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Abstract
Acute liver failure is a multiorgan syndrome with dramatic clinical features and,
often, a fatal outcome. It is characterized by the onset of coma and coagulopathy
within 6 months, and usually in <6 weeks, from onset of illness. Viral hepatitis,
drug-related liver injury, and the alcohol-acetaminophen syndrome are the most common
etiologies. Altered mental status accompanied by jaundice is a hallmark of acute liver
failure. A unique feature is the evolution of increased intracranial pressure due
to cerebral edema. The resulting cerebral ischemia and brainstem herniation account
for approximately 50% of deaths in patients with acute liver failure. Mannitol therapy
may successfully treat most patients with high intracerebral pressure. Most patients
demonstrate features of the multiple organ failure syndrome, including a shock-like
state, renal failure, and occasionally respiratory distress syndrome. Close monitoring
of volume status is necessary, since administration of large quantities of fluid may
be required. Infection is also common; most pathogens are gram-positive, and fungal
infections are also seen. Because an optimum therapy for acute liver failure does
not yet exist, liver transplantation should be considered early, before advanced levels
of coma develop. Alternative, experimental treatment modalities include heterotopic
liver grafting, administration of hepatocyte growth factor, use of an extracorporeal
liver-assist device, and liver cell transplantation, but none of these has attained
widespread use.
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© 1994 Published by Elsevier Inc.
