Thyrotoxicosis-Associated Hypercoagulability Leading to Concurrent Ischemic Stroke and Pulmonary Embolism in Graves’ Disease

Graves' disease is the most common cause of endogenous hyperthyroidism, and it is increasingly recognized as a prothrombotic condition affecting both venous and arterial circulations. We report a 27-year-old male with known but untreated Graves' disease who presented with sudden-onset, left-sided weakness and facial asymmetry, with a National Institutes of Health Stroke Scale score of 9. Brain imaging confirmed multifocal right hemispheric ischemic infarctions with petechial hemorrhagic transformation, and post-contrast T1 black-blood vessel-wall MRI suggested inflammatory arteriopathy. CT pulmonary angiography identified acute pulmonary emboli involving the left upper and right lower lobe segmental pulmonary arteries. Laboratory testing demonstrated overt thyrotoxicosis with reduced Protein S levels, while Protein C, antithrombin III, autoimmune, and antiphospholipid panels were unremarkable. Therapeutic anticoagulation with enoxaparin 1 mg/kg twice daily was initiated and transitioned to apixaban 5 mg twice daily, along with carbimazole 20 mg/day and propranolol 40 mg three times daily. The patient improved clinically and was discharged with near-complete functional recovery. This case underscores that uncontrolled Graves' disease can precipitate simultaneous arterial and venous thrombosis and highlights the importance of early recognition of thyrotoxicosis-associated hypercoagulability, prompt anticoagulation, and initiation of antithyroid therapy. Reassessment of thrombophilia after achieving euthyroidism is advised to guide anticoagulation duration.