Page 912 - Cote clinical veterinary advisor dogs and cats 4th

Hepatic Lipidosis 445

• Cervical ventroflexion ○ Electrolyte abnormalities: hypokalemia, Acute General Treatment
• Ptyalism hypomagnesemia, and hypophosphatemia • Nutritional therapy is crucial and usually
VetBooks.ir Etiology and Pathophysiology ○ Hyperglycemia due to insulin resistance • If an underlying cause of secondary HL Diseases and Disorders
requires a feeding tube.
are common and prognostically significant.
• Poor hair coat
is identified, treatment should be directed
is more likely than hypoglycemia due to
• Hepatic lipidosis can develop rapidly (after
disorders.
2-14 days of inappetence). liver failure in cats. Hypoglycemia is often at it. Often, there is no quick fix for such
recognized in young, toy-breed dogs with
• Anorexia in cats results in a negative energy HL. • Dehydration is common, and fluid resuscita-
balance and deficiency of obligatory essential ○ Mild hypoalbuminemia or low blood urea tion is important, especially in hypovolemic
fatty acids (FAs), amino acids, and vitamins nitrogen (BUN) sometimes identified and hypotensive patients.
and is the primary initiating cause for HL. • Urinalysis: bilirubinuria common, urine often ○ Balanced isotonic crystalloid infusion (0.9%
• An imbalance develops between the influx of minimally concentrated to isosthenuric, and NaCl or Plasmalyte-A) is recommended.
FAs, rate of hepatic FA oxidation for energy, biurate crystals sometimes found ○ Avoid lactated Ringer’s solution because it
and the dispersal of hepatic triglycerides by • Coagulation abnormalities: prolonged pro- contains lactate as a buffer, which requires
excretion of very low-density lipoproteins. thrombin (PT) and activated partial throm- hepatic metabolism and may worsen
• Triglycerides primarily accumulate in the boplastin times (aPTT) are common, as are hyperlactatemia.
liver with HL; however, the exact metabolic clinical bleeding tendencies (45%-73%) ○ Start with small-volume resuscitation
abnormalities causing the accumulation are • Abdominal radiography: ± hepatomegaly (5-10 mL/kg IV bolus given over 30
not completely understood. (not specific for HL) minutes) in hypovolemic cats with serial
• HL has been reported in young, toy-breed, • Abnormal ultrasonography: diffuse hepa- assessment of hydration and perfusion.
anorexic puppies after development of tomegaly with a hyperechoic echogenicity ○ Calculate correction of dehydration (% of
hypoglycemia. Hypoglycemia develops due compared with the falciform fat and normal body weight) + maintenance fluid require-
to inadequate glyconeogenesis to sustain their echotexture. This is a highly sensitive finding, ments (40-60 mL/kg/d) ± ongoing losses
high basal metabolic energy requirements. although it is important to note that healthy (vomiting, diarrhea, polyuria; 2-6 mL/
obese cats and cats with infiltrative liver kg/h), and administer IV over 24 hours.
DIAGNOSIS disease can have similar hepatic ultrasound • Electrolyte abnormalities should be corrected
findings. before starting nutritional therapy.
Diagnostic Overview • Measurement of serum bile acids is not useful • Additional therapies
A presumptive diagnosis is based on the patient’s in icteric patients. ○ Antiemetics often indicated. The following
presentation, clinicopathologic findings, and • Although technically difficult and not can be used alone or in combination.
hepatic ultrasound, with diagnosis confirmed widely used, measurement of blood ■ Maropitant 1 mg/kg IV or SQ q 24h
by hepatic cytology (or less commonly, histo- ammonia can support recognition of hepatic ■ Ondansetron 0.1-0.5 mg/kg IV q 8-12h
pathology). Confirmation is important because encephalopathy. ■ Metoclopramide 0.2-0.5 mg/kg PO,
inflammatory or neoplastic hepatic disease can SQ, or IM q 6-8h or 0.01-0.09 mg/kg/h
have a similar presentation. Because secondary Advanced or Confirmatory Testing IV as a constant-rate infusion (CRI)
HL is common, efforts should be made to • Hepatic cytology (p. 1112) ○ Consider treatment for GI ulceration
identify an underlying disease process. ○ Least invasive and most cost-effective (pantoprazole 1 mg/kg IV q 12h or
○ Small sample size and lack of architectural omeprazole 1 mg/kg PO q 12h).
Differential Diagnosis detail limit diagnostic accuracy for many ○ Vitamin K 1 0.5-1.5 mg/kg PO or SQ q
• Icterus (p. 1243) liver diseases, but cytology often adequate 12h for 3-4 doses if a bleeding tendency
• Inflammatory biliary or hepatopathies, for HL. is noted
including cholecystitis, cholangitis, and ○ Expect abnormal retention of lipids • If necessary, address hepatic encephalopathy
cholangiohepatitis (macrovesicular or microvesicular steatosis) (p. 440).
• Neoplasia (p. 1230) in > 80% of the hepatocytes.
• Hepatotoxins and adverse drug reactions ○ Can rule out some neoplastic and infec- Chronic Treatment
(p. 1231) tious causes of hepatopathy • Maintain tube feeding until appetite
• Infectious hepatopathy (p. 1230): feline infec- • Hepatic biopsy (p. 1128) permits a more normalizes.
tious peritonitis, cholangitis, histoplasmosis, accurate characterization of hepatic pathology • In cats with secondary HL, chronic therapy
liver flukes, toxoplasmosis, cytauxzoonosis but is often unnecessary. is directed at the cause.
• Ischemia/hypoxic injury, including surgical ○ On gross examination, liver is enlarged,
hypotension and hypoxia diffusely pale yellow. Nutrition/Diet
• GI disorders: inflammatory bowel disease, ○ Many cats are at increased surgical risk • Dietary therapy is essential in treating
intestinal neoplasia, foreign bodies (coagulopathy common); assay coagulation primary and secondary HL to reverse the
• Severe systemic or metabolic disorders: acute before biopsy, and prepare for transfusion negative energy balance and catabolic state.
pancreatitis, sepsis, heat stroke, trauma if necessary. • Ideally, initiate a nutrition plan the day of
○ Expect diffuse microvesicular or macrove- admission as soon as severe electrolyte abnor-
Initial Database sicular vacuolation within hepatocytes. malities and hypoperfusion are addressed.
• CBC: low-grade, nonregenerative anemia and • If no clinical signs of HE, provide a diet
leukocytosis, neutrophilic left shift and/or TREATMENT that is high in protein (30%-40% of the
thrombocytopenia, if present, are usually metabolizable energy [ME]), moderate in
secondary to underlying disease. Treatment Overview lipids (approximately 50% of the ME) and
• Serum biochemical profile The cornerstone of treatment of HL is early reduced in carbohydrates (approximately
○ Increased serum alkaline phosphatase nutrition with the goal of achieving a posi- 20% of the ME)
(ALP) activity is extremely common. A tive calorie balance. This usually involves the ○ Most feline veterinary recovery diets meet
greater magnitude of increase in ALP com- placement of an enteral feeding tube. As with these requirements.
pared with gamma-glutamyl transferase all systemically ill cats, correction of hypo- ○ Providing a diet with lower protein content
(GGT) is strongly suggestive of HL. perfusion and electrolyte derangements is very (25% of the ME) was shown to attenuate
○ Hyperbilirubinemia is common. important. but not ameliorate HL.

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