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Feline Hepatic Lipidosis (FHL) is the most prevalent hepatobiliary disorder in cats, distinguished by excessive triglyceride (TG) accumulation within hepatocytes, resulting in hepatic dysfunction and intrahepatic cholestasis. This condition, often precipitated by prolonged anorexia.

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Pathophysiology

FHL is primarily driven by a negative energy balance, which triggers excessive mobilization of fatty acids to the liver. Key metabolic derangements include:

• Impaired β-oxidation: The liver’s inability to process fatty acids effectively.

• Deficiencies: Essential fatty acids (EFAs), amino acids like arginine, taurine, and methionine.

• Insulin Resistance: Elevated glucagon, cortisol, and other counter-regulatory hormones exacerbate the mobilization of non-esterified fatty acids (NEFAs), promoting fat deposition in hepatocytes.

 

Hepatic TG accumulation overwhelms cellular mechanisms, leading to reduced hepatic function and systemic complications such as hepatic encephalopathy (HE) and coagulopathy.

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Clinical Presentation

• Signalment: Middle-aged cats (median age: 7 years), often with a history of obesity.

• Key Signs: Icterus, vomiting, lethargy, dehydration, and significant weight loss.

• Neurological Signs: Mentation changes, ptyalism, or ventroflexion of the neck due to hypokalemia or HE.

 

Diagnostics

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1. Laboratory Findings:

   • Elevated ALP with disproportionate GGT elevation (key differentiator).

   • Hyperbilirubinemia, hyperglycemia, hypoalbuminemia, and electrolyte imbalances (hypokalemia, hypophosphatemia).

2. Imaging:

   • Ultrasonography reveals an enlarged, diffusely hyperechoic liver compared to falciform fat.

3. Definitive Diagnosis:

   • Fine-needle aspirates showing macrovesicular or microvesicular steatosis confirm lipidosis.

 

Treatment Protocol

Early intervention is paramount to successful outcomes:

1. Fluid and Electrolyte Therapy:

   • Correct dehydration and imbalances using isotonic crystalloids.

   • Address hypokalemia and hypophosphatemia prior to initiating feeding.

2. Nutritional Support:

   • Cornerstone of Therapy: Enteral feeding, preferably via nasoesophageal or esophagostomy tubes.

   • High-protein, moderate-fat, low-carbohydrate diets are essential.

   • Gradual caloric introduction prevents refeeding syndrome.

3. Pharmacologic Support:

   • Antiemetics (maropitant, ondansetron) for nausea control.

   • Vitamin K1 for coagulopathy management.

   • Supplements such as L-carnitine (250–500 mg/day) to enhance β-oxidation and reduce TG accumulation.

4. Adjunctive Care:

   • Gastroprotectants to prevent reflux esophagitis.

   • Monitoring for complications like disseminated intravascular coagulation (DIC).

 

Prognosis and NAVLE Insights

• Prognosis: 80-85% survival with early and aggressive treatment.

• Key NAVLE Takeaways:

  • Recognize hallmark lab findings, including ALP:GGT discrepancies.

  • Prioritize early nutritional intervention over forced feeding.

  • Monitor for refeeding syndrome during reintroduction of caloric intake.

  • Understand the association of underlying diseases such as pancreatitis, inflammatory bowel disease, or neoplasia with secondary hepatic lipidosis.

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