Feline hepatic lipidosis

What it is

Feline hepatic lipidosis is the most common liver disease of the cat. When a cat stops eating for several days, adipose tissue releases large amounts of fatty acids that reach the liver. The cat has metabolic peculiarities that make it vulnerable: it needs a lot of protein and essential amino acids (arginine, taurine, methionine, carnitine) to process fat and export it from the liver as lipoproteins, and fasting depletes these nutrients. Triglycerides then accumulate in the hepatocytes, which swell, compress the bile canaliculi and stop working: intrahepatic cholestasis and liver failure follow.

In most cats lipidosis is secondary to another disease that caused the anorexia: pancreatitis, inflammatory bowel disease, cholangitis, diabetes mellitus, hyperthyroidism, neoplasia, kidney disease, foreign bodies or dental problems. When no cause is found, the anorexia was usually triggered by stress: moving house, a diet change, a new animal, hospitalisation.

Who it affects

Middle-aged adult cats of either sex, with greater risk in obese cats that lose weight abruptly. A weight-loss plan that is too fast can also trigger it.

Anatomy involved

• Liver: enlarged, with rounded edges, yellowish colour and a friable, greasy consistency; it floats in formalin. Histologically, more than half of the hepatocytes contain lipid vacuoles that displace the nucleus.
• Bile ducts: intrahepatic cholestasis from compression of the canaliculi; ultrasound shows no extrahepatic obstruction unless the primary disease causes it (for example pancreatitis).
• Adipose tissue and muscle: the cat loses fat and muscle mass, although it may still retain abdominal fat stores.

Clinical signs

Prolonged anorexia (usually more than a few days), weight loss, jaundice, lethargy, vomiting, dehydration and weakness. Ventroflexion of the neck from hypokalaemia may be present and, in severe cases, signs of hepatic encephalopathy (ptyalism, dullness) and bleeding from coagulopathy.

Diagnosis

• Blood work: markedly increased alkaline phosphatase with normal or mildly increased gamma-glutamyl transferase (a characteristic pattern, different from that of cholangitis and biliary obstruction), hyperbilirubinaemia, increased ALT; hypokalaemia, hypophosphataemia and hypomagnesaemia are common; non-regenerative anaemia.
• Ultrasound: enlarged, diffusely hyperechoic liver compared with the falciform fat; it also looks for the primary disease.
• Fine-needle aspiration cytology: hepatocytes with severe lipid vacuolation; it is usually enough for the diagnosis.
• Coagulation profile before any invasive procedure, and a systematic search for the cause of the anorexia.

Treatment

The key is nutrition. Appetite stimulants are not enough and force-feeding by mouth causes food aversion, so a feeding tube is placed: nasoesophageal during the first days while the cat is unstable, then an oesophagostomy tube, which is well tolerated for weeks and allows feeding at home. A high-protein diet is given, starting with a fraction of the energy requirement and increasing over several days, to avoid refeeding syndrome (hypophosphataemia, hypokalaemia and haemolysis). Also: fluid therapy, potassium and phosphate correction, vitamin K for coagulopathy, antiemetics and often vitamin B12, L-carnitine and antioxidant supplements. The primary disease is treated. With early, intensive nutritional support most cats recover within weeks and recurrence is rare; the prognosis depends more on the severity of the disease at presentation (older age, signs of liver failure, hypoalbuminaemia) than on the type of underlying disease.

Key studies

• Center et al. (1993), retrospective study of 77 cats with severe hepatic lipidosis. Females and middle-aged cats predominated. Most had hepatomegaly, jaundice and dehydration and had lost 25% or more of their usual weight; ALT, AST and alkaline phosphatase were increased, with little or no increase in GGT. Coagulation tests were abnormal in 45% of the cats tested, although few bled. Of 42 cats given intensive nutritional and supportive care, 55% survived; a low PCV, hypokalaemia and older age were associated with death.
• Biourge et al. (1994), experimental study in 15 obese cats subjected to prolonged voluntary fasting. Obesity alone did not cause fat to accumulate in the liver, but fasting caused lipidosis in all 15, with clinical disease in 12 after 5 to 7 weeks and a 30–35% loss of body weight. Alkaline phosphatase rose up to 3 weeks before hyperbilirubinaemia.
• Yeager and Mohammed (1992), retrospective study of 36 cats with liver disease and a liver biopsy. A liver hyperechoic to falciform fat was the best ultrasound criterion for severe lipidosis, with 91% sensitivity and 100% specificity.
• Kuzi et al. (2017), retrospective study of 71 cats with hepatic lipidosis and 85 controls with other diseases. 66% were female. A primary disease was found in most cats (gastrointestinal disease, pancreatitis or cholangiohepatitis in 44%, a stressful event in 20%) and 28% were idiopathic. Mortality was 38%. Older age, signs of liver failure, hypoalbuminaemia and, during hospitalisation, effusions or hypotension were associated with death; the type of primary disease was not.
• Wallace et al. (2024), retrospective study of 48 cats. Three-month survival did not differ between cats fed within 12 hours of admission (68%) and those fed later (57%), and the latter were hospitalised for less time; older age and ascites were associated with death. A short stabilisation period before starting enteral feeding does not seem to worsen the outcome, although the study is small.