Acute liver failure (ALF) is defined as the rapid and severe development of liver dysfunction, marked by encephalopathy and coagulopathy in an individual without a prior history of cirrhosis or liver disease.
Acetaminophen is the most common cause of ALF in the United States, and prompt administration of N-acetylcysteine helps to decrease mortality in acetaminophen hepatotoxicity. N-acetylcysteine may also have some benefit in nonacetaminophen hepatotoxicity.
Supportive care remains the mainstay of ALF management. Spontaneous survival rate from ALF is 40% and liver transplantation (LT) remains the only definitive therapy for patients who are unable to achieve timely regeneration of liver mass to maintain life despite adequate supportive care.
Cirrhosis is characterized by progressive hepatic fibrosis that can lead to consequences of portal hypertension including variceal hemorrhage, ascites, renal failure, and encephalopathy.
The combination of pharmacologic therapy and endoscopic variceal ligation is effective in controlling bleeding in up to 90% of patients presenting with acute variceal hemorrhage.
Hepatic encephalopathy is a frequent reason for hospital admissions. Common precipitants, such as infection, dehydration, and bleeding, should be ruled out in any patient presenting with hepatic encephalopathy.
Liver disease results in approximately 35,000 deaths each year, making it the 12th leading cause of death in the United States.1 Patients suffering from ALF or consequences of chronic liver disease are among the sickest in the hospital. These patients often develop problems that require critical care, and physicians should be knowledgeable about the various complications of liver disease that can be encountered in the intensive care unit (ICU).
There are an estimated 2000 cases of acute liver failure (ALF) annually, which accounts for 0.1% of all deaths in the United States. Approximately 6% to 7% of all LTs performed in the United States are secondary to ALF.2,3
ALF is defined as the rapid and severe development of liver dysfunction, marked by encephalopathy and coagulopathy with an elevated prothrombin time (PT) or international normalized ratio (INR), in an individual without a prior history of cirrhosis or liver disease. The exceptions to this definition are in patients who have had previously undiagnosed hepatitis B virus (HBV) infection, hepatitis D virus (HDV) infection with underlying chronic HBV infection, autoimmune hepatitis, or Wilson disease. In these patients, underlying cirrhosis may be present, provided the disease has been recognized for less than 26 weeks.
ALF can be subcategorized by the interval between the development of jaundice and onset of encephalopathy. Common classification cutoffs are: hyperacute (< 7 days), acute (8-28 days), and subacute (28 days-26 weeks). This classification can be clinically useful as cerebral edema is common in hyperacute and acute liver failure whereas complications of portal hypertension are more commonly seen in subacute liver failure.
In the United States, drug-induced hepatitis, especially acetaminophen overdose is the most common cause of ALF in adults. Other causes of ALF are listed in Table 37–1.
Table 37–1Causes of acute liver failure.