Surgical sepsis and intra-abdominal infection

• Surgical sepsis is sepsis that originates in the abdomen or after an operation. The commonest sources are secondary peritonitis, intra-abdominal abscess, and anastomotic leak.
• The underlying problem is spilled or trapped gut organisms and their toxins in a space (the peritoneum) that is normally sterile. Local inflammation can wall off the spill, but uncontrolled spread produces bacteraemia and septic shock.
• A diagnosis is usually clinical: pain, guarding, rigidity, fever, tachycardia and a rising lactate. Imaging confirms depth and containment; it must not delay resuscitation or source control in an unstable patient.
• Treatment has four parts that start together: resuscitate to a perfusion target, give broad-spectrum antibiotics quickly, achieve source control by drainage or surgery, and monitor for response and complications.
• Antibiotics are short when source control is good, typically 4 days after adequate control, and prolonged when the source is uncontrolled or the patient is not improving. ^[2]

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

1. Define peritonitis and distinguish primary, secondary and tertiary peritonitis.
2. Explain the pathophysiology from a gut spill to peritoneal inflammation, abscess formation and sepsis.
3. Recognise secondary peritonitis and anastomotic leak early and know when imaging helps or harms.
4. Choose initial antibiotics and duration by source, severity and risk of resistant organisms.
5. Plan source control: when to drain percutaneously, when to operate early, and what damage control means.
6. Apply sepsis goals and low-resource adaptations confidently.

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection.^[1] Sepsis that begins in the abdomen therefore has two failures at once: the original source leaks organisms and toxins, and the host response injures the patient's own organs. Surgeons and intensivists manage both failures together.

Peritonitis is inflammation of the peritoneum. It is classified by origin:

This page covers all three. It is a curriculum gap topic, so it is written as a standalone clinical reference and cross-checks the infectious disease sepsis page rather than repeating it.

Secondary peritonitis accounts for 1 in 100 urgent or emergent hospital admissions and is the second leading cause of sepsis in intensive care units worldwide. Overall mortality is 6 percent, but rises to 35 percent when severe sepsis develops.^[3] In a large European review of complicated intra-abdominal infections, 21 percent were nosocomial and more than 99 percent of those were due to anastomotic leak.^[3] Colorectal anastomoses accounted for 40 percent of leaks, gastroduodenal 32 percent, biliary 15 percent, pancreatic 11 percent and urinary 2 percent.^[3]

In decompensated cirrhosis, spontaneous bacterial peritonitis affects up to 16.3 percent of patients admitted to liver units, with a mortality of 10 to 32.6 percent.^[6] Outpatients undergoing large-volume paracentesis have a very low prevalence, between 0 and 0.5 percent.^[6]

Risk factors are those that encourage spillage, delay recognition or impede clearance.

• Anatomic: appendicitis, diverticulitis, peptic ulcer disease (including perforation), inflammatory bowel disease, adhesions and strangulated hernias.
• Postoperative: anastomotic leak, especially colorectal, biliary and pancreatic; bile or urine leaks; and retention of devitalised tissue after a first operation.
• Metabolic and host: older age, diabetes, malignancy, HIV, corticosteroid or other immunosuppressant use, chronic liver or kidney disease, hypoalbuminaemia, previous broad-spectrum antibiotics, and prolonged hospital stay.
• Drugs and devices: non-steroidal anti-inflammatory drugs in ulcer disease, peritoneal dialysis catheters, central lines and drains.

Postoperative patients exposed to broad-spectrum antibiotics in the previous 3 months, or with a preoperative hospital stay longer than 5 days, are at higher risk of resistant organisms; exposure to a solid organ transplant, liver or lung disease and a duodenal source add further risk.^[3]

The peritoneum consists of a monolayer of mesothelial cells over a semipermeable membrane. It allows passive exchange of water and solutes and clears particles through lymphatic stomata concentrated on the diaphragm. Primary peritonitis is usually a monomicrobial aerobic infection, whereas secondary peritonitis is polymicrobial.^[3]

A perforated viscus or anastomosis spills organisms, bile, gastric acid, pancreatic enzymes and faecal material into that space. Pattern-recognition receptors on mesothelial and immune cells release tumour necrosis factor alpha, interleukin 1 and interleukin 6; neutrophils arrive within 2 to 4 hours and dominate from 48 to 72 hours. Locally this inflammation is useful: coagulation deposits fibrin and the greater omentum wraps the contamination, encouraging abscess formation. If that containment fails, organisms and mediators reach the diaphragmatic lymphatics and then the bloodstream, producing bacteraemia and septic shock.^[3] A strong local response therefore protects, but once it becomes systemic it is lethal.

Tertiary peritonitis represents secondary peritonitis that remains or returns more than 48 hours after source control, usually in a critically ill patient with a persistent inflammatory and immunosuppressive state. Its flora are commensals and opportunists rather than the usual enteric polymicrobial mixture.^[3]

Secondary peritonitis usually begins as sudden, severe, sharp pain that is worse with movement or coughing and eased by lying still. Visceral peritonitis is more vague and colicky at first and localises only when the parietal peritoneum is involved. Typical accompaniments are nausea, vomiting, fever, inability to pass stool or flatus, and severe malaise. Older patients may present mainly with confusion or falls rather than pain.

Look for guarded or rigid abdomen, rebound tenderness, distension, absent bowel sounds, and tachycardia. Classify the distribution:

• Generalised peritonitis: rigidity or rebound in all four quadrants.
• Localised peritonitis: peritoneal signs in one or two quadrants, often with a contained abscess.

Localised disease with a stable patient can be managed selectively. Generalised peritonitis, or any localised peritonitis with haemodynamic instability, demands urgent operation after resuscitation.^[3]

Primary (spontaneous) peritonitis is suggested by new abdominal pain or tenderness, fever, confusion or renal deterioration in a patient with cirrhosis and ascites. The abdomen need not be rigid; many patients simply feel unwell and deteriorate quietly.

Anastomotic leak usually declares itself between day 3 and postoperative day 10 as fever, tachycardia, ileus, increasing pain, wound or drain discharge, rising inflammatory markers or a sudden change in drain fluid. A sudden change in drain output, a faecal wound discharge or a rising C-reactive protein should prompt early imaging even when the abdomen is soft.

The surgical sepsis that matters is separated from uncomplicated infection and from mimics:

• Uncomplicated gastroenteritis, appendicitis or cholecystitis without peritonitis.
• Non-infectious peritonitis: pancreatitis, ruptured ectopic pregnancy, haemoperitoneum, leaking aneurysm.
• Malignancy, mesenteric ischaemia, volvulus.
• Pelvic inflammatory disease and tubo-ovarian abscess.
• Postoperative infection elsewhere: pneumonia, urinary tract infection, line infection.

The bedside distinction is: a patient with organ dysfunction and abdominal findings that could be infection must be treated as sepsis until infection is excluded, while still pursuing non-infectious causes in parallel.^[1]

Severity comes before diagnosis in an unstable patient.

1. Clinical triage: heart rate, blood pressure, respiratory rate, temperature, oxygen saturation, mental state, urine output and lactate. Generalised peritonitis or instability means resuscitation and early surgery, not a long work-up.^[3]
2. Blood tests: full blood count, urea and electrolytes, creatinine, liver function tests, coagulation screen with platelets, glucose and arterial or venous blood gas. Lactate is trended to judge global perfusion, not to diagnose intestinal ischaemia on its own.^[1][3]
3. Blood cultures: at least two sets when this does not delay antibiotics by more than about 45 minutes.^[1]
4. Imaging in stable patients: ultrasound or computed tomography to find and measure collections, free air, leak and the extent of peritoneal contamination. CT is the more accurate test; ultrasound is often the first step in many pathways and reserves CT for equivocal or high-risk cases. Stable patients with localised peritonitis and findings of a contained process can be handled by limited drainage or conservative management.^[2][3]
5. Anastomotic leak: CT with intravenous, oral and, where tolerated, rectal contrast; a para-anastomotic collection with gas, and careful review for free fluid and oral contrast outside the lumen. Drain output and its biochemical composition help.
6. Primary peritonitis: diagnostic paracentesis in all patients with cirrhosis and ascites admitted as an emergency, even without symptoms. A polymorphonuclear cell count above 250 cells per mm3 is highly suspicious, and a count below 250 cells per mm3 excludes the diagnosis. A subtraction of one cell per 250 red cells is used in haemorrhagic ascites. The ascitic fluid is cultured in aerobic and anaerobic bottles at the bedside before antibiotics are started.^[6]
7. Intra-abdominal cultures: fluid from the source is obtained whenever source control is performed in hospital-acquired or at-risk community-acquired infections or in critically ill patients; uncomplicated appendicitis without a perforated or gangrenous appendix does not routinely need cultures.^[2][4]

A complicated intra-abdominal infection is defined above.^[4] Other useful constructs:

• qSOFA (bedside screen): any two of respiratory rate 22 breaths per minute or more, altered mentation (Glasgow Coma Scale below 15), or systolic blood pressure 100 mm Hg or less. It is a screen for poor outcome, not a definition of sepsis.^[1]
• Sepsis and septic shock: as defined in the infectious disease sepsis topic. In brief, organ dysfunction is an acute Sequential Organ Failure Assessment score increase of 2 points or more from infection; septic shock adds persistent hypotension requiring vasopressors to keep a mean arterial pressure of at least 65 mm Hg, with lactate above 2 mmol per litre after adequate fluid.^[1]
• Severity scoring: the Infectious Diseases Society of America suggests APACHE II within 24 hours of hospital or intensive care admission for adults with complicated intra-abdominal infection. The World Society of Emergency Surgery Sepsis Severity Score, being specific to this condition, is an acceptable alternative. No paediatric cIAI-specific score can be recommended at present.^[4]
• Anastomotic leak severity (practical): small contained leaks with collections under 3 cm; larger collections above 3 cm likely needing percutaneous or surgical drainage; major dehiscence with peritoneal soiling; and leak complicated by septic shock. Management follows stability and size of collection.

Sepsis and septic shock are medical emergencies and treatment begins on recognition.^[1][3]

• Give at least 30 mL per kilogram of intravenous crystalloid within the first 3 hours for sepsis-induced hypoperfusion or septic shock.^[1]
• Target mean arterial pressure 65 mm Hg, using dynamic measures of fluid responsiveness rather than static pressures, and trend lactate. Norms used in one large review include central venous pressure 8 to 12 mm Hg, mean arterial pressure at least 65 mm Hg, urine output at least 0.5 mL per kilogram per hour, mixed venous oxygen saturation of 65 percent and normalising lactate.^{[3] [1]}
• Take blood cultures before antibiotics when this adds no substantial delay (under about 45 minutes).^[1]
• Broad-spectrum antibiotics within 1 hour if septic shock or a high likelihood of sepsis is present; if there is possible sepsis without shock, reassess rapidly and give antibiotics within 3 hours if concern persists.^[1][3]
• Resuscitate before and during any operation; a patient who cannot be stabilised despite fluids, antibiotics and vasopressors has a negligible chance of survival from surgery.^[3]

Empiric therapy is always started before culture results are available. It must cover aerobic Gram-negative bacilli (especially Enterobacteriaceae), aerobic streptococci and obligate anaerobes; anaerobic coverage may not be needed with a straightforward upper gastrointestinal source.^[2] Additional coverage for enterococci should be considered in postoperative infections.^[2]

Selection follows three considerations:

1. Local resistance and individual risk. Hospital or intensive care acquisition, corticosteroid use, organ transplantation, liver or lung disease, prior broad-spectrum antibiotics, ESBL colonisation in the last 90 days, and preoperative stay above 5 days all push toward anti-resistance coverage. Peritoneal fluid cultures guide escalation and de-escalation.^[2]
2. Source. Lower (community) and postoperative (hospital) infections differ in organism profile. Enterococci and candida are more likely in postoperative leaks. Empiric antifungal cover should be considered in critically ill patients with recurrent surgery or leak-related peritonitis.^[3]
3. Severity. In septic shock, broader initial regimens and MRSA coverage when suspected are justified; in mild, contained infection, narrower agents and shorter courses suffice.

Duration is defined by source control:

• For complicated intra-abdominal infection after adequate source control, 4 days of fixed-duration therapy is sufficient; longer courses until all physiological abnormalities resolve added no benefit in a large trial.^[2][5]
• For postoperative intra-abdominal infection in the intensive care unit, 8 days was equivalent to 15 days in a multicentre trial, with more antibiotic-free days and no difference in 45-day mortality.^[2]
• Patients with ongoing signs of infection or systemic illness beyond 5 to 7 days usually warrant imaging or re-operation to find an uncontrolled source or treatment failure.^[2]
• Primary peritonitis is treated with intravenous third-generation cephalosporins (such as cefotaxime or ceftriaxone) for about 5 days; intravenous albumin reduces hepatorenal syndrome and improves survival. Outpatients with mild disease can be treated with oral quinolones.^[6]
• Empiric anastomotic leak regimens that broadly cover gut flora (for example, piperacillin-tazobactam, or a later-generation cephalosporin such as ceftriaxone plus metronidazole) are continued for about 4 days if source control is achieved.^[5]

Source control is the physical elimination of the focus of infection and the restoration of optimal function of the affected area: drainage of pus or infected fluid, debridement of devitalised tissue, resection or repair of a perforated viscus, or removal of an infected organ. Without it, antibiotics have little effect.^[2]

• A specific anatomic diagnosis requiring source control should be identified or excluded as rapidly as possible in septic patients, and the intervention undertaken as soon as medically and logistically possible.^[1][2]
• In septic patients undergoing source control for intra-abdominal infection, delays of only 3 to 6 hours have been associated with increased mortality.^[2]
• Approaches: bedside ultrasound- or CT-guided percutaneous drainage for accessible collections; laparotomy for generalised or unstable disease; resection of the infected organ (appendix, gallbladder) where that is the source; debridement and lavage for necrosis. ^[2]
• Abscess size: small contained collections under 3 cm can often be managed with antibiotics and bowel rest; collections above 3 cm likely need percutaneous drainage; incomplete drainage fails. ^[3][5]
• Between operations, an on-demand relaparotomy strategy is usually preferred to a planned re-laparotomy: fewer procedures, shorter intensive care and hospital stay, and equivalent outcomes, with repeated imaging guiding decisions. ^[2]
• Open abdomen and damage control: deliberately leaving the abdomen open carries fistula and loss-of-domain risk. Negative-pressure temporary closure and definitive closure within about 7 days reduce this risk when the abdomen cannot be closed at the first operation. ^[2]
• Laparoscopic lavage can be considered in selected haemodynamically stable patients with purulent (not faecal) peritonitis from perforated diverticulitis, but re-interventions are more common. ^[3]

• Give intravenous third-generation cephalosporins such as cefotaxime or ceftriaxone for about 5 days, with intravenous albumin. Outpatients with mild disease may take oral quinolones. ^[6]
• Do not perform surgery for uncomplicated spontaneous bacterial peritonitis; operate only when secondary peritonitis cannot be excluded (for example, free air, multiple organisms, or failure to respond).
• Treat hepatorenal risk with albumin early in the course. ^[6]

• Stable, contained leak: bowel rest, broad antibiotics, percutaneous drainage for collections above 3 cm. Small leaks under 3 cm often seal with antibiotics alone. ^[5]
• Unstable patient or generalised peritonitis: resuscitation, broad antibiotics, and expeditious surgery. ^[5]
• Operative options: for a clinically stable patient with a minor defect and minimal contamination, repair and proximal diversion; for a major defect, resection of the anastomosis, usually with an end stoma or redo with diversion; for an unstable patient, a damage-control approach with para-anastomotic drainage and proximal diversion, or Hartmann procedure if accessible. Revision of the anastomosis in an unstable patient is discouraged. ^[5]
• Newer endoscopic options, such as vacuum-assisted rectal drainage or stenting with drainage of the collection, can be useful in stable patients with pelvic collections, but they lack large trial data. ^[5]
• Proximal diversion protects future reconstructive options; whether a loop ileostomy or a colostomy is used depends on stool burden and future reconstruction. ^[5]

Review the clinical trajectory, inflammatory markers, lactate and imaging daily. De-escalate once cultures and sensitivities return, and stop antibiotics when source control is secure and the patient is improving. ^[2] If improvement stalls after 5 to 7 days, search for an undrained collection or persistent spillage. ^{[2] [4]}

• Sepsis and septic shock, with multiple organ dysfunction.
• Undrained collections progressing to tertiary peritonitis with commensal and resistant organisms.
• Acute kidney injury, acute respiratory distress syndrome, coagulopathy.
• Enterococcal and Candida infection in postoperative or recurrent disease. ^[2]
• Anastomotic leak-related fistula, stump blowout, and permanent stoma.
• Long-term post-sepsis catabolism and immunosuppression in survivors. ^[2]
• High mortality in four-quadrant peritonitis (36 percent in one series) and in faecal peritonitis (38 percent), and in patients with diabetes. ^[3]

Prognosis is governed by age, comorbidity, source, extent of peritonitis, delay beyond 24 hours in source control, and whether septic shock develops. Secondary peritonitis has an overall mortality of 6 percent, rising to 35 percent with severe sepsis. Primary peritonitis in cirrhosis carries a mortality of 10 to 32.6 percent. Good recovery follows early, adequate source control and short, targeted antibiotics.

• Children and adolescents: no paediatric severity score specific to complicated intra-abdominal infection can be recommended; adult imaging and antibiotic principles are adapted with weight-based sepsis resuscitation. Suspect appendicitis first in an ill child with acute abdomen. ^[4]
• Pregnancy: ultrasound first, magnetic resonance imaging if needed, and early multidisciplinary involvement. cIAI guidance applies to pregnant adults. ^[4]
• Cirrhosis: treat suspected spontaneous bacterial peritonitis promptly; do not wait for culture results. ^[6]
• Older adults and immunocompromised patients: atypical presentation is common; a low threshold for early antibiotics in shock is sensible, with dose adjustment for renal and hepatic function.
• Neutropenic patients: abdominal pain with fever may be typhlitis; treat as potential sepsis and obtain early surgical and microbiology advice.

• Bedside perfusion markers (heart rate, capillary refill, skin temperature, urine output, mental state) and simple repeated observations substitute for lactate and advanced monitoring.
• Where CT, interventional radiology or pressors are unavailable, rely on ultrasound first, arrange transfer early, and use peripheral surgical drainage to achieve source control by the safest route.
• Drug choice should follow local resistance and availability; appropriate coverage that matches local organisms is better than delay. ^[2]
• Vaccination, infection prevention and good management of chronic disease reduce the surgical sepsis burden more than any bundle. ^[1]

• Sepsis and septic shock (infectious disease)
• Acute abdomen and intestinal obstruction
• Wound healing and surgical site infection
• Perioperative care
• Small bowel obstruction
• Diverticular disease
• Shock and haemodynamic support
• Clostridioides difficile infection
• Cirrhosis, ascites and hepatorenal syndrome