2012年AASLD急性肝衰竭指南

The diagnosis of ALF hinges on identifying that thepatient has an acute insult and is encephalopathic.Imaging in recent years has suggested "cirrhosis," butthis is often an overcall by radiology, because a regenerating massively necrotic liver will give the same nodular profile as cirrhosis. It is vital to promptly get viral hepatitis serologies, including A-E as well as autoimmune serologies, because these often seem to be neglected at the initial presentation. Fulminant Wilson’s disease can be diagnosed most effectively not by waiting for copper levels (too slow to obtain) or by obtaining ceruloplasmin levels (low in half of all ALF patients, regardless of etiology), but by simply looking for the more readily available bilirubin level (very high) and alkaline phosphatase (ALP; very low), such that the bilirubin/ALP ratio exceeds 2.0.The availability of an assay that measures acetaminophen adducts has been used for several years as a research tool and has improved our clinical recognition of acetaminophen cases when the diagnosis is obscured by patient denial or encephalopathy. Any patient with very high aminotransferases and low bilirubin on admission with ALF very likely has acetaminophen overdose, with the one possible exception being those patients who enter with ischemic injury. Obtaining autoantibodies should be routine and a low threshold for biopsy in patients with indeterminate ALF should be standard, given that autoimmune hepatitis may be the largest category of indeterminate, after unrecognized acetaminophen poisoning.