D'sa S R, Victor P, Jagannati M, Sudarsan T I, Carey R A B, Peter J V
Department of Critical Care, Christian Medical College and Hospital , Vellore , India.
Clin Toxicol (Phila). 2014 Sep-Oct;52(8):897-900. doi: 10.3109/15563650.2014.947377. Epub 2014 Aug 12.
Toxin-induced methemoglobinemia is seen in poisoning with oxidizing agents. We report the clinical features and outcome of patients admitted with severe methemoglobinemia due to intentional ingestion of toxicants.
In this observational case series, patients admitted with toxin-induced methemoglobinemia between September 2011 and January 2014 were identified from the institutional poisoning database. Clinical profile and outcome of patients with methemoglobin concentration greater than or equal to 49% is reported.
Of the 824 patients admitted with poisoning, 5 patients with methemoglobin concentration greater than or equal to 49% were included. The implicated compounds were nitrobenzene, benzoylphenylurea, flubendamide and Rishab(TM). One patient refused to name the compound. All patients were managed in the intensive care unit. Altered sensorium [Glasgow coma scale (GCS) < 10] was common (80%); 2 patients presented with a GCS greater than 4. All patients manifested cyanosis, low oxygen saturation and chocolate-brown-colored blood despite supplemental oxygen therapy. The median methemoglobin concentration was 64.7% (range 49.8-91.6%); 2 patients had methemoglobin concentration greater than 70%. One patient needed inotropes. Four patients required mechanical ventilation for 4-14 days. All patients were treated with methylene blue; 4 received more than one dose. Three patients also received intravenous ascorbic acid 500 mg, once daily, for 3 days. Following treatment, there was evidence of haemolysis in all patients; 2 required blood transfusion. All patients survived.
Patients with severe toxin-induced methemoglobinemia present with altered sensorium and cyanosis and may require ventilatory support and inotropes. Though methemoglobin concentrations greater than 70% are considered fatal, aggressive management with methylene blue and supportive therapy can lead to survival.
毒素诱导的高铁血红蛋白血症可见于氧化剂中毒。我们报告因故意摄入毒物导致严重高铁血红蛋白血症而入院患者的临床特征及转归。
在这个观察性病例系列中,从机构中毒数据库中识别出2011年9月至2014年1月期间因毒素诱导的高铁血红蛋白血症入院的患者。报告高铁血红蛋白浓度大于或等于49%的患者的临床资料及转归。
在824例中毒入院患者中,纳入了5例高铁血红蛋白浓度大于或等于49%的患者。涉及的化合物为硝基苯、苯甲酰基苯基脲、氟苯虫酰胺和立杀(商标名)。1例患者拒绝说出化合物名称。所有患者均在重症监护病房接受治疗。意识改变[格拉斯哥昏迷量表(GCS)<10]很常见(80%);2例患者GCS大于4。尽管进行了补充氧气治疗,所有患者均出现发绀、低氧饱和度及巧克力棕色血液。高铁血红蛋白浓度中位数为64.7%(范围49.8 - 91.6%);2例患者高铁血红蛋白浓度大于70%。1例患者需要使用血管活性药物。4例患者需要机械通气4 - 14天。所有患者均接受亚甲蓝治疗;4例接受了不止一剂。3例患者还接受了静脉注射维生素C 500毫克,每日1次,共3天。治疗后,所有患者均有溶血迹象;2例需要输血。所有患者均存活。
严重毒素诱导的高铁血红蛋白血症患者表现为意识改变和发绀,可能需要通气支持和血管活性药物。尽管高铁血红蛋白浓度大于70%被认为是致命的,但积极使用亚甲蓝治疗及支持性治疗可使患者存活。