In the general population, alcohol is the most widely used substance of abuse. Sequelae of ethanol use disorders represent the third leading cause of death in the United States, with an estimated 111,000 deaths per year directly attributable to alcohol ingestion. The most common causes of death in alcohol-related disorders are suicide, cancer, heart disease, and hepatic disease (Schuckit 1999).

The acute action of ethanol in the central nervous system (CNS) derives from two main mechanisms: ethanol facilitates the activation of gamma-aminobutyric acid type A (GABAa) receptors, the main inhibitory neurotransmitter system in the CNS, and inhibits the A-methyl-D-aspartate (NMDA) subtype of glutamate receptors, the main excitatory neurotrans-mitter receptor system in the CNS. The net effects of GABA are thereby potentiated, leading to sedation, and inhibition of NMDA receptors via allosteric modulation appears to be responsible for the intoxicating effects (Schuckit 1999). Sudden cessation of ethanol use in a chronic, heavy drinker often results in an uncomplicated withdrawal syndrome characterized by mild confusion associated with diaphoresis, tremulousness, and increased heart rate, blood pressure, and temperature, all of which can be blocked by administration of GABA-acting drugs such as benzodiaz-epines. In about 5%-10% of patients with alcohol dependence, this syndrome may progress to delirium tremens (DTs), which is characterized by significant autonomic instability, marked confusion, disorientation, agitation, tremulousness, and hallucinations (auditory, visual, and tactile). The mortality rate for untreated DTs is approximately 5%. Alcohol withdrawal seizures ("rum fits") may also develop independently of DTs, typically within the first 24-48 hours after cessation of alcohol use (Schuckit 1998).

Alcohol consumption plays a role in both acute and chronic medical illness through a variety of mechanisms, some or all of which may be operative in a specific individual (Schuckit 1998). Repeated exposure may lead to alcoholic hepatitis and eventually cirrhosis, with secondary cognitive impairment via hepatic encephalopathy in advanced cirrhosis due to the accumulation of nitrogenous compounds that are inadequately metabolized by the compromised liver. The cirrhotic changes of the liver are also manifested in impaired synthetic function (e.g., decreased production of clotting factors) and reduced metabolism of exogenous toxins such as medications. In the CNS, prolonged alcohol abuse leads to cerebellar degeneration in about 1% of chronic alcoholics, presenting as unsteady gait and mild nystagmus. These symptoms are irreversible and often accompanied by global cognitive decline from direct or indirect effects of chronic alcohol consumption (e.g., head injury, nutritional deficiency, direct neurotoxicity). Finally, peripheral neuropathy is seen in approximately 5%-15% of alcoholics due to nutritional deficiency and direct toxic effects of alcohol on neuronal axons (Schuckit 1998).

Alcohol abuse increases blood pressure and serum triglycerides, and may lead to cardiomyopathy and arrhythmias via toxic effects on cardiac muscle (Schuckit 1998). During the acute intoxication period, tests for blood alcohol level, serum electrolytes glucose, aspartate transaminase (AST), alanine transaminase (ALT), gamma-glutamyltransferase (GGT), hematocrit, and amylase can be useful. For the chronic alcoholic, additional laboratory values that should be monitored include albumin, red blood cell indices, white blood cell count, platelet count, prothrombin time, hepatitis B and C screening, vitamin B12, and folate.

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