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 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.