- 1 1. What is hepatic lipidosis?
- 2 2. What is acute hepatitis?
- 3 3. What historical questions should be asked of clients with animals with suspected acute hepatitis?
- 4 4. What population of cats typically develops idiopathic hepatic lipidosis?
- 5 5. What historical complaints are commonly associated with acute hepatitis or lipidosis?
- 6 6. What physical abnormalities are commonly detected in animals with acute hepatitis or lipidosis?
- 7 7. What diagnostic tests should be considered for animals with suspected acute hepatitis or lipidosis?
- 8 8. What routine laboratory abnormalities are most consistent with acute hepatitis or lipidosis?
- 9 9. What ancillary diagnostic tests help to determine the cause of liver disease in animals with suspected acute hepatitis or lipidosis?
- 10 10. Do I need to perform a hepatic biopsy for all animals with suspected acute hepatitis or lipidosis?
- 11 11. What immediate supportive care should be provided to animals with suspected acute hepatitis or lipidosis?
- 12 12. What is the prognosis for recovery from idiopathic hepatic lipidosis?
1. What is hepatic lipidosis?
Hepatic lipidosis is a common disease of cats in which excessive fat accumulates in hepatocytes and may lead to severe intrahepatic cholestasis and progressive liver failure. Most cases in cats are idiopathic. Diabetes mellitus, pancreatitis, cholangiohepatitis, hyperthyroidism, hypertrophic cardiomyopathy, renal disease, chronic cystitis, chronic upper respiratory infections, hyperadrenocorticism, and neoplasia also have been detected in some cats with hepatic lipidosis. Most dogs with hepatic lipidosis have another underlying disease process.
2. What is acute hepatitis?
Acute hepatitis refers to any condition that causes inflammation and swelling of the liver. Injury may be precipitated by drugs, trauma, toxins, and infectious agents. In addition, immune-mediated diseases, inborn errors of metabolism (copper toxicity in Bedlington terriers is an example), and neoplastic diseases may result in acute hepatitis. Acute hepatitis also accompanies acute pancreatitis in both dogs and cats.
3. What historical questions should be asked of clients with animals with suspected acute hepatitis?
Drug administration, trauma, and toxin exposure should be ruled out by history. Many drugs, including potentiated sulfonamides, carprofen, anthelmintics such as metronidazole, and benzodiazepines have been associated with acute hepatitis or acute hepatic necrosis. It should be determined whether the animal has ingested moldy food; aflatoxins produced by some fungi are potent hepatotoxins. Travel and vaccination histories are important; leptospirosis may result in acute hepatitis in dogs and is a direct zoonosis.
4. What population of cats typically develops idiopathic hepatic lipidosis?
Middle-aged cats are primarily affected, but cats of any age may develop hepatic lipidosis. There does not appear to be a breed or sex predisposition. A large percentage of affected cats are obese before onset of clinical signs.
5. What historical complaints are commonly associated with acute hepatitis or lipidosis?
Anorexia occurs in most animals. In cats with idiopathic lipidosis, a stressful episode such as surgery, boarding, moving, or a new member in the household may precede appetite loss. Lethargy, depression, icterus, ptyalism, and vomiting are also commonly reported with acute hepatic diseases. Diarrhea is uncommon with idiopathic lipidosis but occurs in some animals with acute hepatitis. Hepatic encephalopathy (HE), characterized by head pressing, stupor, and coma, occurs in some animals with acute hepatic diseases.
6. What physical abnormalities are commonly detected in animals with acute hepatitis or lipidosis?
Depression, icterus, and dehydration are common. At presentation, most cats with idiopathic hepatic lipidosis have lost as much as 25-50% of their previous body weight. Most animals with acute hepatitis have clinical signs of shock, including elevated heart rate, pale mucous membranes, increased capillary refill time, and weak pulse. Liver size may be normal, increased, or decreased, depending on the primary cause and duration of the disease process before acute presentation. Animals with chronic hepatic disease that present with an acute exacerbation may have abdominal distention due to sustained portal hypertension or hypoalbuminemia-associated transudative ascites.
7. What diagnostic tests should be considered for animals with suspected acute hepatitis or lipidosis?
Complete blood count, platelet count, serum biochemistry panel, activated clotting time, and urinalysis should be assessed on admission. Packed cell volume, total protein, blood glucose, electrolytes, and coagulation should be assessed as soon as possible and emergency treatment initiated as indicated. Coagulation should be assessed because hepatic aspiration or biopsy is often indicated and disseminated intravascular coagulation is common, particularly in animals with acute hepatitis.
8. What routine laboratory abnormalities are most consistent with acute hepatitis or lipidosis?
Although no pathognomonic changes in complete blood count are associated with hepatic lipidosis, mild nonregenerative anemia, neutrophilia, or neutropenia may be noted. Increases in liver enzyme activities are common; any combination of increased activity of alanine transferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), or gamma-glutamyl transferase (GGT) may occur. In most cats, increases in ALP and GGT activities are greater than increases in ALT and AST activities. Lack of increased liver enzyme activities does not exclude the diagnosis of idiopathic hepatic lipidosis. Hyperbilirubinemia and bilirubinuria occur in most cats with idiopathic hepatic lipidosis. Findings are similar with acute hepatitis, but increases in alanine transferase and aspartate aminotransferase activities are usually greater than increases in alkaline phosphatase and gamma-glutamyl transferase activities.
9. What ancillary diagnostic tests help to determine the cause of liver disease in animals with suspected acute hepatitis or lipidosis?
Fasting and postprandial serum bile acids are usually markedly increased but do not need to be measured if hyperbilirubinemia is present. Fasting serum ammonia concentrations may be elevated and can be used for indirect assessment of the presence of hepatic encephalopathy. Abdominal radiographs, hepatic ultrasound, pancreatic ultrasound and trypsin-like immunoreactivity (TL1) tests may be used to narrow the differential list in animals with acute hepatic disease.
10. Do I need to perform a hepatic biopsy for all animals with suspected acute hepatitis or lipidosis?
A presumptive diagnosis of idiopathic hepatic lipidosis in cats may be made by the combination of appropriate history, laboratory abnormalities, and vacuolated hepatocytes on cytologic evaluation of a fine aspirate of the liver. If the cause of hepatitis is determined by history (trauma, drugs, toxins) or other findings (pancreatitis), biopsy may not be needed. However, the reference test for hepatic diseases is hepatic histologic evaluation. If hepatic aspiration or biopsy is performed, samples should be cultured for aerobic and anaerobic bacteria.
11. What immediate supportive care should be provided to animals with suspected acute hepatitis or lipidosis?
Fluid, electrolyte, acid-base, coagulation, and glucose abnormalities should be corrected as discussed in other chapters. Depending on acid-base and electrolyte status, 0.45% NaCl and 2.5% dextrose or Normosol-R are appropriate fluid choices. Potassium supplementation is required for most cases. Antibiotics should be administered to all animals with suspected acute hepatitis because bacterial translocation from the intestines into the liver is common. Penicillin derivatives or first-generation cephalosporins administered parenterally are adequate if clinical findings of sepsis are not present. Enrofloxacin should be considered in animals with suspected gram-negative sepsis. Vitamin K should be given subcutaneously to animals with increased activated clotting time. Supplementation with B vitamins is suggested for most cases. Hepatic encephalopathy, if present, is managed as described for portosystemic shunts (see chapter 83). Appetite stimulants, including cyproheptadine and benzodiazepams, generally are not successful alone. Benzodiazepams may lead to severe sedation if hepatic dysfunction is severe and have been associated with liver failure.
Whether enteral feeding is indicated depends on the cause of the disease. Early, aggressive nutritional therapy is the key to successful treatment of idiopathic hepatic lipidosis in cats. Initial short-term nutritional support may be provided by a nasoesophageal tube. However, because nutritional support is required for at least 3-6 weeks in most cases, a gastrostomy tube is strongly recommended. Multiple small meals should be fed to cats to provide a total of 60-80 kcal/kg/day. Most full-grown cats can handle 50-80 ml of food per feeding when the volume of food at each meal is gradually increased over several days. Protein should not be restricted unless signs of hepatic encephalopathy are present. Food should always be offered by mouth; the tube can be pulled after eating begins and liver enzymes have returned to normal.
12. What is the prognosis for recovery from idiopathic hepatic lipidosis?
The prognosis is guarded to fair, depending on how early the disease is recognized. The conditions can be reversed with aggressive nutritional therapy. Owners must be counseled that recovery may require up to 20 weeks before spontaneous eating occurs. Without treatment, hepatic lipidosis is usually fatal, leading to progressive liver failure.