From 2010 Canine and Feline Health NAVC and WVC Conferences · Disorders of the endocrine system...

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SYMPOSIUM PROCEEDINGS

Critical Updates onCanine and Feline Health

From 2010NAVC and WVCConferences

Wait, Wait, Don’t Tell Me…Controversial and Challenging Feline CasesDeborah S. Greco, DVM, PhD, DACVIM, Senior Research Scientist, Nestlé Purina PetCareOutline of diagnostic approaches that can help practitioners solve three endocrine presentations in cats

Feline IBD: The Good (Diets), the Bad(Bacteria), and the Ugly (Diagnosis)Debra L. Zoran, DVM, PhD, DACVIM-SAIM, College of Veterinary Medicine and Biomedical Sciences,Texas A&M University, College Station, TexasThe role of intestinal bacteria and diet in the diagnosis and management of IBD in cats

Treatment of Liver Disease:Medical and Nutritional AspectsDavid C. Twedt, DVM, DACVIM, College of Veterinary Medicine & Biomedical Sciences, Colorado State University, Fort Collins, ColoradoUnderstanding the major aspects involved in diagnosing and treating canine and feline liver disease

From Problem to Success: A Weight Loss Program That Works, Growing Relationships, Not Girth in CatsMargie Scherk, DVM, DABVP (Feline), Vancouver, BC, Canada Designing a weight loss program that can ensure success—both for the cat and the client

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SymposiumProceedings:

Critical Updates onCanine and

Feline Health

From 2010 NAVC and WVC Conferences

Disorders of the endocrine system are routinely encountered in feline practice.Certain endocrine disorders, such as hyperthyroidismand diabetes mellitus, are relatively simple to diagnosein cats, whereas others, such as hypoadrenocorticism,are more challenging. This article outlines the diagnos-tic approach for three common endocrine presentationsin cats—polydipsia/polyuria (PU/PD), weight gain, andinsulin resistance as reflected by clinical cases in thefield.

Evaluation of Polydipsia/PolyuriaOne of the most common presenting complaints for endocrinedisorders is PU/PD. The major endocrine diseases that causePU/PD are, in order of frequency, diabetes mellitus, hyperthy-roidism, hyperadrenocorticism, acromegaly or hypersomatotro-pism, hypercalcemia resulting from hyperparathyroidism,

hypokalemia associated with hyperal-dosteronism, diabetes insipidus, andpheochromocytoma (Table 1).

The diagnostic approach to polydipsiaand polyuria is shown in Figure 1. In pa-tients presenting with PU or PD, the cli-nician must first document whether thepatient is indeed drinking or urinatingexcessively. The most common conditionmistaken for PU is pollakiuria (Table 2)resulting from urinary tract disease.When the presence of PU/PD is suspect,the clinician should ask several questionsto determine whether the cat is consum-ing or eliminating excessive water. Thepresence of large amounts of urine in thelitter box as opposed to small, more fre-quently eliminated amounts of urinepoints to PU and compensatory PD.

PD may be more difficult to identifythan PU. In general, because cats aredesert species, it is unusual to witnesscats drinking water frequently. In con-trast, dogs are often presented for PDwhen they are, in fact, just “sloppy”drinkers. If the owner can quantitateand measure the amount of water thecat is drinking, any consumption ofwater in excess of 60 to 70 ml/kg/daywould be considered PD.

Evaluation of Weight GainEndocrine causes of weight gain include,in order of frequency, type 2 diabetesmellitus, hyperadrenocorticism, hypothy-

Deborah S. Greco,DVM, PhD, DACVIM,

Senior ResearchScientist,

Nestlé PurinaPetCare

Wait, Wait, Don’t Tell Me…Controversial and ChallengingFeline Cases



Feline Health

Table 1. Causes of PU/PD

Nonendocrine Causes

Chronic renal failure

Hepatic disease (PSS)

Pyometra, pyelonephritis

Hypercalcemia of malignancy, vitamin Dtoxicosis, granulomatous disease, chronicrenal failure, etc

Acute renal failure (nephrotoxicants)

Primary PU

Endocrine Causes

Diabetes mellitus

Hyperthyroidism

Hyperadrenocorticism

Hypercalcemia resulting fromhyperparathyroidism or hypoadrenocorticism

Hyperkalemia associated withhyperaldosteronism

Diabetes insipidus (central, nephrogenic)

Hypersomatotropism (acromegaly)

Pheochromocytoma

2 Wait, Wait, Don’t Tell Me…Controversial and Challenging Feline Cases

PD = polydipsia; PSS = portosystemic shunt; PU = polyuria

Table 2. Distinguishing PU from Pollakiuria and Incontinence

Signs PU Pollakiuria IncontinenceUrination Active Active Passive

Frequency 2–3 times normal More than 3 times normal Nocturia

Urgency Uncommon Common None

Volume of urine Increased Small, multiple Variable

Mucus Rare Common Rare

Concentration of urine Dilute Concentrated Either

Weight loss Common Rare Rare

PU = polyuria

Test

Endocrine disorder

> 100 ml/kg/day H2O;nocturia

fT4 (dialysis)

NORMAL

HIGHhyperthyroidism

Bile acids, ultrasound

RULE OUTPSS

DDAVP®

NO RESPONSE

Water deprivation test

NO RESPONSE

Nephrogenic DI

RESPONSE

Primary PD

RESPONSE

Central DI

ABNORMAL

MDB, CBC, U/A, chemistry TT4, blood pressure

INCREASED BUN/Cr;low USG CRF

INCREASED BUN/Cr;NORMAL/INCREASED USG

INCREASED Ca

ACTH stimulation

NORMAL

RULE OUT ARF

RULE OUTNeoplasia (SCC, LSA)

INCREASED TT4

Hyperthyroidism

Hyperglycemia, glucosuria

NO RESPONSE to insulin

Advanced DM

DECREASED K

Measure aldosterone

RULE OUTacromegaly (IGF)

RULE OUTCushing’s syndrome (LDDS)

ABNORMAL

Addison’s disease

Figure 1. Diagnostic Flowchart for PD and PU

ACTH = adrenocorticotropic hormone; ARF = acute renal failure; BUN = blood ureanitrogen; Ca = calcium; CBC = complete blood count; Cr = creatinine; CRF = chronicrenal failure; DDAVP = brand name for desmopressin acetate; DI = diabetes insipidus; DM = diabetes mellitus; fT4 = free thyroxine; IGF = insulin-like growth factor;K = potassium; LDDS = low-dose dexamethasone suppression; LSA = lymphosarcoma;MDB = minimum database; PD = polydipsia; PSS = portosystemic shunt; PU = polyuria;SCC = squamous cell carcinoma; TT4 = total thyroxine; U/A = urinalysis; USG = urine-specific gravity

Wait, Wait, Don’t Tell Me…Controversial and Challenging Feline Cases 3

(see Nestlé Purina Body Condition System).Creating a diagnostic flowchart of common

rule outs can help eliminate endocrine disordersas diagnostic differentials (Figure 2).

The dietary history is one of the most importantaspects of history taking for weight gain. Theexaminer should ask what type of diet is beingfed—homemade, raw, or commercial. For com-mercial diets, is the cat primarily fed dry food or a mixture of dry and canned food? If the catis being fed a commercial food, also ask aboutthe specific brand, and if the diet is homemade,ask for a complete list of ingredients.

Other important questions include: ■ How long has the diet been fed? ■ When was the diet changed last, and how

frequently is it changed?■ How much is the cat eating, and how is the

food being measured (weighing vs cups)? ■ Is the cat fed ad libitum or restricted? How

many times per day is the cat fed?

roidism, acromegaly, and insulinoma (Table 3).The primary differentials for nonendocrinecauses of weight gain, which are much morecommon, feature overfeeding and the feeding oftreats. Patient records on the body conditionscore (BCS) can help determine whether theweight gain is a result of nonendocrine problems

Table 3. Causes of Weight Gain

Nonendocrine Causes

Overfeeding

Feeding treats

Feeding high caloric density food

Large abdominal tumors

Endocrine Causes


Hypothyroidism

Hypersomatotropism (acromegaly)

Insulinoma

Type 2 diabetes mellitus—early

Weight gain

NORMALappetite

INCREASEDappetite

DECREASEDappetite

RULE OUToverfeeding

Hyperglycemia,increased

fructosamine

NORMALMBD

LOWBG

Low-carbohydrate diet, insulin, oral hypoglycemics

Weight loss dietOM

RULE OUTinsulinoma

RESPONSE NO RESPONSE

Early type 2 DM LDDS, IGF RESPONSE NO RESPONSE

Continue diet to target weight

RULE OUT dietarynoncompliance

Repeat MDB,TSH, TT4

HIGH IGF; acromegaly POSITIVE LDDS;Cushing’s syndrome

NORMAL

MDB MDB, TSH, TT4

Test

Endocrine disorder

NORMAL

LOW TT4 andHIGH TSH

LOW TT4 andLOW TSH

LOW fT4 NORMAL or HIGH fT4

Secondary hypothyroidism

Euthyroidsick syndrome

Hypothyroidism fT4 by dialysis

BG = blood glucose; DM = diabetes mellitus; fT4 = free thyroxine; IGF = insulin-like growth factor; LDDS = low-dose dexamethasone suppression; MDB = minimum database; OM = Purina Veterinary Diets OM Overweight Management Feline Formula; TSH = thyroid-stimulating hormone; TT4 = total thyroxine


Figure 2. Diagnostic Flowchart for Weight Gain

Ribs visible on shorthaired cats; no palpable fat; severe abdominal tuck; lumbar vertebrae and wings of ilia easily palpated.

Ribs easily visible on shorthaired cats; lumbar vertebrae obvious with minimal muscle mass; pronounced abdominal tuck; no palpable fat.

Ribs easily palpable with minimal fat covering; lumbar vertebrae obvious; obvious waist behind ribs; minimal abdominal fat.

Ribs palpable with minimal fat covering; noticeable waist behind ribs; slight abdominal tuck; abdominal fat pad absent.

Well-proportioned; observe waist behind ribs; ribs palpable with slight fat covering; abdominal fat pad minimal.

Ribs palpable with slight excess fat covering; waist and abdominal fat pad distinguishable but not obvious; abdominal tuck absent.

Ribs not easily palpated with moderate fat covering; waist poorly discernible; obvious rounding of abdomen; moderate abdominal fat pad.

Ribs not palpable with excess fat covering; waist absent; obvious rounding of abdomen with prominent abdominal fat pad; fat deposits present over lumbar area.

Ribs not palpable under heavy fat cover; heavy fatdeposits over lumbar area, face and limbs; distention of abdomen with no waist; extensive abdominal fat deposits.

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Call 1-800-222-VETS (8387), weekdays, 8:00 a.m. to 4:30 p.m. CT

Wait, Wait, Don’t Tell Me…Controversial and Challenging Feline Cases 5

Tips for Investigating Weight Gain

✔ In cats, always check the underside of the tarsus for evidence of diabeticneuropathy.

✔ Ask the client to bring photographs of the patient from several years ago forcomparison of skull and facial changes.

✔ Check the patient’s teeth for increased interdental spaces (acromegaly).

✔ Assign a BCS and record each score in the patient’s medical record. Cats innormal body condition (BCS 4–5 on the Nestlé Purina scale) will have ribseasily palpable and normal abdominal tuck.

✔ If necessary, perform the knuckle test (quick BCS). Animals in normal bodycondition have ribs that feel like the tops of the knuckles with the handextended. Overweight patients have ribs that palpate similar to the palm ofthe extended hand.

BCS = body condition score


■ Who feeds the animal, and whatages are the family members (eg,children, grandparents)?

■ Are there other pets in the house-hold, and what diets are they fed?

■ Does the cat have access to theoutdoors?

■ Does the cat receive supplements (eg, treats,vitamins, yogurt)?

It is important to remember that many clients donot perceive treats and additives (eg, table food) aspart of the cat’s diet and, therefore, may forget tomention them.

Another tricky aspect is determining who in the household is responsible for feeding the ani-mal. Many times the primary caregiver is surprisedto find that another family member has been feed-ing a specific food or treat without telling the pri-mary caregiver. In addition, problems may arisebecause owners have preconceived notions aboutpet foods. Clients may indicate that they will notfeed certain flavors of foods or certain ingredientsbecause of “allergies.” Furthermore, it may be diffi-cult to obtain an accurate dietary history becauseclients may be embarrassed or unwilling to divulgeexactly what and how much is being fed. For these

Table 4. Causes of Insulin Resistance

Nonendocrine Causes

Infection (eg, UTI, pulmonary,skin disease)

Cancer

Immune disease

Drugs, pancreatitis, liverdisease, stress

Endocrine Causes

Hyperthyroidism

Hypothyroidism


Hypersomatotropism(acromegaly)

UTI = urinary tract infection

reasons, having clients complete a written ques-tionnaire is often the best and most expedient wayto obtain a dietary history.

Performing a thorough physical examination,comparing the patient’s current weight with itsweight several years ago, and establishing the pa-tient’s BCS are important for determining the rea-son for weight gain (see Tips for InvestigatingWeight Gain).

Evaluation of Insulin ResistanceIt is very rare to obtain a perfect glucose curve ina patient. Generally, problems associated withthe blood glucose curve can be differentiated bythe characteristics of the curve and the insulindose (dosing interval).

If the patient is receiving less than 2.2 U/kgper dose, the blood glucose curve is usually indicative of one of the following:

■ Insufficient insulin dose—Corrective action,increase dose

■ Short duration of action of insulin—Corrective action, change to longer-actinginsulin or twice-daily dose regimen

■ Insulin-induced hypoglycemic hyper-glycemia (Somogyi effect)—Corrective action, reduce insulin dose by 25%

■ Insulin overlap or prolonged insulin action—Corrective action, change toshorter-duration insulin or insulin mixture(ie, 30% regular, 70% NPH)

If the patient is receiving more than 2.2 U/kg of insulin per dose, insulin resistance should beinvestigated (Table 4). In cats, the top diagnos-tic differentials for insulin resistance include hyperthyroidism, hypersomatotropism(acromegaly), and hyperadrenocorticism. ■

Feline inflammatory bowel disease (IBD) applies to a number of poorly understood enteropathiescharacterized by infiltration of inflammatory cells intothe gastrointestinal (GI) mucosa. The cellular infiltrateis composed of variable populations of lymphocytes,plasma cells, eosinophils, and neutrophils that can be distributed throughout the GI tract.1-3 In severely affected cats, this infiltrate may be accompanied bychanges in the mucosal architecture, including villusatrophy, fusion, fibrosis, and lymphangiectasia.

Although IBD appears to be a common clinical problem in cats, little is known about the etiopathogenesis or the local and systemic consequences of the disease, including thedevelopment of lymphoma and nutritional deficiencies.4 Inaddition, the nature of inflammation associated with IBD isjust beginning to be characterized beyond the visible changesin gross histopathology that have been described.5-11

This paper reviews what is known about feline IBD, withparticular focus on the role of commensal and pathogenic in-testinal bacteria as well as diet in the diagnosis and manage-ment of the disease.

Diagnostic ProcessFeline IBD, a commonly diagnosed condition of adult cats,is characterized by persistent clinical signs consistent with GI disease (eg, vomiting, anorexia, weight loss, diarrhea) that occur concurrently with histologic evidence of mucosalinflammation.12 The median age of cats presenting with IBD is around 7 years, and most cats present with a historyof these signs occurring intermittently for weeks to years.Purebred cats, such as the Siamese and Abyssinian, may beoverrepresented, but definitive breed predilections have notbeen reported. There is no reported predilection based onsex.

Diagnosis by exclusion Because clinical signs of IBD can be as-sociated with various primary GI andextra-GI diseases, it is important toconsider broad groupings of differen-tials and obtain a minimum database(ie, CBC, serum biochemical panel,urinalysis) until sufficient data havebeen collected to narrow the list of dif-ferentials. A number of possible causesof intestinal inflammation must beconsidered, however, including infec-tious disease, food sensitivity (allergy)or food intolerance, endocrinopathies(eg, hyperthyroidism), parasitic disease,and neoplastic disease. These differentialsshould be investigated thoroughly beforesettling on a diagnosis of idiopathic IBDand instituting a treatment plan.

Food allergy and intolerance can beparticularly difficult to distinguish fromIBD and other intestinal disorders, es-pecially because of shared clinical signsand identical histopathologic changes inthe bowel. Therefore, appropriate foodtrials are an extremely important com-ponent of both reaching a diagnosis andimplementing therapy in cats with GIdisease or suspected IBD. In addition tofood trials, the diagnostic plan for a catwith chronic vomiting or diarrheashould include multiple fecal examina-tions or therapeutic deworming trialswith broad-spectrum agents, such asfenbendazole, assessment of thyroid and

Debra L. Zoran,DVM, PhD,

DACVIM-SAIM,College ofVeterinary

Medicine andBiomedical

Sciences,Texas A&M

University, CollegeStation, Texas

Feline IBD: The Good (Diets), the Bad (Bacteria), and the Ugly(Diagnosis)



Feline Health

Feline IBD: The Good (Diets), the Bad (Bacteria), and the Ugly (Diagnosis) 7

8 Feline IBD: The Good (Diets), the Bad (Bacteria), and the Ugly (Diagnosis)

FeLV/FIV status, and assessment of GI function,including measuring cobalamin and folate andconducting trypsin-like immunoreactivity (TLI)and pancreatic lipase immunoreactivity (PLI)tests.

Many cats with IBD have concurrent inflam-mation of the liver and pancreas—a phenome-non called triaditis.13 Because chronic pancreatitiscan cause few distinguishing signs and be diffi-cult to diagnose by laboratory testing alone, adegree of clinical suspicion is necessary to care-fully assess cats.14,15 Serum cobalamin levels arecommonly decreased in cats with severe boweldisease or pancreatitis. Furthermore, in cats withhypocobalaminemia, diarrhea does not resolveuntil replacement therapy has been instituted.Cobalamin therapy in some cats may be life-long, whereas in others, once the clinical diseasehas been resolved, supplementation can be dis-continued.

Imaging and exploratory measures In addition to laboratory evaluation, radiographyand ultrasonography are important aspects ofoverall assessment of cats with possible IBD. Al-though abdominal radiographs and ultrasoundfindings cannot confirm IBD, they are essentialfor ruling out other GI problems, including in-

testinal foreign bodies, intussusception, masses,and involvement of other organs, especially theliver and pancreas. Many cats with intestinal in-flammation have thickened loops of bowel,changes in bowel layering, or evidence of mesen-teric lymphadenopathy.16 These changes are notindicative of a specific cause but are further con-firmation of intestinal disease that requires addi-tional assessment.

Abdominal ultrasonography can reveal impor-tant information about the location and severityof lesions, thereby suggesting whether endoscopyor abdominal exploratory surgery might be theappropriate next step. Because intestinal biopsyspecimens obtained either endoscopically orduring exploratory surgery are essential to con-firm the presence of inflammatory infiltrates, ei-ther diagnostic measure is an important part ofthe process. However, a number of problemshave been associated with using histopathologicchanges or findings to diagnose IBD.17

First, problems correlating a pathologist’s interpretation of inflammation found in the GI biopsy specimen with the actual disease have been well documented.5 The presence oflymphocytes and plasma cells in the wall of thegut does not mean the problem is idiopathic,does not necessarily correlate with the cytokineexpression or degree of clinical disease, and does not mean that IBD can be accurately dif-ferentiated from lymphoma. As a result, stan-dards for histopathologic interpretation ofbiopsy specimens have been recommended bypathologists to help improve the utility and consistency of interpreting GI histopathologicfindings5,18 (see WSAVA Guidelines for GIHistopathology).

Inflammatory responseThe basis of the immunologic response in catswith IBD is unknown, and it remains to be deter-mined whether the inflammatory response resultsfrom the presence of undefined pathogens or ex-emplifies an inappropriate response to dietaryantigens or intraluminal commensal bacteria. De-termining the cytokine and immune cell popula-tion in cats with IBD is important from both a

WSAVA Guidelines for GI Histopathology

The WSAVA guidelines offer pertinent information about GIhistopathology.5 Small cell (ie, lymphocytic, low-grade)lymphoma can be extremely difficult to distinguish from IBD.Because the disease can be local (only in the jejunum orileum) or found only in the deeper layers of the intestinal wall(submucosa or muscularis), if during endoscopy, biopsyspecimens are not obtained from the appropriate sites or areinadequate in depth, lesions can be missed. If cats are notresponding to appropriate therapy or were responding totherapy but are now losing weight or having recurrentdiarrhea despite therapy, the possibility of lymphoma shouldbe reconsidered. Several recent reviews on this subjectprovide more details specific to GI lymphoma and itsmanagement.18

WSAVA = World Small Animal Veterinary Association

Abdominalradiographs andultrasoundfindings cannotconfirm IBD butare essential forruling out otherGI problems,such as intes-tinal foreignbodies andintussusception.


pathologic and therapeutic standpoint, as treat-ment of IBD in cats is nonspecific and based ondietary modification, administration of antibi-otics, and suppression of the immune system.

The Role of BacteriaIn humans and experimental animals, recentstudies indicate a strong association between thedevelopment of IBD and a breakdown of normaltolerance mechanisms, host susceptibility, andenteric microflora.19-22 It is likely that these samefactors are important in feline IBD9-11,23 (see AreBacteria a Key Component?). Modulation of theenteric microenvironment in humans with IBD has been shown to reduce proinflammatory cy-tokines in the mucosa and, therefore, decreasethe inflammatory response.24 In humans, IBDtherapy has included antibiotics with immune-modulating capacity, prebiotics, probiotics, andimmunosuppressants as well as other drugs thatmodify cytokine release.22,25

Unfortunately, studies assessing modulation ofenteric flora (using probiotics, prebiotics, or otherspecific therapy for cytokines) in cats with IBDare only in the early stages. Nevertheless, few stud-ies have shown that intestinal microbiota in catswith IBD are clearly different from those in nor-mal cats and often the difference is a decrease innormal commensals (eg, bifidobacteria, lacto-bacilli) and an increase in pathogenic species.6,9 Atthis time, therapy for IBD in cats continues to in-clude inflammatory suppression and antibiotictherapy. The most effective IBD therapies includesteroids (ie, 1 to 2 mg/kg of prednisolone ormethylprednisolone PO Q 12 H) or other drugsthat interrupt the proinflammatory pathways ac-tive in the gut. In cats that are intolerant ofsteroids, budesonide therapy may be a reasonablechoice. Alternatively, in cats in which steroids areno longer effective or are causing morbidity (eg,diabetes), immunosuppressive therapy may benecessary and is often effective. The two drugsmost commonly recommended and effective forcats in this setting are cyclosporine and chloram-bucil.

Antibiotic therapy with 5 to 10 mg/kg ofmetronidazole PO Q 12H has been effective for a

Are Bacteria a Key Component? One group of investigators11 is seeking to determine the effect ofmucosal bacteria and their relationship to cytokine responsesand inflammation in the bowel of cats. Intestinal biopsieswere collected from 17 cats undergoing diagnosticinvestigation of signs of GI disease and from 10 healthycontrols.11 Subjective duodenal histopathology ranged from normal (10) to mild (6) to moderate (8) to severe (3)IBD. The mucosal response was evaluated by objectivehistopathology and cytokine mRNA levels in duodenal biopsies.The number of mucosa-associated Enterobacteriaceae was higherin cats with signs of GI disease than in healthy cats. These pathogens, includingEscherichia coli and Clostridium species, were associated with significant changes inmucosal architecture, principally atrophy and fusion; up-regulation of cytokines,particularly IL-8; and the number of clinical signs exhibited by affected cats.

The study findings indicate that an abnormal mucosa-associated flora isassociated with the presence and severity of duodenal inflammation and clinicaldisease activity in cats. The observations provide a rational basis for futureinvestigations to address the potential causal involvement of mucosa-associatedbacteria. They are perhaps most consistent with a model proposed for the mucosalresponse to gram-negative bacteria, whereby proinflammatory cytokines (eg, IL-1,IL-8, IL-12) produced by epithelial cells in response to such stimuli as gram-negativebacteria are modulated by macrophage production of IL-10. Support for this conceptin the canine GI tract is provided by studies of the small intestines of dogs in whichexpression of IL-10 and IFN-β mRNA by lamina propria cells and the intestinalepithelium was observed in the face of a luminal bacterial flora that was morenumerous than that of control dogs.23

Additional evidence that bacteria are a key component of IBD in cats has beencollaborated by Inness and coworkers,9 who characterized the gut microflora of bothhealthy cats and cats with colonic IBD. Cats with IBD were found to have significantlyhigher populations of Desulfovibrio (a genus of bacteria that produce toxic sulfides)compared with normal cats, which had higher populations of bifidobacteria andbacteroides (normal flora). These authors proposed that modulation of intestinalflora with probiotics and dietary intervention to decrease the production ofpathogenic bacteria were likely important in treating cats with IBD.

Finally, another study10 found that the expression of cytokines in biopsyspecimens from the intestines of cats with IBD represented greater transcriptionof genes encoding IL-6, IL-10, IL-12, TNF-α, and TGF-β than from those of catswith normal intestines. These results also suggested that, in cats with IBD, bothproinflammatory and immune dysregulation features were present.

IBD = inflammatory bowel disease; IFN = interferon; IL = interleukin; TGF = transforming growth factor; TNF = tumor necrosis factor

number of years and continues to be recommendedas initial therapy for IBD.12,26 There is also a widelyheld belief that metronidazole is effective not onlybecause of its antibacterial properties but because ofconcurrent immune-modulating properties. Somedata support these ideas, but the specific role ofmetronidazole as treatment for IBD is still notcompletely known. Because metronidazole may be poorly tolerated and has potential for serious ad-verse effects, it should not be given indefinitely.Another antibiotic that may be useful in cats withpresumed IBD is tylosin at a dose of 10 to 20


mg/kg PO Q 12 H; however, less is known aboutthe effects of tylosin on cats when used long-term.27,28

Finally, data in humans with IBD are increas-ingly showing that probiotics and antioxidantprebiotic nutraceuticals may be important com-ponents of therapy.25 At this time, it is difficultto make specific recommendations concerningthe probiotic or nutraceutical therapy with thegreatest benefit because of the paucity of studiesin cats with IBD and the species-specific natureof probiotics and their effects. However, probi-otics that provide an immune-modulating effector that increase the number of beneficial specieswhile competing against pathogens might be ex-pected to be helpful. In several studies in kit-tens, probiotics containing Enterococcus faecium(SF68) appeared to improve immune functionand had better responses to therapy when ex-posed to enteric protozoa.29 Furthermore,whereas probiotic therapy alone would not beexpected to produce clinical remission, cats un-dergoing long-term therapy for IBD may bene-fit from the addition of probiotics to theirtreatment regimen.

Diets Designed to Promote GI Health

The highly digestible diets from different pet foodmanufacturers have a variety of formulations—different protein and carbohydrate sources, differentlevels of fat, and various additives designed topromote intestinal health (eg, fructooligosaccharide[FOS], mannondigosaccharide [MOS], omega-3 fattyacids, antioxidant vitamins, soluble fiber). If one typeof highly digestible diet has been fed for at least 2weeks with minimal response, then it is entirelyreasonable to try another diet from a differentsource or try an entirely different dietary strategy(eg, high-protein/low-carbohydrate, novel antigen,hydrolyzed diet). In addition, diarrhea may beattributed to carbohydrate intolerance or bacterialchanges resulting from dietary changes. Thus, theaddition of probiotics or prebiotics to help influencemicroflora is a reasonable therapeutic option, as isthe addition of either metronidazole or tylosin.

The Role of Dietary ManagementThe use of diet to help manage GI disease is not a new concept, but the type of diet to use has be-come an increasingly complex issue. In many, if not most, cats with mild IBD, especially thosewithout significant infiltrate of inflammatorycells (mild to moderate infiltrate) or without sig-nificant weight loss or other morbidity, the bestapproach is to feed a highly digestible diet or to change the diet to one with fewer additives,flavorings, or other substances that may be associ-ated with food intolerance. Many cats (nearlytwo-thirds in one study) with chronic diarrheahave complete resolution of clinical signs whenfed a highly digestible diet.30,31

Highly digestible diets are not defined in a reg-ulatory sense but generally indicate a productwith protein digestibility of greater than 85%(typical diets are 78% to 81%) and fat digestibilityof greater than 90% (typical diets are 77% to85%). These diets are designed to provide foodthat is easy to digest because it has moderate to lowfat, moderate to increased protein, and moderateto decreased carbohydrates; may have additives toimprove intestinal health, such as soluble fibers,omega-3 fatty acids, and increased antioxidant vi-tamins; and contain no gluten, lactose, food color-ing, preservatives, and similar additives. Manydifferent brands fall under the category of “highlydigestible,” but they are not all alike.

The protein digestibility of a diet is one of thekey factors that can determine its success in catswith IBD. In general, meat-source proteins anddiets containing meat meals are more digestiblethan plant-source proteins, and animal proteinsare more digestible than meat by-products. Inaddition, to increase digestibility of foods incats, the number and amount of carbohydratesin the food are decreased—a single-source car-bohydrate food is better than foods with manydifferent sources, and highly digestible carbohy-drate sources are better than complex plant-source carbohydrates. Therefore, when one dietfrom this category is not accepted or seems tomake the diarrhea worse, it cannot be assumedthat all diets in this category will be ineffectiveand unaccepted. Diets from different manufac-

Treatment of IBD incats is nonspecificand based ondietary manage-ment, antibiotic treatment, andimmunosuppression.


turers have various formulations (see Diets De-signed to Promote GI Health).

Novel Antigen or Elimination DietsAllergy and intolerance are the most common ad-verse reactions cats have to food. Food allergy orhypersensitivity is an adverse reaction to a food orfood additive with a proven immunologic basis.In contrast, food intolerance is a nonimmunologicabnormal physiologic response to a food or foodadditive. Food poisoning, food idiosyncrasy, andpharmacologic reactions to foods also fall underthe category of food intolerance.

The specific food allergens that cause problemsin cats have been poorly documented, with only10 studies describing the clinical lesions associatedwith adverse reactions.30-33 In these reports, morethan 80% of cases were attributed to beef, dairyproducts, or fish.

The incidence of food allergy in cats remainsunknown but is estimated to be only 15% to 20%of all food-related causes of diarrhea.33 However,food intolerance is believed to contribute to 60%to 65% of feline diarrhea cases. In two separatestudies, a majority of cats responded to dietarytherapy with a highly digestible diet.31,34

The causes of dietary intolerance that need to be carefully considered in feline diets are pri-marily protein and carbohydrates—both sourcesand amounts. The diagnosis of both food allergyand intolerance is based on a dietary eliminationtrial. The major difference between these twotypes of adverse food reactions is the length oftime on the diet required to achieve a response(cats with food allergy may require 6 to 12 weekson the elimination diet before an improvementwill be seen).

Various commercial and homemade eliminationdiets, as well as diets formulated with hydrolyzedproteins, may be used in cats with suspected foodallergy or intolerance. The key is to select a dietthat has a novel protein source based on a carefuldietary history and is balanced and nutritionallyadequate (commercial diets are best for this); how-ever, a homemade elimination diet may be nec-essary to find an appropriate test diet. If ahomemade diet must be used for long-term

therapy, a complete and balanced diet containingthe necessary protein sources should be formulatedby a nutritionist. For most cats with food allergy,avoiding the offending food is most effective andcan result in complete resolution of signs. How-ever, short-term steroid therapy can decrease theconcurrent intestinal inflammation until the ap-propriate food sources can be identified.

GI disease may decrease the availability of anumber of micronutrients, such as vitamins andminerals, thereby having important consequenceson the pathogenesis, diagnosis, and treatment ofthe disease. The diagnostic utility of measuringthe serum concentrations of cobalamin and folatein cats with suspected intestinal disease has re-cently been established. Although the impact ofdeficiencies in cobalamin and folate are not com-

Cobalamin HomeostasisCobalamin homeostasis is a complex, multistep process thatinvolves participation of the stomach, pancreas, intestines, andliver. Following ingestion, cobalamin is released from food inthe stomach. It is then bound to a nonspecific cobalamin-binding protein of salivary and gastric origin calledhaptocorrin. IF, a cobalamin-binding protein that promotescobalamin absorption in the ileum, is produced by thestomach and pancreas in dogs and the pancreas but not thestomach in cats.35

The affinity of cobalamin for haptocorrin is higher at acid pHthan that for IF, so most is bound to haptocorrin in the stomach. After entering theduodenum, haptocorrin is degraded by pancreatic proteases and cobalamin istransferred from haptocorrin to IF.35

A portion of cobalamin taken up by hepatocytes is rapidly re-excreted in bilebound to haptocorrin. This rapid turnover means that cats with cobalaminmalabsorption can totally deplete their body cobalamin stores within 1 to 2months.35

Recent studies indicate that subnormal cobalamin concentrations are common incats with GI disease or exocrine pancreatic insufficiency.4 Investigation of therelationship of subnormal serum cobalamin concentrations to cobalamin deficiencyand the effect of cobalamin deficiency on cats has revealed the clinical significanceof cobalamin deficiency in cats.4

Serum MMA concentrations (median; range) decreased after cobalaminsupplementation. Serum homocysteine concentrations were not significantlyaltered, whereas cysteine concentrations increased significantly. Mean body weightincreased significantly after cobalamin therapy, and the average body weight gainwas 8.2%. Significant linear relationships were observed between alterations inserum MMA and fTLI concentrations and the percentage of body weight change.

There is also emerging evidence that cobalamin supplementation may result inclinical improvement of cats with IBD without recourse to immunosuppressivetherapy.15 In this respect, it is interesting to note that cobalamin deficiency isassociated with altered immunoglobulin production and cytokine levels in mice. Theimpact of cobalamin deficiency on the immune environment of cats remains to beestablished.

fTLI = feline trypsin-like immunoreactivity; IF = intrinsic factor; MMA = methylmalonic acid

B12) in cats with gastrointestinal disease. Simpson KW,Fyfe J, Cornetta A, et al. J Vet Intern Med 15:26-32, 2001.

5. Histopathological standards for the diagnosis of gastrointesti-nal inflammation in endoscopic biopsy samples of the dog andcat: A report from the World Small Animal Veterinary Associa-tion Gastrointestinal Standardization Group. Day MJ, BilzerT, Mansell J, et al. J Comp Pathol 138:1-43, 2008.

6. Molecular characterization of intestinal bacteria in healthycats and cats with IBD. Ritchie L. MS dissertation. TexasA&M University, 2008.

7. Quantitative evaluation of inflammatory and immune re-sponses in cats with inflammatory bowel disease. GoldsteinRE, Greiter-Wilke A, McDonough SP, Simpson KW. AmColl Vet Intern Med Proc, 2003.

8. Immune cell populations in the duodenal mucosa of catswith inflammatory bowel disease. Waly NE, Stokes CR,Gruffydd-Jones TJ, et al. J Vet Intern Med 18:113-122, 2004.

9. Molecular characterisation of the gut microflora of healthyand inflammatory bowel disease cats using fluorescence insitu hybridisation with special reference to Desulfovibrio spp.Inness VL, McCartney AL, Khoo C, et al. J Anim PhysAnim Nutr 91:48-53, 2006.

10. Measurement of cytokine mRNA expression in intestinalbiopsies of cats with inflammatory enteropathy using quan-titative real-time RT-PCR. Van Nguyen N, Tagliner K,Helps CR, et al. Vet Immunol Immunopathol 113:404-414,2006.

11. The relationship of mucosal bacteria to duodenal histopathol-ogy, cytokine mRNA, and clinical disease activity in cats withinflammatory bowel disease. Janeczko S, Atwater D, Bogel E,et al. Vet Microbiol 128:178-193, 2008.

12. Inflammatory bowel disease. Current perspectives. JergensAE. Vet Clin North Am Small Anim Pract 29:501-521, 1999.

13. Relationship between inflammatory hepatic disease and inflam-matory bowel disease, pancreatitis and nephritis in cats. WeissDJ, Gagne JM, Armstrong PJ. JAVMA 209:114-116, 1996.

14. Pancreatitis in cats: Diagnosis and management of a chal-lenging disease. Zoran DL. JAAHA 42:1-9, 2006.

15. Diagnosis of pancreatitis. Steiner JM. Vet Clin North AmSmall Anim Pract 33:1181-1195, 2003.

16. Radiographic, ultrasonographic and endoscopic findings incats with inflammatory bowel disease of the stomach andsmall intestine. 33 cases (1990-1997). Baez JL, Hendrick MJ,Walker LM, Washabau RJ. JAVMA 215:349-354, 1999.

17. Interobserver variation among histopathologic evaluation ofintestinal tissues from dogs and cats. Willard MD, JergensAE, Duncan RB, et al. JAVMA 220:1177-1181, 2002.

18. Feline alimentary lymphoma: Demystifying the enigma. Wil-son HM. Top Companion Anim Med 23(4):177-184, 2008.

19. Chemokine expression in IBD: Mucosal chemokine expres-sion is unselectively increased in both ulcerative colitis andCrohn’s disease. Banks C, Bateman A, Payne R, et al. JPathol 199:28-35, 2003.

20. Bacterial interactions with cells of the intestinal mucosa: Toll-like receptors and NOD2. Cario E. Gut 54:1182-1193, 2005.

21. Experimental models of inflammatory bowel disease revealinnate, adaptive, and regulatory mechanisms of host dia-logue with the microbiota. Elson CO, Cong Y, McCrackenVJ, et al. Immunol Rev 206:260-276, 2005.

22. Inflammatory bowel disease: Epidemiology, pathogenesis,and therapeutic opportunities. Hanauer SB. Inflam BowelDis 12(Suppl 1):S3-S9, 2006.

23. Intestinal cytokine mRNA expression in canine inflamma-tory bowel disease: A meta-analysis with critical appraisal.Jergens AE, Sonea IM, Kauffman LK, et al. Comp Med59:153-162, 2009.


pletely known, the role of cobalamin in normalfunction of the GI tract and in many other aspectsof metabolism is well documented4,15,35 (seeCobalamin Homeostasis). Furthermore, becausecats are obligate carnivores that consume muchhigher amounts of protein in their diet, the im-portance of cobalamin and other B vitamins inmaintaining protein metabolism cannot be over-stated. Therefore, evaluation of all cats with GIdisease, not just cats with IBD, is an importantpart of not only the diagnostic process but also themanagement of these diseases.

Although other vitamin or mineral deficienciesmay occur with longstanding or severe IBD, theyare less likely (because of storage of fat-soluble vi-tamins and some minerals) and supplementationwithout documentation of a deficiency can bedangerous. Thus, supplementation of fat-solublevitamins is not generally recommended unlesssigns of deficiency, such as bleeding from vitaminK deficiency, are occurring or tissue or blood levelsof the vitamin are determined.

Closing RemarksIn conclusion, much remains to be learned

about the complex interplay between GI mi-croflora, dietary antigens, the epithelium, im-mune effector cells, and soluble mediators in thefeline GI tract in health and disease. The devel-opment of feline-specific reagents together withthe growing realization of the nutritional conse-quences of IBD have precipitated a shift beyondreliance on qualitative histology, holding prom-ise for improved understanding, therapy, andprevention in the future. ■

References1. Lymphocytic plasmacytic gastroenteritis in cats: 14 cases

(1985-1990). Dennis JS, Kruger JM, Mullaney TP. JAVMA200:1712-1718, 1992.

2. Lymphocytic plasmacytic enterocolitis in cats: 60 cases(1988-1990). Hart JR, Shaker E, Patnaik AK, et al. JAAHA30:505-514, 1994.

3. Idiopathic inflammatory bowel disease in dogs and cats: 84cases (1987-1990). Jergens AE, Moore FM, Hayness JS, etal. JAVMA 200:1603-1608, 1992.

4. Subnormal concentrations of serum cobalamin (vitamin

Allergy andintolerance arethe most commonadverse reactionscats have to food.The incidence offood allergy incats is unknown,but food intole-rance probablyaccounts for 60%to 65% of felinediarrhea cases.


24. Differential effect of immune cells on non-pathogenic gram-negative bacteria-induced nuclear factor-kappaB activationand pro-inflammatory gene expression in intestinal epithe-lial cells. Haller D, Holt L, Parlesak A, et al. Immunology112:310–320, 2004.

25. Probiotics in gastrointestinal diseases. Guarner F. In Versa-lovic J, Wilson M (eds): Therapeutic Microbiology: Probioticsand Related Strategies —Washington, DC: ASM Press, 2008,pp 255-271.

26. Idiopathic inflammatory bowel disease in cats: Rationaltreatment selection. Trepanier L. J Feline Med Surg 11:32-38, 2009.

27. Inflammatory bowel disease. German AJ. In Bonagura J,Twedt D (eds): Kirk’s Current Veterinary Therapy XIV—St.Louis, MO: Saunders/Elsevier, 2008, pp 501-506.

28. Tylosin responsive diarrhea. Westermarch E. In Bonagura J,Twedt D (eds): Kirk’s Current Veterinary Therapy XIV—St.Louis, MO: Saunders/Elsevier, 2008, pp 507-509.

29. Effect of supplementation with Enterococcus faecium (SF68)

on immune functions in cats. Veir JK, Knorr R, CavadiniC, et al. Vet Ther 8:229-238, 2007.

30. Food sensitivity in cats with chronic idiopathic gastrointestinalproblems. Guilford WG, Strombeck DR, Rogers Q, et al. JVet Intern Med 15:7-13, 2001.

31. Dietary therapy of feline diarrhea. Guilford WG, CenterSA, Strombeck DR, et al. NZ Vet 51:262-265, 2003.

32. Adverse reactions to foods: Allergies versus intolerance. Roude-bush P. In Ettinger SJ, Feldman EC (eds): Textbook of VeterinaryInternal Medicine, ed 6—St. Louis, MO: Elsevier, 2005, p 153.

33. Food allergy in dogs and cats: A review. Verlinden A, HestaM, Millet S, et al. Crit Rev Food Sci Nutr 46:259-273, 2006.

34. Evaluation of two diets in the nutritional management ofcats with naturally occurring chronic diarrhea. LaflammeDP, Martineau B, Jones W, et al. Vet Ther 5:43-51, 2004.

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

Few controlled studies are investigatingtreatments for liver disease in dogs andcats. When recommending specific therapeutic ap-proaches, however, most authors point out the im-portance of linking adequate nutritional support withspecific therapies and general hepatic support. Man-agement of liver-related complications should alsobe addressed if and when they occur. This article cov-ers the major aspects associated with managing liverdisease in small animals and outlines some basictreatment goals (see box).

Nutritional ManagementThe liver is paramount in metabolism and plays a key role inregulating protein, carbohydrates, fat, vitamins, and minerals.Metabolic derangements that occur in dogs and cats with liverdisease can lead to malnutrition, impaired hepatic regeneration,and the clinical consequences of hepatic insufficiency (eg, he-patic encephalopathy [HE], ascites, gastrointestinal [GI] ulcera-tion, coagulopathy, immunosuppression). The liver also has theunique ability to regenerate following injury, a process that oc-curs through appropriate nutrition.

The overall goal of nutritional managementof liver disease is predominately supportiveand requires a fine balance between promotinghepatocellular regeneration and providing nu-trients to maintain homeostasis without ex-ceeding the metabolic capacity that leads toaccumulation of toxic metabolites.

Basic nutritional conceptsOne of the most important aspects of liver dis-ease therapy is ensuring that the patient hasappropriate energy intake to prevent anorexiaand weight loss, thereby minimizing catabo-lism. Adjustments to the diet are required

when malnutrition is present. To thisend, practitioners must first calculatethe patient’s caloric needs.

Calculation of the basal energy re-quirement (BER) is based on theweight of lean body mass; the weight of fat or ascites is not included (seebox). The BER is then multiplied byan illness factor estimated to be 1.0 to 1.4 to achieve daily caloric needs.1

Although no comprehensive studieshave looked at illness factors in dogs or cats with liver disease, studies have

shown that humans with cirrhosis havean energy intake comparable with that ofnormal controls.2 Energy requirementsshould be individually adjusted to main-tain optimal body weight.

It is important to ensure that poordiet palatability is not the reason a pa-tient refuses to eat. Patients can be of-fered an ideal diet for a particularcondition, but I would rather have

David C. Twedt,DVM, DACVIM,

College ofVeterinary

Medicine &Biomedical

Sciences,Colorado State

University, FortCollins, Colorado

Treatment of Liver Disease: Medical and Nutritional Aspects



Feline Health

How to Calculate BER

• For animals weighing < 2 kg:70 x [kg*] 0.75 = kcal/day

• For animals weighing > 2 kg:30 x [kg*] + 70 = kcal/day

• Nutritional requirements for most catscan also be expressed as 50–55 kcal/kgbody weight.

*Of lean body massBER = basal energy requirement

Treatment Goals

✔ Remove or correct incitingcause if identified.

✔ Provide adequate nutrition andprevent malnutrition.

✔ Provide specific treatment forhepatic disease and/or relatedcomplications.

✔ Provide an environment foroptimal hepatic function andregeneration.

14 Treatment of Liver Disease: Medical and Nutritional Aspects

Treatment of Liver Disease: Medical and Nutritional Aspects 15

patients eat almost any diet than nothing at all.When nutritional requirements are not being metby voluntary intake, enteral supplementationshould be considered.

FatA misconception about dietary fat content andliver disease is prevalent, especially in the nutri-tional management of feline hepatic lipidosis. Ingeneral, dogs and cats with liver disease have agood tolerance for dietary fat. Fat not only im-proves palatability but provides important energydensity to the diet. Therefore, lipid restrictiontypically is not necessary for dogs or cats withliver disease; this also holds true for cats with id-iopathic hepatic lipidosis. However, dietary con-trol is probably the most important aspect ofmanaging a case of hepatic lipidosis.

CarbohydratesCarbohydrates should make up no more than35% of the diet’s total calories for cats and 45%for dogs.3 Adequate carbohydrate intake is impor-tant to maintain glucose concentrations, especiallyin dogs with advanced liver disease or when hypo-glycemia is a concern in patients with portosys-temic shunts (PSS). Feeding frequent small mealsthroughout the day may help patients maintainglucose concentrations.

I have observed hypoglycemia in some dogswith cirrhosis and PSS and hyperglycemia in some cats with hepatic lipidosis or cats receivingsteroids. In conjunction with liver disease (andsometimes concurrent steroid therapy), cats withglucose intolerance or a tendency to develop hy-perglycemia after a meal will require a lower-car-bohydrate diet. The best way to prevent hyper- orhypoglycemia is to feed frequent small meals. Ingeneral, I prefer to feed an energy-dense, low-fiberdiet to patients with liver disease. However, man-aging dietary fiber plays a role in how it relates tothe treatment of hepatic encephalopathy.

ProteinA misconception about protein content and liverdisease also exists. It was previously thought thatpatients with liver disease should be placed on a

As a generalrecommendation,dietary proteinshould represent15% to 20% of the digestiblekilocalories in the diet.

Dietary Protein Intake

The goals of dietary protein intake are to:

✔ Adjust quantities and types of nutrients tomeet the patient’s nutrient requirements.

✔ Avoid production of excess nitrogen by-products that cause hepatic encephalopathy.

✔ Provide a high-quality, highly digestibleprotein source.5 Poor-quality proteins mayaggravate hepatic encephalopathy and fail topromote hepatic regeneration.

Protein requirements for patients with liverdisease may be greater than those for normaldogs and cats. Most quality commercial andprescription diets are suitable for this purpose.

protein-restricted diet to reduce the liver’s work-load and the production of detrimental nitroge-nous waste products. This approach is not wellsubstantiated, however. Many veterinary nutri-tionists and gastroenterologists now believe thatrestricting protein could be detrimental, especiallyif patients have a negative nitrogen balance.4

As a general recommendation, dietary proteinshould represent 15% to 20% of the digestiblekilocalories (kcal) in the diet.3 Most highly di-gestible diets (eg, GI diets) are adequate for pa-tients with most liver conditions5 (see DietaryProtein Intake). Protein restriction should only beinstituted in patients with evidence of protein in-tolerance—most often patients with PSS or signsof HE.6 In these situations, lower protein contentand diets with a milk- or plant-based proteinsource rather than a meat source are recommendedto prevent HE and colonic production of excessnitrogen by-products. Because cats have such ahigh protein requirement, I rarely—if ever—limitprotein intake in cats with liver disease, such aslipidosis, and find HE an uncommon consequencein cats.

Basic Therapeutic OptionsAntiinflammatory therapyDecreasing inflammation should be specificallyaddressed in dogs with chronic hepatitis andpossibly in cats with some types of cholangitis.At Colorado State University, our clinical im-pression suggests that antiinflammatory therapyis beneficial in some if not all cases of chronic


hepatitis, but this approach remains controver-sial because no good controlled studies havebeen conducted in dogs.

One retrospective study found that some dogswith chronic hepatitis tend to have a prolongedsurvival when treated with corticosteroids,7 al-though dogs of many different breeds and a di-versity of histology and concurrent therapieswere included. Nevertheless, the use of steroidsversus the use of no steroids offered benefits insome cases (around 25%), and these respondersmay in fact represent dogs with immune-medi-ated liver disease. An initial dose of 1 to 2mg/kg/day of prednisone or prednisolone is sug-gested. When clinical improvement is suspectedor after several weeks of therapy, the dose can begradually tapered to 0.5 mg/kg/day or Q 48 H.

The only accurate way to evaluate response totherapy is to evaluate biopsy specimens in approx-imately 6 to 8 months. It is impossible to deter-mine any improvement based on liver enzymesbecause of concurrent steroid hepatopathy. Al-ternatively, practitioners could stop steroid ad-

ministration and recheck the enzymes in 1 to 2months after the steroid effects on the liver haveresolved. Persistent elevations would suggest thathepatitis is continuing.

Some reports also show improvement of im-mune hepatitis in humans treated with budes-onide.8 These patients had fewer side effects fromsystemic steroids because of the rapid first-pass he-patic metabolism of budesonide. This drug maybe an option in some dogs or cats with inflamma-tory liver disease because it may somewhat lessenthe side effects associated with steroids.

Because of the side effects of corticosteroidsand the failure to successfully monitor liver en-zymes while receiving steroids, other immuno-suppressive therapy, including azathioprine9 andcyclosporine, may represent a more rational ap-proach (see Getting the Most Out of Antiin-flammatory Therapy in Dogs).

Hepatic copper metabolismCopper is an essential trace metal required formany metabolic functions. The liver is quintes-sential in regulating the concentration and ex-cretion of excess copper through bile. Hepaticcopper concentrations can increase in dogs becauseof either a primary genetic defect or diminishedcopper excretion secondary to cholestatic liver dis-ease. Copper accumulation caused by cholestaticdisease does not occur as frequently, and copperconcentrations are lower than in breed-associatedcopper hepatotoxicity. With either mechanism ofcopper accumulation, subcellular damage to hepa-tocytes can result. Damage from copper apparentlyresults in lipid peroxidation and mitochondrialdamage.10

If the liver biopsy of a dog with chronic hepati-tis indicates significant abnormal hepatic copperaccumulation, then dietary copper chelators orzinc therapy should be instituted. Hepatic copperlevels of greater than 1,000 mcg/g of dry weightliver (normal < 400 mcg/g liver) require therapyto reduce copper concentrations.

It is first important to feed diets with a lowercopper content and to avoid nutritional supple-ments with additional copper. A restricted copperintake of about 1.25 mg/1,000 kcal of metaboliz-

Getting the Most Out of Antiinflammatory Therapy in Dogs

Azathioprine is an effective immunosuppressant shown toincrease survival in humans treated for chronic hepatitiswhen administered in conjunction with corticosteroids.9

The therapy may also be beneficial in dogs (do not useazathioprine in cats because of toxicity) by increasing theimmunosuppressive response and enabling reduction ofboth the steroid dose and side effects. Initially, a dose of 2.2mg/kg/day is suggested, followed by Q 48 H after severalweeks. The level of glucocorticoids can frequently be reducedwhen using azathioprine. Of importance, azathioprine has infrequently been associated with drug-induced hepatic necrosis or acute pancreatitis. If the dog worsens clinically or the alanine aminotransferase (ALT) value increasesdramatically, I would stop the medication.

At Colorado State University, we have realized good clinical response whenusing cyclosporine in some dogs with chronic hepatitis. Our experience using 5 mg/kg Q 12 H or Q 24 H (without steroids) has been encouraging in dogs believed to have immune-mediated chronic hepatitis. The veterinary formulation Atopica(www.atopica.com) is a microemulsified preparation with the same properties andbioavailability as the human product Neoral (www.pharma.us.novartis.com) andits generic counterpart. Generally after several days or longer, I will obtain a blood level at the trough (before the next pill). The ideal range of blood levels is400–600 ng/mL.

Many dogs develop gingival hyperplasia when higher concentrations of cyclosporine are administered. Azithromycin at 10 mg/kg/day for 4–6 weeks willoften decrease gingival hyperplasia. With evidence of clinical response at a dose of 5 mg/kg Q 12 H, I often decrease the frequency to Q 24 H and eventually to alternate-day therapy. Using cyclosporine alone, practitioners can follow the level of liver en-zymes and direct therapy based on response without the need for liver biopsy.


able energy (ME) has been suggested.3 The cop-per content is listed on the label of most diets; ifnot, the manufacturer should be able to providethis information. If a homemade diet is used,liver, shellfish, organ meats, and cereals are allhigh in copper content and should be excluded.

Copper-specific chelators (eg, penicillamine,trientine) are the standard therapies used to re-move excess hepatic copper in cases of breed-asso-ciated copper hepatotoxicity. Chelators bind withcopper either in the blood or the tissues and thenpromote copper removal through the kidneys.11-13

Zinc therapy has a number of potential benefitsin dogs with chronic hepatitis. Zinc has antifi-brotic and hepatoprotective properties11,14 (seeThe Role of Oral Zinc Therapy). When zinc isadministered as the acetate, sulfate, gluconate, orother salt, it has proven effective in preventing he-patic copper reaccumulation in humans who haveWilson’s disease and have been decoppered withchelators.4 When these patients received oral zinc,hepatic copper concentrations did not increase.

Choleretic drug therapy Decreasing cholestasis has been shown to be ben-eficial in humans and animals with cholestatic he-patobiliary disease. As serum bile concentrationsincrease (predominately cytotoxic bile acids), cellmembrane permeability changes and fibrogenesiscan occur. Ursodeoxycholic acid (300-mg cap-sules) is a choleretic agent developed to dissolvegallstones but later found to have positive effectsin patients with chronic hepatitis. This synthetichydrophilic bile acid essentially changes the bileacid pool from more toxic hydrophobic bile acidsto less toxic hydrophilic bile acids. Ursodeoxy-cholic acid has been shown to increase bile acid–dependent flow and minimize hepatocellularinflammatory changes, fibrosis, and some im-munomodulating effects.15,16

The hepatoprotective characteristics of ur-sodeoxycholic acid, much like those of antibi-otics, make it good adjunct therapy at a dose of 15mg/kg/day. No toxicity has been observed in dogsor cats at this dose.15,16 However, some practition-ers are concerned about using it if there is a possi-bility of bile duct obstruction (for fear of biliary

rupture). Although with bile obstruction surgicalcorrection is indicated, ursodeoxycholic acid is nota prokinetic and will not worsen the disease. Thisdrug has been shown in controlled studies to bebeneficial in humans with primary biliary cirrho-sis.17 I routinely supplement ursodeoxycholic acidin dogs with hepatitis and cats with cholangitis.

Antifibrotic drug therapy Corticosteroids, zinc, and penicillamine all havesome antifibrotic effects but are used predomi-nately for their other effects. Colchicine, which hasbeen used in treating humans with chronic hepati-tis and other types of liver fibrosis, reportedly in-terferes with the deposition of hepatic collagen andstimulates collagenase activity to break down de-posited fibrous tissue in the liver. It also is shownto have some antiinflammatory properties. How-ever, convincing data on the benefits of colchicinesare lacking for humans and dogs with liver disease.A critical appraisal of colchicine use in humanswith chronic hepatitis now questions its effective-ness; in fact, a large, placebo-controlled study ofchronic hepatitis in humans found no benefits,and the study authors did not recommended itsuse.18

If liver biopsyindicatessignificantabnormal copperaccumulation,then dietarycopper chelatorsor zinc therapyshould beinstituted.

The Role of Oral Zinc Therapy

Oral zinc therapy works by causing an induction of the intestinal copper-binding protein metalloth-ionein. Dietary copper binds to the metallothioneinwith a high affinity that prevents transfer from theintestine into the blood. When the intestinal celldies and is sloughed, the metallothionein-boundcopper becomes excreted through the stool.11

An initial induction dose of 15 mg/kg Q 12 H (or 50–100 mg Q 12 H) of elemental zinc is sug-gested.14 After 1–3 months of induction, the dosecan be reduced by approximately half. The goal isto have serum zinc concentrations greater than200 mcg/dL but less than 500.

Zinc must be administered on an empty stomachand has the frequent side effect of vomiting. Re-placement zinc therapy administered at a dose of2–3 mg/kg/day is given for its antioxidant effectsand replacement value in animals with zinc deple-tion in their liver.


Three case reports of colchicine use in dogs haveindicated questionable results.19-21 However, basedon these reports, a dose of 0.03 mg/kg/day hasbeen suggested. The generic form is inexpensive,with generally only minimal GI side effects notedat high doses.

Recently losartan, an angiotensin-II receptorantagonist used for treating high blood pressure,has shown some effects in preventing hepatic fi-brosis by preventing up-regulation of the stel-late, or collagen-producing, cells in the liver.Clinical response to losartan has been noted inhuman studies of hepatitis.22

Antibiotic therapy Antibiotics are indicated in some patients withprimary hepatic infections, such as bacterial hepa-titis, cholangitis, or leptospirosis. The selection ofappropriate antibiotics is based on culture andsensitivity testing. There is, however, evidence thatsecondary bacterial colonization may take place ina diseased liver.23 Kupffer cells, which are fixed he-patic macrophages, function in filtering the portalblood of bacteria and other toxic products. Kupf-fer cell dysfunction in patients with liver diseasecould account for a secondary bacterial infection.This is supported by studies that have identifiedbacteria in many hepatic cultures.24 Therefore, itmay be prudent to initiate antibiotic therapy forat least a trial of several weeks in patients with sig-nificant hepatic disease (ie, chronic hepatitis).

Amoxicillin, amoxicillin–clavulanic acid, ceph-alosporin, or metronidazole therapy is suggested.Metronidazole may have some immunosuppres-sive properties as well as anaerobic antibacterialmechanisms. Because of hepatic metabolism ofmetronidazole, I recommend a dose of 7.5 to 10mg/kg Q 12 H, which is much lower than thatused for other bacterial infections.

Vitamins and Nutraceuticals for Liver Support Although vitamin and nutraceutical adjunct ther-apies have gained interest in managing certain

types of liver disease, few published reports haveshown their benefit in clinical disease; much ofthe information gathered has been generated fromin vitro studies. Some current information as wellas suggested uses of pertinent vitamins and nu-traceuticals are presented here.

VitaminsBecause vitamin metabolism, specifically vitaminstorage and the conversion of provitamins to ametabolically active state, takes place in hepato-cytes of the liver, the vitamin status of patientswith liver disease needs to be considered.

Fat-soluble vitamins (ie, A, D, E, K) are proneto be deficient because they require bile salts toform intestinal micelles for absorption. In pa-tients with cholestatic liver disease, bile acids ab-normally excrete into the intestine, affecting theuptake of fat-soluble vitamins.25 Water-solublevitamins (ie, B, C) are generally found in highconcentrations in the liver, where many arestored as coenzymes. In patients with liver dis-ease, increased demand for these vitamins, al-tered conversion to the vitamin’s active form, ordecreased hepatic storage may occur.

Vitamin E. Vitamin E (α-tocopherol) func-tions as a cellular membrane-bound antioxidant.Evidence now shows that oxidative damagefrom free radical generation occurs in patientswith liver disease.26 Because cellular damage islikely multifactorial in these patients, free radi-cals may play an important role in initiating orperpetuating this damage.27,28

Vitamin E is inexpensive and safe when sup-plemented at a dose of 10 IU/kg/day: d-α-tocopherol , the natural form of vitamin E, isrecommended because of greater uptake, disper-sion, and bioactivity compared with the morecommon synthetic dl-α-tocopherol. d-α-Tocoph-erol is also retained in tissues by a 2:1 ratio overthe synthetic formulation.25 In patients with sig-nificant cholestatic liver disease, I suggest awater-soluble formulation.

Vitamin C. Vitamin C (ascorbic acid) is an im-portant soluble intracellular antioxidant thathelps convert oxidized tocopherol radicals back toactive α-tocopherol. Vitamin C is also necessary

Fat-solublevitamins A, D, E,and K are proneto be deficientbecause theyrequire bile saltsfor absorption.Water-solublevitamins B and Care generallyfound in highconcentrations in the liver.


for the synthesis of carnitine, which is importantfor transporting fat into mitochondria. Humanswith liver disease often have low hepatic vitaminC concentrations, partially because they cannotsynthesize vitamin C; however, dogs and cats cansynthesize this vitamin.

Although vitamin C supplementation may bebeneficial in treating liver disease, supplementa-tion of excessive amounts of vitamin C may bedeleterious in patients with increased hepaticcopper or iron concentrations because ascorbateis believed to promote oxidative damage causedby these transition metals.26

Vitamin K. Vitamin K stores in the liver canbecome depleted in patients with advanced liverdisease and can result in serious coagulopathy.Deficiency can occur from reduced intestinalabsorption from cholestatic liver disease or asthe result of advanced liver dysfunction with afailure of hepatic conversion to the vitamin K-dependent coagulation factors (ie, factors II,VII, IX, X). This can result in prolongation ofcoagulation as measured by prothrombin timeor activated partial thromboplastin time and cancause significant bleeding.

Vitamin K supplementation is warranted inpatients with liver disease to maintain hepaticstores. With severe cholestasis or overt coagula-tion abnormalities, 0.5 to 2.0 mg/kg of par-enteral vitamin K1 (phytonadione) SC Q 12 Hfor two or three doses (or until normalization ofprothrombin time) is recommended for dogsand cats with hepatic disease. Vitamin K1 sup-plementation is recommended for 24 to 36hours before invasive procedures, such as he-patic biopsy or feeding tube placement.6

Vitamin B. B vitamins are important in manymetabolic functions and may become deficientin both dogs and cats with liver disease. How-ever, deficiencies are difficult to diagnose or ana-lytically document. Because B vitamins arewater-soluble, they are relatively nontoxic andsupplementation using a B-complex formulationis recommended in patients with liver disease.

Cats are particularly prone to vitamin B12(cobalamin) deficiency. Subnormal concentrationsof vitamin B12 have been reported in cats with

liver disease, particularly idiopathic hepatic lipido-sis.29 Cats with cholangiohepatitis frequently haveconcurrent inflammatory bowel disease or chronicpancreatitis and subsequent cobalamin deficiency.The recommended dose of cobalamin for cats is250 mcg SC weekly until normal cobalamin con-centrations have been maintained. There is notenough vitamin B12 in B-complex formulationsto correct its deficiency in cats.

NutraceuticalsThe North American Veterinary NutraceuticalCouncil defines a nutraceutical as “a non-drug sub-stance that is produced in a purified or extractedform and administered orally to patients to provideagents required for normal body structure andfunction and administered with the intent of im-proving the health and well being of animals.”30

Many nutraceuticals used in animals are listed asnutritional supplements. Typical categories include:

■ Antioxidants■ Omega fatty acids■ Amino acids■ Chondroprotective agents■ Herbals■ ProbioticsAlthough some nutraceuticals have shown po-

tential for improving veterinary care, little infor-mation is known about their purity, dosage, safety,side effects, and effectiveness. With a few excep-tions, little has been done to address these issues.

Included here are nutraceutical compoundsthat have shown some scientific evidence forboth effectiveness and relative safety in the man-agement of liver disease.

S-Adenosylmethionine. S-Adenosylmethio-nine (SAMe), a naturally occurring moleculesynthesized in all living cells, is essential in inter-mediary metabolism and has both hepatoprotec-tive and antioxidant properties.

The liver normally produces abundant SAMe,but evidence also suggests conversion from me-thionine to SAMe is hindered in patients withliver disease and, therefore, results in the depletionof glutathione concentrations.31 Orally adminis-tered SAMe (but not oral glutathione) has beenshown to increase intracellular glutathione levels

Although somenutraceuticalshave shownpotential forimprovingveterinary care,informationabout theirpurity, dosage,safety, sideeffects, andeffectivenessremains limited.

in hepatocytes and prevent gluta thione depletionwhen exposed to toxic substances.32 Therefore,SAMe in part acts as an anti oxidant, replenishingthe gluta thione stores. Preliminary veterinarystudies suggest that SAMe supplementation in-creases hepatic glutathione concentrations in nor-mal cats and prevents glutathione depletion indogs with steroid-induced hepatopathy .32 SAMetreatment following acetaminophen administra-tion prevented hepatic glutathione depletion.33

Because SAMe is easily oxidized, it is importantto use products that have been tested for their sta-bility. In addition, product purity can vary fromformulation to formulation, so it is advisable touse products from reputable companies.

N-Acetylcysteine. N-Acetylcysteine, theacetylated variant of the amino acid L-cysteine,is an excellent source of the sulfhydryl groups. It is converted in the body into metabolites thatstimulate glutathione synthesis, thereby promot-ing detoxification and acting directly as free rad-ical scavengers.

N-Acetylcysteine has historically been used as a mucolytic agent for various respiratory ill-nesses but apparently also has beneficial effectsin conditions characterized by oxidative stress ordecreased glutathione concentrations. N-Acetyl-cysteine is currently the mainstay of treatmentfor acetaminophen-induced hepatotoxicity.33 Italso appears to have some clinical usefulness as achelating agent in treating acute metal poison-ing, both as an agent protecting the liver andkidney from damage and as intervention to en-hance elimination of metals.

N-Acetylcysteine is available in a drug formu-lation and as a nutritional supplement. The oraldose recommended for acetaminophen toxicityis 70 mg/kg Q 8 H. The IV loading dose of 140 mg/kg is followed by a dose of 70 mg/kg.N-Acetylcysteine reportedly has extremely lowtoxicity with few side effects. I use N-acetylcys-teine IV when the patient is vomiting or toosick to take oral SAMe, which is my preferenceas maintenance therapy.

Phos pha tidylcholine. Phos pha tidylcholine is aphospholipid used as a nutritional supplement forits hepatoprotective effects. A building block forcell membranes, phosphatidylcholine is requiredfor normal bile acid transport. It is thought to behepatoprotective by improving membrane in-tegrity and function.

In vitro studies have shown that phosphatid-ylcholine increases hepatic collagenase activityand may help prevent fibrosis.34 Clinical trialshave indicated that phosphatidylcholine protectsthe liver against damage from alcohol, viral hep-atitis, and other toxic factors that operate bydamaging cell membranes.34

Several phosphatidylcholine supplements areavailable. No major side effects have been reportedother than occasional nausea or diarrhea. Phos-phatidylcholine is rapidly absorbed, enhances ab-sorption of other compounds, and is included as acarrier in one silybin product.

Given the apparent safety of phosphatidyl-choline, animal studies would be worthwhile.

L-Carnitine. L-Carnitine is a vitamin -like sub-stance found in most cells. Because it is predom-inately synthesized in the liver, liver disease canprecipitate deficiency. Clinically, carnitine defi-ciency has been associated with increased am-monia concentrations, hypoglycemia, and fattylivers.35

In one study, carnitine given to obese cats un-dergoing rapid weight loss from caloric restric-tion was found to protect against hepatictriglyceride accumulation.35 Some studies sug-gest that L-carnitine deficiency may play a rolein the pathogenesis of idiopathic feline hepaticlipidosis; however, carnitine concentrations werehigher in the plasma, liver, and muscle of studycats than in control cats.36

A deficiency of carnitine may lead to impairedmitochondrial function, but studies failed toshow carnitine deficiency in cats with hepaticlipidosis.37 Supplementation with 250 mg/dayof carnitine in cats with lipidosis is reportedlyassociated with better survival rates, but this hasnot been documented.

Silymarin. Silymarin, an active extract of milkthistle, grows wild throughout Europe and has

In preliminarystudies, SAMesupplementationincreased hepaticglutathioneconcentrations innormal cats andpreventedglutathionedepletion in dogswith steroid-inducedhepatopathy.



been used there for more than 2,000 years as amedical remedy for liver disease. In the UnitedStates, silymarin is classified as a nutraceutical.

Mounting evidence suggests that milk thistlehas medicinal benefits for various types of liverdisease as well as a protective effect against hepa-totoxins. A recent poll of liver patients at oneU.S. hepatology clinic found that 31% wereusing alternative agents for their disease and thatmilk thistle was the most common nontradi-tional therapy.38 Several human trials have as-sessed the efficacy of silymarin in the treatmentof liver disease. The data are somewhat difficultto interpret because of the limited number ofpatients, poor study design, variable etiologies,and lack of standardization of preparations withdifferent dosing protocols. However, compellingevidence suggests that silymarin has a therapeuticeffect in humans with acute viral hepatitis, alco-holic liver disease, cirrhosis, and toxin- or drug-induced hepatitis.39

To date, limited clinical studies have evaluatedthe efficacy of silymarin in dogs and cats withliver disease. In one placebo-controlled experi-mental study of dogs poisoned with theAmanita phalloides mushroom, silybin had a sig-nificant positive effect on liver damage and sur-vival outcome.40

The purity and potency of commercial milkthistle products vary by manufacturer, and thetherapeutic dose for dogs and cats is unknown,although suggested doses range from 50 to 250mg/day. Milk thistle reportedly has extremelylow toxicity. When the active isomer silybin iscomplexed with phosphatidylcholine, oral uptakeand bioavailability are greater.41

I recently conducted a pharmacokinetic studyof silybin, specifically evaluating Marin(www.nutramaxlabs.com) in normal cats. Therewas evidence of some oxidative protection in redblood cells but no outward signs of toxicity at adose of 5 mg/kg. A new compound Denamarin(www.denamarin.com) contains SAMe and sily-bin–phosphatidylcholine and is available in achewable formulation. The combination ofcompounds apparently has good absorption andis very stable.

Hepatic Complications Secondary complications can develop as liverdisease becomes advanced. HE, GI ulceration,and ascites are common in patients with advancedhepatitis or cirrhosis.

Hepatic encephalopathyHE results from either portosystemic shunting ofblood (congenital or acquired) or hepatocyte de-pletion from acute or chronic liver disease. Manyfactors can cause HE, most of which are derivedfrom nitrogenous products produced in the GItract. Ammonia is only one of many substancesthat cause HE but is commonly used as its marker.Plasma amino acid concentrations may become al-tered in patients with liver disease. Increased levelsof aromatic amino acids are hypothesized to formfalse neurotransmitters, leading to HE, whereashigher concentrations of branched-chain aminoacids had a more protective effect5 (see HE andDietary Protein3,5,42).

There are three basic therapeutic goals for man-aging HE (see box on page 22). The first step isusing enemas to clean the colon of both bacteriaand protein substrates for ammonia production.Slightly acidic enemas can lower the pH of thecolon, thereby ionizing ammonia and reducing itsabsorption. Povidone-iodine can safely be given by

Mountingevidence suggeststhat milk thistlehas medicinalbenefits forvarious types ofliver disease aswell as protectiveeffects againsthepatotoxins.

HE and Dietary Protein

The importance of the dietary protein source has been studied in humans with HEand several experimental studies in dogs with PSS.42 Vegetable and dairy proteinsources with lower concentrations of aromatic amino acids have produced thebest results in maintaining a positive nitrogen balance with minimal encephalo-pathic signs.5 Foods using soybean meal averted encephalopathic signs in dogswith experimentally created shunts,42 and Purina Veterinary Diet HA Hypoaller-genic formula could be an option in these cases. In addition, dairy products (espe-cially cottage cheese) have been frequently recommended for use in homemadefoods for dogs and cats with PSS and chronic hepatic insufficiency.3 However, theamino acid composition of these protein sources is not significantly different fromthat of meat sources, suggesting that other food factors (eg, digestibility, levels ofsoluble carbohydrate, fermentable fiber) are important.

Fermentable carbohydrates in crease microbial nitrogen fixation, reduce intra-luminal ammonia production in the gut, and promote colonic evacuation. Fer-mentable fiber added to the diet has been shown to decrease ammoniaproduction. Commercial and homemade foods can be supplemented with varioussources of soluble fiber, such as psyllium husk fiber.

HE = hepatic encephalopathy; PSS = portosystemic shunt


enema as a 10% solution (weak-tea color) that willboth acidify the colon and have antiseptic action,thereby reducing bacterial numbers.

Intestinal antibiotics can be used to alter bowelflora and suppress urease-producing organisms important in forming factors that cause HE. An-tibiotic suggestions include oral ampicillin, amino-glycosides (eg, neomycin, kanamycin, gentamicin),or metronidazole. Metronidazole at a dose of 7 to10 mg/kg PO Q 12 H has been useful in control-

ling anaerobic urease-producingbacteria. Practitioners shouldmonitor patients carefully be-cause metronidazole is partiallymetabolized in the liver; thelower dose range is suggested.

A nondigestible disaccharidelactulose given orally can acidifythe colon, convert ammonia toammonium that is poorly ab-sorbable, and thus trap ammoniain the colon. The fermentationproducts of lactulose can also act

as an osmotic laxative and reduce colonic bacteriaand protein substrates. Lactulose is not absorbedsystemically and is considered safe. A dose of 1 to10 ml PO Q 8 H is generally effective, but thedose should be adjusted to cause three or four softstools a day. Lactulose can also be given by enemawhen treating severe cases of HE.

Gastrointestinal ulcerationUlceration in the GI tract, a common occurrencein both advanced acute and chronic liver disease,can cause GI signs, such as vomiting and anorexia.In addition, blood loss into the intestinal tractpromotes HE because blood is an excellent pro-tein source of ammonia production. Gastric ulcersshould be treated with a histamine-2 (H2) blocker,such as 2 to 5 mg/kg of ranitidine Q 8 H to Q 12H and a 1 mg tab/25 kg of oral sucralfate Q 8 Hgiven 1 hour before ranitidine.

Cimetidine should be avoided in patients withliver disease because it is metabolized by the liver

and is an enzyme suppressor that can alter the he-patic metabolism of other drugs. If blood loss is se-vere and there is need for transfusion, only freshblood should be administered because ammoniaconcentrations can increase in stored blood.

Ascites In patients with liver disease, ascites occurswhen portal hypertension, hypoalbuminemia,and renal sodium and water retention work inconcert to cause fluid exudation. The presenceof ascites is a poor prognostic indicator.

Diuretics are the major means of managing as-cites in small animals. Too rapid removal of asciticfluid can cause metabolic complications and pre-cipitate HE. The goal of diuretic therapy shouldbe gentle water diuresis.

The two diuretics most commonly used arefurosemide and spironolactone. The generalconsensus at CSU is that spironolactone is moreeffective with liver disease. The loop diureticfurosemide can, however, cause marked dehy-dration and loss of potassium, which can precip-itate HE. In patients with liver disease, sodiumreabsorption at the distal tubule may be greatand may counter the effects of furosemide at-tributable to elevated aldosterone concentrations(reported to occur in some dogs with liver dis-ease).43 Spironolactone at a dose of 1 to 2mg/kg/day is consequently the first-line diuretic.Furosemide can be added later if necessary. If ananimal has tense ascites, paracentesis should beperformed to decrease intraabdominal pressure,relieve compression of the venous circulation,and improve patient comfort.

Summary It is critical to recognize the complexity of themedical and nutritional needs of patients withliver disease. Practitioners should formulate anindividualized therapeutic and dietary plan ac-cordingly. Because there are few good controlledstudies evaluating liver disease therapy, it is im-portant to carefully monitor each patient andadjust the treatment, based on clinical responseof the patient, laboratory changes, or histologicfindings. ■

Cimetidineshould beavoided inpatients withliver diseasebecause it ismetabolized bythe liver and isan enzymesuppressor thatcan alter hepaticmetabolism ofother drugs.

Basic Therapeutic Goals for HE

1. Recognize and correct precipitatingcauses of HE.

2. Reduce intestinal production andabsorption of neurotoxins, withspecial emphasis on ammonia.

3. Achieve the fine balance betweenproviding too much and too littleprotein.

HE = hepatic encephalopathy


References1. Hepatic disease, nutritional therapy and the metabolic envi-

ronment: Timely topics in nutrition. Bauer JE. JAVMA209:1850-1854, 1996.

2. Energy and protein requirements of patients with chronic liverdisease. Kondrup J, Muller MJ. J Hepatol 27:239-247, 1997.

3. Nutrition and liver disease. Biourge V. Semin Vet Med Surg(Small Anim) 12:34-44, 1997.

4. Nutritional support for dogs and cats with hepatobiliary dis-ease. Center SA. J Nutr 125:2733S-2746S, 1998.

5. Vegetable versus animal protein diet in cirrhotic patients withchronic encephalopathy: A randomized cross-over comparison.Bianchi GP, Marchesini G, Fabbri A, et al. J Intern Med233:369-371, 1993.

6. Nutritional support in hepatic disease. Part II. Dietary man-agement of common liver disorders in dogs and cats. MarksSL, Rogers QR, Strombeck DR, et al. Compend Contin EducPract Vet 16:1287-1290, 1994.

7. Effects of corticosteroid treatment on survival time in dogswith chronic hepatitis: 151 cases 1977-1985. Strombeck DR,Miller LM, Harrold D. JAVMA 193:1109-1113, 1998.

8. Oral budesonide for treatment of autoimmune chronic activehepatitis. Danielsson A, Prytz H. Alimentary Pharm Therapeu-tics 8(6):585-590, 1994.

9. Controlled trial of prednisone and azathioprine in activechronic hepatitis. Murray-Lyon IM, Stern RB, Williams R.Lancet 7;1(7806):735-737, 1973.

10. Copper toxicity and lipid peroxidation in isolated rat hepato-cytes: Effect of vitamin E. Sokol RJ, Devereaux MW, TraberMG, et al. Pediatric Res 25:55-62, 1989.

11. Copper associated hepatopathies in dogs. Rolfe DS, TwedtDC. Vet Clin North Am Small Anim Pract 25:399-417, 1995.

12. Copper-associated hepatitis in Labrador retrievers. Smedley R,Mullaney T, Rumbeiha W. Vet Pathol 46:484-490, 2009.

13. Improvement in liver pathology after 4 months of D-penicil-lamine in 5 Doberman pinschers with subclinical hepatitis.Mandigers PJJ, van den Ingh TSGAM, Bode P, et al. J Vet Intern Med 19(1):40-43, 2008.

14. The use of zinc acetate to treat copper toxicosis in dogs.Brewer GJ, Dick RD, Shall W, et al. JAVMA 201:564-568,1992.

15. Effect of ursodeoxycholic acid administration on bile duct pro-liferation and cholestasis in bile duct ligated rat. Frezza EE,Gerunda GE, Plebani M, et al. Dig Dis Sci 38:1291-1296,1993.

16. Use of ursodeoxycholic acids in a dog with chronic hepatitis:Effects on serum hepatic tests and endogenous bile acid com-position. Meyer DJ, Thompson MB, Senior DF. J Vet InternMed 11:195-197, 1997.

17. Ursodeoxycholic acid for primary biliary cirrhosis. Lindor KD,Poupon RE, Heathcote EJ, et al. Lancet 19:657-658, 2000.

18. Colchicine for alcoholic and non-alcoholic liver fibrosis or cir-rhosis. Rambaldi A, Gluud C. Liver 21(2):129-136, 2001.

19. Idiopathic hepatic fibrosis in 15 dogs. Rutgers HC, HaywoodS, Kelly DF. Vet Rec 133:115-118, 1993.

20. Colchicine therapy for hepatic fibrosis in a dog. Boer HH,Nelson RW, Long GG. JAVMA 3:303-305, 1984.

21. Chronic liver disease: Current concepts of disease mechanisms.Center SA. J Small Anim Pract 40:106-114, 1999.

22. Effects of six months losartan administration on liver fibrosisin chronic hepatitis C patients: A pilot study. Sookoian S, Fer-nández MA, Castaño G. World J Gastroenterol 11(48):7560-7563, 2005.

23. Chronic hepatitis, cirrhosis, breed-specific hepatopathies, cop-per storage hepatopathy, suppurative hepatitis, granulomatous

hepatitis and idiopathic hepatic fibrosis. Center SA. In Guil-ford WG, Center SA, Strombeck DR, et al (eds): Strombeck’sSmall Animal Gastroenterology—Philadelphia: WB Saunders,1996, pp 705-765.

24. Technetium 99M colloid scintigraphy to evaluate reticuloen-dothelial system function in dogs with portosystemic shunts.Koblik PH, Hornof WJ. J Vet Intern Med 9:374-380, 1995.

25. Fat-soluble vitamins and their importance in patients withcholestatic liver disease. Sokol RJ. Pediatr Gastroenterol 23:673-705, 1994.

26. Antioxidants in pediatric gastrointestinal disease. Sokol RJ,Hoffenberg EJ. Pediatr Clin North Am 43:471-488, 1996.

27. Oxidant injury to hepatic mictochondria in patients with Wil-son’s disease and Bedlington terriers with copper toxicosis.Sokol RJ, Twedt D, McKim JM, et al. Gastroenterology107:1788-1798, 1994.

28. Vitamin E protects against oxidatative damage of bile acids inisolated hepatocytes. Twedt DC, Sokol RJ, Devereaux MW, etal. J Vet Intern Med 12:215, 1998.

29. Subnormal concentrations of serum cobalamin (vitamin B12)in cats with gastrointestinal disease. Simpson KW, Fyfe J, Cor-netta A, et al. J Vet Intern Med 15:26-32, 2001.

30. Association of American Feed Control Officials. Official publi-cation, 2007.

31. Liver glutathione concentrations in dogs and cats with natu-rally occurring liver disease. Center SA, Warner KL, Erb HN,et al. Am J Vet Res 63:1187-1197, 2002.

32. Evaluation of the influence of S-adenosylmethionine on sys-temic and hepatic effects of prednisolone in dogs. Center SA,Warner KL, McCabe J, et al Am J Vet Res 66:330-341, 2005.

33. Clinicopathologic evaluation of N-acetylcysteine therapy inacetaminophen toxicosis in the cat. Gaunt SD, Baker DC,Green RA, et al. Am J Vet Res 42:1982-1984, 1981.

34. Nutrition and alcoholic liver disease. Halsted CH. Semin LiverDis 24:289-304, 2004.

35. L-carnitine reduces hepatic fat accumulation during rapidweight reduction in cats (abstract). Armstrong PJ, Hardie EM,Cullen JM, et al. 10th Annu Vet Med Forum Am Coll Vet InternMed Proc, 1992, p 810.

36. Clinical effects of rapid weight loss in obese pet cats with andwithout supplemental L-carnitine (abstract). Center SA, HarteJ, Watrous D, et al. 15th Annu Vet Med Forum Am Coll Vet Intern Med Proc, 1997, p 665.

37. Comparison of plasma, liver, and skeletal muscle carnitineconcentrations in cats with idiopathic hepatic lipidosis and inhealthy cats. Jacobs G, Cornelius L, Keene B, et al. Am J VetRes 51:1349-1351, 1990.

38. Milk thistle and chronic liver disease. Hoofnagel JH. Hepatol-ogy 42:4, 2005.

39. Milk thistle (Silybum marianum) for the therapy of liver dis-ease. Flora K, Hahn M, Rosen H, et al. Am J Gastroenterol93:139-143, 1998.

40. Complementary and alternative medicine in chronic liver dis-ease. Seef LB, Lindsay KL, Bacon BR, et al. Hepatology34:595, 2001.

41. Bioavailability of a silybin-phosphatidylcholine complex in dogs. Filburn CR, Kettenacker R, Griffin DW. J Vet Phar-macol Ther 30:132-138, 2007.

42. Apparent dietary protein requirement of dogs with portosys-temic shunt. Laflamme DP, Allen SW, Huber TL, et al. Am JVet Res 54:719-723, 1993.

43. Sodium retention and ascites formation in dogs with experi-mental portal cirrhosis. Levy M. Am J Physiol 233(6):F572-F585, 1977.

Obesity is the number one nutritionaldisorder in pets in the western world. Twenty-five per-cent of cats seen by veterinarians in the United Statesand Canada are overweight or obese.1 In optimal condi-tion, cats should carry 15% to 20% body fat.

In 1998, Donoghue and Scarlett2 studied diet and obesity incats. Using multivariate statistical analysis controlled for age,they showed that obesity is a risk factor for:

■ Diabetes mellitus■ Skin problems■ Hepatic lipidosis■ Lameness

Other researchers have found that a chronic overweight state,in cats as well as in other species, is associated with an in-creased risk for:3-5

■ Hyperlipidemia ■ Insulin resistance ■ Glucose intolerance ■ Feline lower urinary tract disease ■ Anesthetic complications ■ Dyspnea and Pickwickian syndrome ■ Exercise intolerance ■ Heat intolerance ■ Impaired immune function ■ Exacerbation of degenerative joint disorders■ Dermatologic conditionsInterestingly, mixed-breed cats were found to be at higher

risk for becoming overweight than purebred cats were. Whilethis might be genetic, husbandry and awareness of the catprobably play a role. By keeping cats indoors, we eliminatetheir need to work for food and defend themselves. We leave

them without stimulation for much ofthe day and feed them excessive quanti-ties of palatable, calorie-dense diets.

Neutering has been shown to reducethe energy requirements (resting meta-bolic rate) of cats by 20% to 25%.6,7 Alink has been shown between serum lep-tin levels and weight and fat gains follow-ing gonadectomy.8 Increased leptin levelsmay contribute to the decreased insulinsensitivity seen in overweight cats.9

These tendencies make it importantthat we counsel our clients to measurethe amounts of food being fed and towatch carefully for weight gain and adjustcalorie intake accordingly. Ingesting 10extra pieces of an average maintenancekibble each day above a cat’s energy needscan result in a weight gain of 1 pound ofbody fat in 1 year. Russell and cowork-ers10 showed that the frequency of feed-ing, along with the quantity fed, makes asignificant difference. Feeding smallmeals more often and limiting the num-ber of treats offered together provide themost appropriate feeding strategy, giveninnate feline physiology,11,12 and thus as-sist with weight loss.

Assessing Body Compositionand Condition: ToolsCats reach their adult weight at about 12

Margie Scherk,DVM, DABVP

(Feline),Vancouver, BC,

Canada

From Problem to Success: A Weight Loss Program ThatWorks, Growing Relationships,Not Girth in Cats



Feline Health

24 A Weight Loss Program That Works, Growing Relationships, Not Girth in Cats

A Weight Loss Program That Works, Growing Relationships, Not Girth in Cats 25

to 15 months of age. This can be used as a guide todetermine an individual’s ideal size, assuming opti-mal body condition score (BCS) at that time.

It is easier to prevent weight gain than to loseweight. The prevalence of obesity increases after2 years of age, plateaus until about 12 years, andthen declines thereafter.13 Thus, an approvedstrategy is to:1. Record a body weight at every veterinary visit.2. Calculate the percent weight change to iden-

tify trends. This is a valuable tool for detectingweight change patterns and, in my experience,helpful in identifying cats with early chronicillness, including pancreatitis, cholangitis, andbowel malabsorptive conditions (eg, inflam-matory bowel disease, intestinal lymphoma,adenocarcinoma). Likewise, a percentageweight change that is increasing graduallyhelps to identify cats at risk for obesity.

% Weight change = (Current weight – Previous weight)Previous weight

3. Assess the BCS at every visit, categorizing theindividual’s shape as emaciated, thin, ideal,heavy, or grossly obese on a scale of 1 to 9 (seepage 5) or 1 to 5. For a cat in ideal condition,the bony prominences of the body (ie, pelvis,ribs) can be readily palpated but not seen orfelt above the skin surfaces. There should beinsufficient intraabdominal fat to obscure orinterfere with abdominal palpation.

4. Assess muscle condition using a muscle scoreto help define whether weight is adequatelyproportioned to lean versus fat.

5. In questionable cases, use radiography and ultra-sonography to assess falciform fat deposits, par-alumbar fat, and perirenal fat. In researchsettings, dual energy x-ray absorptiometry(DEXA) evaluation is used for the most accuratebone density, muscle mass, and fat calculations.

What to FeedIt is not enough to simply feed less of a normaldiet. Not only will the patient be unhappy and feel hungry, but all nutrient quantities will be de-creased, not just the calories. A diet should be bal-anced according to energy content. When cats eatenough of the diet to meet energy requirements,

then their protein, vitamin, and mineral needs willbe met as well.

In cats, exceeding protein needs beyond mainte-nance requirements helps to induce satiety. Whenthey were fed a diet with 45% of calories from pro-tein, cats lost more fat and less lean mass comparedwith cats fed a diet with 35% of calories from pro-tein, despite similar total weight loss and rate ofweight loss.14

There are a number of approaches to felineweight loss: 1. High protein protects (minimizes loss of) lean

mass, stimulates cellular energy metabolism andprotein turnover, and may enhance satiety.

2. High moisture can reduce caloric density,which promotes short-term weight loss: Ittakes a few weeks to a few months for cats toadapt to the lower-caloric density (as fed) incanned foods versus dry foods; however, thisonly works for some cats.

3. High fiber can reduce caloric density and inducesatiety. Some cats will self-restrict calorie intakewhen fed a dry, high-fiber, low-calorie diet.

4. Low fat will reduce caloric density. High-fatdiets are a risk factor for inducing obesity andare generally not considered optimum for aweight loss diet. That said, some cats will loseweight on a high-protein, high-fat, low-car-bohydrate diet.Ultimately, it is the calories ingested versus ex-

pended that is required for loss of weight. Giventhe benefits of achieving lean body mass usingthe first approach, a goal of at least 40% protein,dry basis, in a low-fat diet (6% to 10% fat) ormore protein in a higher-fat diet (12% to 16%fat) is a healthy approach to take.

The energy requirement for an individual ismade up of several components: daily energy re-quirement (DER*), resting energy requirement(RER), exercise energy requirement (EER), thermiceffect of food (TEF), and adaptive thermogenesis(AT): DER = RER + EER + TEF + AT. Becausethe RER varies among individuals, a manufacturer’srecommendations may be too high for a given cat.

A goal of at least40% protein, drybasis, in a low-fatdiet (6% to 10%fat) or moreprotein in ahigher-fat diet(12% to 16% fat) is a healthyapproach to take.

*Unlike metabolizable energy requirement (MER), DER includesenergy required for activity, such as work, gestation, and growth, aswell as energy needed for maintaining normal body temperature.

The need for behavior modificationAt the initial extended consultation (a 40-minuteconsultation with the veterinarian), a comprehen-sive physical examination should be performed torule out concurrent medical problems. Baselineblood work may be advisable, depending on theage and condition of the cat. A detailed history isneeded to become familiar with current feedinghabits and routines (see Diet History).

Have the client start a 1- to 2-week feedingjournal; all household members who give the catanything to eat need to record what they havegiven the cat. The amount as well as exact type(brand) of food and treats should be recorded.Clients can be asked to create this diary beforethe appointment and bring it along with them.The diet diary provides the material needed todetermine the calorie intake that the cat has beenreceiving and gaining weight on and will be com-pared with the calorie allowance being recom-mended. As a rule of thumb, to lose weight a catneeds 60% to 70% of the calories required tomaintain his or her ideal weight. In other words: 1. Determine or approximate the cat’s ideal weight.2. Calculate the calories needed to achieve the

ideal weight (wt in kg × 50 kcal/kg/day).3. Multiply this number by 60% to 70% for the

number of calories to feed each day.Discuss with clients the benefits of weight loss

as well as the risks of chronic obesity. Acknowl-edge their concern and praise them for their desireto take action. Be supportive! They are the oneswho will have to do the work. Inform them of thecurrent weight as well as the goal weight. Discusshow long this will take. A safe rate of weight loss isone-quarter to one-half pound per month (0.1–0.25 kg/month). This will help them stay ontrack. A realistic initial goal of 10% to 15% is attainable and will provide health benefits.

Example: Fluffy weighs 18.6 lb (8.4 kg) with aBCS of 9/9 and is currently being fed 375kcal/day. The goal is 12 lb (5.4 kg) for a BCSof 5-6/9.12 lb (5.4 kg) × 50 kcal = 271 kcalFeed 60%-70% × 271 kcal = 163-190 kcal/dayWeight loss of 6.6 lb (3 kg) will take at least12 months.

Have clients keepa feeding diary forat least 1 weekbefore the initialconsultation. Allhouseholdmembers whogive the catanything to eatneed to recordwhat food or treatthey gave.

Key Points to Remember

✔ Schedule an initial 40-minute consultation withthe veterinarian for a comprehensive physicalexamination to rule out medical problems.

✔ Have the client keep a feeding diary (minimum 1 week) to be evaluated during the initial visit.

✔ Evaluate current feeding habits and routines.

✔ Calculate current calorie intake.

✔ Calculate recommended calorie intake: 60% to70% of intake required to maintain goal bodyweight (may need to use 50% if the cat is veryinactive).

✔ Send home a “weight loss pack” with foodsamples (dry and canned) so the cat has aselection to choose from.


■ TEF is the energy spent on digesting andabsorbing food.

■ AT is the energy used to regulate body tem-perature.

■ DER decreases with increasing age until approximately 12 years of age; thereafter,DER increases in this species.13

A Clinic Weight Loss ProgramFor a successful weight loss program, three compo-nents must be in place: diet, exercise, and recheck/follow-up visits. We need to reduce the number ofcalories consumed and increase calorie use andmetabolic rate (exercise). Exercising cats could beseen as an oxymoron; however, any exercise helps.The Association for Pet Obesity Prevention offerssome practical suggestions for clients (for informa-tion, go to www.petobesityprevention.com/images/Weight_Reductionin_Cats_General_Information.pdf).

Success requires commitment on the part ofthe client as well as the veterinary team. Clientsrely on us to educate them about health andobesity as well as on how to modify their ownand their cat’s behavior.

ciently palatable so that a cat eats enthusiasticallyand the consumer will purchase that food again.Many cat foods are very energy-dense, with thecalories coming from fat because fat is palatablefor cats and is a relatively inexpensive ingredient.In addition, because it is convenient to feed ad li-bitum, cats snack all day on high-calorie kibbleand commonly eat more than they need ratherthan 8 to 10 small, 30-kcal (mouse-sized) mealsper day as they would in their native state. Do-mestic cats generally lack exercise when comparedwith the hunter that they are designed to be.

The TEF is the energy cost of digesting and ab-sorbing food. As mentioned earlier, the TEF ishigher when small frequent meals are fed, so feed-ing multiple small meals is preferable to feedingone or two large meals. One way to incorporatethis, as well as give the cat a little challenge (andexercise), is to divide the day’s food amount onto6 or 7 small saucers and place them throughoutthe home as if it were a “treasure hunt.” Thismeans that the cat is less likely to gorge, has tolook for food, and has a higher TEF cost.

But there is more to obesity than energy in andenergy expended. A more holistic approach canprovide a greater chance of success. We must alsoconsider why the cat is eating more. Is the catbored? Is the cat not receiving enjoyable stimulifrom other healthier sources and is, therefore, eat-ing too much? What other aspects of normal be-havior are not available for the cat to participate in? How is the cat meeting his or her “hedonicbudget”? Chronic stress, which may be present inthe confined indoor cat, results in neuroendocrinechanges that predispose to obesity.15

What drives the client? In a very interesting study, Kienzle and Bergler16

found that the “positive strokes” received and thebehaviors of clients toward their cats differ withthe cat’s weight. To quote from the paper itself:

Thirty percent of owners of overweight catscompared with 12% of owners of normal[weight] cats stated that they did not feelvery happy prior to acquiring a cat, and thecat was intended to console and encouragethem. These results are suggestive of (1) a

An alternative option is to utilize the VeterinaryFeeding Guide and Weight Management Pro-gram software package from Purina VeterinaryDiets. The program would start Fluffy on 316kcal/day of Purina Veterinary Diet OM, calcu-lated at 40 kcal/kg/day, targeting for a weight lossof 2% of initial body weight per week. WhenFluffy returns for a recheck after 2 to 4 weeks, thepractice staff enters information about her actualintake and change in body weight over that time.The program can then determine her individualMER and adjust the feeding recommendation ifneeded. Since the MER is based on average, theinitial rate of loss may be more or less than antici-pated. The benefit of this approach is that therecommendation is customized to fit the needsand metabolism of the individual patient.

Discuss with the client why cats become over-weight. Pet food manufacturers make diets suffi-

Key Points to Discuss with Clients

✔ Why cats becomeobese

✔ Risks of obesityversus benefits ofweight loss

✔ Realistic goals

✔ Behaviormodification


Diet History

During the initial weight loss consultation, it isimportant to ask the following questions:

✔ What specific amounts and type of food (all,including treats) are fed to the cat? Does the catdrink milk? Is he/she fed “people” food?

✔ Who feeds the cat’s regular meals? Do familymembers routinely feed treats and table scraps?

✔ How often is the cat fed? Is the food measured?

✔ Does the cat nibble or gorge?

✔ Where is the cat fed?

✔ Does the cat receive any medications? If so, arethe medications given in food or with a treat?

✔ Is the cat indoor or outdoor? If outdoor, doeshe/she routinely hunt?

✔ What other pets are in the household?

✔ Do other pets have access to the overweightcat’s food?

✔ Does the overweight cat have access to the otherpets' food?

✔ What is the activity level of the cat?

✔ Are there any known stress factors in the homeenvironment?

closer relationship between overweightcats and their owners than between nor-mal [weight] cats and their owners, (2)more over-humanization of overweightcats than of normal [weight] cats, (3) a po-tential role of overweight cats as a substi-tute for human companions.

People with overweight or obese cats tend tounderestimate their cat’s BCS and talk aboutdifferent things to their cats than do people liv-ing with cats of normal weight. Not surprisingly,people with overweight cats were more likely toget positive feelings from watching their cats eat,whereas people with cats of normal weight spentmore time playing with their cats. While therewas “no significant difference between the num-ber of meals and snacks and the type of food received by normal and overweight cats, theoverweight cats more often received fresh meatand kitchen scraps or various extra treats addedto their regular food,” and cats of normal weightwere more likely to get moist food than obesecats were.

Somewhat curiously, people with overweightcats were more interested in their own health

than clients with cats of normal weight were,but in reverse, the former group of clients con-sidered preventive care for their cat as less im-portant than the latter group of clients did.

So, in a cat’s weight there is an element ofmeeting the hedonic budget for people who livewith the cat as well. Hence, it is essential that weaddress the behavior of the people who live withand feed the cat. Encouraging alternative“strokes,” things that make people feel goodabout their interactions with the cat, such asplay and feeling proud of achieving weight lossgoals, are not to be taken lightly. Positive feed-back from the veterinary team (the outside envi-ronment) as well as feedback self-generated bythe client are key elements to the success of aweight loss program.

Giving clients the right toolsBehavior modifications required to make aweight loss program successful need all key fam-ily members to play a role. Are there forms ofinteraction that the client can have with the cat,other than feeding? Treats are the downfall ofmany weight control programs. It is best if one

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Weight in pounds

Biweekly Weight Loss Record

Follow-up Is Key!

✔ Assign a technician or nurse as the client’s“buddy’ in charge of follow-up

✔ Review program features

—Unlimited buddy phone support

—Program lasts 6 months and is renewable ifnecessary

✔ Week 1—Support phone call

✔ Week 2 and subsequent biweekly appointments:

—Schedule a 15-minute visit with the programsupervisor and the veterinarian

—Weigh patient biweekly using the same scale

—Talk with owners about highlights or problems

—Update the bar graph and send it home withthe client at each biweekly meeting

✔ After 4 months a plateau may occur, and newcalculations may be needed to promote furthersafe weight loss.


No weight lossprogram iseffective withoutproper follow-up.Assigning atechnician ornurse as a client"buddy" in chargeof follow-up helpsensure success.

person handles all of the feeding and othersbond through other means (eg, catnip, comb-ing, playing). Feeding multiple small meals as atreasure hunt is beneficial. Ask clients whetherthe cat prefers toys that mimic bird movement(flying) or mouse movement (scrambling). Havethem develop a new routine of playing withtheir cat several times a day to add interest andexercise to the cat’s life. The cost of the clinicweight loss program might include a bag of cat-nip and a toy.

Create a bar graph (see Biweekly Weight LossRecord) to be maintained in the computer by staffmembers and included in the cat’s medical record.Update and send the graph home with clients atevery visit as a good reminder of their success.

Follow-up is the key to the success of any weightloss program (see Follow-up Is Key!). A technicianor nurse (program supervisor) should becomethe client’s “buddy” and be in charge of follow-up. No weight loss program is effective withoutproper follow-up. ■

References1. Overweight cats: Prevalence and risk factors. Scarlett JM,

Donoghue S, Saidla J, et al. Intl J Obes Relat Metab Disord18Suppl(10):S22-S28, 1994.

2. Diet and feline obesity. Donoghue S, Scarlett JM. J Nutr128(12 Suppl):2776S-2778S, 1998.

3. The growing problem of obesity in dogs and cats. GermanAJ. J Nutr 136(7):1940S-1946S, 2008.

4. Feline obesity: Pathogenesis and implications for the risk ofdiabetes. Appleton DJ, Rand JS, Sunvold GD. Iams NutrSymp Proc, 81-90, 2000.

5. Obesity. Burkholder WJ, Toll PW. In Hand MS, ThatcherCD, Remillard RL, et al (eds): Small Animal Clinical Nutri-tion, 4th ed — Topeka, KS: Mark Morris Institute, 401-430, 2000.

6. Feline nutrition update. Biourge V. WSAVA Congr Proc, 2001.7. Effects of feeding regimens on bodyweight, composition

and condition score in cats following ovariohysterectomy.Harper EJ, Stack DM, Watson TD, Moxham G. J SmallAnim Pract 42(9):433-438, 2001.

8. Leptin, body fat content and energy expenditure in intactand gonadectomized adult cats: A preliminary study. MartinL, Siliart B, Dumon H, et al. J Anim Physiol Anim Nutr(Berl) 85(7-8):195-199, 2001.

9. Plasma leptin concentrations are independently associatedwith insulin sensitivity in lean and overweight cats. Apple-ton DJ, Rand JS, Sunvold GD. J Feline Med Surg 4(2):83-93, 2002.

10. Influence of feeding regimen on body condition in the cat.Russell K, Sabin R, Holt S, et al. J Small Anim Pract41(1):12-17, 2000.

11. Feline nutrition: Fundamentals and clinical relevance.Michel KE. ABVP Symp Proc, 2002.

12. Weight reduction in cats: Great frustrations in feline nutri-tion. Michel KE. WSAVA Congr Proc, 2001.

13. Effect of nutritional interventions on longevity of seniorcats. Cupp CJ, Jean-Philippe C, Wendell W, et al. Intl JAppl Res Vet Med 4(1):34-50, 2006.

14. Increased dietary protein promotes fat loss and reduces lossof lean body mass during a weight loss in cats. LaflammeDP, Hannah SS. Intl J Appl Res Vet Med 3(2):62-68, 2005.

15. External and internal influences on disease risk in cats. Buff-ington CAT. JAVMA 220(7):994-1002, 2002.

16. Human-animal relationship of owners of normal and over-weight cats. Kienzle E, Bergler R. J Nutr 136(7Suppl):1947S-1950S, 2006. http://jn.nutrition.org/cgi/content/full/136/7/1947/S_-_TBL5.


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From 2010 Canine and Feline Health NAVC and WVC Conferences · Disorders of the endocrine system...

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