Cerebral Venous Sinus Thrombosis With Bilateral Blindness in Systemic Lupus Erythematosus: A Case Report
Md. Gias Uddin, Mohammad Abul Kalam Azad, Md. Masudul Hassan, Md Moinuddin Sohel, Ismail Hossain, Minhaj Rahim ChoudhuryCerebral venous sinus thrombosis (CVST) is an uncommon but potentially life‐threatening neurological complication of systemic lupus erythematosus (SLE) that requires prompt recognition and treatment. We report the case of an 18‐year‐old Bangladeshi woman with established SLE who presented with a 10‐day history of severe headache followed by rapidly progressive bilateral proptosis and sudden, painless bilateral visual loss. Neurological examination revealed complete bilateral visual loss, bilateral ptosis, restricted extraocular movements and multiple cranial nerve deficits. She had active SLE with severe thrombocytopaenia and haematological involvement. Brain magnetic resonance imaging and magnetic resonance venography demonstrated extensive thrombosis involving the superior sagittal, bilateral transverse and sigmoid and cavernous sinuses. Antiphospholipid antibody testing, including lupus anticoagulant, anticardiolipin antibodies and Anti‐β2‐glycoprotein I antibodies, was negative. The patient received therapeutic anticoagulation, high‐dose corticosteroids and immunosuppressive therapy with rituximab, followed by haematological and neurological improvement and subsequent recanalisation of the thrombosed dural venous sinuses. However, bilateral visual loss persisted, with optic disc pallor and optic atrophy. Optical coherence tomography, visual evoked potential testing, dedicated orbital imaging and formal neuro‐ophthalmological assessment were not performed; therefore, the precise mechanism of visual loss could not be definitively established. Nevertheless, ischaemic optic neuropathy was considered the most likely mechanism given the clinical presentation and extensive CVST. This case highlights that extensive CVST may occur in active SLE despite negative antiphospholipid antibody testing. It underscores the importance of early neuroimaging, timely anticoagulation and appropriate immunosuppressive therapy to minimise the risk of persistent neurological and visual sequelae.