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Modalities of diagnosis and management of peritoneal dialysis-related hydrothorax including videothoracoscopy-assisted repair: A single-center experience


1 Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of General Surgery, King George Medical University, Lucknow, Uttar Pradesh, India

Date of Submission05-Apr-2020
Date of Acceptance02-Jul-2020
Date of Web Publication13-Nov-2021

Correspondence Address:
Narayan Prasad,
Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Raebareli Road, Lucknow - 226 014, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijn.IJN_101_20

  Abstract 


Continuous ambulatory peritoneal dialysis (PD)-related hydrothorax (PDRH) is uncommon; however, it is associated with a high discontinuation rate and morbidity. We report clinical characteristics, pleural fluid chemistry patterns, diagnostic modality, management options, and outcomes in 12 patients who have confirmed pleuroperitoneal communication after the inception of the PD program at our institute. The incidence of PDRH in our study was 0.64%. The interval between initiation of PD and hydrothorax ranged from 7 weeks to 40 weeks (average 20.6 weeks). Ten (83.3%) had right-sided, one (8.3%) left-sided, and one (8.3%) bilateral hydrothorax. Most patients (83.3%) had dyspnea with chest symptoms, but two (16.6%) patients were asymptomatic. All patients had confirmed communication either by peritoneal scintigraphy or computed topography peritoneography. PD had to be stopped in two patients and patients were shifted back to hemodialysis. Pleurodesis, through thoracostomy with tetracycline or betadine, was used for four patients. Three patients underwent video-assisted thoracoscopy (VATS) with surgical repair of the diaphragmatic defect, and one underwent VATS assisted talc pleurodesis. All four patients who underwent VATS repair of the defect had successful outcomes. With availability and experience with VATS, most patients had successfully returned to PD with no recurrence and with minimal morbidity.

Keywords: Hydrothorax, peritoneal dialysis, videothoracoscopy



How to cite this URL:
Prasad N, Patel MR, Kushwaha R, Behera MR, Yachcha M, Kaul A, Bhadauria D, Kumar S, Gupta A. Modalities of diagnosis and management of peritoneal dialysis-related hydrothorax including videothoracoscopy-assisted repair: A single-center experience. Indian J Nephrol [Epub ahead of print] [cited 2021 Nov 28]. Available from: https://www.indianjnephrol.org/preprintarticle.asp?id=330349


  Introduction Top


Continuous ambulatory peritoneal dialysis (PD) is an effective and established renal replacement modality for patients with end-stage renal disease (ESRD). Out of various noninfectious complications, CAPD-related hydrothorax (PDRH) is an uncommon event. It occurs due to pleuroperitoneal communication. Though incidence is about 1.6–10% (1, 2), it is associated with a high discontinuation rate of PD and morbidity. Diagnosis is easy; however, it requires a high index of suspicion, particularly in a patient with progressive dyspnea with low ultrafiltration. The condition should be readily differentiated from other causes of pleural effusion, such as congestive cardiac failure, hypoalbuminemia, or fluid overload state, all being a common clinical association in ESRD patients on PD. Herewith, we report a case series of 12 patients with PDRH treated with various treatment modalities, including video-assisted thoracic repair.

We reviewed our hospital CAPD database of patients who have been started on PD from 1998 to 2018. Of the total of 1876 patients, a total of 12 cases (0.64%) had confirmed pleuroperitoneal communication. The clinical data, initial diagnosis, pleural fluid analysis and blood investigations, diagnostic modality, management, and outcomes were analyzed for all patients.


  Cases details Top


Of the 12 cases [Table 1] during the study period, 9 (75%) were males, and 3 (25%) were females, with a median age of 53.5 years (33-75 years). Among causes of ESRD, six (50%) had diabetic nephropathy, two (16.6%) chronic glomerulonephritis, two (16.6%) chronic interstitial nephritis, and one (8.3%) had acute cortical necrosis. The most common clinical presentations were gradually increasing shortness of breath in ten (83.3%), chest pain or discomfort in eight (66.6%), and inadequate ultrafiltration in four (33.3%) patients. In two (16.6%) cases, pleural effusion was detected incidentally on routine chest radiography performed for mild cough. One patient had associated consolidation of lungs and empyema thoracis. The interval between initiation of PD and hydrothorax ranged from 7 weeks to 50 weeks (average 20.6 weeks, in 6 patients; after 20 weeks). Ten (83.3%) had right-sided, one (8.3%) had left-sided, and one (8.3%) had bilateral hydrothorax. Most patients with pleuroperitoneal communication had new-onset pleural effusions by chest radiography after 4 months of the start of PD. In four patients, pleural effusion developed within 2 months, whereas three patients had effusion detected after 10 months of initiation.
Table 1: Clinical characteristics of patients

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Pleural fluid characteristics

The pleural fluid characteristics have been shown in [Table 2]. All patients underwent diagnostic pleurocentesis, and seven (58.3%) patients required therapeutic removal of 1.2 to 2.5 liters of fluid. In 11 (91.6%) cases, fluid was characterized as transudative according to one or more of Lights criteria. In one patient, effusion was categorized as exudative with culture positive for Staphylococcus aureus and empyema requiring multiple paracenteses with tube thoracostomy and prolonged course of intravenous antibiotics. Eight (66.6%) patients had pleural fluid to serum glucose gradient of more than 100 mg/dl, whereas only one had a value of less than 50 mg/dl, and four (33.3%) patients had a value between 50 and 100 mg/dl. Pleural fluid to serum glucose ratio was more than 1 in all (100%) cases. Total cell counts were within 5 to 100 per HPF except for one instance of empyema where counts were higher. Most of the pleural fluid but for one sample was lymphocyte-predominant and culture-negative for bacteria, fungus, and mycobacterium. In two patients initially, empiric antitubercular therapy was started by a local physician, which was stopped after confirmation of peritoneal dialysis-related effusion.
Table 2: Pleural fluid analysis showing glucose, protein, and cell counts

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Imaging and treatment modality

The summary of diagnostic and treatment modalities is shown in [Table 3]. Nuclear scintigraphy was performed in nine (75%) cases, computed tomography (CT) peritoneography in five (41.6%) (representative [Figure 1]), and both nuclear and CT peritoneography in two (16.6%) to confirm the diagnosis of pleuroperitoneal communication. In order to repair the leak, four of them underwent VATS. Two of the patients with PDRH (16.6%) stopped PD, and Tenckhoff catheter was removed as they were not willing to continue PD and shifted back to hemodialysis. Seven (58.3%) patients underwent therapeutic thoracentesis, followed by pleurodesis in five (41.6%) patients with tetracycline in four and betadine in one patient. One patient had a recurrence of pleural effusion on the left side after successful pleurodesis of the right side within 7 days, for which repeat pleurodesis was done on the left side after 2 weeks. Four patients underwent VATS with suturing of the diaphragmatic defect (representative [Figure 2]), and one had VATS assisted talc pleurodesis as well. In all ten cases, willing to continue, PD was successfully restarted after 3-5 weeks of the break-in period after the procedure. All four (100%) patients who underwent VATS repair of the defect had successful outcomes, three of patients still on peritoneal dialysis without recurrence of effusion, and one patient continued for 28 months till she got a renal allograft transplant. None of our patients had undergone open thoracotomy.
Table 3: Summary of diagnosis, management, and outcomes of PD

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Figure 1: (a) Cross-section image of CT peritoneography showing the leak point on the diaphragm (black arrow); (b) coronal section image showing defect on the dome of diaphragm; and (c) hydrothorax on the left side

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Figure 2: (a) Showing the procedure of video-assisted thoracoscopic ports and method; (b) identifying opening at diaphragm; (c) process of taking the suture around the opening defect; and (d) finally closure suture of the defect

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  Discussion Top


Although PDRH is not life-threatening, however, it is associated with morbidity, hospitalization, and a high probability of discontinuation (50%). The incidence of PDRH varies between 1.6 and 10%[1],[2] in adults, and about 3% in a pediatric series.[3] Our center observed an incidence of 0.64%, which is lower than reported in other studies. In our case series, of the 12 patients, only two patients were shifted to HD as they were not willing to continue PD and showed an unwillingness to be investigated and repair of the defect.

Like other studies, the most common clinical presentations were shortness of breath and chest discomfort with reduced UF. However, the clinical presentation may be asymptomatic in about 25% of cases and detected incidentally by routine chest radiography.[1] It manifests as right-sided hydrothorax in 88% within the first few months.[1] Left-sided and bilateral hydrothorax are uncommon. PDRH results due to the migration of dialysis fluid from the peritoneal cavity under positive pressure into the pleural space, which has negative pressure.[4] Increased intraabdominal pressure (IAP) arises either transiently or permanently due to PD solution, which increases further during coughing and straining. IAP reaches 120 – 150 cm H2O with coughing or straining versus 0.5–2.2 cm H2O in controls and 2–10 cm H2O in patients with PD fluid in the peritoneal cavity. Patients with ADPKD have a higher incidence of hydrothorax, possibly due to higher IAP.[5] The exact mechanism by which peritoneal dialysate crosses the diaphragm is not known, possibly due to a pleuroperitoneal communication (congenital or acquired) and/or by lymphatic transport along the aorta or thoracic duct.[6],[7] Congenital defects (i.e., pneumatoenteric recess, infracardiac bursa) explain the preponderance of right-sided hydrothorax because left-sided defects are covered by the heart and pericardium, thereby reducing the possibility of a leak on the left side. In addition, abnormalities in subpleural lymphatic structures predominate in the right hemidiaphragm.[6],[7]

Effusion is usually transudative in nature if not secondarily infected. The condition should be differentiated from other causes of transudative pleural effusion commonly present in the CKD population, such as congestive cardiac failure, hypoalbuminemia of nephrotic state, or cirrhosis of the liver and fluid overload state. Failure to recognize a pleuroperitoneal communication associated with hydrothorax may lead to the inadvertent prescription of hypertonic dialysis fluid exchanges, which may further increase intraperitoneal pressure and aggravate the hydrothorax. It may also unnecessarily lead to the prescription of diuretics or antibiotics, sometimes antitubercular drugs.

However, pleurocentesis, which is easy and inexpensive, is often done for diagnostic purposes or sometimes therapeutically for symptomatic relief. Biochemical and microbiological analysis of pleural fluid is essential to ascertain the transudative nature of effusion and to exclude exudative causes, such as bacterial infections, tuberculosis, and malignancy. Effusion has a low cell, and protein content and Light's criteria for transudative effusion usually holds true in 90% of cases.[8],[9] Although glucose level in pleural fluid is similar to PD fluid and is much higher than serum value, there is no consensus on precise cut off values that can differentiate PDRH from other causes. Pleural fluid glucose may vary with the size of the defect, PD fluid glucose, and reabsorption of glucose by visceral pleura and lymphatics. The PF-S glucose gradient of 50–100 mg/dl is highly suggestive, and a gradient of >100 mg/dl is almost diagnostic PDRH. A PF-S glucose gradient of less than 50 mg/dl may be present in 20% of PDRH. Alternatively, pleural fluid to serum (PF/S) glucose ratio of >1 is more consistent and sensitive for PDRH, whereas the ratio is <1 in other causes of transudative effusion and is <0.5 in exudative effusions. To improve the accuracy of PF-S glucose gradient and PF/S glucose ratio, it is suggested that a pleural tap should be done using a 4.25% dextrose solution within 1 hour of exchange with the patient remaining supine after the exchange.[8],[9]

Confirmation and localization of pleuroperitoneal communication can be done by various modalities. Discoloration of the dialysate with diluted dyes (methylene blue or indocyanine green) followed by thoracocentesis had been abandoned due to the high incidence of chemical peritonitis.[10] Similarly, the detection of icodextrin in the pleural fluid after using it as PD fluid is a simple method to confirms the diagnosis. Peritoneal scintigraphy using Tc-99m macro aggregated albumin or sulfur colloid and detecting movement of the isotope above the hemidiaphragm on the side of the defect was used in the center with nuclear medicine facility.[11],[12],[13] CT peritoneography with intraperitoneal iodinated contrast has become the diagnostic modality of choice for PDRH. Besides, being sensitive, it can often localize the site of the leak. Magnetic resonance imaging with or without contrast has also been used to diagnose leaks.

Conservative management options include shifting the patient to hemodialysis either permanently or temporarily.[14] This alone may be sufficient in 53% of cases.[15] A large pleural effusion may require therapeutic thoracentesis for symptomatic relief.[16],[17] Early leaks with minor defects may heal spontaneously by withholding PD for 4–6 weeks.[18] Conventional pleurodesis or sclerotherapy is performed under local anesthesia through a thoracostomy tube using sclerosing agents.[19] Talc, tetracycline, betadine, fibrin glue, autologous blood all have been used as sclerosant with varying degrees of success. Once the pleural cavity is drained, sclerosant with 1% lignocaine diluted in 50–70 ml of normal saline is administered through a tube, and the patient is positioned lying left, supine, and then to the right for 15 min each then patient is kept flat for 24 hrs. Pain control is usually achieved by both local and systemic analgesics, including opioids. PD is restarted after 2–4 weeks after pleurodesis. The procedure is associated with about 48% success rate in a study.[19],[20]

Open thoracotomy with the repair of the diaphragmatic defect is the most definitive procedure with high success rates (100%) even for larger defects.[14],[15] Usually, this procedure is invasive and associated with high postoperative morbidity in ESRD patients; hence is no longer preferred and used only in exceptional cases.

The VATS-assisted repair has become the procedure of choice as it is both diagnostic and therapeutic and is associated with minimal morbidity.[21],[22],[23] We have successfully performed VATS repair in the last four patients in our series. It permits direct visual identification and repair of diaphragmatic defects. Repair methods can include surgical stapling or suturing, use of a proline mesh or a Teflon patch, use of fibrin glue, or pleurodesis with a sclerosing agent. Intraoperative evaluation for air or fluid leakage assures closure of a pleuroperitoneal communication.[24],[25] VATS allows even distribution of sclerosant like talc (or tetracycline or fibrin glue) between pleura and hence better success rates (80-100%) and less pain compared to conventional pleurodesis. Of the four patients with VATS, one had VATS-assisted sclerotherapy in our series PD usually can be started after 2–4 weeks after the procedure.[21],[26]


  Conclusion Top


Diagnosis of PDRH is easy but requires a high index of suspicion. The condition should be differentiated from other causes of pleural effusion. Management includes temporary withholding of PD for a few weeks, pleurodesis by tube thoracostomy, open thoracotomy, and VATS repair or assisted pleurodesis. With availability and experience with VATS, most patients have successfully returned to PD with no recurrence and with minimal morbidity hence should be considered the modality of choice if conservative management fails.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Nomoto Y, Suga T, Nakajima K, Sakai H, OsawaG, Ota K, et al. Acute hydrothorax in continuous ambulatory peritoneal dialysis—a collaborative study of 161 centers. Am J Nephrol 1989;9:363-7.  Back to cited text no. 1
    
2.
Van Dijk CM, Ledesma SG, Teitelbaum I. Patient characteristics associated with defects of the peritoneal cavity boundary. Perit Dial Int 2005;25:367-73.  Back to cited text no. 2
    
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Kawaguchi AL, Dunn JC, Fonkalsrud EW. Management of peritoneal dialysis-induced hydrothorax in children. Am Surg 1996;62:820-4.  Back to cited text no. 3
    
4.
Mahale AS, Katyal A, Khanna R. Complications of peritoneal dialysis related to increased intra-abdominal pressure. Adv Perit Dial 2003;19:130-5.  Back to cited text no. 4
    
5.
Fletcher S, Turney JH, Brownjohn AM. Increased incidence of hydrothorax complicating peritoneal dialysis in patients with adult polycystic kidney disease. Nephrol Dial Transplant 1994;9:832-3.  Back to cited text no. 5
    
6.
Hausmann MJ, Basok A, Vorobiov M, Rogachev B. Traumatic pleural leak in peritoneal dialysis. Nephrol Dial Transplant 2001;16:1526.  Back to cited text no. 6
    
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Bundy JT, Pontier PJ. Cough-induced hydrothorax in peritoneal dialysis. Perit Dial Int 1994;14:293.  Back to cited text no. 7
    
8.
Chow KM, Sz eto CC, Wong TY, Li PK. Hydrothorax complicating peritoneal dialysis: Diagnostic value of glucose concentration in pleural fluid aspirate. Perit Dial Int 2002;22:525-8.  Back to cited text no. 8
    
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Momenin N, Colletti PM, Kaptein EM. Low pleural fluid-to-serum glucose gradient indicates pleuroperitoneal communication in peritoneal dialysis patients: Presentation of two cases and a review of the literature. Nephrol Dial Transplant 2012;27:1212-9 .  Back to cited text no. 9
    
10.
Macia M, Gallego E, Garcia-Cobaleda I, Chahin J, Garcia J. Methylene blue as a cause of chemical peritonitis in a patient on peritoneal dialysis. Clin Nephrol 1995;43:136-7.  Back to cited text no. 10
    
11.
Rajnish A, Ahmad M, Kumar P. Peritoneal scintigraphy in the diagnosis of complications associated with continuous ambulatory peritoneal dialysis. Clin Nucl Med 2003;28:70-1.  Back to cited text no. 11
    
12.
Wu PS, L ee BF, C hiu NT, YaoWJ, Huang JJ, Wang MC. Peritoneal scintigraphy for the assessment of dialysate leakage in patients on continuous ambulatory peritoneal dialysis. Ann NuclMed Sci 2001;14:11-8.  Back to cited text no. 12
    
13.
Lepage S, Bisson G, Verreault J, Plante GE. Massive hydrothorax complicating peritoneal dialysis. Isotopic investigation (peritoneopleural scintigraphy). Clin Nucl Med 1993;18:498-501.  Back to cited text no. 13
    
14.
Green A, Logan M, Medawar W, McGrath F, Keeling F, Carmody M, et al. The management of hydrothorax in continuous ambulatory peritoneal dialysis. Perit Dial Int 1990;10:271-4.  Back to cited text no. 14
    
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Chow KM, Szeto CC, Li PK. Management options for hydrothorax complicating peritoneal dialysis. Semin Dial 2003;16:389-94.  Back to cited text no. 15
    
16.
Townsend R, Fragola JA. Hydrothorax in a patient receiving continuous ambulatory peritoneal dialysis: Successful treatment with intermittent peritoneal dialysis. Arch Intern Med 1982;142:1571-2.  Back to cited text no. 16
    
17.
Ing A, Rutland J, Kalowski S. Spontaneous resolution of hydrothorax in continuous ambulatory peritoneal dialysis. Nephron 1992;61:247-8.  Back to cited text no. 17
    
18.
Lew SQ. Hydrothorax: Pleural effusion associated with Peritoneal dialysis. Perit Dial Int 2010;30:13-8.  Back to cited text no. 18
    
19.
Moreno A, Suria S, Perez-Valentin MA, Toledo A, Esparza N, Garcia-Canton C, et al. Hydrothorax in peritoneal dialysis. Effective treatment with pleurodesis. Perit Dial Int 1998;18:657-8.  Back to cited text no. 19
    
20.
Benz RL, Schleifer CR. Hydrothorax in continuous ambulatory peritoneal dialysis: Successful treatment with intrapleural tetracycline and a review of literature. Am J Kidney Dis 1985;5:136-40.  Back to cited text no. 20
    
21.
Mak SK, Chan MW, Tai YP, Wong PN, Lee KF, Fung LH, et al. Thoracoscopic pleurodesis for massive hydrothorax complicating CAPD. Perit Dial Int 1991;16:421-5.  Back to cited text no. 21
    
22.
Mak SK, Nyunt K, Wong PN, Lo KY, Tong GM, Tai YP, et al. Long-term follow-up of thoracoscopic pleurodesis for hydrothorax complicating peritoneal dialysis. Ann Thorac Surg 2002;74:218-21.  Back to cited text no. 22
    
23.
Tang S, Chui WH, Tang AW, Li FK, Chau WS, Ho YW, et al. Video-assisted thoracoscopic talc pleurodesis is effective for maintenance of peritoneal dialysis in acute hydrothorax complicating peritoneal dialysis. Nephrol Dial Transplant 2003;18:804-8.  Back to cited text no. 23
    
24.
Tsunezuka Y, Hatakeyama S, Iwase T, Watanabe G. Videoassisted thoracoscopic treatment for pleuroperitoneal communication in peritoneal dialysis. Eur J Cardiothorac Surg 2001;20:205-7.  Back to cited text no. 24
    
25.
Halstead JC, Lim E, Ritchie AJ. Acute hydrothorax in CAPD. Early thoracoscopic (VATS) intervention allows a return to peritoneal dialysis. Nephron 2002;92:725-7.  Back to cited text no. 25
    
26.
Lang CL, Kao TW, Lee CM, Tsai CW, Wu MS. Video-assisted thoracoscopic surgery in continuous ambulatory peritoneal dialysis-related hydrothorax. Kidney Int 2008;74:136.  Back to cited text no. 26
    


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

 
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