Journal of medical toxicology : official journal of the American College of Medical Toxicology
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Nearly all prior studies to delay onset of systemic toxicity and death after snake bite use a model of distal extremity envenomation. In the first of a series of planned studies using snake venoms with different toxicity profiles, the application of a novel device in a new model of torso envenomation in the setting of Eastern Coral Snake (Micrurus fulvius) venom (a potent neurotoxin) envenomation showed promise by delaying systemic intoxication. In this pilot study, we investigated this novel localizing circumferential compression (LoCC) device's ability to delay onset of life threatening systemic toxicity after Eastern Diamondback Rattlesnake (Crotalus adamanteus) envenomation, a potent hemotoxic and myotoxic venom. ⋯ Endpoints included cardiovascular collapse (fatal arrhythmia, loss of mean arterial pressure, or pulse) or respiratory arrest (<3 breaths/min, saturation < 80%) or survival to 7 h. The pigs in the treatment group reached an endpoint at an average time of 355 (+/-65) min compared with control 32 (+/-3.5) min (p < 0.04). In this pilot study, the LoCC device significantly delayed onset of systemic symptoms and death after torso envenomation with Eastern Diamondback Rattlesnake venom in this model.
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Levosimendan (Levo) increases sensitivity of troponin-C to calcium, thus increasing myocardial contractility. It is also a vascular K+-ATP channel agonist producing peripheral vasodilation. Previous research with levosimendan revealed an increase in cardiac output (CO) but not blood pressure (BP) in experimental verapamil poisoning. ⋯ Levosimendan moderately improved CO but not BP in verapamil poisoning. The hypotensive effects of levosimendan were not overcome by coadministration of either 4-AP or CaCl₂. Levosimendan may not be an appropriate agent to use in the treatment of verapamil poisoning.
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The proconvulsive properties of tramadol, bupropion, and nortriptyline have been well documented. Spinal fractures secondary to drug-induced seizures have been rarely reported. ⋯ Sudden onset of back pain during sleep can be an important clue to a seizure complicated by vertebral compression fractures, even in the absence of trauma. Toxicology consultation in seizures of unclear etiology can help discern drugs that offend even in therapeutic doses.
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Unintentional bupropion pediatric exposures uncommonly report severe clinical effects such as seizures. We sought to determine the clinical effects and case outcomes for unintentional bupropion ingestions in children age =6 years. The National Poison Data System was queried for unintentional, acute, single substance bupropion ingestions in children age =6 years for the time period January 1, 2000 to February 27, 2007 for cases followed to a known outcome. ⋯ A mg/kg dose was calculable in 76.1% of cases; the average amount for the no effect/minor cases and moderate/major effect was 13.8 +/- 18.8 and 38.8 +/- 44.0 mg/kg, respectively (p < 0.0001). Average time until development of seizures was 4.2 +/- 3.2 h with a maximum of 14 h. Few children develop toxicity from unintentional reported bupropion ingestions, with about 1.5% of patients developing an ANE.
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Propafenone is an anti-arrhythmic drug used in the management of supraventricular and ventricular arrhythmias. It is metabolised through cytochrome P450 2D6 pathways; the major metabolites possess anti-arrhythmic activity. The cytochrome P450 CYP2D6 is coded by more than 70 alleles resulting in great genetic polymorphism of CYP2D6 isoenzymes, and up to 7% of Caucasian population are poor metabolisers. ⋯ No antidepressant or analgesic drugs were detected in toxicological screen. Propafenone overdose has been reported to be associated with features of severe cardiovascular and CNS toxicity. Aggressive treatment, meticulous monitoring and supportive care was associated with a good outcome in this case.