The symptoms and signs vary with the type and amount of drug as well as with the length of time that has elapsed since it was ingested. Pentobarbital and secobarbital produce their effects quickly and recovery is relatively rapid. Phenobarbital induces coma more slowly and its effects tend to be prolonged. In the case of long-acting barbiturates, such as phenobarbital, the hypnotic-sedative effect lasts 6 h or more after an average oral dose; with the intermediate-acting drugs such as amobarbital, 3 to 6 h; and with the short-acting drugs, secobarbital and pentobarbital, less than 3 h. Most fatalities follow the ingestion of secobarbital, amobarbital, or pentobarbital. The ingestion by adults of more than 3 g of these drugs at one time will prove fatal unless intensive treatment is applied promptly. The potentially fatal dose of phenobarbital is 6 to 10 g. The lowest plasma concentration associated with lethal overdosage of phenobarbital or barbital has been approximately 60 mg/mL and that of amobarbital and pentobarbital, 10 mg/mL.
Severe intoxication occurs with the ingestion of 10 to 20 times the oral hypnotic dose. The patient cannot be roused by any means, that is, the patient is comatose. Respiration is slow and shallow or irregular, and pulmonary edema and cyanosis may be present. The tendon reflexes are usually, but not invariably, absent. Most patients show no response to plantar stimulation, but in those who do, the responses are extensor. With deep coma, the corneal and gag reflexes may also be abolished. Ordinarily the pupillary light reflex is retained in severe intoxication and is lost only if the patient is asphyxiated; but in advanced cases, the pupils become miotic and poorly reactive, simulating opiate intoxication. At this point respiration is greatly depressed and oculocephalic and oculovestibular reflex responses are usually abolished. In the early hours of coma, there may be a phase of flexor or extensor posturing or rigidity of the limbs, hyperactive reflexes, ankle clonus, and extensor plantar signs; persistence of these signs indicates that anoxic damage has been added. The temperature may be subnormal, the pulse is faint and rapid, and the blood pressure is greatly reduced. Failure of respiration to quicken on painful stimulation is an ominous sign.
There are few conditions other than barbiturate intoxication that cause a flaccid coma with small reactive pupils, hypothermia, and hypotension. A pontine hemorrhage may do so, but a hysterical trance or catatonic stupor does not present a problem in differential diagnosis. Serum toxicology studies provide a reliable means of identifying the type and amount of barbiturate in the blood. A patient who has also ingested alcohol may be comatose with relatively low blood barbiturate concentrations. Contrariwise, the barbiturate addict may show only mild signs of intoxication with very high blood barbiturate concentrations.
Management In mild or moderate intoxication, recovery is the rule and special treatment is not required except to prevent aspiration. If the patient is unresponsive, special measures must be taken to maintain respiration and prevent infection. An endotracheal tube should be inserted, with suctioning as necessary. Any risk of respiratory depression or underventilation requires the use of a mechanical ventilator.
Hemodialysis or hemofiltration with charcoal may be used in comatose patients who have ingested long-acting barbiturates and these treatments are particularly advisable if anuria or uremia has developed. Occasionally, in the case of a barbiturate addict who has taken an overdose of the drug, recovery from coma is followed by the development of abstinence symptoms, as described later.
Barbiturate Abstinence, or Withdrawal, Syndrome