Diphenhydramine-induced wide complex dysrhythmia responds to treatment with sodium bicarbonate.

Diphenhydramine, a common ingredient in over-the-counter medications, is often taken in overdose. Toxicity is usually limited to anticholinergic symptoms. However, because diphenhydramine also exhibits type IA sodium channel blockade, cardiac toxicity is also possible. Although it would be expected that, like other type IA toxicities, diphenhydramine-induced cardiotoxicity could be responsive to hypertonic sodium bicarbonate, this finding is largely unappreciated. We describe 3 cases of diphenhydramine-induced cardiac toxicity that were responsive to bicarbonate.

Treatment of methapyrilene toxicity with physostigmine.

Methypyrilene, 40 mg/kg, was administered to male mongrel dogs, resulting in both central and peripheral anticholinergic effects. Physostigmine in doses of 0.5 to 1.0 mg was effective in reversing the central effects completely and the peripheral effects to a limited degree.

Acute poisoning from over-the-counter sleep preparations.

All cases received by the Rocky Mountain Poison Center involving over-the-counter (OTC) sleep preparations were studied during an 18-month period to elucidate 1) the range of toxicity; 2) characteristic symptoms, and 3) the time of onset of symptoms. In 155 cases reviewed retrospectively, the three most commonly ingested agents were Sominex, Nytol and Sleepeze. Multiple ingestions were also involved. Symptomatology was equally divided among no symptoms, mild symptoms and possible life-threatening symptoms. The least amount taken to produce possible life-threatening symptoms was 16 Sominex, 18 Nytol and 15 Sleepeze, although the average amount producing the same symptoms was approximately twice that. These symptoms were seen within six hours in all but three of the 39 cases presenting with these symptoms. There were no deaths.

Sleep aids and sedatives.

Proprietary sleep aids and sedatives can cause delirium, coma and occasionally death in children and adults. The constituents in sleep aids that significantly effect central nervous system activity are bromides, methapyrilene, pyrilamine and scopolamine (hyoscine). Constituent proportions and mixtures vary greatly at different times since manufacturers make frequent adjustments. The effects of toxicity resulting from the misuse of ethylenediamines include nausea, vomiting, blurred vision, incoordination, tremors, dry mouth, constipation and an acute poisoning syndrome. Management of adverse reactions produced by either methapyrilene or pyrilamine consists of dosage reduction or discontinuation. The acute poisoning syndrome requires implementation of general symptomatic and supportive principles.

A fatality involving methapyrilene.

Tissue concentrations of methapyrilene are given in a fatal case. There are no indications that methapyrilene had any synergistic or antagonistic effect with the patient's cardiopulmonary condition, although when taken in high overdosages the pharmacologic effects may be altered. This case was supported by other data in an attempt to elucidate as many contributing factors as possible in evaluating lethal levels.

Methapyrilene toxicity.

Seven cases of drug overdosage involving methapyrilene have been presented, five of which resulted in death. Methapyrilene blood levels ranged fron 1.2 to 3.0 mg% (Table 2). Five of the seven cases involved multiple drug dosage with ethanol, salicylamide, amobarbital, secobarbital, and/or scopolamine. Of the remaining cases, involving only methapyrilene, ome fatality occurred at a blood level of 2.7 mg%. The surviving case involved the reported ingestion of 100 tablets of Sleep-eze (2.5 gm methapyrilene), wherein serial lavage removed 1.1 gm of methapyrilene. Urinalysis revealed 2.52 mg% of methapyrilene in 1300 ml of urine. The methapyrilene blood level was too low to quantitate.