Mann K V, Picciotti M A, Spevack T A, Durbin D R
Philadelphia College of Pharmacy and Science, PA 19104.
Clin Pharm. 1989 Jun;8(6):428-40.
Treatment of severe iron overdose in two children is described, and the pathophysiology of iron toxicity and management of acute iron poisonings are reviewed. An 11-month-old boy was comatose and in shock several hours after ingesting approximately 50 ferrous sulfate tablets (elemental iron 390 mg/kg). He had hyperglycemia and leukocytosis. Lavage was performed with a solution containing deferoxamine and sodium bicarbonate, and deferoxamine was given by continuous i.v. infusion for 48 hours. The initial serum iron (SI) concentration of 14,250 micrograms/dL decreased to 657 micrograms/dL nine hours after i.v. deferoxamine therapy was initiated. A roentgenogram showed tablets in the stomach and small bowel. Packed red blood cells were administered to treat apparent necrotizing gastroenteritis. SI concentration returned to normal by day three [corrected], and the child recovered. A 2.5-year-old boy was examined 1.25 hr after ingesting an estimated 55 tablets of ferrous gluconate 325 mg (elemental iron 130 mg/kg). Initial SI concentration was 134 micrograms/dL, and total iron-binding capacity (TIBC) was 219 micrograms/dL. A roentgenogram indicated iron concretion in the stomach and iron tablets in the small bowel. He underwent lavage with solution containing sodium bicarbonate. An i.m. dose of deferoxamine was administered, followed by i.v. deferoxamine therapy. SI concentration eight hours after the ingestion was 290 micrograms/dL, and whole-bowel irrigation was begun with polyethylene glycol-electrolyte solution. The irrigation and deferoxamine therapy were discontinued 20 hours after the ingestion, when SI concentration was 73 micrograms/dL, and the child recovered. Acute iron ingestions of more than 60 mg/kg are potentially serious. Patient 1 had severe iron intoxication, while aggressive treatment prevented severe toxicity in patient 2. Acute iron toxicity includes effects on the GI tract and the cardiovascular, metabolic, hepatic, and central nervous systems. Guidelines for assessing the severity of an overdose and selecting the most appropriate therapy are provided. The indications for chelation therapy with deferoxamine, gastric decontamination procedures including use of lavage solutions and whole-bowel irrigation, and adjunctive measures are described. Management of acute iron overdose includes supportive care, GI decontamination, and chelation therapy.
本文描述了两名儿童严重铁过量中毒的治疗情况,并对铁中毒的病理生理学及急性铁中毒的处理方法进行了综述。一名11个月大的男童在摄入约50片硫酸亚铁片(元素铁390mg/kg)数小时后昏迷且休克。他出现了高血糖和白细胞增多症。用含去铁胺和碳酸氢钠的溶液进行洗胃,并持续静脉输注去铁胺48小时。静脉注射去铁胺治疗开始9小时后,初始血清铁(SI)浓度从14,250μg/dL降至657μg/dL。X线片显示胃和小肠内有药片。输注浓缩红细胞以治疗明显的坏死性肠胃炎。到第3天[校正后]SI浓度恢复正常,患儿康复。一名2.5岁男童在摄入约55片325mg葡萄糖酸亚铁(元素铁130mg/kg)后1.25小时接受检查。初始SI浓度为134μg/dL,总铁结合力(TIBC)为219μg/dL。X线片显示胃内有铁凝块,小肠内有铁片。用含碳酸氢钠的溶液对其进行洗胃。肌肉注射一剂去铁胺,随后进行静脉去铁胺治疗。摄入8小时后的SI浓度为290μg/dL,开始用聚乙二醇电解质溶液进行全肠灌洗。摄入20小时后,当SI浓度为73μg/dL时停止灌洗和去铁胺治疗,患儿康复。急性铁摄入量超过60mg/kg可能会很严重。病例1发生了严重的铁中毒,而积极治疗预防了病例2出现严重毒性。急性铁中毒包括对胃肠道、心血管、代谢、肝脏和中枢神经系统的影响。本文提供了评估过量中毒严重程度及选择最合适治疗方法的指南。描述了去铁胺螯合治疗的适应证、包括洗胃溶液和全肠灌洗的胃去污程序以及辅助措施。急性铁过量中毒的处理包括支持治疗、胃肠道去污和螯合治疗。