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Acute Peritonitis : Etiology
Name : Vihari Vichakshana Rajaguru
Group : No 32
4th
year 2nd
semester
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.
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.
Causes
• Bacterial  Gastrointestinal & non-
gastrointestinal
• Chemical Bile, Barium
• Allergic  Starch
• Traumatic  Operative Handling
• Ischaemic  Strangulated bowel, vascular
occlusion
• Miscellaneous  Familial Mediterranean fever.
Routes of spreading
• Bowel perforation 

• Transmural Translocation 

• Exogenous contamination 

• Female genital tract 

• Hematogenous spread 
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
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.
Microorganisms
• GASTRO INTESTINAL SOURCE:
– E.coli
– Streptococci
– Bacteroids
– K.pneumonia
• NON GASTROINTESTINAL SOURCE:
– Chlamydia
– Neisseria gonorrheoa
– Streptococci
– Mycobacterium & Fungal
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.
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.
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.
acuteperitonitis SS4 word.docx

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acuteperitonitis SS4 word.docx

  • 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.
  • 3.
  • 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.