Acute myocarditis after massive phenelzine overdose.

BACKGROUND: Monoamine oxidase inhibitors (MAOIs) are uncommonly used due to their high frequency of adverse effects, including tachycardia and hypertension. Recently, there has been renewed interest in the role of this class of drugs in treating a variety of psychiatric disorders. The clinical features of MAOI overdose are poorly characterised. This paper describes a novel cardiac complication of phenelzine toxicity in a previously healthy young adult with no history of cardiovascular disease. METHODS: A 23-year-old woman presented to hospital after massive phenelzine overdose, and the clinical features and pathological findings are discussed in light of existing literature. RESULTS: Clinical features of phenelzine toxicity included reduced consciousness level, seizures, and tachycardia, in keeping with previous reports. Unexpectedly, the patient developed severe and unexplained hypotension and impaired left ventricular function, and died 3 days after initial presentation. Post-mortem examination confirmed high serum phenelzine concentrations (4.1 mg/L) and histopathological features that were consistent with drug-induced acute myocarditis. CONCLUSION: Acute myocarditis was attributed to phenelzine in the absence of any plausible alternative explanation. This possible complication should be considered in patients who develop unexplained hypotension after phenelzine overdose.

"Ping-pong" gaze in severe monoamine oxidase inhibitor toxicity.

Clinical features of monoamine oxidase inhibitor (MAOI) toxicity include hypertension, hyperthermia, tachycardia, and muscular agitation. We report two cases in which some of these signs of severe toxicity were seen in association with a unique periodic alternating gaze disturbance known as "ping-pong" gaze.

Two fatalities involving phenelzine.

Phenelzine is a drug commonly used in the treatment of depression. Fatalities due to phenelzine have been infrequently reported in the medical literature. The authors report two cases in which phenelzine levels in blood at autopsy were 10-50 times greater than therapeutic levels. Although in both cases other drugs were present in elevated levels, the concentrations of phenelzine were so greatly elevated as to be considered as an independent cause of death.

A case of MAO inhibitor/MDMA interaction: agony after ecstasy.

After ingesting 3,4-methylene-dioxy-methamphetamine (MDMA) and the monoamine oxidase (MAO) inhibitor phenelzine, a 50 year old male developed marked hypertension, diaphoresis, altered mental status, and hypertonicity lasting 5-6 hours. This clinical course is typical of interaction between MAO inhibitors and some sympathomimetics including amphetamines. Such interaction has not previously been described involving MDMA. Sympathomimetic-MAO inhibitor interactions can cause excessive release of endogenous bioactive amines (e.g. norepinephrine, serotonin). Hypertensive crisis, intracranial hemorrhage, hypertonicity, and severe hyperthermia have occurred due to sympathomimetic-MAO inhibitor interactions. MDMA shares structural and pharmacologic features with other agents capable of causing this interaction, and this case suggests that MDMA can cause significant toxicity in patients taking MAO inhibitors.

Phenelzine poisoning.

A 46-year-old female with severe phenelzine poisoning was managed successfully by alpha blockade and fluid loading, with the aid of invasive haemodynamic monitoring. The pathophysiology was documented, showing elevated plasma and urinary catecholamines, cardiovascular abnormalities and a contracted blood volume. Most of these changes were reversed following treatment.

Monoamine oxidase inhibitor overdose.

Described is the clinical course of a 26-year-old woman who died following an overdose of the MAO inhibitor phenelzine. Signs and symptoms of toxicity were delayed in onset. Initial findings of excessive neuromuscular activity were followed by severe hyperthermia, coma, cardiovascular collapse, acute renal failure, hemolysis, rhabdomyolysis, and disseminated intravascular coagulation. A review of the literature suggests that these features are not unusual following MAO inhibitor overdosage. The pathophysiology and management of MAO inhibitor poisoning are discussed.

Accidental poisoning with psychotropic drugs in children.

Seventy-seven (0.24%) of 32,005 admissions to the Massachusetts General Hospital pediatric service during the period 1962 to 1973 were due to accidental poisoning. In 27 cases, mostly involving children less than 6 years of age, psychotropic drugs were implicated. These included sedative-hypnotics in six cases, phenytoin in two, major tranquilizers in five, antidepressants in three, stimulants or hallucinogens in three, and drug mixtures in eight. Toxicologic analyses contributed little to diagnosis and initial management. Except for one child who ingested ferrous sulfate, no patient was seriously intoxicated, and all recovered rapidly without sequelae. Although referral of serious poisoning cases to another hospital may have biased the results, the findings suggest that accidental psychotropic drug poisoning is not a major source of childhood morbidity.