A 33-year-old Caucasian woman with end-stage renal failure secondary to systemic lupus erythematosus started PD in December 2008. She had previously been treated with PD without complication 17 years before, in the context of acute kidney injury, from which she recovered. Exact details of PD were unavailable, but it was recalled to be of short duration and probably of small fill volume. The patient denied any history of traumatic injury to the chest or diaphragmatic surgery.\nA Tenckhoff catheter was inserted 28 days before commencement of PD without complication. Her first exchange revealed asymptomatic slightly cloudy dialysate with 210 white cells [82% polymorphonuclear cells] and negative growth and was treated as culture-negative PD peritonitis.\nOne week later, she presented with sudden onset of dyspnea associated with right pleuritic chest pain. Chest X-ray (Figure ) showed right pleural effusion.\nThoracentesis was performed for symptomatic relief. Pleural fluid biochemistry results were consistent with transudate, according to Light's criteria (Table ). Culture of pleural aspirate showed no evidence of infection. Clinically, no evidence of lupus flare or nephrotic syndrome was noted.\nPleural fluid biochemistry results were consistent with PD-related hydrothorax. An effusion reaccumulated with further PD treatment. It was unclear whether poor dialysis (uremia) or ultrafiltration was contributing to the effusion. Tc-99 m DTPA scintigraphy was performed to confirm pleuroperitoneal leakage, showing prompt (within 15 minutes) appearance of tracer in the pleural space on the right side with no evidence of tracer entering the left hemithorax (Figure ). Thus, the etiology of hydrothorax likely was due to congenital diaphragmatic defects, exacerbated by persistently elevated intraabdominal pressure from PD.\nThe patient was temporarily transferred to hemodialysis via a tunneled line and underwent right video-assisted thoracoscopic surgery and talc pleurodesis. An intraoperative methylene blue test failed to identify the pleuroperitoneal defect. Two months after the procedure, she successfully recommenced PD without reoccurrence of hydrothorax.
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. ).