Fatal maprotiline intoxication.

We report a fatal case of drug toxicity associated with torsade de pointes following an overdose of the tetracyclic antidepressant, maprotiline (Ludiomil). Tissue and plasma levels were obtained at autopsy and are noted. In addition, the cardiovascular effects, pharmacokinetics, and toxicity of maprotiline are reviewed and compared with that of tricyclic antidepressants.

Efficacy of ipecac and activated charcoal/cathartic. Prevention of salicylate absorption in a simulated overdose.

Twelve adult volunteers were given 24 81-mg aspirin tablets and were randomly assigned into the following treatment groups: (1) control aspirin, (2) 30 mL of ipecac repeated if vomiting not induced, (3) 60 g of activated charcoal per 15 g of magnesium sulfate (MgSO4), and (4) ipecac repeated if needed, followed by activated charcoal/MgSO4 given 1 1/2 hours after the last vomiting episode. All treatments began 60 minutes following aspirin ingestion. Urine was collected for 48 hours for percent total salicylate excretion. Mean +/- SD recovery of salicylate from urine was as follows: aspirin, 96.3% +/- 7.5%; ipecac 70.3% +/- 11.8%, activated charcoal/MgSO4, 56.4% +/- 12%; and ipecac and activated charcoal/MgSO4, 72.4% +/- 14.1%. Ten subjects completed the study. In group 4, eight of ten subjects vomited the activated charcoal/MgSO4 immediately, making statistical analysis impossible. Analysis revealed that activated charcoal/MgSO4 significantly lowered the absorption of aspirin compared with the control and ipecac-treated groups. Furthermore, ipecac significantly lowered aspirin absorption compared with the control group. We conclude that activated charcoal/MgSO4 used alone is superior to the other treatment modalities at inhibiting the absorption of multiple aspirin tablets.

Crystallization of three phenytoin preparations in intravenous solutions.

The stability of three phenytoin sodium intravenous preparations in two intravenous solutions was compared. Solutions of phenytoin sodium 1.0, 1.5, 4.0. and 10.0 mg/ml were prepared by adding Dilantin, Phenhydan (commercially available in Europe) and Phenytoin Concentrate (available in Europe for research) to 5% dextrose or 0.9% sodium chloride injection. (The two European products contain solubilizers and stabilizers different from those in U.S. formulations.) Four sets of samples were prepared in 10-ml glass blood collection tubes; two sets each were sealed and unsealed. Macroscopic and microscopic observations were made immediately and at various times up to 24 hours. The pH was measured periodically. The three phenytoin sodium preparations also were added to 100-ml polyvinyl chloride bags of 5% dextrose or 0.9% sodium chloride injection in concentrations of 1, 1.5, 4, and 10 mg/ml. Phenytoin concentration was determined spectrophotometrically initially and at 1, 4, 8, 12, and 24 hours. Percent phenytoin crystallization, based on initial concentration, was calculated, and differences among the three phenytoin products were tested using an analysis of variance split-plot factorial design (p less than 0.05). Dilutions of Phenhydan and Phenytoin Concentrate in both solutions were stable (less than 10% crystallization) for at least 24 hours. Percent phenytoin crystallization was significantly greater for Dilantin compared with Phenhydan or Phenytoin Concentrate at each time in 5% dextrose injection and after four hours in 0.9% sodium chloride injection. Phenytoin crystallization was not solely dependent on pH of the solution, concentration, or carbon dioxide absorption. Phenhydan and Phenytoin Concentrate admixtures provided a more suitable environment for phenytoin stability than Dilantin admixtures did.