Abstract Introduction Chronic myeloid leukemia (CML) is usually asymptomatic and found incidentally or presents with constitutional symptoms. The blast phase (BP) of CML resembles acute leukemia, with megakaryoblastic transformation being rare. Due to the limited number of reported BP-CML cases with megakaryocytic transformation, recognizing associated complications such as cardiac tamponade, as seen in this case, remains difficult. Case A 55-year-old woman with a history of chronic myeloid leukemia (CML), previously treated with dasatinib but with multiple lapses in therapy, presented with dyspnea, fever, and productive cough. On admission, she was tachycardic, hypotensive, and required supplemental oxygen. She had a white blood cell count of 431 K/µL, hemoglobin of 8.3 g/dL, platelets of 236 K/µL, and lactate dehydrogenase of 4,422 U/L. Leukapheresis was initiated for cytoreduction. Flow cytometry revealed 52% blasts, and bone marrow biopsy confirmed megakaryocytic transformation. On hospital day 11, she became increasingly tachycardic and hypoxic. Bedside ultrasound showed a pericardial effusion with cardiac tamponade, requiring emergent pericardiocentesis and placement of a pericardial drain. Pericardial fluid analysis, including flow cytometry, showed basophilia without blasts, and infectious studies were negative. Following drainage, the effusion resolved, which was confirmed by a follow-up echocardiogram. The patient was eventually discharged home. Discussion Nonadherence to tyrosine kinase inhibitor therapy is a known risk factor for disease progression and blast-phase transformation in CML. In this case, pericardial fluid analysis revealed basophilia without blasts, suggesting cytokine-mediated inflammation or reactive basophilic proliferation rather than direct leukemic infiltration. Although dasatinib can cause pleural and pericardial effusions, the patient’s discontinuation of therapy supports a disease-related etiology. Prompt recognition of cardiac tamponade is critical, as hemodynamic compromise requires urgent intervention. This case underscores the need for vigilant monitoring during blast crisis, even in the absence of overt leukemic infiltration. Early identification of blast lineage is essential for guiding therapy and prognosis, with megakaryocytic differentiation often indicating a more aggressive course and poorer outcomes. This abstract is funded by: None
Sheikh et al. (Fri,) studied this question.
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