Clinical toxicology : the official journal of the American Academy of Clinical Toxicology and European Association of Poisons Centres and Clinical Toxicologists
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Clin Toxicol (Phila) · Jun 2007
Case ReportsSuccessful organ transplantation after treatment of fatal cyanide poisoning with hydroxocobalamin.
Cyanide-poisoned patients are potential organ donors provided that organs are not damaged by the poison or by antidotal treatment. ⋯ Anoxic cardiac arrest following acute cyanide poisoning treated with hydroxocobalamin (5 g + 5 g) was not a contraindication to organ transplantation after confirmed encephalic death in this patient.
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Clin Toxicol (Phila) · Jun 2007
Development and implementation of an emergency department observation unit protocol for deliberate drug ingestion in adults - preliminary results.
Patients presenting after reported overdose are typically precluded from admission to emergency department observation units (EDOU). The purpose of this study was to describe the initial experience with an EDOU overdose protocol. ⋯ Although initial numbers are too small for meaningful analysis, the results suggest that prolonged observation of this problematic patient subset within an EDOU is feasible.
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Clin Toxicol (Phila) · Jun 2007
Case ReportsRattlesnake envenomation with neurotoxicity refractory to treatment with crotaline Fab antivenom.
Neurotoxicity following rattlesnake envenomation is reported with certain crotaline species. In some instances, crotaline Fab antivenom therapy that effectively halts progression of local tissue edema and hemotoxicity fails to reverse neurologic venom effects. ⋯ We describe two cases of neurotoxicity following rattlesnake envenomation in which treatment with crotaline Fab antivenom adequately obtained initial control of local swelling and hematologic effects, but neurotoxic venom effects remained refractory to antivenom therapy. This phenomenon is anecdotally recognized following certain crotaline species envenomations.
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Clin Toxicol (Phila) · Jun 2007
Case ReportsReversal of salicylate-induced euglycemic delirium with dextrose.
Salicylate poisoning inhibits Krebs cycle enzymes and uncouples oxidative phosphorylation. Under these circumstances, we hypothesize that CNS glucose supply is sometimes unable to keep up with demand resulting in hypoglycorrhacia and delirium even in the face of serum euglycemia. Supporting this conjecture, we report two euglycemic patients with salicylate-induced delirium who responded to boluses of concentrated dextrose with a prompt improvement in mental status.