Stephanopoulos Dimitrios E, Willman David A, Shevlin Douglas, Pinter Larry, Gummin David D
Division of Pediatric Critical Care Medicine, Department of Pediatrics, Southern Illinois University, School of Medicine, Springfield 62794-9658, USA.
Pediatr Crit Care Med. 2002 Jan;3(1):74-80. doi: 10.1097/00130478-200201000-00017.
To describe the toxicokinetics and management of acute pediatric arsenic ingestion.
Case report and literature review.
Tertiary pediatric intensive care unit, St. John's Children's Hospital, Springfield, IL.
A 22-month-old boy ingested approximately twice the estimated lethal dose of arsenic trioxide (As(2)O(3)) ant bait. Only one household arsenical insecticide is available in the United States and is presumed to be shielded from human exposure. He survived without detectable sequelae. Initially, the patient developed signs of acute hemodynamic compromise with tachycardia, hypertension, gastrointestinal symptoms, and poor urine output. He became lethargic with muscle weakness and was somnolent but never developed encephalopathy, seizures, or late onset peripheral neuropathy.
He was stabilized with fluid resuscitation, placed on a sodium bicarbonate intravenous drip, and treated with intramuscular dimercaprol (British anti-Lewisite), 5 mg/kg every 6 hrs for 3 days. When the British anti-Lewisite and the sodium bicarbonate drip were discontinued, oral meso 2,3-dimercaptosuccinic acid (Succimer) was administered three times a day for 5 days and thereafter twice daily until the urine arsenic concentration decreased below 50 microg/L.
Continuous monitoring in the pediatric intensive care unit included continuous electrocardiogram, arterial blood pressure, urine output, vital signs, arterial blood gases, serum and urine arsenic concentrations, electrolytes, electromyography, and determination of arsenic toxicokinetics. The child's serum arsenic concentration was the highest ever reported with survival.
Recovery from arsenic poisoning was attributable to the restoration and maintenance of adequate cardiac output and renal perfusion in early shock, which allowed depot intramuscular British anti-Lewisite to circulate and eliminate the poison. Although an intravenous antiarsenical chelating agent would be advantageous in treating shock from arsenic poisoning, none is currently available. We urge the immediate use of British anti-Lewisite therapy on patient presentation with suspected toxic arsenic ingestion.
描述急性儿童砷摄入的毒代动力学及处理方法。
病例报告及文献综述。
伊利诺伊州斯普林菲尔德市圣约翰儿童医院三级儿科重症监护病房。
一名22个月大的男孩摄入了约两倍于三氧化二砷（As₂O₃）估计致死剂量的杀鼠饵剂。美国仅有一种家用含砷杀虫剂，且推测其可防止人体接触。他存活下来，未出现可检测到的后遗症。最初，患者出现急性血流动力学不稳定的症状，伴有心动过速、高血压、胃肠道症状及少尿。他变得嗜睡、肌肉无力且昏昏欲睡，但从未出现脑病、癫痫发作或迟发性周围神经病。
通过液体复苏使其病情稳定，给予静脉滴注碳酸氢钠，并肌肉注射二巯丙醇（英国抗路易氏剂），剂量为5 mg/kg，每6小时一次，共3天。停用英国抗路易氏剂和碳酸氢钠滴注后，口服消旋2,3 - 二巯基丁二酸（二巯丁二酸），每日3次，共5天，之后每日2次，直至尿砷浓度降至50 μg/L以下。
在儿科重症监护病房进行的持续监测包括连续心电图、动脉血压、尿量、生命体征、动脉血气、血清和尿砷浓度、电解质、肌电图以及砷毒代动力学测定。该患儿的血清砷浓度是有存活记录以来所报道的最高值。
砷中毒得以恢复归因于早期休克时心输出量和肾灌注的恢复及维持，这使得肌肉注射的长效二巯丙醇能够循环并清除毒物。尽管静脉用抗砷螯合剂在治疗砷中毒性休克方面具有优势，但目前尚无此类药物。我们敦促在怀疑有有毒砷摄入的患者就诊时立即使用二巯丙醇治疗。
