Respiratory Medicine CME
Volume 2, Issue 4 , Pages 197-200, 2009

Peritoneal dialysis – An unusual cause of pleural effusion (“sweet hydrothorax”)

  • I. Krivokuca

      Affiliations

    • Department of Respiratory Medicine, Division of Heart & Lungs, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX, Utrecht, The Netherlands
    • Corresponding Author InformationCorresponding author.
    • ,
  • J.-W.J. Lammers

      Affiliations

    • Department of Respiratory Medicine, Division of Heart & Lungs, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX, Utrecht, The Netherlands
    • ,
  • J. Kluin

      Affiliations

    • Department of Cardiothoracic Surgery, Division of Heart & Lungs, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX, Utrecht, The Netherlands

Article Outline

Summary 

Peritoneal dialysis is a rare cause of pleural effusion. It appears, as a complication of continuous ambulatory peritoneal dialysis (CAPD), in approximately 2% of all CAPD patients.

We describe three patients with pleural effusions secondary to CAPD. Because of the late onset of pleural effusion and pulmonary symptoms, i.e. months after CAPD treatment was initiated, the pleural effusion was not directly regarded as a complication of CAPD.

After thoracocentesis with biochemical analysis of crystal clear pleural fluid and in two patients Tc-99 peritoneal scintigraphy/contrast enhanced CT-scanning, which demonstrated pleuroperitoneal communication, we concluded that pleural effusion was secondary to CAPD in these three subjects.

All patients were treated with hemodialysis after cessation of CAPD and because two of them wanted to continue with CAPD, video-assisted thoracoscopic surgery with talc poudrage (chemical pleurodesis) was performed in order to prevent recurrence.

Pleural effusions secondary to CAPD is not a frequent complication of CAPD though a very important one because CAPD must be stopped if it appears. Diagnostic thoracentesis (high glucose concentration) may be the simplest way to make a diagnosis but a contrast enhanced CT-scanning is essential for diagnosis of bigger diaphragmatic defects.

Keywords: Peritoneal dialysis, Hydrothorax, Talc poudrage

 

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Introduction 

The causes of pleural effusion are pulmonary or extrapulmonary diseases.1 The most common cause is congestive heart failure.1, 2 Pleural effusion is rarely caused by peritoneal dialysis. Approximately 2% of all CAPD patients develop massive transudative pleural effusion.3 CAPD-related pleural effusion was first described in 1967 and usually occurs on the right side 4 but sometimes on the left side or on both sides.1

Possible explanation for the right-sided predominance is, in case of congenital diaphragmatic defects, coverage of left-sided diaphragmatic defects by the heart and pericardium, which prevents fluid leakage.3 Not all diaphragmatic defects leading to pleuroperitoneal communications are congenital. Some of them are acquired, due to high intra-abdominal pressure.3

In 2003, Tang et al. described a series of CAPD patients with hydrothorax due to pleuroperitoneal communications. Hydrothorax developed in this group within 5.8 months (median, 5.2 months; range 2 days to 11.2 months) after the start of peritoneal dialysis.5 A hydrothorax did not develop directly after commencing peritoneal dialysis, probably because the formation of acquired pleuroperitoneal communications takes some time. These communications develop secondary to high intra-abdominal pressure due to exchanges of dialysate, which leads to separation of diaphragmal collagen fibres, pleural bleb formation and subsequent rupture of the bleb, resulting in the opening of the pleuroperitoneal communications.6

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Case reports 

Case A 

A 61-year-old man with a history of peritoneal dialysis four months earlier and CAPD peritonitis with uremic pericarditis, was admitted to our hospital because of dyspnea at exertion since one day before admission. He had no fever, cough, sputum production or chest pain. Physical examination revealed shortness of breath with a respiratory rate of 30breaths/min. His body temperature was 37.6°C, his blood pressure was 130/80mm Hg and the pulse rate was 100beats/min. Oxygen saturation was 96% with 3L of additional oxygen.

There was no jugular venous distension and there were no signs of congestive heart failure. Decreased breathsounds were heard on auscultation at the right side. Cardiac examination was normal. A chest X-ray demonstrated a massive right-sided pleural effusion (Fig. 1) Laboratory evaluation demonstrated pronounced renal dysfunction, a white-cell count of 6.3per cubic millimeter and a CRP value of 132mg/l. Arterial blood gas analysis revealed a pH of 7.45, PCO2 was 32mm Hg, PO2 was 59mm Hg, bicarbonate 21mmol/l, and a base deficit of −2.8mmol/l.

Diagnostic thoracentesis revealed crystal clear pleural fluid with a high glucose concentration of 14mmol/l. The pleural-fluid protein was <20g/L and according to Light's criteria the fluid appeared to be a transudate. Cytological and microbiological examination of the pleural fluid showed no abnormalities.

Therapeutic thoracentesis was performed and excess fluid was completely removed. Peritoneal dialysis was temporarily ceased and converted to hemodialysis. The investigation of choice, peritoneal scintigraphy, was performed and pleuroperitoneal communications were seen at the right side. Contrast enhanced CT-scanning did not show diaphragmatic hernias. Subsequently, video-assisted thoracoscopic surgery with talc poudrage was performed to prevent recurrence of the pleural fluid. Peritoneal dialysis was resumed a few weeks after the pleurodesis without recurrence of the pleural fluid.

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Case B 

A 52-year-old female CAPD patient was admitted to our hospital because of dyspnea at exertion and a vague chest pain. Her medical history revealed a polycystic kidney disease and secondary hyperparathyroidism. She was haemodynamically stable and not tachypnoeic, she was afebril and her percutaneous oxygen saturation during room air breathing was 93%. Breathsounds were decreased on auscultation at the right side. Her chest radiograph demonstrated a massive right-sided pleural effusion and basal atelectasis. Diagnostic thoracentesis revealed a transparent pleural fluid with a pleural-fluid glucose level of 6.4mmol/l. The pleural-fluid protein and LD levels were very low indicating the pleural fluid to be a transudate.

Because of the relatively low glucose level in the pleural fluid, peritoneal scintigraphy and contrast enhanced CT-scanning were performed and a pleuroperitoneal leak of peritoneal fluid was detected through a Morgagni's hernia (Fig. 2). Therapeutic thoracentesis was not performed but CAPD treatment was stopped and the patient was treated with hemodialysis for several weeks. The pleural effusion disappeared but directly after peritoneal dialysis was restarted, the pleural fluid recurred. Since conservative treatment failed a video-assisted thoracoscopic talc pleurodesis was performed. At the same time the diaphragmatic hernia was closed. Three months after this procedure hemodialysis was converted to peritoneal dialysis and after one month she had a recurrence of the pleural fluid at the right side. She refused a thoracotomy with pleurectomy and therefore she was again treated with hemodialysis.

  • View full-size image.
  • Figure 2 

    Contrast enhanced CT (A transversal, B coronal, C sagittal image) with intraperitoneal infused contrast-mixed dialysate. A diaphragmatic hernia of the Morgagni foramen was shown at the right side.

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Case C 

A 30-year-old woman presented with symptoms of dyspnea and chest pain precipitated by bending. She was treated already for eleven months with CAPD. Her chest radiograph showed a right-sided pleural effusion and biochemical analysis of clear pleural fluid revealed a low protein concentration and a high glucose concentration of 14mmol/l. The serum glucose concentration was 5mmol/l and therefore the diagnosis was CAPD-related pleural effusion. After termination of CAPD fluid exchange and conversion to hemodialysis, the pleural fluid slowly disappeared. Video-assisted thoracoscopic surgery with talc poudrage was not performed because this patient preferred to continue with hemodialysis.

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Discussion 

Pleural effusion is an uncommon complication of CAPD and VATS with talc pleurodesis is a therapeutic option for these patients as shown in two of our patients (A and B) if they want to continue CAPD.

It is very important to recapitulate that a hydrothorax develops not directly after commencing peritoneal dialysis. So peritoneal dialysis as a cause of a pleural effusion should be included in the differential diagnosis of a hydrothorax of CAPD patients, even if it develops several weeks or months after pleural dialysis was started.

The most frequently used term for diaphragmal fenestration is “pleuro-peritoneal” communication but the flow of dialysate is unidirectional “peritoneo-pleural”. As in transdiaphragmatic migration of ascites (hepatic hydrothorax),9 the fluid flows against the gravity and along a pressure gradient due to a lower pressure of the pleural space compared to the peritoneal space.9 Therefore, the term “peritoneo-pleural” communication would be more appropriate.

Diagnosis 

Diagnostic thoracentesis and pleural-fluid analysis are often diagnostic, revealing a crystal clear pleural fluid with a low protein and a high glucose concentration.3, 10 The term “sweet” hydrothorax is sometimes used because of this high glucose concentration.7, 8 According to Chow a glucose gradient (pleural-fluid glucose level minus simultaneous serum glucose level) of more than 50mg/dL (2.7mmol/l) has a 100% sensitivity and specificity to detect a sweet hydrothorax,3 but some patients had a lower glucose gradient, probably secondary to glucose reabsorption by the pleural mesothelium.5

Analysis of pleural fluid is often sufficient to establish the diagnosis, but in uncertain cases and when the anatomy of the diaphragmal communication needs to be demonstrated, further imaging, such as peritoneal scintigraphy and contrast CT peritoneography, are required.3

Tc-99m sulfur colloid or contrast material can be injected into a 2L dialysate bag and instilled into the peritoneal cavity followed by periodic imaging at 1/2, 1, 2, and 4h, respectively.6

Diaphragmatic defects or blebs can be intraoperatively identified by intraperitoneal infusion of colored CAPD fluid or by CO2 inflation (check-air-leakage method).11

Treatment 

Discontinuation of peritoneal dialysis 

Temporary discontinuation of CAPD, for 1–4 months, as first-line treatment, and temporary transfer to hemodialysis (HD), is usually indicated. This conservative approach can be effective in half of cases.

Chemical or surgical pleurodesis 

Chemical pleurodesis can be performed, via a chest drain, with talc, tetracycline, autologous blood and other agents. This was only successful in 48% of cases.4 A ten-day wait period after pleurodesis is advised before resuming the peritoneal dialysis.

Chemical pleurodesis can also be done as talc insufflation, under video-assisted thoracoscopic guidance. This was successful in 90% (50–100%) of cases.4 Peritoneal dialysis can be resumed after 3–4 weeks.3

There are no data about superiority of any of the mentioned agents for chemical pleurodesis. Systemic absorption of tetracycline from the pleural space is rapid and it has a renal clearance, which is a drawback of tetracycline pleurodesis in this patient group. 4

Adhesions, developed after chemical pleurodesis via a chest drain, can jeopardise subsequent feasibility of successful thoracoscopy.3, 12

The bigger diaphragmatic defects can be closed during thoratocomy by suturing and at the same time, pleurodesis by pleurectomy or pleural abrasion could be performed.3 Pleural abrasion and/or endoscopic closure of the diaphragmatic defects can also be performed by video-assisted thoracoscopy.3

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Conclusion 

CAPD is an uncommon cause of pleural effusion and appears in approximately 2% of all CAPD patients.3 It is an important complication because CAPD must be stopped. Pleural-fluid biochemical analysis is usually diagnostic revealing a crystal clear pleural fluid with a high glucose concentration and a low protein concentration (“sweet” hydrothorax).3, 10

If the diagnosis is not clear, imaging should be performed by either peritoneal scintigraphy or contrast CT peritoneography to detect possible peritoneopleural communications. A conservative approach, which means temporarily conversion of peritoneal dialysis to hemodialysis for a period of 1–4 months, is successful in half of cases.

Pleurodesis, preferentially achieved by talc insufflation under video-assisted thoracoscopic guidance, has a success rate in excess of 90%. This treatment is safe with a low recurrence rate and if necessary can be repeated. Moreover, in case diaphragmatic defects exist, these can be treated at the same time.

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Conflict of interest statement 

None of the authors have a conflict of interest to declare in relation to this work.

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References 

  1. Light RW. Clinical practice. Pleural effusion. N Engl J Med. 2002;346(25):1971–1977
  2. Marel M, Zrustova M, Stasny B, Light RW. The incidence of pleural effusion in a well-defined region. Chest. 1993;104:1486–1489
  3. Szeto CC, Chow KM. Pathogenesis and management of hydrothorax complicating peritoneal dialysis. Curr Opin Pulm Med. 2004;10:315–319
  4. Chow KM, Szeto CC, Li Kam-Tao P. Management options for hydrothorax complicating peritoneal dialysis. Semin Dial. 2003;16(5):389–394
  5. 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(4):804–808
  6. Rajnish A, Ahmad M, Kumar P. Peritoneal scintigraphy in the diagnosis of complications associated with continuous ambulatory peritoneal dialysis. Clin Nucl Med. 2003;28(1):70–71
  7. Michel C, Devy A, Lavaud F, Lavaud S, Lebargy F. A ‘sweet’ hydrothorax. Presse Med. 2001;30(28):1401–1403
  8. Mangana P, Arvanitis D, Vlassopoulos D. Letters and replies acute hydrothorax in peritoneal dialysis patients: diagnosis and treatment options. Nephrol Dial Transplant. 2003;18(11):2451–2452
  9. Lazaridis KN, Frank JW, Krowka MJ, Kamath PS. Hepatic hydrothorax: pathogenesis, diagnosis, and management. Am J Med. 1999;107(3):262–267
  10. Tsunezuka Y, Hatakeyama S, Iwase T, Watanabe G. Video-assisted thoracoscopic treatment for pleuroperitoneal communication in peritoneal dialysis. Eur J Cardiothorac Surg. 2001;20(1):205–207
  11. Yen HT, Lu HY, Liu HP, Hsieh MJ. Video-assisted thoracoscopic surgery for hydrothorax in peritoneal dialysis patients-check-air-leakage method. Eur J Cardiothorac Surg. 2005;28(4):648–649
  12. 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;74:218–221

PII: S1755-0017(08)00110-3

doi:10.1016/j.rmedc.2008.12.001

Respiratory Medicine CME
Volume 2, Issue 4 , Pages 197-200, 2009

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