Acute peritonitis

Acute PeritonitisYuvaraj Karthick R

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.

Visceral Peritoneum: Poorly supplied by blood vessels hence cannot localize pain properly.

Parietal Peritoneum: Richly supplied by blood vessels can localize pain better

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.

Causes of Peritonitis:

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

Route of spread: Bowel perforation

Transmural Translocation

Exogenous contamination

Female genital tract

Hematogenous spread

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

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.

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.

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.

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.

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

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

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

Diagnostic aides: Bedside:

Urine dipstick ECG

Bloods: Baseline U&E CBC S. amylase

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.

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.

Surgery:

Prognosis and complications: Mortality is 10% with modern treatment. Factors responsible for prognosis

Load Age Onset of treatment

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

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.

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