Clinical Features

Mild to moderate barbiturate intoxication closely resembles the drug "high" produced by alcohol. Drowsiness, disinhibition, ataxia, slurred speech, and mental confusion are common features that escalate with increasing dose. The progressive CNS depression seen with severe barbiturate intoxication predictably manifests as a range from stupor to coma to complete neurologic unresponsiveness. Scales gauging the depth of coma are useful in describing patient presentation and monitoring interval changes in the level of consciousness during treatment in overdose settings. 10 The most common vital sign abnormalities seen in overdose are hypothermia, respiratory depression, and hypotension. The abnormal temperature control and respiratory depression are centrally mediated phenomena, whereas hypotension is due primarily to increased vascular capacitance and venous pooling. The end product of these derangements can be a patient who is cold, apneic, and in shock. Pulse rate is not diagnostic; pupil size, light reactivity, nystagmus, and deep tendon reflexes are variable. Gastrointestinal tract motility is slowed, resulting in delayed gastric emptying and ileus. Skin bullae, referred to as barbiturate blisters, are uncommon and may indicate nothing more than the effects of local skin pressure.5!0 Even when it is known that a barbiturate was ingested, it is prudent to consider coingestions and alternate explanations for the observed symptom complex.

Early deaths in barbiturate overdose result from cardiovascular collapse and respiratory arrest. Most common complications are hypoglycemia, followed by the delayed pulmonary problems of aspiration pneumonia, noncardiogenic pulmonary edema, and adult respiratory distress syndrome. Current mortality rates range between 1 and 3 percent and are more often the result of multiple organ system failure. Lethal dose is uncertain, but severe poisoning can be assumed if more than 10 times the hypnotic dose has been ingested in a single exposure.10

Laboratory evaluation in barbiturate overdose should include determination of glucose levels, blood chemistries, complete blood count, arterial blood gas measurement, toxicology screen, chest radiograph, and an electrocardiogram. Barbiturate serum levels are useful in establishing the diagnosis of a comatose patient and should be obtained and used to distinguish long- from short-acting agents because treatment approaches differ. As a rule of thumb, patients presenting with a serum concentration of more than 10 mg/dL for a long-acting barbiturate, more than 7 mg/dL for an intermediate-acting barbiturate, and more than 3 mg/dL for a short-acting barbiturate, left untreated, have a greater risk of death from the exposure. These measurements are not reliable in predicting clinical course in overdose because they do not reflect brain barbiturate concentrations and may underestimate the clinical condition of a patient in the setting of polydrug exposure. Such levels are also invalid in chronic barbiturate abusers who have developed physiologic tolerance and in patients with renal or hepatic disease who have decreased clearance.4,5,!0

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