Demonstrates the impact of pleural effusion diagnosis in patients on peritoneal dialysis, suggesting timely interventions are crucial.
Introduction Pleural effusion is a rare but recognized complication of peritoneal dialysis (PD), occurring in fewer than 5% of patients due to pleuroperitoneal communication, where dialysate leaks into the pleural space. This type of hydrothorax is typically transudative and characterized by high glucose levels from hypertonic dialysate. Risk factors include congenital diaphragmatic defects, increased intra-abdominal pressure, and recent abdominal surgery. We present a case of pleural effusion secondary to peritoneal dialysate leakage following diaphragmatic surgery. Case Presentation A 65-year-old male with ESRD on daily PD for one year, and a history of CAD post-CABG, bioprosthetic mitral valve replacement, and atrial fibrillation with LAA clip, underwent left diaphragm plication one month prior for hemi diaphragmatic paralysis. He presented to emergency department with acute dyspnea and left-sided chest pain. Chest X-ray revealed findings consistent with a moderate-sized left pleural effusion. Chest CT confirmed a moderate left pleural effusion with associated compressive atelectasis of the lower lobe. Thoracentesis drained 1400 ml of clear fluid with pH 7.8, WBC 99/μL (74.8% mononuclear), glucose 246 mg/dL (serum 130 mg/dL), protein 0.4 g/dL (serum 7.4 g/dL), and LDH 52 IU/L (serum 564 IU/L). No organisms or malignant cells were identified. The effusion was transudate based on light’s criteria, and the markedly elevated pleural glucose strongly suggested dialysate leakage. Imaging confirmation was declined by the patient. PD was discontinued, the catheter removed, and he was transitioned to hemodialysis (HD). The effusion resolved within four weeks without recurrence. Discussion PD-related hydrothorax is usually right-sided (90%), but left-sided effusions may occur post-surgical disruption of the diaphragm. The 2022 ISPD guidelines support a presumptive diagnosis based on dyspnea, transudative effusion, and pleural glucose >50 mg/dL above serum. In this case, pleural glucose exceeded serum by > 100 mg/dL, with alkaline pH and low protein/LDH, confirming the diagnosis. Imaging (Tc-99m scintigraphy, CT peritoneography, or methylene blue instillation) is confirmatory but not always necessary. First-line management is PD cessation and switching to HD for 2-6 weeks; over half resolve without recurrence. Surgery (VATS with pleurodesis or suture) is reserved for refractory cases. Conservative approach was curative in our patient. Conclusion Pleural effusion due to PD should be suspected in patients presenting with dyspnea and transudative, high-glucose pleural fluid. Per ISPD guidelines, clinical-biochemical diagnosis is sufficient, and switching to HD is the preferred initial treatment. Early recognition and timely intervention are key to preventing complications. This abstract is funded by: none
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