{"title":"一例致命的先天性碘中毒:护理点氯化物是有用的碘替代标记物吗?","authors":"A. Holford, K. Isoardi","doi":"10.1080/24734306.2023.2272072","DOIUrl":null,"url":null,"abstract":"Abstract Severe toxicity from povidone-iodine is rare, causing metabolic acidosis from the conversion of iodine to sodium iodide and direct tissue destruction. We report a case of fatal iodine toxicity following sclerotherapy. An elderly man presented following ablation of a large renal cyst with 10% povidone-iodine and 100% ethanol. He appeared intoxicated however denied alcohol ingestion. Over hours he developed progressive hypotension despite multiple vasopressor agents. Blood gas analysis demonstrated a metabolic acidosis (pH 7.11, bicarbonate 13 mmol/L) with an apparent hyperchloremia of 124 mmol/L. The ethanol concentration was 55 mmol/L (249 mg/dL). Imaging confirmed large volume residual radio-opaque fluid at the procedure site. The fluid was percutaneously drained and dialysis commenced for iodine toxicity. Iodine concentrations peaked at 8940 µmol/L (reference range 0.32-0.63 µmol/L) 14.5 h post exposure. Point of care chloride concentrations remained elevated (peak 129 mmol/L) following the trend of iodine concentrations, normalising once the iodine concentration was 1559 µmol/L. The patient deteriorated despite maximal therapy and succumbed on day 3. Iodide interferes with point of care testing chloride measurements. Point of care chloride concentrations may have a role as a surrogate marker for iodine but only at very high iodine concentrations (>2000 µmol/L).","PeriodicalId":23139,"journal":{"name":"Toxicology communications","volume":"42 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A fatal case of iatrogenic iodine poisoning: is point of care chloride a useful iodine surrogate marker?\",\"authors\":\"A. Holford, K. Isoardi\",\"doi\":\"10.1080/24734306.2023.2272072\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Abstract Severe toxicity from povidone-iodine is rare, causing metabolic acidosis from the conversion of iodine to sodium iodide and direct tissue destruction. We report a case of fatal iodine toxicity following sclerotherapy. An elderly man presented following ablation of a large renal cyst with 10% povidone-iodine and 100% ethanol. He appeared intoxicated however denied alcohol ingestion. Over hours he developed progressive hypotension despite multiple vasopressor agents. Blood gas analysis demonstrated a metabolic acidosis (pH 7.11, bicarbonate 13 mmol/L) with an apparent hyperchloremia of 124 mmol/L. The ethanol concentration was 55 mmol/L (249 mg/dL). Imaging confirmed large volume residual radio-opaque fluid at the procedure site. The fluid was percutaneously drained and dialysis commenced for iodine toxicity. Iodine concentrations peaked at 8940 µmol/L (reference range 0.32-0.63 µmol/L) 14.5 h post exposure. Point of care chloride concentrations remained elevated (peak 129 mmol/L) following the trend of iodine concentrations, normalising once the iodine concentration was 1559 µmol/L. The patient deteriorated despite maximal therapy and succumbed on day 3. Iodide interferes with point of care testing chloride measurements. Point of care chloride concentrations may have a role as a surrogate marker for iodine but only at very high iodine concentrations (>2000 µmol/L).\",\"PeriodicalId\":23139,\"journal\":{\"name\":\"Toxicology communications\",\"volume\":\"42 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-11-21\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxicology communications\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/24734306.2023.2272072\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology communications","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/24734306.2023.2272072","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
A fatal case of iatrogenic iodine poisoning: is point of care chloride a useful iodine surrogate marker?
Abstract Severe toxicity from povidone-iodine is rare, causing metabolic acidosis from the conversion of iodine to sodium iodide and direct tissue destruction. We report a case of fatal iodine toxicity following sclerotherapy. An elderly man presented following ablation of a large renal cyst with 10% povidone-iodine and 100% ethanol. He appeared intoxicated however denied alcohol ingestion. Over hours he developed progressive hypotension despite multiple vasopressor agents. Blood gas analysis demonstrated a metabolic acidosis (pH 7.11, bicarbonate 13 mmol/L) with an apparent hyperchloremia of 124 mmol/L. The ethanol concentration was 55 mmol/L (249 mg/dL). Imaging confirmed large volume residual radio-opaque fluid at the procedure site. The fluid was percutaneously drained and dialysis commenced for iodine toxicity. Iodine concentrations peaked at 8940 µmol/L (reference range 0.32-0.63 µmol/L) 14.5 h post exposure. Point of care chloride concentrations remained elevated (peak 129 mmol/L) following the trend of iodine concentrations, normalising once the iodine concentration was 1559 µmol/L. The patient deteriorated despite maximal therapy and succumbed on day 3. Iodide interferes with point of care testing chloride measurements. Point of care chloride concentrations may have a role as a surrogate marker for iodine but only at very high iodine concentrations (>2000 µmol/L).