VETgirl December 2024 BEAT e-Magazine

The VETgirl Beat is a quarterly publication available to all subscribed members of VETgirl. The digital newsletter features highlighted webinars (small animal, large animal, veterinary technician, leadership), tech tips, provider spotlights, and recent happenings.

QUARTERLY BEAT / DECEMBER 2024 ISSUE 23 • DECEMBER 2024 BEAT EMAGAZINE

ACUTE ONSET PANCREATITIS

IN DOGS: EVERYTHING YOU NEED TO KNOW IN 30 MINUTES 12

HEARTWORM CAN WE DETECT, PREVENT, AND BETTER MANAGE THESE CASES? 04

TECH TIPS

DOGS AND CATS WITH CYSTOLITHIASIS 08 UNDERSTANDING DIAGNOSTICS & TREATMENT

29 MIND MASSAGE RECAP

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26 BLOG HIGHLIGHTS: HOW TO COORDINATE CHAOS - BECOME AN

beat ISSUE 23 • DECEMBER 2024 TABLE OF CONTENTS

ORGANIZATIONAL MASTER

29 MIND MASSAGE

KEY TAKEAWAYS FROM THE MOST RECENT WEBINARS

04 FEATURED STORY:

16 WEBINAR HIGHLIGHTS: POCUS TO LIVE, LIVE TO POCUS: DIAGNOSING PERICARDIAL EFFUSION IN SECONDS!

32 TECH TIPS

THE REVISED AMERICAN HEARTWORM SOCIETY

NEW DASHBOARD FEATURES TO ENHANCE YOUR VETGIRL EXPERIENCE

FELINE HEARTWORM DISEASE GUIDELINES: CAN WE DETECT,

PREVENT, AND BETTER MANAGE THESE CASES?

34 TEAM SPOTLIGHT MEET VETGIRL'S NEW MARKETING SPECIALIST

FLUID RATES 20

08 FEATURED STORY: UNDERSTANDING DIAGNOSTICS AND

BLOG HIGHLIGHTS: HOW TO CALCULATE

TREATMENT FOR DOGS AND CATS WITH CYSTOLITHIASIS DIET PLAYS A VITAL ROLE IN THE ONGOING TREATMENT AND PREVENTION

12 FEATURED STORY:

24 BLOG HIGHLIGHTS:

35 WHAT'S ON THE CALENDAR

UPDATES IN ACUTE ONSET PANCREATITIS IN DOGS: EVERYTHING YOU NEED TO KNOW IN 30 MINUTES

ESTABLISHING A PATIENT SAFETY CULTURE IN VETERINARY MEDICINE

MUST-SEE EDUCATION TO ADD TO YOUR JANUARY SCHEDULE

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FELINE HEARTWORM DISEASE DIFFERS FROM ITS CANINE COUNTERPART Dogs and cats are both considered susceptible hosts of Dirofilaria immitis , the heartworm parasite. However, because feline patients today are not routinely screened for heartworms, the prevalence of heartworm in cats is not well understood. In a study conducted at a central Florida animal shelter, sets of 100 unprotected dogs and 100 unprotected cats were screened for heartworm infection and/or history of infection using several different diagnostic modalities (antigen and microfilaria tests in dogs; antigen, antibody and microfilaria tests in cats). When comparing the percentage of animals testing positive on any one modality, there was no statistical difference between the two species. 1 Because the feline immune system mounts a more robust response against immature stages, fewer heartworms reach adulthood in cats. This likely contributes to the misconception that heartworm disease is uncommon in cats, when heartworm disease simply follows a different disease process in cats than dogs. In cats, clinical disease first manifests when immature worms reach the lungs—notably before an antigen test can detect infection. From there, potent inflammatory mediators within the lungs mount a response that may create clinical signs like dyspnea, coughing, vomiting, lethargy, anorexia, etc. In fact, it is likely that many cases diagnosed as feline asthma are actually heartworm disease. If the immune system fails to kill all the larval stage worms—and if the cat survives the process—the cat will go on to develop a patent adult heartworm infection. During this phase of infection, the pulmonary damage created by the arrival, and death, of larval stages can lead to long-lasting asthma-like clinical signs. Adult worms also put additional stress on the heart and pulmonary vasculature. When the adult heartworm eventually dies (typically 2-4 years post-infection, compared to 5-7 years in dogs), the risk of sudden respiratory distress, embolism, and death is renewed.

ROUTINE DIAGNOSTIC HEARTWORM SCREENING NOW RECOMMENDED IN CATS Annual heartworm testing in dogs is standard practice in veterinary hospitals, but most cats are not routinely tested. In dogs, annual antigen testing provides a quick, affordable and accurate means of pinpointing heartworm infections. However, because antigen tests detect adult, female worms versus the male-only or immature heartworm infections that are much more common in cats, antigen screening by itself is unlikely to be a sufficient diagnostic strategy. Heartworm antibody testing detects the presence of antibodies produced by cats in response to a previous or existing heartworm infection at any stage from larvae to adults. The limitation of antibody testing is that it cannot distinguish between present and past infections—only that an infection has occurred. The accuracy of antibody tests is also variable and false-negative results are common. Given the inherent shortcomings of antigen and antibody tests described above, tailoring the diagnostic strategy to achieve accurate detection of feline heartworm is critical. After reviewing testing studies from recent years, the AHS recently identified several strategies that can improve the accuracy of heartworm testing in cats. For the first time, the AHS now strongly recommends annual heartworm screening in cats using the following protocol: • A Heska (an Antech company) antibody test , which has been found to be up to 8 times more sensitive than other tests • An antigen test conducted with heat-treated serum . Antigen-antibody immune complexes can produce false-negative heartworm test results in both dogs and cats. Data accrued in recent years have revealed that these immune complexes occur at much higher rates in feline infections than canine infections.

FEATURED STORY

In this VETgirl feature article sponsored* by the American Heartworm Society (AHS), Dr. Jenni Rizzo, reviews what’s new with treating feline heartworm disease. Feline heartworm disease is misunderstood, underdiagnosed, and undermanaged. So, what do you need to know about the revised AHS Feline Heartworm Disease Guidelines? Read on to learn more! * Please note the opinions of this blog are the expressed opinion of the author and not directly endorsed by VETgirl.

THE REVISED AMERICAN HEARTWORM SOCIETY FELINE HEARTWORM DISEASE GUIDELINES: CAN WE DETECT, PREVENT, AND BETTER MANAGE THESE CASES?

BY DR. JENNI RIZZO DVM, President, American Heartworm Society (AHS)

Conventional wisdom among veterinarians has long held that heartworm disease is a serious, ubiquitous issue in dogs. At the same time, while many practitioners also believe that heartworm disease in cats is a serious disease, they view it as relatively uncommon. This assumption has led many practitioners to look for heartworms in feline patients only when overt clinical signs point to the problem, and to refrain from recommending routine heartworm testing and prevention in cats. The result: feline heartworm disease today is misunderstood, underdiagnosed and undermanaged. A recent revision of the American Heartworm Society (AHS) Guidelines on Feline Heartworm Management, which includes updates to the organization’s recommendations for prevention, diagnosis and treatment in cats, is designed to challenge these misperceptions about heartworms in cats and to encourage practitioners to consider a more proactive approach to this serious disease.

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REFERENCES

1. Hays KM, Rodriguez JY, Little SE, Litster AL, Mwacalimba KK, Sundstrom KD, Amodie DM, Serrano MA, Guerios SD, Lane JN, Levy JK. Heartworm prevalence in dogs versus cats: Multiple diagnostic modalities provide new insights. Vet Parasitol. 2020;277S:100027. doi: 10.1016/j. vpoa.2020.100027. Epub 2020 Jun 12. PMID: 34392951. 2. Atkins, CE, DeFrancesco TC, Coats JR, Sidley JA, Keene BW. Heartworm infection in cats: 50 cases 1985-1997). J Am Vet Med Assoc. 2000;217, 355-358.

By conducting these antibody and antigen tests concurrently on a routine basis, practitioners can increase the odds of accurately diagnosing feline patients. Routine testing can also help veterinarians establish a diagnosis when clinical evidence of infection exists, monitor the status of cats already diagnosed with heartworms, establish a baseline prior to beginning a heartworm prevention product, and help veterinarians understand the relative risk of feline heartworm in their geographical practice area. When antigen and antibody tests do not provide a positive diagnosis, radiography, echocardiography and point of care ultrasound can also assist in finding evidence of heartworm disease. It's the AHS’ hope that increased testing will also lead to improved understanding of the disease and increased awareness of its prevalence in cats. Such a shift could also spur research into improved diagnostic and treatment strategies for cats.

The updated AHS feline guidelines now also include a discussion of the importance of vector control in preventing heartworm infection in cats. Because cats are sensitive to many of the pesticide products considered safe for dogs, environmental vector control becomes especially important. Strategies include eliminating sources of standing water or treating sources of standing water with chemical and/or biological tools such as insect growth regulators, Bacillus species and mosquito fish. In addition, owners can limit their cats’ outdoor exposure and utilize local environmental application of insecticidal sprays and fogs, as well as adult mosquito traps. MANAGEMENT OPTIONS FOR CATS WITH FELINE HEARTWORM DISEASE With more routine testing, veterinarians can logically expect numbers of cats diagnosed with heartworms to increase. Because there are no adulticide treatments approved for cats, the AHS guidelines now include updated recommendations for managing cats that have become infected. These recommendations are designed to relieve the clinical signs of disease and, in cases of adult infection, to prevent sudden death of cats. Within the updated guidelines, veterinarians will find specific dose, route, and frequency recommendations for treatment of acutely dyspneic cats, as well as cats with chronic disease or asymptomatic infection.

scientific information that supports a more proactive approach to heartworm diagnosis, as well as greater specificity in prevention and treatment approaches. If these recommendations are widely adopted, we believe it will encourage further advancements in testing, treatment, and prevention for a class of patients that has been historically overlooked. The AHS Heartworm Management Guidelines for dogs and cats are living documents that are updated as appropriate when new information and evidence comes to light. The AHS Board of Directors would like to thank the following board members who serve on the Heartworm Guidelines Committee:

• Charles Thomas (Tom) Nelson, DVM • John McCall, MS, PhD • Andrew Moorhead, DVM, MS, PhD, DACVM (Parasitology) • Lindsay Starkey, DVM, PhD, DACVM (Parasitology) • W. Mark Cousins, DVM, DABVP (Feline Practice) • Marisa Ames, DVM, DACVIM (Cardiology)

When treating infected cats, veterinarians can consider the following medications:

• Prednisolone to relieve coughing and other respiratory signs • Doxycycline to eliminate Wolbachia organisms from heartworms (these endosymbiont bacteria contribute to heartworm pathogenesis in cats as well as dogs)

• Antileukotrienes to prevent respiratory crisis • Macrocyclic lactone preventives to prevent new infection • Supportive therapy with corticosteroids, bronchodilators, oxygen, fluids and thermal support during episodes of respiratory distress The revised AHS recommendations also provide guidance for veterinarians considering surgical removal of adult heartworms in cats, for such cases where it may be deemed necessary. As an organization that is dedicated to reducing the incidence of heartworm disease and its impact on pets, the AHS has long been concerned about the underdiagnosis and undermanagement of heartworm disease in cats. We now have

ROUTINE YEAR-ROUND HEARTWORM PREVENTION NOW INCLUDES VECTOR CONTROL For years, the AHS has recommended routine use of heartworm preventives in cats. Any cat that lives where heartworm-positive dogs and wild canids exist is at risk for heartworm transmission, and with no treatment for adult heartworm infection approved in cats, year-round prevention of heartworms is the best means of protecting these patients from a potentially life-threatening infection. Indoor cats are no exception, as mosquitoes can enter homes and transmit infective heartworm larvae to unprotected animals. In a retrospective study conducted at North Carolina State University, roughly one in four cats found to be heartworm- positive were identified by their owners as “indoor” pets. 2

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the mechanisms for struvite formation in this species are not well understood and likely involves many factors including genetics, sex, environment, diet and hydration. Unfortunately, the pathophysiology of CaOx uroliths in cats and dogs is also not well understood. There are breed predispositions such as the Miniature Schnauzers, Shih Tzu and Bichon Frise 3,5 and Burmese and Persian cats,4 which suggests a genetic basis for mineral formation. Several other factors can increase the risk for CaOx urolithiasis. For example, any comorbidity that contributes to hypercalcemia such as primary hyperparathyroidism can increase serum calcium concentration and result in excess calcium excretion in the urine. However, oftentimes, the reason for the hypercalciuria remains idiopathic 5 and research, including the mechanisms for hypercalciuria, the role of lipids 6,7 and increased body condition score 8 are ongoing. Surgery (e.g., cystotomy) or other minimally invasive procedures (e.g., laser lithotripsy) 9 are usually necessary for CaOx removal and it is a best practice to confirm complete removal by post-procedure radiography. While CaOx uroliths can’t be dissolved by diet, diet should be part of the prevention strategy; medications, such as thiazide diuretics or potassium citrate, might also be needed in select cases. NUTRITION PLAYS A VITAL ROLE Diet plays a crucial role in preventing future stone formation in dogs and cats. In fact, therapeutic diets also can dissolve struvite stones in dogs and cats, 10,11 thereby avoiding unnecessary surgery. When struvite uroliths are suspected in dogs and cats, diets formulated for struvite dissolution are recommended. Due to their differences in pathophysiology, antimicrobials should be administered to dogs (e.g., amoxicillin) but are rarely indicated in cats. The pet should be rechecked in approximately two weeks (cats) or four weeks (dogs) for radiographic evidence of urolith dissolution. If no evidence of dissolution is noted on digital radiography, the stones should be removed by one of the previously mentioned methods. Dissolution can take several months, especially in dogs. Therefore, if uroliths are decreasing in size, dietary therapy should be continued. Fortunately, clinical signs are usually well controlled during this treatment regimen, but analgesics can be provided if warranted. Struvite prevention diets are rarely necessary in dogs, but dietary therapy should be continued for most cats. Therapeutic diets can also be prescribed to reduce the risk of CaOx formation, but “off- label” diets should be considered in pets with comorbidities. Hydration is extremely important for urolith prevention. This can be accomplished by feeding canned food to the pet or adding water to dry kibble or providing additional hydration supplements. Suggested guidelines recommend specific urine dilution levels to reduce the risk of uroliths – consistently less than 1.030 in cats and 1.020 in dogs. 9 Increasing water intake will increase voiding and dilute mineral precursors.

DIFFERENCES BETWEEN CRYSTALLURIA AND UROLITHIASIS Understanding the differences between uroliths and crystalluria is crucial to guide appropriate diagnostics and treatment. Crystalluria refers to the presence of crystals in the urine sediment examination. Struvite, CaOx and amorphous crystals can not only be identified in the urine sediment due to analytical error but also in some healthy animals without any overt lower urinary tract signs (LUTS). Increased storage time and decreased temperature can lead to in vitro struvite and CaOx crystal formation. 1 Therefore, if the clinician is evaluating urine sediment from a pet with LUTS or from a urolithiasis patient, it is crucial to examine the urine appropriately. The urinary sediment should be evaluated within 60 minutes of collection with the specimen at room temperature. Urate and cystine crystals should not spontaneously precipitate and finding these crystals on a urine sediment exam might warrant further diagnostics depending on the pet’s signalment and history. In properly analyzed urine specimens, crystalluria does not always indicate urinary disease. There is no evidence that crystalluria causes any harm to urinary epithelium and healthy dogs and cats can develop crystalluria due to various factors. Moreover, in animals with urolithiasis, crystalluria noted on urine sediment does not accurately correlate with the mineral analysis of the stone. 2 Dietary intervention for pets with only crystalluria is not usually warranted. Urolithiasis involves actual stone formation within the urinary tract, which often leads to LUTS mentioned above. Cystic calculi are a common occurrence in cats and dogs and the two most common uroliths in both species are CaOx and struvite uroliths. 3,4 The pathophysiology for these uroliths is likely multifactorial and are discussed separately below.

FEATURED STORY

In this VETgirl feature article sponsored* by the Purina Pro Plan Veterinary Diets, Dr. Jodi Westropp, DVM, PhD, DACVIM (Internal Medicine) reviews what you need to know about the diagnostic workup and treatment plan for dogs and cats with cystolithiasis. After all, we see and diagnose this all the time, but what do we do for long-term management? * Please note the opinions of this blog are the expressed opinion of the author and not directly endorsed by VETgirl.

UNDERSTANDING DIAGNOSTICS AND TREATMENT FOR DOGS AND CATS WITH CYSTOLITHIASIS DIET PLAYS A VITAL ROLE IN THE ONGOING TREATMENT AND PREVENTION

BY DR. JODI L. WESTROPP PhD, DACVIM University of CA, Davis

Urolithiasis is a common urinary tract disease encountered in dogs and cats. Uroliths are most often diagnosed on plain radiography, ultrasonography or a combination of the two. As veterinarians, we often see patients present with previous history, concerns or clinical signs of lower urinary tract discomfort, such as stranguria, pollakiuria, hematuria or a combination of these signs. Moreover, urolithiasis can be life- threatening and lead to complete urethral or ureteral obstruction in cats and dogs. It is important to understand the underlying pathophysiology for urolith formation as well as diagnostic approaches for evaluating dogs and cats with suspected urolithiasis. This will allow us to formulate better treatment and prevention strategies, including dietary solutions for the most common uroliths in dogs and cats. In this overview, we will focus primarily on the two most common uroliths noted in these species, struvite and calcium oxalate (CaOx).

STRUVITE UROLITHIASIS: BIG DIFFERENCES BETWEEN CATS AND DOGS

In dogs, unlike cats, struvite uroliths typically form due to infections with a urease-producing bacteria, altering urine chemistry and raising urinary pH levels. Struvite urolithiasis in cats usually form in the absence of urinary tract infections. An elevated pH provides the right environment for minerals like magnesium, ammonium and phosphate to precipitate and form struvite stones. The most common urinary pathogen that contributes to struvite urolithiasis in dogs is Staphylococcus spp. Therefore, in dogs with urinary tract calculi, a urine culture is warranted; if Staphylococcus spp. is isolated on aerobic urine culture, the urolith is likely comprised, at least in part, of struvite. Unlike dogs, struvite urolithiasis in cats is usually sterile and

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SCIENTIFIC ADVANCEMENTS POINT TO A PROMISING FUTURE There have been many recent advancements for urinary tract health that are providing new diagnostics, genetic insights and other research regarding diets to prevent uroliths in animals. Ongoing research continues to investigate the connection between cystine stones in intact male dogs, 3,12 urinary microbiome and its role in struvite and CaOx formation, 13,14 and the gut-urinary axis. As procedures and techniques continue to advance, there are minimally invasive techniques and surgeries for improved stone removal.

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Understanding the unique aspects of struvite and CaOx stones allows us to tailor prevention strategies more effectively. By emphasizing hydration, tailored diets for urolith prevention that also address other comorbidities and risk factors, and regular monitoring, we can improve patient outcomes and minimize stone recurrence. Each animal is unique, so individualized approaches are crucial. By staying informed about the latest research and working with other veterinarians, we can optimize animal care and improve health outcomes.

503B outsourcing facilities like Epicur Pharma are not affected by new GFI #256 requirements or new USP guidelines. Learn more about what these new guidelines mean for you and your practice at epicurpharma.com/usp-guidelines

REFERENCES

1. Albasan H, Lulich JP, Osborne CA, et al. Effects of storage time and temperature on pH, specific gravity, and crystal formation in urine samples from dogs and cats. J Am Vet Med Assoc 2003;222:176-179. 2. Dear JD, Shiraki R, Ruby AL, et al. Feline urate urolithiasis: a retrospective study of 159 cases. J Feline Med Surg 2011. 3. Kopecny L, Palm CA, Segev G, et al. Urolithiasis in dogs: Evaluation of trends in urolith composition and risk factors (2006-2018). J Vet Intern Med 2021;35:1406-1415. 4. Kopecny L, Palm CA, Segev G, et al. Urolithiasis in cats: Evaluation of trends in urolith composition and risk factors (2005-2018). J Vet Intern Med 2021;35:1397-1405. 5. Furrow E, Patterson EE, Armstrong PJ, et al. Fasting Urinary Calcium- to-Creatinine and Oxalate-to-Creatinine Ratios in Dogs with Calcium Oxalate Urolithiasis and Breed-Matched Controls. J Vet Intern Med 2015;29:113-119. 6. Paßlack N, Zentek J, Larsen JA, et al. Impact of hyperlipidaemia on intermediary metabolism, faecal microbial metabolites and urinary characteristics of lipoprotein lipase deficient vs. normal cats. J Anim Physiol Anim Nutr (Berl) 2018;102:e139-e146. 7. Paulin MV, Dunn M, Vachon C, et al. Association between hyperlipidemia and calcium oxalate lower urinary tract uroliths in dogs. J Vet Intern Med 2022;36:146-155.

8. Kennedy SM, Lulich JP, Ritt MG, et al. Comparison of body condition score and urinalysis variables between dogs with and without calcium oxalate uroliths. J Am Vet Med Assoc 2016;249:1274-1280. 9. Lulich JP, Berent AC, Adams LG, et al. ACVIM Small Animal Consensus Recommendations on the Treatment and Prevention of Uroliths in Dogs and Cats. J Vet Intern Med 2016;30:1564-1574. 10. Torres-Henderson C, Bunkers J, Contreras ET, et al. Use of Purina Pro Plan Veterinary Diet UR Urinary St/Ox to Dissolve Struvite Cystoliths. Top Companion Anim Med 2017;32:49-54. 11. Dear JD, Larsen JA, Bannasch M, et al. Evaluation of a dry therapeutic urinary diet and concurrent administration of antimicrobials for struvite cystolith dissolution in dogs. BMC Vet Res 2019;15:273. 12. Larsen JA, Hulsebosch S, Henthorn PS, et al. Urinary cystine/ creatinine concentrations in dogs with suspected androgen- dependent cystine urolithiasis before and after castration. In: ACVIM research abstract, Minneapolis, MN 2024. 13. Coffey EL, Gomez AM, Burton EN, et al. Characterization of the urogenital microbiome in Miniature Schnauzers with and without calcium oxalate urolithiasis. J Vet Intern Med 2022;36:1341-1352. 14. Coffey EL, Gomez AM, Ericsson AC, et al. The impact of urine collection method on canine urinary microbiota detection: a cross- sectional study. BMC Microbiology 2023;23:101.

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while a concentration of ≥ 400 ug/L is suggestive of pancreatitis. Spec cPL concentrations between 200 – 400 ug/L are considered equivocal. The SNAP cPL has higher sensitivity (74 – 100%) compared to its specificity (59 – 78%). A normal SNAP cPL correlates with a Spec cPL concentration of < 200 ug/L indicating AP is unlikely and other disease processes should be considered. On the other hand, an abnormal SNAP cPL correlates with a Spec cPL concentration ≥ 200 ug/L (including both the equivocal and the positive results) and should be followed up with a Spec cPL, which is qualitative. Catalytic assays measure sample (serum/plasma) lipase activity by quantifying formation of catalytic product. Catalytic assays are inexpensive and may be included on routine serum chemistry panels. Various substrates are used in catalytic assays including 1,2-diglyceride, 1-oleo-2,3-diacetylglycerol (e.g., Idexx chemistry), 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6’-methylresorufin) ester [DGGR] (e.g., PrecisionPSL), and triolein (e.g., Fuji Dri-Chem v–lip-p). Catalytic lipase assays may detect extra- pancreatic lipases which limits their analytic specificity. 3,4 Diagnostic Imaging Abdominal ultrasound is useful as a non-invasive diagnostic modality to image the pancreas. In dogs, the right limb of the pancreas is more easily identified when compared to the body or left limb. 5 The pancreas may appear enlarged with hypoechoic parenchyma and hyperechoic surrounding mesentery. Other findings may include pancreatic fluid accumulation, extrahepatic bile duct obstruction (EHBDO), gastric or duodenal wall thickening, and peripancreatic fluid accumulation. 6 There appears to be a lag time between the development of pancreatitis and ultrasonographic findings. Other non-inflammatory conditions (such as portal hypertension and hypoalbuminemia) can result in pancreatic edema. 7 TREATMENT UPDATES Acute pancreatitis in dogs can vary in clinical severity. Patients with self-limiting disease can be managed at home while patients that are affected systemically will require intensive care in hospital. Identify Cause(s) Several risk factors of AP have been identified including dietary (high-fat diet), drugs/toxins (L-asparaginase, phenobarbital, potassium bromide, azathioprine), endocrinopathies (Cushing’s, hypothyroid, diabetes mellitus), hypertriglyceridemia (but not hypercholesterolemia), and various breed predisposition and hereditary factors (miniature schnauzers). Often, a specific underlying cause cannot be identified. 8

Fluid Therapy Poor pancreatic perfusion may lead to the progression of self- limiting pancreatitis to severe necrotizing pancreatitis. Therefore, aggressive fluid therapy has been recommended for many years in both human and veterinary pancreatitis patients. Commonly used fluids include normal saline and lactated Ringer’s. Recent meta-analyses in people have shown that lactated Ringer’s, but not aggressive fluid therapy, prevented the progression of mild to moderate/severe AP. 9,10 In fact, the incidence of fluid overload is higher in patients receiving aggressive fluid therapy. 9 There is no evidence to show that the use of colloids or fresh-frozen plasma for AP is helpful. 11 Recognizing and Managing Complications Local complications of AP include pancreatic necrosis, pancreatic fluid accumulations, pancreatitis-associated EHBDO, gastrointestinal dysmotility, amongst others. Systemic complications include aspiration pneumonia, SIRS, MODS, DIC, AKI, or cardiac injury. Antiemetics/Antinausea Vomiting is thought to occur in dogs with AP due to centrally and peripherally mediated mechanisms. Maropitant (NK-1 antagonist) acts on both central and peripheral emetic pathways and is useful in controlling vomiting, but not nausea, in dogs. 12 Ondansetron (5- HT3 receptor antagonist) is reported to have both antiemetic and antinausea properties in dogs. 13 Metoclopramide only has minimal antiemetic properties and is not recommended to be used as an antiemetic in dogs. Analgesics Abdominal pain should be assumed to be present in any dog with a diagnosis of pancreatitis. Opioids are commonly used as a first- line pain management. 14 The author will typically use methadone (0.1 - 0.5 mg/kg IV SC IM q4-8h) or fentanyl (3 mcg/kg/hour IV bolus followed by CRI at 3 – 5 mcg/kg/hour IV) when the patient is hospitalized. Opioid-sparing analgesics (such as lidocaine or ketamine CRI) can be used to reduce side-effects of opioids. Patients that can be discharged should continue to receive pain management at home. In smaller dogs, transdermal buprenorphine (Zorbium®) can be used off-label at 2 mg/kg transdermal. Fentanyl patches can be prescribed to larger-sized dogs, but care must be taken to prevent inadvertent exposure to family members (especially children). Nutrition Delayed enteral feeding can cause enterocyte damage, gut barrier dysfunction, and dysbiosis. 15 Therefore, early enteral nutrition should be provided, and this can be achieved via placement of a temporary feeding tube (nasogastric or nasoesophageal tube) or a semi- permanent esophageal tube. Begin feeding about 1/3 of RER using a liquid diet (such as Royal Canin Veterinary GI Low Fat Liquid [1 kCal/ mL] or low-fat diet (typically <2 g of fat/100 kCal) given in multiple small meals (trickle feeding or boluses q4-6h).

FEATURED STORY

In this VETgirl featured article sponsored* by CEVA, Dr. Sue Yee Lim, PhD, DACVIM (SAIM) discusses what you need to know about updates in canine pancreatitis. From what’s new in the diagnosis to what’s new with treatment of pancreatitis, you’ll want to keep on reading! *Please note the opinions of this article are the expressed opinion of the author and not directly endorsed by VETgirl.

UPDATES IN ACUTE ONSET PANCREATITIS IN DOGS: EVERYTHING YOU NEED TO KNOW IN 30 MINUTES

BY DR. SUE YEE LIM PhD, DACVIM (SAIM) Gastrointestinal Laboratory, Texas A&M University

DIAGNOSTIC UPDATES The diagnosis of acute onset pancreatitis (AP) in dogs should be made based on global assessment of clinical data including history, clinical signs, physical examination findings, clinicopathologic findings (including measurement of pancreatic lipase), and diagnostic imaging findings. 1 Pancreatic Lipase Testing The measurement of pancreatic lipase can be helpful as a non-invasive marker of pancreatic inflammation. There are numerous methods to measure serum (pancreatic) lipase. 2 Common lipase assays are broadly divided into immunologic and catalytic assays. The immunologic assays use pairs of antibodies for canine pancreatic lipase and measure pancreatic lipase concentration. Examples of immunologic assays include Spec and SNAP cPL (Idexx laboratories), VetScan cPL Rapid Test (Zoetis), and Vcheck cPL 2.0 (Bionote). A Spec cPL concentration of < 200 ug/L makes acute pancreatitis unlikely

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Fuzapladib Sodium In the early stages of AP, neutrophils migrate into the pancreas causing further inflammation. Neutrophil migration into the pancreas (or any tissue) is dependent on the rolling, activation, adhesion, and migration of neutrophils within capillaries into tissues (Figure 1). The migration of neutrophils is dependent on the binding of a molecule called leukocyte function-associated antigen type-1 (LFA-1) on the neutrophil with another molecule on the surface of endothelial cells (called ICAM-1). Fuzapladib sodium (Panoquell®-CA1) is an LFA-1 inhibitor, which prevents migration of neutrophils into the pancreas. It has received FDA conditional approval for the treatment of clinical signs of AP in dogs in the US. It is given at a dose of 0.4 mg/kg IV q24h for three consecutive days. CONCLUSIONS Acute-onset pancreatitis is common in dogs and is associated with high morbidity and even mortality. The diagnosis of AP should not depend on a single test in isolation. Rather, a comprehensive clinical picture is important when diagnosing dogs with AP. While the management of AP in the past has been supportive and symptomatic, a new specific therapeutic agent, fuzapladib sodium, is now available in Japan and the USA.

Other supportive management includes identifying the cause of pancreatitis, fluid therapy, early identification and management of complications, antiemetics, and antinausea, analgesia, and nutrition.

FIGURE 1: NEUTROPHIL EXTRAVASATION CASCADE

With permission from Cridge H, Lim SY, Algül H, et al. New insights into the etiology, risk factors, and pathogenesis of pancreatitis in dogs: Potential impacts on clinical practice. J Vet Intern Med. 2022;36:847-864. The author has used Panoquell®-CA1 in outpatient and inpatient settings and have found that it was helpful in avoiding mortality (from euthanasia or from disease progression).

REFERENCES

1. Cridge H, Twedt DC, Marolf AJ, et al. Advances in the diagnosis of acute pancreatitis in dogs. J Vet Intern Med 2021;35:2572-2587. 2. Lim SY, Steiner JM, Cridge H. Understanding lipase assays in the diagnosis of pancreatitis in veterinary medicine. J Am Anim Hosp Assoc 2022;260:1249-1258. 3. Lim SY, Xenoulis PG, Stavroulaki EM, et al. The 1,2-o-dilauryl-rac- glycero-3-glutaric acid-(6'-methylresorufin) ester (DGGR) lipase assay in cats and dogs is not specific for pancreatic lipase. Vet Clin Pathol 2020;49:607-613. 4. Prummer JK, Howard J, Grandt LM, et al. Hyperlipasemia in critically ill dogs with and without acute pancreatitis: Prevalence, underlying diseases, predictors, and outcome. J Vet Intern Med 2020;34:2319- 2329. 5. Stieger-Vanegas, S.M. and P.M. Frank, Peritoneal Space, in Textbook of Veterinary Diagnostic Radiology. 2018. p. 764-791. 6. Cridge H, Sullivant AM, Wills RW, et al. Association between abdominal ultrasound findings, the specific canine pancreatic lipase assay, clinical severity indices, and clinical diagnosis in dogs with pancreatitis. J Vet Intern Med 2020;34:636-643. 7. Lamb CR. Pancreatic edema in dogs with hypoalbuminemia or portal hypertension. J Vet Intern Med 1999;13:498-500. 8. Cridge H, Lim SY, Algül H, et al. New insights into the etiology, risk factors, and pathogenesis of pancreatitis in dogs: Potential impacts on clinical practice. J Vet Intern Med 2022;36:847-864.

9. de-Madaria E, Buxbaum JL, Maisonneuve P, et al. Aggressive or Moderate Fluid Resuscitation in Acute Pancreatitis. N Engl J Med 2022;387:989-1000. 10. Zhou S, Buitrago C, Foong A, et al. Comprehensive meta-analysis of randomized controlled trials of Lactated Ringer's versus Normal Saline for acute pancreatitis. Pancreatology 2021;21:1405-1410. 11. Leese T, Holliday M, Watkins M, et al. A multicentre controlled clinical trial of high-volume fresh frozen plasma therapy in prognostically severe acute pancreatitis. Ann R Coll Surg Engl 1991;73:207-214. 12. Kenward H, Elliott J, Lee T, Pelligand L. Anti-nausea effects and pharmacokinetics of ondansetron, maropitant, and metoclopramide in a low-dose cisplatin model of nausea and vomiting in the dog: a blinded crossover study. BMC Vet Res 2017;13:244. 13. Henze L, Foth S, Meller S, et al. Ondansetron in dogs with nausea associated with vestibular disease: A double-blinded, randomized placebo-controlled crossover study. J Vet Intern Med 2022;36:1726- 1732. 14. Monteiro BP, Lascelles BDX, Murrell J, et al. 2022 WSAVA guidelines for the recognition, assessment and treatment of pain. J Small Anim Pract 2023;64:177-254. 15. Qin HL, Su ZD, Gao Q, Lin QT. Early intrajejunal nutrition: bacterial translocation and gut barrier function of severe acute pancreatitis in dogs. Hepatobiliary Pancreat Dis Int 2002;1(1):150-154.

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CLINICAL SIGNS: Dogs with pericardial effusion often present with a history of vomiting within 24h of presentation, particularly with acute onset. In cases of sub-acute to chronic onset, owners may report vague symptoms such as “ain’t doing right”, weakness, exercise intolerance, lethargy, tachypnea, syncope, cough, abdominal enlargement, or muscle wasting. Clinical signs may vary based on the underlying cause, acuteness of effusion, and severity. Signs can include decreased breath sounds ventrally if pleural effusion is present, muffled or absent heart sounds, and signs of cardiogenic shock. Most affected cats and dogs exhibit signs of right-sided congestive failure, including pleural effusion, ascites, hepatomegaly, and jugular vein distension (with or without jugular pulses). DIAGNOSIS: In dogs with pericardial effusion, low voltage (<1 mV) QRS complexes are the most common ECG finding. Electrical alternans (i.e., variations in QRS complex or occasionally T-wave size) is less common but more specific to pericardial effusion. Some effusions may not cause any changes in the size of the ECG ventricular complex. ECG findings are neither sensitive nor specific. Thoracic radiographs are neither sensitive nor specific for diagnosing pericardial effusion, even if tamponade is present. The cardiac silhouette can sometimes appear normal or may take on a globoid shape on radiographs. In a study of dogs, 22% showed no enlargement of the cardiac silhouette, and 43% lacked a globoid heart despite having pericardial effusion and clinical signs of tamponade. Typical signs of pulmonary edema, such as increased pulmonary densities and distended pulmonary veins, are less likely. Pulmonary nodular changes may indicate metastatic disease. Emergency cardiac POCUS can quickly and accurately identify pericardial effusion with high sensitivity and specificity. Three windows can be used during cardiac POCUS to assess for pericardial effusion: 1) the subxiphoid window, 2) transthoracic right parasternal imaging with the probe situated directly over the heart (often considered the most challenging site for accurately confirming pericardial effusion), and 3) transthoracic imaging just caudal to the heart at the pericardio- diaphragmatic window. Based on the authors’ experiences, the subxiphoid and pericardio-diaphragmatic sites are the easiest for distinguishing between pericardial and pleural effusion. Cardiac POCUS is usually performed in the patient position that is most comfortable for the patient, and the least likely to cause decompensation, which is often in a sternal or standing position. Thus, cardiac POCUS is rarely performed in right lateral recumbency, and patient comfort and stability are prioritized over patient positioning.

1. SUBXIPHOID POCUS (FIG. 1) Place the ultrasound transducer at the subxiphoid position and advanced cranially, slightly under the xiphoid process, rocking the probe until it is nearly parallel to the spine (most often in long axis, but short axis views can also be obtained). The depth is adjusted to visualize both the pleural space and the heart. Fanning the transducer from left to right will aid in localizing the heart. If the left ventricular wall is seen and is continuous with the diaphragm and liver (termed “cardiac blending”), significant clinical pericardial effusion can be ruled out. If a “black ring” (indicating fluid) outlined by a bright white line (the pericardium) is observed around the ventricle (circumferential effusion), the presence of pericardial fluid is confirmed. It's crucial to differentiate pericardial from pleural fluid; from the subxiphoid window, pleural effusion will track along the diaphragm, forming triangular shapes and angles.

POCUS TO LIVE, LIVE TO POCUS: DIAGNOSING PERICARDIAL EFFUSION IN SECONDS!

SØREN BOYSEN AND SERGE CHALHOUB DVM, DACVECC DVM, DACVIM University of Calgary, Faculty of Veterinary Medicine

In this VETgirl Webinar “POCUS to LIVE, LIVE to POCUS: Diagnosing Pericardial Effusion in Seconds!“ on September 24, 2024, Dr. Søren Boysen, DACVECC and Dr. Serge Chalhoub, DACVIM review how to master the art of pericardial POCUS for rapid identification of pericardial effusion! In case you missed the webinar, watch it again HERE or read the cliff notes below!

pericarditis, trauma, left atrial rupture, systemic coagulopathy, congestive heart failure, chronic uremia, intrapericardial cysts, granulation tissue, chylopericardium, or iatrogenic cases. Prognosis varies and depends on the underlying cause as well as treatment options. Dogs with hemangiosarcoma have a guarded to poor prognosis (median survival of 1-4 months), while those with idiopathic pericardial effusion have a good prognosis (up to 4 years). Survival rates in dogs with heart-base tumors will vary; chemodectomas tend to grow slowly and rarely metastasize, with median survival times of 2 years following surgical pericardectomy. Pericardial effusion and tamponade sometimes mimic other life- threatening conditions, which makes rapid diagnosis necessary to improve patient outcome. Without immediate treatment, the mortality rate is 100% for patients exhibiting severe clinical signs. The risks associated with pericardiocentesis are relatively low and reduced further when using ultrasound. Pericardiocentesis should be performed when clinically warranted. With the increasing availability of ultrasound in everyday practice and advances in emergency point-of-care ultrasound (POCUS) by non-specialists, rapid confirmation and treatment of pericardial effusion is now achievable within minutes of presentation.

INTRODUCTION Cardiac tamponade, a result of pericardial effusion leading to intrapericardial pressure that exceeds right ventricular diastolic pressure, is relatively common in dogs with pericardial effusion but rare in cats. (The most common cause of pericardial effusion in cats is hypertrophic cardiomyopathy and this rarely causes clinically significant pericardial effusion). Rapid acute fluid accumulation, resulting from events such as hemorrhage, right atrial rupture or idiopathic causes, can lead to increased intrapericardial pressure despite minimal fluid volume. In contrast, slow fluid accumulations—often seen with idiopathic pericarditis—allows time for the pericardium to stretch, which means larger fluid volumes may be present. In both scenarios, progressive cardiac compression leads to decreased cardiac filling, reduced cardiac output, and lowered arterial blood pressure, potentially resulting in cardiogenic shock. Conditions frequently linked to pericardial effusion in dogs include neoplasia (40-70%) and idiopathic pericarditis (20- 60%); however, some idiopathic cases may be the result of neoplasia that was not detected at the time of assessment. Common cardiac and extracardiac cancers include right atrial hemangiosarcoma and heart-base tumors (e.g., chemodectoma and mesothelioma). Less common causes include infective

Figure 1: In dogs, this allows the operator to visualize the left ventricular free wall blending seamlessly with the diaphragm and liver in the absence of pericardial effusion. When pericardial effusion is present, it appears as fluid curving around the heart’s apex, creating a separation between the heart and the liver and diaphragm, outlined by the pericardium. Image courtesy of Dr. Jantina McMurray with permission.

WEBINAR HIGHLIGHTS

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REFERENCES

Comprehensive echocardiographic assessment of the heart can be conducted if the patient is more stable prior to pericardiocentesis, as the presence of pericardial fluid facilitates the visualization of intra-pericardial masses. However, it is imperative that the patient’s safety not be compromised by delaying the removal of the fluid or by trying to obtain a formal echocardiogram (especially if the patient is not stable). Often, a small amount of effusion remains after pericardiocentesis, aiding in the identification of tumors. Tamponade, which should be diagnosed through clinical examination in any patient showing signs of shock and pericardial effusion, can also be supported by cardiac POCUS. The "trampoline" sign (seeing the right atrium or ventricle bend or deform), indicating right atrial and ventricular collapse, can be seen in both right parasternal long and short- axis views, though it is usually easier to observe in the right parasternal four-chamber long-axis view. TREATMENT: 1. IV fluids: Cardiac tamponade results from inadequate diastolic filling and therefore is different than left-sided congestive heart failure. Administering IV fluids (initially as a challenge with a fluid bolus) to improve diastolic filling can be considered (and is the authors’ preference) until pericardiocentesis can be performed. 2. Pericardiocentesis: Pericardiocentesis is a lifesaving procedure essential for the rapid stabilization of dogs. Indwelling pericardial catheters, which can be quickly placed and are a safe alternative to pericardiocentesis using needles or single tap catheters, require minimal sedation and are not associated with a higher rate of complications. They can be advantageous as they allow for serial drainage if pericardial effusion recurs. In cats, pericardial effusion is most commonly associated with congestive heart failure, is generally well tolerated, and often responds to heart failure management. 3. Other: Following pericardiocentesis, treatment may include surgery, pericardiectomy, chemotherapy, or radiation therapy for heart base, atrial, or intracardiac tumors, as well as antibiotics for infectious pericarditis. Doxorubicin-based chemotherapy has been reported as a viable treatment for dogs with right atrial masses and pericardial effusion. For persistent or recurrent pericardial effusion, pericardiectomy (via thoracotomy or thoracoscopy) or balloon pericardiotomy remains the treatment of choice. Approximately 40% of benign effusions resolve spontaneously after one or two pericardiocentesis procedures.

2. TRANSTHORACIC POCUS (FIG. 2) Position the ultrasound transducer directly over the heart on either or both sides of the chest to assess for pericardial effusion (most often right transthoracic). Care must be taken to differentiate the right ventricle and other cardiac chambers from pericardial effusion. Pericardial effusion appears as a lucent (most often hypoechoic) area surrounding the heart. Increasing the depth of the ultrasound beam allows visualization of the entire left ventricular apex and surrounding structures. When pericardial effusion is present, the heart will completely be encircled by a circumferential ring of fluid, outlined by the bright white pericardium. Be sure to extend the depth to ensure the entire heart AND pericardium are visible when using this window.

3. PERICARDIO-DIAPHRAGMATIC WINDOW (FIG. 3)

Located by sliding the transducer caudal to the heart or identifying the curtain sign (caudal lung and pleural space border seen as a vertical edge artifact created by air-filled lung overlying soft tissue structures of the abdomen) and tracing it ventrally. This window allows the caudal portion of the heart (specifically the left ventricular wall) to be seen alongside the diaphragm in the same image. This site is useful for differentiating between pericardial effusion, which conforms to the heart's contours and curves away from the diaphragm, and pleural effusion, which follows the diaphragm and forms a triangular or sharp point as it fills the costophrenic recess.

1. Côté E, Schwarz LA, Sithole F. Thoracic radiographic findings for dogs with cardiac tamponade attributable to pericardial effusion. J Am Vet Med Assoc 2013 Jul 15;243(2):232-5. 2. Ghaffari S1, Pelio DC, Lange AJ, et al. A retrospective evaluation of doxorubicin-based chemotherapy for dogs with right atrial masses and pericardial effusion. J Small Anim Pract 2014 May;55(5):254-7. 3. Hall DJ1, Shofer F, Meier CK, Sleeper MM. Pericardial effusion in cats: a retrospective study of clinical findings and outcome in 146 cats. J Vet Intern Med 2007 Sep-Oct;21(5):1002-7. 4. Fahey R, Rozanski E, Paul A, Rush JE. Prevalence of vomiting in dogs with pericardial effusion. J Vet Emerg Crit Care (San Antonio) 2017 Mar;27(2):250-252. 5. Cook S, Cortellini S, Humm K. Prospective evaluation of pericardial catheter placement versus needle pericardiocentesis in the management of canine pericardial effusion. J Vet Emerg Crit Care (San Antonio) 2021 Jan;31(1):11-17. 6. Cook S, Cortellini S, Humm K. Retrospective evaluation of pericardial catheter placement in the management of pericardial effusion in dogs (2007-2015):18 cases. J Vet Emerg Crit Care (San Antonio) 2019 Jul;29(4):413-417.

Figure 3: The pericardio-diaphragmatic (PD) window is identified when the transducer is positioned perpendicular to the ribs, marker directed cranially and situated where the heart and the diaphragm are visible within the same sonographic window. It is easy to locate by either sliding the transducer caudally off the heart or locating the curtain sign in the mid thoracic region and following it ventrally until both the diaphragm and heart are visible within the same sonographic image. It should be the only site on the hemithorax where the diaphragm is visible, curving away from the thoracic wall due to the cardiac notch and the presence of mediastinal tissue and fat (MT). The PD window is a good site to differentiate pericardial and pleural effusions. RVL; right ventricular lumen, IVS; intraventricular septum, LVL; left ventricular lumen, LVFW; left ventricular free wall, GB; gall bladder, SC; subcutaneous tissues. Image courtesy Calgary VPOCUS Academy, with permission.

WEBINAR HIGHLIGHTS

Figure 2: Image of a dog depicting transducer location and a radiograph with schematic representation of the right parasternal short axis windows obtained and appearance of pericardial effusion. Images courtesy Calgary VPOCUS Training Academy and Lindsey Strang, with permission.

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