Diagnostic criteria for EPS

In accordance with the UK guideline on EPS (1), we believe that the diagnosis of EPS should be made when two basic criteria are fulfilled:

1. Clinical symptoms of bowel obstruction
2. Radiological findings consistent with a diagnosis of EPS and/or findings consistent with EPS upon surgical inspection of the peritoneum

In addition, no alternative explanation for the symptoms of bowel obstruction should be present (e.g. tumor, peritonitis, paralytic ileus). There should be a low threshold for laparoscopic inspection of the peritoneum as the encapsulation of the bowel may be very localized which may not lead to an abdominal CT-scan confirming the diagnosis of EPS (2).

The diagnostic criteria for EPS are based on a combination of bowel obstruction and features of encapsulation due to peritoneal fibrosis. This combination is chosen as simple peritoneal fibrosis or thickened peritoneal membrane without functional impairment of the bowels may be frequently found after long-term PD (1). Usually, the symptoms consists of anorexia, nausea, vomiting, and weight loss. Changes in peritoneal membrane transport characteristics are frequent. Typically, ultrafiltration capacity falls and there is an increase in peritoneal membrane small solute transport prior to development of EPS. However, absence of these changes does not exclude a diagnosis of EPS. A rise in peritoneal membrane small solute transport and loss of ultrafiltration are commonly observed in patients on long-term PD, the majority of whom do not develop EPS. Other presentations include haemoperitoneum and sterile non-resolving or recurrent PD “peritonitis”. Markers of an inflammatory state including elevated C-reactive protein, anaemia and hypoalbuminaemia may be present, but the degree of systemic inflammation varies(1).

It should be realized that EPS may evolve in an insidious manner with slow progression of abdominal symptoms and radiographical abnormalities of the peritoneum to a variable degree. But it is not known how often suspected or early EPS really develops into definite EPS. To date it is not possible to diagnose with certainty a possible early stage of developing EPS, as specific markers are not available. The Dutch EPS registry includes these possible cases of EPS to increase our knowledge in this area (3).

In recent years, a number of patients have been described with development of EPS shortly after kidney transplantation, an entity known as post-transplantation EPS. It differs from EPS during PD treatment as it develops relatively shortly after transplantation (usually within a year) in previously asymptomatic patients (4). Both the cessation of PD and/or the use of pro-fibrotic drugs may play a role. Increased awareness of post-transplantation EPS is warranted for timely diagnosis and treatment which may lower the high mortality of this condition.


1. UK Encapsulating peritoneal sclerosis clinical practice guidelines, july 2009, www.renal.org
2. Kirkman MA, Heap S, Mitu-Pretorian OM, McGrath S, Pararajasingam R, Tavakoli A, Augustine T. Posttransplant encapsulating peritoneal sclerosis localized to the terminal ileum.Perit Dial Int. 2010;30:480-2
3. Korte MR, Habib SM, Lingsma H, Weimar W, Betjes MG. Posttransplantation encapsulating peritoneal sclerosis contributes significantly to mortality after kidney transplantation. Am J Transplant. 2011;11:599-605
4. Korte MR, Boeschoten EW, Betjes MG; EPS Registry. The Dutch EPS Registry: increasing the knowledge of encapsulating peritoneal sclerosis. Neth J Med. 2009;67:359-62.