Sudden death in association with liver disease is uncommon. Rarely, individuals will die of massive hepatic necrosis caused by fulminating hepatitis. One should always worry in such cases that the hepatitis is of a toxic nature such as that caused by an overdose of acetaminophen. In children, Reye's syndrome can cause relatively rapid death, but the condition is usually diagnosed prior to death.

Another cause of massive hepatic necrosis is ingestion of poisonous mushrooms. Amanita phalloides is one of the most commonly encountered poisonous mushrooms in the United States. It is the most dangerous, accounting for almost all fatalities. It is found in many regions of the U.S., including California, the Pacific Northwest, and the Northeast. It contains cyclopeptide toxins,73 which are potent hepatotoxins with no taste or smell that are not destroyed by cooking. Ingestion of even one mushroom can cause death. Following ingestion, there are no symptoms for several hours. Then, the victims develop nausea, vomiting, severe abdominal cramps, and watery diarrhea. They then seem to be getting better, when they develop hepatic and renal failure, become jaundiced, and develop a coagulopathy and impaired neurologic status. The signs of fulminant hepatic necrosis may not appear for a day or two. The mortality rate for Amanita phalloides poisoning is 20-30%.

In alcoholics with cirrhosis of the liver, there is a relatively obscure entity characterized by massive non-traumatic intra-abdominal hemorrhage. Di Maio reported three cases74 in which no source for the bleeding was found. Of the three, one who was briefly hospitalized showed evidence of a disseminated intravascular coagulopathy. It was the author's opinion that this was the most likely cause of the intra-abdominal hemorrhage in the two other cases and could be attributed to the cirrhosis of the liver. Two of these deaths were obviously sudden and unexpected, with one 44-year-old woman observed to become rigid and collapse while seated in a chair at home. She was found to have 2750 mL of non-clotted blood in her abdominal cavity and advanced micro-nodular cirrhosis. A second individual was a 38-year-old man who collapsed while walking from a convenience store to a parked truck. Again, there was no evidence of trauma, and 4800 mL of non-clotted blood was found in the abdominal cavity. The liver showed micro-nodular cirrhosis of an advanced degree. The third individual, who was hospitalized for 21 h, had between 2500 and 3000 mL of non-clotted blood in his abdominal cavity.

Occasionally, chronic alcoholics die suddenly and unexpectedly, without any anatomical or toxicological cause of death. At autopsy, the only finding is an enlarged liver with severe fatty metamorphosis. The toxicological screen usually shows absence of alcohol. This entity was first described by Le Count and Singer in 1926.75 By tradition, these deaths have been signed out as "fatty metamorphosis of the liver."

Alcohol, in both moderate and heavy doses, has a direct toxic effect on hepatic triglyceride metabolism, with resultant accumulation of triglycerides and phospholipids in the liver cells.76 Large and small vacuoles of fat are present in the hepatocytes and Kupffer cells. While the most common cause of the accumulation of fat in the liver is chronic abuse of alcohol, this condition can also be seen in obesity, diabetes, and viral infections as well as due to toxic compounds of phosphorous and chlorinated hydrocarbons.

While the death is certified as due to fatty metamorphosis, no one seriously believes that it is the actual cause of death. Rather, it is a marker of chronic abuse of alcohol. The present thought is that such deaths are due to cardiovascular etiologies.76 Alcoholics have a tendency to develop arrhythmias. Recent study has also demonstrated an increased QT interval and elevated plasma norepinephrine.77,78 It is thought that the effects of chronic alcoholism on the heart are fatal arrhythmia and death.

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