Thromboembolic complications of thyroid storm.
Min T, Benjamin S, Cozma L -Endocrinology, diabetes & metabolism case reports(2014)
fig1:Initial electrocardiogram (ECG) at presentation to the emergency room: heart rate 160 beats/min and atrial fibrillation.
View Article:PubMed Central - PubMed
Affiliation:ST4 Diabetes and Endocrinology Princess of Wales Hospital Bridgend, CF31 1RQ UK.
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Bottom Line:Early recognition and prompt treatment are essential.Herein, we describe a case of thyroid storm complicated by massive pulmonary embolism.Diagnosis of thyroid storm is based on clinical findings.
Abstract

Unlabelled: Thyroid storm is a rare but potentially life-threatening complication of hyperthyroidism. Early recognition and prompt treatment are essential. Atrial fibrillation can occur in up to 40% of patients with thyroid storm. Studies have shown that hyperthyroidism increases the risk of thromboembolic events. There is no consensus with regard to the initiation of anticoagulation for atrial fibrillation in severe thyrotoxicosis. Anticoagulation is not routinely initiated if the risk is low on a CHADS2 score; however, this should be considered in patients with thyroid storm or severe thyrotoxicosis with impending storm irrespective of the CHADS2 risk, as it appears to increase the risk of thromboembolic episodes. Herein, we describe a case of thyroid storm complicated by massive pulmonary embolism.

Learning points: Diagnosis of thyroid storm is based on clinical findings. Early recognition and prompt treatment could lead to a favourable outcome.Hypercoagulable state is a recognised complication of thyrotoxicosis.Atrial fibrillation is strongly associated with hyperthyroidism and thyroid storm.Anticoagulation should be considered for patients with severe thyrotoxicosis and atrial fibrillation irrespective of the CHADS2 score.Patients with severe thyrotoxicosis and clinical evidence of thrombosis should be immediately anticoagulated until hyperthyroidism is under control.

Mentions
Investigation revealed deranged liver function, normal kidney function and severe thyrotoxicosis with suppressed thyroid-stimulating hormone (TSH) concentration of <0.03 mU/l, free thyroxine (T4) concentration of 71.4 pmol/l and free triiodothyronine (T3) concentration of 27.4 pmol/l. The concentration of TSH receptor antibody was markedly elevated at 38.2 U/l (<1.0). Atrial fibrillation with a rapid ventricular response (heart rate of 165 beats/min) was noted on ECG (Fig. 1).
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