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Feline Idiopathic Hepatic Lipidosis |  |
| Feline idiopathic hepatic lipidosis is the most common cause of feline hepatopathy. The etiology is undetermined but is associated with a period of anorexia (few days to several weeks), especially in obese cats. Factors that may trigger anorexia include a change of diet to initiate weight loss or other stressful events (eg, moving, boarding, death of other pets or owners). Secondary hepatic lipidosis is associated with either a primary metabolic (eg, diabetes mellitus) or GI
disease (eg, inflammatory bowel disease, gastric foreign bodies, pancreatitis, or cholangiohepatitis) that can cause anorexia. Regardless of the inciting cause, the end result is excessive accumulation of triglycerides (fat) within the liver, which leads to severe intrahepatic cholestasis and hepatic failure. |
| Clinical Findings: |
| Clinical signs are variable but can include dramatic weight loss (30-40% of body weight, experimentally) due to anorexia, vomiting, lethargy, and diarrhea. Signs of hepatic encephalopathy are unusual, as are bleeding tendencies, but can be noted in advanced disease. Icterus or pale mucous membranes, ptyalism, hepatomegaly, and decreased body condition with retention of abdominal fat are commonly seen. Laboratory abnormalities include a nonregenerative anemia with
poikilocytosis, stress leukogram, hyperbilirubinemia and bilirubinuria, mild to moderate increases in AST and ALT and marked increase in AP; GGT values are usually normal or mildly elevated. Hypoalbuminemia, prolonged coagulation profile, and hyperammonemia have been reported in advanced disease. If the cat is not icteric, bile acids can be evaluated. Postprandial values may be difficult to obtain if the cat cannot be force-fed. However, in most cases, fasting bile acids will be
abnormal, precluding the need for the postprandial sample. Peritoneal effusion may be seen on radiographs. On ultrasonographic evaluation, the liver often appears diffusely hyperechoic when compared with the falciform ligament. If pancreatitis is also present, abdominal effusion and pancreatic changes can be identified with ultrasonography. Histopathology or cytology reveals vacuolated hepatocytes and cholestasis; lipid is identified within the vacuoles using Sudan black or oil
Red O stain. |
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| Treatment: |
| Treatment is primarily supportive, unless an underlying cause can be found. Fluid therapy, with a polyionic, isotonic solution supplemented with potassium and thiamine, is recommended to correct dehydration. Potassium phosphate should be added if the cat is hypophosphatemic. Administration of dextrose fluids can exacerbate signs of hepatic lipidosis by stimulating hepatic fat synthesis and should be avoided unless the cat is hypoglycemic. Feeding as soon as possible is
essential. Occasionally, appetite stimulants (eg, diazepam or cyproheptidine) may be helpful. However, diazepam can cause fulminant hepatic necrosis and should be used with caution. Usually, placement of a nasoesophageal, pharyngostomy, esophagostomy, or gastrotomy tube is necessary. A nasoesophageal tube can be used initially until the cat is stable and can withstand anesthesia to have a longterm feeding tube placed. A high-protein, calorie-dense, balanced diet is recommended
unless the cat shows signs of hepatic encephalopathy, in which case a low-protein diet should be used. Supplementation with taurine, carnitine, and/or arginine (250 mg of each, bid) can be considered. Initially, feedings are small and given frequently. On the first day, one-third to one-half of the cat’s ideal caloric intake is fed; the amount fed is gradually increased over the next 3-4 days until the total ideal caloric requirement is fed in 3-4 feedings.
Vomiting associated with tube feeding can be controlled with metoclopramide. Another complication associated with tube feeding is hypophosphatemia, which can lead to hemolytic anemia; therefore, phosphorus levels should be routinely evaluated. Gastritis can be controlled with H2 -blockers (eg, famotidine or ranitidine) and carafate. If clinical signs of hepatic encephalopathy are present, lactulose and metronidazole are also recommended. If pancreatitis is
concurrent, total parenteral nutrition may be necessary to prevent pancreatic secretions. Prognosis is good if the diagnosis is made early, treatment is begun, and the underlying disease, if any, can be treated. Concurrent pancreatitis is a poor prognostic indicator. Monitoring AP of obese cats on a weight-reducing diet may be effective in diagnosing preclinical hepatic lipidosis and preventing clinical signs from developing. Early dietary support for obese cats that become
anorectic because of other underlying disease is also recommended to prevent hepatic illness. |
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