Abstract Hyperleukocytosis represents a hematologic emergency in acute leukemia, with pulmonary leukostasis among its most catastrophic complications. Blast cell aggregation within the pulmonary microvasculature leads to impaired gas exchange, endothelial injury, and cytokine-driven inflammation. Once respiratory failure requires mechanical ventilation, mortality exceeds 70%, underscoring the need for early recognition and rapid cytoreduction.We report a 20-year-old man with relapsed Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) who presented with one week of progressive dyspnea, pleuritic chest pain, and fatigue. On arrival, he was febrile, tachypneic, and hypoxemic (SpO2 85% on room air). Chest examination revealed diffuse crackles; imaging showed bilateral interstitial opacities without consolidation. Laboratory results demonstrated WBC 400 × 109/L (72% blasts), hemoglobin 6.6 g/dL, platelets 16 × 109/L, uric acid 16 mg/dL, creatinine 3.7 mg/dL, and phosphorus 10.3 mg/dL—findings consistent with tumor lysis. Arterial blood gas revealed a PaO2/FiO2 ratio of 180.He was admitted to the ICU with suspected pulmonary leukostasis and managed with high-flow oxygen, corticosteroids, rasburicase, aggressive hydration, allopurinol, broad-spectrum antibiotics, and hydroxyurea for cytoreduction. Leukapheresis was urgently planned but could not be initiated before he developed refractory hypoxemia and multiorgan failure, resulting in death within 24 hours of admission.This case highlights the fulminant trajectory of hyperleukocytosis-related respiratory failure in relapsed ALL, a presentation far less described than in AML. Clinicians should suspect leukostasis when extreme leukocytosis coexists with diffuse infiltrates and no clear infection. Prompt cytoreductive therapy, early ICU involvement, and immediate access to leukapheresis—when available—are essential to improve survival. This abstract is funded by: none
Torre et al. (Fri,) studied this question.