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Saudi Journal of Kidney Diseases and Transplantation
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REVIEW ARTICLE  
Year : 2013  |  Volume : 24  |  Issue : 2  |  Page : 223-229
Encapsulating peritoneal sclerosis: Common or rare in peritoneal dialysis?


Kyanous Stavros Patron Dialysis Unit, Patras, Greece

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Date of Web Publication26-Mar-2013
 

   Abstract 

Encapsulating peritoneal sclerosis (EPS) is a serious and often fatal complication of long-term peritoneal dialysis (PD) with severe malnutrition and poor prognosis. It causes progressive obstruction and encapsulation of the bowel loops. As EPS becomes more prevalent with longer duration of PD, large multicenter prospective studies are needed to establish its incidence and identify risk factors, therapeutic approach, and prognosis.

How to cite this article:
Triga K. Encapsulating peritoneal sclerosis: Common or rare in peritoneal dialysis?. Saudi J Kidney Dis Transpl 2013;24:223-9

How to cite this URL:
Triga K. Encapsulating peritoneal sclerosis: Common or rare in peritoneal dialysis?. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2019 Dec 10];24:223-9. Available from: http://www.sjkdt.org/text.asp?2013/24/2/223/109562

   Introduction Top


Encapsulating peritoneal sclerosis (EPS) is a major and often fatal complication of peritoneal dialysis (PD), characterized by progressive obstruction of the bowel and severe malnutrition. It is also called "sclerosing peritonitis," "encapsulating sclerosing peritonitis" and "abdominal coccooning" because the loops of the small intestine are bound and encapsulated by thickened adhesions giving the picture of a cocoon. EPS can occur during chronic renal replacement therapy with PD, usually after long periods or after transfer to hemodialysis or transplantation. The first cases of EPS are reported by Gandhi et al [1] and Denis et al [2] in 1980. The rarity of the condition and the retrospective nature of most reports render it difficult to study; therefore, the exact incidence, etiology and adequate therapy have not been defined yet. In the 2000 ISPD (International Society for Peritoneal Dialysis) meeting, EPS was carefully reviewed. The researchers concluded that this is a clinical syndrome with persistent, intermittent or recurrent intestinal obstruction caused by extensive adhesions of the peritoneum. Morphologically, there is diffuse hypertrophy of the peritoneum and/or sclerosing peritonitis. [3],[4] In the same meeting, other than defining the diagnostic criteria, the name of encapsulating sclerosing peritonitis (ESP) was changed to "encapsulating peritoneal sclerosis (EPS)" because, while peritonitis indicates acute inflammation, sclerosis is the final outcome of EPS.


   Clinical Presentation Top


The symptoms develop in the three phases of the disease: inflammation, calcification, and sclerosis. The inflammation phase is characterized by nonspecific symptoms such as abdominal pain, anorexia, nausea, diarrhea, and weight loss. Nonspecific signs of systemic inflammation, such as fever, leukocytosis, elevated C-reactive protein (CRP), low serum albumin (which is inconsistent with the nutritional state and indicates inflammation), anemia refractory to therapy when other causes of resistance are excluded, bloody PD drainage fluid (recurrent or persistent), and perhaps resistant culture negative nonresolving peritonitis. Eventually, patients will progress to a more obstructive or "sclerosing" phase with abdominal pain, anorexia, nausea, vomiting, weight loss, encapsulated ascites or abdominal mass that refers to intestinal obstruction or intestinal distension proximal to the obstructed bowel, and hemorrhagic PD drainage fluid.

The Scottish registry, [5] in which 46 patients were identified with EPS, indicates that 14 patients presented with signs of inflammation and 11 with intestinal obstruction, whereas the rest of the patients presented with nonspecific symptoms, suggesting that the EPS can occur at various stages. All imaging methods help in diagnosis, including abdominal radiography, abdominal ultrasound, magnetic resonance imaging (MRI) and computed tomography (CT) scans, which is the examination of choice to diagnose EPS.

The laparoscopic findings highlight a fibrotic membrane as part of the peritoneal membrane surrounding the intestinal wall and part of the abdominal wall, creating the image of the "cocoon." However, morphology and thickness of the peritoneal membrane vary among the patients with EPS.


   Pathophysiology Top


EPS is a complex phenomenon and is not identical with simple sclerosis (SS). [3] Simple sclerosis is a mild, clinically subtle illness that occurs following chronic exposure to peritoneal solutions in about 80% of the patients develop SS. [3] Unlike SS, EPS is a rare condition with low incidence of <5/1000/year, [6] but it is dramatic and often fatal. EPS is not an evolution of the SS, as some Japanese researchers claim, [7] but a different disease. This statement results from (a) peritoneal biopsies with absence of intermediate stages, which should appear at lower frequency and (b) the large difference in the incidence of both diseases. With regard to histological features, SS shows morphological variations of the parietal peritoneum (visceral = 1200 mm, parietal = 450 mm) without extensive calcifications; the histology is relatively monotonous with mild vasculopathy. Unlike SS, sclerosis is extensive in EPS and evolves irregularly to encompass the whole peritoneum, particularly the visceral part. [3],[4]

Furthermore, unlike SS, inflammation is present in 100% of the EPS cases [3],[4] and manifests both acute or chronic inflammatory cells, including giant cells, granulation tissue, vasculopathy with vascular occlusion, calcification, and perhaps ossification, which contrasts with the pathology of the SS. Unlike SS, no single risk factor associated with the development of EPS has been identified. The correlation with the duration of PD is often mentioned; however, EPS may develop during the initial years of PD or after discontinuation of the PD renal replacement therapy. Peritonitis is the most common pathogenetic risk factor for developing EPS, which is supported by the epidemiological data but it is not a prerequisite for the development of EPS, as EPS occurs even in patients without a previous history of peritonitis. Specific pathogens, such as Staphylococcus aureus, Candida species, Pseudomonas, and Hemophilus influenza, have been reported as more dangerous than other microorganisms for developing EPS, perhaps due to their ability to promote the production of large amounts of fibrin. The bio-incompatibility of peritoneal solutions is a risk factor of EPS, but it was demonstrated only in a few cases using acetate solutions. Other correlations with clorhexidine, povidone, b-blockers, [8],[9] as well as iodine, catheters, plasticizers, and high-transport status of the peritoneal membrane have not been substantiated. In conclusion, PD is an important but not an essential risk factor for the development of EPS, and the use of bio-compatible solutions lately did not reduce in the incidence of EPS. The disease was reported in non-PD patients.

Finally, EPS was reported in non-PD patients who received b-blockers (atenolol, metoprolol, practolol, propanolol, oxprenlol, and timolol), [8],[9] antiseptics, talc, and in patients with malignancies or inflammatory conditions such as systemic lupus erythematosus (SLE), familial  Mediterranean fever More Details, and sarcoidosis. EPS was also associated with intraperitoneal chemotherapy, gastrointestinal diseases, ascites, and endometriosis or it may be idiopathic.


   Risk Factors for EPS Top


The development of EPS in PD patients is multifactorial. Recurrent infections may contribute to the development of peritoneal injury; however, the severity of peritonitis is more important than frequency, especially if it necessitates the removal of the PD catheter or is associated with certain types of microorganisms. [10]

Duration of PD is a significant risk factor for the development of EPS, although not all studies have demonstrated an increase in the EPS rates with a longer duration of PD. [11],[12],[13] The most accepted theory is Kawanishis "two-hit" hypothesis. It implies that in addition to long-term exposure of the peritoneal membrane to the bio-incompatible solutions (first hit), some additional factors (second hit), which include recurrent or severe peritonitis, exposure of the peritoneal membrane to fibrinogenic therapeutic immunosuppressants that are used after transplantation (calcineurin inhibitors), and genetic predisposition are necessary for the development of EPS. The first "hit" results in peritoneal functional and structural deterioration, [3],[7] and includes factors that relate to glucose-based dialysate solutions, advanced glucation end-products (AGEs), glucose degradation products, acidic dialysate pH (which induce an initial inflammatory reaction), and peritoneal sclerosis associated with upregulation of cytokines such as vascular endothelial growth factor (VEGF), TGF-β, and plasminogen activator inhibitor type-1 (PAI-1). [10] However, more evidence is needed to support the "two-hit" hypothesis. [10],[14],[15],[16],[17],[18] Furthermore, data suggest that use of icodextrin-based dialysis solutions preserves both peritoneal membrane function and mesothelial cell mass. [18],[19] No studies have yet been conducted on the direct association between icodextrin solution and development of EPS.


   Kidney Transplantation and Encapsulating Peritoneal Sclerosis: Is There a Relationship Between Them? Top


The pathophysiology of posttransplantation EPS is probably influenced by multiple factors including preconditioned peritoneum by damaging PD solutions (first hit), and transplantation may impose the second hit. Both termination of PD due to ultrafiltration failure and peritonitis in addition to transplantation-related factors could explain the development of posttransplant EPS. However, that is usually not the case when patients are transferred from PD to kidney transplantation. [20],[21]

First, it has been suggested that after the discontinuation of the PD fluid exchanges, the concentrations of fibrin and proinflammatory and profibrotic mediators such as interleukin-1b, transforming growth factor-beta, and vascular endothelial growth factor in the peritoneal cavity rise and bring about acceleration of inflammation-fibrosis processes. [22],[23] For this reason, it has been proposed to keep the abdomen filled after withdrawal from PD and to continue exchanges of fluids a few times per week. Nevertheless, there is no convincing evidence that this strategy has a beneficial effect on the development or course of EPS. On the other hand, posttransplantation EPS might be related to the concomitant use of profibrotic calcineurin inhibitors CNIs. It is conceivable that these drugs enhance the inflammatory-fibrotic processes already initiated in the peritoneum of patients on long-term PD. On the other hand, corticosteroids may have a beneficial effect on postkidney transplantation EPS. [21]

In this respect, the trend to reduce the corticosteroid load in the recent immunosuppressive treatment regimen may result in a tendency to develop EPS after kidney transplantation. Further multicenter studies including a large number of patients from different centers are necessary to investigate whether the frequency of EPS is increasing and that risk factors can be identified. Special attention should be paid to alterations in the immunosuppressive treatment regimens in kidney transplantation.


   Diagnosis and Prognosis of EPS Top


Diagnosis of EPS is usually delayed, and the combination of malnutrition and end-stage renal disease is a serious risk factor for increased mortality. [24] In addition, the immediate surgical repair to a depleted patient with frozen abdomen can be devastating.

Early diagnostic markers of EPS include regular CA125 measurements or inflammation markers in the peritoneal solution, such as interleukin-6. An acute decrease of concentration of CA125 may indicate extensive damage of the peritoneal membrane.


   Management Top


Treatment of EPS includes total parenteral nutrition (TPN), steroid therapy and other anti-inflammatory agents, [25],[26],[27],[28] and surgical intervention. [29],[30]

The cornerstone of the treatment is adequate food intake, either parenteral or enteral. TPN alone cannot be expected to improve EPS, and long-term TPN can be complicated by catheter-related infection, which may result in sepsis and death. [31]

Nutritional assessment and support is critical to patients' outcome, especially for those who undergo surgical intevention. [32],[33],[34],[35] A study from the UK highlighted the importance of TPN and recommend careful monitoring of the nutritional status by use of markers such as albumin. [36] However, TPN is not a curative therapy as low recovery rates are observed when it is used alone. [12],[37]

The Pan Thames study also observed shorter time to death in the TPN treatment group compared with patients maintained on oral nutrition. [5] Although there was no information on the initial nutritional status or clinical condition of the patients, the difference in survival could be due to TPN-related complications such as infection. [38],[39]

Tamoxifen is a selective estrogen receptor modulator, [40] predominantly used for the treatment of breast cancer. [41],[42],[43] Tamoxifen also influences the activity of the profibrotic cytokine TGF-β and has been shown to be effective in fibrotic diseases as retroperitoneal fibrosis [44] and Riedels' thyroiditis. [45],[46],[47] Success with tamoxifen suggests that estrogen has a permissive role in the development of EPS. [48] However, it is intriguing that so many small case series describe EPS in females, and often young premenopausal females. [49],[50],[51] The reported effects of tamoxifen in EPS are equivocal, and experience is limited to a number of case reports and small series of patients. [5],[52],[53],[54],[55],[56],[57],[58],[59],[60],[61],[62],[63],[64],[65],[66],[67],[68],[69],[70]

All reports demonstrated improvement of the intestinal function and decrease of inflammatory markers, except for a recently published large case series from England. [5] In this latter study, survival time in various treatment groups, including in 31 patients treated with Tamoxifen, was not different compared with patients not given any drug treatment. A controlled study investigating the effect of tamoxifen on survival in a larger population is required.

Surgery may be lifesaving and refers to the lysis of the intestinal adhesions or peritonectomy, depending on the extent of intestinal lesions that vary among patients with EPS. Surgical treatment may reverse intestinal occlusion (two studies indicated 95% success after full enterolysis). [33],[68] Surgical intervention improves the inflammation markers and the nutritional status, but it does not improve the degeneration of the peritoneum. Unfortunately, the relapse rate is high (23.4%), and this is possibly related to the number of peritoneal small vessels, which are increased in patients who relapse. Absolute indications for surgical intervention include symptomatic patients with recurrent ascites, malnutrition, increased CRP, intestinal obstruction, bowel perforation or gangrene, hemoperitoneum, and peritonitis (bacterial/fungal). The view of surgeons in regard to the treatment of EPS is that it is treatable and that the combination of conservative treatment and surgery is the treatment of choice. But, late EPS does not respond to conservative treatment. Corticosteroids may be useful in the early inflammatory phase in order to intercept fibrosis of the peritoneum. [57]

In conclusion, EPS is a rare complication of PD with increased mortality. The duration of PD and its discontinuation are risk factors for developing EPS, but other less-established risk factors are emerging. Prevention and early and correct diagnosis and treatment are challenging. The genetic basis of EPS requires future prospective multicenter studies. Tamoxifen administration appears to be safe, and some patients with EPS may benefit from its use. The role of immunosuppressants and, particularly, calcineurin inhibitors (in steroid free/sparing protocols) needs further investigation.

We need a uniform approach with prospective studies in centers with experience in EPS in order to investigate the incidence, risk factors, treatment, and prognosis of EPS.

 
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Correspondence Address:
Konstantina Triga
Kyanous Stavros Patron Dialysis Unit, Patras
Greece
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DOI: 10.4103/1319-2442.109562

PMID: 23538342

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