Introduced in 1869, chloral hydrate was used as a popular sedative in clinical medicine until the advent of barbiturates largely supplanted their use in the early 1900s. Chloral hydrate is still used effectively for promoting sedation in children because in therapeutic doses it does not depress respiratory drive or circulatory function. Drawbacks include its narrow margin of safety, minimal analgesic activity, and propensity to develop tolerance and physical dependence. Withdrawal symptoms mimic those of alcohol abstinence. Toxic doses produce severe CNS, respiratory, and cardiovascular depression. Ethanol potentiates the sedative effects of chloral hydrate when taken in combination. This observation led to the street use of the two substances for malicious intent, as in slipping someone a "Mickey (Finn)" or "knockout drops." Chloral hydrate is a schedule III drug with recognized abuse potential.
Chloral hydrate absorption occurs rapidly and completely from the GI tract. It is a well-known mucous membrane irritant, especially when taken in quantity or undiluted. Development of GI bleeding is a useful clue in overdose. Chloral hydrate is lipid-soluble and easily transits all cell membranes. Volume of distribution and protein-binding properties are moderate. Metabolism occurs in the liver via alcohol dehydrogenanse and results in the generation of a longer-acting active metabolite, trichloroethanol, thought to be responsible for most of the drug's sedative action. Neither the parent drug nor the metabolite induces hepatic enzyme activity.
Chloral hydrate is a CNS depressant, with an unknown mechanism of action. Toxic doses also depress myocardial contractility, shorten the refractory period, and sensitize the myocardium to catecholamines. These factors create the substrate for resistant ventricular dysrhythmias that are the leading cause of mortality overdose.7
Clinical clues to the ingestion of chloral hydrate are a pearlike breath odor, hypotension, and cardiac dysrhythmias. Because chloral hydrate is radiopaque, abdominal x-rays may help narrow the differential diagnosis and guide decontamination. Serum levels are rarely helpful in guiding clinical management. 7
Barring evidence of caustic injury causing perforation, gastric lavage should be considered and activated charcoal administered. Cardiac monitoring is mandatory, but treatment of ventricular dysrhythmia may prove difficult. There are anecdotal reports of successes using lidocaine and propanolol. Overdrive pacing in the setting of ventricular tachycardia may prove necessary. Avoid b-adrenergic drugs such as epinephrine, isoproterenol, and dopamine, which can potentiate dysrhythmias in the catecholamine-sensitized myocardium. If hypotension does not respond to volume loading, a-acting pressors such as norepinephrine should be used. Hemodialysis and hemoperfusion have been shown to be beneficial in severe overdose.
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