Alcohol and substance abuse

1

How is alcohol absorbed and metabolized?

Alcohol is absorbed across the gastrointestinal mucosa, more so in the small intestine than in the stomach. It enters into the portal vein and proceeds to the liver, where it is metabolized.

Most consumed alcohol is converted to acetaldehyde by the enzyme alcohol dehydrogenase and secondarily by cytochrome P450 2E1, as alcohol blood levels rise. Alcohol metabolism follows Michaelis–Menten zero-order kinetics, meaning that once the enzyme is saturated with ethanol, the rate of metabolism is constant, even though blood alcohol concentration may continue to increase. Some 5% to 10% of consumed alcohol is excreted unchanged in the breath and urine. Alcohol easily crosses the blood-brain barrier. Blood levels of alcohol correlate well with the concentration in lung alveoli, thus the basis of the breathalyzer test used by law enforcement officers.

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 a generalized blunting and eventual 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 effect 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 encephalopathy and Korsakoff psychosis) may be linked to nutritional deficiencies (e.g., thiamine B-1). Alcohol-related neuropathy may be present in the lower extremities, often with concomitant weakness of the intrinsic muscles of the feet. It is a symmetrical, bilateral mixed sensory and motor peripheral neuropathy, often presenting as pain and numbness of the feet. Generalized weakness in the proximal limb musculature may also be noted in chronic alcoholic myopathy.

3

What are the effects of alcohol on the cardiovascular system?

Although controversial, some evidence suggests that small amounts of alcohol may be cardioprotective. However, even modest ingestion over the long-term is associated with atrial fibrillation, hypertension, left ventricular hypertrophy, and cardiomyopathy. “Holiday Heart syndrome,” following an alcohol binge, is well characterized by acute onset of atrial fibrillation. Acutely, moderate ingestion of alcohol produces no significant changes in blood pressure or myocardial contractility. Cutaneous vasodilation generally occurs, and heart rate increases. At high levels of acute 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 over 90 oz per month over a 10-year period may result in cardiomyopathy, with associated pulmonary hypertension, right-sided heart failure, and dysrhythmias. 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 dead-space ventilation. Despite this, alcohol depresses the ventilatory response to carbon dioxide. Chronic alcohol users are susceptible to pulmonary infections because of greater airway colonization, often by staphylococci or gram-negative organisms, associated with frequent aspiration of gastric contents. 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?

Acutely, alcohol use may cause esophagitis, gastritis, and pancreatitis. Chronically, alcohol use leads to delayed gastric emptying and relaxation of the lower esophageal sphincter, increasing the risk of aspiration. Also acutely, the liver undergoes transient and reversible fatty infiltration. Although such changes resolve with abstinence, prolonged alcohol exposure leads to chronic infiltration of fat, which, over time, progresses to necrosis and fibrosis of liver tissue. The initial presentation of fatty liver is hepatomegaly. As necrosis, fibrosis, and cirrhosis progresses, the liver regresses in size. Chronic severe consumption of alcohol leads to irreversible cirrhosis and alcohol-induced hepatitis. Hepatic synthetic function is impaired. Production of albumin and coagulation Factors II, V, VII, X, and XIII are 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?

Chronic alcohol abuse can impair intestinal absorption of essential amino acids and vitamins, especially thiamine and folate. Deficiency of thiamine leads to Wernicke 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?

Acutely, in nonhabituated, intoxicated patients, the minimal alveolar concentration (MAC) of inhalational agents is reduced. For chronic users, the MAC for inhalational agents is increased. Acutely intoxicated patients are also more sensitive to the effects of barbiturates, benzodiazepines, and opioids. Cross-tolerance to intravenous anesthetic agents may also be present in patients who are chronically exposed to alcohol.

8

How does alcohol affect the metabolism of neuromuscular blocking drugs?

Patients with liver disease may have decreased levels of circulating plasma cholinesterase, prolonging the effects of succinylcholine. Cirrhotic patients, with poor liver function, have a greater Volume of distribution V d for injected drugs and thus require larger doses of nondepolarizing neuromuscular blocking drugs (NMBDs). Nondepolarizing 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. Regardless of the NMBD chosen, close monitoring of neuromuscular blockade is recommended.

9

Describe special considerations in the perioperative assessment of 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. Also alcoholic patients are often volume depleted and may require fluid resuscitation. Hypokalemia and hypoglycemia are common. Anemia, thrombocytopenia, and altered coagulation are indicators of significant liver disease and may be present. Instrumentation of the esophagus should be undertaken carefully in patients with known liver disease, as the possibility of rupturing esophageal varices exists.

10

What are the signs and symptoms of alcohol withdrawal?

Alcohol withdrawal presents as anorexia, insomnia, weakness, combativeness, tremors, dilated pupils, disorientation, auditory and visual hallucinations, and convulsions. Onset is usually 10 to 30 hours after abstinence has begun, 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.

11

Review the differences between addiction, dependence, and tolerance according to the American Pain Society.

• Dependence implies “a state of adaptation that is manifested by a drug class–specific withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an antagonist.”

• Opioid tolerance is “a state of adaptation in which exposure to a drug induces changes that result in a diminution of one or more of the drug's effects over time.”

• Addiction “is a primary, chronic, neurobiological disease, with genetic, psychosocial, and environmental factors influencing its development and manifestations. It is characterized by behaviors that include one or more of the following: impaired control over drug use, compulsive use, continued use despite harm, and craving.”