Hu, A.W.

Abstract Lung transplant recipients are at high risk for pleural complications following transplantation. Pleural effusions are nearly universal immediately after transplant, but most resolve spontaneously in the following weeks. For persistent effusions, there is no consensus on the optimal management strategy, and risks of potential procedures must be balanced with long-term complications. A 58-year-old male presented with 3 months of severe fatigue, brain fog, chills without fever, poor appetite, and weight loss. His medical history included bilateral redo lung transplant 7 months prior for chronic lung allograft dysfunction, type II diabetes mellitus, chronic kidney disease stage IIIb, and heart failure with preserved ejection fraction. His immunosuppression regimen included tacrolimus, prednisone, and mycophenolate, with prophylaxis of trimethoprim/sulfamethoxazole and posaconazole. At the follow up visit, spirometry revealed a significant decline in lung function (FVC 2.31 to 1.97; FEV1 1.84 to 1.51). He was admitted for urgent evaluation. A CT scan revealed a large (20 cm) multiseptated left-sided empyema or hematoma causing mass effect on the spleen and distal pancreas. A 12 French locking loop pigtail catheter was placed into the left pleural space, and fluid analysis showed a total nucleated cell count of 23,306/mcL (100% neutrophils), LDH >9000 U/L, total protein of 1.3 g/dL, glucose <2 mg/dL, and pH <6.80, consistent with empyema. Fungal cultures identified Scedosporium species. The patient received six doses of intrapleural lytics, yielding 3.3 liters of serosanguinous drainage. However, repeat CT showed residual thick fibrinous peel surrounding the pleura. Video-assisted thoracoscopic decortication revealed extensive pleural infection with minimal healthy mucosa, allowing only limited decortication due to bleeding risk. He then underwent open-window thoracostomy (Clagett window) for ongoing drainage, followed by three additional debridement procedures and antifungal therapy with liposomal amphotericin B and voriconazole. This case illustrates the insidious onset of empyema in immunocompromised hosts, such as lung transplant patients, and highlights the rare need for open-window thoracostomy in severe pleural infections.

Abstract INTRODUCTION While cardiac comorbidities or factors predisposing infection are common in patients with ESRD, one less common cause for pleural effusion in peritoneal dialysis (PD) patients is pleuroperitoneal communication. We present herein a case of a PD patient with large, right-sided pleural effusion one year after starting PD. CASE REPORT An 82-year-old female with ESRD managed on home continuous cycling peritoneal dialysis (CCPD) for 1 year presented to the Emergency Department (ED) with new-onset dyspnea. She recently completed a course of vancomycin for bacterial peritonitis secondary to PD catheter infection. She also reported that her home CCPD machine was not draining the fill amount in recent weeks. She was afebrile and hemodynamically stable on arrival. CT at the ED showed a large, right-sided pleural effusion. She underwent thoracentesis with pending fluid analysis, and experienced subsequent improvement in her dyspnea. She was then hospitalized and wished to continue PD over pursuing intermittent hemodialysis (iHD) while workup was pending, despite clinical suspicion for pleuroperitoneal fistula (PPF). She started inpatient CCPD, and drains following each dwell showed less than expected volumes with no additional output on manual drains. She reported worsening dyspnea the next morning, and bedside POCUS confirmed reaccumulation of her pleural effusion. Fluid analysis revealed a transudative pleural fluid profile, with pleural glucose of 583mg/dL and serum glucose of 80mg/dL. Given her recent peritonitis, suspicion was greatest for PPF. The patient was transitioned from PD to iHD to allow time for the suspected fistula to heal, and subsequent imaging obtained during her hospitalization did not show reaccumulation of her unilateral pleural effusion. DISCUSSION Pleuroperitoneal communication may occur due to congenital or acquired diaphagmatic defects, or insults such as the case in our patient with recent peritonitis. In fact, diaphragmatic blebs from age related degeneration and chronic increased intraabdominal pressure have been reported to cause hydrothorax in patients undergoing PD. Diagnosis of PD-associated pleural effusions is based on clinical suspicion, with pleural studies showing high pleural fluid to serum glucose gradient, and imaging commonly showing unilateral right-sided pleural effusions. Recent peritoneal dialysis with low drainage further supports PD as the etiology. Most cases of PD-associated pleural effusions occur soon after PD initiation, but cases occurring years after initiation have been reported. Management involves halting PD and thoracentesis for symptomatic relief. Patients may need transitioning to iHD indefinitely, or may resume PD after a pause if the cause of communication is reversible.