A 9-year-old Indonesian boy on CAPD was admitted to the emergency unit of our center due to dyspnea, swelling, and increased body weight. There was no fever, cough, or chest pain. Two years previously, he was diagnosed with end-stage renal disease (ESRD) secondary to bilateral renal hypoplasia; since then, he had been receiving CAPD comprising five cycles of 1-L exchanges with 1.5% dextrose-based solution for 22 months. Furthermore, he had no medical history of heart disease, peritonitis, hernia, thoracic and abdominal trauma, pneumonia, or thoracic and abdominal surgery, except for Tenckhoff catheter insertion. During the previous 3 days, his body weight had increased by 4 kg (12%), and he experienced ultrafiltration failure because although PD fluid at 1 L per cycle was being infused as usual, the effluent drainage was only approximately 0.6 L per cycle.\nPhysical examination revealed a respiratory rate of 34 breaths/min, heart rate of 120 beats/min, and blood pressure of 147/86 mm Hg. Oxygen saturation was 92% with nasal oxygen at 2 L/min. Auscultation of the lungs revealed diminished vesicular sounds in the right chest wall. Cardiac findings were normal. Arterial blood gas analysis results were as follows: pH: 7.467, pCO2: 4.51 kPa, pO2: 22.52 kPa, bicarbonate: 24.8 mmol/L, and base deficit: 2 mmol/L. His hemoglobin level was 131 g/L, albumin level was 34.6 g/L, BUN level was 7.08 mmol/L, and creatinine level was 840.33 µmol/L. Chest radiograph revealed right pleural effusion and bilateral pulmonary infiltrates (Fig. ). The chest tube drained 500 mL of transudative fluid. A comparison of serum, pleural fluid, and peritoneal fluid parameters has been presented in Table .\nAfter the excessive pleural fluid was completely removed, PD was continued via an installed chest tube (Fig. ). Intravenous cefotaxime was administered to treat pneumonia that occurred as an additional complication. Recurrent pleural effusion was subsequently found along with ultrafiltration failure. Pleural fluid culture did not show any microbial growth. Hydrothorax secondary to PPF was suspected, and PD was suspended from the 8th day of hospitalization. Hemodialysis (HD) was subsequently initiated.\nCT peritoneography was performed on the 9th day using 300 mg/mL of iohexol contrast agent immersed in PD fluid. Serial examinations at 30 and 180 min after administering the contrast agent showed excessive fluid in the right pleural cavity (Fig. ). PPF in the right posterolateral side was suspected.\nThe patient underwent VATS on the 20th day of hospitalization; however, no fistula was detected in the right chest cavity. Instead, adhesions between the parietal and visceral pleura with septated appearance were observed (Fig. ). Pleurodesis was performed using 20 mL of bleomycin for the right diaphragm. Following this, pleural effusion of the right lung resolved (Fig. ), and the patient underwent regular HD for 10 weeks. Subsequently, PD was gradually initiated until achieving 1 L of 1.5% dextrose-based dialysate solution with five daily exchanges. A 3-year follow-up showed normal PD without any recurrence of hydrothorax (Fig. ).
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.