A 38-year-old man with untreated hyperthyroidism presented with two-week history of progressively worsening weakness and dyspnea along with a six-month history of unintentional 38 pound weight loss, diarrhea, and palpitations. Exam was notable for confusion, cachexia, diffuse thyromegaly, jugular venous distension, exophthalmos, thyroid bruit, bilateral rales, and tachycardia (HR to 150s). A transthoracic echocardiogram demonstrated newly decreased LV systolic function (EF <20%). Laboratory analysis was notable for TSH 0.02, fT4 4.0, fT3 11.2, and a positive assay for thyroid stimulating antibodies. He was diagnosed with thyroid storm with high-output heart failure and was admitted to the ICU for treatment with methimazole, cholestyramine, beta blockers, steroids, SSKI, and diuresis. He was transferred to the floor medicine service when he began to improve. He developed an acute liver injury, with an elevated INR (1.5) and anemia (Hgb 10.7), but no bleeding was reported. Chemical thromboembolism prophylaxis was held and mechanical prophylaxis was utilized on the lower extremities.
The following day, he developed right upper extremity swelling with erythema and tenderness to palpation. An ultrasound demonstrated an extensive thrombus in the right subclavian and brachiocephalic veins. A continuous infusion of heparin was initiated. The next morning, after developing acute shortness of breath, he underwent a chest CT scan – positive for bilateral pulmonary emboli within both lung bases. Thrombophilia screen revealed elevated levels of Factor VIII and vWF antigen. He was subsequently transferred back to the ICU due to development of cardiogenic shock. Dobutamine was started. Thrombolysis was attempted using tPA; he subsequently developed a hemothorax requiring chest tubes. After failure to control his thyroid hormone levels with oral medications, the patient underwent a thyroidectomy. His symptoms improved following surgery and he was discharged home with levothyroxine.
Discussion:
The increased risk of thromboembolism is a serious and not an uncommon complication associated with hyperthyroidism. In this case, a serious thromboembolic event associated with hyperthyroidism led to hemodynamic instability. It is important to screen for thyroid disorders in patients with unexplained thromboembolic events.
Hyperthyroidism has a significant effect on hemostasis and coagulation factors. There is a positive correlation between the thyroid hormones level and indicators of endothelial damage (such as vWF) as well as Factor VIII. Increased damage to the endothelium promotes a procoagulant state, while increased Factor VIII has been shown to be a dose dependent risk factor for thromboembolism. Fibrinogen and plasminogen activator inhibitor 1 are also elevated in hyperthyroidism. Furthermore, even mild hyperthyroidism can predispose a patient to heart failure, arrhythmias (including atrial fibrillation), and hypertension, thereby increasing the risk of cardiac thrombus formation and subsequent thromboembolism.
Conclusions:
This case demonstrates the risk of thromboembolism associated with hyperthyroidism. Understanding the abnormalities in hemostasis that may predispose patients with hyperthyroidism to hypercoaguability will allow more widespread recognition of the complications of hyperthyroidism.