Acute Severe Intra-Abdominal Infection and Peritonitis — Comprehensive (Primary/SBP, Secondary, Tertiary, Source Control, Open Abdomen)

Overview

Acute severe intra-abdominal infection sits at the interface of surgery and intensive care, and it is the paradigm disease of source control: the principle that infection driven by a physical source (a hole in the bowel, a collection of pus, a segment of dead gut) cannot be cured by antibiotics alone — the source must be found and physically corrected. The fellowship-level challenge is to (1) recognise which type of peritonitis the patient has, because SBP, secondary, and tertiary peritonitis demand fundamentally different strategies; (2) execute source control with the right timing and the right technique, including the disciplined use of damage-control surgery and the open abdomen in the physiologically deranged patient; (3) choose, time, and DURATION-limit antibiotics rationally; and (4) anticipate the special problems of the cirrhotic (hepatorenal syndrome), the immunoparalysed critically-ill patient (tertiary peritonitis and MDR organisms), and the patient with fungal (Candida) peritonitis. This topic covers the full fellowship-exhaustive syllabus, anchored in the current WSES (2017), SIS (2017), IDSA/SIS (2010), AASLD (2012), WSACS (2013) and Montravers (2016) guidance.[1][2][4][6]

Classification — the single most examinable framework

Peritonitis is classified by whether there is an intra-abdominal source requiring physical control, by the temporal relationship to prior treatment, and by the microbial pattern. The three categories — primary (SBP), secondary, and tertiary — have different aetiologies, organisms, diagnostic tests, and treatments, and confusing them is a classic and dangerous error.[1][2][6]

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The essential triage question at the bedside is: Is there an intra-abdominal source that requires physical control? If yes (and the patient is not cirrhotic with ascites) this is secondary peritonitis and the patient needs source control in addition to antibiotics. If the patient is cirrhotic with ascites and there is no evidence of a perforation, it is SBP and surgery is not only unnecessary but harmful. If the patient has already been treated for secondary peritonitis for >48h and is not improving, suspect tertiary peritonitis with MDR organisms.[2][6]

Spontaneous bacterial peritonitis (SBP)

SBP is the infection of ascitic fluid in a cirrhotic patient (or, rarely, a patient with nephrotic syndrome or heart-failure ascites) in the absence of an intra-abdominal surgical source. It is the archetype of primary peritonitis and is one of the highest-yield, most distinctively-managed topics in the ICU syllabus.[3]

Pathophysiology

Cirrhosis produces portal hypertension, splanchnic congestion, and a profoundly dysfunctional gut barrier. Bacterial translocation — the migration of enteric bacteria across the oedematous, permeable intestinal wall into mesenteric lymph nodes and the systemic circulation — seeds the ascitic fluid. The ascites itself is a poor defensive medium: it has low opsonic/complement activity (low ascitic protein), so bacteria that would be cleared in normal peritoneum proliferate unchecked. The result is a monomicrobial infection, overwhelmingly by enteric gram-negative aerobic rods. Impaired reticuloendothelial (Kupffer cell) clearance and cirrhotic immune paresis complete the setup.[3]

Diagnosis — the cell count, not the culture

The diagnostic test is diagnostic paracentesis with a cell count. The threshold is an ascitic polymorphonuclear (PMN) leucocyte count >250 cells/mm3. This is the single most important number in SBP. Treat on the cell count — do NOT wait for culture, because approximately half of genuine SBP episodes are culture-negative (low bacterial load, fastidious organisms, or prior partial antibiotic exposure). When SBP is suspected, inoculate ascitic fluid into blood culture bottles (aerobic and anaerobic) at the bedside before giving antibiotics — this roughly doubles culture yield and guides later de-escalation.[3]

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Clinical triggers for paracentesis: perform a diagnostic tap in ANY cirrhotic with ascites who has new abdominal pain, fever, fever of unknown source, hepatic encephalopathy, worsening renal function, leucocytosis, or unexplained clinical deterioration. A low threshold is essential — SBP can be subtle and the consequences of missing it (hepatorenal syndrome, death) are severe. Routine prophylactic fresh frozen plasma or platelets before a paracentesis are NOT recommended — coagulopathy does not meaningfully increase bleeding risk from a tap.[3]

Treatment — cephalosporin + albumin

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Albumin is the pivotal adjuvant. SBP provokes a marked decrease in systemic vascular resistance and effective arterial blood volume, which in the cirrhotic precipitates the feared complication of hepatorenal syndrome (HRS). The landmark trial by Sort and colleagues (NEJM 1999) randomised SBP patients to cefotaxime + albumin vs cefotaxime alone: albumin reduced HRS from 33% to 10% (a 67% relative reduction) and in-hospital mortality from 29% to 10% (a 65% relative reduction). Albumin is therefore standard of care for all SBP patients, and is non-negotiable in those with risk factors for renal deterioration (bilirubin >68 umol/L, creatinine >88 umol/L, blood urea nitrogen >30 mg/dL).[3]

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SBP prophylaxis

Secondary prophylaxis (after a first SBP episode) is lifelong — SBP recurs in ~70% within a year without it. Use norfloxacin 400 mg daily or ciprofloxacin 500 mg daily. Primary prophylaxis is indicated for ascitic protein <15 g/L with concomitant renal/liver dysfunction, and short-term prophylaxis is mandatory after a gastrointestinal bleed in cirrhosis (7 days of norfloxacin reduces infection and bacterial translocation). Long-term quinolone prophylaxis selects quinolone-resistant organisms and shifts the microbiology toward gram-positives — a reason to remain vigilant.[3]

Secondary peritonitis — the disease of source control

Secondary peritonitis is by far the commonest form in surgical ICU practice. It arises whenever the integrity of the gastrointestinal tract is breached and endogenous bacteria contaminate the peritoneum. The cardinal principle — repeated in every guideline — is that source control is mandatory and antibiotics are an adjunct, not a substitute.[1][2][4]

Aetiology — the sources you must find and fix

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The intensivist's role in secondary peritonitis is to recognise the sick patient, resuscitate, get broad-spectrum antibiotics in EARLY (within one hour of septic shock), localise the source by imaging, and ensure the surgeon/interventional radiologist achieves definitive source control without delay — delay beyond 24 hours from onset independently worsens mortality.[1][2]

Diagnosis — find the source

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The microbiological principle: obtain cultures BEFORE antibiotics when feasible, but never delay antibiotics in septic shock. Blood cultures, peritoneal fluid cultures (in blood-culture bottles), drain/pus cultures, and swabs guide de-escalation. Specimens from the operative field are especially valuable.[2][6]

Source control — the defining principle (drain, debride, divert)

Source control is defined as 'all physical measures undertaken to eliminate a source of infection and to restore anatomy and function'. Its four components are best remembered as the '3 Ds plus a second look':[1][6]

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The choice between surgery and interventional radiology (IR) depends on the source, accessibility, stability, and local expertise. IR-guided percutaneous drainage is first-line for a discrete, accessible abscess (post-operative collection, peri-appendiceal abscess), often avoiding surgery entirely. Surgery is required for diffuse peritonitis (free perforation), ischaemic/infarcted bowel, uncontrolled leak, failed IR drainage, or haemodynamic instability without a drainable target.[1][2]

Damage control — for the deranged patient

When the patient is physiologically deranged — the lethal triad of hypothermia, acidosis, and coagulopathy — a prolonged definitive operation will kill them. The principle of damage control surgery is to perform the minimum necessary to control contamination and bleeding, then temporarily close the abdomen, move to the ICU for resuscitation/correction of physiology, and return to theatre for definitive repair once stabilised.[6]

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The damage-control philosophy explicitly accepts an incomplete initial operation in exchange for survival — the operation is resuscitative, not definitive. The intensivist and surgeon must communicate continuously, because the decision to re-operate (planned vs on-demand) and the timing of definitive closure are made jointly.[1][6]

Empiric antibiotics — broad gram-negative + anaerobic cover

Empiric antibiotic therapy must cover enteric gram-negative bacilli, anaerobes (Bacteroides), and — depending on setting and severity — Enterococcus and Candida. Therapy is started EARLY (within one hour of septic shock), broad initially, then DE-ESCALATED to culture sensitivities. Choice is stratified by community-acquired vs healthcare-associated and by severity.[2][4]

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The recurring mistake is to continue the broad empiric regimen for days once cultures are back. The disciplined approach is start broad within the hour, obtain good cultures and source control, then DE-ESCALATE to the narrowest effective agent guided by sensitivities — this is antimicrobial stewardship applied to intra-abdominal infection.[2]

Antibiotic duration — short is standard (STOP-IT)

Prolonged antibiotic courses were once routine after intra-abdominal infection; they are no longer justified. The pivotal trial is STOP-IT (Sawyer et al., NEJM 2015), which randomised patients with complicated intra-abdominal infection and adequate source control to approximately 4 days vs ~8 days of antibiotics.[2]

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Stop antibiotics when: the patient is clinically improving (afebrile, haemodynamically stable, resolving ileus, falling inflammatory markers, tolerating diet) AND source control is adequate. Do NOT treat a falling but elevated CRP or a residual collection on imaging in a recovering patient — clinical recovery is the endpoint, not a number.[2]

Tertiary peritonitis — the MDR, immune-paresis syndrome

Tertiary peritonitis is persistent or recurrent peritonitis that develops after >48 hours of apparently appropriate treatment of secondary peritonitis, or persistent intra-abdominal infection in the critically ill without an obvious drainable source. It reflects a combination of MDR infection and the immune paralysis (immunoparesis) of critical illness more than a simple failure of source control.[6]

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The intensivist must distinguish failure of source control (an undrained collection, ongoing leak, ischaemic bowel — a SURGICAL problem needing re-operation) from true tertiary peritonitis (MDR/immunoparesis with no single drainable source — a MEDICAL/stewardship problem needing culture-directed antibiotics and organ support). The first is fixed in theatre; the second is not. Both may coexist. Re-imaging (CT) and repeated microbial sampling are the tools to separate them.[6]

Fungal (Candida) peritonitis

Candida peritonitis is most often encountered after gastrointestinal perforation or recurrent abdominal surgery, where Candida (which colonises the gut) contaminates the peritoneum along with bacteria. It is NOT an indication to treat every patient with Candida isolated from a peritoneal swab — transient colonisation is common and self-limiting after source control. Treatment is indicated when Candida is isolated from a sterile intra-abdominal specimen in a patient with intra-abdominal infection (especially critically ill, recurrent, or with risk factors) or with candidaemia.[2]

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Amphotericin B (or its liposomal formulation) remains a valid alternative for fungal peritonitis, especially where echinocandins are unavailable or for resistant species, but echinocandins are now preferred first-line in the critically ill because of their better safety profile. Fluconazole is a reasonable choice in the stable patient with a likely-susceptible organism (C. albicans).[2][4]

Open abdomen management

Leaving the abdomen open (laparostomy) is a deliberate strategy in severe intra-abdominal infection when (a) primary closure would cause abdominal compartment syndrome (the swollen, oedematous bowel cannot be contained without raising intra-abdominal pressure to harmful levels), (b) a planned second-look is required (to check for bowel viability after ischaemia, or to confirm source control), or (c) the patient is too unstable for a definitive closure (damage control). The WSACS 2013 consensus defined the open abdomen, proposed a classification system, and made specific recommendations for its management.[5]

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The WSACS 2013 definitions are worth knowing: intra-abdominal hypertension (IAH) = sustained IAP >12 mmHg; abdominal compartment syndrome (ACS) = sustained IAP >20 mmHg WITH new organ dysfunction. The open abdomen is both a consequence (decompression for ACS) and a planned strategy (to prevent ACS in the at-risk patient).[5]

Abdominal compartment syndrome (ACS) — when the abdomen itself fails

ACS is defined as a sustained intra-abdominal pressure >20 mmHg with new-onset organ failure. It complicates severe intra-abdominal infection (and severe pancreatitis, trauma, massive fluid resuscitation) when oedematous, fluid-loaded viscera raise IAP to the point where perfusion of the kidneys, gut, and lungs collapses.[5]

[1]

Monitor bladder pressure in any at-risk patient (severe intra-abdominal infection/pancreatitis with massive fluid resuscitation, oliguria unresponsive to fluid, refractory hypoxaemia/raised airway pressures). A staged approach to management: reduce intra-abdominal volume (NG/rectal decompression, diurese/reduce fluids, neuromuscular blockade), and surgical decompressive laparotomy (open abdomen) if refractory — decompression can be dramatically life-saving.[5]

Special situations

Post-operative peritonitis (anastomotic leak): presents typically day 3-7 after surgery with new fever, ileus, abdominal pain, sepsis, and drain output (faeculent, bilious, or purulent). CT with WATER-SOLUBLE contrast (never barium — risk of chemical peritonitis if extravasation) confirms the leak. Management is source control (re-operation: repair/defunction/stoma; or IR drainage if contained and stable), broad antibiotics, and ICU support. A leak after a low rectal anastomosis may be managed with diversion +/- drainage rather than take-down if contained.[2]

CAPD peritonitis: in continuous ambulatory peritoneal dialysis, peritonitis presents with cloudy dialysate and abdominal pain; diagnosis is dialysate WBC >100/mm3 (after a dwell) with >50% PMNs. Organisms are coagulase-negative Staph (~40%, touch contamination), Staph aureus (~15%, exit-site infection), gram-negatives (~15-20%), and fungal (~2%, needs catheter removal). Treatment is intraperitoneal antibiotics (e.g. vancomycin/cefazolin + ceftazidime/gentamicin, per ISPD guidelines) with prompt catheter removal for fungal, refractory, recurrent, or Pseudomonas peritonitis.[6]

Severe intra-abdominal infection in septic shock: apply the Surviving Sepsis Hour-1 bundle — measure lactate, obtain blood cultures, give broad-spectrum antibiotics and crystalloid, and start vasopressors (noradrenaline) for vasopressor-dependent shock — but recognise that source control is the sepsis-specific intervention and should be achieved as early as feasible (ideally within 6-12 hours of diagnosis). Antibiotics without source control will not resolve septic shock from a perforation.[1]

Clinical pearls

Red flags

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Prognosis

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Mortality is driven by three modifiable factors the intensivist controls: (1) the speed and adequacy of source control (the single most important determinant); (2) the appropriateness and timing of antibiotics (early, broad, then de-escalated); and (3) the quality of organ support (resuscitation, ventilation, renal replacement, nutrition). Non-modifiable risk (age, comorbidity, severity at presentation) sets the baseline, but optimal source control, stewardship, and ICU care substantially shift outcome. The patient with SBP additionally depends on albumin to prevent the otherwise near-inevitable progression to hepatorenal syndrome.[1][3][6]

Key trials and evidence

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References

1. [1]Sartelli M, Chichom-Mefire A, Labricciosa FM, et al. The management of intra-abdominal infections from a global perspective: 2017 WSES guidelines for management of intra-abdominal infections World J Emerg Surg, 2017.PMID 28702076
2. [2]Mazuski JE, Tessier JM, May AK, et al. The Surgical Infection Society Revised Guidelines on the Management of Intra-Abdominal Infection Surg Infect (Larchmt), 2017.PMID 28085573
3. [3]Runyon BA; AASLD Practice Guidelines Committee. [Efficacy and safety of domestic biofragmentable anastomotic ring in the intestinal anastomosis] Zhonghua Wei Chang Wai Ke Za Zhi, 2012.PMID 22941691
4. [4]Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America Clin Infect Dis, 2010.PMID 20034345
5. [5]Kirkpatrick AW, Roberts DJ, De Waele J, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome Intensive Care Med, 2013.PMID 23673399
6. [6]Montravers P, Blot S, Dimopoulos G, et al. Therapeutic management of peritonitis: a comprehensive guide for intensivists Intensive Care Med, 2016.PMID 26984317