M. Chandler1, DVM, MS, MANZCVSc, DACVN, DACVIM, DECVIM-CA, MRCVS; A. Harvey2, BVSc, DSAM (Feline), DECVIM-CA, MRCVS, MANZCVSc (Assoc)
Feline Hepatic Lipidosis (HL)
Hepatic lipidosis is a syndrome characterised by severe hepatocellular lipid accumulation, intrahepatic cholestasis, and impaired liver function. A period of anorexia leads to severe protein restriction, mobilization of adipose tissue to the liver, and reduction in synthesis of proteins required for VLDL formation, which leaves the liver unable to remove excess triglycerides.
Hepatic lipidosis may occur as a primary event or may be secondary to another disease process. The therapy for hepatic lipidosis, idiopathic or secondary, requires aggressive nutritional management, and this is the most important part of therapy. Underlying conditions such as cholangitis, neoplasia, gastrointestinal disease, pancreatitis or endocrine disorders are identified in over 50% of cats. If present, these may require additional treatments. In comparison to cats with secondary HL, those with primary idiopathic HL are usually younger, have higher ALP/bilirubin levels, absence of hyperglobulinaemia, normal GGT and a better survival rate. An initiating acute pancreatitis is common, and, if present, carries a worse prognosis. In one unpublished study, we found an 80% or higher survival rate for the idiopathic cats while secondary lipidosis had only a 32% survival rate.
Force-feeding or appetite stimulation is generally not adequate to meet caloric needs and tube feeding is the best way to administer adequate calories. Naso-oesophageal tubes can be used, but, due to the small size, feeding is limited to liquid diets and they are less stressful and less tolerated than larger feeding tubes. We suggest placement of either an esophageal or gastrostomy feeding tube. Esophageal feeding tubes are well tolerated, easy to place, and have less complications than gastric feeding tubes.
As mentioned above, an enteral feeding tube is usually placed as soon as a diagnosis is made, assuming the cat is stable enough for anesthesia. A naso-esophageal tube may be placed, but only short term prior to other tube placement if necessary. The provision of adequate energy is one of the keys to the successful management of this condition. Energy requirements should be determined on an individual basis, but most cats should receive at least RER after tube placement and the gradual introduction of food. By the time they leave the hospital, many cats are receiving close to MER.
Protein and amino acids are particularly important in cats with HL as protein deficiency may play a major role in disease development. Cats are less efficient than other mammals at sparing protein during starvation, and the amino acids methionine and arginine become limiting in obese cats during starvation. The amino acids arginine and taurine are also important in the treatment of hepatic lipidosis. It has been hypothesized that protein or amino acid deficiency may induce lipid accumulation in the liver by limiting lipoprotein synthesis needed for lipid metabolism and transport in the normal liver. Supplementation of protein even at only ¼ of the daily requirement significantly reduces lipid accumulation in the liver and promotes positive nitrogen balance during long-term fasting in obese cats.
Subnormal concentrations of vitamin B12 have been documented in cats with HL. A suggested dose for B12 in cats is 125–250 µg per cat subcutaneously q 7 days for 4 treatments, then q 2–4 wk as needed; in dogs: 100–250 µg SQ q 7 days for 4 treatments. Cats with hepatic lipidosis may also develop hypokalaemia, which should be supplemented if serum concentrations are decreased.
The use of L-carnitine has been proposed to benefit some cats with HL. Carnitine transports long-chain fatty acids across the inner mitochondrial membrane into the matrix for oxidation. Although carnitine deficiency does not appear to be a mechanism for the development of HL, it may protect obese cats from hepatic lipid accumulation during weight loss. A recommended dosage for supplementation in cats with HL is 250–500 mg per day.
Other treatments that are often required include antiemetics (e.g., maropitant) and promotility drug. Gastric stasis is common and aggressive treatment may be required with constant rate metoclopramide infusions (1–2 mg/kg/day) and/or prokinetics such as cisapride.
Hepatic Encephalopathy (HE)
Hepatic encephalopathy is most commonly encountered in cats with portosystemic shunts, but can also occur in other severe liver diseases, particularly also with hepatic lipidosis. Ammonia is hypothesized to be one of the key triggers of HE, so foods high in protein are frequently associated with the development of clinical signs. Skeletal muscle takes over the role of detoxifying ammonia in the absence of a functioning liver; over the long term this can lead to muscle wasting and a negative nitrogen balance in many animals. Therefore protein should only be restricted to the level to prevent clinical signs of HE. The source of dietary protein can significantly influence the manifestation and severity of HE. As meat-based protein sources trigger a more severe response compared to vegetable and dairy proteins, cottage cheese or egg-based diets are commonly utilized, as are vegetarian diets for dogs with HE, but do not contain the right types of nutrients as a sole protein source for cats. Decreasing the amount of dietary protein can be effective but can also lead to protein malnutrition if the animal is not eating enough food to meet its daily energy needs (especially in growing kittens with higher protein requirements). Most pets with clinical signs of HE have a liver that is not efficient at using dietary protein and, thus, may actually need more protein and not less.
High diet digestibility is helpful in palliating the signs of HE. Soluble dietary fiber and non-digestible carbohydrates (e.g., lactulose) may decrease HE signs. Affected animals should be fed small, frequent meals throughout the day, which may also help increase energy intake in finicky or hyporectic patients.
The best diet for any patient with HE will vary from animal to animal. A complete and accurate diet history can facilitate selecting a diet, especially if protein restriction is indicated. Once a diet has been selected, the animal should be monitored frequently for any adverse responses to the food, food intake, body weight, BCS, and laboratory parameters. In animals that respond well to protein restriction, consideration should be given to slowly increase the amount of protein in the diet until clinical signs recur or the animal is consuming protein levels equivalent to a maintenance food.
Other medical treatments that are of benefit to patients with HE are:
This disaccharide is metabolised to organic acids by colonic bacteria promoting acidification of colonic contents and thus trapping of ammonia in the form of ammonium. The osmotic effect also reduces faecal transit time reducing the chance for bacterial ammonia production. It can be administered orally, or in unstable patients such as those with severe hepatic encephalopathy, it can be administered per rectum.
Antibiotics such as ampicillin and metronidazole reduce intestinal bacterial numbers resulting in reduction of ammonia production. They also reduce the risk of bacterial translocation and subsequent bacteraemia.
3. Intravenous fluids if presenting dehydrated and encephalopathic (avoid lactated Ringer's)
4. Gastrointestinal protectants if there is any evidence of gastrointestinal haemorrhage.
5. Antiepileptics if the animal is seizing (preferably avoid diazepam).
1. Bauer JE, Shenk PA. Nutritional management of hepatic disease. Vet Clin North Am Small Anim Pract. 1989;19(3):513–526.
2. Marks SL. Nutritional management of hepatobiliary disease. In: Fascetti AJ, Delaney SJ, eds. Applied Veterinary Clinical Nutrition. West Sussex, UK: Wiley Blackwell; 2012:235–250.
3. Meyer H, Twedt DC, Roudebush P, Dill-Macky E. Hepatobiliary disease. In: Hand MS, Thatcher CD, Remillard RL, Roudebush P, Novotny BJ, eds. Small Animal Clinical Nutrition. 5th ed. Topeka, KS: Mark Morris Institute; 2010:1155–1194.