Acute liver disease and hepatoencephalopathy (Proceedings)

Aug 01, 2011

Liver disease is common in both dogs and cats, but acute liver disease is far less common than chronic hepatic disease in either species. Also, it should be noted that many patients with an acute onset of clinical signs suggestive of liver disease actually do have chronic liver disease. This is because chronic liver disease often remains subclinical for quite some time and clinical signs only occur when the disease process becomes more severe or has destroyed a significant portion of hepatic function leading to acute signs of liver failure. One such example would be chronic hepatitis due to phenobarbital administration. Most of these patients have no clinical signs for years even though biochemically hepatic disease is evident. Only when hepatic function has been compromised significantly do these patients present with an apparently acute onset of clinical signs, such as anorexia, vomiting, ascites, hepatoencephalopathy (HE), and even bleeding diathesis. Thus, hepatoencephalopathy and other clinical signs of hepatic failure are not necessarily associated with acute hepatic disease, but are instead associated with hepatic failure.

Acute liver disease – Acute hepatitis

Both infections and toxicities can lead to acute hepatitis. While infections, for example with infectious canine hepatitis or leptospirosis lead to hepatic necrosis and secondary inflammation due to the infectious organism, toxic causes through chemicals or medications lead to hepatocellular necrosis due to the toxic substance with secondary inflammation.

Clinical signs

Acute hepatitis may be associated with fever, anorexia, vomiting, depression, and dehydration. In severe cases, clinical signs of liver failure maybe seen in addition, such as HE, jaundice, ascites, and/or bleeding diathesis. Also, the underlying disease process may affect other organ systems and may thus be associated with additional clinical signs. For example, most cases of canine leptospirosis are associated with renal failure and acute hepatitis.


A serum chemistry profile in patients with acute hepatitis usually shows severe increases of all serum hepatic enzyme activities, most importantly alanine amino transferase (ALT). Biochemical changes can also indicate hepatic failure and may include hyperbilirubinemia, hypoalbuminemia, decreased BUN concentration, or hypoglycemia. Hyperammonemia, thrombocytopenia, and alterations on a coagulation profile may also be observed.

Ultimately, a diagnosis of acute hepatitis is dependent on a biochemical diagnosis of hepatic injury with or without hepatic failure, a history of a potential etiology, and the histopathologic confirmation of hepatic necrosis and inflammation. Histopathology may also be helpful in suggesting a specific etiology (e.g., frequent mitotic figures in canine patients with leptospirosis). Also, serology is useful to diagnose leptospirosis as an underlying cause of the acute hepatitis.


The therapeutic goals in patients with acute hepatitis are to treat a confirmed or suspected underlying cause, administer supportive care, and employ symptomatic therapy for hepatic failure. If leptospirosis is confirmed or heavily suspected the patient should be treated with ampicillin (22 mg/kg IV q 6-8 hrs) or preferably doxycycline (5 mg/kg IV or PO q 12 hrs). In cases of suspected acetaminophen or phalloidin intoxication the patient should be treated with silymarin (50 mg/kg PO q 24 hrs). Also, N-acetylcysteine and vitamin C may be useful to treat patients with acetaminophen intoxication. Patients with mild hyperbilirubinemia, but no evidence of fulminant hepatic failure may benefit from treatment with ursodeoxycholic acid.

Patients with bleeding diathesis need to be treated with fresh frozen plasma. Patients with HE need to be treated as described below.