Venous thromboembolism is a common, yet serious life-threatening condition that has many well-recognized associations which include but are not limited to pregnancy, polycythemia, trauma, immobility, and malignancy. The pathophysiology behind the pro-coagulant effects of hyperthyroidism has been well established; however, there are no current guidelines regarding deep venous thrombosis (DVT) surveillance in patients with hyperthyroidism. In this report, we discuss the case of a 36-year-old female with no significant past medical history (PMH) with the exception of a 15 pack-year smoking history, who presented to us with an extensive, rapidly-progressing lower extremity DVT. Despite aggressive treatment measures, she developed a pulmonary embolus in the hospital. During her stay, she was diagnosed with Graves’ disease by hormone profile and thyroid-stimulating hormone receptor (TSH-R) antibody positivity. Additionally, an incidental thymic mass, likely thymic hyperplasia, was found on imaging and presumed to be associated with Graves’ disease. This case study reports a difficult-to-treat venous thromboembolism in the setting of Graves’ disease along with a review of current literature and pathophysiology on the subject.
Left ventricular thrombus (LVT) is a major complication of acute myocardial infarction (MI). Here, we describe the case of a 36-year-old female with a history of acute anterior MI six years prior to hospitalization, who presented with bilateral vision loss due to a bilateral embolic posterior cerebral artery (PCA) stroke in the setting of a 5.7 x 1.7 cm LVT. She underwent bilateral PCA thrombectomy, which led to improvement of her symptoms. Her LVT was managed non-surgically with apixaban and clopidogrel. Her case highlights the need for more medical education about LVT, as quick initiation of anticoagulation is essential in improving outcomes. We review the existing literature to explain the pathogenesis, diagnosis, and treatment of LVT.
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