Acute Liver and Multi-organ Failure Secondary to Intentional Iron Overdose

Abstract

Introduction: Intentional iron overdoses are rare in adults, but have severe consequences. We report two patients with multi-organ system failure occurring rapidly after large quantity oral iron ingestions. Case Discussion: A 26-year-old woman was transferred from an outside hospital (OSH) for acute liver failure (ALF): 48 hours prior, she had intentionally ingested a large amount of iron supplements. At initial presentation, she had nausea, gastrointestinal bleeding and normal liver enzyme levels. She then developed abdominal pain, tender hepatomegaly, elevated liver enzymes and coagulopathy (see table). No asterixis or encephalopathy was present. Deferoxamine, N-acetylcysteine (NAC) and dialysis were initiated. She progressed to coma, shock, brainstem herniation and death. Case B: A 35-year-old woman with prior gastric bypass surgery, hypertension, iron deficiency anemia and previous suicide attempt was transferred from an OSH with ALF after intentionally ingesting 300 iron pills the evening before. She developed nausea, vomiting, diarrhea and abdominal pain. Initially, she was hypertensive, had a tender abdomen, but no asterixis. Acute kidney injury (AKI) and severe acidosis were managed with intravenous fluids and, eventually, dialysis. She also received a proton pump inhibitor, NAC, polyethylene glycol laxative and deferoxamine. She recovered after 16 days, with liver enzymes and INR near normal. However, she remained dialysis-dependent on discharge, and subsequently has been lost to follow-up. Acetaminophen adducts were negative, and no radio-opaque pills were identified on abdominal x-ray (KUB) in either case. Discussion: Iron overdose causes rapid onset multi-organ failure with high mortality. Iron-induced oxidative damage results from hepatocyte exposure to high quantities of non-transferrin bound iron via the portal venous system, resulting in excessive free radical production. Peak serum iron levels occur 4-6 hours after ingestion. Bowel irrigation is indicated if tablets are identified on KUB. IV deferoxamine should be administered early if systemic signs such as metabolic acidosis are present. NAC can be given empirically. AKI is thought to be from direct mitochondrial injury and lactic acidosis. In case B, survival may, in part, have been due to the history of gastric bypass surgery, which may have limited absorption. These patients were enrolled in the Acute Liver Failure Study Group registry, supported by U-01-58369-014 from NIDDK.Table 5: Liver function tests