dedicated to every aspect of our diverse profession. During the meeting, the 11th World Rabies Day was observed.

One of the WSAVA Foundation’s key projects is the African Small Companion Animal Network (AFSCAN) initiative, which is supporting the development of the veterinary profession across Africa and playing a key role in the fight against rabies on the continent, together with partners such as Worldwide Veterinary Services (WVS) and Mission Rabies. Founded in 2013, Mission Rabies is a charity dedicated to eradicating rabies by 2030 through international vaccination programs. Four years after starting its work in India, this volunteer group is working in 5 different countries, trying to defeat the disease with a combination of vaccination programs, education, technology, research, and a lot of effort. A huge variety of placements are available, with options for volunteers ranging from qualified veterinarians and veterinary nurses to students to people with no prior veterinary experience. Traveling to one of the countries as a volunteer may not suit you for a number of reasons, but there are other ways to get involved.a The globalization of veterinary medicine, including WSAVA’s involvement in the fight against rabies, raises awareness of what veterinarians are doing, and can do, to improve our world. a

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For further information, visit missionrabies.com.

EDITOR’S NOTE

As a profession, most of us find personal fulfillment in giving back—for example, presenting solutions to international crises, such as rabies—even though many of us may not receive comparable financial compensation based on the skills and time that we provide. However, using our skills helps us appreciate the global impact that we can achieve and helps us realize that we are all individually important, regardless of what a certain day may bring or what a difficult owner may say.

As individuals, when we search for inspiration and fulfillment in this profession, we need look no further than the movement to eliminate rabies from this planet.

Global freedom from the threat of dog-mediated rabies is feasible within our lifetime. With the tools, vaccine, and evidence available, veterinarians can be at the forefront of minimizing that threat. What more inspiration do we need than knowing we have the ability to eradicate nearly half of the worldwide human rabies fatalities among children? The financial burden of human treatment far outweighs the costs of mass dog vaccination, which serves to protect whole communities. Studies have shown that culling is an ineffective means of elimination and mass vaccination is most efficacious to reduce rabies incidence. As an example, the Bangladesh canine rabies elimination program focuses on mass dog vaccination to reduce the incidence of human deaths. Since 2011, dog vaccination programs in Bangladesh have resulted in a 50% decrease in human rabies fatalities.1 Let’s aim to make this profession work for us rather than letting it control us. Getting involved in global initiatives to eradicate rabies at any level is using our profession to help the world become a safer place to live in while helping us achieve a sense of personal fulfillment.

Reference 1. Wallace RM, Undurraga EA, Blanton JD, et al. Elimination of dogmediated human rabies deaths by 2030: needs assessment and alternatives for progress based on dog vaccination. Front Vet Sci 2017;4:9.

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References: 1. Levy SA. 2002. “Use of a C6 ELISA test to evaluate the efficacy of a whole-cell bacterin for the prevention of naturally transmitted canine Borrelia burgdorferi infection.”

Vet Ther. 3(4):420–424. 2. Chu H., Chavez L. et al. 1992. “Immunogenicity and efficacy study of a commercial Borrelia burgdorferi bacterin.” J Am Vet Med Assoc. 201(3):403–411 3. Levy S., Lissman B. et al. 1993. “Performance of a Borrelia burgdorferi bacterin in borreliosis-endemic areas.” J Am Vet Med Assoc. 202(11):1834–1838. 4. Levy S., Millership J. et al. 2010.

“Confirmation of presence of Borrelia burgdorferi outer surface protein C antigen and production of antibodies to Borrelia burgdorferi outer surface protein C in dogs vaccinated with a whole-cell Borrelia burgdorferi bacterin.” Intern J Appl Res Vet Med. 8(3):123–128.

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FROM THE FIELD

FROM THE FIELD

Focus on Overweight and Obesity in Dogs Kirk Breuninger, VMD, MPH, DACVPM Banfield Pet Hospital Vancouver, Washington

From the Field shares insights from Banfield Pet Hospital veterinary team members. Drawing from the nationwide practice’s extensive research, as well as findings from its electronic veterinary medical records database and more than 8 million annual pet visits, this column is intended to explore topics and spark conversations relevant to veterinary practices that ultimately help create a better world for pets.

shutterstock.com/Dmitri Ma

Banfield Pet Hospital recently released its 2017 State of Pet Health Report, highlighting a widespread trend of overweight pets nationwide. This is the largest report of its kind, capturing medical data from more than 2.5 million dogs cared for by Banfield in 2016.

According to this year’s report, 1 in 3 pets that visited a Banfield hospital last year was diagnosed as overweight or obese—and in the past 10 years, Banfield witnessed a 158% increase in overweight dogs.

WA 34

MT

ME

ND

27

34

MN

ID

38

22

NV 36

CA

IL

33

CO

34

33

29

KS

AZ 29

OK 31

NM 34

High Risk Medium Risk Low Risk No Banfield Hospital States with Highest Prevalence

TX 29

27

WV

KY

DC 22

26

TN 30

MD 28

SC

20

17

AL 21

GA

31

26

21

FL

PR

17

32

• Give treats in moderation. Advise clients to take note of how many treats they give their dog per day.

• Treats should not make up more than 10% of a dog’s daily caloric consumption.

• Clients can offer rewards other than food, such as belly rubs or playing with a favorite toy.

• If food is given as a reward, clients can substitute low-calorie snacks such as baby carrots for high-calorie treats.

For more client education tools, as well as a host of other resources, visit stateofpethealth.com.

FIGURE 1. 2016 overweight prevalence in dogs.

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• Prevention is key. Remind owners that regular check-ups and nutritional counseling can help keep their dogs at a healthy weight.

29

32

NC

AR

LA

DE

VA

25

MS

Risk Level

NJ

30

34

30

23

31

OH

IN

MO

32

RI

22

CT

PA

32

39

UT

38

IA

NE

28

MI

29 32

NY

WI

SD WY

NH MA

VT

41

Here are some tips and tricks for talking with your clients about their dog’s weight:

• Show, don’t tell. Educate your clients about body condition scoring, and show them how their pet ranks.

Obesity Cats

OR

The top 5 states with the highest prevalence of overweight dogs were Minnesota (41%), Nebraska (39%), Michigan (38%), Idaho (38%), and Nevada (36%). Indiana, New Mexico, Oregon, Utah, and Washington tied for fifth place at 34%. The prevalence estimates for each state are shown in Figure 1. How did your state do?

FROM THE FIELD

HEARTWORM HOTLINE

AHS HEARTWORM HOTLINE

Wolbachia and Heartworm: Why Doxycycline Is Needed in Heartworm Treatment Andy Moorhead, DVM, MS, PhD University of Georgia College of Veterinary Medicine shutterstock.com/otsphoto

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

The treatment of adult heartworm (Dirofilaria immitis) infection in dogs has changed significantly since the days when veterinarians’ only option was injectable thiacetarsamide sodium. First, the introduction of melarsomine dihydrochloride in the mid-1990s revolutionized the treatment of adult heartworm infection by providing superior efficacy via intramuscular administration.1 The next great leap forward in heartworm treatment came with the discovery that some filarial worms harbor a type of bacteria, Wolbachia, and that elimination of these bacteria proved beneficial to the animal and reduced the complications of disease.2

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AHS HEARTWORM HOTLINE

This article explains why Wolbachia are important in the pathogenesis of heartworm disease and why eliminating them through the use of doxycycline is so important to the treatment of the heartworm-infected animal.

WHAT ARE WOLBACHIA AND WHY ARE THEY IMPORTANT TO THE HEARTWORM? Wolbachia bacteria are related to Rickettsia, which are intracellular bacterial parasites that live within certain invertebrates, including some flies and nematodes.3 Wolbachia are bacterial symbionts. As endosymbionts, Wolbachia bacteria require the host organism, the heartworm, to survive; equally, the heartworm requires Wolbachia for its survival.4 The exact function of Wolbachia in heartworms is unknown.5 It has been hypothesized that the presence of these bacteria may aid in energy metabolism.6 Populations of Wolbachia, which are present in all heartworm life stages, expand between the third-stage infectious larvae (L3) and fourthstage larvae (L4). For this reason, it is hypothesized that preventing the expansion of the Wolbachia population will prevent heartworm development.7

HEARTWORM HOTLINE

Wolbachia possess surface proteins (WSPs)8 that are responsible in part for the pathogenesis of heartworm disease. When adult heartworms die naturally or as a result of melarsomine administration, the bacteria and their components, including WSPs, are released.

The WSPs recruit neutrophils and other immune cells; as these cells are recruited on the microscopic level in the blood vessels, partial blockage of vessels can result, which can impede blood flow. Furthermore, inflammation of the dog’s lungs can manifest in clinical signs, such as coughing and dyspnea.2,9 Although we do not understand the complete role of Wolbachia in the pathogenesis of heartworm disease, experimental and clinical trials have shown that elimination of the bacteria using doxycycline decreases both macroscopic and microscopic pathology, as well as clinical signs.2,7,10

WHY IS DOXYCYCLINE IMPORTANT IN HEARTWORM TREATMENT? The American Heartworm Society (AHS) recommends that doxycycline be incorporated into an adulticidal treatment regimen11 to eliminate Wolbachia.

Elimination of Wolbachia has 2 clinical benefits: (1) reducing the WSPs released into the bloodstream, thus decreasing inflammation in the canine host; and (2) reducing worm mass, thereby decreasing the severity of pulmonary thromboembolisms (PTEs) associated with adulticidal treatments.2

Doxycycline not only has effects on adult worms but also decreases numbers of microfilariae and prevents development of heartworm in subsequently infected dogs.

• Decrease in microfilariae • In microfilaremic heartworm-infected dogs administered doxycycline for 30 days at a dose of 10 mg/kg q12h, microfilariae levels slowly declined by 12 to 13 months after administration of doxycycline. In McCall et al,7 elimination of microfilariae was noted in 9 weeks with an increased amount of doxycycline (10 mg/kg q24 h for weeks 1 to 6 and then weeks 10 to 11, 16 to 17, 22 to 25, and 28 to 33).

• Prevention of adult heartworm development in subsequently infected dogs13

• Microfilaremic heartworm-positive dogs were administered doxycycline for 30 days at a dose of 10 mg/kg q12h. At different time points, including 161 days after doxycycline administration, microfilaremic blood was fed to laboratory-reared mosquitoes.

• Sixteen days after feeding, infective L3s were harvested from the mosquitoes and dogs were experimentally infected.

• When the dogs were necropsied at least 7 months after infection, no adults were found in the experimental animals.

The AHS recommendation is based on findings from important clinical studies:

• McCall et al7 demonstrated that in animals

administered prophylactic doses of ivermectin and doxycycline before melarsomine treatment, there were fewer inflammatory infiltrates in the lungs and a lower possibility of development of PTEs (Figure 1). The dose used in this study was 10 mg/kg q24h for an extended period (weeks 1 to 6, 10 to 11, 16 to 17, 22 to 25, and 28 to 33) before melarsomine treatment.

• Kramer et al12 administered doxycycline to dogs

at 20 mg/kg q24h for 30 days, with or without a prophylactic dose of ivermectin. Two months after the end of the doxycycline regimen, animals were administered melarsomine using the standard 3-dose protocol.

In this study, the groups receiving doxycycline had almost no thrombi in their lungs when compared with melarsomine-only controls. This study further supports the use of doxycycline for reducing the pathology associated with Wolbachia released from dying heartworms.

FIGURE 1. Pulmonary pathologic features associated with the death of heartworms in experimentally infected heartworm-positive dogs pretreated with ivermectin and doxycycline before receiving melarsomine injections.

The top two panels are pictures of representative lungs obtained during necropsy. The bottom panels are photomicrographs of hematoxylin-eosin–stained lung sections. Photographs courtesy of John McCall, PhD, and Laura Kramer, DVM, PhD.

NOVEMBER/DECEMBER 2017

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TVPJOURNAL.COM

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HEARTWORM HOTLINE

It is hypothesized that doxycycline had eliminated Wolbachia from microfilariae. Therefore, Wolbachia expansion after the L3 to L4 molt could not occur and heartworms could not fully develop. In essence, the use of doxycycline in heartworm-infected dogs prevented heartworm infection in subsequent animals.

The fact that doxycycline can essentially prevent heartworm transmission makes its use mandatory when macrocyclic lactone resistance is suspected.

HOW SHOULD PRACTITIONERS TIME DOXYCYCLINE ADMINISTRATION? Under the current AHS guidelines (Table 1), a 4-week dose regimen of oral doxycycline should be initiated immediately after diagnosis and concurrent with the first dose of a macrocyclic lactone heartworm

preventive. A second dose of heartworm preventive is given at the end of the doxycycline regimen.11 A month later, the first dose of melarsomine is administered.

However, if there are extenuating circumstances, melarsomine may be administered immediately after the last dose of doxycycline instead of waiting an extra month because at least some of the Wolbachia population will be eliminated by this time.

It is unknown whether the extra month between the end of the last doxycycline dose and the beginning of melarsomine is necessary for the observed reduction in lung pathology associated with Wolbachia elimination. In Kramer et al,2 a lack of arterial lesions was demonstrated after waiting for 2 months after the completion of a 30-day doxycycline regimen. On the basis of this

TABLE 1 American Heartworm Society Treatment Protocol for Dogs DAY

TREATMENT Dog diagnosed and verified as heartworm positive: • Positive antigen (Ag) test verified with microfilaria (MF) test • If no microfilariae are detected, confirm with 2nd Ag test from a different manufacturer

Day 0

Begin exercise restriction.

• The more pronounced the signs, the stricter the exercise restriction If the dog is symptomatic: • Stabilize with appropriate therapy and nursing care • Prednisone prescribed at 0.5 mg/kg BID 1st week, 0.5 mg/kg SID 2nd week, 0.5 mg/kg EOD 3rd and 4th weeks

Day 1

Administer heartworm preventive.

• If microfilariae are detected, pretreat with antihistamine and glucocorticosteroid, if not already on prednisone, to reduce risk of anaphylaxis • O bserve for at least 8 hours for signs of reaction

Days 1–28

Administer doxycycline 10 mg/kg BID for 4 weeks.

• Reduces pathology associated with dead heartworms • Disrupts heartworm transmission

Day 30

Administer heartworm preventive.

Day 60

Administer heartworm preventive.

First melarsomine injection 2.5 mg/kg intramuscularly (IM) Prescribe prednisone 0.5 mg/kg BID 1st week, 0.5 mg/kg SID 2nd week, 0.5 mg/kg EOD 3rd and 4th weeks.

Decrease activity level even further.

• C age restriction/on leash when using yard

Day 90

Administer heartworm preventive.

Second melarsomine injection 2.5 mg/kg IM

Day 91

Third melarsomine injection 2.5 mg/kg IM Prescribe prednisone 0.5 mg/kg BID 1st week, 0.5 mg/kg SID 2nd week, 0.5 mg/kg EOD 3rd and 4th weeks.

Continue exercise restriction for 6 to 8 weeks following last melarsomine injections.

Day 120

Test for presence of microfilariae.

• If positive treat with a microfilaricide and retest in 4 weeks Establish year-round heartworm prevention.

Day 271

Antigen test 6 months after completion; screen for microfilariae.

BID, twice daily; EOD, every other day; SID, once daily. Reprinted by permission from the American Heartworm Society.

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AHS HEARTWORM HOTLINE

HEARTWORM HOTLINE

study, the following questions should be asked:

• Are the Wolbachia completely eliminated after 1

month of doxycycline, or is further time needed?

• Even if Wolbachia are killed during this 1-month time period, have the WSPs, a cause of host inflammation, been completely eliminated?

• Are the clinical benefits of doxycycline dependent on the amount of time (ie, 0, 1, or 2 months) between the end of the doxycycline regimen and the first melarsomine injection?

Further research is needed to answer these questions and to determine whether different doxycycline protocols are effective.

CAN DOXYCYCLINE BE USED IN ALTERNATIVE TREATMENT REGIMENS? The AHS does not recommend the use of multiple doses of macrocyclic lactone heartworm preventives for adulticidal treatment of heartworm infection.11 Nonetheless, in clinical situations where treatment with melarsomine is not feasible, doxycycline and macrocyclic lactones have been used as an alternative treatment. Only studies combining prophylactic doses of ivermectin or topical moxidectin with doxycycline have been reported in the literature.

• In naturally infected dogs, administration of ivermectin (6 mcg/kg q15d for 180 days) plus doxycycline (10 mg/kg q24h) resulted in 8 of 11 (72.7%) dogs becoming antigen negative after 300 days.10

• In an experimental study using 16 dogs (8 treated and 8 controls) that received transplanted adult heartworms, the treated dogs received topical moxidectin (2.5%) plus imidacloprid (10%) for 10 months. Doxycycline (10 mg/kg q12h) was administered concurrently during the first month of moxidectin/imidacloprid treatment.

At the end of the study, dogs were necropsied.

An average of 10.6 heartworms were found in control dogs compared with 0.6 heartworms in experimental dogs. Furthermore, 5 of the 8 experimental dogs had no heartworms.14

Although these regimens have shown some efficacy, the AHS recommends melarsomine in heartworm treatment except when melarsomine administration is not feasible.

These alternative treatment studies do, however, reinforce that doxycycline is extremely important in the treatment of adult heartworm infection.

Andy Moorhead Andy Moorhead, DVM, MS, PhD, is an associate research scientist in the Department of Infectious Diseases at the University of Georgia College of Veterinary Medicine and the director of the Filariasis Research Reagent Resource Center. He received his DVM from North Carolina State University, his MS from Purdue University, and his PhD from Columbia University. His research interests include the potential development of macrocylic lactone resistance in Dirofilaria immitis.

CONCLUSIONS AND LINGERING QUESTIONS Several important questions remain regarding the use of doxycycline in heartworm treatment:

• Is minocycline a viable alternative to doxycycline (Box 1)?

• Is a full month of doxycycline needed for it to

have an effect during heartworm treatment? In other words, what is the minimum dose needed for elimination of Wolbachia from heartworms?

BOX 1. Minocycline Versus Doxycycline in Heartworm Treatment Anecdotally, minocycline has been used in the place of doxycycline for treatment of heartworm, typically at the standard dose of 10 mg/kg q12h for 30 days. Although no formal studies have been published on the effect of minocycline on heartworm, efficacy has been demonstrated in vitro against a related filarial parasite.15 Recent modeling work also suggests that minocycline will be effective as a substitute for doxycycline in the AHS treatment protocol.

Papich16 used pharmacokinetic/ pharmacodynamic analysis to determine potentially effective doses of minocycline for use in heartworm treatment. Results of this analysis suggest that a q12h dose of 5 mg/kg minocycline in dogs will have an effect on Wolbachia in heartworms.

Furthermore, minocycline is more lipophilic and binds less easily to proteins, suggesting that it could have superior tissue penetration compared with doxycycline.

More research is needed, but the hope is that minocycline can be used for heartworm treatment when doxycycline use is not possible for cost or availability reasons.

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HEARTWORM HOTLINE

Chewable Tablets

• Would a different regimen of doxycycline be more effective in the adulticidal regimen?

Brief Summary: Please consult full package insert for more information.

INDICATIONS: Tri-Heart® Plus chewable tablets are indicated for use in prevention of canine heartworm caused by Dirofilaria immitis and for the treatment and control of ascarids (Toxocara canis, Toxascaris leonina) and hookworms (Ancylostoma caninum, Uncinaria stenocephala, Ancylostoma braziliense) in dogs and in puppies 6 weeks of age and older.

PRECAUTIONS: All dogs should be tested for existing heartworm infection before starting treatment with Tri-Heart® Plus chewable tablets. A mild hypersensitivity-type reaction, presumably due to dead or dying microfilariae and particularly involving a transient diarrhea has been observed in clinical trials with ivermectin alone after treatment of some dogs that have circulating microfilariae.

Keep this and all drugs out of the reach of children. In case of ingestion by humans, clients should be advised to contact a physician immediately.

Physicians may contact a Poison Control Center for advice concerning cases of ingestion by humans.

ADVERSE REACTIONS: The following adverse reactions have been reported following the use of ivermectin at the recommended dose: depression/ lethargy, vomiting, anorexia, diarrhea, mydriasis, ataxia, staggering, convulsions and hypersalivation.

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

HOW SUPPLIED: Tri-Heart® Plus chewable tablets are available in three dosage strengths for dogs of different weights. Each strength comes in convenient packs of 6 chewable tablets.

Store at controlled room temperature of 59-86˚ F (15-30˚ C). Protect product from light.

• Does a regimen of doxycycline increase the efficacy of melarsomine administration?

Answering these questions will advance our knowledge of the practical applications of doxycycline in the heartworm treatment protocol. Even without these answers, we know that Wolbachia are a significant contributor to pathology in dogs infected with heartworm. Because doxycycline can eliminate Wolbachia and reduce inflammation and PTEs, it should be used whenever possible in the treatment of heartworm-infected animals. Don’t let a heartworm-positive dog leave the clinic without it.

References 1.

McTier TL, McCall JW, Dzimianski MT, et al. Use of melarsomine dihydrochloride (RM 340) for adulticidal treatment of dogs with naturally acquired infections of Dirofilaria immitis and for clinical prophylaxis during reexposure for 1 year. Vet Parasitol 1994;55(3):221-233.

2. Kramer L, Grandi G, Leoni M, et al. Wolbachia and its influence on the pathology and immunology of Dirofilaria immitis infection. Vet Parasitol 2008;158(3):191-195.

3. Bandi C, Anderson TJ, Genchi C, et al. Phylogeny of Wolbachia in filarial nematodes. Proc Biol Sci 1998;265(1413):2407-2413.

4. Bandi C, Trees AJ, Brattig NW. Wolbachia in filarial nematodes: evolutionary aspects and implications for the pathogenesis and treatment of filarial diseases. Vet Parasitol 2001;98(1-3):215-238.

5. Kozek WJ. What is new in the Wolbachia/Dirofilaria interaction? Vet Parasitol 2005;133(2-3):127-132.

6. Voronin D, Bachu S, Shlossman M, et al. Glucose and glycogen metabolism in Brugia malayi is associated with Wolbachia symbiont fitness. PLoS One 2016;11(4):e0153812.

7. McCall JW, Genchi C, Kramer L, et al. Heartworm and Wolbachia: therapeutic implications. Vet Parasitol 2008;158(3):204-214.

8. Kramer LH, Tamarozzi F, Morchon R, et al. Immune response to and tissue localization of the Wolbachia surface protein (WSP) in dogs with natural heartworm (Dirofilaria immitis) infection. Vet Immunol Immunopathol 2005;106(3-4):303-308.

9. Kramer L, Simon F, Tamarozzi F, et al. Is Wolbachia complicating the pathological effects of Dirofilaria immitis infections? Vet Parasitol 2005;133(23):133-136.

10. Grandi G, Quintavalla C, Mavropoulou A, et al. A combination of doxycycline and ivermectin is adulticidal in dogs with naturally acquired heartworm disease (Dirofilaria immitis). Vet Parasitol 2010;169(3-4):347-351.

11. American Heartworm Society. Current canine guidelines for the diagnosis, prevention, and management of heartworm (Dirofilaria immitis) infection in dogs. 2014. heartwormsociety.org/veterinary-resources/american-heartwormsociety-guidelines. Accessed May 2017.

For Technical Assistance, call Merck Animal Health: 1-800-224-5318

12. Kramer L, Grandi G, Passeri B, et al. Evaluation of lung pathology in Dirofilaria immitis-experimentally infected dogs treated with doxycycline or a combination of doxycycline and ivermectin before administration of melarsomine dihydrochloride. Vet Parasitol 2011;176(4):357-360.

Manufactured for: Intervet Inc. a subsidiary of Merck & Co. Inc., Summit, NJ 07901 Manufactured by: Diamond Animal Health, Inc., a wholly owned subsidiary of Heska Corporation, Des Moines, IA 50327

13. McCall JW, Kramer L, Genchi C, et al. Effects of doxycycline on heartworm embryogenesis, transmission, circulating microfilaria, and adult worms in microfilaremic dogs. Vet Parasitol 2014;206(1-2):5-13.

2016 Heska Corporation. ©2013 All rights reserved.

14. Savadelis MD, Ohmes CM, Hostetler JA, et al. Assessment of parasitological findings in heartworm-infected beagles treated with Advantage Multi(R) for dogs (10% imidacloprid + 2.5% moxidectin) and doxycycline. Parasites Vectors 2017;10(1):245.

02260-1 ANADA 200-338, Approved by FDA

15. Townson S, Tagboto S, McGarry HF, et al. Onchocerca parasites and Wolbachia endosymbionts: evaluation of a spectrum of antibiotic types for activity against Onchocerca gutturosa in vitro. Filaria J 2006;5:4.

16. Papich MG. Considerations for using minocycline vs doxycycline for treatment of canine heartworm disease. Parasit Vectors [In press, 2017].

14

AHS HEARTWORM HOTLINE

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PRACTICAL TOXICOLOGY

PRACTICAL TOXICOLOGY

Christmas Plants: Hazards, History, and Holiday Dangers Charlotte Means, DVM, MLIS, DABVT, DABT ASPCA Animal Poison Control Center University of Illinois shutterstock.com/Chris Hill

Welcome to Practical Toxicology, brought to you in partnership between Today’s Veterinary Practice and the ASPCA Animal Poison Control Center (APCC) (aspcapro.org/poison). This column provides practical clinical information about diagnosing and treating pets that have been exposed to potentially harmful substances.

The APCC: •P rovides 24-hour diagnostic and treatment recommendations by specially trained veterinary toxicologists •P rotects and improves animal lives through toxicology education, consulting services, and case data review •D eveloped and maintains AnTox, an animal toxicology database system that identifies and characterizes toxic effects of substances in animals •W orks closely with human poison control centers to provide animal poisoning information •O ffers extensive veterinary toxicology consulting to organizations in industry, government, and agriculture.

If treating a patient that requires emergency care for poisoning, call the APCC at 888-426-4435.

The Christmas season is filled with wonderful scents, lights, and music. Homes are filled with family and friends. Plants and bouquets are frequently presented as gifts, and homes are decorated with more flowers and plants than at many other times of the year. Dogs and cats, being curious, are likely to investigate new plants.

Cats tend to nibble on them, while dogs are more likely to ingest the entire plant, including the soil, roots, or bulb. In all cases of plant ingestion, it is important to identify the ingested plant, ideally with the genus and species name.

When obtaining a medical history for a pet with clinical signs of toxicosis, also obtain a list of plants in the home or yard. If clinical signs fit a potential exposure to a known plant in the environment, the plant can be included in the rule-out list and appropriate therapy initiated. If clinical signs are not consistent with plant ingestion, the owner should be asked about other substances, such as insecticides and fertilizers, that might have been added to soil. Owners are not always aware whether a pet has ingested a leaf, eaten the dirt around the plant, or drunk from a pot reservoir.

Water in the reservoir of pots may contain the toxic principle of poisonous plants (like cardiac glycosides) or added substances (like insecticides).

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PEER REVIEWED

AMARYLLIS (AMARYLLIS OR HIPPEASTRUM SPECIES) Amaryllis is native to South America. It can be forced to bloom in winter, generally during the holiday season. The flowers come in a variety of colors, with red being popular for Christmas.

Like other members of the Amaryllidaceae family, amaryllis contains the phenanthradine alkaloids lycorine and tazetine. These alkaloids reach concentrations of up to 0.5% in the bulb and leaves. Lycorine is the toxic principle responsible for most of the clinical effects. Lycorine acts on neurokinin-1 receptors, with some effect on the 5-hydroxytryptamine receptors.

Many other alkaloids are present in the plant as well.

A lycorine study in dogs demonstrated that 0.5 to 2 mg/kg SC causes nausea and vomiting.2 At 2 mg/kg SC, 100% of dogs vomited. The gastrointestinal effects of lycorine in the study lasted 2.5 hours. However, the oral bioavailability of lycorine in dogs is only 40%.

Clinical signs would likely last longer when plant material is ingested and remains in the gastrointestinal tract.

For most pets, ingesting leaf material results only in mild gastrointestinal upset, with clinical signs that may include mild to moderate vomiting, diarrhea, anorexia, and hypersalivation. Ingestion of portions of the bulb may cause more intense clinical signs, such as restlessness, tremors, or dyspnea, while large or massive bulb ingestions could cause hypotension, seizures, and sedation.

Most cases of vomiting are managed at home by withholding food and water for several hours; additional treatment is rarely required. Moderate to severe vomiting can be managed with antiemetics.

Maropitant (Cerenia; zoetisus.com) is a neurokinin-1 receptor antagonist and is the antiemetic of choice.

In a study of lycorine-induced vomiting in beagles, maropitant completely blocked vomiting when given before lycorine was administered.1,2 On the basis of ASPCA Animal Poison Control Center data, maropitant is an effective antiemetic for pets that begin vomiting after amaryllis ingestion.

Other antiemetics (ondansetron, metoclopramide) are not as effective as maropitant in these cases.

Other supportive care includes IV fluids and, in severe cases, correction of electrolyte imbalances.

Large ingestions of leaves and bulbs may require

18

PRACTICAL TOXICOLOGY

decontamination with induction of emesis (if within an appropriate time frame). Massive ingestions may require blood pressure monitoring. Prognosis is generally good for amaryllis ingestions, and, in most cases, signs resolve within 24 hours.

CHRISTMAS CACTUS (SCHLUMBERGERA TRUNCATA) Christmas cactus is a native Brazilian plant and a member of the cactus family (another common name is crab’s claw cactus). The plant is light sensitive and can be forced to bloom seasonally.

In dogs and cats, the most common clinical signs of toxicosis include vomiting, lethargy, anorexia, diarrhea, and hypersalivation. Bloody vomiting and diarrhea can also occur. Ataxia has been reported in cats. Clinical signs are generally mild and resolve within a few hours.

Treatment is generally managed at home by withholding food and water and giving the gastrointestinal tract a chance to recover. If vomiting or diarrhea is moderate to severe, the animal may require antiemetics and correction of dehydration or electrolyte imbalances. A bland diet may be indicated for several days.

CHRISTMAS TREES Christmas trees are the ultimate Christmas season plants. Common species include firs (Abies and Pseudotsuga species), pines (Pinus species), cypresses (Cupressus species), spruces (Picea species), and cedars (Juniperus and Cedrus species). Most Christmas trees are cut before being brought into the house, although some have a root ball so the tree can be planted outdoors after the holidays. Cut trees are usually placed in a stand with a reservoir for water. Frequently, preservatives containing dextrose and fertilizers are added to the water.

Drinking the preservative–water mix typically causes only mild, self-limiting gastrointestinal upset. If the water is not routinely changed, bacterial or fungal overgrowth can occur.

Pets may ingest needles, cones, branches, and bark. Most Christmas trees contain essential oils (concentration and specific oils vary by species). Ingestion of large quantities of needles, cones, and parts of the tree may result in a gastrointestinal foreign body.

PRACTICAL TOXICOLOGY

CHRISTMAS CACTUS (Schlumbergera

shutterstock.com/Smileus

shutterstock.com/Kopytin Georgy

KALANCHOE (Kalanchoe blossfeldiana)

MISTLETOE (Phoradendron species)

shutterstock.com/Mattia ATH

shutterstock.com/Margo Harrison

HOLLY (Ilex aquifolium)

POINSETTIA (Euphorbia pulcherrima)

CHRISTMAS TREES

truncata)

shutterstock.com/rossella

species)

ROSEMARY (Rosmarinus officinalis)

shutterstock.com/Ann Baso

AMARYLLIS (Amaryllis or Hippeastrum

shutterstock.com/Simone Andress

shutterstock.com/and-g

shutterstock.com/Maren Winter

Common Christmas Plants

STAR OF BETHLEHEM (Ornithogalum species)

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Although long-term ingestion by livestock causes reproductive losses and concentrated essential oils and extracts can cause central nervous system signs, such as seizures, the amount of essential oil a pet is likely to ingest is minimal. The most common clinical signs of ingestion include vomiting, anorexia, abdominal pain, and depression. Some trees have sharp needles, which can cause mechanical irritation and trauma to the mucosa of the alimentary tract. Signs are generally mild and self-limiting.

Typical signs of a foreign body (abdominal distension, persistent vomiting) may occur.

Most cases are managed at home by withholding food and water for several hours. For severe or protracted vomiting, antiemetics may be indicated.

Gastrointestinal protectants (sucralfate slurries for mucosal irritation) may be helpful for large ingestions or protracted vomiting. If dehydration is present, replace fluids and correct any electrolyte abnormalities. If a foreign-body obstruction develops, surgical or endoscopic removal of the plant material may be required. In most cases, prognosis is good.

HOLLY (ILEX AQUIFOLIUM) Holly has shiny green leaves with sharp spines and bright red drupes (generally referred to as berries). It is used in wreaths and other decorative trimming. Holly is also planted in gardens.

The sharp leaves can cause mechanical damage.

Several potentially toxic substances are found in holly, including methylxanthines and cyanogens, as well as saponins. Significant intoxication usually involves ingestion of concentrated extracts. In plant ingestions, the primary toxic effect in dogs and cats is gastrointestinal irritation from the saponins.

Some animals may ingest enough leaf material to cause a foreign-body obstruction, but this is rare.

20

smacking), rinse the mouth with water and administer sucralfate slurries. Evaluate and treat as needed for a foreign-body obstruction if vomiting is protracted.

Prognosis is good. Most cases resolve in a few hours.

KALANCHOE (KALANCHOE BLOSSFELDIANA) Kalanchoe has only recently been associated with Christmas. These plants can be forced to bloom during winter, and red kalanchoes are popular Christmas gifts.

Because this is a year-round houseplant, ingestions can occur at any time. Dwarf varieties are used as houseplants.

Kalanchoe is a cardiotoxic plant; other cardiotoxic agents are listed in Box 1. The toxic principle is bufadienolides, which are found in all parts of the plant, but are concentrated in the flowers. Bufadienolides inhibit the Na-K adenosine triphosphatase in the myocardial cell membrane. This causes an increase in intracellular sodium and a decrease in intracellular potassium. The net result is a reduction in the normal membrane resting potential, which reduces the myocardium’s ability to act as pacemaker. The loss of the normal myocardial electrical function can result in asystole. Hyperkalemia is seen in severe toxicosis. Dogs are reported to be especially sensitive to the cardiotoxic effects of bufadienolides. However, most of the potted dwarf varieties of kalanchoe cause only mild gastrointestinal effects; cardiovascular signs are uncommon.

The most common clinical signs in dogs and cats are vomiting, depression, lethargy, and diarrhea.

Other reported signs include weakness, dyspnea, anorexia, tachycardia, and vocalization. Neurologic

BOX 1. Diagnostic Differentials for Kalanchoe Ingestion

Typical clinical signs include hypersalivation, vomiting, diarrhea, head shaking, lip smacking, and potential mechanical injury resulting in mild oral ulceration or laceration.

Ingestion of any of the following may cause cardiotoxic clinical signs.

Most holly ingestions can be managed at home. If large quantities of plant material were ingested, bulk up the diet (eg, with bread). Emesis may be attempted for significant ingestions. Mild vomiting can be treated by withholding food and water. Prolonged or significant vomiting can be treated with antiemetics.

If oral discomfort is present (head shaking, lip

• Oleander (Nerium oleander)

PRACTICAL TOXICOLOGY

• Digoxin • Digitoxin • Lily of the valley (Convallaria majalis) • Foxglove (Digitalis purpurea) •C ane toad (Rhinella marina; formerly Bufo marinus) secretions • Fireflies (Photinus species)

PRACTICAL TOXICOLOGY

signs have been reported in dogs and include nystagmus, tremors, seizures, and disorientation.

Ingestion of kalanchoe warrants decontamination (asymptomatic pets only). Monitor pets for clinical signs at a veterinary hospital. In most cases, signs develop within a few hours, but onset can be delayed up to 12 hours. Any pet developing clinical signs after kalanchoe ingestion should have heart rhythm, blood pressure, and electrolytes monitored. Hyperglycemia has been reported in kalanchoe intoxications, although many cardiotoxic substances cause hypoglycemia instead. Gastrointestinal signs are managed as needed, and fluids should be administered. Add dextrose to the fluids if hyperkalemia is present. Manage vomiting and gastrointestinal clinical signs with antiemetics and histamine-2 blockers.

Antiarrhythmic drugs (Table 1) should be used as needed. Treat the specific arrhythmia. A digoxin-specific immune Fab (Digibind; DigiFab, digifab.us) is indicated when serum K+ >5 mEq/L or if arrhythmias do not respond to standard therapy.

In most veterinary cases, the initial dose is 1 to 2 vials empirically. The vials should be reconstituted in sterile water and then added to 50 mL of saline.

Administer IV over 30 minutes (improvement is noted within 20 minutes to a few hours).

Monitor potassium and electrocardiograms while maintaining fluid therapy. Sometimes, the toxin redistributes in tissues and signs reappear. The prognosis is excellent if only mild gastrointestinal signs develop. If significant cardiovascular signs and/ or hyperkalemia develop, the prognosis is guarded.

MISTLETOE (PHORADENDRON SPECIES) There has been significant confusion over the years between European and American mistletoe; the genus discussed here, Phoradendron, is the American mistletoe.

The plants are semiparasitic and live on tree branches.

One theory suggests toxicity may vary depending on the species of tree in which the mistletoe grows.

Mistletoe contains a variety of potentially toxic compounds, although serious signs are uncommon. Human poison control centers have published retrospective studies of mistletoe ingestions. Most people remained asymptomatic, and gastrointestinal effects were the primary clinical signs in symptomatic cases. In rare cases, hypotension, collapse, ataxia, seizures, and death were reported.4–6 Mistletoe contains glycoprotein lectins, which are same type of toxin found in castor beans (Ricinus communis). Mistletoe lectins (phoratoxin and ligatoxin A) are significantly less toxic than ricin.

The toxins act as a cardiac depressant, causing hypotension, bradycardia, and decreased contractility.

The most common clinical signs include vomiting, depression, and diarrhea. Rarely, with large ingestions, hypotension may be seen. Most ingestions are managed at home by withholding food and water. Large ingestions warrant decontamination. Pets experiencing more than mild gastrointestinal upset should be evaluated for hypotension. Prognosis is generally good.

POINSETTIA (EUPHORBIA PULCHERRIMA) Poinsettia is an especially popular Christmas plant. The upper leaves come in a variety of colors and resemble a flower. The flowers are the tiny yellow structures resembling stamens. Poinsettias have received a great deal of negative publicity based on a probable urban legend from 1919.

All Euphorbia plants produce a milky sap containing latex irritants. However, poinsettias are much less potent than many Euphorbia species. Diterpenoid euphorbol esters and steroids with saponin-like

TABLE 1 Antiarrhythmic Therapies for Dogs and Cats ARRHYTHMIA

DRUG

DOSAGE

Bradycardia

Atropine

0.04 mg/kg IV

Tachycardia

Propranolol

0.02 mg/kg slow IV

Tachycardia with hypertension

Atenolol (β1-specific blocker) or

0.25–1 mg/kg PO q12h (dogs) 6.25 mg/cat q12h (cats)

Esmolol (β1-specific blocker)

0.25–0.5 mg/kg IV loading dose, then 10–200 mcg/kg/min IV as a continuous rate infusion3

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Charlotte Means Charlotte Means, DVM, MLIS, DABVT, DABT, is Director of Toxicology at the ASPCA Animal Poison Control Center (APCC). She received her DVM and undergraduate degree from Oklahoma State University and a master’s degree in library and information science from University of Oklahoma. Dr. Means worked in small animal practice and as a clinical medical librarian before joining the ASPCA APCC.

properties in the sap are the toxic principle and have a “soapy” effect on tissues. Dermal exposures in pets can cause pruritus, erythema, and irritation.

Ocular exposure may lead to conjunctivitis. Ingestion irritates the mucosa, resulting in hypersalivation, vomiting, and possibly diarrhea. Clinical signs are expected to be mild and self-limiting, and frequently no medical treatment is required.

Large ingestions can be diluted with milk and water.

Owners should withhold food and water for several hours if vomiting occurs. The pet should be bathed with a mild shampoo and water if sap is on the coat.

In cases of ocular exposure, flush eyes with saline or tepid tap water. Prognosis for full recovery is excellent.

ROSEMARY (ROSMARINUS OFFICINALIS) Rosemary is known as the herb of love and remembrance. A small evergreen shrub, it has a rich, pungent flavor and a pleasant aroma.

Although exposure to rosemary occurs year round, rosemary is often trimmed into a pine tree shape for a miniature Christmas tree.

Rosemary contains a variety of volatile essential oils. In small quantities (such as the amount used in cooking), no toxic effects are seen. However, large ingestions of extracts or oils can result in gastrointestinal upset and irritation, as well as renal and neurologic effects. The mechanism of toxicity is not well understood. Gastrointestinal signs are most likely due to a direct irritant effect.

The hypotensive effects are due to the spasmolytic action on smooth and cardiac muscles. Finally, the convulsant effect is theorized to be caused by monoterpene ketones. Reproductive effects are possible but rarely a concern in dogs and cats.

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PRACTICAL TOXICOLOGY

Small to moderate ingestions may cause nausea and vomiting, as well as diarrhea. Large ingestions, in addition to gastrointestinal signs, may cause hypotension, weakness, pale mucous membranes, depression, acute kidney injury, and seizures (humans).

Seizures are most likely due to monoterpene ketones.7 Most cases causing significant clinical signs involve concentrated oils and extracts. Ingestion of the plant typically causes only mild gastrointestinal upset, which can be managed by a pet owner at home by withholding food and water for 1 to 2 hours. If vomiting and diarrhea worsen, the animal should be transported to the veterinarian. In cases of large ingestion, induce emesis. Antiemetics, fluid therapy, and pressor agents (drugs that raise the arterial blood pressure, such as epinephrine or norepinephrine) should be used in cases of hypotension. Obtain a complete blood count and chemistry profile and manage seizures if needed.

STAR-OF-BETHLEHEM (ORNITHOGALUM SPECIES) Star-of-Bethlehem is a perennial plant that grows from a bulb. Most plants are grown outdoors, although some dwarf varieties are potted. Because of the star-shaped petals, this plant is frequently included in bouquets around the Christmas holidays. All parts of the plant are toxic, although the toxins are concentrated in the bulb.

This plant contains 2 alkaloids: convallatoxin and convalloside. These are cardiac glycosides.

Clinical signs and treatment are similar to those for kalanchoe ingestion. Pets generally have access only to the foliage, and most ingestions of cut flowers result in mild clinical signs.

SUMMARY Although pets are more likely to be exposed to these plants at Christmas, ingestions are unlikely to cause serious, life-threatening signs. Most cases can be managed at home. Advise clients to gift pet-safe bouquets and houseplants to friends and family members who have pets.

Some common safe houseplants include African violets and orchids. Suggestions for cut flowers include roses, Alstroemeria species (Peruvian or Brazilian lily), Gerbera daisies (Gerbera jamesonii), snapdragons, and sunflowers.

PRACTICAL TOXICOLOGY continued on page 28

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NUTRITION NOTES

ACVN NUTRITION NOTES

Diabetic Diets for Dogs and Cats: Assessing the Evidence Deborah E. Linder, DVM, MS, DACVN Cummings School of Veterinary Medicine at Tufts University shutterstock.com/Sidarta

Nutritional management can be an important adjunct to medical management of canine and feline diabetes. Once a pet has been stabilized on an insulin regimen, a change in diet may provide benefits to disease management. Consideration of

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, written 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 •E stablish requirements for certification in veterinary nutrition

essential nutrients of concern can help to optimize diabetic control and obtain ideal body condition.

There is no “one-diet-fits-all” approach to diabetes.

Species, body condition, pet preferences, and comorbid diseases guide the optimal diet choice.

Although controversy exists and approaches for optimal nutrition in pets differ, this article reviews the evidence behind various approaches to diabetic diets.

NUTRIENTS OF CONCERN Before selecting a “diabetic diet,” consider the nutrients of concern that will guide the optimal nutrient profile. Common nutrients of concern in dogs and cats are shown in Box 1.

•E ncourage continuing education for both specialists and general practitioners • Promote evidence-based research •E nhance 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.

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ACVN NUTRITION NOTES

BOX 1. Nutrients of Concern in Diabetes • Water

• Carbohydrates

• Calorie density

• Protein a

• Fiber

• Fata

a

Depends on patient and comorbidities.

NUTRITION NOTES

Many pets with diabetes have increased thirst or may experience polydipsia/polyuria, so fresh, clean water should be available at all times. Energy (calorie density) depends on body condition and whether the pet needs to gain or lose weight to obtain ideal body condition.

Although not yet directly linked to outcomes in diabetes, protein and fat should be considered in pets with some comorbid conditions. For example, dogs with concurrent pancreatitis or hyperlipidemia may need dietary fat restriction, while overweight cats and dogs may need increased protein to ensure that their essential needs are met while they undergo calorie restriction. Chromium, a trace mineral, has been evaluated as a potential nutrient of concern because of its involvement in glucose regulation, but studies have not shown clinical benefit to supplementation.1 Optimal levels of fiber and carbohydrates differ between species and are discussed in detail below.

UNDERSTANDING FIBER Different types of fiber can have different properties and benefits (or adverse effects). Fiber types can be defined in a few ways. In a clinical setting, however, describing fibers by their solubility in water is the most relevant.

Soluble fibers, such as pectins and gums, are best at absorbing water. Adding soluble fiber can promote healthy colonic mucosa and immune function in the colon, but this type of fiber is not as active in glucose control.

Insoluble fibers, such as cellulose, have less water-holding capacity, but by adding bulk, they can slow absorption of dietary carbohydrate, which can be a benefit to glucose regulation in diabetic dogs. Some ingredients, such as beet pulp, are mixed-fiber sources and may have some of the benefits of both soluble and insoluble fibers.

Although the term “high-fiber diet” can be confusing, a rough estimate of the amount of insoluble fiber in a food is the crude fiber content. Of note, percentages on pet food labels are “guaranteed analyses” and thus indicate only a maximum or minimum; they cannot be compared between diets of different moisture or calorie content.a

CANINE DIABETES Although terminology varies, this article uses the clinically applicable terms insulin-dependent diabetes For more information on fiber and comparing fiber contents of diets, see “Featuring Fiber: Understanding Types of Fiber and Clinical Uses” in the 2017 January/February issue of Today’s Veterinary Practice on tvpjournal.com. a

mellitus (IDDM) and non–insulin-dependent diabetes mellitus (NIDDM). Dogs are more commonly diagnosed with IDDM; thus, while diet can play an integral role in management, it should be used in conjunction with medical management.

The first aspect of dietary management to consider should be calorie density. Dogs with diabetes can present underweight, overweight, or even at ideal weight, so focusing on achieving or maintaining ideal body weight can guide diet choice based on calorie density. Calorie density is also intricately associated with another important nutrient of concern for diabetic dogs, fiber, which is commonly used to dilute calorie density. Diet selection based on individual pet needs can therefore be critical. For example, a food high in fiber and low in calorie density would be contraindicated for an underweight dog that cannot eat enough of the food to meet its energy needs.

The Case for Fiber Although it would seem logical to reduce dietary carbohydrates in both dogs and cats for better glucose control, research has shown that for dogs, carbohydrate content in diets is not as clinically beneficial as fiber content. In fact, a study showed no difference in diabetic control in dogs fed canned diets that differed in carbohydrates by a factor of 9 (ie, 2% carbohydrate metabolizable energy [ME] vs 26% ME).2 Research shows that the effect of insoluble fiber on diabetic control in dogs is more promising. Researchers found that dogs with naturally occurring IDDM had better fasting blood glucose and urinary glucose excretion while on a high-fiber diet (6.0 g/100 kcal) compared with a lower-fiber diet (2.6 g/100 kcal).3 Another clinical trial comparing diets with differing soluble and insoluble fiber concentrations showed that dogs with naturally occurring IDDM had better glycemic control while on the diet with high insoluble fiber.4 A challenging confounder in these studies is the correlating caloric dilution that results from the addition of fiber. It is not known whether the mechanism of action providing benefit is the addition of insoluble fiber itself, the subsequent lower calorie density, or the combination of the two. For dogs in which higher fiber is not contraindicated, the evidence suggests that diets with higher insoluble fiber may help with diabetic control after dogs are stabilized with medical management.

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Clinical Considerations in Dogs • At each visit, obtain a full dietary history that includes treats, chews, table scraps, and food used for medication administration to help ensure consistency and improve diabetic control. Sample diet history forms, as well as other helpful nutrition resources for veterinarians and clients, can be found online at the World Small Animal Veterinary Association Nutrition Toolkit site (wsava.org/nutrition-toolkit).5 • When higher-fiber diets are considered, let clients know in advance that the increased fecal bulk will result in more frequent need to eliminate. For dogs, this may mean that clients need to schedule more walks during the day to avoid accidents.

• Commercial diets are a better source of fiber supplementation because they can be formulated to still provide the appropriate essential nutrients to pets (added fiber can decrease absorption of nutrients from the diet). Canned pumpkin is popular with clients as a fiber supplement, but the amount needed to see an effect may unbalance the total diet (ie, the pumpkin would provide substantially more than 10% of the pet’s total calories).

• Avoid fiber supplements containing added flavors or sweeteners, such as xylitol, which can be harmful to pets.

FELINE DIABETES Unlike dogs, cats can be diagnosed with IDDM or NIDDM, although the typical presentation is overweight cats with NIDDM. Also contrary to dogs, some cats with NIDDM can achieve remission.

Obesity has been associated with NIDDM in cats and should be an initial consideration in selecting diets (ie, diets with lower calorie density that are appropriate for weight loss if necessary in obese cats).

Any dietary change, especially one incorporating weight loss, should be introduced only after the cat has been stabilized on an insulin regimen.

Regardless of overweight status, adequate protein should remain a priority throughout diabetic management. Protein needs may change during weight loss (because of caloric restriction and relative nutrient density) or as a result of the catabolism that can accompany uncontrolled diabetes. The exact needs of each cat will differ and should be monitored by assessing muscle condition and altering protein content of the diet as needed.

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Fiber Versus Carbohydrates: What’s the Evidence?

Only a handful of published studies address optimal diet composition (particularly fiber and carbohydrates) for cats with naturally occurring diabetes. Most have evaluated the effect of lower-carbohydrate diets. However, a study in cats with NIDDM fed a diet high in insoluble fiber (5.8 g/100 kcal) showed improved glycemic control compared with a diet low in insoluble fiber (1.1 g/100 kcal).6 Other studies have shown a positive effect of lowcarbohydrate diets (<5 g/100 kcal), including improved glycemic control and diabetic remission, in cats with naturally occurring NIDDM.7–10 Although it may seem that a low-carbohydrate diet has solid evidence to support its use, almost all of these studies have noteworthy limitations, such as not controlling for caloric intake or weight loss, small sample size, or comparison of diets that differed in more than just carbohydrate content. With at least some evidence to support both low-carbohydrate and high–insoluble-fiber approaches, the bottom line from the available studies is that both approaches may have some benefit in the regulation of feline diabetes, although low-carbohydrate diets look more promising.

Low-carbohydrate diets may not be appropriate for every cat. For example, many low-carbohydrate dry diets tend to be higher in calories because of the need for fat and protein to replace the carbohydrates.

High-calorie foods, even if low carbohydrate, would be contraindicated in an obese cat with NIDDM because diabetes is so closely associated with obesity. Each cat should be evaluated individually, with considerations made for overall health.

Clinical Considerations in Cats • Although it is not as common for cats to be given a variety of treats, clients often switch out flavors or textures, assuming that diets within the same line or product name are similar. These can have drastically different nutrient profiles, and clients should be instructed to carefully read labels and not switch foods without consulting with the veterinarian first.

• Similarly, dry and canned diets, even of the same product (veterinary therapeutic diets included), may not have the same nutrient profile and should not be used interchangeably without ensuring the nutrient profile meets the needs of the pet.

NUTRITION NOTES

• One approach owners may find on the internet is to use “any kitten diet,” which wrongly assumes that all canned diets made for growing kittens are low in carbohydrates. This is not always the case, and, again, flavors and consistency can be concerns in over-the-counter diets that are not formulated and produced to be exactly the same from batch to batch.

BOX 2. Client Communication Tip 5 What determines a high-quality pet food company? The World Small Animal Veterinary Association has created guidelines for pet owners and veterinarians to help determine companies producing high-quality products. One example is employing board-certified veterinary nutritionists and PhD-level animal nutrition scientists to properly formulate and test foods using their training in animal nutrition, physiology, and biochemistry. A full list of the guidelines can be found at wsava.org/nutrition-toolkit.

PREVENTION Although multiple studies show obesity is strongly associated with diabetes, the other risk factors for diabetes (and, thus, possible strategies for prevention) are less clear and have been considered controversial.

Of the epidemiologic studies available, it appears risk factors for diabetes include obesity, male sex, physical inactivity, and indoor confinement, but not dry-food feeding or carbohydrate content.11–13

Veterinary Therapeutic Versus Over-the-Counter Diets Some veterinary therapeutic diets require a prescription because they are outside the Association of American Feed Control Officials guidelines for a healthy pet, but high–insoluble-fiber or low–carbohydrate-diet nutrient profiles can also be found in over-the-counter foods. Of consideration, however, is the consistency and strict processing protocols in veterinary diets that may not be found in over-the-counter diets, which may have more batch-to-batch variability. This variability may be fine for a healthy pet, but the consistency a veterinary therapeutic diet has for diabetic regulation may be beneficial. More peer-reviewed studies are warranted to further support this notion.

Regardless of prescription diet status, all clients should be warned about the risks of substituting flavors, textures, or even dry and canned versions of the same food (Box 2). Each product may have a drastically different nutrient profile and should be evaluated before switching. Additionally, a study has shown that semi-moist foods, especially those with sucrose, fructose, or other simple carbohydrates, resulted in higher postprandial blood glucose and insulin responses and should be avoided in pets with diabetes.14

MORE TIPS FOR CLINICAL MANAGEMENT OF DIABETES • For clients who really want to provide treats, encourage the same treat at the same time each day or use a portion of the daily kibble as treats.

• Setting expectations is crucial, and it is helpful to discuss with clients that dietary management alone may not be successful.

• Clients sometimes seek home-cooked diets.

Consistency can vary because diets are made daily or weekly by owners and will have mild variability with each batch. As a result, such diets may not be ideal.

Recommend a consultation with a board-certified veterinary nutritionist (acvn.org) to ensure the diet is formulated properly without any deficiencies.15 References 1.

Schachter S, Nelson RW, Kirk CA. Oral chromium picolinate and control of glycemia in insulin-treated diabetic dogs. J Vet Intern Med 2001;15(4):379-384.

2. Fleeman LM, Rand JS, Markwell PJ. Lack of advantage of high-fibre, moderate-carbohydrate diets in dogs with stabilised diabetes. J Small Anim Pract 2009;50(11):604-614.

3. Nelson RW, Duesberg CA, Ford SL, et al. Effect of dietary insoluble fiber on control of glycemia in dogs with naturally acquired diabetes mellitus. JAVMA 1998;212(3):380-386.

4. Kimmel SE, Michel KE, Hess RS, Ward CR. Effects of insoluble and soluble dietary fiber on glycemic control in dogs with naturally occurring insulin-dependent diabetes mellitus. JAVMA 2000;216(7):1076-1081.

5. Freeman L, Becvarova I, Cave N, et al. WSAVA nutritional assessment guidelines. Compend Contin Educ Vet 2011;33(8):E1-E9.

Deborah E. Linder Deborah E. Linder, DVM, MS, DACVN, is a research assistant professor in clinical nutrition at Tufts Cummings School of Veterinary Medicine and head of the Tufts Obesity Clinic for Animals. Her interests include obesity management and effective client education, and she has focused her research on safe and effective weight loss strategies for pets as well as the effect of obesity on pet and human well-being. Dr. Linder received her DVM from Tufts Cummings School of Veterinary Medicine.

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ADVERTISER INDEX

NUTRITION NOTES 6. Nelson RW, Scott-Moncrieff JC, Feldman EC, et al. Effect of dietary insoluble fiber on control of glycemia in cats with naturally acquired diabetes mellitus.

JAVMA 2000;216(7):1082-1088.

7.

Mazzaferro EM, Greco DS, Turner AS, et al. Treatment of feline diabetes mellitus using an alpha-glucosidase inhibitor and a low-carbohydrate diet. J Feline Med Surg 2003;5(3):183-189.

8. Frank G, Anderson W, Pazak H, et al. Use of a high-protein diet in the management of feline diabetes mellitus. Vet Ther 2001;2(3):238-246.

9. Bennett N, Greco DS, Peterson ME, et al. Comparison of a low carbohydratelow fiber diet and a moderate carbohydrate-high fiber diet in the management of feline diabetes mellitus. J Feline Med Surg 2006;8(2):73-84.

Boehringer Ingelheim boehringer-ingelheim.com/animal-health Vision and Value . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 Dechra dechra-us.com Vetoryl . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3, 4

11. Prahl A, Guptill L, Glickman NW, et al. Time trends and risk factors for diabetes mellitus in cats presented to veterinary teaching hospitals. J Feline Med Surg 2007;9(5):351-358.

Elanco elanco.com Duramune Lyme . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

13. Backus RC, Cave NJ, Ganjam VK, et al. Age and body weight effects on glucose and insulin tolerance in colony cats maintained since weaning on high dietary carbohydrate. J Anim Physiol Anim Nutr 2010;94(6):e318-328.

14. Holste LC, Nelson RW, Feldman EC, et al. Effect of dry, soft moist, and canned dog foods on postprandial blood glucose and insulin concentrations in healthy dogs. Am J Vet Res 1989;50(6):984-989.

15. Stockman J, Fascetti AJ, Kass PH, et al. Evaluation of recipes of homeprepared maintenance diets for dogs. JAVMA 2013;242(11):1500-1505.

PRACTICAL TOXICOLOGY continued from page 22

References 1.

Kretzing S, Abraham G, Seiwert B, et al. In vivo assessment of antiemetic drugs and mechanism of lycorine-induced nausea and emesis. Arch Toxicol 2011;85(12):1565-1573.

2. Kretzine S, Abraham G, Seiwert B, et al. Dose-dependent emetic effects of the Amaryllidaceous alkaloid lycorine in beagle dogs.

Toxicon 2011;57:117-124.

3. Plumb DC. Plumb’s Veterinary Drug Handbook. 8th ed. Hoboken, NJ: Wiley-Blackwell; 2015.

4. Hall AH, Spoerke DG, Rumack BH. Assessing mistletoe toxicity. Ann Emerg Med 1986;15(11):1320-1323.

5. Krenzelok EP, Jacobsen TD, Aronis J. American mistletoe exposure.

Am J Emerg Med 1997;15:516-520.

6. Spiller HA, William DB, Gorman SE, et al. Retrospective study of mistletoe ingestion. J Toxicol Clin Toxicol 1996;34(4):405-408.

7. DerMarsodiam A, Beutler JA. The Review of Natural Products. 3rd ed.

St. Louis, MO: Facts and Comparisons; 2002: 626-628.

elanco.com Ultra Duramune Lyme . . . . . . . . . . . . . . . . . . . . . . . . back cover elanco.com Bronchi-Shield . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 Henry Schein Vet Solutions poweringsuccessfulpractices.com Business solutions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Interson Corporation interson.com Interson Sonography System . . . . . . . . . . . . . . . . . . . . . . . . . . 45 Masterfoods royalcanin.com/vet/gi Royal Canin Gastrointestinal Low Fat diet . . . . . . . . . . . . 9 Merck bravectovets.com Bravecto . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33, 34 merck.com Tri-Heart Plus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14, 15 Midmark midmarkanimalhealth.com/TVP1117 Midmark products . . . . . . . . . . . . . . . . . . . . inside front cover NAVC navc.com/vmx Conference . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .55 navc.com/institute Institute . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Nestle Purina purinaproplanvets.com FortiFlora . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Nutramax denamarinadvanced.com Denamarin Advanced . . . . . . . . . . . . . . . inside back cover Pet Health Pharmacy pethealthpharmacy.com Pharmacy services . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67

Suggested Reading •B urrows GE, Tyrl RJ. Toxic Plants of North America. 2nd ed. Ames, IA: John Wiley & Sons; 2013.

•F rohne D, Pfänder HJ. Poisonous Plants. 2nd ed. Portland, OR: Timber Press; 2005.

•G waltney-Brant S. Christmastime plants. In: Peterson ME, Talcott PA, eds. Small Animal Toxicology. 3rd ed. St. Louis, MO: Elsevier; 2013: 400-511.

•V olmer PA. How dangerous are winter and spring holiday plants to pets? Vet Med 2002;97:879-884.

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Bayer Healthcare bayerdvm.com/claro Claro . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . front cover

10. Hall TD, Mahony O, Rozanski EA, et al. Effects of diet on glucose control in cats with diabetes mellitus treated with twice daily insulin glargine. J Feline Med Surg 2009;11(2):125-130.

12. Slingerland LI, Fazilova VV, Plantinga EA, et al. Indoor confinement and physical inactivity rather than the proportion of dry food are risk factors in the development of feline type 2 diabetes mellitus. Vet J 2009;179(2):247253.

PRACTICAL TOXICOLOGY

Antech Diagnostics antechdiagnostics.com Lab diagnostics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59

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PNC Financial Services pnc.com/hcprofessionals Financial services . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 VetFolio vetfolio.com VetFolio.com . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Ultimed ulticare.com iPet Pro . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 Zoetis AlphaTRAKmeter.com AlphaTRAK . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

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IMAGING ESSENTIALS

IMAGING ESSENTIALS

Ultrasonography of the Urinary Tract: Kidneys and Ureters Elizabeth Huynh, DVM, and Clifford R. Berry, DVM, DACVR University of Florida

Welcome to our series of articles on small animal abdominal ultrasonography. The initial articles provided an overview of basic ultrasonography principles and a discussion about how to perform a systematic scan of the abdomen. The rest of the series discusses ultrasound evaluation of specific abdominal organs/systems.

Read the other small animal abdominal ultrasonography articles published in Today’s Veterinary Practice at tvpjournal.com.

NORMAL ULTRASONOGRAPHIC FEATURES Kidneys The kidneys are paired structures located in the retroperitoneal space and surrounded by adipose tissue.

Normal kidneys are symmetric in size and shape; they can be oval shaped in cats and bean shaped in dogs.

The cranial pole of the left kidney is adjacent to the greater curvature of the stomach and dorsomedial to the craniodorsal extremity of the spleen (seen cranial and lateral). In dogs, the right kidney is located more cranially than the left kidney and lies within

the renal fossa of the caudate lobe of the liver. In cats, the right kidney is often separated from the caudate lobe of the liver by retroperitoneal fat.

The widely accepted normal ultrasonographic measurement for kidneys in a cat varies between 3 and 4.3 cm in length. One report proposed that feline kidneys can measure 3.2 to 4.1 cm in length, 2.2 to 2.8 cm in width, and 1.9 to 2.5 cm in height.1 Currently, there is no widely accepted method for determining ultrasonographically normal kidney size for dogs. Ultrasonographic size is usually subjective. The following are proposed methods of measuring normal canine kidney size that have been discussed in recent reports: • The ratio of the left and right kidney to the length of L5 or L6, with normal being 1.3 to 2.72 • The ratio of kidney length to aortic diameter, with normal ranging from 5.5 to 9.13 When viewing the kidneys in sagittal orientation, the renal sinus, medulla, and cortex can be identified.

The renal medulla is the least echogenic region, followed by the renal cortex, and then the renal sinus with hyperechoic fat (Figure 1).4 When assessing for changes of the renal parenchyma, the corticomedullary NOVEMBER/DECEMBER 2017

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distinction should be readily identified. At the corticomedullary junction, the interarcuate vessels can be identified normally in some dogs and cats.

The normal renal cortex in dogs can be slightly hyperechoic to the liver.5 In normal cats, however, it is not unusual for the renal cortices to be isoechoic or hyperechoic to the hepatic parenchyma. The

renal medulla is homogeneous but often has a coarser echotexture than the renal cortex.

The renal vessels (artery and vein) can be seen entering the renal hilum. Within the renal hilum, extending into the renal sinus, fat can be deposited (hyperechoic), especially in cats. Normally, the renal pelvis is not dilated, but a small amount of

A

B

C

D

E

F

FIGURE 1. Imaging planes of the left kidney in a dog: (A) long axis dorsal, (B) long axis sagittal, (C) short axis transverse. Imaging planes of the left kidney in a cat: (D) long axis dorsal, (E) long axis sagittal, (F) short axis transverse. The different parts of the kidney are labeled in each image. The renal cortex is equal in thickness with the renal medulla and is hyperechoic relative to the renal medulla.

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1 DOSE. 12 WEEKS.* IMPROVED CLIENT COMPLIANCE. THE DIFFERENCE OF 12-WEEK* FLEA AND TICK PROTECTION Only Bravecto® takes care of killing fleas and ticks on dogs for 12 weeks* with just one convenient chew.1 Easier pet owner adherence – nearly 3X longer compliance per dose than monthly treatments1 Fast-acting efficacy – kills 100% of fleas and ticks in 12 hours2,3 Proven-safety – clinically proven for breeding, pregnant and lactating dogs1 Discover the difference at BravectoVets.Com

ASK YOUR MERCK ANIMAL HEALTH REP ABOUT BRAVECTO AND OUR UPCOMING ADDITION TO THE BRAVECTO PORTFOLIO

* Bravecto Chew kills fleas, prevents flea infestations, and kills ticks (black-legged tick, American dog tick, and brown dog tick) for 12 weeks and also kills lone star ticks for 8 weeks.

IMPORTANT SAFETY INFORMATION: The most common adverse reactions recorded in clinical trials were vomiting, decreased appetite, diarrhea, lethargy, polydipsia, and flatulence. Bravecto has not been shown to be effective for 12-weeks’ duration in puppies less than 6 months of age. Bravecto is not effective against lone star ticks beyond 8 weeks after dosing.

PLEASE SEE FULL PRESCRIBING INFORMATION ON REVERSE SIDE. References: 1. Bravecto Chew for Dogs [prescribing information]. Madison, NJ: Merck Animal Health; 2014.

2. Burgio et al. Parasites & Vectors (2016) 9:626. 3. Taenzler et al. Parasites & Vectors (2014) 7:567.

Copyright © 2017 Intervet Inc., d/b/a Merck Animal Health, a subsidiary of Merck & Co. Inc. All rights reserved.

Clinical Pharmacology: Peak fluralaner concentrations are achieved between 2 hours and 3 days following oral administration, and the elimination half-life ranges between 9.3 to 16.2 days. Quantifiable drug concentrations can be measured (lower than necessary for effectiveness) through 112 days. Due to reduced drug bioavailability in the fasted state, fluralaner should be administered with food.

Flavored chews for dogs.

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

Description: Each chew is formulated to provide a minimum dose of 11.4 mg/lb (25 mg/kg) body weight.

The chemical name of fluralaner is (±)-4-[5-(3,5-dichlorophenyl)-5-(trifluoromethyl)-4,5- dihydroisoxazol-3yl]-2-methyl-N-[2-oxo-2-(2,2,2-trifluoroethylamino) ethyl]benzamide.

Indications: Bravecto kills adult fleas and is indicated for the treatment and prevention of flea infestations (Ctenocephalides felis) and the treatment and control of tick infestations [Ixodes scapularis (blacklegged tick), Dermacentor variabilis (American dog tick), and Rhipicephalus sanguineus (brown dog tick)] for 12 weeks in dogs and puppies 6 months of age and older, and weighing 4.4 pounds or greater.

Bravecto is also indicated for the treatment and control of Amblyomma americanum (lone star tick) infestations for 8 weeks in dogs and puppies 6 months of age and older, and weighing 4.4 pounds or greater.

Dosage and Administration: Bravecto should be administered orally as a single dose every 12 weeks according to the Dosage Schedule below to provide a minimum dose of 11.4 mg/lb (25 mg/kg) body weight.

Bravecto may be administered every 8 weeks in case of potential exposure to Amblyomma americanum ticks (see Effectiveness).

Bravecto should be administered with food.

Dosage Schedule Body Weight Ranges (lb)

Fluralaner Content (mg)

Chews Administered

4.4 – 9.9

112.5

One

>9.9 – 22.0

250

One

>22.0 – 44.0

500

One

>44.0 – 88.0

1000

One

>88.0 – 123.0*

1400

One

*Dogs over 123.0 lb should be administered the appropriate combination of chews Treatment with Bravecto may begin at any time of the year and can continue year round without interruption.

Contraindications: There are no known contraindications for the use of the product.

Warnings: Not for human use. Keep this and all drugs out of the reach of children. Keep the product in the original packaging until use, in order to prevent children from getting direct access to the product.

Do not eat, drink or smoke while handling the product. Wash hands thoroughly with soap and water immediately after use of the product.

Precautions: Bravecto has not been shown to be effective for 12-weeks duration in puppies less than 6 months of age. Bravecto is not effective against Amblyomma americanum ticks beyond 8 weeks after dosing (see Effectiveness).

Adverse Reactions: In a well-controlled U.S. field study, which included 294 dogs (224 dogs were administered Bravecto every 12 weeks and 70 dogs were administered an oral active control every 4 weeks and were provided with a tick collar); there were no serious adverse reactions. All potential adverse reactions were recorded in dogs treated with Bravecto over a 182-day period and in dogs treated with the active control over an 84-day period. The most frequently reported adverse reaction in dogs in the Bravecto and active control groups was vomiting.

Percentage of Dogs with Adverse Reactions in the Field Study

Mode of Action: Fluralaner is for systemic use and belongs to the class of isoxazoline-substituted benzamide derivatives.

Fluralaner is an inhibitor of the arthropod nervous system. The mode of action of fluralaner is the antagonism of the ligand-gated chloride channels (gamma-aminobutyric acid (GABA)-receptor and glutamate-receptor).

Effectiveness: Bravecto began to kill fleas within two hours after administration in a well-controlled laboratory study. In a European laboratory study, Bravecto killed fleas and Ixodes ricinus ticks and reduced the numbers of live fleas and Ixodes ricinus ticks on dogs by >98% within 12 hours for 12 weeks. In a well-controlled laboratory study, Bravecto demonstrated 100% effectiveness against adult fleas 48 hours post-infestation for 12 weeks. In wellcontrolled laboratory studies, Bravecto demonstrated ≥93% effectiveness against Dermacentor variabilis, Ixodes scapularis and Rhipicephalus sanguineus ticks 48 hours post-infestation for 12 weeks. Bravecto demonstrated ≥90% effectiveness against Amblyomma americanum 72 hours post-infestation for 8 weeks, but failed to demonstrate ≥90% effectiveness beyond 8 weeks.

In a well-controlled U.S. field study, a single dose of Bravecto reduced fleas by ≥99.7% for 12 weeks. Dogs with signs of flea allergy dermatitis showed improvement in erythema, alopecia, papules, scales, crusts, and excoriation as a direct result of eliminating flea infestations.

Palatability: In a well-controlled U.S. field study, which included 559 doses administered to 224 dogs, 80.7% of dogs voluntarily consumed Bravecto within 5 minutes, an additional 12.5% voluntarily consumed Bravecto within 5 minutes when offered with food, and 6.8% refused the dose or required forced administration.

Animal Safety: Margin of Safety Study: In a margin of safety study, Bravecto was administered orally to 8- to 9-week-old puppies at 1, 3, and 5X the maximum label dose of 56 mg/kg at three, 8-week intervals. The dogs in the control group (0X) were untreated.

There were no clinically-relevant, treatment-related effects on physical examinations, body weights, food consumption, clinical pathology (hematology, clinical chemistries, coagulation tests, and urinalysis), gross pathology, histopathology, or organ weights. Diarrhea, mucoid and bloody feces were the most common observations in this study, occurring at a similar incidence in the treated and control groups. Five of the twelve treated dogs that experienced one or more of these signs did so within 6 hours of the first dosing. One dog in the 3X treatment group was observed to be dull, inappetant, with evidence of bloody diarrhea, vomiting, and weight loss beginning five days after the first treatment. One dog in the 1X treatment group vomited food 4 hours following the first treatment.

Reproductive Safety Study: Bravecto was administered orally to intact, reproductively-sound male and female Beagles at a dose of up to 168 mg/kg (equivalent to 3X the maximum label dose) on three to four occasions at 8-week intervals. The dogs in the control group (0X) were untreated.

There were no clinically-relevant, treatment-related effects on the body weights, food consumption, reproductive performance, semen analysis, litter data, gross necropsy (adult dogs) or histopathology findings (adult dogs and puppies). One adult treated dog suffered a seizure during the course of the study (46 days after the second treatment). Abnormal salivation was observed on 17 occasions: in six treated dogs (11 occasions) after dosing and four control dogs (6 occasions).

The following abnormalities were noted in 7 pups from 2 of the 10 dams in only the treated group during gross necropsy examination: limb deformity (4 pups), enlarged heart (2 pups), enlarged spleen (3 pups), and cleft palate (2 pups). During veterinary examination at Week 7, two pups from the control group had inguinal testicles, and two and four pups from the treated group had inguinal and cryptorchid testicles, respectively.

No undescended testicles were observed at the time of necropsy (days 50 to 71).

In a well-controlled field study Bravecto was used concurrently with other medications, such as vaccines, anthelmintics, antibiotics, and steroids. No adverse reactions were observed from the concurrent use of Bravecto with other medications.

Storage Information: Do not store above 86°F (30°C).

How Supplied: Bravecto is available in five strengths (112.5, 250, 500, 1000, and 1400 mg fluralaner per chew). Each chew is packaged individually into aluminum foil blister packs sealed with a peelable paper backed foil lid stock.

Product may be packaged in 1, 2, or 4 chews per package.

Adverse Reaction (AR)

Bravecto Group: Percentage of Dogs with the AR During the 182-Day Study (n=224 dogs)

Active Control Group: Percentage of Dogs with the AR During the 84-Day Study (n=70 dogs)

Vomiting

7.1

14.3

Decreased Appetite

6.7

0.0

Diarrhea

4.9

2.9

Distributed by: Intervet Inc (d/b/a Merck Animal Health) Madison, NJ 07940

Lethargy

5.4

7.1

Made in Austria

Polydipsia

1.8

4.3

Flatulence

1.3

0.0

Copyright © 2014 Intervet Inc, a subsidiary of Merck & Company Inc. All rights reserved

In a well-controlled laboratory dose confirmation study, one dog developed edema and hyperemia of the upper lips within one hour of receiving Bravecto. The edema improved progressively through the day and had resolved without medical intervention by the next morning.

For technical assistance or to report a suspected adverse drug reaction, contact Merck Animal Health at 1-800-224-5318. Additional information can be found at www.bravecto.com. 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.

NADA 141-426, Approved by FDA

154545 R1

IMAGING ESSENTIALS

anechoic fluid can occasionally be seen; in the transverse plane, the pelvic width can measure up to 2 mm in dogs and 1.6 mm in cats.6

Ureters The proximal and mid portions of the ureters extend along the retroperitoneal space lateral to the aorta and caudal vena cava. When examining the urinary bladder, the distal ureters, if seen, can be evaluated as they enter the ureteral papillae in the region of the trigone. Ureteral jets into the bladder lumen can often be detected when scanning the area of the papillae, and detection of the jet may be enhanced by use of color Doppler.

SCANNING TECHNIQUE To optimize images of the urinary tract, the patient’s hair must be clipped and ultrasonic gel applied to the skin before examination.

As discussed in “A Tour of the Abdomen: Part 1” (January/February 2016), the urinary tract is examined in a clockwise fashion, beginning with the left kidney, urinary bladder, proximal urethra, and then right kidney. Each kidney is evaluated in its long and short axis; these often correspond to the long and short axis of the patient, although, in some cases, the kidneys are oriented obliquely relative to the patient’s sagittal and transverse planes, requiring some adjustment of the ultrasound imaging plane to obtain true renal sagittal and transverse images.

There are 3 renal imaging planes: 2 long axis (dorsal and sagittal) and 1 short axis (transverse).

Within the dorsal plane (Figure 1), the renal pelvis is located in the far field of the image, and within the sagittal plane, the long axis of the kidney is seen but the renal pelvis is not. Typically, imaging the kidney from the lateral abdominal wall creates the dorsal plane, and imaging the kidney from the ventral aspect of the abdomen creates the sagittal plane.

The transverse plane can be created by rotating the transducer 90°. Mild renal pelvic dilation is usually best seen in the transverse plane when centered on the renal hilum.

Be sure to evaluate each kidney from medial to lateral or dorsal to ventral in one of the long axis imaging planes and from cranial to caudal in the

transverse imaging plane. Any abnormalities should be documented with static images or short video clips.

Left Kidney The left kidney is easier to localize than the right kidney because of its lateral location along the mid abdomen. Occasionally, it is seen deep to the spleen (located in the near field). The transducer is initially placed in the left cranial abdomen and is moved medially and caudally until the left kidney is visible in a long axis.

Right Kidney The right kidney is typically more difficult to image due to its craniodorsal location in the abdomen in dogs; it is especially difficult in deep-chested dogs. The transducer is placed in the right dorsolateral subcostal region to visualize the right kidney. However, a lateral approach through the 11th or 12th intercostal space might be needed, especially in deep-chested dogs.

The presence of gas and gastrointestinal contents within the stomach, descending duodenum, and/or the ascending colon can affect the image of the right kidney.7

URINARY TRACT ABNORMALITIES Congenital Abnormalities of the Kidneys Renal Agenesis or Hypoplasia Unilateral renal agenesis is rare, but has been reported in dogs and cats.8 If only one kidney exists, compensatory hypertrophy of that kidney may occur. In this instance, the kidney is enlarged but retains normal internal architecture.

Congenital Renal Dysplasia This defect can be hereditary or result from neonatal infection, such as feline panleukopenia virus or canine herpesvirus. Renal dysplasia is defined as the disorganized development of renal parenchyma leading to misshapen and fibrosed kidneys.9 These kidneys can be normal in size or small, irregular, and hyperechoic with reduced corticomedullary distinction.

Renal Ectopia Congenital malposition of one or both kidneys may occur. The etiology is unknown. Classification is based on the ectopic kidney’s anatomic position: NOVEMBER/DECEMBER 2017

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pelvic, iliac, or abdominal.10 Ectopic kidneys are structurally and functionally normal, but they can be abnormally small, and a short ureter may be kinked, predisposing to obstruction, secondary hydronephrosis, or pyelonephritis.11 Ectopic Ureters This congenital condition results in an abnormal vesicoureteral orifice at the urinary papilla and can be bilateral or unilateral. Ectopic ureters is the most common congenital condition causing dilated ureter and renal pelvis.12 It is more common in female dogs. Ectopic ureters may be dilated due to ileus, concurrent infection, or partial obstruction at the point of entry to the urethra or vagina/vestibule.

Autosomal Dominant Polycystic Kidney Disease This is an inherited disease reported mostly in Persian or Persian-cross cats, cairn terriers, and bull terriers.13,14 Persian cats and bull terriers inherit this disorder as an autosomal dominant trait. In Persian cats, this disease can be detected as early as 6 to 8 weeks of age, but absence of cysts does not preclude development of cysts later on in life.

Ultrasonographically, these cysts are rounded, centrally anechoic, and have smooth, sharply demarcated thin walls with distal acoustic enhancement (Figure 2). The cysts are located in the renal medulla and cortex, but most are within the cortex or at the corticomedullary junction. Occasionally, these cysts may be found in the liver as well as the pancreas.

FIGURE 2. Long axis sagittal image of the left kidney in a ragdoll cat. Multiple smoothly marginated, rounded, anechoic foci with distal acoustic enhancement are seen throughout the entire renal parenchyma (white arrows).

These cystic structures are distorting the entire internal architecture of the kidney. The caudal pole of the kidney is indicated by the white arrowhead.

36

IMAGING ESSENTIALS

Focal Abnormalities of the Renal Parenchyma Renal Cysts Renal cysts may be solitary or multiple, involving both kidneys.15â&#x20AC;&#x201C;17 This condition may be congenital, as explained previously, or acquired. Renal cysts are round to oval in contour and anechoic, and they have smooth, sharply demarcated thin walls with a distinct far wall border and distal acoustic enhancement.

Cysts may deform the renal capsule if they become large enough or if autosomal dominant polycystic kidney disease is present. Also, they can contain internal echoes in association with hemorrhage or necrotic debris. Diagnostic differentials for solitary cysts include hematoma, abscess, and solid or cavitary mass. The presence of cystic lesions of the kidneys in some breeds, such as German shepherds, should raise concern for some neoplasms, such as renal cystadenocarcinoma, which can be associated with cutaneous paraneoplastic fibrotic nodular lesions (nodular dermatofibrosis).18 Renal Hematoma Renal hematomas typically occur in a young animal with a clotting disorder or recent trauma. They may contain a mixture of anechoic, hypoechoic, and hyperechoic components within the renal cortex or medulla. Differentiation from some neoplastic lesions, such as renal hemangiosarcoma, can be ultrasonographically challenging.

FIGURE 3. Short axis transverse image of the left kidney in an Alaskan malamute. This renal abscess is located within a portion of the kidney and is irregularly shaped with a thick wall containing anechoic and echogenic fluid (black arrowheads); the hyperechoic component is forming a sediment in the dependent portion of the abscess, causing a fluid-fluid line. More normal renal architecture is still present (white arrow).

IMAGING ESSENTIALS

Renal Abscess A renal abscess can occur in conjunction with fever and leukocytosis. Abscesses appear as poorly demarcated cavitary lesions that are irregular in contour with internal echoes and sedimentation, and they have variable degrees of distal acoustic enhancement (Figure 3). Typically, the renal pelvis is enlarged.

Renal Infarctions Ultrasonographically, organized infarcts are well-defined, wedge-shaped, cortical lesions located perpendicular to the capsule and extending centrally to the renal pelvis (Figure 4). The base of the wedge-shaped lesion is

directed toward the renal capsule while the apex points towards the hilus. They vary in appearance and, at the chronic phase, are typically hyperechoic and cause focal cortical depressions secondary to contracture and fibrosis.

Renal Mineralization (Nephrocalcinosis) Renal mineralization can be seen in older dogs and cats. It is classified based on its location. Renal diverticular mineralization is caused by dystrophic mineralization. Renal parenchymal mineralization, however, is caused by mineralization of the renal cortex from deposition of calcium salts or other minerals (eg, ethylene glycol toxicosis).

Mineralization is identified as hyperattenuating foci with distal acoustic shadowing within the renal diverticuli, pelvis, and/or cortex (Figure 5); however, if there are punctate foci of hyperechogenicity, distal acoustic shadowing may not be evident.

Renal Cystadenocarcinomas These tumors are commonly found in German shepherds and are associated with paraneoplastic nodular dermatofibrosis (neurofibromas).

Ultrasonographically, one to several fluid-filled cavities (cysts) can be detected, and a solid tissue component can infiltrate the kidney and protrude into the cyst.19 Other Renal Neoplasia

FIGURE 4. Long axis sagittal image of the left kidney in a domestic shorthaired cat. A focal, hyperechoic, wedgeshaped, focally concave, renal cortical infarction is seen extending from the cortex to the corticomedullary junction (white arrowheads) along the caudal pole of the kidney.

Solid soft tissue masses may appear in a variety of ways: • Homogeneous or heterogeneous • Hypoechoic, isoechoic, or hyperechoic • Regular or irregular with variable margins (Figure 6) • Altered renal internal architecture • Hypoechoic halo at the periphery of the cortex • Hyperechoic foci or striations throughout the medulla • Pyelectasia • Hypoechoic medullary or cortical nodules or masses20

FIGURE 5. Long axis sagittal image of the left kidney in a Siamese cat. Overall, the kidney is irregularly shaped, lobulated, and small. There is a large, hyperechoic, smoothly marginated nephrolith with distal acoustic shadowing located within a renal diverticulum (white arrow). Note the renal pelvis distended with anechoic fluid (white arrowhead).

The differential diagnosis of hypoechoic nodules or masses includes lymphoma and malignant histiocytosis.21 Other neoplasms that can affect kidneys include adenocarcinomas, hemangiomas, nephroblastomas, hemangiosarcomas, and metastases.22 The most common renal tumor in the dog is renal cell carcinoma (Figures 6 and 7). The most common renal tumor in the cat is renal lymphoma NOVEMBER/DECEMBER 2017

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(Figure 8), where diffuse changes can be seen. The kidneys are usually enlarged, irregular, hyperechoic, with hypoechoic subcapsular thickening.23

Diffuse Abnormalities of the Renal Parenchyma

corticomedullary junction (Figure 9); this appearance is consistent with mineralization, necrosis, congestion, and/or hemorrhage.20

A

Ethylene Glycol Toxicosis Ethylene glycol toxicosis causes a severe increase in cortical and, to a lesser extent, medullary hyperechogenicity (Table 1). In addition, there can be a medullary rim sign, which is denoted as a circumferential hyperechoic band located in the medulla, parallel to the

B

FIGURE 6. Long axis sagittal image of the right kidney in a Rhodesian ridgeback. There is a large, lobulated, heterogeneous mass located in the cranial pole of the kidney. The margins of this mass are well demarcated (white arrowheads). More normal renal parenchyma can still be identified in the caudal pole of the kidney (white arrow). This mass was diagnosed as a renal cell carcinoma.

FIGURE 7. Long axis sagittal image of the left kidney in a Labrador retriever. There is an expansile, well demarcated, lobulated, heterogeneously hyperechoic mass in the caudal pole of the kidney, causing distortion of the renal architecture and shape. This dog was diagnosed with renal cell carcinoma.

38

IMAGING ESSENTIALS

FIGURE 8. (A) Long axis sagittal and (B) short axis transverse images of the right kidney in a domestic shorthaired cat. The cortex is thickened and hyperechoic, and its margin is irregular. Anechoic fluid is detected within the mildly to moderately distended renal pelvis (white arrowheads). A very small amount of anechoic to hypoechoic fluid surrounds the kidney (white arrow). This cat was diagnosed with renal lymphoma.

FIGURE 9. Long axis sagittal image of the right kidney in a mixed-breed dog. The renal cortex is severely hyperechoic.

There is also a hyperechoic band within the medulla traversing parallel to the corticomedullary junction (white arrows).

This dog was diagnosed with ethylene glycol toxicosis.

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TABLE 1 Differential Diagnoses of Diffuse Renal Cortical and Medullary Hyperechogenicity DIFFERENTIAL DIAGNOSIS IN DOGS

DIFFERENTIAL DIAGNOSIS IN CATS

Cortical hyperechogenicity

• • • • • • •

I nterstitial or glomerular nephritis Pyelonephritis24 Leptospirosis Acute tubular necrosis Ethylene glycol toxicosis25 End-stage renal disease Nephrocalcinosis

• Interstitial or glomerular nephritis • Ethylene glycol toxicosis25 • Diffuse renal lymphoma (Figure 8) • Feline infectious peritonitis • Cryptococcosis • Amyloidosis

Cortical and medullary hyperechogenicity (reduced corticomedullary distinction)

• • • •

ongenital renal dysplasia C J uvenile boxer nephropathy26 Chronic renal disease End-stage kidney disease

•C ongenital renal dysplasia • Chronic renal disease • End-stage kidney disease

Caution should be used when interpreting the medullary rim sign; it should not be considered an accurate indicator of renal disease, although it could represent sentinel signs of early renal disease or past renal insult.27 It has also been detected in clinically normal dogs and cats.27,28 Chronic Interstitial Nephritis Kidneys become small, irregular, and diffusely hyperechoic from fibrosis.16 When kidneys are diffusely hyperechoic, the corticomedullary demarcation becomes difficult to delineate.

Capsular or Pericapsular Diseases Perirenal or Subcapsular Fluid The differential diagnosis for perirenal or subcapsular fluid includes: • Urine leakage

29

Subscapular perirenal pseudocysts are formed by accumulation of a transudate between the capsule and parenchyma of the kidney due to underlying parenchymal disease.32 This is more common in cats.

Abnormalities of the Renal Pelvis and Proximal Ureter Pyelectasia Pyelectasia is a dilation of the renal pelvis (Figure 11).33 Pyelectasia may be caused by intravenous fluid administration, diuretic administration, increased diuresis from renal insufficiency, distended urinary bladder or lower urinary tract obstruction, pyelonephritis, ureteritis, ectopic ureter, or another congenital malformation.

Pyelonephritis Pyelonephritis can affect one or both kidneys and is usually a result of ascending ureteral infection

• Hemorrhage30 • Abscess31 • Acute renal failure29 • Ureteral obstruction29 • Ethylene glycol toxicosis29 • Leptospirosis29 • Amyloidosis • Cryptococcosis Perinephric (Perirenal) Pseudocysts Ultrasonographically, perirenal pseudocysts appear as an accumulation of anechoic fluid around one or both kidneys, most commonly between the capsule and the renal cortex (Figure 10).32

40

IMAGING ESSENTIALS

FIGURE 10. Long axis sagittal image of the right kidney in a domestic shorthaired cat. The kidney is abnormally shaped, lobulated, and contains multiple hyperechoic, wedge-shaped defects within its cortical margin. The diverticuli contains multiple ovoid, hyperechoic foci (black arrowheads) with distal acoustic shadowing. There is a large amount of anechoic fluid surrounding the kidney, consistent with a perinephric pseudocyst (white arrows).

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from the urinary bladder. Ultrasonographic changes associated with pyelonephritis include: • Mild renal enlargement and mild to moderate pelvic and ureteral dilation34 • Hyperechoic mucosal margin parallel to the wall of the renal pelvis and proximal ureter24 • Echogenic medullary band at the corticomedullary junction • Focal hyperechoic areas in the renal medulla and patchy, focal hypoechoic or hyperechoic areas in the renal cortex24 Urine echogenicity may increase and even contain sedimentation due to pyuria. In chronic cases, renal pelvic and diverticula distortion and a hyperechoic rim can be seen.

Hydroureter If ureters are filled with fluid, they are easily identified beginning at the renal hilus. Ureters can be abnormally distended secondary to ectopia, ureteritis, obstruction, or congenital conditions.36 In chronic obstructions, the distended ureters can become severely enlarged and tortuous, making it possible to follow them caudally to the level of the obstruction. If ureteroliths (ureteral calculi) are suspected to be the inciting cause, smoothly to irregularly marginated, hyperechoic foci with distal acoustic shadowing can be identified within the abnormally distended ureteral lumen.

Other tubular structures are also located in the renal hilus, such as the renal vein and artery. To differentiate

Hydronephrosis Hydronephrosis occurs when the renal pelvis and diverticuli become dilated, distorting and compressing the renal parenchyma.33 The renal diverticuli become rounded and appear as anechoic finger-like projections extending from the anechoic renal pelvis (Figure 12).

Possible causes of hydronephrosis include congenital malformation, lower urinary tract obstruction, and ureteral or renal pelvic obstruction from a calculus, stricture, or trigonal or retroperitoneal mass.

In chronic cases, the renal pelvis is distended, and the renal parenchyma can atrophy. Hydroureter is often seen in combination with hydronephrosis.

Hydronephrosis may progress to pyonephrosis, caused by urinary stasis and subsequent infection.35

FIGURE 11. Short axis transverse image of the right kidney in a domestic shorthaired cat. The retroperitoneal fat is hyperechoic. There is poor corticomedullary distinction. The renal pelvis is mildly distended with slightly echogenic fluid.

This cat was diagnosed with presumptive pyelonephritis.

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IMAGING ESSENTIALS

FIGURE 12. Long axis sagittal image of the left kidney in a domestic shorthaired cat. The renal pelvis (P) and proximal ureter (U) are moderately distended with anechoic fluid.

Note the rounded renal diverticuli (white arrowheads). This cat was diagnosed with obstructive hydronephrosis and hydroureter secondary to ureteral calculi.

FIGURE 13. Long axis sagittal image of the right ureter at the level of the apex of the urinary bladder in a domestic shorthaired cat. The ureter is distended with anechoic fluid.

Note the lack of color Doppler flow within the ureter and the subjectively thickened ureteral wall.

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be seen with accumulation of urine or blood, following trauma to the kidneys and/or ureters.

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

Clifford R. Berry Clifford R. Berry, DVM, DACVR, is a professor of diagnostic imaging at University of Florida College of Veterinary Medicine. His research interests include cross-sectional imaging of the thorax, nuclear medicine, and biomedical applications of imaging. He received his DVM from University of Florida and completed a radiology residency at University of Californiaâ&#x20AC;&#x201C;Davis.

hydroureter from a normal renal vessel, color Doppler or power Doppler can be used, focusing on the renal hilum (Figure 13); the anechoic tubular structures with flow within their lumen are vascular and should not be mistaken for the abnormally distended ureter.

Abnormalities of the Retroperitoneum Retroperitoneal transudate appears as linear, triangular, or oval anechoic to hypoechoic foci adjacent to the kidneys. These changes can

Retroperitoneal exudate and acute hemorrhage are usually more echogenic because of their higher cell count. Inflammatory processes, such as acute pyelonephritis and ureteritis, can cause the retroperitoneal fat to become hyperechoic and hyperattenuating.

Retroperitoneal abscesses can be caused by migrating plant awns in some regions of the country.

They have thickened, irregular walls and often present as anechoic to hypoechoic masses, with or without septae and internal echogenic debris.37 Retroperitoneal masses may occur secondary to granulomas, neoplasia, or enlarged sublumbar lymph nodes. They can be variable in size, shape, and echogenicity. Hemangiosarcoma is a common neoplasm of the canine retroperitoneal space (Figure 14).38

SUMMARY Abnormalities of the kidneys and ureters are commonly seen when urinary bladder abnormalities are present. A systematic examination of the urinary system is a routine part of the complete abdominal evaluation.

References 1.

Walter PA, Feeney DA, Johnston GR, Fletcher TF. Feline renal ultrasonography: quantitative analyses of imaged anatomy. Am J Vet Res 1987;48(4):596-599.

2. Barella G, Lodi M, Sabbadin LA, Faverzani S. A new method for ultrasonographic measurement of kidney size in healthy dogs. J Ultrasound 2012;15(3):186-191.

3. Mareschal A, dâ&#x20AC;&#x2122;Anjou MA, Moreau M, et al. Ultrasonographic measurement of kidney-to-aorta ratio as a method of estimating renal size in dogs. Vet Radiol Ultrasound 2007;48(5):434-438.

4. Hart DV, Winter MD, Conway J, Berry CR. Ultrasound appearance of the outer medulla in dogs without renal dysfunction. Vet Radiol Ultrasound 2013;54(6):652-658.

5. Ivancic M, Mai W. Qualitative and quantitative comparison of renal vs. hepatic ultrasonographic intensity in healthy dogs. Vet Radiol Ultrasound 2008;49(4):368-373.

6. D'Anjou MA, Bedard A, Dunn ME. Clinical significance of renal pelvic dilatation on ultrasound in dogs and cats. Vet Radiol Ultrasound 2011;52(1):88-94.

7. Nyland TG, Widmer WR, Mattoon JS. Urinary tract. In: Mattoon JS, Nyland TG, ed. Small Animal Diagnostic Ultrasound. 3rd ed. St. Louis: Elsevier Saunders; 2015:557-607.

FIGURE 14. Long axis sagittal image of the right retroperitoneal space in an Australian shepherd. There is an irregularly shaped, heterogeneous mass with anechoic foci (white arrowhead) within the retroperitoneal space. The crosshairs demarcate the peripheral extremities of this mass in this view. A malignant neoplasm, such as hemangiosarcoma, was highly suspected; however, no cytology or histopathology was performed to confirm this suspicion.

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IMAGING ESSENTIALS

8. Hoskins JD. The Urinary System. In: Hoskins JD, ed. Veterinary Pediatrics: Dogs and Cats from Birth to Six Months. 3rd ed.

Philadelphia: Saunders; 2001:371-395.

9. Burder MC, Shoieb AM, Shirai N, et al. Renal dysplasia in beagle dogs: four cases. Toxicol Pathol 2010;38(7):1051-1057.

10. Allworth MS, Hoffmann KL. Crossed renal ectopia with fusion in a cat.

Vet Radiol Ultrasound 1999;40(4):357-360.

11. Hecht S. Diagnostic imaging of lower urinary tract disease. Vet Clin North Am Small Anim Pract 2015;45(4):639-663.

IMAGING ESSENTIALS 12. Lamb CR, Gregory SP. Ultrasonographic findings in 14 dogs with ectopic ureter. Vet Radiol Ultrasound 1998;39(3):218-223.

13. Reichle JK, DiBartola SP, Leveille R. Renal ultrasonographic evaluation and computed tomographic appearance, volume, and function of cats with autosomal dominant polycystic kidney disease. Vet Radiol Ultrasound 2002;43(4):368-373.

The CLEAR choice in portable ultrasound technology...

14. McKenna SC, Carpenter JL. Polycystic disease of the kidney and liver in the Cairn Terrier. Vet Pathol 1980;17(4):436-442.

15. Konde LJ. Sonography of the kidney. Vet Clin North Am Small Anim Pract 1985;15(6):1149-1158.

16. Walter PA, Feeney DA, Johnston GR, O’Leary TP. Ultrasonographic evaluation of renal parenchymal diseases in dogs: 32 cases (19811986). JAVMA 1987;191(8):999-1007.

17. Walter PA, Johnston GR, Feeney DA, O’Brian TD. Applications of ultrasonography in the diagnosis of parenchymal kidney disease in cats: 24 cases (1981-1986). JAVMA 1988;192(1):92-98.

18. Lium B, Moe L. Hereditary multifocal renal cystadenocarcinomas and nodular dermatofibrosis in the German shepherd dog: macroscopic and histopathologic changes. Vet Pathol 1985;22(5):447-455.

19. Moe L, Lium B. Hereditary multifocal renal cystadenocarcinomas and nodular dermatofibrosis in 51 German shepherd dogs. J Small Anim Pract 1997;38(11):498-505.

20. Konde LJ, Wrigley RH, Park RD, Lebel JL. Sonographic appearance of renal neoplasia in the dog. Vet Radiol Ultrasound 1985;26(3):74-81.

21. Taylor AJ, Lara-Garcia A, Benigni L. Ultrasonographic characteristics of canine renal lymphoma. Vet Radiol Ultrasound 2014;55(4):441-446.

22. Bryan JN, Henry CJ, Turnquist SE, et al. Primary renal neoplasia of dogs. J Vet Intern Med 2006;20(5):1155-1160.

23. Valdes-Martinez A, Cianciolo R, Mai W. Association between renal hypoechoic subcapsular thickening and lymphosarcoma in cats. Vet Radiol Ultrasound 2007;48(4):357-360.

24. Neuwirth L, Mahaffey M, Crowell W, et al. Comparison of excretory urography and ultrasonography for detection of experimentally induced pyelonephritis in dogs. Am J Vet Res 1993;54(5):660-669.

25. Adams WH, Toal RL, Breider MA. Ultrasonographic findings in dogs and cats with oxalate nephrosis attributed to ethylene glycol intoxication: 15 cases (1984-1988). JAVMA 1991;199(4):492-496.

26. Chandler ML, Elwood C, Murphy KF, et al. Juvenile nephropathy in 37 boxer dogs. J Small Anim Pract 2007;48(12):690-694.

27. Mantis P, Lamb CR. Most dogs with medullar rim sign on ultrasonography have no demonstratable renal dysfunction. Vet Radiol Ultrasound 2000;41(2):164-166.

SiMPLi Series

28. Yeager AE, Anderson WI. Study association between histologic features and echogenicity of architecturally normal cat kidneys. Am J Vet Res 1989;50(6):860-863.

Ultra Simple USB Ultrasound

29. Holloway A, O'Brien R. Perirenal effusion in dogs and cats with acute renal failure. Vet Radiol Ultrasound 2007;48(6):574-579.

Runs on Windows Laptop or Tablet

30. Whittemore JC, Preston CA, Kyles AE, et al. Nontraumatic rupture of an adrenal gland tumor causing intra-abdominal or retroperitoneal hemorrhage in four dogs. JAVMA 2001;219(3):324, 329-333.

Lightweight, Handheld and Mobile

31. HyeYeon L, JinHwa C, JooHyun J, et al. Unilateral renal subcapsular abscess associated with pyelonephritis in a cat. J Vet Clin 2010;27:7982.

Plug & Play – Instant Real-Time Imaging 100% Manufactured in the USA

32. Ochoa VB, DiBartola SP, Chew DJ, et al. Perinephric pseudocysts in the cat: a retrospective study and review of the literature. J Vet Intern Med 1999;13(1):47-55.

Diagnostic Procedures

33. Stedman TL. Stedman's Pocket Medical Dictionary. 1st ed.

Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2010.

• • • • •

34. Felkai C, Voros K, Fenyves B. Lesions of the renal pelvis and proximal ureter in various nephro-urological conditions: an ultrasonographic study. Vet Radiol Ultrasound 1995;36(5):397-401.

35. Choi J, Jang J, Choi H, et al. Ultrasonographic features of pyonephrosis in dogs. Vet Radiol Ultrasound 2010;51(5):548-553.

36. Lamb CR. Ultrasonography of the ureters. Vet Clin North Am Small Anim Pract 1998;28(4):823-848.

37. Hylands R. Veterinary diagnostic imaging. Retroperitoneal abscess and regional cellulitis secondary to a pyelonephritis within the left kidney. Can Vet J 2006;47(10):1033-1035.

Fine-Needle Aspiration Pregnancy Diagnosis Abdominocentesis Cystocentesis Liver Biopsy

7150 Koll Center Parkway | Pleasanton, CA 94566 925.462.4948 | sales@interson.com

38. Liptak JM, Dernell WS, Ehrhart EJ, et al. Retroperitoneal sarcomas in dogs: 14 cases (1992-2002). JAVMA 2004;224(9):1471-1477.

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Chronic Vomiting in Cats: When to Recommend Endoscopy Kyle Restle, DVM, and Jacqueline Whittemore, DVM, PhD, DACVIM University of Tennessee School of Veterinary Medicine

Chronic vomiting is a common presenting sign for cats, and evaluation can be frustrating for both owners and veterinarians because of the long differential list. Chronic vomiting has previously been defined as vomiting 3 or more times per month for at least 3 months.1 Vomiting of trichobezoars (hairballs) should not be dismissed, particularly in cats without long hair, because their development could reflect altered gastrointestinal (GI) motility due to underlying disease.2

Vomiting should first be differentiated from regurgitation. Vomiting is an active process with retching or heaving, and it is often preceded by nausea or hypersalivation. Vomitus may contain partially digested food and be discolored because of the presence of bile. In contrast, regurgitation is a passive process; regurgitated food is typically undigested, might have a mucus coating, and lacks bile.

After confirmation of chronic vomiting, the next step is crafting an appropriate differential list based on the patientâ&#x20AC;&#x2122;s signalment, environment and husbandry, history, and physical examination findings because this can drastically alter the diagnostic approach.

For example, although metabolic evaluation is generally warranted in older cats before abdominal imaging, immediate performance of abdominal radiography might be more appropriate in a young cat because of increased risk for linear foreign body ingestion.5

Endoscopy can be a valuable tool in achieving a final diagnosis, but it is not inexpensive or completely without risk. Additionally, premature performance of endoscopy can result in misdiagnosis because histologic findings do not differentiate among types of chronic enteropathy, such as food responsive disease (FRD) and inflammatory bowel disease (IBD).3,4 Thus, when evaluating a cat for chronic vomiting, clinicians must follow a systematic approach.

PET PEEVES Chronic vomiting in cats is a frustrating condition, and accurate diagnosis hinges on use of a systematic approach. Endoscopy is warranted after systemic diseases have been ruled out, particularly in cases without solitary jejunal disease.

shutterstock.com/Stefano Garau

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Tables 1 and 2 present the systemic and GI diseases most commonly associated with chronic vomiting in cats. An exhaustive review of causes of vomiting in cats, along with a ranking of the level of evidence supporting each association, has been published by Batchelor et al.8

SIGNALMENT AND CLINICAL HISTORY Retrospective analysis suggests that the prevalence of urinary, neoplastic, cardiovascular, and GI diseases increases with age, whereas the prevalence

TABLE 1 Extragastrointestinal or Systemic Diseases Associated With Chronic Vomiting in Cats SIGNALMENT AND CLINICAL SIGNS

PHYSICAL EXAMINATION FINDINGS

POSSIBLE RELEVANT DIAGNOSTIC TEST RESULTS

Parasitic (eg, heartworm, hepatic and pancreatic flukes, Toxoplasma)

Young cat that hunts Outdoor exposure Exposure to raw meat

Potbelly Underweight

↓ Albumin ↑ Globulins ↑ Liver enzymes + H eartworm test, echocardiogram

Viral (FeLV, FIV, FIP)

Young to adult, geriatric Outdoor exposure Multicat environment History of cat fights

Anterior uveitis or chorioretinitis Fever Peritoneal effusion Thickened intestines Underweight

↓ Hct ↓ WBC ↑ Globulins without ↓ albumin ↑ Liver enzymes and bilirubin Positive viral test results

Chronic kidney disease

PUPD Hyporexia/food aversion Weight loss

Hypothermia (without shock) Hypertension, retinal hemorrhages Poor hair coat Irregular, small kidneys

↓ Hct ↑ BUN, creatinine ↑ tCa, PO4, ↑/↓ K+ Isosthenuria/minimally concentrated urine ↑ UPC

Diabetes mellitus

Burmese Polyphagia PUPD

Ill-kempt coat Obese Plantigrade stance

↑ Glucose, fructosamine Glucosuria

Hepatobiliary disease (eg, lymphocytic cholangitis, suppurative cholangitis)

Middle-aged Weight loss (lymphocytic)

Dehydration and fever (suppurative) Jaundice Peritoneal effusion Underweight (lymphocytic)

↓ ↓ ↑ ↑

Heart murmur Hypertension Palpable goiter Thickened intestines6

n/↑ Hct ↑ Liver enzymes n/↑ BUN, creatinine Isosthenuria/minimally concentrated urine ↑ UPC 7 ↑ T4/fT4 GI thickening

Middle-aged Hyporexia/food aversion Weight loss

Ill-kempt coat Cranial abdominal pain Peritoneal effusion Thickened intestines

↑ Liver enzymes ↑ fPL/DGGR lipase Widened gastroduodenal angle, loss of serosal detail Hypoechoic or heterogenous pancreas, hyperechoic mesentery, duodenal corrugation

Hepatic and pancreatic

Adult Hyporexia/food aversion Weight loss

Cranial abdominal organomegaly Underweight

↓ Hct ↑ Liver enzymes Organomegaly on radiography Mass on ultrasonography

Round cell tumors (lymphoma, mast cell tumor)

Any age Hyporexia Weight loss

Cranial abdominal organomegaly (uncommon)

Variable Gastric ulceration (mast cell)

CAUSE INFECTIOUS

METABOLIC

Behavioral changes Polyphagia PUPD Weight loss

Hyperthyroidism

Pancreatitis

Hct (lymphocytic) Albumin Globulins Liver enzymes, bilirubin

NEOPLASTIC

BUN, blood urea nitrogen; DGGR, 1,2-o-dilauryl-rac-glycero glutaric acid-(6'-methylresorufin) ester; fPL, feline pancreas-specific lipase; fT4, free thyroxine; GI, gastrointestinal; Hct, hematocrit; n, normal; PUPD, polyuria and polydipsia; T4, thyroxine; tCa, total calcium; UPC, urine protein-to-creatinine ratio; WBC, white blood cell.

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CHRONIC VOMITING IN CATS

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TABLE 2 Gastrointestinal Diseases Associated With Chronic Vomiting in Cats DISEASE

SIGNALMENT AND CLINICAL SIGNS

PHYSICAL EXAMINATION FINDINGS

POSSIBLE RELEVANT DIAGNOSTIC TEST RESULTS

History of foreign-body ingestion Long-hair coat Vomiting associated with food ingestion

Mass effect Intestinal plication String under tongue

Mass effect Intestinal plication

ANATOMIC Obstruction (gastric or linear foreign body, trichobezoars, neoplasia) Pseudoobstruction (hypomotility)

Large, fluid-filled stomach on imaging

INFECTIOUS

Bacterial (spiral bacteria)

Hyporexia, food aversion

Generally normal

Demonstration of organisms on biopsy (with lack of gross or histologic abnormalities in the small intestine)

Fungal (Histoplasma species)

Geographic location Outdoor/bird exposure Lameness Respiratory signs Weight loss

Anterior uveitis or chorioretinitis Bone pain Fever, jaundice Abnormal lung sounds Thickened intestines Splenomegaly

↓ Hct/WBC/platelets ↑ Globulins, ↓ albumin ↑ Liver enzymes Pulmonary infiltrates Thickened intestines, lymphadenomegaly FeLV positivity

Parasitic (Physaloptera, Ollulanus, Ancylostoma, Toxocara, Toxascaris, and Dipylidium species)

Hunter Outdoor exposure New cat or dog introduced into home Cattery History of fleas

Generally normal Thickened intestines

↑ Eosinophils Positive fecal test result Microscopic visualization in vomitus or gastric lavage samples Direct visualization

Outdoor exposure Multicat environment

Anterior uveitis or chorioretinitis Fever Thickened intestines Underweight

↓ Hct ↑ Liver enzymes and bilirubin ↑ Globulins without ↓ albumin Positive viral test results GI thickening, scant perinephric effusion

FRD

Behavioral changes Diarrhea Hyporexia, food aversion Polyphagia Weight loss

Dermatologic abnormalities Ill-kempt coat Thickened intestines Underweight

↑ BUN with normal creatinine ↓ Albumin ↑ Eosinophils GI thickening, muscularis thickening Response to diet trial

IBD (including ESF)

Behavioral changes Diarrhea Hyporexia, food aversion Polyphagia Weight loss

Ill-kempt coat Thickened intestines Underweight

↑ Eosinophils GI thickening ± muscularis thickening (primarily duodenal), loss of wall layering Mass effect (ESF)

Carcinoma

Older animals Hyporexia, food aversion Polyphagia Weight loss

Mass effect Thickened intestines

Focal mass effect Gastric ulceration GI thickening/mass effect ± loss of wall layering

Lymphoma

FeLV positivity Diarrhea Hyporexia, food aversion Polyphagia Weight loss

Abdominal pain Nausea Mesenteric lymphadenomegaly Thickened intestines

Gastric ulceration GI thickening ± muscularis thickening (primarily jejunal), loss of wall layering, mass effect, mesenteric lymphadenomegaly

Viral (dry form FIP)

INFLAMMATORY/IMMUNE

NEOPLASTIC

BUN, blood urea nitrogen; ESF, eosinophilic sclerosing fibroplasia; FeLV, feline leukemia virus; FIP, feline infectious peritonitis; FIV, feline immunodeficiency virus; FRD, food responsive disease; GI, gastrointestinal; Hct, hematocrit; IBD, inflammatory bowel disease; WBC, white blood cell.

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of infectious and traumatic diseases decreases.9 Cats with outdoor access often have greater exposure to parasites and retroviruses, although all cats should be considered at risk. Although these trends can help guide the formation of an appropriate initial diagnostic plan, atypical presentation is possible.

Cats with chronic vomiting should be assessed for the changes listed in Box 1. Polydipsia with polyuria should be differentiated from polydipsia in the absence of polyuria. The latter can result from increased GI water loss, which is not always accompanied by diarrhea. Fecal scoring charts should be reviewed with clients to determine fecal consistency. If present, diarrhea should be categorized (small, large, or mixed bowel) and the presence of blood determined. Weight loss should be subdivided into changes to fat stores, muscle mass, or both.

If GI disease is diagnosed, the feline chronic enteropathy activity index should be calculated to quantitate the severity of disease,10 thereby facilitating more accurate evaluation of the patient’s response to therapy.

PHYSICAL EXAMINATION Although physical examination is often unremarkable in cats with chronic vomiting, abnormalities can aid in winnowing the differential list.

Cats with chronic GI disease are typically euvolemic but can have decreased skin turgor due to dermal aging changes or depletion of fat stores. Conversely, oral mucous membranes can be moist in dehydrated

BOX 1. Pertinent Historical Changes in Cats With Chronic Vomiting • Activity level and appetite • Water intake

Abnormalities on thoracic auscultation or abdominal palpation might alter initial testing. The thorax should be auscultated for cardiac murmurs, rhythm disturbances, and abnormal bronchovesicular sounds.

Gentle but thorough abdominal palpation might reveal nausea (licking of lips, excessive swallowing, resistance to palpation), hepatomegaly, cranial abdominal pain, irregularity or asymmetry of the kidneys, an enlarged urinary bladder, or peritoneal effusion, increasing prioritization of abdominal imaging.

Careful attention should be paid to GI abnormalities, such as diffuse thickening or mass effects.

Rectal temperature should be determined regardless of patient temperament; alterations such as hypothermia and fever generally suggest systemic disease. Hematochezia or melena might be identified on inspection of the thermometer or sedated rectal examination.

INITIAL DIAGNOSTIC TESTS As noted above, the diagnostic approach for each case should be customized after assessment of the patient’s history, physical examination findings (including metabolic stability), and differential diagnosis. The typical baseline diagnostics are discussed below. Although a second-tier test for most cases of chronic vomiting, abdominal radiography might be the initial diagnostic test performed when obstruction or an abdominal mass effect is suspected.

Fecal Flotation/Empirical Deworming

• Urine output • Fecal consistency • Weight •B ody and muscle condition score (eg, client reports that the cat is “hollow in the belly” or “skinny”) •D emeanor and activity, (eg, hyperactivity, irritability, pruritus, excessive vocalization)

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cats because of ptyalism. The nictitans, sclera, and mucous membranes should be carefully assessed for jaundice. The base of the tongue should be elevated to check for linear foreign bodies, particularly in younger cats and cats with a history of pica. The breath should be checked for uremic halitosis and the mouth surveyed for periodontal disease, calculus, ulcers, and masses. Complete ophthalmic evaluation might reveal anterior uveitis, chorioretinitis, vascular tortuosity, or retinal hemorrhage. The ventral neck should be carefully palpated for thyroid nodules.

CHRONIC VOMITING IN CATS

Fecal flotation and empirical deworming should be performed in all cases, regardless of outdoor exposure.

A minimum of 2 g of feces, a solution with a specific gravity greater than 1.240, and centrifugation should be used for fecal flotation to decrease the likelihood of falsenegative results (by up to 10-fold for some parasites).11

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A broad-spectrum parasiticide, such as fenbendazole (generally given for 3 days, repeated at 3 weeks and 3 months), should be administered in cases with negative fecal flotation results because of the poor sensitivity of this test.12 In cases with direct or indirect flea exposure, treatment for Dipylidium species should also be administered. When Physaloptera species are suspected, multiple pyrantel treatments are recommended.13

Diet Trial Half of cats in a study of chronic enteropathy experienced clinical cure after diet change, with almost immediate cessation of vomiting.3 Other GI signs, if present, resolved in most cats within 3 days.

Because serial diet trials often do not need to exceed 7 to 14 days each, it is reasonable to perform them before pursuing the remaining first-tier diagnostic tests in cats without evidence of systemic disease.

Although the phrase “diet trial” is often used interchangeably with the term “novel protein trial”— suggesting that FRD is uniformly triggered by protein sources—grains, feed additives, and nonspecified changes associated with commercial processing can trigger clinical signs in some cats.3 Thus, over-thecounter and highly digestible diets can be used in addition to novel or hydrolyzed protein diets.

During each dietary trial, cats should not receive treats, human food, flavored medications, or vitamins or feast on prey. If clinical cure is noted, rechallenge with the cat’s initial diet is important to determine whether long-term dietary modification is necessary to prevent recrudescence. In 1 trial, 40% of cats with FRD remained in clinical remission in the face of rechallenge with their initial diet, while the rest experienced recurrence of signs within 3 to 4 days.3

Noninvasive Blood Pressure Measurement Hypertension may indicate the presence of systemic disease, such as chronic kidney disease or hyperthyroidism. To avoid misdiagnosis, blood pressure should be measured in a relaxed environment after a 10-minute acclimation period to the environment and personnel. Use of Doppler method is recommended because it has better accuracy and precision in awake cats compared with oscillometry.14 Additionally, the coccygeal artery should be used in cats with low muscle condition scores because of a confounding influence of sarcopenia on radial artery measurements.15

Complete Blood Count Normocytic, normochromic, nonregenerative anemia is a nonspecific finding. In contrast, regenerative anemia and microcytic, hypochromic anemia occur secondary to chronic GI bleeding, often without hematochezia or melena. Erythrocytosis in apparently euvolemic patients can result from hyperthyroidism,16 although subclinical dehydration should be considered. Eosinophilia and basophilia are common in cats with GI disease and/ or parasitism, but they are nonspecific findings.

Serum or Plasma Biochemical Profile Abnormalities should be considered in light of magnitude, proportionality of change, and physical examination findings. For example, discordant increases in blood urea nitrogen and creatinine generally suggest GI bleeding but can also occur in cats with cachexia due to chronic kidney disease.

Discordant elevation of globulin over albumin might indicate systemic disease, while proportional elevation is more consistent with total body water losses and dehydration. Hypochloremia, hyponatremia, hypokalemia, and hypophosphatemia might occur as sequelae of vomiting, while hypercalcemia and hyperphosphatemia generally reflect underlying systemic disease. Ionized calcium measurement is occasionally necessary to differentiate between hemoconcentration-associated increases in total calcium and true hypercalcemia.

Liver enzyme activity increases are more significant in cats than in dogs because of shorter enzyme halflives and the lack of a glucocorticoid-induced alkaline phosphatase isoform in this species. Discrimination between hepatocellular and cholestatic liver enzyme patterns is a crucial step to guide clinical reasoning.

Additional information regarding liver enzyme assessment can be found in McAtee and Lidbury.17

Urinalysis Urine concentration should be interpreted in light of the water content of the patient’s diet, as well as the patient’s hydration status. Minimally concentrated urine in a cat eating a dry commercial diet suggests extragastrointestinal disease. Proteinuria should be quantified by urine protein:creatinine ratio in patients with negative urine sediment and culture results, with values 0.2 to 0.4 considered borderline proteinuria and >0.4 considered NOVEMBER/DECEMBER 2017

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significant proteinuria. If proteinuria is present, thorough evaluation for systemic disease is generally warranted before pursuing primary GI disease.

Heartworm and Retroviral Testing Geographic location dictates prioritization of heartworm testing, although it should be considered a first-tier test in areas where heartworms are endemic. Serum antigen testing is generally considered more specific but less sensitive than antibody testing18 because it assesses the presence of worm antigen versus historical exposure. However, a recent study found serum antigen testing to be more sensitive and specific than serum antibody testing.19 Combination testing has the highest sensitivity, although false-negative results still occur.20 Retroviral status should be confirmed as part of initial diagnostic screening, even for indoor-only cats.21 Confirmatory testing is recommended for cats that are positive on initial screening. Care should be taken to ascertain FIV vaccination status because not all point-of-care antibody tests can accurately differentiate between prior vaccination and infection.22 A positive FIV result from an antibody test with unknown differentiation ability should be confirmed via Western blot or polymerase chain reaction (PCR).

Thyroid Hormone Quantitation Screening for hyperthyroidism is warranted regardless of age, given reports of clinical hyperthyroidism in cats as young as 8 months.23 Measurement of total thyroxine (T4) concentration is diagnostic for hyperthyroidism in approximately 95% of cases. Free T4 concentration determination is recommended for cats suspected of hyperthyroidism that have total T4 concentrations in the upper half of the reference range. Elevated free T4 in the presence of total T4 measurements in the upper half of the reference range suggests hyperthyroidism.24

Radiographs are evaluated for alterations in organ size, the presence of mass effects and foreign bodies, GI abnormalities suggestive of obstruction or motility disorders, and peritoneal effusion.

Such findings are generally specific, although their absence does not rule out significant disease.

Advantages of ultrasonography in evaluation of patients with GI signs include the ability to detect homogenous and heterogenous changes to the parenchyma of various viscera; visualize the biliary tree and its path through the pancreas; differentiate between the GI lumen and various layers of the wall, as well as localize and quantitate any thickening present; assess intestinal motility, corrugation, and plication; identify mesenteric lymphadenomegaly, foreign bodies, and masses; and guide noninvasive tissue and fluid sampling. Care should be taken in differentiating between dilatation and simple dilation of the common bile duct (an aging-related change in cats).

Assuming hyperthyroidism has been ruled out, changes in GI wall layering or thickness suggest primary GI disease (eg, FRD, IBD, neoplasia, histoplasmosis). It is generally accepted that small intestinal wall thickening of 0.28 cm or greater is clinically significant; such thickening has been associated with both lymphoma and IBD.1,2,25,26 Wall thickening can be focal, diffuse, or segmental. Although focal thickening can suggest neoplasia, ulceration and IBD also can be associated with focal defects and warrant consideration. Segmental thickening has been found with multiple abnormalities, such as concurrent IBD and lymphoma.26 Thickening can affect all wall layers or specific layers (Figure 1).

Thickening of the muscularis propria (greater than half the thickness of the submucosa) is more likely in cats with lymphocytic lymphoma, although it

SECOND-TIER DIAGNOSTIC TESTS If the cause of vomiting remains unknown after completion of the preceding tests, second-tier diagnostics are warranted.

Abdominal Imaging To optimize diagnostic accuracy, abdominal radiography and ultrasonography should be performed after a routine fast. Inadequate fasting particularly complicates assessment for motility disorders.

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CHRONIC VOMITING IN CATS

FIGURE 1. Diffuse muscularis thickening (arrows) in a cat with chronic vomiting diagnosed with hyperthyroidism.

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also can be seen in normal cats or those with IBD.27 Additionally, loss of intestinal wall layering, masslike lesions, and/or reduced wall echogenicity have been associated with lymphoblastic lymphoma.27

Markers of Dysbiosis, Vitamin Deficiency, and Pancreatic Inflammation Hypocobalaminemia is present in 61% of cats with primary GI disease,28 and vomiting has been reported as the only clinical sign in some cats with hypocobalaminemia.29 Hypocobalaminemia also has been reported in cats with extragastrointestinal disease, such as hepatitis and hyperthyroidism.27,30,31 It is important that cobalamin deficiency be detected and addressed because failure to do so can result in persistence of clinical signs despite treatment of the primary disease.27 Some cats have been diagnosed with clinical cobalamin deficiency based on the presence of increased methylmalonic acid concentrations without hypocobalaminemia.28 Consequently, supplementation should be considered for cats with values in the low end of the reference range.

Folate is absorbed in the proximal small intestine only. Elevated serum folate concentrations can be secondary to small intestinal bacterial overgrowth (resulting from GI disease or dysbiosis) or coprophagia (feces have high folate concentrations).32 Decreased serum folate concentrations can be secondary to focal proximal or diffuse small intestinal disease, but they also have been noted in cases of pancreatitis or cholangiohepatitis.27 Low serum folate concentrations also can be seen in clinically healthy cats.27 Concurrent low cobalamin and folate concentrations have been associated with severe diffuse GI disease.33 Some patients with high serum folate and low cobalamin concentrations experience normalization of folate concentrations after cobalamin supplementation.29 Reevaluation of folate concentration after correction of hypocobalaminemia might, therefore, be prudent in some cases.

Exocrine pancreatic disease can be divided into exocrine pancreatic insufficiency (EPI) and pancreatitis.

EPI is diagnosed based on decreased serum trypsinlike immunoreactivity concentration. Although feline EPI historically has been considered rare, the apparently low prevalence could reflect inadequate surveillance for the disease, according to a recent

report.34 Clinical signs in cats with EPI in that report included poor body condition, weight loss, loose stools or diarrhea, and polyphagia, but also lethargy, anorexia, and vomiting. The study found a high frequency of low cobalamin and high folate concentrations.

Elevated trypsin-like immunoreactivity also can be seen in cats with small intestinal disease, pancreatitis, and kidney failure. Sensitivities (42% to 80%) and specificities (63% to 100%) of the validated lipase assays for pancreatitis vary dramatically, depending on the criteria for diagnosis (histologic inflammation, clinical signs and ultrasonographic changes, or some combination thereof ).35–38 A semiquantitative point-of-care feline pancreatic-specific lipase test is available, but its sensitivity, specificity, and accuracy have not been independently validated. None of the biomarkers for pancreatic inflammation are a substitute for clinical judgment, and clinical signs and other diagnostic test results should be integrated into the diagnosis of feline pancreatitis.

Urine Histoplasma Antigen Histoplasma urine antigen concentration (miravistalabs.com) should be quantitated in cases with appropriate clinical history and exposure, laboratory findings, and abdominal imaging changes.

Histoplasma infections primarily occur in the Ohio River Valley and southeastern United States. The assay has good sensitivity (94.4%), although negative test results do not rule out infection.39 Cross-reactivity with other systemic infectious agents is possible.39

Helicobacter Species Testing Helicobacter species have been identified in biopsy specimens from both clinically ill and healthy cats.40–44 Prevalence increases with age,43 although the organisms have been noted in animals as young as 6 weeks.45 Because of the high prevalence of Helicobacter species within healthy populations, treatment is generally withheld unless concurrent histopathologic abnormalities have been identified and other causes of gastritis have been ruled out.45 Treatment consists of multimodal antibiotics with or without gastric acid suppression.45–47

WHEN TO RECOMMEND ENDOSCOPY Direct evaluation of the GI tract should be considered when the preceding testing does not reveal a systemic cause for vomiting and diet trials have failed or the cat has evidence of focal disease that warrants focused NOVEMBER/DECEMBER 2017

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investigation. This can be accomplished via endoscopy, laparoscopy, or laparotomy. The decision to perform endoscopy over laparotomy is multifactorial, and advantages of each approach are listed in Box 2.

Investigating Imaging Findings No Abnormalities Endoscopy is generally preferable as an initial sampling technique for patients without abnormalities on imaging because it is less invasive and might reveal focal mucosal lesions that would be missed by laparotomy.

Diffuse Changes Endoscopy should be considered for cases with diffuse or accessible focal GI changes, whereas laparotomy is prioritized for patients with ultrasonographic abnormalities limited to the jejunum. Although the muscularis is inaccessible endoscopically, thickening on ultrasonography does not necessarily dictate use of more invasive sampling techniques, such as laparotomy. Diffuse ultrasonographic thickening is often associated with IBD and lymphoma (Figure 2),49,50 which are regularly diagnosed via endoscopic biopsy.

Focal Thickening Focal thickening of the muscularis propria has been associated with mast cell tumor,51 which might be amenable to endoscopic sampling depending on location. Because muscularis thickening can occur in cats without GI disease, sampling is not warranted in the absence of clinical signs.52 Similarly, although focal mass effects on examination or diagnostic imaging are most suggestive of neoplasia, disorders such as GI eosinophilic sclerosing fibroplasia and (rarely) fungal infection should not be overlooked.

Because the location of lesions can substantially complicate surgical removal and positive, long-term responses can be achieved by using a combination of diet and medical therapies,53 it is reasonable to rule out GI eosinophilic sclerosing fibroplasia via endoscopy before proceeding to laparotomy.

Identifying Lesions for Surgery Endoscopy can be useful for localizing and targeting mucosal lesions for surgical intervention, although it is very reasonable to proceed directly to laparotomy in cases with concurrent abnormalities in the liver, pancreas, or other organs. If financial limitations are present,

BOX 2. Advantages of Endoscopy versus Laparoscopy or Laparotomy48 Advantages of endoscopy •A llows direct, continuous visualization of the gastrointestinal tract (Figure A) without disruption of normal anatomy, thereby enhancing detection of:

o Primary and secondary esophageal diseases (eg, esophagitis)

o Gastroduodenal reflux

o Erosions and ulcerations

o Multifocal and highly localized lesions

o Alterations in gastrointestinal motility

•U ses natural orifices for access, allowing more rapid recovery and avoiding risk of dehiscence Advantages of laparoscopy or laparotomy • Ability to obtain full-thickness samples •A bility to sample neighboring structures (eg, liver, pancreas, regional lymph nodes) •A bility to access lesions aborad to approximately 50% of the duodenum or orad to the ileum •A bility to achieve cure through surgical resection of focal neoplasms or other masses

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FIGURE A. Endoscopic image of a prominent duodenal papilla (arrow) and generalized mild duodenal edema in a cat with chronic hyporexia and vomiting due to lymphocytic IBD.

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Kyle Restle Kyle Restle is a small animal surgery resident at the University of Tennessee’s small animal teaching hospital. He is a 2016 graduate of Auburn University’s College of Veterinary Medicine. His primary interests are veterinary surgery, 3-dimensional printing, and medical technology/instrumentation.

Jacqueline Whittemore Jacqueline Whittemore is an associate professor at the University of Tennessee College of Veterinary Medicine, where she also serves as the minimally invasive procedures service chief and the Acree Research Chair in Small Animal Medicine. She received her DVM from the University of California, Davis, and completed her residency and PhD at Colorado State University. Her major research foci are identification and amelioration of adverse effects of exogenous therapies (particularly antiplatelet, immunosuppressive, and antibiotic) on the gastrointestinal tract, development of simulators for veterinary training, and validation of minimally invasive diagnostic techniques to decrease patient morbidity and improve patient outcome.

laparotomy with biopsies of all possibly affected organs is generally recommended to avoid missing the primary disease process or a chance to achieve surgical cure.

Collecting Samples for Biopsy Endoscopically collected biopsy samples can be both highly sensitive and specific for GI disease, depending on the histologic quality of the samples.48 To be considered histologically adequate, samples

must contain 3 or more villi and lamina propria extending to the mucosa–muscularis mucosa border.

A 99% likelihood of detecting cellular infiltrates and villus blunting in the stomach and duodenum can be achieved with as few as 6 adequate samples;54 if samples are histologically inadequate, 18 to 26 specimens are required for this level of confidence. Histologic quality cannot be determined on the basis of gross appearance; therefore the endoscopist should collect a reasonable number of biopsy samples and follow best practices for sample alignment to avoid overlooking a subtle lesion.48 Sensitivity of endoscopic biopsy for detection of lymphoma does not vary according to sample quality,54 although distinguishing between lymphoma and lymphoplasmacytic enteritis can be difficult regardless of sample quality.55 The use of immunohistochemistry and PCR for antigen receptor rearrangements can help differentiate between the two differentials.56–59 Simultaneous collection of ileal biopsy specimens increases the chance of detecting regional disease, particularly with regard to ileal lymphoma.60 Because this necessitates colonoscopy, clinical judgment should be used in deciding whether the increase in patient preparation, anesthesia time, costs, and potential complications is warranted.

CONCLUSION Chronic vomiting in cats is a frustrating condition, and accurate diagnosis hinges on use of a systematic approach. Endoscopy is warranted after systemic diseases have been ruled out, particularly in cases without solitary jejunal disease. In the absence of other findings, the presence of muscularis thickening does not indicate a need for laparotomy. As technology advances and endoscopy becomes more sophisticated, it may become more useful or reliable in obtaining samples and performing interventional techniques.

REFERENCES 1. Norsworthy GD, Estep JS, Hollinger C, et al. Prevalence and underlying causes of histologic abnormalities in cats suspected to have chronic small bowel disease: 300 cases (2008-2013). JAVMA 2015;247(6):629-635.

2. Norsworthy GD, Scot Estep J, Kiupel M, et al. Diagnosis of chronic small bowel disease in cats: 100 cases (2008-2012). JAVMA 2013;243(10):1455-1461.

3. Guilford WG, Jones BR, Markwell PJ, et al. Food sensitivity in cats with chronic idiopathic gastrointestinal problems. J Vet Intern Med 2001;15(1):7-13.

4. Washabau RJ, Day MJ, Willard MD, et al. Endoscopic, biopsy, and histopathologic guidelines for the evaluation of gastrointestinal inflammation in companion animals. J Vet Intern Med 2010;24(1):10-26.

FIGURE 2. Diffuse muscularis thickening (arrows) and lymphadenopathy (caliper markings) in a cat with chronic vomiting due to lymphoma.

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5. Felts JF, Fox PR, Burk RL. Thread and sewing needles as gastrointestinal foreign bodies in the cat: a review of 64 cases. JAVMA 1984;184(1):56-59.

6. Nussbaum LK, Scavelli TD, Scavelli DM, et al. Abdominal ultrasound examination findings in 534 hyperthyroid cats referred for radioiodine treatment between 2007-2010. J Vet Intern Med 2015;29(4):1069-1073.

CONTINUING EDUCATION 7. Williams TL, Peak KJ, Brodbelt D, et al. Survival and the development of azotemia after treatment of hyperthyroid cats. J Vet Intern Med 2010;24(4):863-689.

8. Batchelor DJ, Devauchelle P, Elliott J, et al. Mechanisms, causes, investigation and management of vomiting disorders in cats: a literature review. J Feline Med Surg 2013;15(4):237-265.

9. Egenvall A, Nødtvedt A, Häggström J, et al. Mortality of life-insured Swedish cats during 1999–2006: age, breed, sex, and diagnosis. J Vet Intern Med 2009;23(6):1175-1183.

10. Jergens AE, Crandell JM, Evans R, et al. A clinical index for disease activity in cats with chronic enteropathy. J Vet Intern Med 2010;24(5):1027-1033.

11. Dryden MW, Payne PA, Ridley R, et al. Comparison of common fecal flotation techniques for the recovery of parasite eggs and oocysts.

Vet Ther 2005;6(1):15-28.

12. Little S, Adolph C, Downie K, et al. High prevalence of covert infection with gastrointestinal helminths in cats. JAAHA 2015;51(6):359-364.

13. Companion Animal Parasite Council. Phylasoptera spp. Available at: capcvet.org/guidelines/physaloptera-spp/. Accessed September 2017.

14. Binns SH, Sisson DD, Buoscio DA, et al. Doppler ultrasonographic, oscillometric sphygmomanometric, and photoplethysmographic techniques for noninvasive blood pressure measurement in anesthetized cats. J Vet Intern Med 1995;9(6):405-414.

15. Whittemore JC, Nystrom MR, Mawby DI. Effects of various factors on Doppler ultrasonographic measurements of radial and coccygeal arterial blood pressure in privately owned, conscious cats. JAVMA 2017;250(7):763-769.

16. Broussard JD, Peterson ME, Fox PR. Changes in clinical and laboratory findings in cats with hyperthyroidism from 1983 to 1993. JAVMA 1995;206(3):302-305.

17. McAtee B, Lidbury J. Continuing education: liver enzyme interpretation and liver function tests. Today Vet Pract 2017;7(3):28-38.

18. Snyder PS, Levy JK, Salute ME, et al. Performance of serologic tests used to detect heartworm infection in cats. JAVMA 2000;216(5):693-700.

19. Berdoulay P, Levy JK, Snyder PS, et al. Comparison of serological tests for the detection of natural heartworm infection in cats. JAAHA 2004;40(5):376-384.

20. Jones S, Graham W, von Simson C, et al. Current feline guidelines for the prevention, diagnosis, and management of heartworm (Dirofilaria immitis) infection in cats. Batavia, IL: American Heartworm Society; 2014.

21. Levy J, Crawford C, Hartmann K, et al. 2008 American Association of Feline Practitioners' feline retrovirus management guidelines. J Feline Med Surg 2008;10(3):300-316.

22. Westman ME, Malik R, Hall E, et al. Determining the feline immunodeficiency virus (FIV) status of FIV-vaccinated cats using point-of-care antibody kits. Comp Immunol Microbiol Infect Dis 2015;42:43-52.

23. Gordon JM, Ehrhart EJ, Sisson DD, et al. Juvenile hyperthyroidism in a cat. JAAHA 2003;39(1):67-71.

24. Peterson ME, Melian C, Nichols R. Measurement of serum concentrations of free thyroxine, total thyroxine, and total triiodothyronine in cats with hyperthyroidism and cats with nonthyroidal disease. JAVMA 2001;218(4):529-536.

25. Goggin JM, Biller DS, Debey BM, et al. Ultrasonographic measurement of gastrointestinal wall thickness and the ultrasonographic appearance of the ileocolic region in healthy cats. JAAHA 2000;36(3):224-228.

26. Lingard AE, Briscoe K, Beatty JA, et al. Low-grade alimentary lymphoma: clinicopathological findings and response to treatment in 17 cases. J Feline Med Surg 2009;11(8):692-700.

27. Reed N, Gunn-Moore D, Simpson K. Cobalamin, folate and inorganic phosphate abnormalities in ill cats. J Feline Med Surg 2007;9(4):278-288.

28. Dossin O. Laboratory tests for diagnosis of gastrointestinal and pancreatic diseases. Topics Compan Animal Med 2011;26(2):86-97.

29. Ruaux CG, Steiner JM, Williams DA. Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia. J Vet Intern Med 2005;19(2):155-160.

32. Suchodolski JS, Steiner JM. Laboratory assessment of gastrointestinal function. Clin Tech Small Animal Pract 2003;18(4):203-210.

33. 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(1):26-32.

34. Xenoulis PG, Zoran DL, Fosgate GT, et al. Feline exocrine pancreatic insufficiency: a retrospective study of 150 cases. J Vet Intern Med 2016;30(6):1790-1797.

35. Oppliger S, Hilbe M, Hartnack S, et al. Comparison of serum spec fPL() and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6'-methylresorufin) ester assay in 60 cats using standardized assessment of pancreatic histology. J Vet Intern Med 2016;30(3):764-770.

36. Oishi M, Ohno K, Sato T, et al. Measurement of feline lipase activity using a dry-chemistry assay with a triolein substrate and comparison with pancreas-specific lipase (Spec fPL(TM)). J Vet Med Sci 2015;77(11):1495-1497.

37. Oppliger S, Hartnack S, Riond B, et al. Agreement of the serum spec fPL and 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6'-methylresorufin) ester lipase assay for the determination of serum lipase in cats with suspicion of pancreatitis. J Vet Intern Med 2013;27(5):1077-1082.

38. Oppliger S, Hartnack S, Reusch CE, et al. Agreement of serum feline pancreas-specific lipase and colorimetric lipase assays with pancreatic ultrasonographic findings in cats with suspicion of pancreatitis: 161 cases (2008-2012). JAVMA 2014;244(9):1060-1065.

39. Cook AK, Cunningham LY, Cowell AK, et al. Clinical evaluation of urine Histoplasma capsulatum antigen measurement in cats with suspected disseminated histoplasmosis. J Feline Med Surg 2012;14(8):512-515.

40. Neiger R, Dieterich C, Burnens A, et al. Detection and prevalence of Helicobacter infection in pet cats. J Clin Microbiol 1998;36(3):634-637.

41. Jalava K, Hielm S, Hirvi U, et al. Evaluation of a molecular identification scheme based on 23S rRNA gene polymorphisms for differentiating canine and feline gastric Helicobacter spp. Lett Appl Microbiol 1999;28(4):269-274.

42. Norris CR, Marks SL, Eaton KA, et al. Healthy cats are commonly colonized with "Helicobacter heilmannii" that is associated with minimal gastritis. J Clin Microbiol 1999;37(1):189-194.

43. Otto G, Hazell SH, Fox JG, et al. Animal and public health implications of gastric colonization of cats by Helicobacter-like organisms. J Clin Microbiol 1994;32(4):1043-1049.

44. Papasouliotis K, Gruffydd-Jones TJ, Werrett G, et al. Occurrence of 'gastric Helicobacter-like organisms' in cats. Vet Rec 1997;140(14):369-370.

45. Neiger R, Simpson KW. Helicobacter infection in dogs and cats: facts and fiction. J Vet Intern Med 2000;14(2):125-133.

46. DeNovo R, Magne M, eds. Current concepts in the management of Helicobacter-associated gastritis. In: Proceedings of the 13th Annual Veterinary Medical Forum-American College of Veterinary Internal Medicine; 1995 Lake Buena Vista, Florida, USA. 47. Khoshnegah J, Jamshidi S, Mohammadi M, et al. The efficacy and safety of long-term Helicobacter species quadruple therapy in asymptomatic cats with naturally acquired infection. J Feline Med Surg 2011;13(2):88-93.

48. Jergens AE, Willard MD, Allenspach K. Maximizing the diagnostic utility of endoscopic biopsy in dogs and cats with gastrointestinal disease. Vet J 2016;214:50-60.

49. Daniaux LA, Laurenson MP, Marks SL, et al. Ultrasonographic thickening of the muscularis propria in feline small intestinal small cell T-cell lymphoma and inflammatory bowel disease. J Feline Med Surg 2014;16(2):89-98.

50. Zwingenberger AL, Marks SL, Baker TW, et al. Ultrasonographic evaluation of the muscularis propria in cats with diffuse small intestinal lymphoma or inflammatory bowel disease. J Vet Intern Med 2010;24(2):289-292.

51. Laurenson MP, Skorupski KA, Moore PF, et al. Ultrasonography of intestinal mast cell tumors in the cat. Vet Radiol Ultrasound 2011;52(3):330-334.

52. Winter MD, Londono L, Berry CR, et al. Ultrasonographic evaluation of relative gastrointestinal layer thickness in cats without clinical evidence of gastrointestinal tract disease. J Feline Med Surg 2014;16(2):118-124.

30. Cook AK, Suchodolski JS, Steiner JM, et al. The prevalence of hypocobalaminaemia in cats with spontaneous hyperthyroidism. J Small Animal Pract 2011;52(2):101-106.

53. Linton M, Nimmo JS, Norris JM, et al. Feline gastrointestinal eosinophilic sclerosing fibroplasia: 13 cases and review of an emerging clinical entity.

J Feline Med Surg 2015;17(5):392-404.

31. Geesaman BM, Whitehouse WH, Viviano KR. Serum cobalamin and methylmalonic acid concentrations in hyperthyroid cats before and after radioiodine treatment. J Vet Intern Med 2016;30(2):560-565.

54. Willard MD, Mansell J, Fosgate GT, et al. Effect of sample quality on the sensitivity of endoscopic biopsy for detecting gastric and duodenal lesions in dogs and cats. J Vet Intern Med 2008;22(5):1084-1089.

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PEER REVIEWED 55. Willard MD, Jergens AE, Duncan RB, et al. Interobserver variation among histopathologic evaluations of intestinal tissues from dogs and cats. JAVMA 2002;220(8):1177-1182.

58. Pohlman LM, Higginbotham ML, Welles EG, et al. Immunophenotypic and histologic classification of 50 cases of feline gastrointestinal lymphoma. Vet Pathol 2009;46(2):259-268.

56. Kiupel M, Smedley RC, Pfent C, et al. Diagnostic algorithm to differentiate lymphoma from inflammation in feline small intestinal biopsy samples. Vet Pathol 2011;48(1):212-222.

59. Gabor LJ, Canfield PJ, Malik R. Immunophenotypic and histological characterisation of 109 cases of feline lymphosarcoma. Austral Vet J 1999;77(7):436-441.

57. Moore PF, Rodriguez-Bertos A, Kass PH. Feline gastrointestinal lymphoma: mucosal architecture, immunophenotype, and molecular clonality. Vet Pathol 2012;49(4):658-668.

60. Scott KD, Zoran DL, Mansell J, et al. Utility of endoscopic biopsies of the duodenum and ileum for diagnosis of inflammatory bowel disease and small cell lymphoma in cats. J Vet Intern Med 2011;25(6):1253-1257.

Chronic Vomiting in Cats: When to Recommend Endoscopy LEARNING OBJECTIVE

After reading this article, participants will be able to categorize common causes of chronic vomiting in cats, create a systematic diagnostic plan, and distinguish when endoscopy is warranted.

The article you have read has been submitted for RACE approval for 1 hour of continuing education credit and will be opened for enrollment when approval has been received.

To receive credit, take the approved test online for free at vetfolio.com/journal-ce. Free registration on VetFolio.com is required. Questions and answers online may differ from those below. Tests are valid for 2 years from the date of approval.

1. Vomiting can be distinguished from regurgitation by a. association with eating. b. presence of food in vomitus. c. frequency of occurrence. d. presence of nausea or ptyalism.

6. A duration of _____ is appropriate for a diet trial to rule out food responsive disease in most cats. a. 2 days b. 2 weeks c. 2 months d. 4 months

2. _______ testing has the highest sensitivity for detecting heartworm infection in cats. a. Modified Knott b. Serum antibody c. Serum antigen d. Serum antibody with antigen

7. Approximately what percentage of cats with food responsive disease relapse when rechallenged with their original diet? a. 25% b. 50% c. 75% d. 100%

3. Thyroid hormone quantitation should be performed in _____ cats with chronic vomiting. a. juvenile b. adult c. geriatric d. all 4. Diffuse thickening of the muscularis mucosa without concurrent clinical signs of disease necessitates advanced diagnostics such as endoscopy. a. True b. False 5. Ultrasonographic small intestinal thickening of _____ cm is generally considered clinically significant. a. ≥0.08 b. ≥0.10 c. ≥0.18 d. ≥0.28

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8. Tissue in which area of the gastrointestinal tract is inaccessible via endoscopy? a. Stomach b. Duodenum c. Ileum d. Jejunum 9. Because endoscopy does not allow collection of full-thickness biopsy specimens, it has low diagnostic value for cases with diffuse muscularis propria thickening. a. True b. False 10. Fenbendazole is ineffective for treatment of which of the following parasites? a. Ancylostoma species b. Dipylidium species c. Toxascaris species d. Trichuris species

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ADVANCES IN FELINE CARDIAC DIAGNOSTICS

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Advances in Feline Cardiac Diagnostics Brent Aona, DVM, and Darcy Adin, DVM, DACVIM North Carolina State University College of Veterinary Medicine

The diagnosis of cardiac disease in cats can be challenging and may require a combination of history, physical examination, laboratory evaluation, electrocardiography, diagnostic imaging, and systemic workup. This article presents 2 clinical cases, 1 with and 1 without clinical signs of heart disease, to highlight the use of tailored diagnostics to diagnose cardiac disease in cats.

CASES Case 1: Tux Tux is a 4-year-old male, castrated, domestic medium-haired cat presented for routine vaccination.

His physical examination is unremarkable except for a new grade II/VI left parasternal systolic murmur.

What recommendations should be made?

Case 2: Elvis Elvis is an 8-year-old male, castrated, domestic long-haired cat presented for labored breathing, first noted by his owner this morning. A limited physical examination reveals regular tachycardia (heart rate, 220 beats/min), dyspnea, pale mucous membranes, and hypothermia (temperature, 99.0°F). Lung sounds are harsh dorsally and dull ventrally. A murmur is not auscultated.

What recommendations should be made?

PHYSICAL EXAMINATION Although exceedingly important, physical examination alone cannot be used to rule in or rule out heart disease in cats. A murmur is an important indicator of heart disease; however, cardiac auscultation alone can be

THE RIGHT COMBINATION The diagnosis of cardiac disease in cats can be challenging and may require a combination of history, physical examination, laboratory evaluation, electrocardiography, diagnostic imaging, and systemic workup.

shutterstock.com/Elena Glezerova

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misleading in the diagnosis of feline cardiac disease.

Murmurs can be auscultated in cats with and without underlying heart disease, and up to half of all feline murmurs are found in cats without primary cardiac disease.1 Conversely, cats can exhibit heart disease, potentially severe, without a murmur.

Case notes: The presence of a new murmur in Tux does not equate to heart disease but does warrant further investigation. Likewise, the inability to auscultate a murmur in Elvis does not rule out heart disease.

Additional physical examination findings that may prompt cardiac diagnostic testing include a precordial thrill, muffled heart and lung sounds, gallop sound, arrhythmia, changes in pulse quality, pulse deficits, or jugular venous distention or pulsation. Diastolic heart sounds are abnormal in small animals, and S4 gallops, in particular, are often associated with advanced heart disease in cats. This extra sound in diastole indicates atrial contraction into a stiff ventricular cavity. Common arrhythmias in cats include sinus tachycardia, premature beats, and, in cases of severe heart disease and atrial enlargement, atrial fibrillation.

Pulse deficits may accompany some of these arrhythmias. Jugular venous distention or pulsation indicates elevated right atrial pressures or arrhythmias demonstrating atrioventricular dissociation.

Case notes: Tux does not have physical examination abnormalities other than a murmur. Elvis, on the other hand, is tachycardic, tachypneic, and hypothermic and has dull ventral lung sounds, all of which could be consistent with congestive heart failure (CHF). He should be placed in an oxygen cage after a brief examination.

natriuretic peptide (NT-proBNP) would be a reasonable screening test (see Biomarkers).

Case notes: Echocardiography should be offered to Tuxâ&#x20AC;&#x2122;s owner to determine whether heart disease is present, whether any medications are indicated, and when he should be rechecked.

The most common cardiac disease in cats is hypertrophic cardiomyopathy (HCM), which is characterized by primary left ventricular concentric hypertrophy detected by echocardiography (Figure 1). Secondary causes of hypertrophy (eg, systemic hypertension, hyperthyroidism) should be ruled out before HCM is diagnosed.

Other, less common cardiac diseases in cats are listed in Box 1. Although treatment of CHF is similar regardless of the underlying cause, more tailored treatment recommendations and prognostic information may be obtained by determining the underlying cardiac disease with echocardiography (eg, taurine analysis and supplementation for dilated cardiomyopathy).

In addition to facilitating a definitive diagnosis, echocardiography can also be used to determine disease severity, monitor progression, and guide treatment. For example, the severity of HCM can be assessed by the thickness of the left ventricle, the size of the atria, left atrial appendage velocity, and the presence or absence of spontaneous echo contrast. Estimating thromboembolic risk based on left atrial parameters is pertinent in light of a

ECHOCARDIOGRAPHY Echocardiography is used to definitively diagnose heart disease in cats and to determine disease severity. It provides information on cardiac size and function, as well as blood flow direction and speed. It is reasonable to recommend echocardiography as the first test in a cat with a murmur but without clinical signs of heart disease and then pursue further guided testing if the echocardiogram is abnormal. Detection of cardiac disease at this preclinical stage is considered important because medications can be initiated in an attempt to reduce thromboembolic risk, and the client can be educated regarding monitoring and further evaluations. If echocardiography is not pursued initially, then N-terminal pro B-type

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FIGURE 1. Two-dimensional short-axis ultrasonographic view of Tux showing concentric left ventricular hypertrophy and papillary muscle hypertrophy, consistent with hypertrophic cardiomyopathy. His left atrium was normal in size on other images. LV, left ventricle.

PEER REVIEWED

recent report showing that clopidogrel prolonged the time to recurrent thromboembolism in cats with cardiomyopathy.2 Other medications, such as atenolol, may be initiated in a cat with preclinical heart disease, especially if left ventricular outflow obstruction is detected echocardiographically. However, minimal evidence supports this recommendation.

For dyspneic cats, point-of-care cage-side thoracic ultrasonography is useful to aid in the clinical decision to treat for heart failure or respiratory disease. This is performed in the emergency department, often in the oxygen cage, with the cat in sternal recumbency to reduce stress. The goals of brief ultrasonography in this situation are to determine whether the left atrium is enlarged, screen for pericardial and pleural effusion, and determine whether hyperechoic lung artifacts (B-lines) are present, which could indicate interstitial fluid (Figures 2 and 3). A recent study showed high sensitivity and specificity of B-lines to detect CHF in cats (87% and 89%, respectively).3 Cage-side ultrasonography may also be useful to briefly assess left ventricle size and function; however, routine echocardiography is required to fully assess the underlying cardiac disease.

Case notes: Because of Elvis’s clinical instability, cageside thoracic ultrasonography is indicated to assess left atrial size and screen for pleural effusion, which is clinically suspected on the basis of physical examination.

Full echocardiography should be postponed until Elvis is stabilized; however, this initial assessment indicates the need for thoracocentesis and medical intervention for suspected CHF. The presence of B-lines suggests concurrent pulmonary edema, and the enlarged left atrium supports CHF as the diagnosis.

RADIOGRAPHY Initial diagnostic imaging for cardiac disease may include thoracic radiography because it is relatively inexpensive and available to most veterinarians.

Moderate to severe cardiac enlargement can be appreciated on thoracic radiography; however, this modality is insensitive for the detection of mild cardiac disease and cannot depict concentric hypertrophy of the ventricle.

Case notes: Thoracic radiography is not a good screening tool for cats like Tux. Thoracic radiography is the test of choice for dyspneic cats to determine whether respiratory signs are caused

by CHF. Cardiomegaly, pulmonary vascular distention,

FIGURE 2. Two-dimensional cage-side thoracic ultrasonogram from Elvis showing pleural effusion and an enlarged left atrium (LA). LV, left ventricle; RA, right atrium.

BOX 1 Cardiac Diseases That Can Cause Congestive Heart Failure in Cats • Hypertrophic cardiomyopathy • Restrictive cardiomyopathy • Dilated cardiomyopathy • Unclassified cardiomyopathy •A rrhythmogenic right ventricular cardiomyopathy • Valvular disease • Congenital disease

FIGURE 3. Cage-side thoracic ultrasonogram from Elvis showing B-lines consistent with interstitial edema. Rib shadows are noted. Photo courtesy of Teresa DeFrancesco, DVM, DACVIM (Cardiology), DACVECC, North Carolina State University, College of Veterinary Medicine.

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and pulmonary edema or pleural effusion support a diagnosis of CHF (Figure 4). Pulmonary infiltrates in cats with CHF often appear as an unstructured interstitial to alveolar pattern with no typical distribution (in contrast to the appearance in dogs).

Thoracic radiography is useful to document response to diuresis and to monitor for recurrent CHF. In most situations, radiography is the initial test to determine the underlying cause of respiratory distress. However, when patient instability precludes radiography, pointof-care, cage-side thoracic ultrasonography can provide important information on the likelihood of CHF. Case notes: Point-of-care ultrasonography is the best choice to initially evaluate Elvis; however, after thoracocentesis and improved clinical stability, thoracic radiography is indicated to continue diagnostic evaluation for CHF.

ELECTROCARDIOGRAPHY Electrocardiography is the test of choice for the diagnosis of arrhythmias and conduction disturbances but is relatively insensitive as a screening tool for the detection of heart disease in cats. It is recommended when an arrhythmia is auscultated or suspected (eg, syncope).

BIOMARKERS A biomarker is a parameter that can be accurately measured and is an indicator of a normal or pathologic process, or a pharmacologic response to therapeutics.4 The two most commonly used cardiac biomarkers in veterinary medicine are cardiac troponin I (cTnI) and NT-proBNP.

A

B

FIGURE 4. (A) Right lateral and (B) dorsoventral thoracic radiographs from Elvis after thoracocentesis was performed. A small amount of residual pleural effusion is present, obscuring the cardiac silhouette in the dorsoventral view. The cardiac silhouette is enlarged and the pulmonary vasculature is enlarged. A mild interstitial pattern is present in the caudal lung fields, consistent with pulmonary edema.

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Cardiac troponin I is a regulatory protein that binds actin and myosin in cardiac myocytes. When these cells are damaged, cTnI is released into the bloodstream and can be measured. Because of its exclusivity to cardiac cells, an increase in blood cTnI concentration is relatively specific for cardiac cell damage; however, elevations do not indicate a specific disease process.5 Cardiac troponin I has been reported to be higher in cats with moderate to severe HCM than in healthy cats, but because of the substantial overlap between groups this test is not considered a good screening tool for feline cardiomyopathy.6,7 Similarly, cTnI is higher in cats with respiratory distress due to CHF than in cats with a noncardiac cause of respiratory distress; however, values overlap enough that clinical utility of cTnI for this purpose is limited.7,8 The detection of arrhythmias or abnormal echocardiographic wall motion may prompt evaluation of cTnI as an indicator of acute myocardial damage.

B-type natriuretic peptide (BNP) is a hormone released in response to cardiac stretch associated with heart disease. The natriuretic action of BNP helps to control fluid homeostasis in the body by renal sodium excretion and so counteracts the volume-retaining effects of the renin-angiotensin-aldosterone system.

The breakdown product of BNP (NT-proBNP) can be measured as an indicator of myocardial stress.9 Several studies have demonstrated the ability of NT-proBNP to help distinguish between normal cats and cats with preclinical heart disease with good sensitivity and specificity (76% to 92% and 71% to 93%, respectively).10â&#x20AC;&#x201C;12 Because these studies compared the performance of NT-proBNP to that of echocardiography as the gold standard, this test is not additive if echocardiography is performed. Rather, it can be used as a screening test for patients at risk for cardiac disease.

Although NT-proBNP is sensitive and specific for the detection of cardiac disease, it cannot be used to determine the type of disease. Additional diagnostics are often required if the value is elevated.

The negative predictive value of NT-proBNP is very high (ie, heart disease is unlikely if the NT-proBNP level is normal); however, diseases such as hyperthyroidism, hypertension, or renal disease can elevate NT-proBNP concentrations in the absence of cardiac disease. Thus, results of biomarker testing should be interpreted in conjunction with other clinical information.

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BOEHRINGER INGELHEIM

Vision and Value: Leading the Way to Support Practices Part Two in a Series

Following is an interview with Tim Bettington, North American region head of commercial operations at Boehringer Ingelheim What is your vision for the new Boehringer Ingelheim pet business?

Our vision is to be the company of choice for veterinarians, technicians and practice managers.

We’ve made a start toward realizing that vision with offerings including innovative products, couponing and direct-to-consumer advertising, which drives pet owners to the veterinarian.

As a leader in the pet healthcare space, we are now starting to focus on better understanding how we can support clinics to make the experience of pet healthcare as engaging and enjoyable as possible. Looking at our interactions with veterinarians and veterinary practices, we want to make sure we are engaging at the right times, in the right way and with the right people. Our goal is to be the first company a practice calls for products, scientific questions and business support.

What’s an example of how understanding the customer experience will benefit veterinarians and veterinary practices?

One example is managing our pet owner coupon programs; a lot of what we do today is still very much a manual process and quite labor-intensive. If a client signs up for one of our programs at a veterinary practice, the front office staff has to administer those programs and it’s all manual.

How do we improve that and make it easier for the staff so they don’t have to enter and track manually? How do we continue to make the experience smoother and easier for the clinic staff and the pet owner?

We are also looking at initiatives that help bring clients into the practice more often. If the veterinarian gets to see a patient twice a year for a prescription for one of our products, that supports compliance. The biggest obstacle with any preventive is compliance.

For example, heartworm preventives have been available for decades and, to this day, roughly 70 percent of clients leave the clinic without a heartworm preventive for their dogs.

As you think about where the company is going, are you more focused on helping solve a veterinarian’s problem, or bringing them something they didn’t know they needed?

If we focus only on solving problems, we’ve failed already, because we’re not bringing veterinarians anything new.

That’s where we need to have a nice mix of products, technology, and automation that can really help practices.

If we can walk into a vet clinic and demonstrate to the owner or practice manager that the clinic may be able to generate more income through using tools we offer, we can make a difference in that practice.

If our representative comes in and says, “Here’s a tool we have to help drive profitability,” and the practice owners and managers experience increased sales and pet owner compliance, then we have something that can really help.

It doesn’t even have to come from us. We can be the third or fourth party. But if it’s something we bring because of the scope we have, and we can bring offerings we weren’t able to bring before, that adds value.

Are there other examples where you are managing change or areas where you see the need for change moving forward?

We want to lead the way with strategies on how practices generate revenue in the future that will be positive and sustaining. Different types of customers want to buy things very differently. We’re looking at ways to connect with those people, both practices and pet owners, to offer options. That should be our No. 1 focus. We want to provide the No. 1 brands in all our chosen product categories, and we want to be on the forefront to support veterinarians and pet owners as we make positive changes today and for years to come.

“IF WE FOCUS ONLY ON SOLVING CUSTOMERS’ PROBLEMS, WE’VE FAILED ALREADY, BECAUSE WE’RE NOT BRINGING THEM ANYTHING NEW.” -Tim Bettington, North American region head of commercial operations

Visit boehringer-ingelheim.com/animal-health

PEER REVIEWED

Brent Aona Brent Aona is a cardiology resident at North Carolina State University College of Veterinary Medicine. He completed his undergraduate and graduate studies at The Ohio State University, where he received his DVM. This was followed by a small animal rotating internship at Tufts University, after which he began his residency in cardiology at North Carolina State University. His clinical research is focused on echosonography of congenital cardiac defects, and his main clinical interest is interventional cardiology.

Darcy Adin Darcy Adin is a clinical assistant professor of cardiology at North Carolina State University College of Veterinary Medicine. She received her DVM from Cornell University. She completed a rotating internship at VCA South Shore Animal Hospital and a cardiology residency at the University of California, Davis, with ACVIM board certification in cardiology in 2000. Dr. Adin has held positions in both academic and private specialty practice. Her clinical research focuses on the investigation of neurohormonal modulation of and new treatment options for congestive heart failure.

Case notes: Evaluation of NT-proBNP would be a reasonable first step if Tux’s owner were not able to pursue echocardiography. An NT-proBNP level <100 pmol/L would provide assurance that significant heart disease is not associated with Tux’s new heart murmur. An NT-proBNP value >100 pmol/L could be consistent with the presence of heart disease and should prompt echocardiography or close monitoring.

Assessment of NT-proBNP also provides valuable information for differentiating between cardiac and noncardiac causes of respiratory distress.13,14 An NT-proBNP level >265 pmol/L suggests CHF in a cat with respiratory distress.12,14 Values <265 pmol/L but >100 pmol/L could indicate a noncardiac cause of dyspnea and concurrent heart disease.

A feline SNAP BNP test (idexx.com) is available and can be helpful in an urgent care setting to determine whether a dyspneic cat is likely to have CHF. A negative SNAP result correlates to an NT-proBNP level <100 pmol/L, indicating that CHF is unlikely in a dyspneic cat. A positive SNAP result correlates to an NT-proBNP level >270 pmol/L, supporting CHF in a dyspneic patient; however, concurrent respiratory causes of dyspnea and

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preclinical heart disease could also be the cause of a positive SNAP result. The final SNAP result should always be interpreted in light of the clinical examination and other diagnostic tests. Analysis of BNP in pleural fluid also correlates well to blood concentrations and may prove useful in some clinical situations.15 Case notes: Biomarker testing is not indicated for Elvis because other diagnostic testing rapidly yields his diagnosis of CHF.

GENETICS Genetic testing using blood or cheek swab samples is available for known mutations associated with HCM in 2 cat breeds. Both mutations are single nucleotide substitutions in the cardiac myosin-binding protein C gene. The A31P substitution is found in the Maine coon breed, and the R820W mutation is found in ragdoll cats.16,17 Genotype determination may help guide breeding programs and cardiac therapy, but it should not be used as a substitute for echocardiography because other, undiscovered mutations are associated with HCM in both of these breeds.18–20 In addition, because of the many factors that can influence disease expression, genotype does not always equate to phenotype in individual patients.

Case notes: Because Tux and Elvis are mixedbreed cats, genetic testing is not recommended.

SYSTEMIC DISEASE WORKUP The hallmark echocardiographic finding of HCM is left ventricular hypertrophy. However, other disease processes can also induce wall thickening. The most common systemic causes of left ventricular hypertrophy include systemic hypertension and hyperthyroidism.

Less common causes include acromegaly, infiltrative myocardial diseases (eg, lymphoma), and left ventricular outflow obstructions (eg, aortic stenosis or mitral valve dysplasia causing systolic anterior motion). The echocardiographic finding of left ventricular hypertrophy should therefore prompt an assessment of blood pressure and thyroid concentration in any middleaged to older cat. Treatment of systemic hypertension or hyperthyroidism is expected to improve or resolve echocardiographic abnormalities, but coexisting primary HCM and systemic disease is possible.

Case notes: Blood pressure and thyroid status should be evaluated in Elvis. However, thyroid testing is not necessary in Tux given his young

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age. Although the test is low yield, he should be screened for systemic hypertension.

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References 1. Wagner T, Fuentes VL, Payne JR, et al. Comparison of auscultatory and echocardiographic findings in healthy adult cats. J Vet Cardiol 2010;12(3):171-182.

2. Hogan DF, Fox PR, Jacob K, et al. Secondary prevention of cardiogenic arterial thromboembolism in the cat: the double-blind, randomized, positive-controlled feline arterial thromboembolism; clopidogrel vs. aspirin trial (FAT CAT). J Vet Cardiol 2015;17 Suppl 1:S306-S317.

3. Ward JL, Lisciandro GR, Keene BW, et al. Accuracy of point-of-care lung ultrasonography for the diagnosis of cardiogenic pulmonary edema in dogs and cats with acute dyspnea. JAVMA 2017;250(6):666675.

4. Strimbu K, Tavel JA. What are biomarkers? Curr Opin HIV AIDS 2010;5(6):463-466.

5. Liquori ME, Christenson RH, Collinson PO, Defilippi CR. Cardiac biomarkers in heart failure. Clin Biochem 2014;47(6):327-337.

6. Connolly DJ, Cannata J, Boswood A, et al. Cardiac troponin I in cats with hypertrophic cardiomyopathy. J Feline Med Surg. 2003;5(4):209216.

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7. Herndon WE, Kittleson MD, Sanderson K, et al. Cardiac troponin I in feline hypertrophic cardiomyopathy. J Vet Intern Med 2002;16(5):558564.

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8. Connolly DJ, Brodbelt DC, Copeland H, et al. Assessment of the diagnostic accuracy of circulating cardiac troponin I concentration to distinguish between cats with cardiac and non-cardiac causes of respiratory distress. J Vet Cardiol 2009;11(2):71-78.

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9. van Kimmenade RRJ, Januzzi JL. The evolution of the natriuretic peptides – current applications in human and animal medicine. J Vet Cardiol 2009;11 Suppl 1:S9-S21.

Photo © David Schrichte

Photo © David Schrichte

10. Connolly DJ, Soares Magalhaes RJ, Syme HM, et al. Circulating natriuretic peptides in cats with heart disease. J Vet Intern Med 2008;22:96-105.

11. Fox PR, Rush JE, Reynolds CA, et al. Multicenter evaluation of plasma N-terminal probrain natriuretic peptide (NT-pro BNP) as a biochemical screening test for asymptomatic (occult) cardiomyopathy in cats. J Vet Intern Med 2011;25(5):1010-1016.

12. Wess G, Daisenberger P, Mahling M, et al. Utility of measuring plasma N-terminal pro-brain natriuretic peptide in detecting hypertrophic cardiomyopathy and differentiating grades of severity in cats. Vet Clin Pathol 2011;40(2):237-244.

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13. Connolly DJ, Soares Magalhaes RJ, Fuentes VL, et al. Assessment of the diagnostic accuracy of circulating natriuretic peptide concentrations to distinguish between cats with cardiac and noncardiac causes of respiratory distress. J Vet Cardiol. 2009;11 Suppl 1:S41-S50.

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14. Fox PR, Oyama MA, Reynolds C, et al. Utility of plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) to distinguish between congestive heart failure and non-cardiac causes of acute dyspnea in cats. J Vet Cardiol. 2009;11 Suppl 1:S51-S61.

15. Janda S, Swiston J. Diagnostic accuracy of pleural fluid NT-pro-BNP for pleural effusions of cardiac origin: a systematic review and metaanalysis. BMC Pulm Med 2010;10(1):58.

16. Meurs KM, Sanchez X, David RM, et al. A cardiac myosin binding protein C mutation in the Maine Coon cat with familial hypertrophic cardiomyopathy. Hum Mol Genet 2005;14(23):3587-3593.

17. Meurs KM, Norgard MM, Ederer MM, et al. A substitution mutation in the myosin binding protein C gene in ragdoll hypertrophic cardiomyopathy. Genomics 2007;90(2):261-264.

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18. Li RHL, Stern JA, Ho V, et al. Platelet activation and clopidogrel effects on ADP-induced platelet activation in cats with or without the A31P mutation in MYBPC3. J Vet Intern Med 2016;30(5):1619-1629.

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19. Wess G, Schinner C, Weber K, et al. Association of A31P and A74T polymorphisms in the myosin binding protein C3 gene and hypertrophic cardiomyopathy in Maine coon and other breed cats. J Vet Intern Med 2010;24(3):527-532.

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20. Borgeat K, Stern J, Meurs KM, et al. The influence of clinical and genetic factors on left ventricular wall thickness in Ragdoll cats. J Vet Cardiol 2015;17 Suppl 1:S258-S267.

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CANINE HOUSE SOILING: BACK TO BASICS

PEER REVIEWED

Canine House Soiling: Back to Basics Kelly C. Ballantyne, DVM, DACVB Veterinary Behavior at Illinois, Chicago, IL

Despite the general ease of house training, house soiling is a common behavior problem, reported in approximately 20% of pet dogs.1 House soiling degrades the human–animal bond and is a common reason for pet relinquishment.1–3

These goals can be achieved with close owner supervision, scheduled frequent elimination opportunities, and confinement (Box 1) when the dog cannot be supervised. Although some mistakes will happen even with careful management, frequent mistakes should be avoided because the dog or puppy may develop learned preferences for indoor elimination sites.

Screening patients for behavioral issues at every visit is recommended to identify problems early and institute treatment before the human–animal bond is strained or broken.

When house soiling is identified, the first step in developing an effective treatment plan is to determine the underlying cause or motivation for soiling because several medical and behavioral differentials exist.

Initially, the new dog or puppy should be taken on supervised trips to the chosen elimination site on the following schedule:

PREVENTION: HOUSE TRAINING

BOX 1 Confinement Options for House Training • Confine the dog or puppy to a crate or pen • Tether it to a specific area of the house

With appropriate preventive counseling, most puppy and new dog owners are able to house train their dogs within 1 to 2 months of adoption.4 There are 2 important house training goals:

•T ether it to a family member (also known as umbilical cord training) Introduction of confinement should be done gradually and should be paired with positive experiences to prevent separation or confinement distress.

• Make elimination in the desired location easy.

• Prevent mistakes.

LOCATION, LOCATION, LOCATION If the dog or puppy is caught in the act of eliminating indoors, the owner can attempt to interrupt by clapping or whistling, and then immediately bringing the pet to the desired location.

shutterstock.com/Elena Glezerova

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PEER REVIEWED

• Every 2 to 3 hours • Immediately upon waking and before confinement • Within 10 to 15 minutes of meals and playtime Use of positive reinforcement—for example, giving a treat immediately after elimination in the desired location—can further strengthen preferences for elimination at the desired location.

If the dog or puppy is caught in the act of eliminating indoors, the owner can attempt to interrupt by clapping or whistling, and then immediately bringing the pet to the desired location. Counsel clients to avoid verbal or physical punishment because it can cause fear, anxiety, and aggression and does not teach the dog or puppy where to eliminate. Any soiled indoor sites should be thoroughly treated with an odor-eliminating or enzymatic cleaner as residual odor may encourage resoiling. Once the dog has not soiled indoors for at least 8 weeks, the frequency of scheduled elimination trips and stringency of supervision can be gradually reduced.

DIAGNOSTIC DIFFERENTIALS Medical conditions should be the top differentials for soiling in puppies refractory to house training, cases with acute onset, or soiling in adult and geriatric dogs that were previously house trained. Conditions that can contribute to house soiling include anything that increases the urgency or frequency of elimination, causes pain on elimination, or affects mobility or voluntary control of elimination. Cognitive dysfunction syndrome is a common condition affecting senior dogs that may result in loss of house training via progressive decline in cognitive functioning.5,6 Lack of house training is a common behavioral cause of house soiling.5,6 Soiling occurs for the purpose of relieving pressure on the bladder or bowels. Learned preferences for one or more indoor elimination sites may develop as elimination is a self-reinforcing behavior.

Urine marking is elimination for the purpose of communication.5,6 When urine marking, dogs typically deposit small amounts of urine on vertical surfaces. This behavior is most common in intact male dogs5,6 but can be observed in intact females and neutered males and females. Urine marking may also be a sign of anxiety, triggered by stressful situations or territorial threats.

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Excitement or submissive urination occurs during interactions with other animals, including humans.

In this context, a rapidly wagging tail or signs of appeasement, such as lip licking, lowered head, and caudally deflected ears, accompany urination.

Excitement or submissive urination is most common in puppies6 and young female dogs.5,7 Fear and anxiety disorders that may result in house soiling include separation anxiety, noise aversions, and fear of the outdoors.7 Dogs with separation anxiety may soil during even brief owner absences, whereas dogs with noise aversion may do so during loud noise events, such as thunderstorms or fireworks. Dogs with noise aversion or fear of the outdoors may refuse to go outdoors to eliminate, or their emotional state may prevent or interrupt complete elimination when outdoors. Treatment of the primary condition can help to decrease the frequency or resolve the house soiling.

HISTORY A thorough history helps to differentiate these conditions. Specific questions to focus on include the following: • Who is soiling? In multidog/multianimal households, avoid making assumptions. If the soiling occurs only in the owner’s absence, using a video camera to monitor the soiled area can definitively determine the culprit and ensure the correct patient receives treatment.

• What is it: urine, feces, or both? Domestic dogs rarely mark with feces, so the presence of stool suggests a medical condition, lack of house training, or a fear or anxiety disorder.

• Where is the dog soiling? A consistent location or surface pattern suggests lack of house training,8 while in the author’s experience an inconsistent pattern of soiling throughout the home may indicate a response to fear or anxiety.

• When does the soiling occur, and are there identifiable triggers? Is the owner present, absent, or both? Soiling only in the absence of the owner, even for brief periods, suggests separation anxiety, while soiling during owner interactions suggests excitement or submissive urination.5,6 Determining the frequency of house soiling will also establish the baseline with which to measure treatment success.

• How does the timing of soiling relate to opportunities to eliminate and meal times? Learned preferences for indoor sites may develop when

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dogs are not allowed frequent access to an outdoor elimination site and if elimination opportunities are not offered after meals, play, and sleeping.

• How does the dog eliminate? Signs of discomfort, such as straining or difficulty posturing to eliminate, suggest medical conditions, whereas signs of fear or anxiety while the dog is outdoors suggest an emotional condition.

DIAGNOSTICS A veterinarian should evaluate all dogs presenting with house soiling issues. The minimum database for dogs younger than 5 years includes a physical examination, urinalysis via cystocentesis, and imaging of the lower urinary tract. Dogs aged 5 years and older should also have a complete blood count and chemistry profile. Intestinal parasite screening and a rectal examination are recommended if the dog is defecating indoors. Additional diagnostics, such as water quantitation and a urine cortisol/ creatinine ratio, may be needed depending on the patient’s signalment and clinical signs.

TREATMENT Lack of House Training Lack of house training can be addressed with the same methods used in prevention. Additionally, access to the dog’s preferred indoor elimination site should be restricted. If this is not possible, the owner can attempt to change the function of the site by placing bedding or food and water bowls in the area. Dogs with long histories of house soiling may require several months of careful management to become completely house trained. Complete house training is not established until no house soiling episodes have occurred for 8 weeks or more.

sight, or sound of other dogs or other arousing stimuli, such as mail or package delivery. Medications, such as tricyclic antidepressants or selective serotonin reuptake inhibitors, can help to reduce the marking dog’s emotional arousal and decrease urine marking when combined with environmental management.

Excitement and Submissive Urination Treatment strategies for excitement and submissive urination include environmental management, behavior modification, and, in some cases, medical therapy.

Environmental management requires identification of triggers for urination so they can be eliminated or reduced. Triggers may include the following: • Approach of familiar or unfamiliar people • Standing, reaching, or leaning over the dog • Petting • Speaking in a loud, excited, or harsh tone Clients should be counseled to avoid these types of interactions; call the puppy or dog over to them, rather than approaching; and keep greetings calm. The dog or puppy should also be given an opportunity to eliminate outdoors immediately before the arrival of visitors and should be confined away from visitors who cannot follow the calm greeting routine.

Behavior modification strategies focus on teaching the puppy or dog greeting behaviors that are incompatible with urination, such as lying down or retrieving a toy. Medications that reduce emotional arousal (tricyclic antidepressants or selective serotonin reuptake inhibitors) or increase urethral sphincter

Urine Marking Castration reduces the frequency of urine marking in 50% to 80% of male dogs, regardless of age at time of castration.9 If the castration status of a male dog with marking behavior is undetermined, abdominal ultrasound may help to identify or rule out cryptorchidism. Environmental management strategies for urine marking involve restricting the dog’s access to marked sites, cleaning soiled areas with odor-elimination products, and identifying triggers for marking so they may be eliminated or reduced.

Triggers for marking in dogs may include the smell,

Suggested Client Resources on House Training •H orwitz DF, Ciribassi J, Dale S, eds: Decoding Your Dog: The Ultimate Experts Explain Common Dog Behaviors and Reveal How to Prevent or Change Unwanted Ones. New York: Houghton Mifflin Harcourt; 2014.

•M artin KM, Martin D. Puppy Start Right: Foundation Training for the Companion Dog. Waltham, MA: Karen Pryor Clickertraining; 2011.

• The Ultimate Puppy Toolkit: ultimatepuppy.com

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PEER REVIEWED

Kelly C. Ballantyne Kelly C. Ballantyne, DVM, DACVB, is a clinical assistant professor at the University of Illinois College of Veterinary Medicine. She received her DVM from the University of Illinois and completed a non-traditional residency in veterinary behavior under the mentorship of Dr. John Ciribassi. Her research interests include dog bite prevention and the impact of companion animal behavior on the humanâ&#x20AC;&#x201C;animal bond.

tone (phenylpropanolamine) may aid treatment of excitement or submissive urination.

SUMMARY House soiling is a common behavior problem in dogs that affects the humanâ&#x20AC;&#x201C;animal bond.

A veterinarian should evaluate all house-soiling dogs because several medical conditions can cause elimination issues. Lack of house training is a common behavioral cause of house soiling, and prognosis for improvement is excellent with the use of careful environmental management.

References 1. Wells DL, Hepper P. Prevalence of behaviour problems reported by owners of dogs purchased from an animal rescue shelter. Appl Anim Behav Sci 2000;69(1):55-65.

2. Salman MD, Hutchison J, Ruch-Gallie R. Behavioral reasons for relinquishment of dogs and cats to 12 shelters. J Appl Anim Welf Sci 2000;3(2):93-106.

3. New JC Jr, Salman MD, King M, et al. Characteristics of shelterrelinquished animals and their owners compared with animals and their owners in US pet-owning households. J Appl Anim Welf Sci 2000;3(3):179-201.

4. Herron ME, Lord LK, Reisner IR. Effects of preadoption counseling for owners on house-training success among dogs acquired from shelters. JAVMA 2007;231(4):558-562.

5. Landsberg GM, Hunthausen W, Ackerman L. Canine house soiling.

In: Behavior Problems of the Dog and Cat. 3rd ed. Philadelphia: Saunders Limited; 2013:269-279.

6. Houpt K. House soiling by dogs. In: Horwitz DF, Mills DS, eds.

BSAVA Manual of Canine and Feline Behavioural Medicine. 2nd ed.

Gloucester: British Small Animal Veterinary Association; 2010:111-116.

7. Overall K. Abnormal canine behaviors and behavioral pathologies not primarily involving pathological aggression. In: Manual of Clinical Behavioral Medicine for Dogs and Cats. St. Louis, MO: Elsevier Health Sciences; 2013:231-311.

8. Horwitz DF, Neilson JC. House soiling: canine. In: Blackwell's FiveMinute Veterinary Consult Clinical Companion: Canine and Feline Behavior. Ames, IA: Wiley-Blackwell; 2007:320-328.

9. Neilson JC, Eckstein RA, Hart BL. Effects of castration on problem behaviors in male dogs with reference to age and duration of behavior. JAVMA 1997;211(2):180-182.

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