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

Type	Definition	Key Features
Primary (Spontaneous)	No apparent source of GI contamination	Usually monomicrobial; gram-negatives dominant
Secondary	Arises from an identifiable intraabdominal source	Polymicrobial; gram-negatives + anaerobes
Tertiary	Persistent/recurrent peritonitis after treatment	Often 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:

Early phase - rapid influx of polymorphonuclear leukocytes (PMNs) driven by resident-cell chemokine synthesis
Exudative phase - serous fluid accumulates, becomes turbid, then frankly purulent
Fibrinous phase - fibrin plaques coat viscera and abdominal wall, loops of bowel adhere to each other and to the parietes
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

Investigation	Finding / Purpose
CT abdomen (with contrast)	Investigation of choice; identifies source, free gas, collections
Erect CXR	Subdiaphragmatic free gas (pneumoperitoneum) in perforation
Lateral decubitus XR	Alternative to erect CXR in unstable patients
Abdominal ultrasound	Limited specificity except for tubo-ovarian pathology
FBC	Leukocytosis with left shift (band forms)
CRP, procalcitonin	Support diagnosis; rarely diagnostically specific
Ascitic fluid tap (SBP)	Cell count >250 PMN/µL is diagnostic; culture in blood culture bottles
Laparoscopy	If CT/USS inconclusive
Peritoneal fluid Gram stain	Insensitive for bacteria; useful mainly for early yeast detection

Microbiology Summary

Setting	Organisms
SBP / cirrhosis	E. 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 peritonitis	Candida spp. (PD patients; immunocompromised)
Mycobacterial	M. 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):

Abdominal pain
Cloudy peritoneal effluent / WBC >100/mm³ (>50% PMN)
Positive culture of dialysis effluent

Routes of infection:

Transluminal (through catheter lumen) - most common
Pericatheter route
Transmural bacterial migration (associated with constipation, diarrhoea, recent colonoscopy, diverticulitis)
Haematogenous spread
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

Type	Key Features
Tuberculous peritonitis	Chronic; granulomatous; reaction typically remains superficial
Fungal (Candida) peritonitis	PD 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 peritonitis	Dense fibrosis; may represent IgG4-related disease
Familial Mediterranean fever	Episodic, 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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