Peritonitis

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Peritonitis

Definition

Peritonitis is inflammation of the peritoneum - the serous membrane lining the abdominal cavity and covering the viscera. It is a life-threatening event that is often accompanied by bacteremia and sepsis syndrome.
  • Harrison's Principles of Internal Medicine 22E, p. 1113
  • Bailey and Love's Short Practice of Surgery 28th Ed., p. 1109

Classification

By extent:
  • Localised - inflammation confined to a specific area; patient may have normal vital signs but shows local guarding and rebound tenderness
  • Diffuse (generalised) - inflammation of large regions of the parietal peritoneum; life-threatening, typically from viscus perforation or major vascular catastrophe
By aetiology:
  • Primary (spontaneous) bacterial peritonitis (SBP/PBP) - no identifiable intra-abdominal source
  • Secondary peritonitis - from a definable intra-abdominal source
  • CAPD-associated peritonitis - from peritoneal dialysis catheter
Causes of peritoneal inflammation (Bailey & Love):
CategoryExamples
Bacterial (GI)Perforated ulcer, appendix, diverticulum
Bacterial (non-GI)PID, haematogenous spread
ChemicalBile, pancreatic enzymes, barium
AllergicStarch peritonitis
TraumaticOperative handling, open trauma
IschaemicStrangulated bowel, vascular occlusion
MiscellaneousFamilial Mediterranean fever, endometriosis

Pathogenesis

Intraperitoneal infections arise when a normal anatomic barrier is disrupted - by perforation of appendix, diverticulum, or ulcer; bowel wall weakening from ischaemia, tumour, or inflammation; or adjacent processes like pancreatitis or PID leaking into the peritoneal space.
The peritoneal cavity is large but functionally divided:
  • Upper and lower cavities divided by the transverse mesocolon
  • The greater omentum lines the lower peritoneal cavity
  • Pancreas, duodenum, and ascending/descending colon are in the anterior retroperitoneal space
  • Kidneys, ureters, and adrenals are in the posterior retroperitoneal space
Normally the peritoneal fluid contains <30 g/L protein and <300 WBCs/µL (mainly mononuclear). In bacterial infection, a massive neutrophilic response is mounted.
Fluid circulation: During expiration, peritoneal fluid travels upward toward the diaphragm - bacteria can be absorbed through lymphatic pores in the diaphragmatic peritoneum within minutes. This explains abscesses anatomically remote from the primary site. The most common sites for collection are the pelvis (gravity while standing) and subdiaphragmatic spaces (gravity while recumbent).

Primary (Spontaneous) Bacterial Peritonitis (PBP)

Associations

  • Most common in cirrhosis (alcoholic, post-necrotic, chronic active hepatitis)
  • Also: metastatic malignancy, congestive heart failure, SLE, lymphoedema, nephrotic syndrome in children
  • Occurs in ≤10% of cirrhotic patients with ascites

Pathogenesis

  • Haematogenous spread facilitated by impaired hepatic filtration
  • Deficient complement cascade proteins in cirrhotic ascitic fluid
  • Reduced PMN opsonic/phagocytic activity in advanced liver disease
  • Gut microbiota alterations (increased Enterobacteriaceae), small bowel bacterial overgrowth → bacterial translocation

Microbiology (PBP)

  • Usually single organism
  • Enteric gram-negative bacilli: E. coli (most common)
  • Gram-positives: streptococci, enterococci, pneumococci
  • Anaerobes: uncommon (multiple organisms + anaerobes → reconsider diagnosis, seek secondary source)
  • Emerging concern: ESBL-producing Enterobacteriaceae and gram-positive organisms from quinolone prophylaxis

Diagnosis of PBP

  • Fever in up to 80% of patients
  • Abdominal pain, ascites, peritoneal irritation
  • Subtle cases: malaise, fatigue, encephalopathy, jaundice, AKI without another cause
  • Key criterion: >250 PMNs/µL in ascitic fluid (diagnostic)
  • Single organism on culture

Secondary Peritonitis

Microbiology is mixed flora including anaerobes (contrast with PBP).
Most common organisms: E. coli, streptococci, S. aureus, enterococci, C. perfringens
Pathology (Robbins):
  • Dense neutrophils and fibrinopurulent debris coat the viscera and abdominal wall
  • Serous fluid accumulates, becomes suppurative as infection progresses
  • Subhepatic and subdiaphragmatic abscesses may form
  • Reaction generally remains superficial (except in tuberculous peritonitis)

CAPD-Associated Peritonitis

  • Most common reason for discontinuation of CAPD
  • Organisms: skin flora - Staphylococcus species (~45%), predominantly coagulase-negative; S. aureus in nasal carriers; gram-negative bacilli; Candida spp.
  • Pathogenesis: skin organisms migrate along the catheter
  • Diagnosis: cloudy dialysate with >100 WBCs/µL with >50% neutrophils (or >50% PMNs regardless of absolute count if dwell time is short)
  • Multiple organisms on culture should prompt search for secondary peritonitis

Clinical Features

FeatureDetail
Abdominal painWorse on movement, coughing, deep respiration
ConstitutionalAnorexia, malaise, fever, lassitude
GI upsetNausea ± vomiting
PyrexiaMay be absent
TachycardiaCommon
Abdominal signsTenderness, involuntary guarding, rebound tenderness ("board-like rigidity" in diffuse peritonitis)
Bowel soundsAbsent or reduced (paralytic ileus)
Hippocratic faciesPatient lies still to minimise fluid movement (diffuse peritonitis)
Pelvic tendernessOn rectal/vaginal examination
Referred painShoulder tip pain if subdiaphragmatic (C5 dermatome)
Late signsHypotension, SIRS, MODS, septic shock
Signs may be limited or absent in obese patients or those on immunosuppressive medications.

Investigations

  • CT scan (contrast-enhanced) - investigation of choice; identifies underlying cause, perforation, abscess
  • Erect chest X-ray - identifies subdiaphragmatic free gas (perforation)
  • Lateral decubitus X-ray - alternative if CT unavailable and patient too unwell to sit erect
  • Ultrasound - useful for tubo-ovarian pathology; lacks specificity otherwise
  • Ascitic fluid tap - PMN count and culture (essential in PBP)
  • Laboratory - FBC, CRP, LFTs, renal function, lactate, blood cultures (biomarkers support but are rarely diagnostically specific)
  • Laparoscopy - if above investigations inconclusive

Treatment

General management (Bailey & Love summary)

  1. General care of the patient
  2. Correction of fluid and electrolyte imbalance (IV resuscitation)
  3. Nasogastric tube (decompression) + urinary catheter (monitoring)
  4. Broad-spectrum antibiotics (IV)
  5. Analgesia
  6. Surgery - to remove the underlying cause and lavage residual contamination

Antibiotic regimens

PBP treatment:
  • Cefotaxime 2 g IV every 8 h (or another third-generation cephalosporin) for 5 days
  • Albumin infusion (1.5 g/kg at diagnosis, 1 g/kg on day 3) reduces risk of hepatorenal syndrome
  • Consider ESBL coverage in nosocomial or quinolone-prophylaxis patients
PBP prophylaxis (secondary):
  • Norfloxacin 400 mg/day orally (long-term) in high-risk cirrhotic patients
  • TMP-SMX (double-strength once daily) as alternative
CAPD peritonitis empirical therapy:
  • Cover S. aureus, coagulase-negative staphylococci, and gram-negative bacilli
  • Often: first-generation cephalosporin (e.g. cefazolin) for gram-positives + fluoroquinolone or third-generation cephalosporin (e.g. ceftazidime) for gram-negatives
  • High MRSA areas: vancomycin substituted for cefazolin
  • Administered intraperitoneally

Surgical management

  • Aim: remove underlying cause + lavage/dilute residual contamination
  • Operative findings: reddened, thickened peritoneum with velvety texture; yellow/white fibrin plaques causing bowel adhesion; turbid exudate ± frank pus

Complications

  • Intra-abdominal abscess (subphrenic, pelvic, paracolic)
  • Septic shock and multi-organ failure
  • Hepatorenal syndrome (in PBP/cirrhosis)
  • Ileus (paralytic)
  • Adhesions and bowel obstruction (long-term)
  • Death - without treatment, diffuse peritonitis is uniformly fatal

Special Types

TypeKey Features
Tuberculous peritonitisGranulomatous inflammation; NOT superficial - can be deep and chronic; may have "doughy" abdomen
Bile peritonitisSterile initially, intense chemical irritant; quickly complicated by bacterial superinfection
Pancreatic peritonitisSterile peritonitis from pancreatic enzyme leak; fat necrosis; bowel wall damage allows secondary bacterial spread
Foreign body peritonitisTalc, sutures → granulomas + fibrous scarring
Sclerosing peritonitisDense fibrosis; often IgG4-related disease (Ormond disease equivalent)

Sources:
  • Harrison's Principles of Internal Medicine 22E (2025), Chapter 137
  • Bailey and Love's Short Practice of Surgery 28th Edition, Chapter 65
  • Robbins, Cotran & Kumar Pathologic Basis of Disease, Chapter on Peritoneal Cavity
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