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Peritoneal Dialysis
Dr. Mohamed Abbass
Consultant Nephrology
PGDD,CARDIFF,UK 1
ENCAPSULATING
PERITONEAL SCLEROSIS
(EPS)
 EPS is an uncommon but serious
complication of long term peritoneal
dialysis  partial or completes intestinal
obstruction.

2
ENCAPSULATING
PERITONEAL SCLEROSIS
(EPS)
 The risk factor
 Duration of PD therapy, significant after 5 years and more
after 10 years.
 Onset of PD at young age.
 No association of EPS with the type or number of episodes
of PD peritonitis or with the type or strength of PD solutions
3
Pathophysiology
 In a healthy person, the peritoneum is very thin , so the
intestinal loops move easily and food passes through
 In peritoneal dialysis patient, the membrane becomes thick
and fibroses (sclerosed)
 The food is no longer passing through the blocked intestine
which causes abdominal pain, nausea, vomiting and weight
4
Pathophysiology
 There are two phases:
 The early inflammatory phase

Vague abdominal discomfort and Bloody effluent

Rapid transport status

Signs of inflammation (erythropoietin- resistant anemia
and elevated CRP).
 Sclerosing phase: the membrane becomes thick and
fibroses (sclerosed) over time till restrict the intestinal
movement and become blocked 5
Clinical picture
 Most commonly symptoms occur after quitting PD.
 Symptoms of intestinal obstruction (abdominal pain,
intermittent constipation, vomiting), weight loss,
ascites (which can be haemorrhagic).
 An inflammatory process  raising CRP.
 If patient still on PD; UF failure, Length of time on
PD, Rapid transport status , Severe peritonitis.
6
Clinical course
• Severe cases progress rapidly complete
bowel obstruction  severe malnutrition (on
parenteral nutrition) death.
• Moderate cases intermittent course with
nutrition maintained  small amounts frequently
with oral nutritional supplements.
• Mild cases improve all their symptoms over
time and not require any dietary manipulations.
7
Diagnosis
 Should be early during inflammatory stage.
 Clinical features:
 HX of change to HD or transplanted after many
years on PD
 Unexplained haemorrhagic ascites
 Unexplained high CRP with abdominal pain
 Unexplained weight loss.
8
Diagnosis
 Abdominal CT scan (with contrast) standard
method
 Peritoneal thickening and calcification
 Thickened and Dilated bowel loops with bowel
pulled into center of abdominal cavity (‘fist sign')
 MRI scan has been suggested as a useful tool.
 Abdominal X-ray is not helpful only may show
9
10
Abdominal CT scan from a patient with EPS. Red arrows
indicate thickened parietal peritoneum with calcification.
Green arrows indicate thickened visceral peritoneum forming a
cocoon containing loops of bowel.
Treatment
 Drug treatment: in inflammatory phase
 Corticosteroid : moderate dose, duration of
treatment is unclear and should be titrated to the
symptoms.
 Tamoxifen for its antifibrotic effects.
 Sirolimus :no evidence of any benefit.
 Surgery: in sclerosing phase


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ENCAPSULATING PERITONEAL SCLEROSIS (EPS)

  • 1. Peritoneal Dialysis Dr. Mohamed Abbass Consultant Nephrology PGDD,CARDIFF,UK 1
  • 2. ENCAPSULATING PERITONEAL SCLEROSIS (EPS)  EPS is an uncommon but serious complication of long term peritoneal dialysis  partial or completes intestinal obstruction.  2
  • 3. ENCAPSULATING PERITONEAL SCLEROSIS (EPS)  The risk factor  Duration of PD therapy, significant after 5 years and more after 10 years.  Onset of PD at young age.  No association of EPS with the type or number of episodes of PD peritonitis or with the type or strength of PD solutions 3
  • 4. Pathophysiology  In a healthy person, the peritoneum is very thin , so the intestinal loops move easily and food passes through  In peritoneal dialysis patient, the membrane becomes thick and fibroses (sclerosed)  The food is no longer passing through the blocked intestine which causes abdominal pain, nausea, vomiting and weight 4
  • 5. Pathophysiology  There are two phases:  The early inflammatory phase  Vague abdominal discomfort and Bloody effluent  Rapid transport status  Signs of inflammation (erythropoietin- resistant anemia and elevated CRP).  Sclerosing phase: the membrane becomes thick and fibroses (sclerosed) over time till restrict the intestinal movement and become blocked 5
  • 6. Clinical picture  Most commonly symptoms occur after quitting PD.  Symptoms of intestinal obstruction (abdominal pain, intermittent constipation, vomiting), weight loss, ascites (which can be haemorrhagic).  An inflammatory process  raising CRP.  If patient still on PD; UF failure, Length of time on PD, Rapid transport status , Severe peritonitis. 6
  • 7. Clinical course • Severe cases progress rapidly complete bowel obstruction  severe malnutrition (on parenteral nutrition) death. • Moderate cases intermittent course with nutrition maintained  small amounts frequently with oral nutritional supplements. • Mild cases improve all their symptoms over time and not require any dietary manipulations. 7
  • 8. Diagnosis  Should be early during inflammatory stage.  Clinical features:  HX of change to HD or transplanted after many years on PD  Unexplained haemorrhagic ascites  Unexplained high CRP with abdominal pain  Unexplained weight loss. 8
  • 9. Diagnosis  Abdominal CT scan (with contrast) standard method  Peritoneal thickening and calcification  Thickened and Dilated bowel loops with bowel pulled into center of abdominal cavity (‘fist sign')  MRI scan has been suggested as a useful tool.  Abdominal X-ray is not helpful only may show 9
  • 10. 10 Abdominal CT scan from a patient with EPS. Red arrows indicate thickened parietal peritoneum with calcification. Green arrows indicate thickened visceral peritoneum forming a cocoon containing loops of bowel.
  • 11. Treatment  Drug treatment: in inflammatory phase  Corticosteroid : moderate dose, duration of treatment is unclear and should be titrated to the symptoms.  Tamoxifen for its antifibrotic effects.  Sirolimus :no evidence of any benefit.  Surgery: in sclerosing phase 