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Introduction

Feline hepatic lipidosis (FHL) is a common and potentially fatal hepatopathy of cats characterized by excessive accumulation of triglycerides in the liver, with associated severe intrahepatic cholestasis and hepatic dysfunction (Zoran 2012).

The primary form of the disease is idiopathic hepatic lipidosis (IHL) where over-conditioned cats that become anorexic are at increased risk, but the syndrome can also be seen secondary to other underlying disease conditions directly causing a catabolic state and prolonged ano­rexia. These diseases may include other liver diseases such as cholangio-hepatitis and extra-hepatic bile duct obstruction, but may also include diseases of other organ systems such as diabetes mellitus, neoplasia, hyper­thyroidism, renal disease, pancreatitis, and small intestinal disease (Center 2005). The pathogenesis remains incompletely under­stood, but involves an imbalance between peripheral fat stores mobilized to the liver, hepatic use of fatty acids for energy, and hepatic dispersal of triglycerides (Armstrong and Blanchard 2009).

Anorexia, ranging from a few days to several weeks, often precedes development of FHL and is the most common presenting com­plaint. Anorexia in otherwise healthy cats may occur due to forced overly rapid weight loss, unintentional food deprivation, change to a diet unacceptable to the cat, a sudden change in lifestyle or stress such as boarding or sur­gery, but may also be associated with other systemic diseases (Armstrong and Blanchard 2009). Rapid weight loss is common and can be profound (often >25% of body weight), with concurrent sarcopenia. Other clinical signs include lethargy, depression, vomiting, diarrhea or constipation, and an unkempt, poor quality hair coat (Armstrong and Blanchard 2009). As the disease progresses and hepatic function deteriorates, icterus (about 70% of cases) and signs of hepatic encephalopathy such as severe depression, ptyalism, and seizures ((Center 2005); however, the solution is com­monly used with success by many clini­cians (Hill and Armstrong 2014)

o Avoid dextrose supplementation unless hypoglycemia is present, as dextrose supplementation promotes hepatic lipid deposition, inhibits fatty acid oxidation, and worsens electrolyte depletion (Hill and Armstrong 2014)

o Correct all fluid and electrolyte imbal­ances before anesthesia is attempted for feeding tube placement (Armstrong and Blanchard 2009)

• Vitamin Ki: 0.5-1.5mg∕kg SC BID for three injections to treat coagulopathy

î Allow adequate response interval after initiation of Vitamin K therapy before fine needle aspirates or biopsies of the liver are obtained (Center 2005)

• Supplement water-soluble vitamins

î B-complex vitamins: Add to IV fluids (1-2 ml∕L)

î Cobalamin (Vitamin B12): 250 μg SC once weekly for six weeks if decreased serum cobalamin is documented; this happens primarily where there is under­lying gastrointestinal disease (Hill and Armstrong 2014)

î Thiamine: 50-100 mg PO/cat/day for one week if severe ventroflexion of the neck is present (Center 2005)

• Enteral feeding

î Enteral feeding must be initiated as early as possible.

Oral forced feeding is not advised, as it is generally inadequate to provide enough calories to reverse FHL. Force-feeding can also be stressful and may exacerbate nausea and vomiting. It can also result in aversion to food, which may delay the return to voluntary food intake (Zoran 2012)

î Provision of adequate calories to reverse the progression of FHL usually requires placement of a feeding tube. In critically ill cats with FHL, the stress of general anes­thesia may be fatal thus the initial feeding should be given via a naso-esophageal tube (Hill and Armstrong 2014)

î Once the cat is more stable, general anesthesia for long-term feeding tube placement can be safely accomplished (Zoran 2012)

• Appetite stimulants

î Oral appetite stimulants such as mir­tazapine or cyproheptadine are not rec­ommended, as they are unreliable for ensuring the adequate caloric intake that is required for successful therapy for FHL (Hill and Armstrong 2014)

î Oral diazepam should be avoided, as it can also cause idiosyncratic hepatic necrosis in cats (Zoran 2012)

• Blood transfusions are sometimes required for treatment of severe anemia (Center 2005)

Chronic Therapy

• Place an esophagostomy (or gastrostomy) tube for chronic long-term feeding

î An esophagostomy (or gastrostomy) tube allows feeding of a blended solid canned food diet in the home environ­ment until the FHL is resolved and ade­quate voluntary food intake resumes (Zoran 2012)

î Diets selected for cats with FHL should ideally be high in protein and have lower amounts of carbohydrates, with the remaining calories coming from fat (Zoran 2012). Many commercially avail­able diets meet these requirements including Maximum Calorie (IAMS Veterinary Formula) and Prescription Diets a/d or m/d (Hill's Pet Nutrition). Maximum Calorie is often preferred for tube feeding because of its high caloric density - it provides 2.1 kcal/ml, while most other commercial recovery­formula foods typically provide about 1kcal/ml.

A higher caloric density food allows daily energy requirements to be met with a lower total food volume (Hill and Armstrong 2014)

î Do not restrict dietary protein unless overt signs of hepatic encephalopathy are present (Hill and Armstrong 2014)

î Provide 40-60 kcal/kg/day. Start with tube feeding of ¼ to ½ of daily require­ments, divided into four to six feed­ings. Gradually increase to daily requirements over three to four days (Zoran 2012)

î Tube feeding is usually required for 3-6 weeks, pending clinical and biochemical improvement - total bilirubin concen­tration is expected to decrease by at least 50% within 7-10 days, although serum liver enzyme activities often require longer to decrease (Armstrong and Blanchard 2009) î Remove feeding tube only when the cat is eating on its own for at least a week (Zoran 2012).

• Control vomiting

î Vomiting is a common problem in cats with FHL and often persists during the first week of re-feeding despite gradual introduction of increasing meal volumes

î Maropitant 1 mg/kg SID IV, SC or PO is the drug of choice (Zoran 2012); however as the liver metabolizes maropitant, a dosage of 0.5 mg/kg is sometimes used. Maropitant may also provide visceral analgesia, which would be useful in cases with concurrent pancreatitis (Hill and Armstrong 2014)

î Metoclopramide 0.2-0.5 mg/kg TID SC/ PO or CRI 1-2 mg/kg/day. Metoclo­pramide is a weak antiemetic in cats, but is commonly used for its prokinetic effects (Hill and Armstrong 2014)

î Ondansetron 0.1-1 mg/kg SID-BID IV/ PO or dolasetron 0.5-1 mg/kg q SID-BId IV/PO is advised if vomiting persists (Zoran 2012)

î Famotidine 0.5-1mg/kg q SID-BID IV/ PO, a H2 receptor antagonist, can be added in persistently vomiting cats to protect the lower esophagus from acid damage (Armstrong and Blanchard 2009)

• Dietary supplements (used empirically): Supplementation with specific micronutri­ents has been suggested by some authors (Center 2005). Until more evidence becomes available, the use of these supple­ments is based purely on clinician prefer­ence and experience.

Clinicians should also consider that prescribing multiple supplements and medications might risk decreasing client compliance with feeding instructions.

î S-Adenosylmethionine (SAMe): 20 mg/ kg PO OID (Zoran 2012)

î SAMe is an important hepatocellular metabolite and glutathione donor with hepatic and systemic antioxidant effects (Center 2005) î L-carnitine: 250-500 mg PO SID. L-carnitine is an essential cofactor for fatty acid oxidation; a relative carnitine deficiency is believed to exist in FHL (Center 2005)

î Taurine: 250-500 mg PO SID for the ini­tial 7-10 days of treatment. Taurine is an essential amino acid for cats and is required for bile acid conjugation; plasma taurine levels have been found to be decreased in many cats with FHL (Center 2005) Some recovery formula diets (for example Hill's a/d) are already high in taurine (Hill and Armstrong 2014)

î Vitamin E (water soluble form): 50-100 units/cat PO SID, which is an important antioxidant (Center 2005).

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Source: Gram W.D., Milner R.J., Lobetti R. (eds.). Chronic Disease Management for Small Animals. Wiley,2018. — 357 p.. 2018

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