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) · Dec 2010
ReviewDelayed neurological sequelae from ethylene glycol, diethylene glycol and methanol poisonings.
Ethylene glycol, diethylene glycol and methanol are widely available chemicals and are found in a variety of common household products including antifreeze, windshield washer fluid, brake fluid and lubricants. Following ingestion of these glycols and methanol, patients frequently develop an early neurological syndrome consisting of inebriation, ataxia, and if severe, seizures and coma. Though uncommon, a neurological syndrome may also develop as a delayed complication. ⋯ Uncommonly, delayed neurological syndromes may develop as complications of poisoning due to ethylene glycol, diethylene glycol and methanol; the onset of such neurological damage is often days or even weeks post-ingestion. Further research is required to explain why the facial nerve is the cranial nerve most commonly involved and why the basal ganglia are predisposed to injury.
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Clin Toxicol (Phila) · Dec 2010
Usefulness of the serum lactate concentration for predicting mortality in acute beta-blocker poisoning.
Serum lactate measured in the emergency department was recently assessed as an excellent prognosticator of drug-overdose fatality, with the optimal lactate cutoff point being 3.0 mmol/L. However, lactate's role has never been specifically studied in beta-blocker poisonings. ⋯ Serum lactate elevation in beta-blocker poisoning is relatively mild on admission despite the presence of significant cardiovascular symptoms. Even if raised in severe poisonings and alone correlate well with prognosis, lactate concentration is not an absolute predictor of beta-blocker-overdose fatality.
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Clin Toxicol (Phila) · Nov 2010
Case ReportsStatus epilepticus and wide-complex tachycardia secondary to diphenhydramine overdose.
Diphenhydramine is an H1 histamine antagonist that is commonly used for allergic reactions, colds and cough, and as a sleep aid. In addition to anticholinergic and antihistaminergic effects, sodium channel blockade becomes evident following diphenhydramine overdose. While seizures may occur following overdose of a diphenhydramine, status epilepticus is distinctly uncommon. We report a case with both status epilepticus and wide-complex dysrhythmias following an intentional diphenhydramine overdose. ⋯ Diphenhydramine overdose may cause status epilepticus and wide-complex tachycardia. Management should focus on antidotal therapy with sodium bicarbonate and supportive neurological management with appropriate anticonvulsants and airway protection if clinically indicated.
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Botulism is a neuroparalytic illness caused by botulinum toxin, a product of the Clostridium botulinum bacteria and characteristically presents as an acute, symmetrical, descending flaccid paralysis. Albeit it is the most poisonous substance known, which even poses a major threat as biological weapons, purified and highly diluted botulinum toxin can be used to treat a wide variety of conditions associated with muscular hyperactivity, glandular hypersecretions and pain. There are six clinical presentations associated with current occurring botulism, each results from absorption of botulinum toxin into the bloodstream. ⋯ Early diagnosis and management rely on history and physical examination. Delay in treatment may allow progression of paralysis, protracted hospitalization and deaths of long-term mechanical ventilation and intensive care unit care. The clinicians must take this disease into consideration of a possible outbreak. Awaiting laboratory confirmation is an egregious error, while awareness of the clinical sign and symptoms of botulism is critical for early diagnosis. Rapid management and followed public health surveillance may greatly alleviate disease severity and decrease mortality rates.