Acute peritonitis

1. Acute Peritonitis : Etiology
Name : Vihari Vichakshana Rajaguru
Group : No 32
4th
year 2nd
semester

2. What’s peritoneum ?
• Made of mesothelium.
• Largest cavity in the body
• Composed of flattened polyhedral cells,
resting on fibro-elastic membrane.
• Beneath the peritoneum lies loos areolar
tissue which has rich supply of capillaries and
lymphatics.

4. Introduction
• Defined as inflammation of the peritoneum.
• May be localized or generalized.
• In most cases there is bacterial invasion hence
when it is said that there is peritonitis 
Bacterial peritonitis.
• Even in patients with non bacterial peritonitis
like those d/t Pancreatitis  Eventually gets
infected d/t transmural spread from the gut.

5. Causes
• Bacterial  Gastrointestinal & non-
gastrointestinal
• Chemical Bile, Barium
• Allergic  Starch
• Traumatic  Operative Handling
• Ischaemic  Strangulated bowel, vascular
occlusion
• Miscellaneous  Familial Mediterranean fever.

6. Routes of spreading
• Bowel perforation 

• Transmural Translocation 

• Exogenous contamination 

• Female genital tract 

• Hematogenous spread 

7. Microbiological aspect
• Peritoneal infection is usually caused by more than 2
strains of bacteria.
• Gram negative  endotoxins (lipopolysaccharides) 
TNF
 Tissue perfusion
Endotoxic shock
• These organisms are present in the lower GI tract and
do respond to Penicillins rather to metronidazole and
clindamycin and cephalosporins

8. Non gastrointestinal causes
• Pelvic infection via fallopian tubes are one of the
major causes of Non GI cause of peritonitis.
• The most common organisms being Chlamydia or
gonococcus.
• Chlamydia  Fitz Hugh Curtis Syndrome
(perihepatitis)
• Fungal Peritonitis  In severely ill patients or
Immuno-compramised patients.

9. Microorganisms
• GASTRO INTESTINAL SOURCE:
– E.coli
– Streptococci
– Bacteroids
– K.pneumonia
• NON GASTROINTESTINAL SOURCE:
– Chlamydia
– Neisseria gonorrheoa
– Streptococci
– Mycobacterium & Fungal

10. Localized Peritonitis
• Anatomical and pathological factors help confining infection to
localized areas.
• Greater sac is divided into
– Subphrenic space
– The pelvis
– Peritoneal cavity proper.
• Supracolic and infracolic (division by transverse colon and
transverse mesocolon)
• When supracolic compartment overflows, it does so over to
infracolic region/paracolic gutters/pelvis.

11. Peritoneum
• Inflammed peritoneum loses sheen
Fibrin
• Flakes of fibrin appear  loops of intestine become
adherent to each other
Leukocytes
• Outpouring of serous fluid rich in leukocytes which later
becomes frank pus  Ileus  Prevents spread of infection
 Greater omentum seals the area.

12. Diffuse peritonitis
• Factors favoring spread of peritonitis.
– Speed of peritoneal contamination
– Ingestion of food.
– Virulence of infecting organism
– Young children with small omentum.
– Disruption of localized collection
– Immune deficiency
• With appropriate treatment localized disease will
resolve
– About 20% progress to abscess.