Disseminated intravascular coagulation: An uncommon initial manifestation of AML presenting with embolic stroke

Abstract Introduction: Disseminated intravascular coagulation (DIC) is classically associated with acute promyelocytic leukemia (APL), but is rarely seen at initial presentation in other subtypes of acute myeloid leukemia (AML). We present an unusual case of non-APL AML manifesting with early DIC and embolic stroke. Case Description: A woman in her 60s with atrial fibrillation and hypertension presented to urgent care with worsening back pain. Initial labs revealed WBC 113.8 x 10⁹/L, platelets 43 x 10⁹/L, and INR 4.3. She was referred to the emergency department but presented the following day. On admission, she was febrile, tachycardic, mildly hypotensive, and required supplemental oxygen. She reported several months of fatigue, night sweats, dyspnea, and weight loss, though no prior hematologic workup had been performed. Repeat labs confirmed persistent hyperleukocytosis, thrombocytopenia, and a markedly elevated D-dimer (>12,000 ng/mL), with preserved fibrinogen and prolonged INR, findings concerning for an early prothrombotic phase of DIC. Imaging revealed borderline splenomegaly and hepatic hypodensities suggestive of marrow infiltration. Hematology was consulted, and empiric hydroxyurea and allopurinol were ordered for suspected AML. Peripheral smear confirmed AML, without promyelocytes, excluding APL. Shortly after initial evaluation, while the patient was stable, alert, and eating, she developed sudden neurologic deficits at 1:19 PM. CT angiography revealed a left MCA (M1/M2/M3) occlusion with significant perfusion mismatch. Mechanical thrombectomy was performed, but her condition deteriorated, and she died in the ICU. Cytoreductive or anticoagulant therapy had not yet been initiated. Discussion: This case illustrates a rare presentation of non-APL AML with early DIC manifesting as embolic stroke. While DIC is commonly associated with hemorrhagic complications, its early or subacute phases may be dominated by procoagulant activity. This may result from increased tissue factor expression driven by cytokine-mediated endothelial injury and decreased fibrinolysis via elevated plasminogen activator inhibitor-1 (PAI-1). Despite thrombocytopenia and prolonged INR, the markedly elevated D-dimer and embolic stroke support an underlying hypercoagulable state rather than a bleeding-predominant coagulopathy. Although leukostasis is a more commonly discussed etiology of neurologic events in AML, this case lacked classic leukostasis symptoms such as visual disturbances or dyspnea, and neuroimaging revealed a large-vessel occlusion without findings suggestive of microvascular obstruction. Instead, the presence of an arterial thromboembolism points to an alternative, likely DIC-mediated, thrombotic mechanism. The coexistence of thrombosis and coagulopathy highlights the diagnostic and therapeutic complexity of early DIC in AML. This case underscores the importance of recognizing prothrombotic DIC as a potentially life-threatening early manifestation of non-APL AML, particularly when accompanied by hyperleukocytosis and cytopenias. It reinforces the need for heightened clinical suspicion, early interdisciplinary coordination, and raises important questions regarding stroke risk stratification and anticoagulation strategies in patients presenting with leukemia-associated coagulopathy.