From:
https://www.merckvetmanual.com/dige...ase-in-small-animals/feline-hepatic-lipidosis
Nutritional support is the cornerstone of recovery (see
Nutrition in Hepatic Disease in Small Animals). Feeding is initiated after the cat is rehydrated and has reasonable electrolyte balance, because these are requisite factors enabling normal enteric motility.
Because cats with HL are in metabolic liver failure, appetite stimulants are inappropriate; diazepam, oxazepam, cyproheptidine, and mirtazepine should not be used and will not recover an affected cat. Occasionally, an appetite stimulant may help initiate feeding early in syndrome development.
A palatable odiferous food should be offered initially. If the cat salivates or objects, all food should be removed because of the risk of inducing a "food aversion syndrome." If oral feeding is not tolerated, feeding a liquid diet (eg, CliniCare®) with supplements via a nasoesophageal tube is cautiously initiated as a first step. A 5–10 mL volume of tepid water is administered first to assess the cat’s tolerance and response. If no vomiting or signs of discomfort are noted, the process is repeated with liquefied food. After a few days of nasoesophageal feeding, if the cat is judged to be a reasonable anesthetic risk, an esophagostomy tube (E-tube) is placed with the distal tip 2–4 cm craniad to the esophageal-gastric junction. This should be documented with a lateral thoracic radiograph.
A high-protein, calorie-dense, balanced feline diet is recommended for E-tube feeding. Only rarely should a protein-restricted diet be used, because protein restriction can aggravate hepatic lipid accumulation. Rather, use of lactulose and oral amoxicillin or low-dose metronidazole (7.5 mg/kg, bid) can optimize nitrogen tolerance to allow feeding of a normal feline diet (these measures modify enteric flora, substrate utilization, and increase colonic catharsis or cleansing). A number of metabolic supplements have improved recovery of affected cats: taurine (250–500 mg/cat/day), medical grade liquid oral l-carnitine (250–500 mg/cat/day), vitamin E (10 IU/kg/day), and potassium gluconate (if hypokalemia is persistent).
Initial feedings are small and given frequently or by constant-rate infusion. On the first day, one-third to one-half of the cat’s energy requirements are fed; the amount fed is then gradually increased over the next 2–4 days to the ideal intake. If vomiting occurs, electrolytes must be rechecked, feeding tube position verified, and factors relevant to the underlying disease process considered. Metoclopramide (0.05–0.1 mg/kg, IM, up to tid, or 0.25–0.5 mg/kg divided per day as a constant-rate infusion), ondansetron (0.025 mg/kg, IV, up to bid), or maropitant (1 mg/kg/day, no more than 5 days) may be used as antiemetics. Enteric motility may be stimulated by exercise during owner visits.
To avert development of hypophosphatemia induced by re-feeding, which can cause weakness, hemolysis, encephalopathy, and other adverse effects, serum phosphorus concentrations should be serially monitored and supplemental potassium phosphate judiciously provided. Routine IV potassium phosphate supplementation is administered when feeding is initiated to obviate persistent or feeding-induced hypophosphatemia. If gastritis is suspected, an H2-blocker (eg, famotidine or ranitidine) may be used, and carafate administered PO (but not via E-tube). If the cat tolerates oral medications, SAMe at 40 mg/kg/day is given between meals once N-acetylcysteine treatment is completed. SAMe supplementation must be accompanied by sufficient B12, folate, and other water-soluble vitamins to ensure optimal metabolic benefit (metabolism to glutathione and methyl group donation for transmethylation reactions). Use of ursodeoxycholate in HL may be detrimental because TSBAs are extraordinarily high in these cats and because bile acid profiles resemble those associated with EHBDO (increased secondary bile acids). All bile acids are toxic to cells in high concentrations and, in HL, bile acids are seemingly trapped by canalicular compression.
In the rare circumstance that signs of HE are encountered, lactulose, amoxicillin, or low-dose metronidazole (≤7.5 mg/kg, PO, bid) may be useful. In symptomatic pancreatitis, feeding distal to the pancreas is done using a constant-rate infusion of CliniCare® mixed with supplemental pancreatic enzymes through a jejunostomy tube. Alternatively, parenteral nutrition can be provided, although this may delay recovery and provoke hepatic triglyceride retention.
Prognosis for cats with HL is good with early diagnosis, full treatment support, and control of underlying disease. Monitoring liver enzymes has no value in predicting recovery. However, a decline in total bilirubin by 50% within the first 7–10 days portends an excellent chance of full recovery. Concurrent pancreatitis is a poor prognostic indicator. Monitoring ALP of obese cats undergoing weight reduction may identify emerging HL that will allow suspension of the weight loss program and early treatment intervention. Recurrence of HL is rare in recovered cats.
