Alcoholism is rampant in U.S. and world. People like you reading this page know someone who is alcoholic. They can be your relatives, friends or co-workers. We are all familiar with the alcohol associated problems in our daily life. These include alcohol related social, occupational, or legal difficulties such as alcohol related blackouts, argument with friends/family, marital problems, poor job performance, decreased life quality and so on. Health professionals may be familiar with the definition of alcohol abuse or alcohol dependence (as indicated in DSM-III), alcohol related health problems such as alcohol withdrawal, alcohol hepatitis, cirrhosis, GI bleeding, cardiomyopathy, and CNS complications (delirium tremens, generalized seizures), etc. However, few people are aware of the sudden death syndrome associated with alcoholism. The sudden, unexpected death associated with alcoholism is one of the most mystifying complications of the abuse of alcohol and it is an entity so poorly understood that it does not even bear a generally accepted label or name. In general, death associated with alcohol may be classified as following categories:

1. Acute alcoholism and acute alcohol poisoning
2. Chronic alcoholism
3. Increased susceptibility to diseases and conditions of all manner
4. Aggravation of existing diseases (hepatic or extra hepatic conditions)
5. Alcohol obscuring co-existing disease or injury
6. Coincidental death (alcohol use and death due to other causes)
7. Sudden, unexpected death associated with alcoholism

Alcohol associated sudden death syndrome is also termed as unexpected death associated with fatty liver syndrome. This death situation is one of the more frequent among medical examiner cases. Typically, the body was found alone at his residence and the death could not be explained with apparent reasons. Often times, victim was physically active days or even hours before the accident. Complete autopsy workup may reveal an enlarged, fatty liver plus other subtle characteristics of chronic alcoholism. Toxicological analyses revealed little or no alcohol and no other drugs, poisons, or unnatural chemicals. The victim always had a background as a heavy drinker, but has not had a drink in the previous 12 to 36 hours prior to the sudden event. Occasionally these deaths were witnessed. On these occasions, the clinical picture was one of lack of coherence, chills or minor tremors, pallor, sweating, and collapse. In medical examiner's office, it has been traditional to certify these deaths as "fatty liver," "hepatic failure," or simply "chronic alcoholism." The manner of death was ordinarily certified as natural (the classification of death includes natural, accident, suicide or homicide). Various explanations to the sudden unexpected death have been offered and there has been little data to support each of these. Speculations were generally in the area of metabolic derangements such as hypoglycemia, hypocalcemia, magnesium deficiency, alkalosis, or alcoholic ketoacidosis. Some suggested a possible relationship of death to delirium tremens although the mechanism and pathogenesis of delirium tremens are unknown. The once held theory of massive fat embolization to the lung from the fatty liver as a cause of death was not substantiated by autopsy findings.

Medical research to date has attempted, but was unable to reveal the cause of alcohol associated sudden death syndrome. For example, the study on the relationship of alcohol to sudden natural death found only associations between alcohol and fatty liver (May, 1980). Of 172 sudden nontraumatic deaths, 16 were attributed to fatty liver alone and 74 to other causes with concomitant fatty liver, while 82 had no fatty liver. A study of victims of alcohol abuse was performed on the case files of the Office of the Medical Examiner of Metropolitan Dade County in Miami, Florida (Copeland 1985). During the year 1983, all cases in which alcoholism, either acute or chronic, was the cause of death primarily or contributory in a natural or accidental manner of death were collected. These 118 cases were then analyzed as to the age, race, sex, and cause of death of the victim along with the blood alcohol content, the drugs detected at autopsy, the scene circumstances, the geographic location of the terminal incident, noting whether or not there was a history of drinking prior to the terminal incident, the average weights of key target organs, and the histopathology of the liver. The most common victim is an older, white male who dies from "chronic alcoholism" with a terminal negative blood alcohol. This victim is usually "found dead" at home with a past history of drinking, and histopathologically the liver depicts fatty metamorphosis rather than cirrhosis. Hepatic fatty change is a common lesion. Two forms are recognized: micro- and macrovesicular steatosis, the former being much less frequent and more serious than the latter.

Taff suggested that sudden death may be due to delayed rupture of hepatic subcapsular hepatoma. He indicated that rupture of a hepatic subcapsular hematoma is a relatively rare cause of sudden death following minor blunt abdominal trauma. Death may be delayed several days to weeks.  A case of alcoholic who died of a ruptured hepatic subcapsular hematoma was presented in the paper (Taff, 1990). The death investigation of the case revealed that the victim had sustained blunt abdominal trauma during a fall a few days prior to death.

Yoshida suggested the association of sudden death and alcohol withdrawal (Yoshida 1990). He described a 50-year-old driver was arrested in a drunken stupor while he was driving a track. The driver suddenly died after five days of the arrest in a jail. As time went by, various symptoms of alcohol withdrawal appeared. He was in the state of delirium treatments for about a day before he died. Gross and microscopical examination revealed fibrosis and fatty degeneration of liver and heart lesions representing chronic and acute ischemia. The cause and the mechanism of the death in the case were discussed.

Randall proposed that the cause of sudden death may be related to the hyperacute ethanol withdrawal. He noticed that there is a generally unrecognized epidemic of sudden, nonviolent deaths among alcohol abusers, largely due to fatty liver-related sudden deaths. Using data from the North Carolina Office of the Chief Medical Examiner, 411 cases of fatty liver-related sudden deaths were identified from 1972 through 1976. He suggested a alcohol related sudden death rate of epidemic proportions, considering a low autopsy rate among nonviolent alcohol abuser deaths and the lack of awareness of such death. The study revealed the high incidence of low-level (1 to 50 mg/dL) blood ethanol levels among these sudden death as compared with control groups. Author concluded that low blood alcohol level in alcohol related sudden death was in consistent with theory linking these deaths to some form of acute or hyperacute ethanol withdrawal phenomenon (Randall 1980b).

Yuzuriha suggested that the extensive microvesicular fatty change superimposed on macrovesicular fatty change could be a cause of sudden death. They have scrutinized both the clinical and pathological data of 11 subjects who died under such circumstances between 1987 and 1993 (Yuzuriha, 1997). It was described that death may follow several days of uninterrupted drinking often with little dietary intake. The notable clinical features at the emergency room were disturbance of consciousness, hypotension, hypothermia, hypoglycaemia, metabolic acidosis, renal dysfunction and hyperammonaemia. The common hepatic pathology was the extensive appearance of numerous microvesicular fatty droplets in the hepatocytes together with varying degrees of macrovesicular fatty change. Some subjects had an underlying cirrhosis. Author suggested that the death undoubtedly results from a variety of metabolic disturbances triggered by the combination of massive ethanol intake and starvation. The appearance of extensive microvesicular fatty change superimposed on macrovesicular fatty change was considered to be an associated phenomenon.

In a review article, Randall proposed several mechanisms of sudden fatty liver deaths from nonviolent causes, including ethanol withdrawal induced hypoglycemia or hypomagnesemia, pulmonary fat embolization from fatty liver, other facets of the alcohol withdrawal syndrome, or ethanol dependent maladaptive derangements of neurotransmitters. It was also indicated that all the theories of fatty liver death were essentially untested, owing to uncontrolled postmortem conditions and the lack of awareness of fatty liver deaths within the scientific community (Randall, 1980a).

Eaton described certain biochemical effects in the pathogenesis of alcoholic fatty liver. It was stated that the pathogenesis of alcoholic fatty liver is unknown, but several causes have been proposed based on biochemical findings (Eaton, 1997). These include the metabolism of alcohol leading to a shift in the cytosolic NAD+/NADH ratio to reduction, which in turn causes a direct inhibition of beta-oxidation and enhanced triacylglycerol formation via the [glycerol-3-phosphate]/[dihydroxyacetone phosphate] ratio. There are also chronic effects of ethanol on hepatic enzyme activities. Thus, increased activity of phosphatidate phosphohydrolase, an increased amount of fatty acid binding protein, decreased secretion of very low-density lipoprotein and impairment of the respiratory chain as a result of decreased protein synthesis or decreased amounts of ubiquinone could all lead to fat accumulation and steatosis. The interplay of each of these with nutritional and genetic factors would then lead to the heterogeneity of the severity and characteristics of the steatosis observed in human alcoholics.
 
 

Conclusion

It is apparent that we do not know all of the answers about alcoholism. We even know less about the sudden death syndrome associated with alcoholism. The etiology and pathogenesis of this condition is so poorly understood to this date. Perhaps this homepage has provided reader with some information into the scope of the problem.  In a broader picture, one should be aware of that 17% US residents are suffering with depression, 14% with alcoholism, 13% with social anxiety and 11% are drug dependent. We also realize the life span of an alcoholic victim is shortened by an average of 15 years with the leading causes of death, in decreasing order, being heart disease, cancer, accidents and suicide. One's personal philosophy might be either that alcoholism is the cause of many ills or that it is a symptom or manifestation of other problems. In any event, the abuse of alcohol is in itself a monumental problem in this world.
 
 

Reference

Copeland, A. R. (1985). "Sudden death in the alcoholic." Forensic Sci Int 29(3-4): 159-69.
Eaton, S., C. O. Record, et al. (1997). "Multiple biochemical effects in the pathogenesis of alcoholic fatty liver." Eur J Clin Invest 27(9): 719-22.
May, S. J., L. H. Kuller, et al. (1980). "The relationship of alcohol to sudden natural death. An epidemiological analysis." J Stud Alcohol 41(7): 693-701.
Randall, B. (1980a). "Fatty liver and sudden death. A review." Hum Pathol 11(2): 147-53.
Randall, B. (1980b). "Sudden death and hepatic fatty metamorphosis. A North Carolina survey." Jama 243(17): 1723-5.
Taff, M. L., A. A. Wolodzko, et al. (1990). "Sudden death due to delayed rupture of hepatic subcapsular hematoma following blunt abdominal trauma." Am J Forensic Med Pathol 11(3): 270-4.
Yoshida, K., M. Funahashi, et al. (1990). "Sudden death of alcohol withdrawal syndrome--report of a case." Nippon Hoigaku Zasshi 44(3): 243-7.
Yuzuriha, T., M. Okudaira, et al. (1997). "Alcohol-related sudden death with hepatic fatty metamorphosis: a comprehensive clinicopathological inquiry into its pathogenesis." Alcohol Alcohol 32(6): 745-52.
EtOH: ethyl alcohol
 

Suggested Readings

The Alcoholic Republic: An American Tradition If you don't understand drinking, you don't understand American history. Colonial Americans drank like fish. The average whiskey consumption was one pint a day. In the early 1800s, they went on a bigger binge, mostly on hard liquor and drinking alone, rather than sociably like in the old days. Rorabaugh says this explains how the temperance movement came up just then, & it was the stress of industrialization & frontier loneliness & inflated dreams for the new nation. Readable & smart & has the good modern historical perspective on alcoholism.

Alcoholism : The Facts  Goodwin's accessible, effortless style, which he used so well in previous editions, carries the reader nicely through the intricacies of one of the world's most popular drugs and its associated disorders. Excerpts from literature and case studies provide a superb feel for the phenomenology of addiction. Numerous entertaining quotes appear from everyone from Kissinger to Humpty Dumpty. Goodwin provides a thorough look at alcohol itself, the problems associated with excess consumption, common theories designed to account for these problems, and many of the available treatments. Through simple explanations of the correct interpretations of available data, Goodwin not only provides a great deal of meaningful information, but he teaches the reader to become a good consumer of research. This book is refreshingly scientific and lacks the horribly moralistic tone many books on this topic take.

Alcohol and You (Impact Book) The physiological, emotional, and sociological effects of teenage drinking, alcoholism, and recovery are thoroughly discussed in a revised volume that includes updated statistics.

Heavy Drinking : The Myth of Alcoholism As a Disease Author writes a cool and logical prose that argues persuasively that all our preconceptions about "the alcoholic" are scientifically invalidated. Instead of viewing alcoholism as a disease with a single cause, single outcome, and single treatment, he discusses "heavy drinking" as a behavior problem that can effect each drinker differently. he writes that drinking must be viewed as a response the drinker has developed to his particular life's problems, and must be considered together with those other problems. along the way he debunks such ideas as that alcoholics have an irresistable urge to drink, cannot stop drinking once they have begun, will do anything to get a drink, and that abstinence alone solves their problems. since his view contradicts AA tenets, the book is certainly provocative.

Addiction, Change & Choice: The New View of Alcoholism The author is affiliated with Rational Recovery which is an alternative to Alcoholics Anonymous. He covers the questions and controversies in the field-what alcoholism is, what treatments work and don't work, and how the multi-billion-dollar treatment industry functions.

Alcohol : How to Give It Up and Be Glad You Did  This book is an insightful and practical approach to help the reader eliminate their alcohol or substance abuse. Dr. Philip Tate, the author, presents logical and detailed rational principles while he examines irrational thought processes as a basis for addictions. Dr. Tate not only gives sound principles, but he also offers many specific ideas about how to deal with the main unhelpful emotions.