TextbookSurgeryPeritonitis

Peritonitis

Peritonitis is inflammation of the peritoneum, most commonly secondary to perforation of a hollow viscus. It is a surgical emergency with high mortality if untreated.

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Key Facts

Primary peritonitis (spontaneous bacterial peritonitis — SBP): Infection without perforation, typically in ascites (liver cirrhosis); treat with IV cefotaxime 2g TDS Secondary peritonitis: Perforation of hollow viscus (perforated appendix, peptic ulcer, diverticular disease) — requires surgical intervention Tertiary peritonitis: Persistent/recurrent infection after adequate surgical treatment — often nosocomial organisms Clinical features: Board-like rigidity, absent bowel sounds, tachycardia, fever, rebound tenderness Erect CXR: Free air under diaphragm (pneumoperitoneum) — ~80% sensitive for perforation CT abdomen/pelvis is the investigation of choice for identifying source of secondary peritonitis Sepsis 6 pathway should be initiated immediately: Lactate, blood cultures, IV antibiotics, IV fluids, O₂, urine output monitoring Mortality increases significantly with delayed surgical intervention — source control is the surgical priority

Overview

Key Facts

Peritonitis is a critical surgical condition requiring prompt recognition, resuscitation, and usually surgical intervention. The distinction between primary and secondary peritonitis guides management.

Epidemiology

Secondary peritonitis is the most common form. SBP occurs in ~10-30% of hospitalised patients with ascites from liver cirrhosis. Peritonitis carries overall mortality of ~10-20% (higher in elderly, immunocompromised, and delayed presentation).

Aetiology

Primary (SBP): Haematogenous/lymphatic bacterial translocation — usually E. coli, Klebsiella, Streptococcus pneumoniae. Secondary: Perforation (appendicitis, peptic ulcer, diverticulitis, trauma, anastomotic leak), post-operative. Tertiary: Failed source control — Enterococcus, Candida, coagulase-negative staphylococci.

Pathophysiology

  • Peritoneal contamination → intense inflammatory response → fluid sequestration (third-spacing) → hypovolaemia
  • Bacterial proliferation → systemic inflammatory response → sepsis → organ failure
  • Peritoneal membrane has large surface area (~1.7m²) — inflammation causes massive fluid shifts and cytokine release
  • Fibrin deposition may localise infection (abscess) or lead to adhesion formation

Clinical Presentation

Clinical Features

  • Pain: Severe, constant, worsened by movement or coughing
  • Guarding: Involuntary muscular rigidity — board-like in generalised peritonitis
  • Rebound tenderness: Pain on releasing palpation
  • Absent bowel sounds: Paralytic ileus
  • Fever, tachycardia, tachypnoea: Systemic sepsis
  • Lying still: Movement exacerbates peritoneal irritation
  • Distension: From ileus and fluid accumulation

SBP (Primary)

  • Often insidious in cirrhotic patients — may present as worsening ascites, encephalopathy, or renal failure
  • Fever, abdominal pain/tenderness, altered mental status
  • May be clinically silent — maintain high index of suspicion

Red Flags

  • Board-like rigidity — generalised peritonitis, likely perforation
  • Haemodynamic instability — septic shock requiring immediate resuscitation
  • Absent bowel sounds with fever — late presentation
  • Free air on erect CXR — perforation confirmed

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Perforated peptic ulcerSudden epigastric pain, board-like rigidityErect CXR (free air), CT
Perforated appendicitisRIF pain progressing to generalisedCT abdomen, bloods
Perforated diverticulitisLIF pain, elderly patientCT abdomen
SBPKnown cirrhosis/ascitesAscitic fluid analysis (WCC >250/mm³ neutrophils)
PancreatitisEpigastric pain radiating to backAmylase/lipase
Mesenteric ischaemiaPain out of proportion to examination, AFCT angiography, lactate

Diagnosis / Investigation

Bedside

  • Observations: NEWS2 — likely high-scoring
  • Erect CXR: Free air under diaphragm
  • Urine dipstick, β-hCG: Exclude urological/gynaecological cause

Bloods

  • FBC, CRP: Leucocytosis, raised inflammatory markers
  • U&Es, LFTs: Organ function
  • Amylase/lipase: Exclude pancreatitis
  • Lactate: Severity marker for sepsis (>4 mmol/L = severe)
  • Blood cultures: Before antibiotics
  • Coagulation, G&S/crossmatch: Pre-operative
  • ABG/VBG: Acid-base status

Imaging

  • CT abdomen/pelvis with IV contrast: Investigation of choice — identifies source, free fluid, free air
  • Erect CXR: Quick screen for pneumoperitoneum

Special Tests

  • Ascitic tap (SBP): WCC >250 neutrophils/mm³ confirms SBP; send for culture, albumin, protein

Management

Initial Resuscitation (Sepsis 6)

  1. High-flow oxygen
  2. Blood cultures
  3. IV antibiotics: Co-amoxiclav 1.2g IV TDS + metronidazole 500mg IV TDS (or piperacillin-tazobactam 4.5g IV TDS per local protocol)
  4. IV crystalloid fluid resuscitation
  5. Lactate measurement
  6. Urine output monitoring (catheter)

Surgical Management (Secondary Peritonitis)

  • Source control is paramount — laparotomy or laparoscopy
  • Repair perforation (e.g., omental patch for perforated peptic ulcer)
  • Resection of diseased segment (e.g., perforated appendix, sigmoid colon)
  • Peritoneal washout with warm saline
  • May require temporary stoma (e.g., Hartmann's procedure for perforated diverticulitis)
  • Planned relook laparotomy in severe cases

SBP Management

  • IV cefotaxime 2g TDS (or co-amoxiclav) — 5-7 days
  • IV albumin 1.5g/kg at diagnosis, 1g/kg at day 3 (reduces mortality — Sort & Levacher trial)
  • Prophylaxis with ciprofloxacin 500mg OD or norfloxacin after SBP episode (secondary prophylaxis)

Referral Criteria

  • All secondary peritonitis — urgent surgical team
  • ICU referral for organ support
  • SBP — hepatology/gastroenterology

Prognosis

  • Secondary peritonitis: Mortality ~10-20% with timely surgery; increases to >50% if delayed
  • SBP: In-hospital mortality ~20-30%; 1-year mortality ~50-70% (reflects underlying liver disease severity)
  • Anastomotic leak: Mortality ~10-20%
  • Elderly and immunocompromised patients have significantly higher mortality
  • Post-operative adhesions are a common long-term complication

Other Relevant Information

Causes of Pneumoperitoneum

Common CausesLess Common
Perforated peptic ulcerPost-operative (normal up to 7 days)
Perforated diverticulitisPeritoneal dialysis
Perforated appendicitisPneumatosis intestinalis
Traumatic bowel injuryPer-vaginal (post-coital, rare)