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Chapter: Modern Medical Toxicology: Neurotoxic Poisons: Inebriants

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Ethanol: Clinical Features - Inebriant Neurotoxic Poisons

Initially, ethanol produces excitement which progresses to loss of restraint, behavioural changes, garrulous-ness, slurred speech, ataxia, unsteady gait, drowsiness, stupor, and finally coma.

Clinical Features

Acute Poisoning (Intoxication, Inebriation):

·              Initially, ethanol produces excitement which progresses to loss of restraint, behavioural changes, garrulous-ness, slurred speech, ataxia, unsteady gait, drowsiness, stupor, and finally coma (Table 14.2).


·              Rarely, alcohol induces allergic reactions (usually in the form of urticaria, nasal congestion, headache, etc.), which may be severe and may even result in death.

·              There are also reports of cardiac dysrhythmias (espe-cially atrial fibrillation) associated with binge drinking.

·              Through all the 7 stages of ethanol intoxication, a distinct odour is perceptible in the breath of the indi-vidual. It is however not the alcohol itself which imparts this odour but other nonalcoholic constituents that give a particular flavour depending on the type of beverage consumed (wine, beer, whisky, etc.). It is important to remember that even after a person has completely sobered up from the effects of ethanol, the odour may persist in the breath for a considerable period of time.

·              Ethanol is a mydriatic, but towards terminal stages (stages of stupor and coma), the pupils may become constricted, only to dilate once again at about the time of death. The McEwan sign* is highly unreliable and must not be depended upon for diagnosis of alcoholic coma.

·              Hypothermia is common.

·              Hypotension and tachycardia may be present. Atrial fibrillation and atrioventricular block have been reported with acute overdose. Cardiac output may be decreased in persons with pre-existing cardiac disease. After consuming recreational amounts of alcohol, persons suffering from variant angina may experience chest pain due to coronary artery spasm or myocardial ischaemia. Sudden cardiac failure, arrhythmias, subclin-ical left ventricular dysfunction, and other morphologic abnormalities of the heart can occur with chronic heavy abuse. Alcoholic cardiomyopathy has insidious onset and can be clinically inapparent. Symptoms of alco-holic cardiomyopathy are often present for an average of 10–12 months before diagnosis, but as much as 85% of cases have not been diagnosed through routine screening, unless angiography was performed.

·              Bradypnoea may occur early, and tachypnoea may develop in cases of metabolic acidosis.

·              Poor control of eye movements, with diplopia and nystagmus may occur and alter vision and performance. Acute overdoses of ethanol have caused spontaneous (not gaze-evoked) horizontal nystagmus. Amblyopia due to peripheral neuritis has been reported in chronic alcoholics.

·              Bilaterally decreased vision occurs. Vitamin deficiencies correlate with the ocular defects and early administration of B vitamins causes recovery in some patients.

·              Lactic or ketoacidosis may occur. Acidosis may occur due to metabolic disturbances, such as NADH over- production, oxidation of ethanol, decreased lactate utilisation, and inhibition of hepatic gluconeogenesis. Hypoglycaemia which can result in seizures and coma is a serious complication of acute alcoholic intoxication, especially in children.

·              Medicolegally, stages 3 and 4 of alcoholic intoxication (stages of excitement and confusion) are the most impor-tant, since most of the offences associated with drinking are committed during these two stages. It is pertinent to mention that stage 7 (death) is extremely rare in pure ethanol ingestion. In most cases there is recovery after prolonged sleep, with some residual after effects (hang-over), consisting of headache, irritability, lethargy, nausea,and abdominal discomfort. While the last mentioned is mainly due to gastritis produced by ethanol, the other symptoms are actually the result of congeners and impu-rities present in alcoholic beverages which cause mild cerebral oedema. Part of the hangover may also be the result of hypoglycaemia induced by ethanol.

·              While the subject of some professional dispute, some data indicate that a small number of people may be exceptionally sensitive to ethanol, exhibiting combative and irrational behaviour after ingesting non-intoxicating amounts. This has been termed pathological intoxica-tion or ethanol idiosyncratic intoxication.

·              Alcoholic intoxication (through all the stages) can mimic several conditions which can lead to errors in diagnosis. Table 14.3 lists the differential diagnosis for acute ethanol intoxication.



 

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