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) · Jan 2008
Multicenter Study Comparative StudyAcute poisonings treated in hospitals in Oslo: a one-year prospective study (II): clinical outcome.
The changing pattern of acute poisoning may affect complications and outcome in these patients. An update study on acute poisonings was therefore performed and compared to similar data from 1980. ⋯ In-hospital mortality in poisoned patients remained low, few patients entailed complications, and most patients survived without permanent sequelae. Drug- and alcohol-abuse related poisonings were most severe.
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Clin Toxicol (Phila) · Jan 2008
Case ReportsRecurrent life-threatening ventricular dysrhythmias associated with acute hydrofluoric acid ingestion: observations in one case and implications for mechanism of toxicity.
Hydrofluoric acid (HF) is a weak inorganic acid used for etching and as rust remover. Systemic toxicity is manifested as ventricular dysrhythmias. The mechanisms for these dysrhythmias are not well elucidated. ⋯ Ventricular dysrhythmias due to HF toxicity seem to be independent of either hypocalcemia or hyperkalemia. Systemic toxicity after ingestions may be delayed and precipitous.
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Clin Toxicol (Phila) · Jan 2008
Comparative StudyTreatment of experimental verapamil poisoning with levosimendan utilizing a rodent model of drug toxicity.
Levosimendan is an inotropic agent used in the treatment of heart failure. It is a myocardial calcium sensitizer, binding to cardiac troponin-C, and a vascular K+ATP-channel agonist producing peripheral vasodilatation. ⋯ Levosimendan increased CO in this model of verapamil poisoning to a similar degree as CaCl2 alone, but it did not improve BP from time of maximal toxicity. The addition of CaCl2 to Levosimendan did not appear to result in any further improvement in CO and BP compared to CaCl2 alone. The failure of levosimendan to improve BP may result from vasodilation induced by levosimendan peripheral vascular K+ATP-channel agonism. This may compound the vasodilatory effects of verapamil and offset any hemodynamic improvements produced by increased cardiac output.