Abbreviations: ECG, electrocardiography; CVVHDF, continuous veno-venous hemo dia filtration; ARDS, acute respiratory distress syndrome
IntroductionGlyphosate-surfactant herbicide is one of the most frequently used herbicides. Glyphosate kills plants by suppressing the shikimic metabolic pathway. 1 The mechanism of toxicity of glyphosate in mammals has been proposed to be the uncoupling of oxidative phosphorylation.2 Surfactants are inert ingredients that are added to herbicides to precisely increase the absorption of the active component. Surfactants may contribute to the toxicity of the active substance.1 An experiment in dogs found that hypotension is primarily caused by myocardial depression with surfactant. 3 The ingestion of small amounts of glyphosate-surfactant herbicide usually causes only mild symptoms. However, when large volumes of concentrates are ingested intentionally, it can generate potentially fatal symptoms that are refractory to the treatment. 4 The treatment for glyphosatesurfactant herbicide poisoning is primarily of a supportive nature.
5Early continuous veno-venous hemodiafiltration (CVVHDF) contributes to the survival.
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Case reportAt noon, a 45-year-old man deliberately drank a ½-liter of glyphosate-surfactant herbicide (trade name Cidokor). Cidokor is formulated as a liquid concentrate for solution and contains 480g/ L±24g/L (41.5% approx. weight) monoizopropylamine glyphosate salt (monoizopropylamine salt of N-phosphonomethyl-glycine). Other ingredients include ethoxylated fatty amines (mixture of n-alkyl (C 14 +C 16 +C 18 )-N, N, -bis (poliethoxylated) fatty amines 176g/L±11g/L (15.5% approx. weight). Cidokor is manufactured by Monsanto Europe SA, Brussels, Belgium. Immediately after drinking the poison, his wife gave him a few deciliters of milk to drink. For many years, the patient had suffered from psychosis, which was recently in a deterioration (paroxetine and risperidone were not taken regularly). He consumed alcohol. After poisoning he was transported by boat from the island to the hospital. He was admitted into the Gastroenterology Department at 3 p.m. Upon admission, he was conscious, complained of pain in the throat and epigastric area. Treatment was started, and diuresis was stimulated by furosemide. Hyperkalemia was corrected with an infusion of glucose and insulin, sodium bicarbonate and calcium gluconate. The patient received pantoprazole, amiodarone and oxygenation through a facemask with a bag. Despite treatment, his consciousness deteriorated into a coma (Glasgow coma score 3), and the patient demonstrated dilated pupils and no reaction to light. Chest X-rays showed confluent opacities and the development of ARDS. Cardiovascular collapse developed (blood pressure 80/50mmHg). Anuric acute renal failure, hyperkalemia and metabolic acidosis also developed. ECG showed progressive hyperkalemia. Nasogastric retention of bloody content was large. Rhabdomyolysis developed. For further treatment, he was admitted to the intensive care unit. Orotracheal intubation was performe...
Low-dose mannitol administration appears to be efficacious for improving the indicators of disturbed circulation in a TBI (FV-min increase, PI decrease). The maximum decrease in the PI was recorded 1 hour after the administration of mannitol and was 10.9% of the initial value. The maximum increase in the FV-min was recorded 1 hour after administration and was 29.7% of the initial value. These changes were significant ∼ 2 hours later.
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