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Feline Hepatic Lipidosis
(Fatty Liver Syndrome)

Hepatic lipidosis, or fatty liver, is a common syndrome characterized by excess fat accumulation in the liver of cats. It can occur in cats of any age or breed and may affect more females than males. Hepatic lipidosis classically occurs after a period of anorexia (loss of appetite) of at least 2 weeks duration. When an additional disease state is found to be the cause of the anorexia, the hepatic lipidosis is defined as "secondary." The term "primary" or "idiopathic" hepatic lipidosis is used when an additional disease state cannot be identified. This is the case in approximately 50 per cent of cats diagnosed with the disorder. Obesity before the period of anorexia increases the chances of a cat developing clinical hepatic lipidosis. The decrease in appetite causing secondary hepatic lipidosis can occur for a variety of reasons. The more common of the predisposing disease states are diabetes mellitus, pancreatitis (inflammation of the pancreas), cancer, and other liver diseases. Behavioral or stress-related causes of anorexia are also common; they include the owners being away on vacation, family members leaving or new people or pets being introduced into the household, boarding, and dietary changes. Unfortunately, once this disease develops, cats feel ill and may not begin to eat again even if the, initial cause of their loss of appetite has been eliminated. Without aggressive medical intervention, this vicious circle can, lead to death in over 90 per cent of the cats.

Cats are unique in their tendency to develop this disorder. Excessive amounts of fat are broken down from the cat's peripheral fat storage tissue during fasting. This fat is then transported to the liver. The liver should then process this fat and export it to the rest of the body in a new form. In cats that develop hepatic lipidosis this process is impaired and the rate of fat export from the liver is much slower than the rate of fat intake, resulting in liver fat accumulation. Damage to the liver is caused by swelling of liver cells filled with fatty deposits as well as additional processes.

Symptoms commonly seen with this syndrome are anorexia, weight loss, lethargy, vomiting, jaundice (yellow tinge to the skin, inside of the ears, and gums), and occasionally behavioral or neurologic signs such as excessive drooling, blindness, semicoma or coma, and seizures. The suspicion that a cat is suffering from liver disease is confirmed by physical examination and appropriate abnormalities in blood work. Imaging techniques such as x-rays or ultrasound examination of the abdomen are helpful in demonstrating the size and appearance of the liver, as well as ruling out other disease states. The definitive diagnosis of hepatic lipidosis requires visualization of fat globules in liver cells obtained via liver biopsy or needle aspiration.

The treatment of hepatic lipidosis varies depending on its severity and the existence of other diseases. Prevention is extremely important. Any anorexic cat, especially if obese, should be seen by a veterinarian. Thus, the development of hepatic lipidosis can be caught in its early stages or prevented entirely with appropriate therapy. Hospitalization, fluid therapy, and supportive care may be required initially when the disease develops. Additional therapy such as antibiotics, vitamin K, and the treatment of other diseases may also be necessary.

The cornerstone of therapy, the only way to reverse the process of fat accumulation in the liver, is aggressive feeding to supply your cat with his or her full caloric requirements. Offering different diets and appetite-stimulating medications may induce a cat to eat in the initial phases of anorexia but will most likely not be of benefit once clinical signs of hepatic lipidosis develop. Appetite stimulating drugs, such as benzodiazepines (diazepam [valium], oxazepam) and cyproheptadine (Periactin), are primarily effective for stimulating appetite in those cats that are only partly anorectic, that continue to show some interest in food (even if not eating), and that are not severely ill.  There is no place for these appetite-stimulating drugs in the treatment of feline HL. Furthermore, benzodiazepines may trigger or worsen hepatic encephalopathy, they require hepatic metabolism for excretion, and they may produce excessive sedation in cats with HL.   In addition, chronic administration (>7 days) of diazepam PO to cats has been associated with fulminant hepatic necrosis.

Force feeding is usually not a good idea.  Most cats resent force feeding, are uncooperative, become stressed, and rarely eat sufficient amounts of food for effective treatment.  Cats with HL are very ill and severely stressed; thus, additional stress should be avoided. Cats also seem to develop food aversions rapidly, and the association between food and the unpleasant experience of forcing may delay the cat's return to eating. Therefore, in the clinical phase of the disease the only reliable treatment option is tube feeding.

Tube Feeding.  The use of long-term tube feeding has changed the outcome in this disease from over 90 per cent mortality to less than 30 per cent. There are three types of feeding tubes commonly used for this disease. Nasoesophageal, esophagostomy, and gastrostomy tubes (percutaneous endoscopic gastrostomy [PEG tube]).   Nasoesophageal (NE) tubes are easy to place through the nose into the stomach and require no surgery and minimal or no sedation.  Although NE tubes are well tolerated by many cats, nasal pain, irritation, and sneezing may be a problem with extended use as is generally required for treating HL.  For this reason, NE tubes are best suited for short-term nutritional support (i.e., days rather than weeks) and/or in preparation for gastrostomy tube placement. Esophagostomy tubes. Cats often are uncomfortable with esophagostomy tubes and the associated neck wrap. This is evidenced by gagging, drooling, and facial expressions consistent with discomfort and stress. Since avoidance of stress is one of the major concerns, esophagostomy tubes are not recommended for enteral nutrition in cats. Jejunostomy tubes enter the abdominal wall and end in the small intestine (jejunum). Jejunostomy tubes are rarely used in HL unless the cat has other complicating factors.

Although percutaneous endoscopic gastrostomy (PEG) tube placement involves surgery or it can be endoscopically placed through the body wall directly into the stomach, it is a relatively safe, simple, cost-effective clinical procedure that offers several advantages over nasoesophageal and esophagostomy tubes for both, the cat and the caregiver.  Percutaneous endoscopic gastrostomy tubes are considered the treatment of choice for cats with HL by the vast majority of veterinarians.  Some of the major advantages of a gastrostomy tube for enteral nutrition in feline HL are the large-diameter tube (up to 18F), the ability to easily administer commercial cat foods through the tube once they have been put through a blender, allows accurate and consistent delivery of nutrients, does not interfere with the cat's ability to swallow, and the apparent patient comfort with the tube; a light bandage wrap or no wrap at all can be used.  Cats typically become so adapted to gastrostomy tube feeding that tube feeding needs to be withheld periodically to evaluate the cat for a return of appetite.

DIET The composition of an ideal therapeutic diet for cats recovering from IHL has not been determined. Signs of hepatic dysfunction begin to resolve as soon as the cat is receiving adequate protein and energy intake. However, most cats require 3 to 6 weeks of intense dietary therapy before laboratory values normalize, clinical improvement occurs, and the cat's appetite returns. Because it appears that acquired food aversion is a component of the anorexia seen in many cats with IHL, oral feeding should not be introduced until tube feeding is well established and the cat voluntarily shows a strong interest in food when it is presented.

A variety of diets have been recommended, including blenderized high-protein cat diets, human enteral products, and veterinary enteral products. Because it is generally accepted that the provision of optimal levels of dietary protein is essential, a product that provides 30% to 50% of metabolizable energy (ME) calories as protein, 30% to 40% as fat, and 20% to 30% as digestible carbohydrate is recommended.  Cats that show clinical signs of hepatoencephalopathy initially need to be fed a reduced-protein diet. Protein content can be gradually increased as neurological signs resolve. 

An accepted formula for estimating energy requirements is: 1.5 X [30 X body weight (kg) + 70].  Therefore, a cat weighing 5 kg needs approximately 1.5 X [30 X 5 + 70 = 330 kilocalories (kcal) per day or approximately 65 kcals/kgBW/day divided into 4 to 6 feedings per day.  For the first 12 hours, only small amounts of water should be flushed through the gastrostomy tube (10 to 15 ml every 6 hours). During this time, energy requirements should be estimated and a feeding plan developed.

Cats have a high maintenance requirement for dietary protein.  Protein malnutrition may play a role in the development of HL or be a consequence of prolonged anorexia. Thus, protein should not be restricted in cats with HL, except when overt signs of hepatic encephalopathy are present. Protein (5 to 10 g/250kcal) should be added to commercially available human liquid diets as fed to cats.

Because of the absolute requirement of cats for taurine and arginine, these amino acids should be supplemented. Taurine and arginine may be purchased at health food stores, and supplemented at 500 mg/day for taurine and 300 to 1,000 mg/day for arginine.  If a blenderized balanced commercial feline diet is fed, supplementation of these amino acids may be discontinued after a few weeks. Supplementation should be continued if a human liquid diet is fed. The role of carnitine in the pathogenesis of HL is unresolved, so supplementation of the diet with carnitine (250 to 500 mg/day) seems reasonable pending clarification of the role of this amino acid in HL.

Vitamin K deficiency may develop in cats with HL due to decreased intake and reduced intestinal synthesis. Coagulation screens may normalize in some cats with HL when supplemented with vitamin K, (5 mg PO q24h tapered over 2 weeks). Thiamine administration is also advocated (50 to 100 mg PO q24h for 1 week).

Hypokalemia is often present in cats with HL.  Potassium concentration may be corrected initially by adding potassium chloride to parenteral fluid solutions. If potassium supplementation is required beyond the initial rehydration period, potassium gluconate may be added to the diet. Potassium concentration should be measured frequently during potassium supplementation so that supplementation can be adjusted as needed.

The initial tube feeding should provide 1/4 to 1/2 of the cat's calculated ME requirement. This is gradually increased over a 1-week period to the cat's ME requirement. A minimum of four feedings should be provided per day.   Intestinal villi undergo atrophy during prolonged fasting; thus, a short adaptive period is recommended when feeding begins, such that 25 to 50 percent of the total daily caloric requirement is fed initially. Daily volume increments may be made until the desired caloric goal is reached. Most adult cats can accommodate 30 to 50 ml of food per feeding when the volume of the feedings is gradually increased to this level over several days.

Before each feeding, the tube should be aspirated and the amount of residual food and water measured. If the quantity aspirated is significant (>20% of the volume of the previous meal), a feeding should be skipped to lessen the chances of vomiting from excessive gastric distention.  The most common complication is vomiting after feeding.  The frequency of vomiting can be reduced by slowing the rate of food administration (10 to 15 minutes per feeding), warming the food to body temperature in a microwave oven, and pretreating with metoclopramide (Reglan, A.H. Robins Co.) 30 minutes before feeding.  After food administration, the tube should be flushed with 10 to 15 ml of warm water and capped. This regimen supplies approximately I ml of water per milliliter of food slurry administered. Therefore, it is generally unnecessary to administer additional fluids for maintenance.

If the cat's progress is good, the caregiver should periodically withhold one or more feedings in order to "challenge" the cat to eat on her own. Offering the cat's favorite foods or special treats is one way of evaluating whether the cat may be regaining her appetite. As the cat's appetite returns, the frequency of tube feedings should be slowly decreased until the cat is consuming adequate calories voluntarily.  The caregiver should carefully estimate how much food the cat is eating so that adequacy of caloric intake can be determined. When the cat is consuming all or almost all her daily caloric needs, the gastrostomy tube should be removed.

Caregiver education and periodic rechecks while the gastrostomy tube is in place are especially important. Caregivers need to thoroughly understand all aspects of food preparation and administration, including flushing of the tube with water after each feeding. They should visually inspect the tube exit site daily and gently clean off accumulated debris with a warm water compress. They should report the development of excessive, foul-smelling material to the veterinarian immediately to circumvent complications from the development of purulent cellulitis

When vomiting can be controlled and long-term adequate protein and calorie intake is ensured, treatment is usually successful.   However, because many cats refuse to eat voluntarily for a period of weeks to several months, management can be difficult for pet owners and prognosis will be guarded until the cat begins to eat voluntarily. Supportive treatment involves minimizing any stress that the cat may experience.  Although some veterinarians advocate supplying supplemental carnitine during tube feeding, recent evidence indicates that this is probably unnecessary. Throughout the treatment period, frequent monitoring of liver-associated enzymes in serum can be used as an indicator of hepatic recovery.

Because most cats with IHL have a history of obesity, it is prudent to prevent weight regain following recovery. If the cat is still overweight, a weight loss protocol that allows a slow rate of weight loss and includes a diet containing optimal levels of protein should be followed. Veterinary supervision is warranted to ensure a slow rate of weight loss and prevent the recurrence of IHL. Most importantly, the cat's lifestyle and living conditions should be managed to minimize or prevent stressful events that may lead to subsequent episodes of anorexia.

The feline liver has the remarkable ability to regenerate. Therefore, in cats with idiopathic hepatic lipidosis recurrence is rare, and the cats that recover go on to live normal lives.

 

Related Topics

Managing PEG Tubes and Feeding Tubes

Hepatic Lipidosis Laboratory Profile


Main Subject Index

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Adapted in part from:

Hepatic Lipidosis in Cats. Goldstein RE DVM, Diplomate, ACVIM. 2000

Therapy for Hepatic Lipidosis. Cornelius LM, DVM, Diplomate, ACVIM; Bartges JW, DVM, Ph.D, Dipl. ACVIM, ACVN. 2000

Hepatic Lipidosis. Bunch SE, DVM, PhD, Diplomate ACVIM. 1998

Hepatic Lipidosis
. Strombeck, Donald R., DVM, PhD, Diplomate. ACVIM. 1996

Idiopathic Hepatic Lipidosis in Cats. Deorah G. Day, DVM, Ph.D., Professor of Small Animal medicine. 1994

Small Animal Surgery 2nd ed. Fossum, Theresa Welch, DVM, MS, PhD, Diplomate ACVSHedlund, Cheryl S., DVM, MS, Diplomate ACVS 2002

J Feline Med Surg. 1999 Dec;1(4):215-20; Willard MD, Weeks BR, Johnson M.; Fine-needle aspirate cytology suggesting hepatic lipidosis in four cats with infiltrative hepatic disease

Am J Vet Res. 2000 May;61(5):566-72.Sunvold GD, Kelleher JK, Bruckner GG; Effect of dietary protein quality and fatty acid composition on plasma lipoprotein concentrations and hepatic triglyceride fatty acid synthesis in obese cats undergoing rapid weight loss.

J Vet Intern Med. 2000 Jan-Feb;14(1):20-6;  Brown B, Mauldin GE; Metabolic and hormonal alterations in cats with hepatic lipidosis.

J Nutr. 1998 Dec;128(12 Suppl):2733S-2746S. Review;  Center SA; Nutritional support for dogs and cats with hepatobiliary disease.

J Am Vet Med Assoc. 1998 Jul 1;213(1):94-8; Newell SM, Selcer BA; Correlations between ultrasonographic findings and specific hepatic diseases in cats: 72 cases
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J Vet Intern Med. 1997 Jul-Aug;11(4):238-42; Hall JA, Barstad LA, Connor WE; Lipid composition of hepatic and adipose tissues from normal cats and from cats with idiopathic hepatic lipidosis

Semin Vet Med Surg (Small Anim). 1997 Feb;12(1):28-33. Review.  Dimski DS. Feline hepatic lipidosis.

J Vet Intern Med 7:266, 1994;  Adams LG, Hardy RM, Weiss DJ, et al: Hypophosphatemia and hemolytic anemia associated with diabetes mellitus and hepatic
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J Vet Intern Med 7:349, 1993.; Center SA, Crawford MA, Guida L, et al: A retrospective study of 7 cats with severe hepatic lipidosis: 1975-1990.

J Am Med Assoc 209:618, 1996; Center SA, Elston TA, Rowland PH, et al: Fulminant hepatic fail associated with oral administration of diazepam in I I cats. .

Vet Clin North Am 25:357, 1995; Dimski DS, Taboada J: Feline idiopathic hepatic lipidosis. .

J Nutr 2002 Feb;132(2):204-10; Blanchard G, Paragon BM, Milliat F, Lutton C: Dietary L-carnitine supplementation in obese cats alters carnitine metabolism
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