Abstract: PO1049
Rare Cause of Pleural Effusion in a Dialysis Patient
Session Information
- Vascular Access Arena: Challenges, Progress, and Prospects
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Dialysis
- 703 Dialysis: Vascular Access
Authors
- He, Mingyue, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
- Khan, Waqas Ahmad, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
- Lee, Iris J., Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
- Rakhman, Ilay, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
- Constantinescu, Serban, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
Introduction
The most common causes of pleural effusion in dialysis patients are congestive heart failure, infections, and tumors. However, in some dialysis patients, identifying the rare cause of pleural effusion requires careful consideration.
Case Description
A 29-year-old African American female with ESRD secondary to Lupus Nephritis (LN) s/p deceased donor kidney transplant, developed allograft failure and restarted dialysis. Upon initiating dialysis and weaning of immunosuppression she had episodes of fever, myalgias, synovitis and pleural effusions thought to be manifestations of lupus flare. Despite restarting immunosuppression, she presented frequently with dyspnea and recurrent bilateral transudative pleural effusions requiring repeat thoracenteses. Her physical exam was notable for swelling of bilateral upper extremities and face with minimal lower extremity edema. Lupus serologies were normal. Echo was unrevealing. CT angiogram (CTA) revealed complete occlusion of the distal superior vena cava (SVC) with extensive collateralization in the chest and abdominal wall.
Discussion
Her initial symptoms were attributed to volume overload and lupus serositis. However, inactive serologies, ongoing immunosuppression, and the transudative nature of the effusion were not consistent with lupus flare. Aggressive UF also failed to prevent recurrent pleural effusion. Given CTA and clinical findings, we concluded that the persistent pleural effusion is a manifestation of the SVC syndrome in our patient. The occlusion of the SVC was below the junction of the arch of the azygos vein. Venous blood flow from the upper body and extremities was shunted into the azygos system and flowed counter-current, returning to the right heart through the inferior vena cava. This results in increased hydrostatic pressure in the intercostal veins, contributing to the development of edema of the head, upper chest, bilateral upper extremities, and pleural effusions. Our patient had multiple central venous catheters increasing her risk for SVC syndrome. Clinicians should consider SVC stenosis as a potential cause of recurrent pleural effusions in a dialysis patient.