Acute peritonitis

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

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