Journal of toxicology. Clinical toxicology
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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.
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J. Toxicol. Clin. Toxicol. · Jan 2000
Multicenter StudyA nationwide survey of the management of unintentional-low dose tricyclic antidepressant ingestions involving asymptomatic children: implications for the development of an evidence-based clinical guideline.
The triage of unintentional tricyclic and cyclic antidepressant ingestions involving children <6 years seems based on single cases or small studies. Walsh, in describing 2 cases involving 15-20 mg/kg ingestions, recommended hospitalizing all children ingesting tricyclic and cyclic antidepressants. ⋯ This survey demonstrates that most children with tricyclic and cyclic antidepressant ingestions will be sent to the emergency department, regardless of the amount ingested. A prospective study is needed to determine the probable dose of tricyclic and cyclic antidepressant ingestions that requires observation at a health care facility.
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J. Toxicol. Clin. Toxicol. · Jan 2000
ReviewPyrethroid insecticides: poisoning syndromes, synergies, and therapy.
Pyrethroid insecticides are widely used, but there have been relatively few reports of systemic poisoning. These reports have, however, shown that pharmacotherapy is difficult and that the duration of poisoning can be unexpectedly long. Pyrethroids are ion channel toxins prolonging neuronal excitation, but are not directly cytotoxic. ⋯ Hence, the unauthorized pyrethroid/organophosphate mixtures marketed in some developing countries may precipitate human poisoning. Pyrethroid paresthesia can be treated by decontamination of the skin, but systemic poisoning is difficult to control with anticonvulsants. Pentobarbitone, however, is surprisingly effective as therapy against systemic type II pyrethroid poisoning in rats, probably due to its dual action as a chloride channel agonist and a membrane stabilizer.
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J. Toxicol. Clin. Toxicol. · Jan 2000
Case ReportsAcute elevation of blood lead levels within hours of ingestion of large quantities of lead shot.
Ingestion of elemental lead foreign bodies is felt to have a low risk of clinically significant lead absorption unless gastrointestinal pathology and/or prolonged transit time are present. We present a case of ingestion of a large quantity of small diameter lead shot accompanied by rapid elevation of blood lead levels. ⋯ Acute elevations of blood lead concentrations may occur rapidly after ingestion of multiple small elemental lead objects.
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J. Toxicol. Clin. Toxicol. · Jan 2000
Review Case ReportsIntermediate syndrome after malathion ingestion despite continuous infusion of pralidoxime.
A 33-year-old female ingested an unknown quantity of malathion in a suicide attempt. Cholinergic signs consistent with severe organ, phosphate intoxication developed and were treated within 6 hours of ingestion. Intravenous atropine and a continuous infusion of pralidoxime (400 mg/h) were administered. ⋯ Despite an initial clinical improvement and the presence of plasma pralidoxime concentrations exceeding 4 microg/mL, the patient developed profound motor paralysis consistent with the diagnosis of Intermediate Syndrome. In addition to the dose and frequency of pralidoxime administration, other factors including persistence of organophosphate in the body, the chemical structure of the ingested organophosphate, and the time elapsed between ingestion and treatment may limit the effectiveness of pralidoxime as an antidote in organophosphate ingestions. This case study suggests that these factors should be taken into account in assessing the risk of Intermediate Syndrome after intentional organophosphate ingestions.