1735: CARDIAC ARREST SECONDARY TO EXCESSIVE COW’S MILK INGESTION AND SEVERE IRON DEFICIENCY ANEMIA

Abstract

Learning Objectives: While iron-deficiency anemia (IDA) is commonly asymptomatic, some cases progress to cardiorespiratory compromise necessitating critical care interventions. We present a toddler with high-output heart failure and subsequent cardiac arrest secondary to excessive cow’s milk consumption and severe IDA. Methods: A 16-month-old previously healthy female was transferred to our ICU from an outside hospital with respiratory distress. Physical exam revealed an irritable and pale-appearing child, with bilateral decreased breath sounds and retractions, normal perfusion, and normal pulses. Within 30 minutes of arrival, she had an acute hypoxic, bradycardic arrest with ~25 minutes of chest compressions prior to return of spontaneous circulation. ECMO was deployed but not utilized. Initial laboratory studies drawn prior to arrest were notable for inability to result a complete blood count due to insufficient sample viscosity, with undetectable hemoglobin levels, and significantly low iron, ferritin, and transferring levels. Echocardiogram showed mild mitral regurgitation, mild left ventricular dilation, and low normal left ventricle systolic dysfunction. A respiratory viral panel was positive for adenovirus. On further review, her mother described a milk intake of approximately 4 gallons per week and a predilection for eating paper. Following arrest, the patient developed acute respiratory distress syndrome and acute kidney injury with eventual escalation to veno-venous extracorporeal membrane oxygenation, as well as continuous veno-venous hemodialysis. Three months following her arrest, her respiratory failure resolved, but she continues with renal failure requiring peritoneal dialysis, as well as mild cognitive deficits and global volume loss on magnetic resonance imaging. Results: Congestive heart failure is a recognized sequela of severe anemia, though rarely to the level of heart failure and cardiac arrest. Recent animal and human myocyte studies have shown iron deficiency itself also contributes to cardiac dysfunction, with or without anemia. Notably, multiple studies illustrate the rapid reversibility of IDA-induced cardiac dysfunction with iron therapy and/or blood transfusion. It is imperative to appreciate potential life-threatening complications of severe IDA prior to significant cardiorespiratory events.