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Fatality after deliberate ingestion of the pesticide rotenone: a case report
Authors:David?Michael?Wood  author-information"  >  author-information__contact u-icon-before"  >  mailto:dwood@sghms.ac.uk"   title="  dwood@sghms.ac.uk"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author,Hadi?Alsahaf,Peter?Streete,Paul?Ivor?Dargan,Alison?Linda?Jones
Affiliation:(1) Specialist Registrar in General Medicine and Clinical Pharmacology, Department of Pharmacology and Clinical Pharmacology, St George's Hospital Medical School, London, UK;(2) Consultant in Anaesthetics and Intensive Care Medicine, Kingston Hospital, Kingston, Surrey, UK;(3) Head of Clinical &; Forensic Toxicology Section, Medical Toxicology Laboratory, Guy's and St. Thomas' NHS Foundation Trust, London, UK;(4) Consultant Clinical Toxicologist, National Poisons Information Service (London), Guy's and St. Thomas' NHS Foundation Trust, London, UK;(5) Director and Clinical Toxicologist, National Poisons Information Service (London), Guy's and St. Thomas' NHS Foundation Trust, London, UK
Abstract:Rotenone is a pesticide derived from the roots of plants from the Leguminosae family. Poisoning following deliberate ingestion of these plant roots has commonly been reported in Papua New Guinea. However, poisoning with commercially available rotenone in humans has been reported only once previously following accidental ingestion in a 3.5-year-old child. Therefore, the optimal management of rotenone poisoning is not known. After deliberate ingestion of up to 200 ml of a commercially available 0.8% rotenone solution, a 47-year-old female on regular metformin presented with a reduced level of consciousness, metabolic acidosis and respiratory compromise. Metformin was not detected in premortem blood samples obtained. Despite intensive supportive management, admission to an intensive care unit, and empirical use of N-acetylcysteine and antioxidant therapy, she did not survive. Poisoning with rotenone is uncommon but is potentially fatal because this agent inhibits the mitochondrial respiratory chain. In vitro cell studies have shown that rotenone-induced toxicity is reduced by the use of N-acetylcysteine, antioxidants and potassium channel openers. However, no animal studies have been reported that confirm these findings, and there are no previous reports of attempted use of these agents in patients with acute rotenone-induced toxicity.
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