Peritoneum

• Serosal membrane with area equivalent to body surface

area, I.e. 1 to 2 metres2 •
• 80% is visceral peritoneum and gets its vascular supply via
the mesenteric arteries and portal veins
• 20% is parietal peritoneum and gets its vascular supply via
arteries and veins of abdominal wall •
Normal peritoneum
• Normal parietal peritoneum is consisted of mesothelial cells (surface
lining), the submesothelial interstitial layer and underlying peritoneal
adipose tissue and the peritoneal fascia
Mesothelial cell layer

Sub Mesothelial
interstitial layer
Peritoneal adipose
tissue layer
Peritoneal fascia
• Normal parietal peritoneum is consisted of mesothelial cells (surface
lining), the submesothelial interstitial layer and underlying peritoneal
adipose tissue or peritoneal fascia
• The high elasticity and plasticity of the peritoneum are a result of that
action of the mesothelial cells covering the peritoneal surface.
• These cells have fine microvilli (3–12 μm) on their surface and
synthesize and secrete various lubricating substances such as
hyaluronic acid
Submesothelial compact zone (SMC)
Width of the submesothelial compact zone was defined as a distance
from the mesothelial surface to the upper border of peritoneal adipose
tissue or peritoneal fascia.
The width of submesothelial compact zone is regarded as the thickness
of parietal peritoneum.
The vascular network

• The vascular network of parietal peritoneum is mainly located

between the submesothelial interstitial layer and peritoneal adipose
tissue and is composed of small artery, arteriole, capillary, post-
capillary venule and veins), occasionally with lymphatic vessels.
Post-capillary venule (PCV)
• Post-capillary venules (PCVs) are blood vessels, connecting capillaries
to small veins.
• The diameter of PCVs ranges approximately from 20 to 100
• The PCV has a thin wall structure containing a few slender smooth
muscle cells within the wall, and usually co-localizes with arterioles
• hyalinizing vasculopathies in the PD peritoneum primarily affect PCVs
Peritoneal fascia
• The peritoneal fascia is composed of dense connective tissue that
appears as a compact assemblage of collagen bundles.
• Sometimes, the peritoneal fascia is adjacent to the submesothelial
interstitial layer without the intercalation of peritoneal adipose tissue
Dialysate is believed to be the culprit
• Peritoneal injury induced by the PD dialysate is thought to be a major
cause of peritoneal deterioration.
• 18% of overall technique failure and transfer to hemodialysis
• It is widely assumed that alteration in peritoneal function is related to
structural changes in the peritoneal membrane
• The acidity, high concentration of lactic acid, high osmotic pressure,
and high glucose concentration in the peritoneal dialysate, and
glucose degradation product (GDP) can be cited as the factors
contributing to peritoneal deterioration
DIALYSAT
E
Changes in Peritoneum post dialysis
• Peritoneal disorders in PD can be pathologically designated into 2
categories:
• simple peritoneal sclerosis and
• encapsulating peritoneal sclerosis (EPS),
• These histologic changes are associated with changes in peritoneal
membrane function
Simple Peritoneal
Sclerosis
• (SPS) is a mild, clinically subtle illness that occurs following chronic
peritoneal irritation
• Also called hyalinizing peritoneal sclerosis (HPS)”
• Parietal peritoneum and the visceral peritoneum have shown uniform
fibrous thickening of the submesothelial interstitium ranging from 200
to 500 μm and sometimes up to 1 mm, along with the degeneration of
the collagenous fibers and vascular wall sclerosis
• Hyalinizing vasculopathy is defined as hyalinization of vascular walls
with or without narrowing or obstruction ofthe lumen (
• It primarily affects PCVs and capillaries
• Larger vessels; such as small arteries, arterioles and veins can be
involved inmore advanced cases.
Encapsulated peritoneal sclerosis
• It is defined by the International Society for Peritoneal Dialysis as “a
syndrome continuously, intermittently, or repeatedly presenting with
symptoms of intestinal obstruction caused by adhesions of a diffusely
thickened peritoneum”

EPS can be divided into primary (idiopathic) or secondary in which a

trigger for the inflammatory process can be identified.
•
Encapsulated peritoneal sclerosis
• It is pathologically defined by the encapsulation of intestines or entire
abdominal organs with cocoon like thin white encapsulating
membranes.
• It is often accompanied by edema of intestinal walls, ascites and
adhesions to the abdominal wall (parietal peritoneum) in advanced
cases.
• The encapsulating membrane is a newly-formed fibrous membranous
structure that covers the visceral surface of the intestines and other
abdominal organs
• Primary EPS was classically thought to afflict adolescent women in
tropical and subtropical areas leading to theories of retrograde
menstruation or gynecologic infection as the cause
• Secondary EPS, a local or systemic factor can be identified as
triggering peritoneal inflammation. medications, infection,
mechanical or chemical intraperitoneal irritants,cirrhosis, organ
transplantation, endometriosis, gynecologic neoplasms, dermoid cyst
rupture, and systemic rheumatologic and inflammatory disorders
• In peritoneal dialysis, the annual incidence of EPS varies from 0.14%
to 2.5%
Microscopy
• Histologically, the encapsulating membrane is composed of fibrin
deposits
• There is loss of mesothelial layer
• EPS also shows swelling and the proliferation of peritoneal fibroblasts
and fibroblast like cells, inflammatory cell infiltration both acute and
chronic, angiogenesis and
• fibrosis and hyalinization similar to that of simple sclerosis
• Calcification, positive iron stains and hemorrhage may also be seen.
Peritonitis
• Peritonitis is an inflammation of the peritoneum, the tissue that lines
the inner wall of the abdomen
• Peritonitis is usually caused by infection from bacteria or fungi.
• he first symptoms of peritonitis are typically poor appetite and nausea
 and a dull abdominal ache that quickly turns into persistent, severe 
abdominal pain, which is worsened by any movement.
• Abdominal tenderness or distention
• Chills
• Fever
• Fluid in the abdomen
• Not passing any urine, or passing significantly less urine than usual
• Difficulty passing gas or having a bowel movement
• Vomiting
Causes of Peritonitis
• The two main types of peritonitis are primary spontaneous peritonitis,
an infection that develops in the peritoneum; and secondary
peritonitis, which usually develops when an injury or infection in the
abdominal cavity allows infectious organisms into the peritoneum. 
• The most common risk factors for primary spontaneous peritonitis
include:
• Liver disease with cirrhosis. Such disease often causes a buildup of
abdominal fluid (ascites) that can become infected.
• Kidney failure getting peritoneal dialysis. This technique, which
involves the implantation of a catheter into the peritoneum, is used to
remove waste products in the blood of people with kidney failure. It's
linked to a higher risk of peritonitis due to accidental contamination of
the peritoneum by way of the catheter.
• Common causes of secondary peritonitis include:

• A ruptured appendix, diverticulum, or stomach ulcer

• Digestive diseases such as Crohn's disease and diverticulitis
• Pancreatitis
• Pelvic inflammatory disease
• Perforations of the bowel, stomach, intestine, gallbladder, or appendix
• Surgery
• Trauma to the abdomen, such as an injury from a knife or gunshot wound
• Noninfectious causes of peritonitis include irritants such as bile, blood, or foreign
substances in the abdomen, such as barium.
Infectious causes
• In most cases of perforation of a hollow viscus, mixed bacteria are
isolated; the most common agents include Gram-negative bacilli (e.g.,
Escherichia coli) and anaerobic bacteria (e.g., Bacteroides fragilis
• In trauma / surgical wound, /continuous ambulatory 
peritoneal dialysis, and intra-peritoneal chemotherapy. mixed 
bacteria are isolated; the most common agents include
cutaneous species such as Staphylococcus aureus, and 
coagulase-negative staphylococci, and fungi such as Candida.
[10]
Non infectious causes
• Leakage of sterile body fluids into the peritoneum, such as blood (e.g.,
endometriosis, blunt abdominal trauma), gastric juice (e.g., peptic
ulcer, gastric carcinoma), bile (e.g., liver biopsy), urine (pelvic
trauma), pancreatic juice (pancreatitis), or even the contents of a
ruptured dermoid cyst.
• It is important to note that, while these body fluids are sterile at first,
they frequently become infected once they leak out of their organ,
leading to infectious peritonitis within 24 to 48 hours.
Tests can help the doctor diagnose peritonitis
• Complete blood count (CBC), can measure your white blood cell count
(WBC). A high WBC count usually signals inflammation or infection.
• A blood culture can help to identify the bacteria causing the infection
• If there is a buildup of fluid in the abdomen(ascites), a needle is used
to remove some and send it to a laboratory for fluid analysis.
Culturing the fluid can also help identify bacteria.
• Imaging tests, such as CT scans and X-rays, can show any perforations,
Peritonitis changes dialysis fluid appearence
• Is cloudy or has an unusual color
• Contains white flecks
• Contains strands or clumps (fibrin)
• Has an unusual odor, especially if the area around the tube (catheter)
is red or painful.
Complications
• Sepsis