van Schie Saskia, Hardjo Sureiyan, Haworth Mark
School of Veterinary Science, The University of Queensland, Gatton, Queensland, Australia.
J Vet Emerg Crit Care (San Antonio). 2025 May-Jun;35(3):302-307. doi: 10.1111/vec.13478. Epub 2025 Jun 25.
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.
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.
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.
磷化锌是一种广泛使用的商用非抗凝血灭鼠剂。然而,兽医文献中缺乏关于其毒性作用的详细信息。本病例报告的目的是全面描述一只接受早期去污处理的狗因磷化锌中毒的情况。
一只5岁绝育雄性混种狼犬在摄入磷化锌4小时后就诊。主人在送医前曾试图通过给狗口服一汤匙食盐进行去污处理。初次检查时,狗表现为黏膜充血和明显腹痛。记录到轻度高乳酸血症(2.3毫摩尔/升)。初始治疗包括静脉注射马罗匹坦(1毫克/千克)、埃索美拉唑(1毫克/千克)和复方乳酸钠(6毫升/千克/小时)。摄入毒素14小时后,狗发生全身性惊厥,用静脉注射地西泮(0.5毫克/千克)控制。发现低血糖并给予葡萄糖推注和持续输注治疗。代谢性酸中毒用碳酸氢钠治疗,尽管进行了此治疗,代谢性酸中毒仍持续存在,高乳酸血症恶化至8.0毫摩尔/升。根据凝血酶原时间延长、唇部裂伤出血过多、低血糖以及丙氨酸氨基转移酶活性和总胆红素浓度严重升高,推测诊断为急性肝衰竭。开始用维生素K和N - 乙酰半胱氨酸治疗。低血压对保守的液体推注无反应,结合急性肝衰竭,促使注重成本的主人选择实施安乐死。
这是第一份详细描述狗磷化锌中毒综合征和急性肝衰竭确诊病例的报告。一项对潜在暴露情况的回顾性研究提示预后良好;然而,本报告表明,即使在就诊时症状似乎仅限于胃肠道,摄入磷化锌也应进行积极监测和治疗。