Abstract
RECENT clinical studies have demonstrated that osmotic diuresis, with or without urinary alkalinization, will accelerate the renal excretion of drug in patients with barbiturate intoxication.1 2 3 4 5 When the intoxication is due to a long acting barbiturate — for example, phenobarbital — urinary excretion plays a major part in drug disposal. The augmented excretion achieved with this regimen is of sufficient magnitude to accelerate the fall in plasma barbiturate concentration and shorten the duration of coma.1 , 3 The claim that a similar beneficial effect can be obtained when coma is due to a short acting barbiturate such as pentobarbital or secobarbital is less . . .