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Peritonitis

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Peritonitis

Peritonitis is inflammation of the peritoneum - the serous membrane lining the abdominal cavity and viscera. It is a potentially life-threatening condition that may be localised or diffuse, acute or chronic, bacterial or chemical.
Intraperitoneal spaces and fluid circulation - showing subphrenic, subhepatic, paracolic, pelvic, and lesser sac compartments with arrows indicating fluid flow and potential abscess sites
Intraperitoneal compartments and fluid circulation pathways - pelvic space, subphrenic spaces (R & L), and Morrison's pouch are the most common sites for abscess formation. (Harrison's Principles, Fig. 137-1)

Classification

By Source

TypeDefinitionKey Features
Primary (Spontaneous)No apparent source of GI contaminationUsually monomicrobial; gram-negatives dominant
SecondaryArises from an identifiable intraabdominal sourcePolymicrobial; gram-negatives + anaerobes
TertiaryPersistent/recurrent peritonitis after treatmentOften drug-resistant organisms, fungi

By Extent

  • Localised - involves a focal area; parietal peritoneal involvement causes somatic pain with guarding and rebound
  • Diffuse (generalised) - involves large regions of the parietes; signifies life-threatening pathology

Causes / Aetiology

Bacterial (most common):
  • Perforation of abdominal viscus (peptic ulcer, appendix, diverticulum, colon in obstruction)
  • Transmural bacterial translocation without frank perforation (pancreatitis, ischaemic bowel, primary bacterial peritonitis)
  • Exogenous contamination (peritoneal dialysis catheters, trauma, open surgery)
  • Female genital tract (pelvic inflammatory disease, salpingitis)
  • Haematogenous spread (rare)
Chemical (sterile initially):
  • Bile leakage - highly irritating, usually complicated by secondary bacterial infection
  • Pancreatic enzymes (acute haemorrhagic pancreatitis) - fat necrosis and enzymatic peritonitis
  • Barium (from contrast studies)
Other:
  • Starch peritonitis (allergic/foreign body reaction to surgical glove powder)
  • Endometriosis (haemorrhage acts as irritant)
  • Ruptured dermoid cysts (keratin-induced granulomatous reaction)
  • Familial Mediterranean fever
  • Bailey and Love's Short Practice of Surgery, 28th Ed., p. 1109
  • Robbins, Cotran & Kumar Pathologic Basis of Disease

Pathophysiology

Normal peritoneal fluid contains <30 g/L protein and <300 WBC/µL (mainly mononuclear). When bacteria or chemical irritants enter the peritoneal cavity:
  1. Early phase - rapid influx of polymorphonuclear leukocytes (PMNs) driven by resident-cell chemokine synthesis
  2. Exudative phase - serous fluid accumulates, becomes turbid, then frankly purulent
  3. Fibrinous phase - fibrin plaques coat viscera and abdominal wall, loops of bowel adhere to each other and to the parietes
  4. Late phase - frank pus, abscess formation in dependent spaces (pelvis, subphrenic, Morrison's pouch), or systemic sepsis/bacteraemia
At surgery the inflamed peritoneum appears reddened, thickened and has a velvety texture, with yellow/white fibrin plaques and turbid exudate.
Harrison's Principles of Internal Medicine, 22e, p. 1113-1114

Primary (Spontaneous) Bacterial Peritonitis (SBP)

Epidemiology: Occurs in ≤10% of cirrhotic patients with ascites. Also seen in nephrotic syndrome (children), congestive heart failure, SLE, and lymphoedema.
Pathogenesis:
  • Haematogenous seeding of ascitic fluid (a good growth medium)
  • Diseased liver + altered portal circulation → defective bacterial filtration
  • Reduced opsonic/phagocytic capacity of PMNs in advanced liver disease
  • Gut dysbiosis with increased Enterobacteriaceae + small intestinal bacterial overgrowth → pathologic bacterial translocation
  • Reduced Paneth cell defensins, portal hypertensive enteropathy
Microbiology: Monomicrobial - E. coli most common; also streptococci, enterococci, Klebsiella. Anaerobes are rare (their presence should prompt reconsideration of the diagnosis toward secondary peritonitis). Important current trend: increasing gram-positive bacteria and ESBL-producing Enterobacteriaceae due to widespread quinolone prophylaxis.
Clinical features:
  • Fever (up to 80% of patients) - most common sign
  • Abdominal pain and peritoneal signs may be present but are often subtle
  • Non-localising symptoms: malaise, fatigue, hepatic encephalopathy, acute kidney injury, jaundice
Diagnosis: Sample peritoneal fluid in any cirrhotic patient with ascites and fever. >250 PMN/µL in ascitic fluid is diagnostic (this threshold does not apply to secondary peritonitis).
Treatment:
  • IV third-generation cephalosporin (e.g., cefotaxime, ceftriaxone)
  • IV albumin (1.5 g/kg at diagnosis + 1 g/kg on day 3) to reduce acute kidney injury and mortality
  • Prophylaxis with norfloxacin in high-risk patients (low-protein ascites, prior SBP episode)

Secondary Peritonitis

The most common form, arising from a perforated or inflamed intraabdominal viscus. It is polymicrobial - aerobic gram-negative bacilli (E. coli, Klebsiella) plus anaerobes (Bacteroides fragilis, C. perfringens) are the rule.

Clinical Features

Localised peritonitis:
  • Pain in the affected region (somatic - parietal peritoneum is extensively innervated)
  • Involuntary guarding (reflex abdominal wall muscle contraction)
  • Rebound tenderness (pain on releasing examiner's hand)
  • Pyrexia and tachycardia
Diffuse peritonitis (surgical emergency):
  • Severe, generalised abdominal pain, worse on movement, coughing, and respiration
  • Patient lies motionless, often with knees drawn up
  • "Board-like rigidity" - entire abdominal musculature in reflex contraction
  • Hippocratic facies (gravely ill appearance)
  • Generalised ileus → abdominal distension
  • Haemodynamic instability: hypotension, tachycardia, fever
  • Progressive confusion → loss of consciousness if untreated
Additional features:
  • Shoulder tip ("phrenic") pain if inflammation reaches the diaphragm - referred via C5 dermatome
  • Pelvic tenderness on digital rectal/vaginal examination if pelvic source
  • Signs may be blunted in obese patients or those on immunosuppressants
Bailey and Love's Short Practice of Surgery, 28th Ed., pp. 1109-1111 Harrison's Principles of Internal Medicine, 22e, p. 1114
Summary of clinical features (Bailey & Love):
  • Abdominal pain, worse on movement, coughing and deep respiration
  • Constitutional upset: anorexia, malaise, fever, lassitude
  • GI upset: nausea +/- vomiting
  • Pyrexia (may be absent)
  • Raised pulse rate
  • Tenderness +/- guarding / rigidity / rebound

Investigations

InvestigationFinding / Purpose
CT abdomen (with contrast)Investigation of choice; identifies source, free gas, collections
Erect CXRSubdiaphragmatic free gas (pneumoperitoneum) in perforation
Lateral decubitus XRAlternative to erect CXR in unstable patients
Abdominal ultrasoundLimited specificity except for tubo-ovarian pathology
FBCLeukocytosis with left shift (band forms)
CRP, procalcitoninSupport diagnosis; rarely diagnostically specific
Ascitic fluid tap (SBP)Cell count >250 PMN/µL is diagnostic; culture in blood culture bottles
LaparoscopyIf CT/USS inconclusive
Peritoneal fluid Gram stainInsensitive for bacteria; useful mainly for early yeast detection

Microbiology Summary

SettingOrganisms
SBP / cirrhosisE. coli, streptococci, Klebsiella (monomicrobial)
Secondary (GI perforation)E. coli, streptococci, S. aureus, enterococci, C. perfringens, Bacteroides (polymicrobial)
Peritoneal dialysis (PD)S. epidermidis (mild), S. aureus, gram-negatives, fungi
Fungal peritonitisCandida spp. (PD patients; immunocompromised)
MycobacterialM. tuberculosis (chronic presentation)

Treatment

Surgical / Interventional (Secondary Peritonitis)

  • Expedient surgical intervention - remove the underlying cause (seal perforation, resect gangrenous bowel, drain abscess)
  • Peritoneal lavage - dilute and evacuate contamination
  • At laparotomy: drain all pus, irrigate, consider open abdomen / "damage control" surgery in severe cases

Antibiotic Therapy

Community-acquired, mild-to-moderate:
  • Piperacillin/tazobactam 3.375 g IV q6h, OR
  • Ticarcillin/clavulanate 3.1 g IV q4-6h, OR
  • Fluoroquinolone (e.g., levofloxacin 750 mg IV q24h) OR ceftriaxone 2 g IV q24h + metronidazole 500 mg IV q8h
Health-care-associated / ICU / severe:
  • Imipenem 500 mg IV q6h, OR
  • Meropenem 1 g IV q8h, OR
  • Piperacillin/tazobactam 4.5 g IV q6h (higher dose), OR
  • Cefepime/ceftazidime 2 g IV q8h + metronidazole
Enterococcal coverage (add if very ill, cephalosporin-based regimen): ampicillin or vancomycin; use linezolid/daptomycin for VRE.
Antifungal coverage: warranted if Candida grows from a sterile site.
Newer agent: Eravacycline (tetracycline class) 1 mg/kg IV q12h - FDA-approved for complicated intraabdominal infections.
Harrison's Principles of Internal Medicine, 22e, p. 1115

Peritonitis in Peritoneal Dialysis (PD-Related)

A distinct and important entity in nephrology:
Diagnosis (requires 2 of 3):
  1. Abdominal pain
  2. Cloudy peritoneal effluent / WBC >100/mm³ (>50% PMN)
  3. Positive culture of dialysis effluent
Routes of infection:
  1. Transluminal (through catheter lumen) - most common
  2. Pericatheter route
  3. Transmural bacterial migration (associated with constipation, diarrhoea, recent colonoscopy, diverticulitis)
  4. Haematogenous spread
  5. Ascending via female genital tract
Key points:
  • S. epidermidis causes milder symptoms than S. aureus or gram-negatives
  • Fungal peritonitis (Candida) is an indication for catheter removal
  • PD-related peritonitis is rarely associated with bacteraemia (unlike surgical peritonitis)
  • Gram stain of effluent is insensitive; culture by inoculating 5-10 mL into blood culture bottles
Brenner and Rector's The Kidney, 2-Volume Set; Comprehensive Clinical Nephrology, 7th Ed.

Complications

  • Intraabdominal abscess formation - subphrenic (R > L due to falciform ligament barrier), subhepatic (Morrison's pouch), pelvic
  • Sepsis syndrome / bacteraemia - especially in secondary peritonitis
  • Paralytic ileus
  • Adhesions - risk of future bowel obstruction
  • Multi-organ failure - in advanced or untreated cases
  • Death - untreated diffuse peritonitis is rapidly fatal

Special Forms

TypeKey Features
Tuberculous peritonitisChronic; granulomatous; reaction typically remains superficial
Fungal (Candida) peritonitisPD patients; immunocompromised; mandates catheter removal
Chemical (bile/pancreatic enzyme)Sterile initially; intense peritoneal reaction; secondary infection common
Eosinophilic peritonitis>10% eosinophils in effluent; early after PD catheter placement or drug reactions
Sclerosing peritonitisDense fibrosis; may represent IgG4-related disease
Familial Mediterranean feverEpisodic, self-limiting sterile peritonitis
Sources:
  • Harrison's Principles of Internal Medicine, 22e (2025), Chapter 137
  • Bailey and Love's Short Practice of Surgery, 28th Ed., Chapter 65
  • Robbins, Cotran & Kumar Pathologic Basis of Disease
  • Brenner and Rector's The Kidney, 2-Volume Set
  • Comprehensive Clinical Nephrology, 7th Ed.
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