Aggressive resuscitative efforts were needed to support this patient, including mechanical ventilation and inotropic support with dopamine, dobutamine, and epinephrine infusions. The poor prognosis for this child was discussed with his parents, and they requested that no further interventions be done. Approximately 13 hours after his initial presentation to the community hospital, the patient was pronounced dead. This patient had severe toxic effects from acute iron intoxication, which resulted in his death despite aggressive efforts. The pathophysiology of iron intoxication has been well described in the literature.
Gastrointestinal effects are due to direct corrosive effects on the mucosa.
Pathologic specimens reveal venous thrombosis, ulceration, infarction, diffuse edema, and hemorrhage within the mucosa. These effects are manifested in a patient as nausea, vomiting, diarrhea, abdominal pain, melena, and hematemesis. Hepatic effects result from the accumulation of free iron within hepatocytes during the first absorptive pass. Once free iron has accumulated in mitochondria, oxygen free radicals are generated, lipid peroxidation begins, and aerobic metabolism is disrupted. Clinically, these effects are manifested as coagulopathy, aminotransferase elevation, and direct hyperbilirubinemia.