Class for undergrad med students

1. Acute Peritonitis
Yuvaraj Karthick R

2. Peritnoeum
 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.  Visceral Peritoneum: Poorly supplied by blood vessels hence
cannot localize pain properly.
 Parietal Peritoneum: Richly supplied by blood vessels  can
localize pain better

4. Peritonitis
 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 of Peritonitis:
 Bacterial  Gastrointestinal & non- gastrointestinal
 Chemical Bile, Barium
 Allergic  Starch
 Traumatic  Operative Handling
 Ischaemic  Strangulated bowel, vascular occlusion
 Miscellaneous  Familial Mediterranean fever.

6. Route of spread:
 Bowel perforation 
 Transmural Translocation 
 Exogenous contamination 
 Female genital tract 
 Hematogenous spread 

7. Microbiology: (Those from GI tract)
 Peritoneal infection is usually caused by more than 2 strains of
bacteria.
 Gram negative  endotoxins (lipopolysaccharides)  TNF
Endotoxic shock  Tissue perfusion
 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 of Peritonitis
 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
Immunocompramised 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. Pathological
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.

13. Clinical features of localized peritonitis
 Symptoms and signs are those of the affected organ.
 Abdominal pain, specific GI symptoms, malaise, anorexia & nausea.
 Then peritoneum gets inflamed
 Pain worsens,
 Increased temp and pulse rate.
 Localized guarding ++
 Rebound tenderness ++
 If inflammation under the diaphragm  Shoulder tip Pain+
 Pelvic inflammation: Abdominal signs but severe tenderness of P/R or
P/V

14. Diffuse peritonitis
 Early
 Pain  Worsened by movement
 Initially at the site of lesion then followed by spread elsewhere.
 Tenderness and generalized guarding
 Decreased bowel sounds as Paralytic ileus sets in
 Increased temperature and pulse

15. Late peritonitis
 Abdomen becomes rigid.
 Distension +
 Bowel sounds –ve
 Shock  Cold clammy extremities
 Sunken eyes, dry tongue
 Rapid thread pulse
 Anxious facies.

16. Diagnostic aides:
 Bedside:
 Urine dipstick
 ECG
 Bloods:
 Baseline U&E
 CBC
 S. amylase

17. Imaging
 Erect X-ray abdomen – Air under the diaphragm
 Supine X-ray – Distended bowel loops
 CECT – To localize the condition.
 USG abdomen – To localize the condition.

18. Management
 General Care for the patient
 Correction of fluid loss and circulating volume.
 Urinary catheterization and output monitoring.
 Antibiotic therapy.
 Analgesia
 Specific treatment for the condition.
 Early surgery following localization of the lesion
 In case of causes relating to non GI like Salpingitis or Pancreatitis then
non-operative treatment.

19. Surgery:

20. Prognosis and complications:
 Mortality is 10% with modern treatment.
 Factors responsible for prognosis
 Load
 Age
 Onset of treatment

21. Complications:
 Systemic complications:
 Bacterimic or endotoxic shock
 SIRS
 MODS
 Abdominal Complications:
 Paralytic ileus
 Residual/recurrent abscess/ Inflammatory mass
 Portal pyemia/ Liver abscess
 Adhesions  Small bowel obstruction

22. Bile peritonitis:
 Usually occurs following Lap. Cholecystectomy on damaging the
biliary tract or a duodenal stump blow out.
 Extravasated bile gets collected and causes local chemical
peritonitis  laparotomy and evaluation
 Source of bile leak should be identified and treated.
 Laparotomy wound is not closed unless the leak is dealt with.
 Usually dealt with placement of drain and ERCP and stenting of the
CBD.

23. Primary peritonitis or Spontaneous bacterial
peritonitis:
 D/t Pneumococci  occurs in Cirrhosis or Nephrotic syndrome.
Rarely in Female children (3-9 yrs)
 Sudden onset with pain over lower abdomen
 Raised temp
 Vomiting but after 24-48 hrs  Profuse diarrhea
 Peritonism + but less than perforation peritonitis.
 Investigations:
 Leukocytes >30k with > 90 % polymorphs
 If peritoneal fluid is odourless and sticky then almost certain diagnosis
 Peritoneal fluid can be sent for evaluation