Abstract
Background: Cerebral venous thrombosis (CVT) accounts for <1% of strokes. In most cases, there is a predisposition to hypercoagulability; however, in about 30% of cases there is no identifiable etiology. Risk factors include pregnancy, puerperium, oral contraceptives, and coagulopathies and rarely hyperthyroidism. To the best of our knowledge there is no reported cases of CVT in uncontrolled hyperthyroidism with no underlying hypercoagulable disorder. We present a case where a woman developed CVT in the setting of uncontrolled hyperthyroidism. Clinical Case: A 24 year-old Caucasian woman was diagnosed with hyperthyroidism during 1st trimester of pregnancy based labs and was treated with propylthiouracil (PTU) 150 mg bid. At 34 weeks of pregnancy her FT4 normalized and PTU was discontinued. Three and half months post-partum she presented with left frontal headache, photophobia, phonophobia and transient visual loss on the right. Physical exam revealed right homonymous hemianopia without meningismus and an enlarged thyroid. Vitals showed BP 108/57 mm of Hg, HR 162 beats/min, RR of 23/min. CT head without contrast showed 8 mm focal hyperdensity along the left tentorium projecting at the left occipital lobe. She developed seizures after admission. MRI brain with and without contrast showed diffusely small left transverse and sigmoid sinus with a focal area of dural sinus thrombosis. MRI venogram of head confirmed CVT. She was started on levetiracetam and low dose heparin drip. Further workup showed: TSH <0.005 UIU/ml with FT4>8 ng/dl, TSH receptor antibodies 11.10 (normal range 0.00 - 1.75 IU/L), thyroid peroxidase antibody >1300 (normal range <=59 u/ml), and thyroid stimulating antibodies 6.85 (0.00 - 0.55 IU/L) suggestive of Graves disease. She was initiated on PTU 200 mg Q8hrs, propranolol 80 mg Q8hrs and lugol’s iodine 5 drops Q8hrs. Hypercoagulable workup except for protein C and S returned unremarkable. Over the next several days, thyroid levels improved significantly. She was discharged home on warfarin and methimazole. Conclusion: The exact pathophysiology of CVT in hyperthyroidism remains unclear. Some proposed mechanisms include increased activity of pro coagulative plasma constituents including Von Willebrands Factor, Factor IX, X, antithrombin, and fibrinogen as well as an increased aPTT and a decrease in thrombolytic factors like t-PA. These changes result in an increased risk of thrombosis. This case demonstrates the potential development of CVT as a result of untreated overt hyperthyroidism. It highlights the importance of treatment and close follow up of Graves’ disease to prevent severe complications. Further studies need to be done to understand the process of coagulation in hyperthyroidism and this could allow clinicians to better identify hyperthyroid patients at risk for clotting.
Development of a dural arteriovenous fistula subsequent to cerebral venous thrombosis by venous hypertension
