Renal Cell Carcinoma Presenting as Syncope due to Saddle Pulmonary Tumor Embolism

Abstract

Pulmonary embolism (PE) is defined as the obstruction of the pulmonary artery or one of its branches by a blood clot, tumor, air, or fat emboli originating elsewhere in the body. A saddle PE occurs when the obstruction affects the bifurcation of the main pulmonary artery trunk. We present a case of a 46-year-old man who presented to our hospital due to an episode of syncope. Computed tomography angiography (CTA) of the chest showed extensive PE and abdominal CT scan showed a large 8 cm left renal mass with inferior vena cava (IVC) thrombus. Emergent embolectomy, left total nephrectomy, and IVC tumor removal were performed yielding the diagnosis of clear cell renal cell carcinoma (RCC). Interestingly, our patient did not experience any symptoms related to his RCC until the diagnosis of PE due to syncope, and the asymptomatic tumor was found out to be the possible cause of this PE due to the presence of tumor cells constituting the tumor embolus. It is thus recommended to improve the early screening process for RCC. Besides, clinicians should pay attention to patients presenting with uncharacteristic symptoms of RCC who might present with symptoms of saddle PE.

Pulmonary Arterial Tumor Embolism From Recurrent Metastatic Renal Cell Carcinoma on FDG PET/CT

“…With respect to RCC, available reports describe pulmonary tumor embolism only when a primary tumor is present or in the perioperative setting. To our knowledge, this is the first report in which the patient had long-term remission and recurrence manifested as pulmonary tumor emboli secondary to RCC 12–20 …”

“…To our knowledge, this is the first report in which the patient had long-term remission and recurrence manifested as pulmonary tumor emboli secondary to RCC. [12][13][14][15][16][17][18][19][20]…”

Renal vein thrombosis in a patient secondary to high grade Rhabdoid renal cell carcinoma: a case report and review of literature

“…RCC can continuously grow, penetrate capillary walls, and enter the renal vein, eventually migrating into the inferior vena cava. There are different mechanisms that explains how malignancy can cause venous thromboembolism namely external compression by solid tumours, tumour invasion and malignancy related hypercoagulability 17 – 19 . Inflammatory mediators in response to malignancy prompt the activation of coagulation cascade while simultaneously suppressing anticoagulatory pathways.…”