An 80-year-old gentleman on treatment with PD was admitted with increasing dyspnea and progressive reduction in ultrafiltration volumes over the previous week. His end-stage kidney disease was secondary to hypertension; he had also previously had a left nephrectomy for cancer. His comorbidities included systemic hypertension, stroke, glaucoma, prostatic hypertrophy, and osteoarthritis. He had started PD 3 months prior to admission. During the previous 2 weeks, he had switched from CAPD with daytime exchanges to nocturnal cycler-assisted automated peritoneal dialysis (APD).\nOn initial assessment, he was tachypneic and hypoxic. The jugular venous pressure was elevated; there was also peripheral edema. On auscultation, he had reduced breath sounds over the right lower hemithorax, with dullness on percussion. His electrocardiogram (ECG) and initial blood tests were unremarkable. The chest X-ray showed a large right pleural effusion ().\nTherapeutic thoracentesis was performed. 3 litres of fluid were drained; his clinical status improved markedly. A repeat chest X-ray showed complete resolution of pleural effusion ().\nBiochemical analysis of pleural fluid showed high concentrations of sugar and creatinine, and negligible protein, consistent with peritoneal dialysate fluid ().\nTreatment was changed temporarily to hemodialysis via a tunneled central venous catheter. He underwent video-assisted thoracoscopic surgery and talc pleurodesis, which he tolerated well. At the time of the procedure, most pleural fluids had been drained. There was no fresh drainage of fluid into the pleural space. Some pleural thickening was described.\n4 weeks later, PD was recommenced, in CAPD mode, with small fill volumes and avoidance of nightly dwells. He subsequently tolerated CAPD without complications and was recommenced on APD. Hemodialysis was successfully discontinued.
A 25-year-old female patient on longstanding continuous ambulatory peritoneal dialysis (CAPD), due to end stage renal disease (ESRD) complicating lupus nephritis, presented with respiratory distress following dialysate infusions. Repeated chest X-rays showed recurrent large right pleural effusions (), requiring repeated therapeutic taps.\nAs a result of her shortness of breath, a clinical diagnosis of pulmonary embolus (PE) was considered. Computed tomography pulmonary angiogram (CTPA) was performed and excluded pulmonary embolus. The CTPA confirmed large right pleural effusion with some underlying consolidation () and small left pleural and large pericardial effusion (). Although the right pleural effusion was large and out of keeping with a systemic cause, the presence of the pericardial effusion and very small left pleural effusion suggested the diagnosis of fluid overload.\nHowever, the patient did not improve with clinical management for fluid overload and at that stage, the possibility of communication between the peritoneal and pleural cavity was considered. Peritoneal scintigraphy was performed using 3mCi Technetium Tc-99m Macroaggregated Albumin (Tc-99m MAA) injected into the abdominal dialysate port. The scan demonstrated a progressive increase in activity in the right lung, confirming the diagnosis of pleuroperitoneal leak (). Peak activity values were measured to quantify the leak, which would be beneficial in treatment decision making as well as in monitoring her progress. Our patient was managed conservatively by changing to biweekly haemodialysis and monitoring her progress closely.