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Hepatic Lipidosis in Cats

 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.

Force feeding is usually not a good idea. Even with the most cooperative cat, it is virtually impossible to feed adequate amounts in this fashion. 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.

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. A tube placed through the nose into the stomach or esophagus can be used temporarily. Long-term feeding is achieved with a tube surgically placed in the esophagus or, more commonly, a tube surgically or endoscopically placed through the body wall directly into the stomach.

A commercially available maintenance diet is used for most cats. Your veterinarian will supply you with a feeding plan aimed at meeting your cat's nutritional requirements. Additional medications to control vomiting are sometimes necessary. Frequent rechecks with your veterinarian will be required to assess the tube location, possible infection, your cat's clinical state, and blood work. Liver parameters usually improve within 2 to 8 weeks after initiating feeding. Oral food should not be offered until that time.

Once your cat begins to eat, tube feedings can be gradually reduced over a few weeks and eventually discontinued. Most cat's tubes can be removed 3 to 4 months after placement. In cats with idiopathic hepatic lipidosis recurrence is rare, and the cats that recover go on to live normal lives.

The above is general veterinary information. Do not begin any course of treatment without consulting your regular veterinarian. All animals should be examined at least once every 12 months.

About the author:

From the Textbook of Veterinary Internal Information: Client Information Series. Copyright © 2000 by W.B. Saunders Company. All rights reserved.

Linda Mar Veterinary Hospital and its cat-only affiliate, Coastal Cat Clinic, are small animal practices located in Pacifica, California. To find a veterinarian or to learn more about the vet clinic and our staff, visit:[http://lindamarvet.com/]

 Richard E. Goldstein, DVM

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