Among patients receiving CAPD, the incidence of PPC is 1.6%, and about 50% of these patients are compelled to terminate CAPD and turn into hemodialysis due to secondary hydrothorax[1, 2]. Hydrothorax occurs prevalently in women and on the right side[3], similar to our study. The nosogenesis of hydrothorax is still not clear. Possible mechanisms include drainage disorder of diaphragmatic lymphatics, thoracic duct, congenital or acquired diaphragmatic defects or blebs, and pleuro-peritoneal pressure gradient[4]. Patients commonly present dyspnoea and cough, but some of them can be asymptomatic[1]. Also there is a continuous reduction in ultrafiltration in these patients. In the present study, all twelve patients had reduction of ultrafiltration volume and eleven patients occurred shortness of breath, and seven patients developed cough at the same time.
Based on the close relationship between pleural effusion, clinical presentations and implementation of CAPD, the diagnosis is usually not difficult. The commonly preoperative diagnostic methods include: biochemical analysis of pleural effusion, the methylene blue dye test, isotopic scanning and contrast computerized tomography (CT) peritoneography and so on[5, 6]. A high glucose concentration in the pleural effusion, which is similar to the level in the dialysis solution, indicates the diagnosis of PPC complicating CAPD[7]. Chow et al. found that there was 100% sensitivity and specificity for differentiating hydrothorax caused by pleuroperitoneal communication from other reasons when the difference between the concentration of glucose in pleural effusion and that in serum exceeded 50 mg/dl[2]. Also Momenin et al. showed that there was a low pleural fluid-to-serum glucose gradient in the diagnosis of PPC complicating CAPD[8]. In our study, we used a high glucose concentration in the pleural effusion as a diagnostic marker. And all patients existed a high pleural effusion glucose level and the pleural fluid-to-serum glucose concentration difference exceeded 50 mg/dl. Some studies reported that the methylene blue test was negative in the tested patients[4, 5], and could cause abdominal pain and even chemical peritonitis[9]. In the present study, the methylene blue test was positive among these tested cases and there was no evident discomfort in them. CT peritoneography is not sensitive in detecting PPC and is expensive for patients[10]. Tang et al. reported that only one patient was positive in three patients undergoing CT peritoneography[4]. And CT peritoneography was negative in the tested subject in our study. The reason may be that the high intrapleural pressure produced by massive pleural effusion impedes tracer migration.
There are many varying therapeutic methods like: conservative approach (temporary discontinuation of CAPD, temporary change to hemodialysis, reduction of the CAPD exchange volume, repeated thoracocentesis)[2], pleurodesis (mechanical rub pleurodesis[11] and chemical pleurodesis adopting talc[12], tetracycline[13], fibrin glue[14], OK-432[13], autologous blood[15] et al), and surgery[4, 5, 7] according to reports until now. No matter what kind of therapeutic method was adopted, the required pleural adhesion could not always be firmly formed, leading to the recurrence of hydrothorax[3]. There is still no consensus on the choice of the standard method of management. In our study, we chose to perform video-assisted thoracoscopic direct closure of the defective diaphragm and mechanical rub pleurodesis, and pseudomonas aeruginosa injection was infused into the thoracic cavity postoperatively to further promote pleural adhesion in all patients.
Video-assisted thoracoscopic surgery can well display the entire parietal pleura and diaphragm surface with minimal incisions, and realize diaphragmatic defects diagnosis. Direct visualization, infusion of colored dialysate into the peritoneal and cavity check-air-leakage method under the thoracoscopy can be used to detect diaphragmatic lesions including small defects, bleblike lesions, and thin walls, making a definite diagnosis of PPC[14, 16]. Not all cases can find obvious defects, perhaps because these defects are too small to be found[17]. In our study, we discovered bleblike lesions in all patients with direct inspection and obvious holes in two patients through check-air-leakage method under the thoracoscopy. Currently, thoracoscopic surgery includes diaphragm repair[18], mechanical rub pleurodesis and chemical pleurodesis[4], with different degrees of effect. Most studies only used one or two of these methods. However, in our study, we chose all of them. Video-assisted thoracoscopic direct closure of the defective diaphragm and mechanical rub pleurodesis was performed in all patients, and pseudomonas aeruginosa injection was infused into the thoracic cavity postoperatively to further promote pleural adhesion. It was these triple means that ensured the success rate and finally achieved 100% success rate. There were no complications related to surgery, and no recurrence of hydrothorax and transformation to hemodialysis during the follow-up period (mean: 9.0 months). Chemical pleurodesis using pseudomonas aeruginosa injection was a novel method, which was firstly reported in our study. It was the innovation of our study. In patients infusing pseudomonas aeruginosa injection, only three cases occurred fever with remission after 2–3 days of symptomatic treatment, and there was no evident discomfort in the rest patients. The reaction to pseudomonas aeruginosa injection was mild and manageable.
In conclusion, direct closure of the defective diaphragm and mechanical rub pleurodesis under the thoracoscopy plus chemical pleurodesis using pseudomonas aeruginosa injection postoperatively is a safe and effective option for the treatment of pleuroperitoneal communication complicating continuous ambulatory peritoneal dialysis with 100% success rate. However, the effectiveness of our findings requires more larger randomized controlled trials to confirm because of the small sample size.