Hepatic lipidosis can occur as either a primary idiopathic disease syndrome or secondary to a number of other primary non-hepatic conditions. Lipid accumulation in the liver is simply the result of nutritional, metabolic or toxic insults to the liver and this process is reversible.¹ An example of a common secondary disease associated with significant hepatic triglyceride accumulation is diabetes mellitus. Hepatic lipid accumulation can also result secondary to a number of disease syndromes associated with anorexia and weight loss such as pancreatitis, inflammatory bowel disease or other major organ dysfunction.² These secondary conditions generally have less severe lipidosis than the idiopathic form and the prognosis is based on the underlying disease. The idiopathic lipidosis syndrome has no identifiable etiologic factor, however obesity is a common risk factor. Often in the history an inciting stress factor is identified.

The therapy for idiopathic hepatic lipidosis requires aggressive management.³ I believe an 80% or higher survival rate should be expected in cats given appropriate therapy and when no underlying disease is present. Initial therapy requires rehydration with balanced electrolyte solutions. Replacement of potassium deficits is imperative as normokalemia improves survival.⁴ Some cats may also require magnesium and phosphorus supplementation.³ The common practice of adding B-vitamins to the fluids may be unwarranted because their prolonged exposure to light in the fluid bag could inactivate them. Parenteral administration is a better option.

Adequate nutrition is the most important part of the primary therapy for hepatic lipidosis. Force-feeding or appetite stimulation is generally not adequate to meet caloric needs and tube feeding is the best way to administer adequate calories.⁵ Nasogastric tubes can be used but are often not well tolerated and because of their small size feeding is limited to liquid diets. I suggests placement of either an esophageal or gastrostomy feeding tube. In our practice we find esophageal tubes to be well tolerated and have less complications than gastric tubes. One should refer to specific articles describing tube placement techniques. I find a 20 French soft red rubber feeding tube ideal for the esophagus.

The nutritional recommendations for idiopathic hepatic lipidosis are completely empirical and poorly documented. There are numerous reports suggesting various diets (with a variety of protein and fat content recommendations). In general, dietary fat and protein should not be restricted in these cats because calories and protein are so important in providing nutritional balance. I feed blenderized canned recovery formulations or prescription diets. The caloric needs should be calculated (approximately 60 Kcal/kg/day for the average cat) and fed in 4-6 meals a day. The first day I give only 25% of their calculated requirements, then slowly increase to total caloric needs over 5-7 days. There is also no good data showing benefit of various dietary supplements. Carnitine is required for transport of long chain fatty acids into the mitochondria for subsequent oxidation for energy production. There is evidence that L-carnitine replacement in cats protects against hepatic lipid accumulation in experimental weight reduction studies and therefore may be an appropriate dietary adjunct for cats with lipidosis.⁶ However, one report failed to show carnitine deficiency to occur in cats with idiopathic hepatic lipidosis.⁷ A suggested dose is 250mg/day. Some cats with hepatic lipidosis have or will develop cobalamin deficiency. Experimental cobalamin deficiency results in lethargy, anorexia and weight loss, all common signs observed with lipidosis. My impression is that cats appear to improve faster when cobalamin is given 250 µg SQ weekly. Serum cobalamin levels should be determined to document the presence of a deficiency prior to therapy, and at recovery.

Other therapies suggested include S-adenosylmethionine (SAMe), an intermediary molecule involved in the metabolism of glutathione (GSH), in lipid membrane integrity and cell regeneration. Exogenous administered SAM has been shown to increase intracellular GSH levels in hepatocytes and prevents GSH depletion thus acting indirectly as an important antioxidant.⁸ The benefit of SAMe or other antioxidants in hepatic lipidosis is unknown. Another antioxidant and hepatic protector is milk thistle or its extract silymarin or the active isomer silibinin (available as a silibinin-phosphatidylcholine combination). Milk thistle products are very safe and are frequently used in hepatic support therapy.

The prognosis may be guarded for recovery, however with aggressive nutritional therapy many, if not most, cats do recover. Several complications that can occur with therapy include a re-feeding syndrome and vomiting. The re-feeding syndrome is associated with the development of often life-threatening electrolyte disturbances that occurs within 24 to 48 hours from the start of enteral feeding.⁹ With the introduction of nutrition there is a resultant increased insulin level that drives potassium, phosphorous and magnesium into the cells causing a critical depletion of these electrolytes in the blood. This is prevented by first correcting electrolytes and then by slowly introducing food. Vomiting is also a frequent complication associated with feeding too much and too fast. If vomiting persists I will sometimes use maropitant or other antiemetics. Maropitant is metabolized by the liver and the dose I use in cats with hepatic lipidosis is lower (0.25-0.5 mg/kg SO q 24 h), with my normal cat dose being 1.0 mg/kg SQ q 24 h. Metoclopramide is not an effective antiemetic in cats. We have also used mirtazapine (Remeron^TM), a tricyclic antidepressant for humans that in cats has both antiemetic and appetite stimulant effects (approximate dose is 1/8 of a 15 mg tablet every 2 days).

When the cat is consuming adequate calories without the need for tube supplementation the feeding tube can be removed. Tube feeding time may extend for up to 4-6 weeks in some cases and consequently most cats are managed by the owner at home.

References

1.  Center SA, et al. Veterinary Clinics of North America Small Animal Practice. 2005; 246.

2.  Akol KG, et al. J Vet Intern Med 1993; 7(4):205-9.

3.  Holan KM. Kirk's Current Veterinary Therapy XIV 2008; 570.

4.  Center SA, et al. J Vet Intern Med 1993; 7:349.

5.  Griffin B. Compend Cont Educ Pract Vet 2000; 22(10):910.

6.  Center SA, et al. J Vet Intern Med 2000; 14(6):598.

7.  Jacobs GB, et al. Am J Vet Res 1990; 51(9):1349.

8.  Justin RB, et al. J Vet Intern Med 1995, 9:228.