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 twenty-four-year-old Irish male with a background history of congenital deafness, intellectual impairment and repair of a posterior urethral valve initially presented to the paediatric nephrology services with nephrotic syndrome. A renal biopsy revealed secondary focal segmental glomerulosclerosis and significant tubuleinterstitial fibrosis. Following introduction of Renin-Angiotensin-Aldosterone system blockade, his proteinuria was controlled.\nDespite this, his chronic kidney disease progressed. Ten years later, he was approaching end-stage kidney disease. A Tenckhoff catheter was inserted without complication. Six weeks later, PD training was initiated. A bicarbonate/lactate buffered solution was used to avoid infusion pain, which he would be unable to verbalise. The following months were complicated by dialysis-associated pericarditis that resolved with intensive haemodialysis for a number of weeks. His baseline PD prescription consisted of seven cycles of two litre exchanges with 1.36% dextrose solution. He was also prescribed an icodextrin-based daytime dwell.\nFive months later, he was admitted with clinical and radiological evidence of a large, rightsided pleural effusion with pleural thickening. The exact duration of the effusion was unclear as he was unable to verbalise symptoms. It was thought to have developed over weeks given the apparent absence of symptoms and the degree of pleural thickening. A chest radiograph four months earlier showed normal lung fields.\nHe was afebrile and systemically well. His serum biochemistry and haematology were unchanged and his inflammatory markers were not raised. ECG and echo were normal. A diagnostic pleural aspirate was performed under ultrasound guidance. This yielded serous fluid and also identified numerous loculations within the collection.\nThe pleural fluid biochemistry was atypical for that seen with pleuroperitoneal leak (). However, as the patient was so well clinically, and numerous pleural fluid cultures were sterile, it was felt that the effusion was not related to infection. It was also felt that the effusion was not due to volume overload given the degree of loculation within the effusion and the absence of other clinical signs of volume overload. The low pleural fluid glucose and high lactate dehydrogenase (LDH) were difficult to interpret as the sampled fluid was walled off within a loculation, probably for many weeks. A clinical diagnosis of pleuroperitoneal leak was made and PD was discontinued.\nThe effusion did not resolve with drainage of the peritoneal cavity, and a chest drain was inserted. This drained minimal serous fluid due to the highly loculated nature of the effusion. A second drain was inserted and intrapleural alteplase administered. This drain became dislodged and was replaced by a third drain with further intrapleural alteplase administration. At this point, however, a chest radiograph confirmed persistence of the large, loculated effusion with a small pneumothorax and a thick pleural rind.\nVideo-assisted thorascopic surgery with decortication was performed. A rapid postoperative recovery ensued and the postoperative chest drains were removed without event. A chest radiograph six weeks later showed a well-expanded right lung, without effusion or pleural abnormality. HD is ongoing without complication.