Anticoagulation in lobar ICH management for patients with antiphospholipid syndrome

Introduction Lobar intracerebral hemorrhage (ICH) in the elderly typically raises concern for cerebral amyloid angiopathy (CAA), especially when it is accompanied by cerebral microbleeds. However, in patients with prothrombotic disorders like antiphospholipid syndrome (APLS), these presentations could be a sign of an altogether different process with significantly different therapeutic implications. We present a case which emphasizes diagnostic and therapeutic dilemma of resuming anticoagulation in a patient with a history of lobar ICH and microbleeds—where the etiology may not always be as assumed. Materials/Methods We report the case of a 69‐year‐old woman with a history of APLS (positive lupus anticoagulant and anticardiolipin antibodies), prior ischemic stroke, hypertension, and seizure disorder, on long‐term warfarin. Two months after a right parietal lobar ICH, she presented with new onset vertigo and headache. The rest of her neurological exam was unremarkable. Workup included head CT, brain MRI with and without contrast, and CT venography. Management involved decision‐making due to imaging findings that were concerning for both residual venous thrombosis versus possible cerebral amyloid angiopathy, which required careful reconsideration of anticoagulation strategy. Results Initial head CT confirmed stability of the prior right parietal hemorrhage. CT venography revealed a nonocclusive filling defect in the distal right transverse sinus, which raised concern about lingering thrombosis. Brain MRI revealed a small acute infarct in the right centrum semiovale and several cerebral microbleeds, involving both lobar and deep structures, such as basal ganglia and thalami. While these findings had initially raised concern for cerebral amyloid angiopathy (CAA), the distribution of microbleeds along with her medical history were more consistent with hypertensive or, more likely, APLS‐associated vasculopathy. With her double‐positive APLS status and thrombotic risk, anticoagulation was resumed with a bridging regimen of low molecular weight heparin and warfarin, to a therapeutic INR of 2.5‐3. The patient was neurologically intact and discharged with close outpatient follow‐up in coordination with neurology, hematology, and an APLS specialist. Conclusion In patient with lobar ICH and microbleeds, one needs to consider non‐CAA diagnoses—especially if the imaging and clinical scenario don't quite add up. APLS‐associated vasculopathy may produce a similar MRI appearance, but the treatment implications are entirely different. This case emphasizes the value of individualized decision‐making in weighing hemorrhagic and thrombotic risk, particularly in complex patients with pre‐existing prothrombotic disease.