Journal of toxicology. Clinical toxicology
-
J. Toxicol. Clin. Toxicol. · Jan 1996
ReviewBenefits of extracorporeal membrane oxygenation for hydrocarbon pneumonitis.
To review the therapeutic benefits of extracorporeal membrane oxygenation for the management of hydrocarbon pneumonitis. ⋯ The need for extracorporeal membrane oxygenation is rare owing to the generally good outcome of most cases of hydrocarbon ingestions and pneumonitis. Only with further research on the nature and clinical course of severe hydrocarbon pneumonitis, refinement of extracorporeal membrane oxygenation criteria, and evaluation of alternative therapies, will the benefits of extracorporeal membrane oxygenation be better defined.
-
J. Toxicol. Clin. Toxicol. · Jan 1996
An evaluation of unleaded petrol as a harm reduction strategy for petrol sniffers in an aboriginal community.
In mid 1989, leaded petrol was replaced by unleaded petrol to reduce lead toxicity in petrol sniffers in Maningrida, a remote Aboriginal community in Northern Australia. RETROSPECTIVE REVIEWS: Hospital admissions between 1987 and 1992 due to petrol sniffing were compared for Maningrida and a community using only leaded petrol. ⋯ The elimination of tetraethyl lead from petrol resulted in a significant decrease in hospitalization of petrol sniffers.
-
J. Toxicol. Clin. Toxicol. · Jan 1996
Effect of calcium chloride and 4-aminopyridine therapy on desipramine toxicity in rats.
Hypotension is a major contributor to mortality in tricyclic antidepressant overdose. Recent data suggest that tricyclic antidepressants inhibit calcium influx in some tissues. This study addressed the potential role of calcium channel blockade in tricyclic antidepressant-induced hypotension. ⋯ The administration of CaCl2 or 4-aminopyridine did not reverse tricyclic antidepressant-induced hypotension in rats. CaCl2 therapy may possibly worsen both cardiovascular and central nervous system toxicity. These findings do not support a role for calcium channel inhibition in the pathogenesis of tricyclic antidepressant-induced hypotension.
-
J. Toxicol. Clin. Toxicol. · Jan 1996
Review Case ReportsHemolysis after acetaminophen overdose in a patient with glucose-6-phosphate dehydrogenase deficiency.
A sixteen year-old-male with a history of glucose-6-phosphate dehydrogenase deficiency ingested an unknown amount of acetaminophen and presented to an emergency department 7.5 h later. He was afebrile. His serum acetaminophen level was 184 micrograms/mL, and his urine toxicologic screen was otherwise negative. Vomiting led to enrollment in a experimental protocol of intravenous N-acetylcysteine. He developed no evidence of subsequent chemical hepatitis but did develop a significant Coomb's negative hemolytic anemia. Hemoglobin on presentation was 14 g/dL and reached a nadir of 9.4 g/dL on admission day 4. ⋯ Patients with glucose-6-phosphate dehydrogenase deficiency who overdose with acetaminophen should be monitored for the possible development of subsequent drug-induced hemolysis.
-
J. Toxicol. Clin. Toxicol. · Jan 1996
Review Case ReportsSalicylism from topical salicylates: review of the literature.