Delayed recovery from dazzle

Prolonged reaction time & lack of colour discrimination

Inaccurate cornering

Fig. 10.3 Alcohol and driving.

of warmth that follows taking the drug. Body heat loss is increased so that it is undesirable to take alcohol before going out into severe cold for any length of time, but it may be harmlessly employed on coming into a warm environment from the cold to provide quickly a pleasant feeling of warmth.

Blood pressure. An acute dose of 4-5 units raises the blood pressure which parallels the blood concentration. The mechanism appears to involve centrally mediated sympathetic stimulation.

Diuretic effect. Alcohol acts by inhibiting secretion of antidiuretic hormone by the posterior pituitary gland. The reason it is useless as a diuretic in heart failure is that the diuresis is of water, not of salt.

Gastric mucosa. Injury occurs because alcohol allows back diffusion of acid from the gastric lumen into the mucosa. After an acute binge the mucosa shows erosions and also petechial haemorrhages (recovery may take 3 weeks) and up to 60% of chronic alcoholics show chronic gastritis.

Vomiting. This common accompaniment of acute alcoholism seems to be partly a central effect, for the incidence of vomiting at equivalent blood alcohol concentrations is similar following oral or i.v. administration. This is not to deny that very strong solutions and dietary indiscretions accompanying acute and chronic alcoholism can cause vomiting by local gastric effects. That said, when death occurs, it is commonly due to suffocation from inhaled vomit.

Glucose tolerance. Alcohol initially increases the blood glucose, due to reduced uptake by the tissues. This leads to increased glucose metabolism.

But alcohol also inhibits gluconeogenesis and a person whose hepatic glycogen is already low, e.g. a person who is getting most of his calories from alcohol or who has not eaten adequately for 3 days, can experience hypoglycaemia that can be severe enough to cause irreversible brain damage. Hypoglycaemia can be difficult to recognise clinically in a person who has been drunk, and this adds to the risk.

Hyperuricaemia occurs (with precipitation of gout) due to accelerated degradation of adenine nucleotides resulting in increased production of uric acid and its precursors. Only at high alcohol concentrations does alcohol-induced high blood lactate compete for renal tubular elimination and so diminish excretion of urate.

Effects on sexual function. Nothing really new has been said since William Shakespeare wrote that alcohol 'provokes the desire, but it takes away the performance'. Performance in other forms of athletics is also impaired. Prolonged substantial consumption lowers plasma testosterone concentration at least partly as a result of hepatic enzyme induction;

féminisation may be seen and men have been threatened with genital shrinkage.

Source of energy. Alcohol may be useful as an energy source (rather than a food) in debilitated patients. It is rapidly absorbed from the alimentary tract without requiring digestion and it supplies 7 calories31 per gram as compared with 9 from fat and 4 from carbohydrate and protein. Heavy doses cause hyperlipidaemia in some people.

Tolerance to alcohol can be acquired and the point has been made that it costs the regular heavy drinker 2.5 times as much to get visibly drunk as it would cost the average abstainer. This is probably due both to enzyme induction and to adaptation of the central nervous system.

Intolerance. Inter-ethnic variation in tolerance to alcohol is well recognised, for Asian persons, particularly Japanese, develop flushing, headache and nausea after what are, by Caucasian standards, small amounts of the substance. Genetic deficiency of aldehyde dehydrogenase with slow metabolism of (toxic) acetaldehyde may explain these features.

Acute alcohol poisoning is a sufficiently familiar condition not to require detailed description. It is notorious that the characteristic behaviour changes, excitement, mental confusion (including 'blackouts'), incoordination and even coma, can be due to numerous other conditions and diagnosis can be extremely difficult if a sick or injured patient happens to have taken alcohol as well. Alcohol can cause severe hypoglycaemia (see above). Measurement of blood alcohol may clarify the situation.

If sedation is essential, diazepam in low dose is least hazardous. Alcohol dialyses well, but dialysis will only be used in extreme cases.

Acute hepatitis, which may be extremely severe, can occur with extraordinarily heavy acute drinking bouts. The serum transaminase rises after alcohol in alcoholics but not in others. The single case-report that after a binge the cerebrospinal fluid tasted of gin remains unconfirmed.

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