A41-13 When Oxygen Turns Red: Diffuse Alveolar Hemorrhage During Induction Therapy for Secondary Acute Myeloid Leukemia

Background Acute myeloid leukemia evolving from myelodysplastic syndrome (MDS) represents a high risk hematologic malignancy marked by ineffective hematopoiesis, genetic instability, and profound cytopenias. The combination of Liposomal Daunorubicin and Cytarabine (Vyxeos) with Venetoclax has improved remission rates in older adults, however the regimen’s depth of myelosuppression predisposes patients to infectious and hemorrhagic complications. Diffuse alveolar hemorrhage (DAH), though rare, is a catastrophic pulmonary event requiring urgent recognition and multidisciplinary management. Case Presentation A 67-year-old female with MDS diagnosed in 2020 presented with progressive transfusion requirements. Bone marrow biopsy confirmed transformation to AML, and induction therapy with Vyxeos plus Venetoclax was initiated. Initially her hospitalization was uneventful except for a superficial fungal skin infection treated with topical Nystatin. On day 21 of therapy, she developed a new-onset cough. Chest computed tomography revealed bilateral ground-glass opacities concerning for pneumonia, acute respiratory distress syndrome (ARDS), or early DAH. The following day, she developed acute hypoxemia with oral and nasal bleeding requiring intubation. DAH was suspected, and she was promptly treated with recombinant activated factor VII, high dose corticosteroids, and Tranexamic acid, achieving stabilization. Her course was further complicated by septic shock from a bloodstream infection requiring vasopressors and broad spectrum antibiotics. After four weeks of mechanical ventilation, she was successfully extubated. Follow-up bone marrow biopsy confirmed complete remission, and she was discharged to inpatient rehabilitation. Discussion DAH in AML arises from injury to the alveolar-capillary membrane due to profound thrombocytopenia, endothelial damage, and inflammatory cytokine release. Cytotoxic therapy and Venetoclax induced marrow aplasia amplify microvascular fragility and disrupt hemostasis, while infection driven cytokine surges further increase vascular permeability. These events culminate in alveolar flooding with erythrocytes and fibrin, impairing gas exchange and precipitating respiratory failure. Early corticosteroid administration mitigates capillary inflammation, while NovoSeven and Tranexamic acid help restore hemostasis. Supportive strategies lung-protective ventilation, infection control, and timely cytopenia correction are critical for recovery. Conclusion This case underscores the importance of early recognition and prompt, multidisciplinary intervention in DAH during AML induction therapy. Time sensitive management, guided by understanding the underlying pathophysiology, can transform a potentially fatal event into a story of remission and recovery.