Finnegan, K.

Abstract Introduction: Hemolytic uremic syndrome (HUS) is especially uncommon in adults and can manifest as devasting complications including severe acute kidney injury (AKI) and microangiopathic hemolytic anemia (MAHA). Transfusion-related acute lung injury (TRALI) is a rare complication of blood product transfusion that is characterized by the rapid development of noncardiogenic pulmonary edema. We present a rare case of HUS complicated by TRALI requiring mechanical ventilation. Case Description: A 41-year-old female farmer, who occasionally drank raw cow's milk, was admitted with abdominal pain and distension, bloody diarrhea, poor appetite, decreased urine output and fatigue. She was found to have MAHA and stage 3 AKI. Imaging demonstrated pancolitis and workup revealed Shiga toxin-producing E. coli, O157:H7 serotype which was consistent with a diagnosis of HUS. Tests for DIC, TTP and atypical HUS were negative. She was not a candidate for dialysis, plasma exchange or eculizumab. With supportive measures including 3 units of packed red blood cell (pRBC), her symptoms, renal function, and bicytopenia improved and she was discharged. Two days post-discharge, she presented to the ED for unilateral vision changes, left hemiparesis, and lower extremity tremor. After negative neurological evaluation, this was attributed to encephalopathy secondary to HUS. She received 1 unit of pRBCs for a hemoglobin of 6.8. Within 3 hours of transfusion, she developed acute respiratory distress requiring intubation and ICU transfer. CT chest angiogram was negative for pulmonary embolism but demonstrated diffuse bilateral lower lobe dependent consolidations concerning for TRALI (Figure 1). After diuresis, she was able to be extubated within 48 hours with return to her respiratory and neurologic baselines soon after. Discussion: The pathophysiology of TRALI involves neutrophil sequestration and priming in the pulmonary vasculature with subsequent neutrophil activation by donor blood product factors where active infection is a known risk factor. Active HUS likely contributed to neutrophil priming through endothelial damage and systemic inflammation, predisposing this patient to TRALI. There are few reports of similar cases in the literature. TRALI can be subdivided into type I and type II; type I has no risk factors for acute respiratory distress syndrome (ARDS) while type II does. TRALI must also be distinguished from ARDS and transfusion-associated circulatory overload; these distinctions are predominantly made based on timing of respiratory symptom onset. This case highlights the importance of keeping TRALI in the differential for all patients with active or recent infection, including HUS, who develop acute-onset respiratory decompensation after transfusion.