A Chollet, J Muszynsky, C Bismuth, J Pham, M El Khouly, R Surugue
{"title":"[百草枯中毒中的低氧。[6例]。","authors":"A Chollet, J Muszynsky, C Bismuth, J Pham, M El Khouly, R Surugue","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The toxicity of the weed-killer paraquat is related to the formation of superoxyde radicals responsible of a progressive and usually lethal pulmonary fibrosis. Recognition of lipid peroxidation of membrane bilayers by free radicals as the causative factor pointed to oxygen as an important cofactor in the severity of paraquat poisoning. It has been shown that any FiO2 over 21% accelerates this process and increases the the mortality of rats and humans. FiO2 21% gave a significant reduction of mortality in rats (DOUZE 1976). We proposed this therapy (1978-1879) in 6 cases of paraquat poisoning. It was conducted with induction of a barbiturate coma, hypothermia, curarisation and hypo-oxygenation (FiO2 around 14% thanks to the adjunction of nitrogen to assisted ventilation). In 5/6 patients, these technics did not prevent the evolution towards death. This evolution was in fact predicted, according the following prognostic factors: suicide, more than a mouthful ingestion, oesophago-gastric burns detected by endoscopy, organic renal failure, high plasma paraquat level. Associated methods of elimination (Fuller's earth, provoked diarrhea, furosemide, hemoperfusion and hemodialysis) did not change the early established prognosis. The only survival was observed in an accidental poisoning with undetectable plasma paraquat and isolated oral burns: the herbicide had been probably spit out. This survival cannot be related to hypo-oxygenation. This failure is not definitive, according to us: this therapy should be undertaken only after minimal, accidental poisoning possibly evolving to pulmonary fibrosis. It appears unuseful in massive, suicidal poisonings, leading readily to a lethal circulatory failure.</p>","PeriodicalId":23153,"journal":{"name":"Toxicological European research. Recherche europeenne en toxicologie","volume":"5 2","pages":"71-5"},"PeriodicalIF":0.0000,"publicationDate":"1983-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Hypo-oxygenation in paraquat poisoning. Apropos of 6 cases].\",\"authors\":\"A Chollet, J Muszynsky, C Bismuth, J Pham, M El Khouly, R Surugue\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The toxicity of the weed-killer paraquat is related to the formation of superoxyde radicals responsible of a progressive and usually lethal pulmonary fibrosis. Recognition of lipid peroxidation of membrane bilayers by free radicals as the causative factor pointed to oxygen as an important cofactor in the severity of paraquat poisoning. It has been shown that any FiO2 over 21% accelerates this process and increases the the mortality of rats and humans. FiO2 21% gave a significant reduction of mortality in rats (DOUZE 1976). We proposed this therapy (1978-1879) in 6 cases of paraquat poisoning. It was conducted with induction of a barbiturate coma, hypothermia, curarisation and hypo-oxygenation (FiO2 around 14% thanks to the adjunction of nitrogen to assisted ventilation). In 5/6 patients, these technics did not prevent the evolution towards death. This evolution was in fact predicted, according the following prognostic factors: suicide, more than a mouthful ingestion, oesophago-gastric burns detected by endoscopy, organic renal failure, high plasma paraquat level. Associated methods of elimination (Fuller's earth, provoked diarrhea, furosemide, hemoperfusion and hemodialysis) did not change the early established prognosis. The only survival was observed in an accidental poisoning with undetectable plasma paraquat and isolated oral burns: the herbicide had been probably spit out. This survival cannot be related to hypo-oxygenation. This failure is not definitive, according to us: this therapy should be undertaken only after minimal, accidental poisoning possibly evolving to pulmonary fibrosis. It appears unuseful in massive, suicidal poisonings, leading readily to a lethal circulatory failure.</p>\",\"PeriodicalId\":23153,\"journal\":{\"name\":\"Toxicological European research. Recherche europeenne en toxicologie\",\"volume\":\"5 2\",\"pages\":\"71-5\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1983-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxicological European research. Recherche europeenne en toxicologie\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicological European research. Recherche europeenne en toxicologie","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
[Hypo-oxygenation in paraquat poisoning. Apropos of 6 cases].
The toxicity of the weed-killer paraquat is related to the formation of superoxyde radicals responsible of a progressive and usually lethal pulmonary fibrosis. Recognition of lipid peroxidation of membrane bilayers by free radicals as the causative factor pointed to oxygen as an important cofactor in the severity of paraquat poisoning. It has been shown that any FiO2 over 21% accelerates this process and increases the the mortality of rats and humans. FiO2 21% gave a significant reduction of mortality in rats (DOUZE 1976). We proposed this therapy (1978-1879) in 6 cases of paraquat poisoning. It was conducted with induction of a barbiturate coma, hypothermia, curarisation and hypo-oxygenation (FiO2 around 14% thanks to the adjunction of nitrogen to assisted ventilation). In 5/6 patients, these technics did not prevent the evolution towards death. This evolution was in fact predicted, according the following prognostic factors: suicide, more than a mouthful ingestion, oesophago-gastric burns detected by endoscopy, organic renal failure, high plasma paraquat level. Associated methods of elimination (Fuller's earth, provoked diarrhea, furosemide, hemoperfusion and hemodialysis) did not change the early established prognosis. The only survival was observed in an accidental poisoning with undetectable plasma paraquat and isolated oral burns: the herbicide had been probably spit out. This survival cannot be related to hypo-oxygenation. This failure is not definitive, according to us: this therapy should be undertaken only after minimal, accidental poisoning possibly evolving to pulmonary fibrosis. It appears unuseful in massive, suicidal poisonings, leading readily to a lethal circulatory failure.