Journal of toxicology. Clinical toxicology
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J. Toxicol. Clin. Toxicol. · Jan 1995
Case ReportsProlonged neuromuscular blockade when mivacurium and pancuronium were administered in series.
Long acting non-depolarizing neuromuscular blockade is useful in many clinical circumstances, especially during surgical procedures. Reinstitution of the blockade for short periods to facilitate the completion of clinical tasks can be accomplished in different ways. We present a case wherein a short-acting non-depolarizing neuromuscular blocker used after a long-acting one resulted in an unusual prolongation of the neuromuscular blockade.
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J. Toxicol. Clin. Toxicol. · Jan 1995
Case ReportsColchicine toxicity--clinical features and treatment. Massive overdose case report.
This is a report of colchicine poisoning in a 24-year-old woman. She developed multiple organ failure and bone marrow suppression after the suicidal ingestion of 50 (1 mg) colchicine tablets. The pancytopenia responded to granulocyte colony-stimulating factor 300 micrograms on days 4, 5, 6, and 8. Although anticolchicine monoclonal antibody administration is the only specific therapy described, intensive supportive care including granulocyte colony-stimulating factor administration can facilitate recovery from severe colchicine intoxication.
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Non-depolarizing neuromuscular blocking agents have been used with increasing frequency in critically ill patients. Recently, numerous reports have described patients with prolonged muscle weakness after use of these agents for more than two days. Brief weakness lasting several hours to several days is likely the result of prolonged neuromuscular blockade, while more prolonged weakness lasting several weeks to months is likely caused by a myopathy. ⋯ Selective loss of thick myofilaments on muscle biopsy has been produced experimentally in rats by combing denervation with high doses of corticosteroids. As this disorder likely leads to additional respiratory compromise, difficulty weaning from the ventilator, and prolonged hospitalization, prevention is warranted. Methods of prevention include minimizing the dosage of non-depolarizing neuromuscular blocking agents and of other drugs with an effect on the neuromuscular junction, twitch monitoring with a peripheral nerve stimulator and allowing patients to come to an unparalyzed state for brief periods.
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Aluminum phosphide poisoning is common in the rural belt of Northern India. The release of cytotoxic phosphine gas primarily affects the heart, lungs, gastrointestinal tract and kidneys, although all organs can be involved. ⋯ Treatment consists of early gastric lavage, vasopressors and supportive care. Specific therapy with intravenous magnesium sulphate is recommended.
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For many physicians an antidote is an antidote. According to the International Programme on Chemical Safety definition, an antidote is a therapeutic substance used to counteract the toxic action(s) of a specified xenobiotic. Given this wide definition, the efficacy of an antidote may vary considerably depending on which toxic action(s) being counteracted and the level of counteracting power. ⋯ This may be particularly important in severe poisoning when the antidote may only be considered as an important adjunct to supportive care, e.g. deferoxamine in acute iron poisoning. Unless this is stressed, the unexperienced physician may rely too much on the antidote and pay insufficient attention to the supportive care. The varying efficacy levels will be discussed based on the presently ongoing International Programme on Chemical Safety/Commission of the European Communities evaluation program on antidotes.