DP21: SEVERE VITAMIN K DEFICIENCY BLEEDING AND TRANSFUSION-RELATED ACUTE LUNG INJURY IN AN INFANT: A CASE REPORT
Taylor L Carto1; Alecia Sabartinelli Stein, MD2
1University of Miami Miller School of Medicine; 2University of Miami Jackson Health System
Background: Vitamin K deficiency bleeding (VKDB) remains a rare but potentially devastating cause of hemorrhagic stroke in infants, particularly when neonatal vitamin K prophylaxis is declined. Late-onset VKDB, occurring between 2 weeks and 6 months of age, often presents with life-threatening intracranial hemorrhage. We present a previously healthy 2-month-old infant who developed a giant left intraparenchymal hemorrhage and profound coagulopathy, likely from parental refusal of neonatal vitamin K.
Case Presentation: A previously healthy 2-month-old, 5.3 kg infant presented to the ED unresponsive. CT imaging revealed a giant left intraparenchymal hemorrhage with midline shift. The patient was intubated upon arrival due to depressed mental status. Neurosurgery was consulted for emergent decompression; however, surgery was delayed after discovering severe coagulopathy (hemoglobin 5.5 g/dL, INR >15, PTT >200). Immediate resuscitation in the pediatric intensive care unit (PICU) was initiated, including a massive transfusion protocol (MTP) with red blood cells, cryoprecipitate, fresh frozen plasma, platelets, and vitamin K to correct coagulopathy. After stabilization, the patient was taken to the OR for decompressive left hemicraniectomy.
Patient arrived to the OR with O2 saturations in the 50s. The endotracheal tube (ETT) was noted to contain frothy pinkish-red exudate on transfer. High positive end-expiratory pressure (PEEP), low tidal volumes, and 100% FiO2 were required to maintain O2 saturations in the 80-90s. ABG showed severe acidosis (pH 7.18, pCO2 92, pO2 54). After ruling out severe bronchospasm, a working diagnosis of transfusion-related acute lung injury (TRALI) versus fluid overload pulmonary edema was made. A postoperative chest X-ray showed multifocal opacities and bilateral mid-to-upper lung haziness. In the PICU, the patient required high-frequency oscillatory ventilation (HFOV). Given the administration of 11 units of blood products (167.3 ml/kg) during MTP, TRALI was suspected as the primary cause of respiratory failure.
The patient improved with HFOV and inhaled nitric oxide. Gradual recovery allowed weaning to SIMV and later BiPAP. The patient was extubated successfully and discharged. Two months later, the patient returned for left cranioplasty, demonstrating significant recovery with mild right-sided weakness and normal neurological function
Implications: Parental refusal of vitamin K prophylaxis is rising, with estimates suggesting 0.3–3% of U.S. newborns do not receive it. Infants without prophylaxis have an 81-fold increased risk of late VKDB, with up to 50% presenting with intracranial hemorrhage. As this trend continues, more cases of preventable hemorrhagic stroke may emerge.
TRALI remains an underrecognized but life-threatening transfusion complication. While its precise incidence in neonates is not well established, it’s estimated to occur in 1 in 5,000 transfusions, with an increased risk associated with FFP and platelet-rich products. Early recognition and ventilatory support is critical to improving outcomes.
Conclusion: This case underscores the consequences of vitamin K refusal and demonstrates the importance of recognizing TRALI as a significant transfusion-related complication in infants, particularly in massive transfusion settings. As parental refusal of vitamin K prophylaxis increases, proactive education and preventive strategies are essential to mitigate future cases of VKDB and its associated complications.