National Hospital, Colombo, Sri Lanka.
BMC Pharmacol Toxicol. 2017 May 25;18(1):37. doi: 10.1186/s40360-017-0144-7.
Run Rat® is a rodenticide widely used against small mammals. It comprises of a minimum of 32% zinc phosphide which is highly toxic in acute exposures to humans. It may be consumed accidentally or intentionally. It enters the body via skin, respiratory and gastrointestinal tracts. Zinc phosphide is hydrolyzed by the gastric acid and is transformed into phosphine gas. Phosphine is a respiratory toxin that inhibits cytochrome C oxidase system resulting in renal failure and liver failure.
A 35 year old Sri Lankan female presented following ingestion of 2.5 g of Run Rat®, which is a branded preparation of zinc phosphide, resulting in 61 mg/kg poison load. She developed severe acute kidney injury with acute tubular necrosis, subnephrotic ranged proteinuria and tubulointerstitial nephritis for which she underwent haemodialysis three times along with other measures of resuscitation. She also developed elevated liver enzymes with hyperblirubinaemia, hypoalbuminaemia, acute pancreatitis and mild myocarditis. She improved with supportive therapy over a period of 3 weeks.
Run Rat® is a commonly used rodenticide and the toxic effects are mediated through conversion of phosphide to phosphine gas. The majority of the deaths had occurred in the first 12 to 24 h and the main causes identified are refractory hypotension and arrhythmias. The late deaths (beyond 24 h) had been commonly due to adult respiratory distress syndrome, liver and renal failure. The outcome is poorer with delayed presentation, development of coagulopathy, hyperglycaemia and multiorgan failure with elevated liver enzymes. In our patient, Zinc phosphide poisoning caused severe acute kidney injury, abnormal liver profile, pancreatitis and possible myocarditis. The patient improved with repeated haemodialysis. The renal biopsy revealed acute tubulointerstitial nephritis with acute tubular necrosis. In tropical countries, the rural population engaged in agriculture has easier access to the compound, as it is available at a lower cost. Furthermore, the lack of an antidote and advanced resuscitative measures such as inotropic supportive therapy and renal replacement facilities at most of the peripheral hospitals pose a major challenge in providing timely interventions to prevent deaths.
Run Rat®是一种广泛用于小型哺乳动物的杀鼠剂。它至少含有 32%的磷化锌,对人类急性暴露具有高度毒性。它可能是意外或故意摄入的。它通过皮肤、呼吸道和胃肠道进入人体。磷化锌被胃酸水解,并转化为磷化氢气体。磷化氢是一种呼吸毒素,它抑制细胞色素 C 氧化酶系统,导致肾衰竭和肝功能衰竭。
一名 35 岁的斯里兰卡女性因摄入 2.5 克 Run Rat®而就诊,这是一种含有磷化锌的品牌制剂,导致 61mg/kg 的毒药负荷。她出现严重的急性肾损伤,伴有急性肾小管坏死、亚肾病范围蛋白尿和肾小管间质性肾炎,为此她接受了三次血液透析以及其他复苏措施。她还出现了肝酶升高、高胆红素血症、低白蛋白血症、急性胰腺炎和轻度心肌炎。她在 3 周的时间内通过支持性治疗得到了改善。
Run Rat®是一种常用的杀鼠剂,其毒性作用是通过将磷化物转化为磷化氢气体来介导的。大多数死亡发生在最初的 12 至 24 小时内,主要识别出的原因是难治性低血压和心律失常。晚期死亡(超过 24 小时)通常是由于成人呼吸窘迫综合征、肝肾功能衰竭。延迟出现、凝血功能障碍、高血糖和多器官衰竭以及肝酶升高会导致预后更差。在我们的患者中,磷化锌中毒导致严重的急性肾损伤、异常的肝功能谱、胰腺炎和可能的心肌炎。患者通过反复血液透析得到改善。肾活检显示急性肾小管间质性肾炎伴急性肾小管坏死。在热带国家,从事农业的农村人口更容易获得这种化合物,因为它的成本更低。此外,大多数外围医院缺乏解毒剂和先进的复苏措施,如正性肌力支持治疗和肾脏替代治疗设施,这在提供及时干预以防止死亡方面构成了重大挑战。