Alcohol and substance abuse

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James Duke, MD, MBA

1. How is alcohol absorbed and metabolized?

Alcohol is absorbed across the gastrointestinal mucosa, more so in the small intestine than in the stomach. The volume of distribution (Vd) of alcohol is that of body water. Alcohol easily crosses the blood-brain barrier. Arterial blood levels of alcohol correlate well with concentrations in lung alveoli, thus the basis of the breathalyzer test used by law-enforcement officers.

Alcohol is metabolized primarily in the liver. Most consumed alcohol is converted to acetaldehyde by the enzyme alcohol dehydrogenase. Alcohol metabolism follows Michaelis-Menten zero-order kinetics. When alcohol dehydrogenase is saturated with ethanol, the rate of metabolism is constant, although alcohol concentration may increase. A 5% to 10% amount of consumed alcohol is excreted unchanged in the breath and urine.

2. What are the acute and chronic effects of alcohol on the nervous system?

Acutely alcohol depresses the central nervous system by inhibiting polysynaptic function, which is characterized by generalized blunting and loss of higher motor, sensory, and cognitive function. Although the behavioral effects of alcohol consumption may seem excitatory or stimulating to observers and users, this impression is probably caused by a depressive effect on inhibitory pathways (disinhibition).

Chronic alcohol use is associated with peripheral nerve and neuropsychiatric disorders, many of which (e.g., Wernicke's encephalopathy and Korsakoff's psychosis) may be linked to nutritional deficiencies. Alcohol-related neuropathy usually involves pain and numbness in the lower extremities, often with concomitant weakness of the intrinsic muscles of the feet. Patients may exhibit hypalgesia in a stocking-foot distribution, and the Achilles tendon reflex may be absent. Generalized weakness in the proximal limb musculature may also be noted.

3. What are the effects of alcohol on the cardiovascular system?

Moderate acute ingestion of alcohol produces no significant changes in blood pressure or myocardial contractility. Cutaneous vasodilation occurs, and heart rate increases. At toxic levels of acute alcohol ingestion, a decrease in central vasomotor activity causes respiratory and cardiac depression.

The leading cause of death in chronic users of alcohol is cardiac dysfunction. Consumption of 60 oz of ethanol per month (8 pints of whiskey or 55 cans of beer) may lead to alcohol-induced hypertension. An intake >90 oz per month over a 10-year period may result in congestive cardiomyopathy with associated pulmonary hypertension, right-heart failure, and dysrhythmias (usually atrial fibrillation and premature ventricular contractions). Ventricular tachydysrhythmias, ventricular fibrillation, and sudden death are also risks.

4. How does alcohol affect the respiratory system?

Acute alcohol intake may cause hyperventilation via disinhibition of central respiratory regulation centers and increases in dead-space ventilation. Despite hyperventilation, alcohol depresses the ventilatory response to carbon dioxide. Aspiration of gastric contents is a risk. Chronic alcohol users are susceptible to pulmonary infections, often by staphylococci or gram-negative organisms. There is also a generalized decrease in all lung capacities (vital, functional residual, and inspiratory capacity).

5. How does alcohol affect the gastrointestinal and hepatobiliary systems?

Acute alcohol use may cause esophagitis, gastritis, and pancreatitis. Chronic alcohol use leads to delayed gastric emptying and relaxation of the lower esophageal sphincter, increasing the risk of aspiration. The liver undergoes transient and reversible fatty infiltration during acute alcohol use. Although such changes resolve with abstinence and the cycle can repeat itself many times, prolonged alcohol exposure leads to chronic infiltration of fat, which overtime progresses to necrosis and fibrosis of liver tissue. The initial presentation of fatty liver is hepatomegaly. When necrosis, fibrosis, and cirrhosis become apparent, the liver regresses in size. Chronic severe consumption of alcohol leads to irreversible cirrhosis and alcohol-induced hepatitis. Hepatic synthetic function is also impaired. Production of albumin and coagulation factors II, V, VII, X, and XIII is decreased. Reduction of albumin results in lower intravascular oncotic pressure and may lead to tissue edema. A reduction in circulating coagulation factors may predispose to bleeding, which is evidenced by a prolonged prothrombin time.

6. Which nutritional deficiencies are seen in chronic alcohol users?

Deficiency of thiamine leads to Wernicke's encephalopathy, polyneuropathy, and cardiac failure characterized by high cardiac output, low systemic vascular resistance, and loss of vasomotor tone. Folic acid deficiency causes bone-marrow depression and thrombocytopenia, leukopenia, and anemia.

7. What are the effects of alcohol on inhalational anesthetics?

In acutely intoxicated, nonhabituated patients, the minimal alveolar concentration (MAC) of inhalational agents is reduced. For chronic users of alcohol the MAC for inhalational agents is increased.

Acutely intoxicated patients are more sensitive to the effects of barbiturates, benzodiazepines, and opioids. Cross-tolerance develops to intravenous agents with chronic alcohol exposure.

8. How does alcohol affect muscle relaxants?

Patients with liver disease may have decreased levels of circulating plasma cholinesterase, and the effects of succinylcholine may be prolonged. Cirrhotic patients with poor liver function have a greater Vd for injected drugs and thus require a larger dose of nondepolarizing relaxants. Relaxants that rely on hepatic clearance may have a prolonged duration of action. Muscle relaxants that are metabolized independently of organ function (e.g., cisatracurium) are good choices for patients with liver disease.

9. Describe special considerations in the perioperative assessment ol alcohol-abusing patients.

Special consideration must be given to the cardiovascular system of chronic alcohol users. Tachycardia, dysrhythmias, or cardiomegaly may indicate alcohol-related cardiac dysfunction; and a 12-lead electrocardiogram (ECG) should be evaluated. Patients with alcohol-induced cardiac disease are less sensitive to endogenous or parenteral catecholamines. Hypokalemia and hypoglycemia are common, as are anemia, thrombocytopenia, and altered coagulation. These patients are often volume depleted and will require fluid resuscitation. Insert a urinary catheter to follow urine output. Intravascular monitoring should be individualized. Instrumentation of the esophagus should be avoided in patients with known liver disease because of the possibility of rupturing esophageal varices.

10. How should sober chronic alcohol abusers be anesthetized?

Sober chronic alcohol users can tolerate intravenous and inhalational anesthetics. Isoflurane may be the best inhalational agent for maintaining hepatic blood flow. In general, a balanced anesthetic technique using amnestics, opioids, muscle relaxants, and an inhalational agent will suffice.

11. What are the signs and symptoms of alcohol withdrawal?

Alcohol withdrawal presents as anorexia, insomnia, weakness, combativeness, tremors, disorientation, auditory and visual hallucinations, and convulsions. Onset is usually 10 to 30 hours after abstinence, and the symptoms may last for 40 to 50 hours. Prolonged abstinence may lead to delirium tremens or autonomic hyperactivity (tachycardia, diaphoresis, fever, anxiety, and confusion). Alcohol withdrawal syndrome may occur while under anesthesia and manifest as uncontrolled tachycardia, diaphoresis, and hyperthermia. The treatment is administration of benzodiazepines or intravenous infusion of ethanol.

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