Fulminant Hepatic Failure

Unfortunately, a small percentage of patients with toxic acetaminophen ingestions will develop fulminant hepatic failure. The mortality rate for these patients (without NAC therapy) is estimated to be 58 to 80 percent. Most fatalities occur on days 3 to 5 after overdose and are attributed to hepatic complications such as cerebral edema, hemorrhage, shock, acute respiratory distress syndrome, sepsis, and multiorgan failure. Patients who eventually survive fulminant hepatic failure generally begin to show evidence of their recovery by days 5 to 7. Eventually, all survivors will develop complete hepatic regeneration without any persistence of hepatic impairment.

NAC also appears to be beneficial in the treatment of acetaminophen-induced fulminant hepatic failure. When compared with controls, NAC therapy was associated with increased survival (48 vs 20 percent), decreased cerebral edema (40 vs 68 percent), and decreased vasopressor requirements (40 vs 80 percent). 12 NAC appears to be beneficial in the treatment of other forms of hepatic failure, too, including viral hepatitis and alcoholic cirrhosis. 16

Prognostic indicators have been developed to determine those patients with the highest risk of mortality from acetaminophen-induced fulminant hepatic failure. As a result, they also serve as early predictors of patients who will subsequently require liver transplantation. A variety of laboratory and clinical markers have been used, including serum pH, prothrombin time (PT), serum creatinine, and mental status evaluation. The presence of a metabolic acidosis, pH < 7.3, despite fluid and hemodynamic resucitation, or a combination of coagulopathy (PT > 100), renal failure (creatinine > 3.3 mg/dL), and encephalopathy (grade III or IV) is extremely useful in predicting patients who will die without liver transplantation. 17

Treatment for acetaminophen-induced fulminant hepatic failure includes NAC therapy, aggressive correction of coagulopathy and acidosis, monitoring for and aggressive treatment for cerebral edema, and early patient referral to a liver transplant center. Unlike the treatment of early acetaminophen toxicity, NAC therapy should be continued past the 72-h standard regimen until the patient recovers, receives a liver transplant, or dies. Since all clinical studies supporting the use of NAC to treat fulminant hepatic failure utilized the IV administration of NAC, IV NAC therapy may be preferable to oral NAC. IV NAC should be administered at the same dosage as oral NAC. Because of the risk of anaphylactoid reaction, IV NAC infusions should be administered slowly and adjusted based on repeated blood pressure measurements to prevent hypotension.

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