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.
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.