{"title":"犬迟发性磷化锌中毒。","authors":"Saskia van Schie, Sureiyan Hardjo, Mark Haworth","doi":"10.1111/vec.13478","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Objective</h3>\n \n <p>Zinc phosphide is a widely used, commercial, non-anticoagulant rodenticide. However, there is a lack of detailed information in veterinary literature regarding its toxic effects. The purpose of this case report is to provide a comprehensive description of toxicosis caused by zinc phosphide in a dog that underwent early decontamination.</p>\n </section>\n \n <section>\n \n <h3> Case Summary</h3>\n \n <p>A 5-year-old neutered male Wolfhound mix presented 4 h after ingesting zinc phosphide. The owners had attempted decontamination by giving the dog one tablespoon of table salt orally before arrival. On initial examination, the dog showed injected mucous membranes and apparent abdominal pain. Mild hyperlactatemia (2.3 mmol/L) was documented. Initial treatment included IV administration of maropitant (1 mg/kg), esomeprazole (1 mg/kg), and compound sodium lactate (6 mL/kg/h). Fourteen hours after toxin ingestion, a generalized seizure occurred, which was controlled with diazepam (0.5 mg/kg IV). Hypoglycemia was identified and treated with a glucose bolus and continuous infusion. Metabolic acidosis was treated with sodium bicarbonate, and despite this treatment, metabolic acidosis persisted and hyperlactatemia worsened to 8.0 mmol/L. Acute hepatic failure was presumptively diagnosed based on increased prothrombin time, excessive bleeding from a lip laceration, hypoglycemia, and severely increased alanine aminotransferase activity and total bilirubin concentration. Treatment with vitamin K and <i>N</i>-acetylcysteine was initiated. Hypotension, which did not respond to a conservative fluid bolus, in combination with acute hepatic failure, prompted the cost-conscious owners to elect humane euthanasia.</p>\n </section>\n \n <section>\n \n <h3> New or Unique information Provided</h3>\n \n <p>This is the first report detailing a confirmed case of zinc phosphide toxidrome and acute liver failure in a dog. A retrospective study of potential exposures suggested good outcomes; however, this report demonstrates that even when signs appear limited to the gastrointestinal tract at presentation, ingestion of zinc phosphide should be aggressively monitored and treated.</p>\n </section>\n </div>","PeriodicalId":17603,"journal":{"name":"Journal of veterinary emergency and critical care","volume":"35 3","pages":"302-307"},"PeriodicalIF":1.2000,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/vec.13478","citationCount":"0","resultStr":"{\"title\":\"Delayed Zinc Phosphide Toxicosis in a Dog\",\"authors\":\"Saskia van Schie, Sureiyan Hardjo, Mark Haworth\",\"doi\":\"10.1111/vec.13478\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Objective</h3>\\n \\n <p>Zinc phosphide is a widely used, commercial, non-anticoagulant rodenticide. However, there is a lack of detailed information in veterinary literature regarding its toxic effects. The purpose of this case report is to provide a comprehensive description of toxicosis caused by zinc phosphide in a dog that underwent early decontamination.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Case Summary</h3>\\n \\n <p>A 5-year-old neutered male Wolfhound mix presented 4 h after ingesting zinc phosphide. The owners had attempted decontamination by giving the dog one tablespoon of table salt orally before arrival. On initial examination, the dog showed injected mucous membranes and apparent abdominal pain. Mild hyperlactatemia (2.3 mmol/L) was documented. Initial treatment included IV administration of maropitant (1 mg/kg), esomeprazole (1 mg/kg), and compound sodium lactate (6 mL/kg/h). Fourteen hours after toxin ingestion, a generalized seizure occurred, which was controlled with diazepam (0.5 mg/kg IV). Hypoglycemia was identified and treated with a glucose bolus and continuous infusion. Metabolic acidosis was treated with sodium bicarbonate, and despite this treatment, metabolic acidosis persisted and hyperlactatemia worsened to 8.0 mmol/L. Acute hepatic failure was presumptively diagnosed based on increased prothrombin time, excessive bleeding from a lip laceration, hypoglycemia, and severely increased alanine aminotransferase activity and total bilirubin concentration. Treatment with vitamin K and <i>N</i>-acetylcysteine was initiated. Hypotension, which did not respond to a conservative fluid bolus, in combination with acute hepatic failure, prompted the cost-conscious owners to elect humane euthanasia.</p>\\n </section>\\n \\n <section>\\n \\n <h3> New or Unique information Provided</h3>\\n \\n <p>This is the first report detailing a confirmed case of zinc phosphide toxidrome and acute liver failure in a dog. A retrospective study of potential exposures suggested good outcomes; however, this report demonstrates that even when signs appear limited to the gastrointestinal tract at presentation, ingestion of zinc phosphide should be aggressively monitored and treated.</p>\\n </section>\\n </div>\",\"PeriodicalId\":17603,\"journal\":{\"name\":\"Journal of veterinary emergency and critical care\",\"volume\":\"35 3\",\"pages\":\"302-307\"},\"PeriodicalIF\":1.2000,\"publicationDate\":\"2025-06-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1111/vec.13478\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of veterinary emergency and critical care\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/vec.13478\",\"RegionNum\":3,\"RegionCategory\":\"农林科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"VETERINARY SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of veterinary emergency and critical care","FirstCategoryId":"97","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/vec.13478","RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"VETERINARY SCIENCES","Score":null,"Total":0}
Zinc phosphide is a widely used, commercial, non-anticoagulant rodenticide. However, there is a lack of detailed information in veterinary literature regarding its toxic effects. The purpose of this case report is to provide a comprehensive description of toxicosis caused by zinc phosphide in a dog that underwent early decontamination.
Case Summary
A 5-year-old neutered male Wolfhound mix presented 4 h after ingesting zinc phosphide. The owners had attempted decontamination by giving the dog one tablespoon of table salt orally before arrival. On initial examination, the dog showed injected mucous membranes and apparent abdominal pain. Mild hyperlactatemia (2.3 mmol/L) was documented. Initial treatment included IV administration of maropitant (1 mg/kg), esomeprazole (1 mg/kg), and compound sodium lactate (6 mL/kg/h). Fourteen hours after toxin ingestion, a generalized seizure occurred, which was controlled with diazepam (0.5 mg/kg IV). Hypoglycemia was identified and treated with a glucose bolus and continuous infusion. Metabolic acidosis was treated with sodium bicarbonate, and despite this treatment, metabolic acidosis persisted and hyperlactatemia worsened to 8.0 mmol/L. Acute hepatic failure was presumptively diagnosed based on increased prothrombin time, excessive bleeding from a lip laceration, hypoglycemia, and severely increased alanine aminotransferase activity and total bilirubin concentration. Treatment with vitamin K and N-acetylcysteine was initiated. Hypotension, which did not respond to a conservative fluid bolus, in combination with acute hepatic failure, prompted the cost-conscious owners to elect humane euthanasia.
New or Unique information Provided
This is the first report detailing a confirmed case of zinc phosphide toxidrome and acute liver failure in a dog. A retrospective study of potential exposures suggested good outcomes; however, this report demonstrates that even when signs appear limited to the gastrointestinal tract at presentation, ingestion of zinc phosphide should be aggressively monitored and treated.
期刊介绍:
The Journal of Veterinary Emergency and Critical Care’s primary aim is to advance the international clinical standard of care for emergency/critical care patients of all species. The journal’s content is relevant to specialist and non-specialist veterinarians practicing emergency/critical care medicine. The journal achieves it aims by publishing descriptions of unique presentation or management; retrospective and prospective evaluations of prognosis, novel diagnosis, or therapy; translational basic science studies with clinical relevance; in depth reviews of pertinent topics; topical news and letters; and regular themed issues.
The journal is the official publication of the Veterinary Emergency and Critical Care Society, the American College of Veterinary Emergency and Critical Care, the European Veterinary Emergency and Critical Care Society, and the European College of Veterinary Emergency and Critical Care. It is a bimonthly publication with international impact and adheres to currently accepted ethical standards.