Title
Syncope Shadows: Unraveling the Link with SVC Syndrome
Introduction
Superior Vena Cava Syndrome (SVC Syndrome) is when blood flow through the SVC is obstructed or compressed. The syndrome manifests as clinical signs and symptoms secondary to diminished blood return to the heart (1). The most common cause of SVC Syndrome is malignancy, which can compress or invade the SVC. Another reason is the frequent use of central venous catheters and devices, leading to thrombosis (2). Patients with SVC Syndrome often present with a constellation of symptoms, including facial swelling, shortness of breath, cough, and chest pain (3). The condition is a diagnostic challenge and a critical juncture in patient care, especially if malignancy is the underlying cause. Understanding the causes, clinical presentation, and potential complications of SVC Syndrome is crucial for timely diagnosis and appropriate management, ensuring better outcomes for affected patients.
Clinical Case
A 22-year-old female presented to the hospital after a syncopal episode at home. She has a medical history of mixed germ cell tumor of the ovary and recently underwent her third etoposide/cisplatin chemotherapy cycle. On presentation to the emergency department, she was hypotensive with systolic blood pressures ranging from 52-75 mmHg. Pulse oximetry was 85% on 4 L/min of oxygen, and the heart rate was 90 beats per minute. She required peripheral vasopressor support on presentation with norepinephrine. Physical exam was notable for a “violaceous color to the skin of the head and neck.” Her labs were notable for a serum lactate of 3.3. An urgent CTA demonstrated a sizeable hypodense structure extending from the tip of her port catheter in the lower SVC into the right atrium, 3.4 cm by 2.6 cm. Blood cultures did not demonstrate evidence of bacteremia. Subsequently, she underwent transesophageal echo-directed catheter-based suction embolectomy (Angio Vac). The transesophageal echocardiogram during the procedure confirmed the presence of a bulky thrombus prolapsing from the superior vena cava into the right atrium. Shen then had a successful Angio Vac of the thrombus in the right atrium; however, there was a significant thrombus in the superior vena cava with minimal flow, and initial SVC pressure was 40 mmHg. An angioplasty of the SVC at the cavoatrial junction was performed with serial dilations with 16-millimeter and 20-millimeter balloons. There was improvement in SVC pressure to 25 mmHg. The following day, her physical exam was notable for improvement in her color and vital signs.
Discussion
In SVC Syndrome, obstruction of the vena cava leads to impaired venous return from the upper body to the heart. While the body may initially compensate for the insufficient flow by dilating collateral veins, the compensation is limited (4). In the absence of timely intervention, reduced preload can compromise cardiac output and lead to shock, although this is rare (5). The incidence of shock in the setting of SVC syndrome is unknown and limited to a few case reports. In our patient’s case, her shock was likely obstructive as there was likely impaired blood flow returning to the right ventricle from the rest of the body.