Ethchorvynol

Ethchlorvynol, a schedule IV drug, was marketed initially in 1955 as an alternative to barbiturates, possessing a more rapid onset and shorter duration of action. However, the drug's high abuse potential, coupled with its tendency toward tolerance, physical dependence, and life-threatening withdrawal, overshadowed any claim of superior efficacy. The drug is available as a liquid-filled capsule, allowing both intravenous and oral abuse.

Ethchlorvynol is absorbed rapidly from the GI tract. It is highly lipophilic, concentrates in the CNS, and possesses a large volume of distribution. Its biphasic distribution is characterized by an initial period of adipose tissue deposition, 3 to 5 h after ingestion, with sedative effects disappearing only to resurface 7 to 10 h later when the drug redistributes from fat stores. Ethchlorvynol is moderately protein-bound and hepatically metabolized but does not induce microsomal enzymes. It also crosses the placenta and causes neonatal withdrawal symptoms. Mechanisms of CNS sedative action and hepatic degradation are unknown. Ethanol potentiates CNS depressant effects.

Distinguishing clinical clues in oral and intravenous overdose are a vinyl-like breath odor (although the patient may report a mintlike taste in the mouth), dypsnea, and dry cough. CNS effects include nystagmus, lethargy, and extremely prolonged coma. Isoelectric electroencephalographic (EEG) tracings have been reported but do not preclude full recovery. Hypothermia, hypotension, and relative bradycardia signal hemodynamic instability. Noncardiogenic pulmonary edema can be seen in massive oral overdose, although it is more characteristic of intravenous overdose. Polydrug exposures that potentiate CNS depression can result in respiratory arrest and cardiovascular collapse. Psychological and physical dependence develop rapidly. Chronic abusers may present with a variety of neurologic symptoms: ataxia, dysarthria, tremors, facial numbness, confusion, weakness, and visual disturbances (e.g., toxic amblyopia and central scotomata). Abstinence symptoms resembling those seen with alcohol withdrawal include states reminiscent of delirium tremens, with psychotic hallucinations, seizures, agitation, confusion, hypertension and tachycardia.

Successful treatment of ethchlorvynol overdose centers on the usual attention to supportive care and general decontamination. Serum levels of ethchlorvynol are not helpful in guiding management except to confirm diagnosis or trigger use of an extracorporeal elimination method in refractory cases. Charcoal hemoperfusion is superior to hemodialysis because of the drug's degree of protein binding and redistribution characteristics. Forced diuresis is not recommended because the risk of inducing pulmonary edema outweighs the minimal enhancement of drug cleared by the kidney.

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