Ethanol (alcohol)

Cardiovascular

Alcohol is one of many drugs that cause or aggravate systemic hypertension. Acute alcohol exposure has an inconsistent effect on blood pressure, but cross-sectional population studies have shown a relation between chronic alcohol consumption and blood pressure, and the prevalence of hypertension up to three times higher in heavy drinkers [ ]. Although the mechanism of hypertension caused by chronic alcohol consumption is not known, it is suspected that it is partly related to repeated episodes of acute withdrawal, causing increased sympathoadrenomedullary activity, an increase in plasma renin activity, and increased ACTH secretion, which may be sufficient to have a mineralocorticoid effect [ ].

It has been suggested that there are individual differences in subjective responses to alcohol and an exaggerated cardiac response to alcohol has been suggested to be a marker of increased sensitivity to its stimulant properties. The relation between cardiac reactivity to alcohol measured on the ascending limb of the Blood Alcohol Concentration (BAC) curve and its subjective stimulant and sedative effects throughout the BAC curve has been examined in 39 male social drinkers [ ]. Cardiac responses to ethanol correlated positively with stimulant effects at numerous times during the ascending and descending limbs of the BAC curve. There were no associations between the cardiac changes and alcohol-related sedative effects at any time.

The effects of potentially lethal serum concentrations of ethanol on features of the electrocardiogram that may be associated with cardiac dysrhythmias have been studied in 84 patients with assumed acute ethanol intoxication and 27 hospitalized controls [ ]. In subjects with moderately increased to high serum osmolality, the PR and QT _c intervals were prolonged compared with sober subjects. The authors suggested that ethanol at high to very high concentrations in the blood causes several electrocardiographic changes that might be associated with an increased risk of dysrhythmias.

Respiratory

In 36 patients with inoperable cancers of the esophagus who were treated by endoscopic injection of alcohol, complications included mediastinitis in one patient and tracheoesophageal fistulas in two [ ].

Nervous system

Peripheral nerve block is created by injecting ethanol around the selected nerve. The effect of alcohol on nerve tissue has been examined in animal models and in postmortem specimens from patients who received neurolytic blocks [ , ]. In general, alcohol causes destruction of nerve fibers, with subsequent Wallerian degeneration. The basal lamina around the Schwann cell usually remains intact. This leaves a tract available for axon regeneration without the formation of a neuroma. If the cell bodies are completely destroyed, regeneration will not occur. Contact of alcohol with unintended nerve roots underlies many of the more serious complications. Involvement of anterior rootlets sufficient to interrupt motor nerve function will result in muscle weakness or paralysis. Interruption of parasympathetic fibers in the anterior roots of the three middle sacral segments can result in bowel and bladder dysfunction and can cause urinary retention and anal sphincter paralysis.

In one study of 82 patients over a 20-year period who received repeated peripheral alcohol nerve blocks for trigeminal neuralgia, although moderate swelling and discomfort were invariable, significant complications occurred in only three of 413 nerve blocks [ ]:

• avascular necrosis, leading to a sequestrum, possibly due to repeated injections;

• necrosis of the lateral aspect of the nose, attributed to intravascular injection of alcohol;

• pallor and faintness after the injection followed by diplopia, which took 5 months to resolve.

Alcohol relatively commonly causes less serious complications, such as vomiting, headache, and paresthesia, which are but fortunately of limited duration, while loss of proprioception and profound numbness are disconcerting but almost always preferable to the pain that the alcohol injection has relieved [ ].

Cerebellar degeneration has been attributed to alcoholism [ ]. Alcoholic cerebellar degeneration is one of the most common neurological complications in alcoholics. As far as it is known, however, only four Japanese autopsy cases have been reported, and only limited pathological data are now available in Japan. Alcoholic cerebellar degeneration has been studied in six Japanese autopsy cases of ACD, including three asymptomatic cases, in order to elucidate the pattern of progression of the cerebellar lesions. The findings suggested that in alcoholic cerebellar degeneration, severe lesions develop successively in the anterior superior vermis, the anterior superior hemisphere, the anterior inferior hemisphere, and the anterior inferior vermis. In addition, cerebellar symptoms can often occur if the anterior superior and anterior inferior hemispheres are involved, in addition to the anterior superior vermis.

The association between blood alcohol concentration and the presence and degree of amnesia has been investigated in actively drinking subjects [ ]. A questionnaire was administered regarding any recent alcohol-associated arrest with a documented blood alcohol concentration over 80 mg/dl (14.3 mmol/l) for public intoxication, driving under the influence, or under-age drinking. Memory of the drinking episode was evaluated to determine if there had been either a grayout (partial anterograde amnesia) or blackout (complete anterograde amnesia). There were differences in (1) the mean total number of drinks ingested before the arrest; (2) gulping of drinks; and (3) blood alcohol concentration at the time of arrest for those who had blackouts compared with no amnesia; while there were differences in drinking more than planned between those without amnesia and those with grayouts. There was a strong linear relation between blood alcohol concentration and the predicted probability of memory loss, particularly for blackouts. Subjects with a blood alcohol concentration of 310 g/dl or greater have a 0.50 or greater probability of having an alcoholic blackout.