Case Presentation: Patient is a 64 male with a past medical history of coronary artery disease who was experiencing two months of syncopal episodes with increasing frequency. Associated with these episodes were instances where he would wake up at night, face flushed and diaphoretic. He would also note bradycardia to the 30’s. He had an extensive work up both as an outpatient and inpatient where he had an unremarkable EKG, stress test, carotid duplex scan, and echocardiogram. Furthermore, patient had negative orthostatic vital signs, CT of the head, and TSH. He left AMA after his first hospitalization then presented back to the hospital after having passed out on the street, found cool and diaphoretic with a blood pressure in the 80’s/50’s, which responded to IV fluids. He had a CT Pulmonary Embolism protocol done which showed a 4.3 x 4.6 x 3.6 cm soft tissue mediastinal mass encasing the left main pulmonary arteries causing compression left main and upper lobe pulmonary arteries. Cytology showed lung adenocarcinoma. He has since received chemotherapy and radiation therapy with a substantial decrease in tumor burden and improvement in syncopal symptoms.
Discussion: Syncope accounts for 1-1.5% of emergency room visits (1). The differential diagnosis of recurrent syncope can range from its most common benign cause, neural/reflex (situational), to life-threatening cardiac arrythmias. Initial syncope work-up is targeted towards these. Identification of etiology is found in approximately 76% of these cases with non-invasive diagnostic tools but can be extremely challenging for the remaining group (2). Syncope mediated by vagal nerve activation due to mechanical compression by a head or neck mass is not uncommon, but compression by a mediastinal mass is rare. Only a few cases of small cell lung cancer have been reported to cause syncope (3,4), but there are even fewer reports of pulmonary adenocarcinoma being the cause, as it tends to be a peripherally dominant cancer (5,6). We present an atypical case of pulmonary adenocarcinoma presenting with recurrent syncopal episodes. Our patient had a rare, reversible case of recurrent syncope and initially had a negative workup. His cardiac history was a red herring and led to a cardiogenic syncope workup. He did, however, have B symptoms concerning for a malignancy and the substantial bradycardia did suggest a vagal mediated syncope. While he eventually received a CT showing a mass compressing his vagal nerve, more prompt work up could have prevented an additional episode of syncope and possible complications (fractures, hemodynamic instability, hypoxia, etc.). Furthermore, an earlier CT could have allowed earlier detection of the malignancy, increasing the chances of a therapeutic response to chemotherapy and radiation. This case highlights how recurrent syncope, especially with systemic symptoms and a negative initial work-up, deserves further evaluation.
Conclusions: Recurrent syncope, especially with systemic symptoms and a negative initial work-up, deserves further evaluation.