N.Acetylcysteine and deferoxamin as an antidotal therapy in a gastrectomized patient with iron poisoning

Objective: Iron poisoning leads to systemic organ damage being potentially lethal. We describe an iron intoxication in a gastrectomized patient and the use of N-acetylcystein and deferoxamine as a successful antidotal therapy. Case report. A 48 year old gastrectomized woman was admitted to the hospital two hours after voluntary ingestion of 40 iron sulfate tablets (525 mg). On admission the patient showed no clinical evidence of iron poisoning. Gastric and whole bowel irrigation were quickly performed. Laboratory findings showed normal values. Metabolic acidosis and hypokalemia quickly appeared and were rapidly treated. Seven hours after the ingestion, the patient presented pyrosis, rectal bleeding, hypotension and tachycardia. Laboratory findings revealed increased liver enzymes (AST 220 ALT 70 U/L; peak level AST 6020, ALT 2860 at 32 hours), and D-dimers (56923 mcg/L); INR 2.2; hemoglobin 9.6 g/dl. As serum iron concentration was 4636 microg/dl, intravenous deferoxamin 10 mg/kg/h for 12 h and longastatin 0.025 mg/h for 72 h were started. Fresh frozen plasma and concentrated red blood cells were infused together with electrolytic solution and vitamin K. The upper GI endoscopy performed 10 hours after iron ingestion revealed hemorrhagic enteritis and bleeding from the anastomotic loop. Colonoscopy was negative. Twenty-two hours after poisoning, intravenous infusion of N-acetylcysteine was started at 40 mg/kg/h and prolonged for 66 hours. The patient’s conditions improved and she was eventually discharged from hospital 12 days after the intoxication with a negative upper GI endoscopy and normal laboratory findings. Conclusion: Ferrous iron salts are responsible for direct corrosive effects on GI tract and are absorbed from the small and large intestine. Once absorbed, free iron can catalyze redox reactions with free radical formation and lipid peroxidation leading to possible acute liver failure. Hence, the association of an iron chelator and a free radical scavenger should be considered in order to prevent free radicals secondary damages in iron poisoning.