Clinical features

Patients with acute liver failure are jaundiced as the liver fails to conjugate and excrete bilirubin. Their laboratory values demonstrate marked transaminase elevation (AST and ALT in the range of 1000-5000), as liver cells are injured. Synthetic function is compromised and coagulopathy occurs as a consequence of clotting factor depletion. Disseminated intravascular coagulation (DIC) can also contribute to clotting abnormality.

Life threatening hypoglycemia may develop secondary to impaired gluconeogenesis and depletion of glycogen stores.

Hepatic encephalopathy is a key feature of FHF. Four clinical grades are recognized:

• Grade 1: Awake, mild confusion, altered personality.

• Grade 2: Awake, agitated, disoriented, hallucinations.

• Grade 4: Comatose, but with intact pupillary reflexes and usually ability to withdraw to pain.

Importantly, hepatic encephalopathy in the acute setting differs from that of encephalopathy related to cirrhosis and chronic liver failure. In chronic hepatic failure, encephalopathy is related to increased ammonia levels. Conversely, encephalopathy in FHF is related to cerebral edema. Thus, worsening of encephalopathy in patients with FHF is a sign of progressive edema and a poor prognostic indicator. Progression to central herniation is possible in these patients.

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