Case Presentation: A 50-year-old woman with history of ESRD on PD, CHF, and recent invasive pulmonary aspergillosis on posaconazole presents with three days of gradually progressive shortness of breath and right-sided chest pain. The chest pain was associated with coughing and deep breathing, but non-exertional with no hemoptysis. The patient lived with her sister and denied recent travel, alcohol abuse, or recent toxic ingestion. Notably, she was admitted 4 months prior with similar chest pain and found to have a cavitary lung mass, positive for aspergillosis. She followed in ID clinic and was expected to be on posaconazole for a twelve month course.On admission, vital signs were notable for reduced oxygen saturation (83%) which improved to 96% on 5 L of O2, absent breath sounds on the right side, and mild tenderness surrounding the PD site. Laboratory studies were remarkable for poor kidney function (Cr 11.1 mg/dl, baseline 12), elevated BNP 4,922 pg/ml, (baseline 4,000), and mild leukocytosis 12.3 K/uL. Imaging included CT CAP which showed resolved LUL cavitary lesions, worsening R sided pleural effusion with complete opacification of R lung (Figure 1). The working diagnosis included complication of PD (recently started few months PTA), transudative effusion from CHF, or infection, though patient did not appear toxic. Patient was treated with therapeutic and diagnostic thoracentesis which resolved symptoms. Pleural fluid analysis showed evidence of transudative effusion.Chest X-Ray (Figure 1) after thoracentesis showed decreased right pleural effusion with improved aeration of the right lung. Patient endorsed resolved symptoms and O2 saturation improved to the 90s on RA. On the evening of hospital day 2, decision was made to restart PD. Renal service had elected to hold PD until after her presenting symptoms had resolved. On hospital day 3, patient endorsed return of initial presenting symptoms and need for O2 requirement. Repeat Chest X-Ray (Figure 1) showed interval re-accumulation of the right pleural effusion, and Nuclear Medicine study (Figure 2) confirmed pleuroperitoneal shunt (Figure 2). Unifying diagnosis of hydrothorax due to pleuroperitoneal leak as a complication of PD was made. Patient was discharged home with central line placed for hemodialysis and followed by renal clinic.
Discussion: Hydrothorax in the setting of PD is a rare, yet documented complication in the literature occurring in about 1.6 to 10 percent (1-3) of patients. This diagnosis should be considered in patients that present with nontoxic dyspnea and/or chest pain with recent transition to PD (within 1 year). Its etiology is unclear, yet linked to congenital or environmental causes, specifically the increases in intraabdominal pressure associated with PD dialysate. If not recognized early, patients can be subject to metabolic complications of inadequate PD as well as clinical sequelae of worsening pleural effusion. First-line treatment involves immediate cessation of PD, and acute thoracentesis is used sparingly for symptom resolution. While our patient had other comorbidities that may have also presented with pleural effusion, her lack of significant vital signs and lab findings suggested a noninfectious, non-cardiac etiology.
Conclusions: Hydrothorax in the setting of PD should be considered with the appropriate clinical picture; if on the differential, perhaps waiting to restart peritoneal dialysis until after confirmation with further imaging is in the patient’s and management team’s best interest.
