Immediately following withdrawal, the patient seemingly improves over a period of 8 to 12 h, as the symptoms of intoxication diminish. Then a new group of symptoms develops, consisting of nervousness, tremor, insomnia, postural hypotension, and weakness. With chronic phenobarbital or barbital intoxication, withdrawal symptoms may not become apparent until 48 to 72 h after the final dose or it does not occur at all because of the slow metabolism and long half-life of these drugs. Generalized seizures with loss of consciousness may occur, usually between the second and fourth days of abstinence, but occasionally as long as 6 or 7 days after withdrawal. There may be a single seizure, several seizures, or, rarely, status epilepticus. Characteristically, in the withdrawal period, there is a greatly heightened sensitivity to photic stimulation, to which the patient responds with myoclonus or a seizure accompanied by paroxysmal changes in the EEG. The convulsive phase may be followed directly by a delusional-hallucinatory state or, as occurred in one of our cases (Romero et al), a full-blown delirium indistinguishable from delirium tremens. Death has been reported under these circumstances. The abstinence syndrome may occur in varying degrees of completeness; some patients have seizures and recover without developing delirium, and others have a delirium without preceding seizures.
This is the oldest and one of the safest, most effective, and most inexpensive of the sedative-hypnotic drugs. After oral administration, chloral hydrate is reduced rapidly to trichloroethanol, which is responsible for the depressant effects on the CNS. A significant portion of the trichloroethanol is excreted in the urine as the glucuronide, which may give a false-positive test for glucose.
Tolerance and addiction to chloral hydrate develop only rarely; for this reason, it was in the past commonly used for insomnia. Poisoning with chloral hydrate is a rare occurrence and resembles acute barbiturate intoxication except for the finding of miosis, which is said to characterize the former. Treatment follows along the same lines as for barbiturate poisoning. Death from poisoning is because of respiratory depression and hypotension; patients who survive may show signs of liver and kidney disease. Combining alcohol and chloral hydrate, the popular “Mickey-Finn” of detective stories in the mid-last century, produced severe intoxication and amnesia. Paraldehyde, another member of this group of sedative drugs, is no longer being manufactured in the United States, and chloral hydrate is now available mainly as an elixir for pediatric use.
With the introduction of chlordiazepoxide in 1960 and the benzodiazepine drugs that followed (particularly diazepam), the older sedative drugs (barbiturates, paraldehyde, chloral hydrate) have become virtually obsolete. Indeed, the benzodiazepines are among the most commonly prescribed drugs in the world today. According to Hollister (1990), 15 percent of all adults in the United States use a benzodiazepine at least once yearly and about half this number use the drug for a month or longer.