Journal of toxicology. Clinical toxicology
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J. Toxicol. Clin. Toxicol. · Jan 2000
Sources of information for acute poisoning in accident and emergency departments in Dublin, Ireland.
Access by accident and emergency staff to up-to-date information on poisoning is essential for optimal management of acute poisoning. Apart from the National Poisons Information Centre, other information sources can be used. The objectives of the study were to identify sources of information on acute poisoning in accidents and emergencies and satisfaction with their use. ⋯ For the optimal management of acute poisoning, direct access to computerized information databases in accidents and emergencies combined with telephone access to the National Poisons Information Centre is required, with information available in hard copy.
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J. Toxicol. Clin. Toxicol. · Jan 2000
A descriptive study of an epidemic of poisoning caused by heroin adulterated with scopolamine.
Adulterants, contaminants, and diluents are all examples of additives to street drugs. Some of these additives may be pharmacologically active; however, it is unusual for them to cause toxic side effects. In the spring of 1995, a new form of heroin appeared in New York City, spreading to other East Coast cities, that was adulterated with scopolamine. It caused severe anticholinergic toxicity in heroin users with patients often presenting to emergency departments in great numbers. This is a report of the demographics and clinical characteristics of the epidemic. ⋯ Adulteration of street drugs can lead to toxic epidemics. Poison centers are essential for identification of these trends and are the primary source of information on diagnosis and treatment.
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A case of combined, massive overdose of both atenolol and diltiazem in an adult male is reported. Cardiac arrest ensued which was responsive to cardiopulmonary resuscitation. Bradycardia, hypotension, and oliguria followed which were resistant to intravenous pacing and multiple pharmacologic interventions, including intravenous fluids, calcium, dopamine, dobutamine, epinephrine, prenalterol, and glucagon. Adequate mean arterial pressure and urine output were restored only after addition of phenylephrine to therapy with multiple agents and transvenous pacing. The patient survived until discharge after a hospital course complicated by nontransmural myocardial infarct on hospital day 4 and pneumonia. Laboratory testing subsequently revealed high serum levels of both atenolol and diltiazem. The atenolol level of 35 microg/mL in this patient is the highest reported associated with survival. ⋯ This case illustrates severe cardiovascular toxicity after overdose of both atenolol and diltiazem. Oliguria, which has previously been reported in severe atenolol overdose, was successfully treated without hemodialysis by the addition of phenylephrine to aggressive therapy with pacing, inotropic, and pressor support.
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J. Toxicol. Clin. Toxicol. · Jan 2000
Case ReportsFelbamate overdose complicated by massive crystalluria and acute renal failure.
We report a 20-year-old woman who developed altered mental status, massive crystalluria, and acute renal failure following an intentional overdose of felbamate and sodium valproate. Peak plasma concentrations of felbamate and sodium valproate were 200 microg/mL and 470 microg/mL, respectively. ⋯ Following parenteral hydration, the crystalluria and acute renal failure resolved and the patient recovered. The frequency and significance of crystalluria in felbamate intoxication is unknown.
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J. Toxicol. Clin. Toxicol. · Jan 2000
Case ReportsCentral nervous system toxicity and early peripheral neuropathy following dermal exposure to methyl bromide.
We describe a case of early peripheral neuropathy and central nervous system toxicity as a result of acute predominantly dermal exposure to methyl bromide. A 32-year-old male was admitted after an accidental predominantly dermal exposure to methyl bromide while fumigating soil for pest control. The patient suffered dermal burns and vesicles on the upper and lower limbs. One week following exposure, he developed progressive weakness of the lower limbs, ataxia, paresthesiae of both legs and the left arm, hyperactive tendon reflexes in the lower limbs, and left Babinski sign. Nerve conduction velocity testing was compatible with axonal neuropathy. The patient recovered gradually from his burns. Three months postexposure he showed no signs of central nervous system toxicity, but the peripheral neuropathy was still present. ⋯ Neurological effects primarily referable to the central nervous system following severe inhalation of methyl bromide have frequently been reported. The patient described in this study developed an unusual early peripheral neuropathy following dermal exposure. Peripheral neuropathy can be an outcome of methyl bromide intoxication, but is usually a late sequela of acute central nervous system toxicity or an aftereffect of repetitively inhaled chronic exposure. In this case, exposure to methyl bromide through abraded skin caused early peripheral neuropathy and central nervous system toxicity.