背景:磷化锌(ZnP)是世界范围内容易获得的几种杀虫剂的基本成分。故意或意外中毒可能导致严重的并发症和多器官功能衰竭,导致高死亡率。目前没有已知的解毒剂。铁螯合和抗氧化作用是α-硫辛酸(ALA)的众所周知的特征,虽然其在ZnP中毒治疗中的应用以前没有文献记载。我们描述了一例严重的ZnP中毒伴多器官衰竭的患者,ALA也包括在患者的支持治疗中。
方法:一名65岁的男子摄入125克Arvalin®(含5克ZnP)并被送往急诊科,伴有呼吸功能不全和意识下降。他出现了低钾血症,低钙血症,白细胞计数低,C反应蛋白水平升高,混合性酸中毒,肝肾损害,空肠壁增厚,和肺不张,这也是随之而来的细菌性肺炎的基础。提供抗生素和足够的支持治疗。实验室检查显示肝损伤(肝酶略有增加,假胆碱酯酶水平低;第2天706U/L),可能是由患者的慢性酒精中毒或ZnP毒物本身引起的,因此,肝保护剂,连续6天施用具有N-乙酰半胱氨酸的ALA(ThiogammaTurbo-Set®)。假胆碱酯酶值增加了六倍,直到第二周的护理结束。入院后15天,病人被转移到精神科,生命功能稳定,清晰的意识,炎症标志物下降,和改善肝功能。一个月后他出院了,完全恢复。
结论:我们的病例是匈牙利首次记录的自愿和严重的ZnP中毒。我们的病人出现了多器官衰竭和肺不张,可能导致观察到的呼吸道感染。细菌性肺炎的发展突出了磷化氢引起的肺不张的危险。ALA在我们病人的情况下的使用,作为抗氧化剂和金属螯合剂,表明该药物可能是预防和治疗ZnP诱导的肝损伤的有前途的工具。
BACKGROUND: Zinc phosphide (ZnP) is the basic component of several insecticides easily accessible worldwide. Intentional or accidental intoxication may lead to severe complications and multiple organ failure, resulting in high mortality. No known antidote is currently available. The iron-chelation and the antioxidative effects are well-known features of alpha-lipoic acid (ALA), although its use in the treatment of ZnP poisoning has not been documented previously. We describe the
case of a patient with serious ZnP poisoning with multiple organ failure, where ALA was also included in the patient\'s supportive therapy.
METHODS: A 65-year-old man ingested 125 g of Arvalin® (containing 5 g ZnP) and presented to the Emergency Department, with respiratory insufficiency and decreased consciousness. He developed hypokalemia, hypocalcemia, low white blood cell count, elevated C-reactive protein level, mixed acidosis, hepatic and kidney damage, thickening of the jejunal wall, and lung atelectasis, which served as a basis for the ensuing bacterial pneumonia. Antibiotics and adequate supportive therapy were provided. Laboratory tests indicated liver damage (slightly increased liver enzymes, low pseudocholinesterase levels; 706 U/L on day 2), possibly caused by the patient\'s chronic alcoholism or the ZnP poison itself, therefore, hepatoprotective agents, ALA (Thiogamma Turbo-Set®) with N-acetylcysteine were administered for six consecutive days. Pseudocholinesterase values increased sixfold until the end of the second week of care. Fifteen days after admission, the patient was relocated to the department of psychiatry with stable vital functions, clear consciousness, declining inflammatory markers, and improved liver function. He was discharged 1 month later, fully recovered.
CONCLUSIONS: Our
case is the first documented voluntary and severe ZnP poisoning in Hungary. Our patient developed multiple organ failure and atelectasis, possibly resulting in the observed respiratory infection. The development of bacterial pneumonia highlighted the dangers of phosphine-induced atelectasis. The use of ALA in our patient\'s
case, as an antioxidant and agent for metal chelation, suggested that this agent could be a promising tool in the prevention and treatment of ZnP-induced hepatic damage.