背景:本案例研究报道了涉及吲哚沙卡和维生素C的自杀未遂。吲哚沙卡是一种神经毒性杀虫剂,用于农业和宠物中的跳蚤控制剂。棉花,蔬菜,水果用吲哚沙卡威处理,一种可以在室内和室外使用的杀虫剂。会引起皮肤过敏,高铁血红蛋白血症,和溶血性贫血.它也归因于通过摄入的过敏反应,吸入,身体接触,和跨层运动。该病例报告重点介绍了在因吲哚沙卡威中毒引起的高铁血红蛋白血症中使用维生素C。Indoxacarb中毒可能非常严重,甚至致命。在这种情况下,患者在尝试自杀时摄入含吲哚沙卡的物质后,最初没有症状。然而,进一步的测试显示高铁血红蛋白血症和低氧水平。
方法:一名28岁的东南亚女性患者摄入了含有5.25%诺瓦龙的杀虫剂,4.5%吲哚沙卡威,和25%的噻虫嗪,并报告说,她注意到浑浊的棕色尿液,但没有出现活跃的迹象或中毒症状。经检查,病人完全清醒,警报,血液动力学稳定,但氧饱和度为84%.进行了胃灌洗,血液调查显示,血液样本呈褐色,高铁血红蛋白水平为12%。患者接受大剂量维生素C治疗,并有明显改善,高铁血红蛋白水平下降到1.2%,氧饱和度增加到97%。
结论:Indoxacarb中毒可引起严重的高铁血红蛋白血症。维生素C可能是由吲哚沙卡威引起的高铁血红蛋白血症的有用治疗选择,特别是在传统的亚甲蓝治疗禁忌或不耐受的情况下。因此高剂量的抗坏血酸,也就是说,维生素C,给病人服用,降低了他们的高铁血红蛋白水平,改善了氧气水平,没有太多安全问题。
结论:本实施例强调了吲哚沙卡威中毒早期检测和治疗的重要性,以及在高铁血红蛋白血症治疗中使用抗坏血酸的可能优势,并强调使用维生素C治疗因吲哚沙卡中毒引起的高铁血红蛋白血症。因此,对于医疗保健专业人员来说,重要的是要意识到吲哚沙卡威可能导致高铁血红蛋白血症,并考虑将维生素C作为治疗选择.
BACKGROUND: This
case study
reports on a suicide attempt involving indoxacarb and vitamin C. Indoxacarb is a neurotoxic insecticide used in agriculture and as a flea controller in pets. Cotton, vegetables, and fruits are treated with indoxacarb, an insecticide that can be applied both indoors and outdoors. It causes skin allergies, methemoglobinemia, and hemolytic anemia. It is also attributed to allergic reactions through ingestion, inhalation, physical contact, and translaminar action. This
case report highlights use of vitamin C in methemoglobinemia caused by indoxacarb poisoning. Indoxacarb poisoning has the potential to be extremely serious and even lethal. In this instance, the patient initially had no symptoms after ingesting a substance containing indoxacarb in an attempt at suicide. However, further tests revealed methemoglobinemia and low oxygen levels.
METHODS: A 28-year-old south-east Asian female patient ingested an insecticide containing 5.25% novaluron, 4.5% indoxacarb, and 25% thiamethoxam, and reported that she noticed muddy brown urine but presented with no active signs or symptoms of poisoning. Upon examination, the patient was fully conscious, alert, and hemodynamically stable, but had an oxygen saturation of 84%. Gastric lavage was performed, and blood investigations revealed a muddy-brown-colored blood sample and methemoglobin levels of 12%. The patient was treated with high-dose vitamin C and showed significant improvement, with a drop in methemoglobin levels to 1.2% and an increase in oxygen saturation to 97%.
CONCLUSIONS: Indoxacarb poisoning can cause severe methemoglobinemia. Vitamin C may be a useful treatment option for methemoglobinemia caused by indoxacarb, particularly in cases in which traditional treatment with methylene blue is contraindicated or not tolerated. Hence high doses of ascorbic acid, that is, vitamin C, were administered to the patient, which lowered their methemoglobin levels and improved oxygen levels without much safety concerns.
CONCLUSIONS: This example emphasizes the significance of early indoxacarb poisoning detection and treatment as well as the possible advantages of utilizing ascorbic acid in the management of methemoglobinemia, and highlights the use of vitamin C in the treatment of methemoglobinemia caused by indoxacarb poisoning. Therefore, it is important for healthcare professionals to be aware of the potential for indoxacarb to cause methemoglobinemia and to consider vitamin C as a treatment option.