P2.113: Intracardiac Air Embolism Associated with Necrotizing Enterocolitis in a Premature Infant: A Case Report

Introduction: Necrotizing enterocolitis (NEC) is a devastating gastrointestinal emergency primarily affecting premature infants, with mortality rates ranging from 20-30%. While pneumatosis intestinalis and portal venous gas are well-documented radiographic findings in NEC, intracardiac air embolism is a rare and typically fatal complication. This case report describes a former 29-week premature infant who experienced sudden cardiopulmonary collapse associated with massive intracardiac air embolism in the setting of evolving NEC, highlighting the importance of recognizing this complication for neonatologists and pediatric intensivists.

Case Description: A former 29-week preterm infant with a tenuous gastrointestinal course characterized by intermittent feeding intolerance and abdominal distension but no previous evidence of NEC experienced sudden decompensation on day of life 34 (at PMA 34weeks). At the time of NEC episode infant was on full enteral feeds and also minimal dextrose-containing intravenous fluids via a peripherally inserted central catheter (PICC) for mild persistent hypoglycemia. Patient suffered a sudden profound desaturation and bradycardia event that progressed to cardiopulmonary arrest and did not respond to any aggressive resuscitation efforts. Imaging studies obtained during resuscitation revealed appropriate position of lines and devices, intracardiac air bubbles, extensive portal venous gas, and gaseous distension of multiple bowel loops. These findings suggested an acute NEC event with translocation of intraluminal gas into the portal venous system and subsequently into the cardiac chambers, resulting in massive air embolism and cardiovascular collapse refractory to resuscitation efforts.

Discussion: This case illustrates the rare but catastrophic complication of intracardiac air embolism associated with NEC in premature infants. The pathophysiological mechanism likely involves intestinal mucosal disruption allowing gas from gas-forming bacteria to invade the bowel wall and enter the portal venous circulation. Subsequently, gas emboli can travel through the liver's portal venous system to the inferior vena cava and into the right heart chambers, potentially crossing into the left heart through a patent foramen ovale or other septal defects common in premature infants. Intracardiac gas embolism creates an air-lock phenomenon that severely compromises cardiac output and leads to rapid hemodynamic collapse resistant to resuscitation measures. Virtual autopsy (postmortem imaging attached) confirmed the diagnosis. Literature review reveals few reported cases of this complication, underscoring the need for increased awareness among clinicians caring for this vulnerable population.

Conclusion: Intracardiac air/gas embolism represents a rare but frequently fatal complication of NEC in premature infants. The rapid clinical deterioration and poor response to standard resuscitation measures in this case emphasize the importance of early recognition of this entity. Further research is needed to develop preventive strategies and potentially effective interventions for this devastating complication. This case contributes to the current limited literature on the association between NEC and intracardiac air/gas embolism, providing valuable insights for clinicians managing premature infants with gastrointestinal compromise.