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Chapter: Modern Medical Toxicology: Neurotoxic Poisons: Inebriants

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Methaqualone - Inebriant Neurotoxic Poisons

Methaqualone is a non-barbiturate sedative- hypnotic with anticonvulsant, anaesthetic, antihistaminic and antispasmodic properties.

Methaqualone

Methaqualone is a non-barbiturate sedative- hypnotic with anticonvulsant, anaesthetic, antihistaminic and antispasmodic properties. It was extensively abused in the past ( Mandrax,Quaalude, Sopor), which led to its withdrawal from themarket. Combination of methaqualone with wine (“luding out”) is said to produce powerful euphoria with feelings of invincibility.

Absorption of this drug after oral administration is rapid and metabolism occurs in the liver leading to the formation of numerous hydroxy metabolites. Methaqualone is completely metabolised by the hepatic microsomal enzyme system, primarily by hydroxylation. Methaqualone is highly lipid soluble, and also has a slow biotransformation, leading to a long half-life.

Dizziness, ataxia, slurred speech, and drowsiness are common in mild intoxication with methaqualone. Overdose is characterised by ataxia, lethargy, coma (sometimes preceded by delirium), hyperreflexia, and respiratory arrest. In severe poisoning, pyramidal signs such as hypertonicity, limb hyperreflexia, clonus, flailing limb motions, myoclonia and upgoing Babinski responses are common. Hypotension, absence of EEG activity, muscular hyperactivity, and respira-tory depression are also common phenomena. Tachycardia, hypotension, and myocardial infarction have been reported in severe cases. Reversible ECG changes may occur. Pupils may be somewhat mydriatic and sluggishly responsive, or may be miotic.

Usual fatal dose is around 8 grams. Acute ingestion of greater than 800 mg in an adult is usually considered toxic. Ingestion of as little as one tablet in a child can cause toxicity.

In severely intoxicated patients monitor CBC, liver and renal function tests, platelets, coagulation tests, electrolytes, arterial blood gases, and ECG. Consider prehospital adminis-tration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Early gastric lavage is also beneficial. Treatment is essentially supportive, with emphasis on control of convulsions and hypotension. Although haemodialysis and haemoperfusion are effective in removing methaqualone, they should be reserved for life-threatening situations. Many patients have been success-fully treated without the aid of dialysis. Forced diuresis is contraindicated because of the possibility of precipitating pulmonary oedema.

Abrupt withdrawal following chronic use causes nausea, vomiting, abdominal cramps, weakness, anxiety, restlessness, tachycardia, hyperreflexia, agitation, convulsions, and delirium. Death may occur if severe withdrawal is not treated.


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