Cerebral Infarction As a Complication of a Hypercoagulable State in the Setting of Hyperthyroidism: A Case Presentation

Introduction

Studies have demonstrated a significant association between hyperthyroidism and a hypercoagulable state. Hyperthyroidism, characterized by the excessive production of thyroid hormones, can influence the hemostatic balance, leading to an increased risk of thrombosis. Additionally, hyperthyroidism is a well-known risk factor for atrial fibrillation and cardiomyopathy, both of which can contribute to the development of thromboembolic events. Although rare, cerebral infarction has been reported in patients with hyperthyroidism, particularly due to the hypercoagulable state induced by the excessive thyroid hormones. This case presentation illustrates such an instance, highlighting the complex interplay between thyroid dysfunction and coagulation abnormalities.

Case presentation

A 23-year-old male with a history of Type 1 Diabetes Mellitus, uncontrolled hyperthyroidism due to Graves' disease, and asthma presented with decreased consciousness and possible seizure activity. He was diagnosed with diabetic ketoacidosis (DKA), thyrotoxicosis, cardiogenic shock, a large middle cerebral artery (MCA) infarction, and pulmonary infarction. Transesophageal echocardiogram showed no vegetations. He was initiated on propranolol, methimazole, and hydrocortisone. Hypercoagulable panel, including PT/INR, aPTT, antithrombin III activity, protein C/S, factor V Leiden, G20210A, lupus anticoagulant, homocysteine, and anticardiolipin, was unremarkable. With normalization of thyroid function, cardiac function steadily improved, and no further progression of pulmonary embolism or cerebral infarction was observed. Due to the significant MCA infarction, long-term rehabilitation was required.

Discussion

A hypercoagulable state associated with hyperthyroidism is not commonly recognized but has been documented in several cases. The proposed mechanisms include the upregulation of clotting factors, increased platelet activation, endothelial dysfunction, a hyperadrenergic state, and reduced fibrinolysis. Clinicians should maintain a high index of suspicion for hyperthyroidism as a potential cause of thromboembolic events. Prompt treatment of hyperthyroidism is essential to prevent complications.

No relevant conflicts of interest to declare.