Beruflich Dokumente
Kultur Dokumente
10 October 2000
Feline Hepatic
FOCAL POINT Lipidosis: Treatment
★ Cats with hepatic lipidosis (HL)
require aggressive nutritional
support; careful monitoring is
Recommendations*
needed because life-threatening
complications may arise within Auburn University
72 hours of initiation of Brenda Griffin, DVM, MS
nutritional therapy.
ABSTRACT: Aggressive nutritional support is the mainstay of treatment for feline hepatic lipi-
KEY FACTS dosis. The ideal diet would fulfill all basic protein and nutrient requirements, provide a positive
energy balance, promote liver regeneration, and facilitate recovery from the metabolic de-
rangements and clinical signs associated with the syndrome. For most cats, a high-protein
■ In contrast to the usual dietary diet is indicated. Patients should be monitored closely during the initial 72 hours of nutritional
recommendations for small therapy, the period during which most serious complications occur.
animals with liver disease, most
cats with HL should be fed high-
F
protein diets. eline hepatic lipidosis (HL), a syndrome in which hepatocellular lipid ac-
cumulation leads to intrahepatic cholestasis and liver dysfunction, is a
■ Virtually all cats with HL require common hepatobiliary disease in domesticated cats. All cats with HL need
enteral nutritional support via a thorough systematic evaluation to rule out primary diseases that may be under-
feeding tube. lying their condition.
Therapy for HL is aimed at reversing fat and protein catabolism, managing
■ Icteric cats with severe HL electrolyte abnormalities, and treating the clinical signs of hepatic disease as well
must be considered to be in as any underlying or concurrent conditions. Aggressive nutritional support is the
critical condition at the time cornerstone of treatment and is the only known effective therapy for cats with
of presentation. HL. The mortality rate associated with HL ranges from 10% to 40% in cats
treated with aggressive nutritional therapy and is as high as 90% in cats not
■ Life-threatening hypokalemia treated aggressively.1–3 Recurrence is rare.4
and hypophosphatemia may
occur after initiating nutritional DIET
therapy in cats with HL. The ideal diet for treatment of HL is unknown. The best clinical results are
obtained with high-protein diets containing adequate calories and nutrients to
■ Hypokalemia and meet known requirements.5 The need for increased dietary protein in patients
hypophosphatemia may with HL is in contrast to dietary recommendations in many other liver diseases
worsen despite adequate in which increased protein may precipitate hepatoencephalopathy. In one study
supplementation. in which HL was induced by feeding 25% of maintenance energy requirements,
cats fed calories as protein developed less lipid accumulation than did cats fed
carbohydrate or fat,6 suggesting that protein improves mobilization of fat from
hepatocytes.
*A companion article entitled “Feline Hepatic Lipidosis: Pathophysiology, Clinical Signs,
and Diagnosis” appeared in the September 2000 (Vol. 22, No. 9) issue of Compendium.
Compendium October 2000 Small Animal/Exotics
TABLE I
Commercially Available Diets Used in the Treatment of Feline Hepatic Lipidosis
For Cats without Clinical Signs For Cats with
Manufacturer of Hepatoencephalopathy Hepatoencephalopathy
Abbott Laboratories Clinicare®—Feline Liquid Dieta Clinicare® RF—Specialized Feline
(Abbott Park, IL) Liquid Dieta
Hill’s Pet Nutrition Prescription Diet® Feline p/d®b,c; Prescription Diet® Feline l/d™b,e
(Topeka, KS) Prescription Diet® Canine/Feline a/d™b,d
The IAMS Company Maximum-Calorie™/Felinea,f None
(Dayton, OH)
Ralston Purina Company CNM CV-Formula®b,c CNM NF-Formula®b,c
(St. Louis, MO)
Waltham (Vernon, CA) Waltham® Veterinary Diet Waltham® Veterinary Diet
Feline Selected Proteinb,c,g Feline Low Proteinb,c
a
Recommended for use with nasoesophageal and jejunostomy tubes.
bRecommended for use with esophagostomy and gastrostomy tubes.
cMust be blenderized with water to make a gruel.
d May be fed undiluted using an 18-Fr or larger tube.
eMay be fed undiluted using a 20-Fr or larger tube.
f May be fed undiluted using an 8-Fr or larger tube.
g Contains novel protein and carbohydrate sources (venison and rice) and may be useful in cats with concurrent inflammatory bowel
disease.
When selecting a diet, one should consider that cats firmed with a fasting ammonia concentration. Admin-
are true carnivores.7 Their physiology and metabolism istration of oral lactulose (0.67-mg/ml solution, 0.5 to
require diets high in protein and fat and low in carbo- 1 ml/4.5 kg, three times daily) is often helpful because
hydrate. Cats do not have the ability to synthesize such it lowers colonic pH, trapping ammonia as ammonium
essential nutrients as taurine, arginine, vitamin A, nia- and thereby decreasing its absorption into portal circu-
cin, and arachidonic acid that would be present in prey. lation. In addition, oral metronidazole (7.5 to 15
Commercially prepared feline diets should be used to mg/kg twice daily), oral neomycin (20 mg/kg three to
avoid nutritionally incomplete rations (Table I). Diets four times daily), or oral amoxicillin (22 mg/kg two to
formulated for humans or other species require the ad- three times daily) may be used to reduce intestinal bac-
dition of such supplements as the essential amino acid terial flora, thereby decreasing ammonia synthesis in
arginine, which is required for ammonia detoxification the intestinal tract.
in cats.
Cats have much higher protein requirements than do ENTERAL SUPPORT
humans and dogs. Protein should provide at least 20% Virtually all cats with HL require enteral support via
of a diet’s calories.7 Because protein is required to sup- a feeding tube. Nasogastric, esophagostomy, gastrosto-
port a positive nitrogen balance and liver regeneration my, or jejunostomy tubes may be used (Figure 1). Icter-
and because protein supplementation is known to re- ic cats with severe HL must be considered to be in criti-
duce hepatic lipid accumulation during rapid weight cal condition at the time of presentation. Because most
loss in obese cats, cats with HL should receive the high- cats that die of HL do so within the first few days of
est level of protein they can tolerate as soon as possi- therapy, treatment—including nutritional support—
ble.6,7 Feline renal diets provide approximately 22% of needs to be initially provided in noninvasive and non-
calories as protein.7 Most cats with liver disease can tol- stressful ways. Treatment for severe HL should be di-
erate higher dietary protein levels (up to 35% to 45%, vided into an initial stabilization phase followed by a
which is typical of most commercial cat foods).7 long-term phase.2 Investigators using this approach re-
Cats with overt signs of hepatoencephalopathy (se- port lower mortality rates and recovery rates of 90%.1,2
vere depression and ptyalism), however, should be fed a During the initial stabilization phase (usually the first
reduced-protein diet, such as one designed to manage few days of therapy), dehydration and electrolyte imbal-
renal failure. Before feeding, diagnosis should be con- ances should be corrected and monitored. Cats often look
successful, 2 to 4 ml of a carbonated beverage (e.g., this time, cats expressing an interest in eating can be of-
cola) may be flushed into the tube, followed in 5 to 10 fered small amounts of a novel food.
minutes by 10 ml of warm water.9 During the long-term phase of therapy, serum bio-
Food aversion may be a complicating factor in cats chemical profiles should be monitored every 1 to 2
with HL.7 Cats that refuse to eat a diet they associate weeks depending on the patient’s stage of recovery. Res-
with nausea may continue to avoid the diet even after olution of icterus and hepatic function begins once the
full recovery. Exposing cats with HL to different com- cat is receiving adequate energy and protein intake, but
mercial diets during tube feeding may predispose them most cats require 3 to 6 weeks of diet therapy before
to aversion of those diets. No food should be offered clinicopathologic values normalize and the appetite re-
orally for the first 10 days of nutritional support.7 After turns.7 When biochemical parameters normalize, most
cats begin eating on their own stasis, many cats may not have
and tube feedings can gradually had a bowel movement for days
be reduced. Tube removal is per- to weeks before presentation.
formed only after a cat is consis- Removal of hard fecal material
tently eating its full caloric re- from the colon with a small
quirement for 1 week. glycerin enema or suppository
may promote normal gastroin-
ADDITIONAL THERAPEUTIC testinal motility.
RECOMMENDATIONS Cats with non–vitamin K re-
Several vitamin and dietary sup- sponsive coagulopathies may re-
plements, including carnitine, quire transfusions of plasma or
arginine, taurine, and antioxi- fresh whole blood. Appetite stim-
dants, have been advocated in the Figure 3A ulants (e.g., oxazepam, cyprohep-
treatment of feline HL (see Cur- tadine) are seldom useful and are
rent Recommendations for Di- not recommended until the re-
etary Supplements). Controlled covery phase of the disease, if at
studies of these supplements are all.1,3,5 Antibiotic therapy is indi-
needed for specific recommen- cated when secondary infection is
dations.1 present. Because of their catabolic
Cats presenting with signs con- effects, corticosteroids are con-
sistent with thiamine deficiency traindicated unless indicated to
(e.g., ventroflexion of the head treat an underlying disease.
and neck; Figure 4) should re- Ursodeoxycholic acid (Acti-
ceive two or three doses of sup- gall®, Novartis, East Hanover, NJ)
plemental thiamine (50 to 100 is used in humans with various liv-
mg intramuscularly, twice daily).1 er diseases and may be beneficial
Lipotropic compounds that may Figure 3B in cats with HL. 12 Ursodeoxy-
potentiate hepatoencephalopathy Figure 3—Cat with a gastrostomy tube in place. cholic acid promotes bile flow
(e.g., choline, methionine) are The tube may be covered with a bandage or prefer- through modulation of bile acids
contraindicated and should not ably with a T-shirt. Elizabethan collars are rarely and may increase hepatic peroxi-
be used.11 necessary. Shirts (which may be fashioned from cast somes and mitochondria. The rec-
Other therapies include the stockinet or human infant clothing) offer the ad- ommended dose is 50 mg/cat/day
use of antiemetics and promotil- vantages of comfort and easy tube access and may orally; however, controlled studies
ity drugs. Although vomiting be changed and washed by owners at home. are needed to evaluate the efficacy
may occur for many reasons of this drug in cats with HL.
(e.g., electrolyte imbalances, liv-
er dysfunction, secondary to underlying diseases), gas- COMPLICATIONS
tric stasis caused by prolonged anorexia is common in Complications frequently occur during nutritional
cats with HL. The absence of normal gut sounds (bor- therapy of feline HL, usually during the initial 72 hours,
borygmi) on abdominal auscultation is consistent with and include tube-associated problems, hypokalemia, hy-
gastric stasis. Gastric stasis can be treated with pro- pophosphatemia, and induction of hepatoencephalopa-
motility drugs and by allowing ample time for the thy. Because complications may be life threatening,
stomach to empty between feedings. Metoclopramide careful in-hospital monitoring of patients is essential
(0.2 to 0.4 mg/kg) can be administered through the during the initial stabilization phase of therapy.
feeding tube every 6 to 8 hours or subcutaneously 30 to
60 minutes before feedings or intravenously (1 to 2 Tube-Associated Problems
mg/kg/day, constant-rate infusion); oral cisapride (0.1 Tube-associated complications include local irritation
to 0.5 mg/kg every 8 to 12 hours, or 1⁄4 of a 10-mg and infection, improper placement, and premature re-
tablet for an average-sized cat) can also be used. Four moval. Nasoesophageal tubes often cause sneezing and
daily feedings are adequate, tend to reduce the inci- nasal discomfort. Vomiting of the tube, aspiration
dence of vomiting, and are practical for owner compli- pneumonia, and esophageal reflux are potential risks
ance. A volume of 10 ml/lb/feeding should not be ex- with nasoesophageal and esophagostomy tubes. 10
ceeded. Because of prolonged anorexia and gastric Esophagostomy, gastrostomy, and jejunostomy tubes
tend to be well tolerated by patients; cats rarely require clinical signs (e.g., severe depression, ptyalism) that de-
Elizabethan collars with these tubes. Minor stomal in- velop after the initial feeding. This complication is un-
fections are common with both esophagostomy and gas- common cats with HL14; if it occurs, it may be treated
trostomy tubes.10 Owners should be instructed to check with low-protein diets and lactulose as discussed. Fast-
and clean the tube stoma daily to prevent infection. ing at this time to obtain an ammonia concentration to
Improper placement of a gastrostomy tube may result document hepatoencephalopathy is not recommended.
in obstruction of the pylorus and vomiting associated Smaller, more frequent feedings may be helpful. Cats
with feeding. Tube placement should be checked in per- should be monitored for exacerbation of hepatoen-
sistently vomiting cats by administering a radiopaque, cephalopathy-associated clinical signs after feedings. In
iodinated contrast solution through the tube. Although most cases, clinical signs resolve within a few days, after
rare, premature tube extraction (less than 5 days) or which time most cats can be gradually switched to a
tube migration may result in peritonitis (gastrostomy higher-protein diet.
tube) or local infection (esophagostomy tube). Tube-as-
sociated complications are very rare when jejunostomy Electrolyte Imbalances
tubes are placed using newly described techniques.13 Hypokalemia and hypophosphatemia are life-threaten-
ing electrolyte imbalances that may be sequelae to ali-
Hepatoencephalopathy mentation.15 The presumed mechanisms of hypokalemia
Induction of hepatoencephalopathy is evidenced by and hypophosphatemia in cats with HL are similar. At
presentation, hypokalemia is
Current Recommendations
the most common elec-
trolyte abnormality in cats for Dietary Supplements
with HL ; clinical signs of ■ Oral L-carnitine (DL-carnitine may be toxic):
14
12 to 72 hours after initiation of enteral alimentation.16 unless vomiting is present.17 Serum phosphate levels
If severe (serum phosphorus concentration below 2.2 should be monitored every 12 hours until cats stabilize.
mg/dl), hypophosphatemia can result in massive, acute Oral supplementation may be accomplished by feeding
hemolysis. Because cats may be more sensitive to hy- skim milk or commercial oral phosphate supplements.
pophosphatemia-induced hemolysis than are other Cow’s milk contains 0.029 mmol/ml of phosphate.15
species and because hemolytic anemia and hypophos- The oral phosphorus dose is 0.5 to 2.0 mmol/kg/day. An
phatemia have been reported in cats with HL, careful average 4-kg cat requires just over 2 oz of milk/day for
postalimentation monitoring of hematocrit and serum adequate supplementation. Although many cats can tol-
phosphorus concentrations is indicated.17 (Experimen- erate this quantity of milk, using lactose-free milk (Lac-
tally, serum phosphorus concentrations must be reduced taid®, distributed by H. P. Hood, Chelsea, MA) and di-
to less than 0.5 mg/dl to induce hemolysis in dogs.16) viding the milk dose over the day are recommended to
Adenosine triphosphate (ATP) depletion is the pro- prevent diarrhea caused by lactose intolerance.
posed mechanism by which hypophosphatemia causes
hemolysis.16,17 ATP is necessary to maintain erythrocyte CONCLUSION
membrane integrity, shape, and deformability. ATP de- Cats with HL require aggressive nutritional support
pletion causes malfunction of the sodium–potassium for recovery. In most cases, high-protein diets are indicat-
pump, resulting in decreased cell deformability and os- ed. Underlying diseases, if present, must be diagnosed
motic lysis. The spleen and liver may contribute by re- and treated concurrently. Icteric cats with HL must be
moving rigid erythrocytes. considered to be in critical condition. Their treatment
Cats with severe hypophosphatemia (below 2.2 mg/dl) should be divided into an initial stabilization phase fol-
should receive IV potassium phosphate or sodium phos- lowed by a long-term phase.2 Investigators using this
phate at 0.01 to 0.06 mmol/kg/hour. The higher dose is treatment approach report recovery rates of 90%.1,2 Re-
often needed in severely affected cats.16 Parenteral potas- currence of HL is rare.4 Patients should be monitored
sium phosphate supplements contain 3 mmol of phos- closely during the initial 72 hours after alimentation be-
phate and 4.4 mEq/ml of potassium, whereas sodium cause most serious complications, including life-threat-
phosphate solutions provide 3 mmol of phosphate and 4 ening hypokalemia and hypophosphatemia, occur dur-
mEq/ml of sodium. These phosphate supplements should ing this period. Without aggressive nutritional support
be administered in calcium-free solutions (e.g., 0.9% and monitoring, most cats with HL die.1–3
saline) to prevent precipitation of insoluble calcium
phosphate. The amount of supplemental potassium in
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Vet Intern Med 7:349–359, 1993. About the Author
15. Macintire DK: Disorders of potassium, phosphorus, and Dr. Griffin is affiliated with the Scott-Ritchey Research
magnesium in critical illness. Compend Contin Educ Pract Center, College of Veterinary Medicine, Auburn Universi-
Vet 19(1):41–48, 1997. ty, Alabama. She is a Diplomate of the American College
16. Justin RB, Hohenhaus AE: Hypophosphatemia associated
with enteral alimentation in cats. J Vet Intern Med 9:228– of Veterinary Internal Medicine.
233, 1995.