VETgirl Q1 2022 Beat e-Magazine

beat

ISSUE 12 | APRIL 2022

CONTENTS APRIL 2022

ARTICLES

When patients are back in business, your staff is, too

20 Helpful Tips on Performing a Feline Orthopedic Exam 21 On Simone Biles, Emotional Agility, and Leading with Mental Health 04 Strategies to Avoid Surgery for Canine Osteoarthritis 06 Top 10 Human Medications Poisonous to Dogs and Cats 12 What if Your Superpower was the Ability to Stop Acute Pain? 16 Healthy Weight Loss in Pets: Help Clients Turn Intent In To Action

Using Cerenia injectable perioperatively is good for dogs—and your practice

Benefits to your patients Help ease a dog’s recovery by adding Cerenia to your perioperative protocol, to prevent vomiting and enable a quick return to normal feeding. 1

Benefits to your practice A third of practice owners reported the impact of cleaning up after patients that vomit. With Cerenia, less cleaning can mean more time for patient care, leading to greater dog owner satisfaction. 2,3

23 TECH TIP 24 UPCOMING CONTENT WHAT’S NEW

“Happier patients, happier clients, a happier team!” – Dr. Sue Ettinger, DVM, DACVIM (oncology)

An expert panel recommends the use of Cerenia. Download your copy at www.RelievePOV.com

IMPORTANT SAFETY INFORMATION: Use Cerenia Injectable subcutaneously for acute vomiting in dogs 2 to 4 months of age or either subcutaneously or intravenously in dogs 4 months of age and older. Safe use has not been evaluated in dogs with gastrointestinal obstruction, or those that have ingested toxins. Use with caution in dogs with hepatic dysfunction. Pain and vocalization upon injection is a common side effect. In people, topical exposure may elicit localized allergic skin reactions, and repeated or prolonged exposure may lead to skin sensitization. Please see full Prescribing Information. References: 1. Ramsey D, Fleck T, Berg T, et al. Cerenia prevents perioperative nausea and vomiting and improves recovery in dogs undergoing routine surgery. Intern J Appl Res Vet Med . 2014;12(3):228-237. 2. Data on file. Cerenia Quick Poll Infographic. 2017 Zoetis Inc. 3. Data on file. Rethinking Perioperative Vomiting in Dogs Proceedings. April 2019 Zoetis Inc.

All trademarks are the property of Zoetis Services LLC or a related company or a licensor unless otherwise noted. © 2022 Zoetis Services LLC. All rights reserved. CER-00535

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is pro-inflammatory (e.g., arachidonic acid) and therefore bad. Diets with higher concentrations of omega-3 fatty acids (fish oils, flaxseeds, walnuts) showed significantly improved lameness over dogs fed a conventional diet, 6 so veterinary therapeutic dog food manufacturers strive for a low omega-6/omega-3 ratio. (Table One – BLUE W+M versus Other Mobility Diets). Roughly speaking, the recommended dose of EPA and DHA for dogs with OA is about 1000mg/day for every twenty pounds of body weight, so check the label on over-the-counter fish oil products to make sure they are cost effective and don’t require regular dosing of dozens of stinky capsules. THE TRUTH ABOUT GLUCOSAMINE AND CHONDROITIN SULFATE Both glucosamine and chondroitin sulfate are building blocks for the cartilage matrix and based on in vitro studies, they also appear to suppress proteolytic enzymes and inflammatory cytokines. But do they offer anything beyond a placebo effect for our arthritic dogs? One randomized double-blind study showed arthritic dogs treated with glucosamine and chondroitin sulfate demonstrated significant improvement in weight bearing, pain and severity of lameness some 70 days after starting treatment, but this was based on subjective assessment. 7 And then there’s the question of dosage regimes and bioavailability, with a paucity of information on exactly how much glucosamine and chondroitin sulfate actually finds its way to synovial joint to work their magic. 8 Despite these frustrations, there is enough imperfect evidence to suggest chondroprotective supplements are a worthwhile addition to a treatment plan to offset canine OA, so long as you bear the following in mind. Glucosamine and chondroitin sulfate are better at prevention, so start your patients on these supplements as soon as you make a diagnosis e.g., elbow or hip dysplasia, to try to get ahead of cartilage damage. Both supplements can take eight to twelve weeks before an owner appreciates a clinical benefit, so stress patience, and if cartilage erosion and arthritic change is severe, chances are you’re way too late for these supplements to be helpful. Bottom line, when it comes to canine OA, proactive trumps a reactive approach every time, so work with your clients to find a multi-modal approach that combines a plan to prevent or minimize existing disease through a combination of healthy diet and lifestyle.

References: 1.

SPONSORED ARTICLE

Smith GK, Paster ER, Powers MY, et al. Lifelong diet restriction and radiographical evidence of osteoarthritis of the hip joint in dogs. J Am Vet Med Assoc 2006, 229: 690-693. 2. Marshall WG, Hazewinkel HAW, Mullen D, et al. The effect of weight loss on lameness in obese dogs with osteoarthritis. Vet Res Commun 2010, 34(3): 241-253. 3. Chapman M, Woods GRT, Ladha C, et al. An open-label randomized clinical trial to compare the efficacy of dietary caloric restriction and physical activity for weight loss in overweight pet dogs. Vet J 2019, 243: 65-73. 4. Mlacnik E, Bockstahler BA, Muller M, et al. Effects of calorie restriction and a moderate or intense physiotherapy program for treatment of lameness in overweight dogs with osteoarthritis. J Am Vet Med Assoc 2006, 229(11): 1756-60. 5. Frye CW, Shmalberg JW, Wakshlag JJ. Obesity, Exercise and Orthopedic Disease. Vet Clin Small Anim 46 2016: 831-841. 6. Roush JK, Cross AR, Renberg WC, et al. Evaluation of the effects of dietary supplementation with fish oil omega-3 fatty acids on weight bearing in dogs with osteoarthritis. J Am Vet Med Assoc 2010, 236: 67-73. 7. McCarthy G, O’Donovan J, Jones B, et al. Randomized double- blind, positive controlled trial to assess the efficacy of glucosamine/ chondroitin sulfate for the treatment of dogs with osteoarthritis. Vet J 2007, 174(1): 54-61. 8. Comblain F, Serisier S, Barthelemy N, et al. Review of dietary supplements for the management of osteoarthritis in dogs in studies from 2004 to 2014. J Vet Pharmacol Therap 2015, 39: 1-15.

Strategies to Avoid Surgery for Canine Osteoarthritis

NICK TROUT , MA, VETMB, MRCVS, DIPLOMATE ACVS, DECVS Angell Animal Medical Center, Boston, MA

Whether we are talking about our own health, or our pets, if there’s a decent medical treatment option for a disease, with a good chance of avoiding surgery, we’re going to jump all over it. Osteoarthritis (OA) is one such disease. It remains incurable, and progressive, and when it comes to dogs, reportedly affects twenty percent over one year of age, therefore producing a major negative impact on mobility and quality of life for a huge chunk of our patient population. Be it elbows, hips, knees, or spine, trying to minimize the progression of degenerative changes in synovial joints, for as long as possible, has universal appeal, and there are three major ways to make this happen, long before you are forced to reach for a bottle of anti-inflammatories.

BLUE RUNS NOTMOGUL FIELDS! If you’ve got bad knees but you still want to ski, best to choose the runs that are a little less challenging, a little gentler on your joints. Unfortunately, when it comes to dogs, way too many go black diamond every time, paying the price for days to come. We need to apply our own appreciation of the cost of excessive exercise to our canine friends and impose limitations, starting with a discovery of what constitutes “good” versus “bad” activity. Clients should begin with leash walks, getting longer and longer by five minutes every couple of days, looking for the ‘switch’ between well tolerated walks and those resulting in soreness, stiffness, or other markers of discomfort. If thirty minutes is “good”, but forty minutes means the climb upstairs that evening will be a challenge; stick with thirty minutes. Recommend playing with terrain—grass, asphalt, woodland, beach, inclines, and declines—and how it impacts post-exercise recovery, before working on length and type of exercise off leash, alone in the backyard, or with dogs at a dog park or doggy day care. Often this is easier said than done, but by careful observation and trial and error, over a period of weeks, clients can be closer to finding a healthy level of activity that avoids the cumulative effects of soreness, and deterioration of the affected joints. A DECISION TO TRY While food motivated dogs may not like it, maintaining (or acquiring) a healthy body weight and condition score can have a profound impact on lameness secondary to osteoarthritis (OA). One study took a preventative approach by offering different amounts of food to two groups of eight-week-old Labs; group one was fed ad lib (control), the second group fed twenty-five

percent less (restricted). 1 Followed over a lifetime, the median age of radiographic evidence of hip OA was significantly lower in the control group (six years), compared to those on restriction (twelve years). Arguably a more “real world” study demonstrated how weight loss in obese dogs can have a profound impact on lameness secondary to OA. Subjectively, a 6.1% weight reduction onwards produces a significant decrease in lameness. Objectively, that number increases to 8.85% when using kinetic gait analysis. 2 Either way, modest and doable weight loss can be a game changer both to protect against the progression of OA and improve function and comfort in the face of it. Some owners will ask, if my dog is overweight or obese (body condition score 6-9/9) which approach works best—dietary caloric restriction or increased physical activity? The answer is diet, 3 although adding in some intense physical therapy has proven to enhance osteoarthritic joint mobility while facilitating weight loss. 4 MORE THAN JUST BODYWEIGHT The interplay between OA and obesity is far more complicated than just extra body weight increasing load on synovial joints that exacerbates cartilage damage. In humans, there is a strong correlation between obesity and OA in the hand, despite the hand being a non-weight bearing joint, prompting concerns that obesity may contribute to the inflammatory process through direct cell signaling, and interaction with immune cells. 5 Although the role of inflammatory mediators released from adipose tissue remains unclear, the role of polyunsaturated fatty acids (PUFAs) in the canine diet is well documented. Keeping it simple, where OA is concerned, omega -3 (e.g., eicosapentanoic acid {EPA} and docosahexanimic acid {DHA}) are good, anti-inflammatory, whereas omega-6

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WEBINAR HIGHLIGHTS

Top 10 Human Medications Poisonous to Dogs and Cats

JUSTINE LEE , DVM, DACVECC, DABT VETgirl Co-Founder

output becomes reduced, and secondary severe hypoperfusion and acute kidney injury (AKI) can potentially develop. 3-5 With ACE-inhibitors, severe overdoses can cause hypotension, dizziness, and weakness.. In general, there is a wider margin of safety with ACE-inhibitors, which are typically considered much safer. Pets ingesting small amounts of ACE-inhibitors can potentially be monitored at home, unless they have underlying disease (e.g., kidney failure, cardiac disease, etc.). With ACE- inhibitors, ingestions > 10-20X a therapeutic dose are generally considered toxic, and can result in severe clinical symptoms (e.g., hypotension). 5 Treatment for any cardiac medication includes decontamination (e.g., emesis induction, gastric lavage, activated charcoal (AC) administration), blood pressure monitoring, aggressive IV fluid therapy if hypotension is detected, and blood work monitoring. With severe toxicosis, the use of high-dose insulin therapy or intravenous lipid emulsion may be warranted as a potential antidote for calcium channel blocker toxicosis. 3 SELECTIVE SEROTONIN RE-UPTAKE INHIBITORS (SSRI) Selective serotonin re-uptake inhibitors (SSRIs) are a class of medications that are commonly used in human medicine for depression. Common examples include the following drugs fluoxetine (Prozac® in human beings; Reconcile™ in veterinary medicine), citalopram (Celexa®), paroxetine (Paxil®) and sertraline (Zoloft®). Other similar drugs include selective norepinephrine re-uptake inhibitors (SNRIs), which include common drugs like duloxetine (Cymbalta®), nefazodone (Serzone®), and venlafaxine (Effexor®). SNRI and SSRI drugs result in similar clinical signs of toxicosis, and therefore are treated the same. In veterinary medicine, SSRIs are used for a wide array of behavioral problems, including feline urine spraying, canine separation anxiety, lick granulomas, etc. These SSRI drugs work by blocking the reuptake of serotonin in the pre-synapse, thereby increasing the levels of serotonin in the pre-synaptic membrane. In small animal patients, common clinical signs from SSRIs include the following:

Need a review of poisoning cases in dogs and cats? Missed the last toxicology webinar by Dr. Justine Lee, DACVECC? Get the highlights here on “Top 10 human medications poisonous to dogs and cats,” Dr. Justine Lee, DACVECC, DABT reviews the importance common human medications that dogs - and even cats - ingest! Each year, the ASPCA Animal Poison Control Center (APCC) manages hundreds of thousands of poisoning calls. At the ASPCA APCC, an estimated 50% of pet poisonings comprise human over the counter (OTC) and prescription medications. In the veterinary poisoned patient, the goal of decontamination is to “inhibit or minimize further toxicant absorption and to promote excretion or elimination of the toxicant from the body.” 1,2 When treating the poisoned patient, the clinician should have an understanding of the toxic dose (if available), the pharmacokinetics (including absorption, distribution, metabolism, and excretion), the underlying mechanism of action, and the potential clinical signs that can be observed with the toxicant. 2 This will help determine appropriate decontamination and therapy for the patient. While some of these human medications are VERY common (e.g., antidepressants, amphetamines, acetaminophen), a few are less common but more deadly (e.g., 5-FU, isoniazid). CALCIUM CHANNEL BLOCKERS, BETA- BLOCKERS, ACE-INHIBITORS, STATINS AND DIURETICS Certain cardiac medications include broad categories such as calcium channel blockers (CCB), beta-blockers (BB), and angiotensin-converting enzyme (or “ACE”) inhibitors. These medications are commonly used in both human and veterinary medicine to treat underlying cardiac disease or hypertension. Each category of cardiac medication has different margins of safety. CCB and BB toxicosis should be treated aggressively, as these two categories of medications have a narrow margin of safety. Toxicosis of these agents can result in myocardial failure, severe bradycardia, and hypotension; untreated, cardiac

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metabolite NAPQI by providing additional glutathione substrate. 7 Baseline blood work and follow-up biochemical panels should be performed to monitor for the presence of metHb, Heinz body anemia, or evidence of hepatotoxicity. Generally, prognosis is fair to excellent with therapy. If clinical signs resolve and liver enzymes are within normal limits after 48 hours of NAC therapy, patients can be discharged with SAMe (for 30 days). Those with severe hepatic failure have a poorer prognosis. ASTHMA INHALERS (e.g., ALBUTEROL) Asthma inhalers are often used in both human and veterinary medicine. Various types of medications may be used, including steroids (e.g., fluticasone) or beta agonists (e.g., albuterol, salbutamol, etc.). When beta-agonist inhalers are accidentally chewed and punctured by dogs, they can result in a severe, life-threatening, acute toxicosis. (Inhaled steroids are not a large toxicity issue). Because inhalers often contain approximately 200 metered, concentrated doses, a massive amount of beta- agonist is released with just one puncture. Clinical signs include cardiac (e.g., tachycardiac, a “racing heart rate” per the owner, injected gums, hypotension, hypertension, severe arrhythmias), electrolyte changes (e.g., severe hypokalemia, hyperglycemia), GI (e.g., vomiting), and CNS (e.g., mydriasis, agitation, weakness, collapse, death). Treatment includes stat electrolyte monitoring, IV fluids, potassium supplementation, blood pressure and ECG monitoring, sedation/anxiolytics (if the patient is agitated, hypertensive, and tachycardiac), anti-arrhythmics such as beta-blockers (e.g., propranolol, esmolol, etc.), and symptomatic supportive care. Treatment for 24-36 hours is typically necessary, until clinical signs resolve. DECONGESTANTS Cold and flu medications (e.g., “Claritin-D”) often carry decongestants such as pseudoephedrine (PSE) and phenylephrine (PE). The exact mechanism of how these drugs work is unknown but thought to stimulate alpha and beta-adrenergic receptors by releasing norepinephrine. Phenylephrine is typically considered to be less toxic than PSE as it is less bioavailable with oral ingestion. Clinical signs seen with decongestant ingestion include cardiac (e.g., tachycardia, hypertension, reflex bradycardia), CNS (e.g., mydriasis, agitation, trembling, seizures), and various miscellaneous signs (e.g., hyperthermia). With PSE, moderate to severe clinical signs can be seen at 5-6 mg/kg, while death has been reported at 10-12 mg/kg. With phenylephrine, similar clinical signs can be seen, although GI signs such as vomiting are the most common sign observed. Treatment includes decontamination (if appropriate), administration of one dose of charcoal with a cathartic, IV fluid therapy (to enhance urinary elimination), blood pressure monitoring, anti-emetics, sedatives/anxiolytics (e.g., acepromazine), muscle relaxants for tremoring (e.g., methocarbamol 22-100 mg/kg, IV PRN), anticonvulsants (e.g., phenobarbital 4-6 mg/kg, IV, PRN), and rarely, anti-hypertensives (e.g., hydralazine).

and toxic dose was ingested. For example, in dogs, ibuprofen results in GI signs at doses as low as 16-50 mg/kg, while severe GI signs may be seen at 50-100 mg/kg. 6 Renal compromise may be seen at doses of 100-250 mg/kg (resulting in potential AKI), and fatalities have been reported at doses > 300 mg/kg. 6 This differs tremendously from naproxen sodium (dogs), where severe clinical signs can be seen at doses as low as 5 mg/kg. 6 Clinical signs of NSAID toxicosis include anorexia, vomiting, hematemesis, diarrhea, melena, abdominal pain, lethargy, malaise, uremic halitosis, dehydration, etc. Treatment includes decontamination, the use of activated charcoal (often multiple doses due to enterohepatic recirculation, if appropriate), GI protectants (e.g., H2 blockers, sucralfate), aggressive IV fluid therapy (to help maintain renal blood flow), anti-emetic therapy, and symptomatic and supportive care. With high doses, anticonvulsants may also be necessary if CNS signs develop. ACETAMINOPHEN Acetaminophen (N-acetyl-p-aminophenol), a cyclooxygenase (COX)-3 inhibitor, is a popular OTC analgesic and antipyretic medication used frequently in humans. It is not considered a true NSAID as it lacks anti-inflammatory properties. Normally, part of this drug is metabolized into non-toxic conjugates via the metabolic pathways (glucuronidation and sulfation); 7 some is metabolized into the toxic metabolite, N-acetyl-para- benzoquinoneimine [NAPQI] via the cytochrome P-450 enzyme pathway. 7 Typically, NAPQI is detoxified by conjugation with glutathione in the liver. 7 Toxicosis occurs when glucuronidation and sulfation pathways are depleted; this results in toxic metabolites building up and secondary oxidative injury occurring. 7 While this drug is very safe for human use, it has a narrow margin of safety in dogs and cats; the severity of toxicosis and development of clinical signs is species dependent. Cats have an altered glucuronidation pathway and a decreased ability to metabolize acetaminophen, making them much more susceptible to toxicosis. In cats, red blood cell (RBC) injury is more likely to occur in the form of methemoglobinemia (metHb), and toxicity can develop at doses as low as 10 mg/kg. 7 In cats, lethargy, swelling of the face or paws, respiratory distress, brown mucous membranes, cyanosis, vomiting, and anorexia may be seen secondary to metHb. In dogs, hepatic injury is more likely to occur; acetaminophen toxicosis can occur at doses > 100 mg/ kg, while metHb can develop at doses of > 200 mg/kg. 7 Dogs may develop clinical signs of keratoconjunctivitis sicca (dry eye), malaise, anorexia, hepatic encephalopathy, vomiting, melena, and icterus secondary to hepatotoxicity. Treatment includes decontamination, administration of activated charcoal (AC), anti-emetic therapy, IV fluid therapy, treatment for hypoxemia (e.g., oxygen, blood transfusion, etc.), antioxidant therapy (e.g., Vitamin C), provision of a glutathione source (S-adenosyl-methionine or SAMe), and the antidote n-acetylcysteine (NAC, ideally IV) to limit formation of the toxic

WEBINAR HIGHLIGHTS

Top 10 Human Medications Poisonous to Dogs and Cats

JUSTINE LEE , DVM, DACVECC, DABT VETgirl Co-Founder

toxicosis, secondary stimulation of certain body systems can result in significant clinical signs: GI (e.g., vomiting, diarrhea, hypersalivating), CNS (e.g., agitation, mydriasis, tremors, seizures), cardiovascular (e.g., tachycardia, hypertension), and respiratory (e.g., panting). Both clinical signs and treatment for amphetamine toxicosis are similar to SSRI toxicosis, and include IV fluids, cooling measures, sedation (e.g., with acepromazine or chlorpromazine), muscle relaxants, anticonvulsants, thermoregulation, blood pressure monitoring, and symptomatic/ supportive care. NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS) NSAIDs are competitive inhibitors of prostaglandin synthesis (cyclooxygenase or “COX” inhibitors) and result in decreased prostaglandin, which is important for normal homeostatic function (including maintaining renal blood flow, maintaining mucous production in the stomach, etc.). Common OTC human NSAIDs include active ingredients such as ibuprofen and naproxen sodium. Examples of human NSAIDs include Advil®, Aleve®, certain types of Motrin®, etc. Common prescription veterinary NSAIDs can also result in toxicosis, particularly when available in the chewable, palatable formulation. Examples of veterinary NSAIDs include carprofen, deracoxib, etogesic, previcoxib, etc. With NSAID toxicosis, the GI tract, kidneys, CNS, and platelets can be affected. Cats and certain breeds of dogs (e.g., German shepherds) seem to be more sensitive to NSAIDs and should be treated aggressively. With cats, severe acute kidney injury (AKI) is often more clinically seen with NSAID toxicosis at lower doses (as compared to dogs). With dogs, signs secondary to GI ulceration (e.g., vomiting, diarrhea, melena, hematemesis, etc.) are more commonly seen initially, followed by secondary AKI. With NSAID toxicosis, it is important to keep in mind that each NSAID has a different toxic dose, margin of safety, half-life, and route of excretion, and the ASPCA Animal Poison Control Center should be contacted to identify what specific NSAID

• • • •

Sedation or central nervous system (CNS) stimulation

Anorexia Lethargy

Serotonin syndrome

Clinical signs of serotonin syndrome include gastrointestinal (GI) signs (e.g., hypersalivation, vomiting, diarrhea, abdominal pain) and CNS signs (e.g., stimulation, mydriasis, tremors, seizures, hyperthermia secondary to tremoring and seizures). Treatment for antidepressants includes decontamination (ideally done at a veterinarian, due to the rapid onset of clinical signs), sedation (e.g., with acepromazine or chlorpromazine), intravenous (IV) fluid therapy, blood pressure and electrocardiogram (ECG) monitoring, thermoregulation, muscle relaxants (for tremors; methocarbamol 22-55 mg/kg, IV, PRN), anticonvulsants (e.g., phenobarbital 4-16 mg/kg, IV, PRN; diazepam 0.25-0.5 mg/kg, IV, PRN), serotonin antagonists [e.g., cyproheptadine (1.1 mg/ kg for dogs or 2-4 mg total per cat) PO or rectally q. 6-8], and supportive and symptomatic care. In general, the prognosis for antidepressant toxicosis is excellent. AMPHETAMINES Amphetamines are used for a variety of medical and illicit reasons. Legal forms include prescription medications for attention-deficit disorder/attention deficit-hyperactivity disorder (ADD/ADHD), weight loss, and narcolepsy. Examples of amphetamines include dextroamphetamine, amphetamine (Adderall®), d-amphetamine (Dexedrine®), methamphetamine (Desoxyn®) and lisdexamfetamine (Vyvanse®). Illegal forms of amphetamines include street drugs like methamphetamine, crystal meth, and ecstasy. This class of drugs acts as sympathomimetic agents, meaning they stimulate the sympathetic system. Amphetamines also cause stimulation of alpha and beta-adrenergic receptors and stimulate release of serotonin and norepinephrine; this results in increased catecholamine stimulation in the synapse. Amphetamines also increase release of serotonin from the presynaptic membrane, resulting in serotonin syndrome. With amphetamine

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SEE THE DIFFERENCE Pain and dysphoria don’t have to be part of the post-op experience. *

ISONIAZID Isoniazid (commonly known as INH) is a human medication used for tuberculosis. While it is used in veterinary medicine to treat Mycobacterium or Actinomyces, it has a narrow margin of safety in dogs and cats. This drug works by blocking the synthesis of mycolic acid. INH depletes the CNS of pyridoxine and also decreases levels of GABA within the brain. Many assume that since this is an “antibiotic” that it is safe; however, when accidentally ingested in dogs (and rarely, cats), it can result in severe CNS signs (e.g., tremors, refractory seizures, coma, death). The LD 50 in dogs is estimated to be as low as 50 mg/kg; at this same dose, seizures can be seen. One 300 mg tablet can result in severe poisoning in a 10-pound dog. Other clinical signs include GI signs (e.g., hypersalivating, vomiting, diarrhea), acid-base disturbances (e.g., metabolic acidosis), hyperthermia (secondary to tremors or seizures) and organ injury (e.g., hepatic injury, acute kidney injury, etc.). Due to the rapid onset of clinical signs, it is often too late to decontaminate the patient. Gastric lavage under anesthesia may be necessary. Treatment also includes IV fluids, ant-emetics, anticonvulsants, muscle relaxants, supportive care, and the antidote pyridoxine hydrochloride (typically available as 100 mg/ml) (Dose: suggested dose of 71 mg/kg IV, diluted to 5-10%, slow over 30-60 minutes). Clinicopathologic monitoring should include a biochemistry panel and recheck hepatic panel (3-5 days later). 5-FLUOROURACIL (5-FU) The most life-threatening topical toxin to dogs and cats is 5-fluorouracil (5-FU). 5-FU, commonly known by the brand names Efudex®, Carac®, Adrucil®, and Fluoroplex®, is a prescription anti-neoplastic medication that is often used for treatment of actinic keratosis or superficial basal cell carcinoma in humans. It is commonly sold in low concentration products (e.g., 0.5-5%), and works by inhibiting DNA and RNA synthesis and production, resulting in programmed cell death. 8 While IV administration of 5-FU is occasionally used as a chemotherapeutic agent in dogs (e.g., for mammary gland tumor, etc.), it is not recommended for use in cats. Decades ago, topical 5-FU was used in cats for the treatment of squamous cell carcinoma; however, it resulted in severe toxicosis and death due to its narrow margin of safety. Clinical signs of 5-FU toxicosis can often be seen within 30 minutes up to 6 hours; death has been reported as early as 7 hours. 8 Clinical signs include acute GI signs (e.g., hypersalivation, anorexia, vomiting, abdominal pain, diarrhea, bloody diarrhea, etc.), CNS signs (e.g., ataxia, tremors, seizures), and bone marrow suppression (e.g., anemia, leukopenia, thrombocytopenia). 8 The lowest reported toxic (oral) dose in dogs is 6 mg/kg, while the minimal reported lethal dose is 20 mg/kg. One case report did have a dog survive ingestion of 46 mg/kg of 5-FU. 8 That said, the prognosis with 5-FU toxicosis is typically grave in cats and guarded in dogs (with a reported survival in dogs of approximately 25%). Death typically occurs

due to secondary complications from the 5-FU such as sepsis (due to leukopenia), increased intracranial pressure (due to persistent seizures), intracranial hemorrhage (due to severe thrombocytopenia), or DIC (due to severe seizures). Unfortunately, most patients present with severe clinical signs, where it is too late to perform decontamination. Therefore, treatment should be aimed at symptomatic supportive care, anti-convulsant therapy, anti-emetics, anti-diarrheals, IV fluids (to help maintain perfusion), thermoregulation, broad-spectrum antibiotics, clinicopathologic monitoring, and symptomatic supportive care. If the patient is able to survive the acute crisis, clinicopathologic monitoring is necessary every 3-4 days thereafter for 2-3 weeks, until bone marrow function returns to normal. 8 CONCLUSION Pet owners should be appropriately educated on how to pet-proof the house and be trained on what common human medications can be toxic to pets. Pet owners should also be appropriately educated on crate training to help minimize toxin exposure. When in doubt, the ASPCA Animal Poison Control Center should be consulted for toxic ingestions that veterinarians are unaware of.

References available upon request.

LEARN MORE

Controls Pain to Help Post-Op Return to Function

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Recovery care begins with Nocita™

Indications For single-dose infiltration into the surgical site to provide local postoperative analgesia for cranial cruciate ligament surgery in dogs. For use as a peripheral nerve block to provide regional postoperative analgesia following onychectomy in cats. Important Safety Information NOCITA is for use in dogs and cats only. Do not administer concurrently with bupivacaine HCl, lidocaine or other amide local anesthetics. The safe use of NOCITA in dogs and cats with cardiac disease or with hepatic or renal impairment has not been evaluated. The safe use in dogs or cats younger than 5 months of age, that are pregnant, lactating, or intended for breeding has not been evaluated. The most common adverse reactions in dogs were discharge from incision, incisional inflammation and vomiting. The most common adverse reactions in cats were elevated body temperature and infection or chewing/licking at the surgical site. Please see accompanying brief summary for product safety information. *In a field trial, Nocita reduced the need for post-op rescue pain treatment with opioids **Cranial cruciate ligament Nocita, Elanco and the diagonal bar logo are trademarks of Elanco or its affiliates. ©2021 Elanco or its affiliates. PM-US-21-1709

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NOCITA ® (bupivacaine liposome injectable suspension) 13.3 mg/mL For local infiltration injection in dogs only For use as a peripheral nerve block in cats only Local anesthetic Single use vial Caution: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian. Before using this product, please consult the Product Insert, a summary of which follows: DOG Indication: For single-dose infiltration into the surgical site to provide local postoperative analgesia for cranial cruciate ligament surgery in dogs. CAT Indication: For use as a peripheral nerve block to provide regional postoperative analgesia following onychectomy in cats. DOG Dosage and Administration: NOCITA is for single dose administration only. A dose of 5.3 mg/kg (0.4 mL/kg) is administered by infiltration injection into the tissue layers at the time of incisional closure for dogs. A single dose administered during surgical closure may provide up to 72 hours of pain control. CAT Dosage and Administration: NOCITA is for administration only once prior to surgery. Administer 5.3 mg/kg per forelimb (0.4 mL/kg per forelimb, for a total dose of 10.6 mg/kg/cat) as a 4-point nerve block prior to onychectomy. Administration prior to surgery may provide up to 72 hours of pain control. Contraindications: Do not administer by intravenous or intra-arterial injection. If accidental intravascular administration occurs, monitor for cardiovascular (dysrhythmias, hypotension, hypertension) and neurologic (tremors, ataxia, seizures) adverse reactions. Do not use for intra-articular injection. In humans, local anesthetics administered into a joint may cause chondrolysis. Warnings: Not for use in humans. Keep out of reach of children. NOCITA is an amide local anesthetic. In case of accidental injection or accidental topical exposure, contact a physician and seek medical attention immediately. Wear gloves when handling vials to prevent accidental topical exposure. Precautions: Do not administer concurrently with bupivacaine HCl, lidocaine or other amide local anesthetics. A safe interval from time of bupivacaine HCl, lidocaine or other amide local anesthetic administration to time of NOCITA administration has not been determined. The toxic effects of these drugs are additive and their administration should be used with caution including monitoring for neurologic and cardiovascular effects related to toxicity. The safe use of NOCITA in dogs or cats with cardiac disease has not been evaluated. The safe use of NOCITA in dogs or cats with hepatic or renal impairment has not been evaluated. NOCITA is metabolized by the liver and excreted by the kidneys. The ability of NOCITA to achieve effective anesthesia has not been studied. Therefore, NOCITA is not indicated for pre-incisional or pre-procedural loco-regional anesthetic techniques that require deep and complete sensory block in the area of administration. The safe use of NOCITA in dogs for surgical procedures other than cranial cruciate ligament surgery has not been evaluated. The safe use of NOCITA in cats for surgical procedures other than onychectomy has not been evaluated. The safe use of NOCITA has not been evaluated in dogs or cats younger than 5 months old. The safe use of NOCITA has not been evaluated in dogs or cats that are pregnant, lactating or intended for breeding. DOG Adverse Reactions: Field safety was evaluated in 123 NOCITA treated dogs. The most common adverse reactions were discharge from incision (3.3%), incisional inflammation (2.4%), and vomiting (2.4%). CAT Adverse Reactions: Field safety was evaluated in 120 NOCITA treated cats. The most common adverse reactions were elevated body temperature (6.7%), surgical site infection (3.3%), and chewing/licking of the surgical site (2.5%). Storage Conditions: Unopened vials should be stored refrigerated between 36° F to 46° F (2° C to 8° C) NOCITA may be held at a controlled room temperature of 68° F to 77° F (20° C to 25° C) for up to 30 days in sealed, intact (unopened) vials. Do not re-refrigerate. Do Not Freeze. How Supplied: 13.3 mg/mL bupivacaine liposome injectable suspension in 10 mL or 20 mL single use vial. 10 mL supplied in 4-vial carton. 20 mL supplied in a single vial carton and 4-vial carton. NADA 141-461, Approved by the FDA US Patent: 8,182,835; 8,834,921; 9,205,052 4 Most of the commonly used blocks in veterinary practice (e.g., incisional, oral/dental, manus/pedus, intraperitoneal, testicular, etc.) can be done with knowledge of anatomy and the ability to palpate anatomical landmarks. Easy-to- follow, detailed, open-access resources that describe the anatomy relevant to the blocks are available 3,4 and should be downloaded and placed in the work area where the blocks are done. There are also advanced techniques that are most effectively done using nerve finders or ultrasound guidance if you want to expand your power. 5 If nothing else, block the incision or traumatic injury site. The skin is highly innervated and a major source of pain.

1 General anesthesia and local anesthetic blockade are completely different. Only perception is blocked with general inhalant anesthesia while the rest of the pain (or nociceptive) pathway is fully functional. Whether the patient is awake or anesthetized, the pathophysiologic adverse effects of pain are still occurring. This can be demonstrated by the fact that physiologic markers, like changes in heart rate, blood pressure, serum cortisol concentrations, etc., are used as pain (nociceptive) indicators in research studies on anesthetized patients undergoing painful procedures. Clinically, pain can make maintenance of the patient at an appropriate plane of anesthesia more difficult, while local blockade allows a lower dose of inhalant anesthetic, which improves dose-dependent anesthetic safety. 2 As with all drugs, the adverse effects of local anesthetics are uncommon when the drug is administered at the correct dose using proper technique. Adverse effects are most likely to occur when supra-clinical doses are administered IV, 1 which is not the injection site for local/regional blocks. Carefully calculate the dose and use good injection technique, meaning gentle insertion of the needle into tissue and aspiration prior to injection every single time a local anesthetic (or any other drug) is injected into the tissue. 3 To make your superpower a habit, put ‘local/regional block’ on a checklist (Figure 2) of analgesic drugs/procedures that the patient needs. Increasing awareness that a block should be used will increase the likelihood that doing the blocks will become habit. Date Preanesthesia (fill in drug name) Dose/Route/Time Administered Opioid: Analgesic Protocol For Procedure

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What if Your Superpower was the Ability to Stop Acute Pain?

TAMARA GRUBB , DVM, PHD, DACVAA, PRESIDENT-ELECT IVAPM Adjunct Professor at Washington State University; Founder of VetAACE.com; Consultant

Imagine, a room full of patients that have suffered trauma or have undergone surgery and are in pain, suffering, probably in silence and trying to hide their misery. The pain is causing adverse health effects (e.g., tachycardia, hypertension), behavior (e.g., anxiety, aggression) and welfare/quality of life issues (e.g., anorexia, insomnia). And in you step, with the super powerful class of drugs - the local anesthetics – to use your superpower of stopping acute pain.

Pain is most effectively controlled when a multimodal protocol is used with drugs chosen based on their mechanism and location of action in the pain pathway. For acute pain, opioids, non-steroidal anti-inflammatory drugs (NSAIDs) and local anesthetics are the most potent drugs included in the protocol. As a quick review of the pain pathway and where drugs work (Figure 1), NSAIDs work primarily in the transduction phase of the pathway, opioids in modulation and perception, and local

mediated in the brain. A recent review paper described the powerful impact of local anesthetics: decreased nociceptive responses intraoperatively; lower inhalant doses for anesthetic maintenance; lower postoperative pain scores overall, even when used alone (which isn’t the goal); decreased need for rescue analgesia, like opioids, so decreased opioid-mediated sedation and gastrointestinal effects; and potential prevention of chronic pain from the acute pain source. 1 So given this superpower, wouldn’t local anesthetics be used for every patient undergoing every painful procedure? Unfortunately, and inexplicably, no. In a recent veterinary

anesthetics in transmission. All of these are very potent drugs and are effective at their site of action, but the site of action itself can be quite complicated as there are numerous pain generators and propagators in most phases and the drugs acting there may not control all of them. The exception is transmission. In transmission, the pain (or nociceptive) impulse is propagated from the periphery to the central nervous system

Alpha-2 agonist:

survey, local anesthetic blocks were used in only 0.17%, 0.24% and 0.23% of cats undergoing ovariohysterectomy or castration, major soft tissue surgery, or orthopedic surgery, respectively. 2 Yes, that abysmally low number is correct. In addition, veterinarians indicated that, if they were to use

NSAID:

Other: INTRAOPERATIVE Drug bolus:

Figure 1: The pain pathway and site of action of various drugs/ treatments for acute pain

Local/regional block:

Infusion:

by the one way that any other nerve signal is propagated, the opening of voltage-gated sodium channels with subsequent nerve depolarization. Our superpower is the ability to use local anesthetics to block the pain by blocking sodium channels. This has a unique and profound effect on the pain pathway. Opioids modulate, i.e., decrease pain once it reaches the central nervous system (CNS), while local anesthetics prevent the pain impulse from reaching the CNS. The power of this is not only decreased pain itself, but also decreased behavioral and effective components of pain since those are

opioids more, they would use local anesthetics even less, which is not capitalizing on the superpower – or on multimodal analgesia. Why is this happening? Why isn’t every veterinarian using their superpower? In an informal survey by the author, veterinarians stated these reasons for not routinely using local anesthetics: 1) no perceived need for local anesthesia if the patient is under general anesthesia; 2) fear of adverse effects; 3) use of blocks ‘not a habit’ so often forgotten; 3) uncertain which drug to use and 4) unsure of the proper local/regional blockade technique. Let’s clear out the kryptonite and start using our superpower!

Other: RECOVERY/DISCHARGE Bolus:

Infusion:

Manufactured for: Aratana Therapeutics, Inc., Leawood, KS 66211 Additional Information is available at www.aratana.com or by calling Aratana Therapeutics at 1-844-272-8262. NOCITA is a registered trademark of Aratana Therapeutics, Inc. © Aratana Therapeutics, Inc. NOC-0088-2 August 2018

NSAID:

Other:

Figure 2: An example of a patient checklist that includes the use of local/ regional blocks. Not all drugs listed are appropriate for all patients

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SAVED YOU A SEAT.

5 The clinical properties of the local anesthetic drugs are listed in Table 1. Choose the drug that fits your needs. Lidocaine has the fastest onset, but shortest duration, of action, which is often less than ideal. In most instances longer duration drugs should be chosen to decrease pain both intraoperatively and in recovery. Bupivacaine and ropivacaine provide slightly slower onset than lidocaine but longer duration. The onset time can be countered by doing the block early, e.g., prior to final surgical scrub. For the longest duration blockade, liposome-encapsulated bupivacaine (NOCITA® is the only veterinary drug in this category) provides analgesia for up to 72 hours. This has a further benefit in that pain after discharge can be controlled, in part, by the local anesthetic. More information on the drugs, including NOCITA®, and appropriate blocks is available. 1,3

Recommended reading: 1.

Grubb T, Lobprise H. Local and regional anaesthesia in dogs and cats: Overview of concepts and drugs (Part 1). Vet Med Sci. 2020 May;6(2):209-217. https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC7196681/ Proprietary market research, Elanco Animal Health, 2021. 2. Grubb T, Lobprise H. Local and regional anaesthesia in dogs and cats: Descriptions of specific local and regional techniques (Part 2). Vet Med Sci. 2020 May;6(2):218-234. Grubb T, Lobprise H. Local and regional anaesthesia in dogs and cats: Overview of concepts and drugs (Part 1). Vet Med Sci. 2020 May;6(2):209-217. https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC7196681 Proprietary market research, Elanco Animal Health, 2021. 2. References: 1. Grubb T, Lobprise H. Local and regional anaesthesia in dogs and cats: Descriptions of specific local and regional techniques (Part 2). Vet Med Sci. 2020 May;6(2):218-234. https://pubmed.ncbi.nlm.nih.gov/31965749/ 3. Mathews K, Kronen PW, Lascelles D, Nolan A, Robertson S, Steagall PV, Wright B, Yamashita K. Guidelines for recognition, assessment and treatment of pain. J Small Anim Pract. 2014 Jun;55(6):E10-68. https://wsava.org/Global-Guidelines/Global-Pain-Council-Guidelines/ 4. Otero P, Portela DA. (2018). Manual of small animal regional anesthesia: Illustrated anatomy for nerve stimulation and ultrasound-guided nerve blocks. 5. https://www.elanco.us/products-services/dogs/nocita, Accessed March 1, 2022.

Now you are ready to help all painful patients by using your superpower – the local anesthetics!

Table 1: Clinical properties of commonly used local anesthetic drugs

DOSE (mg/kg)

ONSET (mins)

DURATION 9hrs)

DRUG

Lidocaine

4-6 dogs; 2-4 cats

< 5

1-2

Bupivacaine

1-2 dogs; 0.5-1 cats 5-10

4-6

OK, maybe there won’t be a cat in your chair. But you will get 20+ hours of RACE-approved CE in our TED-talk like, case-based program, with topics ranging from surgery to anesthesia to emergency to derm to ophtho! Plus you’ll be treated right. Awesome speakers, relaxing evening events, free daycare and free swag! AUG 25-28, 2022 | RADISSON BLU, MINNEAPOLIS, MN

Ropivacaine

1-2 dogs; 0.5-1 cats 5-10

4-6

Mepivacaine

3-5 dogs; 2-3 cats

2-5

2-3

NOCITA® (bupivacaine)

5.3 dogs; 5.3/foreleg for 10.6 total cats

Within 2-5*

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*Human data (Apseloff et al. 2013). not measure in animals

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future intervention programs that promote healthier and more active lifestyles for both people and their dogs; for example, incorporating dogs into weight-loss interventions for shared “One Health” benefits. STUDY 2: THE LINK BETWEEN FELINE OBESITY AND REDUCED QUALITY OF LIFE Obese dogs have been shown to have a diminished quality of life, but there has been less evidence characterizing the impact of obesity on the quality of life of cats. The second study* I was involved in set out to determine the impact of obesity on quality of life in companion cats and to examine owner perception of feline obesity. Thirty-three cats participated in our study and were either at healthy weights (BCS of 4 or 5 out of 9; 60.6% of the cats) or obese (BCS of 8 or 9; 39.4% of the cats).7 Owners were asked to self-report their cat’s quality of life as measured by a 16-item scale. 7 For example, one question owners were asked was: In the past four weeks, my cat has been curious and shown an interest in its surroundings (e.g., looking outdoors, watching surroundings, looking under furniture, sniffing objects). Owners could select between five answers: “Not at all,” “A little,” “Somewhat,” “Quite a bit,” or “A great deal.” 7 Significant findings 7 included: • 77% of owners of obese cats reported that obesity was a high risk to their cat’s health and less frequently cited the primary caretaker as a cause of cat obesity compared to owners of healthy weight cats. • 85% of owners of obese cats said they would implement a weight-loss plan for their cat, but only 47% had done so previously (emphasizing a gap between owner intent and action that the veterinary health care team could address). • 93% of owners preferred to focus on diet and exercise as weight-loss tools for their cat rather than medications, supplements, support groups and surgical interventions. • 97% of all participants believed that veterinarians should play a role in weight loss for cats. While these results indicate a communications gap between veterinarians and clients on the topic of feline nutrition, weight management and pet obesity, the good news is that nearly all of the owners believed that veterinarians should play a role in feline weight loss, citing health and quality of life concerns as motivations. This desire for support on the part of cat owners also presents an excellent opportunity for the veterinary team to work with owners to help their cats lose weight and improve their health and quality of life. Quality-of-life questionnaires similar to those distributed to cat owners in our study could be provided by

veterinarians as a tool to better align veterinarian and owner cat health goals.

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Making the complex achievable: With so many—and often competing—elements in play, it may seem daunting to identify individual strategies to help overweight or obese patients lose weight. And while I won’t say that pet weight loss isn’t challenging, it is absolutely achievable. Following are tips I’ve found helpful: 1. ACKNOWLEDGE THE EMOTION. Sometimes, the relationship between clients and their pets seems confounding. That’s because it’s often based on emotion, not logic. In my experience, successful weight management in pets comes down to understanding the type of relationship the owner has with his or her pet. For example, one of my clients was a personal trainer who brought in a cat that weighed more than 20 pounds. I admit I was a little perplexed about how to help him as he knew everything I was about to say! I then asked the owner what he would “tell” his cat if she were one of his clients. He replied that he’d tell her to stop snacking on kibble. When I asked why he couldn’t do that, he looked at me and said, “She meows at me.”

Healthy Weight Loss in Pets: Help Clients Turn Intent In To Action

DEBORAH E. LINDER , DVM, MS, DACVIM (NUTRITION) Research Assistant Professor - Department of Clinical Sciences Cummings School of Veterinary Medicine, Tufts University

In this VETgirl online veterinary continuing education feature article sponsored by Purina® Pro Plan® Veterinary Diets, Deborah E. Linder, DVM, MS, DACVIM (Nutrition) and Board-Certified Veterinary Nutritionist®, discusses the importance of achieving healthy weight loss in dogs and cats and how this might even benefit the health of pet owners.

The human-animal bond has long been powerful. But during the last two years, it has grown even stronger between the patients and clients I see at the Tufts Obesity Clinic for Animals. Because many people have been home more due to the COVID-19 pandemic, they’ve spent additional time with their pets. In some cases, this led to increased exercise time for both parties—particularly dog owners and their dogs. In other cases, clients hunkered down and indulged in treats more and exercised less, resulting in weight gain for all concerned. Human and pet obesity are not new phenomena. We know that the prevalence of human obesity has consistently risen since 1999 and it is predicted that by 2030, 78% of American adults, 33% of children and 50% of adolescents will be either overweight or obese. 1 But what about pet obesity? Is there a connection between the weight of owners and the weight of their dogs? And how does excess weight affect quality of life for cats? I’ve been involved in recent preliminary studies that explored each of these topics. I’d like to share the results we have so far with you and offer some tips for encouraging pet owners to be more proactive about the health of their pets—and, maybe by default, their own—and make healthy lifestyle changes that improve quality of life for everyone. STUDY 1: DO OVERWEIGHT CLIENTS HAVE OVERWEIGHT DOGS? Let’s start with the obvious: Pet obesity is a serious and growing concern. In 1995, 34.1% of adult dogs seen in private practice in the United States were overweight or obese. 2 More recent studies estimate that the prevalence of overweight and

obesity in dogs has increased to more than 50% of the U.S. canine population. 3,4

But what does this have to do with obesity in humans? A study out of the Netherlands found that adult pet owners being overweight correlated with excess weight in their pet dogs. 5 These findings reinforce the idea that owners may apply their own health choices, particularly regarding food and exercise, to their dogs. 5 With these findings in mind, my colleagues and I conducted a preliminary study to determine if there was data to support a possible correlation between the body composition of dogs and the body composition of their owners in the United States. We collected data from 38 owners and their dogs at pet festivals at several locations in Central New England, determining dog owner body composition by calculating body mass index (BMI) and dog body composition by measuring body condition score (BCS). 6 The median BMI of dog owners was 26 (with a range of 17 to 53), which is slightly overweight; while the median BCS of dogs was 6 out of 9 (with a range of 4 to 9), again, slightly overweight. 6 Frequency of overweight and obesity in dog owners was 31.6% and 26.3%, respectively; and 50.0% and 13.2% in dogs, respectively. 6 Owner body mass was positively correlated with dog body condition score (r = 0.60, p < 0.001). 6 While these findings may not be representative of the general U.S. population of dog owners and dogs, they provide perspective that some health behaviors may be shared among dog owners and their dogs. This perspective can help us build on current knowledge and allow for improvement in

It was a moment that changed everything I do at the Tufts Obesity Clinic for Animals.

This client didn’t need information about feline weight loss. He wanted a certain relationship with his cat. And if a weight-loss program was going to alter that relationship in a way he felt would harm or threaten their bond, he didn’t want to do it. In the end, we worked out a plan together that included their “non-negotiables,” meaning including foods or routines he felt were critical to providing his cat an excellent quality of life and that strengthened their bond. In order to create a weight-loss program that’s right for an individual patient and client, it’s important to perform a full nutritional assessment (which includes an extensive diet history) from the client of an overweight cat or dog. (Resources to help with this assessment are described below). Most of the time, that turns out to be more of a lifestyle assessment for the pet and family environment. In my work with overweight pets, I ask about the household, what a typical day is like, what the pet and the family like to do. 2. PROVIDE A CUSTOMIZED WEIGHT-LOSS PROGRAM.

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