Comment on "Pediatric fatality following ingestion of Dinitrophenol: postmortem identification of a 'dietary supplement'".
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Biomedical subjects
Publications and source records attributed to Donna Seger.
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In the US, two antivenins are marketed for the treatment of snake envenomation. The horse-derived serum-globulin-based Antivenin (Crotalidae) Polyvalent (ACP) has been available since 1954. There are few data on the efficacy and incidence of adverse events that occur following the administration of ACP. Most of the data are retrospective, anecdotal, or case reports. In 2000, ovine-derived serum-globulin-based ACP (Crofab) became available. Crofab is said to cause fewer reactions than ACP, but there are few comparative data to substantiate this claim. Although both antivenins ameliorate the systemic symptoms following snake envenomation, the efficacy of either antivenin in decreasing oedema and swelling is unknown for a number of reasons. Clinical trials are small and have not included control arms. The degree of oedema, as well as the efficacy of the antivenin in decreasing oedema, may depend on the genera of the snake (usually unknown) that envenomated the patient. This article compares available data on clinical aspects of the two antivenins. More prospective data are needed to determine the comparative efficacy of the two antivenins, or the efficacy of Crofab in preventing tissue oedema. There are still unanswered questions regarding the optimal dosing regimen of Crofab.
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Single-dose activated charcoal (SDAC) is frequently administered to poisoned patients. The assumption is that toxin absorption is prevented and that toxicity (as defined by morbidity and mortality) of the poisoning is decreased. Yet there is no evidence that SDAC improves outcome. Risks of this procedure have not been determined. The reported adverse events following SDAC administration are reviewed and risk:benefit ratio for this procedure is discussed.
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Limited data exist on overdose with new antiepileptic drugs. We reviewed the medical records of two patients who took a topiramate overdose as a suicide attempt. We recorded their medical and seizure histories, concomitant antiepileptic medications, neurologic examination, and laboratory findings at the time of presentation following the overdose. We also recorded their progress and the evolution of laboratory abnormalities. Both patients progressed to coma and had generalized convulsive status epilepticus, requiring intubation and treatment with benzodiazepines. Both patients recovered within 2 days but had a non-anion-gap metabolic acidosis that persisted for 5-6 days. Physicians should carefully monitor patients treated with topiramate who develop signs of clinical depression. The non-anion-gap metabolic acidosis observed may be due to inhibition of renal cortical carbonic anhydrase.