Peritonitis and the acute abdomen

• Peritonitis is inflammation of the peritoneum, the serous membrane that lines the abdominal cavity and covers the organs. It is a sign of disease, not a diagnosis, and the causes range from a tiny sealed perforation to diffuse faecal contamination.
• Secondary peritonitis, by far the commonest surgical form, begins when a hollow viscus loses its integrity and gastrointestinal contents (acid, enzymes, bacteria, food) spill into a sterile cavity. The peritoneum's huge surface area turns a local hole into a body-wide inflammatory and septic response.
• Because the cavity is so reactive, the same process can look local and silent in one patient and fulminant in another: only about two-thirds of patients with a perforated peptic ulcer show generalised peritonitis. ^[1]
• The management is simultaneous, not sequential: recognise sepsis, resuscitate, image when it is safe to do so, and obtain source control (drain, repair or remove the leak) before antibiotics alone have to carry the whole load. Antibiotics without source control rarely cure established secondary peritonitis.
• Perforation is uncommon compared with bleeding, but it is the most common reason for emergency operation in peptic ulcer disease and accounts for roughly four in ten ulcer-related deaths. ^[1]

By the end of this page you should be able to:

1. Distinguish primary, secondary and tertiary peritonitis, and spontaneous (primary) peritonitis from surgical ones.
2. Explain why a small hole in the stomach or bowel can produce generalised peritonitis and septic shock.
3. Take a focused history and perform an examination that picks up (and does not miss) peritonitis, especially in older patients.
4. Choose and interpret the appropriate imaging for suspected perforation or peritonitis, and know when imaging should be skipped.
5. Resuscitate to explicit physiological targets and name the qSOFA and SOFA concepts used to grade severity.
6. Decide on the urgency of source control, and choose between non-operative, laparoscopic and open management for a perforated hollow viscus.
7. Plan empirical antimicrobial therapy, including how long to give it, and state when antifungals are justified.
8. Describe the special challenges of postoperative and tertiary peritonitis, and of the immunocompromised and older patient.

The peritoneum has an enormous surface area and is richly supplied with somatic (parietal) and visceral nerves. Irritation of the parietal layer produces the sharp, well-localised, movement-worsened pain that makes patients rigidly still, breathe shallowly and resist any movement of the bed. That is why "peritonitis" is the central physical sign of an acute surgical abdomen rather than a separate disease.

A whole companion topic, "Acute abdomen and intestinal obstruction", covers the general approach to sudden severe abdominal pain: history, examination, red flags, investigation and obstruction. This page complements it by focusing on peritoneal sepsis and perforation — the "septic abdomen" — where the driver of illness is contamination of the peritoneal cavity and the question is usually not "which organ?" but "how much contamination, how sick is the patient, and when do we control the source?"

The peritoneal cavity is not simply a bag. It absorbs water, electrolytes and, importantly, bacteria and endotoxin into the bloodstream through the diaphragmatic lymphatics and the mesenteric veins. Within hours of a perforation the chemical irritant (gastric acid, pancreatic juice, bile) produces a chemical peritonitis that is rapidly joined by a bacterial peritonitis as enteric flora translocate. Fluid shifts from the intravascular space into the peritoneum (third spacing), so the patient can be simultaneously hypovolaemic, febrile and hyperdynamic. That is why sepsis from a perforated peptic ulcer behaves like sepsis from a pneumonia, and why the same lactate, vasopressor and bundle logic applies. ^[3]

Primary peritonitis is uncommon on a surgical ward and is usually managed with antibiotics and drainage of ascites. It is mentioned here so that the two are not confused: a cirrhotic patient with new abdominal pain and ascites has primary peritonitis until proven otherwise, but a patient with peritoneal signs after a perforation has secondary peritonitis and needs a surgeon. ^[2]

Tertiary peritonitis deserves a separate warning. It is not a new disease but secondary peritonitis that has lasted, selected harder organisms (often multidrug-resistant or Candida species) and produced an organ failure that did not settle. Mortality is high. Repeated, fruitless laparotomy in a septic patient who is not improving is one of the most dangerous traps in abdominal surgery. ^[2]

Secondary peritonitis has one essential requirement: a breach. The breach may be a macroscopic hole (perforated peptic ulcer, ruptured diverticulum), a necrotic wall (strangulated hernia, volvulus, mesenteric ischaemia), or a controlled micro-perforation that has sealed and localised as an abscess.

Peptic ulcer disease has a lifetime prevalence of about 5% to 10% and an incidence of 0.1% to 0.3% per year. Complications occur in 10% to 20% of those patients. ^[1] Bleeding is by far the commoner complication — the perforation-to-bleeding ratio is about 1 to 6 — but perforation is the commonest reason for emergency operation and causes about 40% of all ulcer-related deaths. ^[1] Its reported 30-day mortality is a sample size-weighted average of 23.5%, rising with every hour of pre-operative delay. ^[1]

Two points matter for a first-time student. First, the same disease can produce either generalised peritonitis or a localised abscess, depending on how well the omentum and adjacent loops wall it off; an elderly patient may therefore have surprisingly little pain with a large abscess. Second, perforation can be "sealed" — the leak stops because omentum plugs the hole — and those patients are the only ones in whom a carefully selected non-operative plan is realistic. ^[1]

Because most of the published guidance on peritonitis targets this entity, it is worth tracing one case:

1. A chronic duodenal (or gastric) ulcer erodes through the full thickness of the wall.
2. Gas and fluid enter the peritoneum suddenly; some patients describe pain that peaks within seconds, but only about 47% of older patients report that sudden onset. ^[4]
3. Peritoneal irritation may be local only at first (epigastric guarding), then generalises; generalised peritonitis is present in only about two-thirds of patients. ^[1]
4. Chemical peritonitis dominates early; bacterial peritonitis (polymicrobial, enteric) develops over hours.
5. Fluid shifts and third spacing produce tachycardia, hypotension and oliguria; lactate rises.
6. Without source control the process becomes an intra-abdominal abscess, then tertiary peritonitis, then multi-organ failure.

Ask the patient (or a relative) to tell the story, then fill the gaps. The pattern matters more than any single symptom.

• Onset: sudden versus gradual. Sudden maximal pain that "hits like a lightning bolt" suggests perforation, ruptured aneurysm, torsion or volvulus. In older patients, slower onset does not exclude perforation. ^[4]
• Pain that worsens with movement, coughing or a bumpy ride means peritoneal irritation. ^[4]
• Rigidity and the "board-like" abdomen are late but serious signs; in patients over 70, epigastric rigidity occurs in only about one-fifth of proven perforated ulcers. ^[4] Ageing blunts abdominal wall tone and the inflammatory response.
• Associated features: fever (often absent early), anorexia, vomiting, inability to pass flatus, diarrhoea (which does not exclude obstruction or perforation), dizziness, confusion.
• Risk factors: peptic ulcer symptoms or NSAID/aspirin use, steroid use, Helicobacter pylori (not always tested acutely), previous surgery, immunosuppression, cirrhosis, dialysis, vascular disease.
• In women of childbearing age, pregnancy must be excluded.

• General appearance and posture: a patient lying perfectly still, knees drawn up, breathing shallowly, is protecting a peritoneum. Conversely, an elderly, well-looking patient can still have a sealed perforation.
• Vital signs: tachypnoea (chest disease or metabolic acidosis from ischaemic bowel), tachycardia, fever (absent in over 30% of appendicitis and in most cholecystitis), hypotension. ^[4]
• Inspection: scars, distension, hernias, Cullen (periumbilical) and Grey Turner (flank) bruising, skin changes.
• Palpation: localised tenderness first, then generalised; look for guarding that does not relax on inspiration (involuntary), rebound and percussion tenderness. Indirect tests such as the cough test are at least as useful as traditional rebound testing, which has high sensitivity but low specificity. ^[4]
• Auscultation is optional and brief: silence late in the illness suggests ileus or a catastrophe; high-pitched tinkling suggests early small-bowel obstruction.
• Adjuncts: rectal and pelvic examination when indicated, hernial orifices, testes, chest and back.

QSOFA is a bedside screen: 2 or more of (i) respiratory rate more than 22 breaths per minute, (ii) systolic pressure under 100 mmHg, (iii) altered consciousness (Glasgow Coma Scale under 15). ^[3] It is not a replacement for clinical judgement but a prompt to act. SOFA scores six organ systems (respiration, coagulation, liver, cardiovascular, central nervous system, renal) from 0 to 4 each; an increase of 2 or more in the SOFA score from baseline defines sepsis in the Sepsis-3 scheme. ^[2]

This is the single most important prognostic idea in this topic, and the numbers come from the WSES intra-abdominal infection consensus: ^[2]

• No sepsis: about 1.2% mortality
• Sepsis only: about 4.4%
• Severe sepsis: about 27.8%
• Septic shock (vasopressor to maintain a mean arterial pressure of at least 65 mmHg and lactate above 2 mmol/L in the absence of hypovolaemia): about 67.8% ^[2]

Abdominal infections overall carry a hospital mortality of about 23% to 38%, and are the second most common cause of sepsis-related death. ^[3]

A "medical" abdomen can still be a surgical one. Diabetic ketoacidosis, hypercalcaemia, Addison disease, sickle cell crisis, uremia, lead poisoning, acute intermittent porphyria and methanol toxicity can all produce severe abdominal pain with an unremarkable or confusing examination. Thoracic disease (myocardial infarction, basal pneumonia, pulmonary embolism, aortic dissection) also refers pain to the abdomen. Gynaecological emergencies (ectopic pregnancy, ovarian torsion) are non-negotiable exclusions in women of childbearing age.

Investigations run in parallel with resuscitation; a negative test never excludes a high-probability diagnosis. ^[2]

• Arterial (or venous) blood gas: acid-base status, anion gap, lactate, glucose, electrolytes. Lactate is raised in bleeding or ischaemia and is both a target and a marker of severity.
• Full blood count: anaemia, leukocytosis (which can be normal in severe infection).
• Urea and electrolytes, creatinine: dehydration, renal impairment, the vomiting alkalosis of pyloric outlet obstruction.
• Liver function and bilirubin: biliary or hepatic disease (any source of "medical" abdomen).
• Lipase: preferred for pancreatitis.
• C-reactive protein and procalcitonin: support the inflammatory picture; procalcitonin is useful to guide the duration and cessation of antibiotics, particularly once source control has been achieved. ^[3]
• Coagulation profile and group and save, plus blood cultures before antibiotics whenever feasible. ^[3]
• Urine dipstick/culture; pregnancy test in any woman who could be pregnant.

A chest radiograph plus an abdominal film or decubitus view is a fast, pragmatic test:

• Free air under the diaphragm, air-fluid levels, calcified aneurysm, radio-opaque stones.
• Free air is present in roughly 30% to 85% of perforations, depending on the series; a plain film therefore misses many. ^[1]
• Useful when CT is unavailable or delayed, or when a single finding (free air with peritonitis) would already mandate operation. ^[1]

Ultrasound is the study of first choice for many acute abdomens, particularly in pregnancy, because it is bedside, rapid, radiation-free and operator-dependent. It identifies focal peritoneal fluid, abscess, gallbladder and gynaecological causes, and can show free air in skilled hands. Its sensitivity drops with obesity, ileus and free intraperitoneal gas. ^[2]

Contrast-enhanced CT is the imaging study with the highest sensitivity and specificity for the acute abdomen and for perforation, and should generally use intravenous contrast. ^[2] It can show the site and size of a leak, the cause, free fluid and air, collections amenable to drainage, and ischaemic bowel (see CT angiography for mesenteric ischaemia). Oral contrast rarely helps acutely and delays imaging; water-soluble contrast given orally or via nasogastric tube is reserved for detecting whether a perforation has sealed. ^{[1] [2]}

Important caveats:

• Up to about 12% of perforations have a normal CT scan. If clinical suspicion remains, a triple-contrast study (oral or nasogastric water-soluble contrast) improves detection. ^[1]
• CT should not delay life-saving care in an unstable, peritonitic patient. If free air and generalised peritonitis are already present, the operating theatre is the next destination, not the scanner.
• In pregnancy, ultrasound first; MRI (usually without contrast) is the next step for a stable patient to limit fetal radiation. ^[2]

When history, examination and imaging leave an acute intra-abdominal problem undiagnosed (roughly a quarter of cases), diagnostic laparoscopy has very high sensitivity, specificity and accuracy (about 86% to 100% in unselected patients), permits treatment in most cases and reduces unnecessary laparotomy. It is contraindicated in diaphragmatic rupture and in the haemodynamically unstable patient. ^[2]

Abscesses up to about 3 to 6 cm in maximum diameter may be treated with intravenous antibiotics alone in selected patients; larger or symptomatic collections generally need percutaneous (or surgical) drainage. ^[3]

Resuscitation and diagnosis are simultaneous, and resuscitation must never be deferred for imaging. ^[2]

Follow the sepsis logic (quoted in the 2024 Bova review of intra-abdominal infection): ^[3]

• Sepsis without shock: empirical broad-spectrum antimicrobial within about 3 hours of recognition.
• Septic shock or high likelihood of sepsis: antibiotics immediately, ideally within about 1 hour. ^[3]
• Aim for an initial mean arterial pressure of 65 mmHg, with fluids and vasopressors as needed.
• In unstable perforated-peptic-ulcer patients specifically: mean arterial pressure of at least 65 mmHg, urine output of at least 0.5 mL/kg/h, and normalisation of lactate. ^[1]

Practical steps:

1. Position, airway, oxygen, monitoring, two large-bore cannulae.
2. Crystalloid resuscitation (blood products if there is haemorrhage), correcting electrolyte abnormalities; use cautious vasopressors to keep the mean arterial pressure at 65 mmHg or above once adequate filling has been given.
3. Adequate analgesia, including opioids, early. Analgesia does not obscure the diagnosis and is part of good care.
4. Nil by mouth, antiemetics, nasogastric tube if vomiting or obstruction.
5. Broad-spectrum antibiotics covering Gram-negative enteric organisms; add anaerobic cover for colonic or perforated sources. ^{[2] [4]}
6. Venous thromboembolism prophylaxis once bleeding is controlled; type and cross-match anyone who may need blood.
7. Repeat examination and repeated lactate. The abdomen changes over time, and a deteriorating examination after fluids is often the most important finding.

Antibiotics are necessary but not sufficient. The cure of secondary peritonitis is control of the source: closure or resection of the perforation, drainage of pus, debridement of necrotic bowel, and removal of a gangrenous organ. The delay from admission to surgery matters: in a large Danish series of perforated ulcers, every hour of delay was associated with an adjusted 2.4% drop in the probability of survival compared with the previous hour, and operating within 24 hours of onset carried no observed mortality in one series, versus beyond 48 hours. ^[1] Generalised peritonitis is an indication to operate without waiting for complete diagnostic certainty. ^{[1] [2]}

The general principle of source control "as soon as possible" translates into three levels of urgency: ^[3]

• Emergent: mandatory, as soon as feasible — extensive peritonitis, septic shock, strangulated or ischaemic bowel, uncontrolled haemorrhage.
• Urgent: can be delayed for up to about 24 hours to optimise the patient with fluids and broad-spectrum antibiotics — localised infection without systemic inflammation.
• Delayed: postponed until the process is well defined — a stable patient with localised, contained disease and low risk.

Source control should not be delayed beyond about 24 hours in a localised infection if appropriate antimicrobial therapy is given, and it should happen as soon as possible in extensive peritonitis. ^[3]

• Laparoscopy is appropriate for a contained leak in a stable patient, small perforations with minimal contamination, and for diagnostic purposes. It reduces wound complications and recovery time when conditions are favourable. ^{[1] [2]}
• Laparotomy is preferred for generalised purulent or faecal peritonitis, large perforations (about 2 cm or more), haemodynamic instability, dense adhesions, or when ischaemia or necrosis must be excluded and bowel resected. ^[1]
• Damage-control surgery (abbreviated laparotomy, packing, temporary closure with negative-pressure dressing, planned second look) is reserved for the unstable patient in whom a full definitive repair would be lethal; enteric fistula occurs in roughly 14% with negative pressure. ^[3]
• Non-operative management of a perforated peptic ulcer is not routine. It can be considered in an extremely selected patient whose perforation has sealed on water-soluble contrast (no leak), with normal vital signs and no peritonitis or sepsis, under repeated clinical and laboratory surveillance and with readiness to operate. The components are nil by mouth, intravenous hydration, nasogastric decompression, acid suppression (proton-pump inhibitor), intravenous antibiotics, and follow-up endoscopy at 4 to 6 weeks. Caution is advised in patients over 70 years. ^[1]
• Endoscopic treatment (clipping, sealing, stenting) is not recommended for perforated peptic ulcer in most situations. ^[1]

Risk scores such as Boey, PULP and ASA can be adopted to stratify patients and predict outcome after perforated peptic ulcer, although none is perfect; hypoalbuminaemia remains a strong single predictor of mortality. ^[1] Damage-control and second-look decisions belong to the experienced surgical team.

Antibiotics are a pillar of treatment, not the whole treatment. ^{[2] [3]}

• Community-acquired infections in a non-severe patient: combinations such as piperacillin/tazobactam or a third-generation cephalosporin plus metronidazole remain reasonable empirical broad-spectrum choices in many settings; local resistance (extended-spectrum beta-lactamases, Enterobacteriaceae) must guide selection. ^[3]
• Healthcare-associated or severe sepsis: broader empirical cover (including combinations or carbapenems) is appropriate, with de-escalation once cultures and antibiograms return. ^[3]
• Cultures from the site of infection should be taken before antibiotics in critically ill or healthcare-associated cases so that the regimen can be expanded or narrowed. ^[3]
• Antifungals: empirical antifungal cover (for Candida species) is not recommended in community-acquired intra-abdominal infection, except in immunocompromised patients. Reserve it for patients with intra-abdominal signs of infection and major risk factors — recent abdominal surgery, tertiary peritonitis from anastomotic leak, or necrotising peritonitis. ^[3]
• Duration: a single pre-operative dose is as effective as multiple doses in uncomplicated infection (such as uncomplicated appendicitis or acute cholecystitis) once source control is adequate; complicated intra-abdominal infection and postoperative peritonitis respond to a short course (median of about 8 days versus 12 days, with no benefit from continuation to about 15 days in one randomised trial). ^[3]
• Monitoring: reassess daily; use clinical status and biomarkers such as procalcitonin to guide stopping; prolong therapy only for documented uncontrolled or unknown sources, and then look again for an undrained collection. ^[3]
• Pharmacokinetic awareness: sepsis produces a "third spacing" dilution for hydrophilic antibiotics (beta-lactams, aminoglycosides, glycopeptides), requiring higher loading doses; lipophilic drugs (fluoroquinolones, tetracyclines) usually need standard loading. ^[3]

Drug doses, interval and exact regimen follow local microbiology, resistance patterns and formulary: check the hospital antibiogram and national sepsis bundle before prescribing any drug by name.

Postoperative peritonitis carries excess mortality from three independent sources: an atypical, late presentation due to muted signs (steroids, analgesia, age), severe underlying comorbidity, and multidrug-resistant organisms and Candida. ^[2] It must be suspected when a patient worsens or fails to improve after an apparently adequate operation, especially if the bowel leaks from an anastomosis. Re-laparotomy is sometimes needed, but only after resuscitation, imaging and multidisciplinary discussion; repeated operation without a clear source deepens the problem.

Tertiary peritonitis, as noted earlier, is not a separate disease. It is secondary peritonitis that persists beyond 48 hours after good source control, usually with multidrug-resistant or Candida organisms, in the immunocompromised or critically ill. Its mortality is high. Palliation becomes the right conversation for patients with accumulated risk factors (very high age, severe disease on presentation, septic shock). ^[2]

• Older adults: pain may be mild, rigidity and fever often absent, and presentation late. Mortality is high. Investigate aggressively and lower the threshold for CT and surgical consultation. ^{[1] [2] [4]}
• Pregnancy: ultrasound first, then MRI for a stable patient; operate when indicated on both obstetric and surgical grounds. Appendix, ectopic pregnancy and ovarian torsion remain important differential diagnoses.
• Immunocompromised and neutropenic patients: signs are muted, fungal peritonitis is more likely, CT is usually justified, and a multidisciplinary (or tertiary) team should be involved early. ^[3]
• Low-resource settings: bedside ultrasound, careful repeated clinical assessment, and the same principles of airway/breathing/circulation, antibiotics and source control carry most of the diagnosis and management; plain film and contrast studies (water-soluble) fill the gap where CT is unavailable. Early transfer for mesenteric ischaemia or high-grade sepsis is valuable. ^{[2] [3]}

• Peritonitis is inflammation of the peritoneum; secondary peritonitis from a perforated or necrotic viscus is the commonest surgical form and requires both antibiotics and source control. ^[2]
• Only about two-thirds of patients with a perforated peptic ulcer show generalised peritonitis; a sealed perforation can present with little or no peritoneal sign. ^[1]
• Perforation is about one-sixth as common as bleeding in peptic ulcer disease but causes roughly 40% of ulcer-related deaths; 30-day mortality is about 23.5%. ^[1]
• Abdominal infection mortality rises steeply with sepsis severity: about 1.2% with no sepsis, 4.4% with sepsis, 27.8% with severe sepsis and 67.8% with septic shock. ^[2]
• Overall intra-abdominal infection hospital mortality is about 23% to 38%, and abdominal infections are the second most common cause of sepsis-related death. ^[3]
• Free air is seen on plain film in roughly 30% to 85% of perforations; contrast-enhanced CT is the investigation of highest sensitivity and misses up to about 12%. ^{[1] [2]}
• Treat to explicit targets: mean arterial pressure at least 65 mmHg, urine output at least 0.5 mL/kg/h, normalised lactate, in parallel with source control. ^{[1] [3]}
• Antibiotics within about 3 hours for sepsis without shock, and within about 1 hour (or immediately) for septic shock, quoting the Surviving Sepsis Campaign 2021 as recorded in the 2024 intra-abdominal infection review. ^[3]
• Source control is the cure: emergent for extensive peritonitis or shock, urgent (up to about 24 hours) for localised disease, never later than about 24 hours for localised disease on antibiotics. ^[3]
• Every hour of delay in a perforated ulcer is associated with an adjusted 2.4% drop in the probability of survival compared with the previous hour (large Danish series, 2688 patients). ^[1]
• Abscesses of about 3 to 6 cm maximum diameter may be treated with antibiotics (with or without percutaneous drainage) in selected patients. ^[3]
• Complicated and postoperative infections need only a short course of antibiotics (median about 8 vs 12 days); uncomplicated single dosing is enough once source control is adequate. ^[3]
• Empirical antifungals are not routine in community-acquired infection; reserve them for immunocompromised patients or major risk factors such as postoperative leaks. ^[3]
• Tertiary peritonitis is secondary peritonitis persisting beyond 48 hours after adequate control, often with multidrug-resistant or Candida organisms; its mortality is high. ^[2]

Acute abdomen and intestinal obstruction; acute appendicitis; acute diverticulitis; acute mesenteric ischaemia; perforated peptic ulcer disease; peptic ulcer disease; intra-abdominal abscess; sepsis and septic shock; abdominal tuberculosis; intestinal obstruction; hernias; strangulated bowel; postoperative complications; enhanced recovery after surgery; imaging and surgery in pregnancy.