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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is presented of a fatal drug interaction caused by ingestion of clozapine (Clozaril) and fluoxetine (Prozac). Clozapine is a tricyclic dibenzodiazepine derivative used as an "atypical antipsychotic" in the treatment of severe paranoid schizophrenia. Fluoxetine is a selective serotonin reuptake inhibitor used for the treatment of major depression. Clinical studies have proven that concomitant administration of fluoxetine and clozapine produces increased plasma concentrations of clozapine and enhances clozapine's pharmacological effects due to suspected inhibition of clozapine metabolism by fluoxetine. Blood, gastric, and urine specimens were analyzed for fluoxetine by gas chromatography/mass spectrometry (GC/MS) and for clozapine by gas-liquid chromatography (GLC). Clozapine concentrations were: plasma, 4.9 micrograms/mL; gastric contents, 265 mg; and urine, 51.5 micrograms/mL. Fluoxetine concentrations were: blood, 0.7 microgram/mL; gastric contents, 3.7 mg; and urine 1.6 micrograms/mL. Norfluoxetine concentrations were: blood, 0.6 microgram/mL, and none detected in the gastric contents or urine. Analysis of the biological specimens for other drugs revealed the presence of ethanol (blood, 35 mg/dL; vitreous, 56 mg/dL; and urine 153 mg/dL) and caffeine (present in all specimens). The combination of these drugs produced lethal concentrations of clozapine and high therapeutic to toxic concentrations of fluoxetine. The deceased had pulmonary edema, visceral vascular congestion, paralytic ileus, gastroenteritis and eosinophilia. These conditions are associated with clozapine toxicity. The combined central nervous system, respiratory and cardiovascular depression of these drugs was sufficient to cause death. The death was determined to be a clozapine overdose due to a fatal drug interaction.
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PMID:A fatal drug interaction between clozapine and fluoxetine. 972 31

Electroconvulsive therapy (ECT) was scheduled for a 61-yr-old woman with major depression who had been taking a beta-blocker for hypertension. She underwent the first ECT under thiamylal anesthesia uneventfully. The second ECT was performed under propofol anesthesia on the next day. Immediately after ECT, the heart rate dropped from 56 to 19 beats.min-1, which was remedied by intravenous atropine. Then, the blood pressure increased to 204/108 mmHg but it was controlled by nicardipine. However, the SpO2 decreased to 84-88% under oxygen administration by mask at a rate of 3 l.min-1. The patient complained of chest discomfort and had a bloody secretion from the trachea. A chest X-ray showed a butterfly shadow. The patient was diagnosed as having neurogenic pulmonary edema and was treated in the ICU by artificial ventilation and administration of diuretics and catecholamines. These treatments proved to be successful, and the patient was discharged from the ICU 4 days later uneventfully. This case indicates that hemodynamics should be carefully monitored following ECT and that care should be taken to prevent the occurrence of complications after ECT.
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PMID:[A case of pulmonary edema after electroconvulsive therapy under propofol anesthesia]. 1142 71

A 42-year-old right-handed man with major depression, posttraumatic stress disorder, gastroesophageal reflux disease, and hypertension received 7 treatments of right unilateral electroconvulsive therapy, with the only complications being elevated blood pressure up to 180/120 mm Hg and agitation upon awakening. During eighth treatment, he experienced blood pressures as high as 210/130 mm Hg with severe agitation upon awakening from anesthesia followed by pulmonary edema. Pulmonary edema is rarely seen as a complication in electroconvulsive therapy, but if the airway becomes obstructed or there is excessive sympathetic discharge during the procedure, pulmonary edema may be more likely to occur.
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PMID:Pulmonary edema after electroconvulsive therapy. 1861 64

Acute pulmonary edema complicating electroconvulsive therapy is an extremely uncommon event that has rarely been described in the literature. Different theories, including one suggesting a cardiogenic component, have been proposed to explain its genesis. The present report describes a classic presentation of this condition with review of its potential mechanisms and diagnostic approach. After successful completion of a session of electroconvulsive therapy, a 42-year-old woman with major depressive disorder developed acute systemic high blood pressure, shortness of breath, and hemoptysis. A chest radiograph demonstrated diffuse bilateral pulmonary infiltrates. Initially cardiogenic pulmonary edema was presumed, but an extensive diagnostic work-up demonstrated normal systolic and diastolic left ventricular function, and with only supportive measures, a complete clinical and radiographic recovery was achieved within 48 hours. The present case does not support any cardiogenic mechanism in the genesis of this condition.
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PMID:Non-cardiogenic pulmonary edema complicating electroconvulsive therapy: short review of the pathophysiology and diagnostic approach. 2203 75