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Endocrine Abstracts (2019) 62 P26 | DOI: 10.1530/endoabs.62.P26

Norfolk and Norwich University Hospital, Norwich, UK.


Background: Evidence suggested a hypercoagulable state in the context of hyperthyroidism. We presented a case of cerebral venous thrombosis (CVT), a rare but potentially fatal complication of the already high mortality thyroid storm.

Case History: A 16year old boy with Asperger’s syndrome was admitted with one-month history of non-specific illness and weight loss followed by 2 weeks of progressive frontal headaches and vomiting, weakness in left arm and left leg for few days. He previously attended A&E twice with headache and vomiting. Examination revealed a dense left-sided hemiparesis with upper motor neurone signs, prominent exophthalmos, a temperature of 38C and sinus tachycardia.

Investigations: Thyroid biochemistry evidenced severe thyrotoxicosis: TSH < 0.01 mU/L [0.35–3.50], FT4 56 pmol/L [8-21] and FT3 > 46.1 pmol/L [3.8–6.0]. Burch-Wartofskyscore was calculated at 55 suggestive of probable thyroid storm. CT head showed features in-keeping with dural venous sinus thrombosis. Lupus anticoagulant (DRVV ratio) was positive (but normalised 10 months after presentation). PNH, Homocysteine, Methionine, Protein C, Protein S, Antithrombin mutation, Factor V leiden mutation, JAK2 mutation, Prothrombin time, APTT and Vasculitis antibodies were all normal. His factor VIII was high at 428% [59–200%].

Management: He was treated with Propylthiouracil, Propranolol, IV hydrocortisone and therapeutic anticoagulation with Dalterparin 12500 units followed by warfarin. High frequency of seizure activity within 24 hours of admission prompted an escalation of treatment to Lugol’s iodine in addition to high dose antiepileptic medications (Phenytoin, Levetiracetam). The patient’s neurology was completely resolved by his first follow-up appointment. He was also maintained in a euthyroid state on Carbimazole. He was treated with Warfarin for 12 months and then changed to aspirin. It was felt that CVT was primarily driven by the hyperthyroid state.

Discussions: Thyroid storm can be triggered by infection, post-surgery, post radioiodine and delayed treatment. The background of Asperger Syndrome in this case might have caused delayed presentation and diagnosis leading to thyroid storm. The hypercoagulable state in hyperthyroidism is multifactorial due to the increased activity of factor VIII (as in this case), Von Willebrand factor, fibrinogen and tissue plasminogen activator. There have been 19 cases of CVT with hyperthyroidism reported. One other case has been reported of antiphospholipid syndrome and Grave’s leading to cerebral venous and arterial thrombosis. It is hypothesised that anticardiolipin antibodies may cross-react with thyrotropin receptor stimulating antibodies. Thus, we should have a low threshold for checking venous thromboembolism in hyperthyroidism.

Volume 62

Society for Endocrinology Endocrine Update 2019

Society for Endocrinology 

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