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Abstract: PO1003

Peritoneal-Mediastinal Communication Complication in Peritoneal Dialysis

Session Information

  • Peritoneal Dialysis
    November 04, 2021 | Location: On-Demand, Virtual Only
    Abstract Time: 10:00 AM - 12:00 PM

Category: Dialysis

  • 702 Dialysis: Home Dialysis and Peritoneal Dialysis

Authors

  • Sy-Go, Janina Paula Tiulentino, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Androga, Lagu A., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Qureshi, Fawad, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Kattah, Andrea G., Mayo Clinic Minnesota, Rochester, Minnesota, United States
Introduction

Increased intra-abdominal pressure is a well-recognized non-infectious complication of peritoneal dialysis (PD) resulting from instillation of dialysate fluid into the peritoneal cavity. Peritoneal-pleural communication causing hydrothorax is well-described in the literature, but cases of peritoneal-mediastinal communication are scarce.

Case Description

A 36-year old Caucasian man with end-stage kidney disease secondary to calcineurin inhibitor nephrotoxicity and BK virus nephropathy transitioned to continuous cycler peritoneal dialysis (CCPD) after one year of intermittent hemodialysis (iHD). He presented to our institution nine months after starting CCPD primarily because of complications related to prior heart transplantation. He underwent cardiac surgery and did not have any problem with his CCPD in the immediate post-operative period and was discharged. One month later, however, he presented with increased serous drainage from his sternal incision site and reduced ultrafiltration. A chest CT scan revealed a partially loculated anterior chest wall subcutaneous fluid collection. He was taken to the operating room and was found to have a peritoneal-mediastinal communication. He was successfully managed with “low-pressure” PD by using reduced fill volumes for all his exchanges, which also allowed optimal healing of the muscle flap closing the communication. Transition to iHD was considered, but he had no vascular access options because of multiple prior thromboses. He was able to subsequently return to his outpatient CCPD prescription about two months after his surgery by doing very gentle uptitration of his fill volumes. Unfortunately, one and a half months after his last hospitalization, he succumbed to septic shock secondary to trans-lumbar PICC-associated Candida glabrata fungemia.

Discussion

A peritoneal-mediastinal communication should be suspected in an otherwise asymptomatic patient on PD with reduced ultrafiltration who underwent any form of chest surgery. Clinical suspicion can be confirmed either through CT peritoneography or intraoperatively. Management with a trial of “low-pressure” PD is feasible and can be successful, particularly if iHD is not an option. A multi-disciplinary approach involving our surgical colleagues is also crucial to ensure appropriate patient care.