Intra-Abdominal Infection & Peritonitis

Meet the patient

Two patients arrive in the same hour. The first is a 60-year-old man with known alcoholic cirrhosis and ascites, brought in confused and febrile, his abdominal exam deceptively soft — the senior's instinct is to tap the ascites before attributing the encephalopathy to "just decompensation". The second is a 50-year-old previously well woman who rolled over in bed and felt something tear; she now lies board-like, motionless, sweating, with absent bowel sounds and free gas under the diaphragm on the erect chest X-ray.[1][2]

The two questions these patients force you to answer are the two that decide every peritonitis case: is there a surgical source I must fix? (the cirrhotic with SBP has none; the perforated ulcer is a theatre job in the next hour) and can I keep the patient perfused and oxygenated while I find and control the source? (resuscitation and antibiotics run concurrently with imaging, never after). Hold those two questions and every section below slots into place.[1][6]

Three diseases, one peritoneum — the classification that drives everything

Peritonitis is inflammation of the parietal and visceral peritoneum — the serous membrane that lines the abdominal cavity and invests its organs, with a total surface area of about 1.7 m² in an adult, comparable to the skin. Intra-abdominal infection (IAI) extends the term to include infection of the abdominal viscera or the peritoneal space, with or without abscess formation. The two overlap and are managed by the same principles — antibiotics plus source control plus resuscitation — but the aetiology, organisms, definitive treatment and prognosis differ sharply between the major subtypes.[4][5]

The clinical art in peritonitis is NOT making the diagnosis — acute generalised peritonitis is unmistakable at the bedside — but in distinguishing the three mechanistic classes, because that distinction drives everything that follows:[1][5]

• A cirrhotic with ascites and fever or encephalopathy needs a diagnostic tap and cefotaxime plus albumin — SBP is a medical peritonitis; surgery will not help.
• A previously well patient with sudden severe peritonism and sepsis needs CT, broad-spectrum antibiotics and urgent surgery or source control — secondary peritonitis from a perforated viscus.
• A critically ill ICU patient with persistent fever, leucocytosis and organ dysfunction despite prior source control has tertiary peritonitis with MDR organisms and needs broadened empiric cover and re-operation.[1]

In all three, the unifying principles are early antibiotics, source control and resuscitation; in secondary peritonitis specifically, delay in source control is fatal. The two biggest process levers in mortality reduction are (1) diagnostic paracentesis in every cirrhotic with ascites (catches SBP while still treatable) and (2) early source control in secondary peritonitis within hours of recognition.[1][6]

[14] [16] [18] [4] [5]

Etymology for viva gold: peritoneum is from the Greek peri (around) and teinein (to stretch) — "the stretched membrane around the bowels". Ascites is from the Greek askos, a wine-skin; the cirrhotic abdomen was likened to a bulging skin of wine by Hippocrates. Both names describe what the clinician sees, and both have outlived the millennium that coined them.[5]

Variants of ascitic infection — the AASLD distinctions

In cirrhosis, three related variants of ascitic infection are distinguished by ascitic PMN count and culture (first codified by Hoefs and Runyon):[14]

• SBP — ascitic PMN over 250 cells per mm³ with a positive culture (monomicrobial, no surgical source).
• Culture-negative neutrocytic ascites (CNNA) — ascitic PMN over 250 cells per mm³ with negative culture, in a symptomatic patient; treated identically to SBP.
• Bacterascites — positive culture with a normal ascitic PMN (under 250 cells per mm³); treat if symptomatic or repeat the tap.
• Secondary bacterial peritonitis — polymicrobial ascites OR a very high PMN with total protein over 1 g per dL, glucose under 50 mg per dL and LDH above the upper limit of normal for serum (the perforation criteria — 100 percent sensitive for gut perforation), with ascitic CEA over 5 ng per mL a further perforation marker — implies a perforation; search for the source with CT.[16][17]

How common, who, and why SBP keeps killing cirrhotics

Spontaneous bacterial peritonitis complicates cirrhotic ascites: in a prospective cohort of 127 patients with cirrhotic ascites, the probability of a first episode was 11 percent at one year and 15 percent at three years — rising to 24 percent at three years when the ascitic protein is under 1 g per dL (versus 4 percent when it is over). Without prophylaxis, the one-year recurrence probability after a first episode is 68 percent, falling to 20 percent on norfloxacin. In the cefotaxime randomised trials, hospital survival was 69 to 79 percent.[13][12][11]

[12] [14] [13] [11]

The risk factors for SBP combine low ascitic defence (low opsonic activity) with bacterial over-translocation:[1]

• Low ascitic total protein (under 1 g per dL) — the only independent predictor in multivariate analysis (24 percent versus 4 percent three-year risk of a first episode); it reflects the poor antimicrobial capacity of low-protein ascites.
• Advanced liver disease — increased serum bilirubin, increased AST and reduced prothrombin activity each predicted a first SBP episode on univariate analysis.
• Poor nutritional status — a further univariate predictor.
• Prior SBP — recurrence probability 68 percent at one year without secondary prophylaxis.
• Acute gastrointestinal bleeding and hospitalisation — the classic high-risk settings in which prophylaxis is indicated.
• Severe intrahepatic shunting — marked redistribution of activity from liver to spleen and bone marrow on liver-spleen scan.[13][12][14][18]

Secondary peritonitis is the commonest surgical abdominal emergency. Causes by age: appendicitis dominates in the young; perforated peptic ulcer, perforated diverticulitis and mesenteric ischaemia dominate in the elderly. Post-operative anastomotic leak is an increasingly important cause in the surgical ICU.[2][5]

Tertiary peritonitis arises in the critically ill: prolonged ICU stay, prior broad-spectrum antibiotics, immunosuppression, post-operative state, multi-organ failure. The organisms are MDR by selection.[5]

The three mechanisms — translocation, perforation, failure of source control

All three subtypes begin with bacteria reaching the peritoneum by different routes, and all three converge on the SIRS to sepsis to septic shock to MODS cascade.[1][5]

Primary peritonitis (SBP) — bacterial translocation. The hallmark is infection of ascitic fluid without an intra-abdominal surgical source, and the pathogenesis runs in four steps:[1]

1. Bacterial translocation — enteric bacteria cross the disrupted mucosal barrier and reach mesenteric lymph nodes, then the bloodstream — the first of the three key pathogenetic steps.
2. Depressed reticuloendothelial (Kupffer cell) phagocytic system activity in cirrhosis — bacteria that reach the portal or systemic circulation are not cleared.
3. Decreased antimicrobial capacity of the ascitic fluid — low-protein cirrhotic ascites is particularly susceptible to infection (protein under 1 g per dL carries a 24 percent three-year risk of a first episode versus 4 percent when it is over).
4. Bacterial seeding of ascites — the result is a monomicrobial infection, typically a single enteric aerobic Gram-negative bacillus (recurrent SBP is overwhelmingly caused by aerobic Gram-negatives). Anaerobes are rare in SBP; polymicrobial growth should prompt a search for secondary bacterial peritonitis.[18][13][12][16]

Secondary peritonitis — polymicrobial contamination. The peritoneum is flooded by enteric contents from a perforated or translocating viscus. The cascade:[5]

1. Contamination — gastric juice, bile, small bowel contents, faecal matter or blood enters the peritoneum. Initial inflammation may be chemical (sterile) but becomes bacterial within hours.
2. Mesothelial and peritoneal macrophage activation — release of IL-1, IL-6, TNF-alpha, leukotrienes and complement activation.
3. Neutrophil influx into the peritoneal cavity (ascitic PMN rises sharply).
4. Cytokine amplification — local cytokines spill into the systemic circulation, producing SIRS, then sepsis, septic shock and multi-organ dysfunction syndrome (MODS).
5. Splanchnic vasodilation, capillary leak and third-spacing — large volumes sequester into the peritoneum; hypovolaemia, abdominal compartment syndrome and shock follow.
6. Localisation or walled-off infection — omentum and adjacent loops wall off contamination, forming an intra-abdominal abscess if source control fails.[1]

The microbial load is polymicrobial: any perforation distal to the ligament of Treitz yields Gram-negative aerobes (E. coli, Klebsiella, Proteus), anaerobes (Bacteroides fragilis — the dominant anaerobe), and Enterococcus. Pseudomonas emerges with healthcare exposure.[4]

Tertiary peritonitis — failure of source control. In the critically ill, prior broad-spectrum antibiotics and impaired immunity select for low-virulence but multi-drug-resistant organisms — Pseudomonas aeruginosa, Enterococcus (including VRE), Candida species, MRSA, Acinetobacter, Stenotrophomonas. The peritoneum is unable to clear even modest contamination; biofilm on foreign material and necrotic tissue sustain infection. Clinical signs are often blunted in the ICU patient (sedation, analgesia, mechanical ventilation mask the peritonism).[5]

In cirrhosis, SBP is the classic precipitant of hepatorenal syndrome (HRS-AKI): the systemic inflammatory response causes splanchnic vasodilation, effective arterial underfilling, activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, and intense renal vasoconstriction — the rationale for IV albumin in every treated episode.[1][3]

The clinical picture — three bedside phenotypes

Generalised (secondary) peritonitis — the classic acute abdomen

The patient lies still, motionless, with shallow breathing because any movement worsens the pain. The key features:[5]

• Severe, constant, poorly localised abdominal pain that is worse on movement, coughing and deep inspiration. Pain may be referred to the shoulder from diaphragmatic irritation.
• Peritonism — tenderness, guarding (voluntary then involuntary), rigidity (board-like abdomen) and rebound tenderness.
• Absent or markedly reduced bowel sounds (paralytic ileus).
• Fever, tachycardia, tachypnoea, then hypotension, oliguria and altered mental status as sepsis progresses.
• Signs of the underlying source — epigastric guarding and free gas (perforated peptic ulcer); RIF signs (appendicitis); LIF signs (diverticulitis); RUQ (cholecystitis); distension and obstipation (obstruction or ischaemia).[5]

Spontaneous bacterial peritonitis — the subtle presentation in cirrhosis

SBP may present overtly (fever, abdominal pain) but is frequently subtle or asymptomatic. A diagnostic tap is therefore mandatory in any cirrhotic with ascites who has any of the following:[1]

• Abdominal pain or tenderness.
• Fever (over 37.8 degrees C) or rigors.
• New or worsening hepatic encephalopathy (confusion, drowsiness, asterixis).
• Worsening renal function (rising creatinine, falling urine output).
• GI bleeding, paralytic ileus, diarrhoea or worsening ascites.
• Routine tap on admission in any cirrhotic with ascites hospitalised for any reason.[1]

A high index of suspicion is essential because SBP may present without any clinical manifestation — diagnosis requires a low threshold for paracentesis.[14]

Atypical presentations

[1]

Localising signs by source:[1]

• Right upper quadrant — perforated peptic ulcer, acute cholecystitis, cholangitis.
• Right iliac fossa — appendicitis (most common surgical cause in the young), Meckel diverticulitis, right-sided colonic pathology.
• Left iliac fossa — perforated diverticulitis (most common in the elderly), sigmoid pathology.
• Pelvic — pelvic abscess: diarrhoea, urinary frequency, tenesmus, a tender boggy anterior mass on digital rectal examination.
• Diffuse — perforated peptic ulcer (free gas throughout), ischaemic bowel, post-operative leak, primary peritonitis.[1]

The mimics of the acute abdomen — the eight you must separate

The differential of the acute abdomen with peritonism is broad. The discriminating features below separate the commonest mimics.[2][5]

[2]

Distinguishing SBP from secondary peritonitis in ascitic fluid (the most examinable tap-level distinction):[1]

| Fluid feature | SBP (primary) | Secondary |[1] |---|---|---| | PMN | over 250 cells per mm³ | very high | | Culture | monomicrobial (single organism) | polymicrobial (incl. anaerobes) | | Glucose | normal (over 50 mg per dL) | under 50 mg per dL | | LDH | normal | high (over serum) | | Total protein | variable | over 1 g per dL | | CEA | normal | over 5 ng per mL (or alkaline phosphatase over 240 units per L) | | Amylase | normal | high (gut origin) |

[16] [17]

The one-line discriminator: polymicrobial ascites with glucose under 50 mg per dL, LDH above the serum limit and CEA over 5 ng per mL is a perforation — find the source, do not treat it as SBP.[16][17]

The bedside round — vital signs, peritonism, the source

• Vital signs and qSOFA — assess severity early. qSOFA: 2 or more predicts a high risk of poor outcome (respiratory rate 22 or more per minute, altered mentation (GCS under 15), systolic blood pressure 100 mmHg or less).
• General — posture (lying still), facial expression (anxious, in pain), hydration, signs of chronic liver disease (palmar erythema, spider naevi, jaundice, ascites, caput) if SBP is suspected.

[1]

Abdominal examination — the peritonitic signs:[1]

• Inspection: motionless abdomen; distension (ileus, ascites, third-spacing); visible peristalsis suggests obstruction, not peritonitis.
• Palpation:
  • Tenderness — localised or generalised.
  • Guarding — voluntary (the patient tenses up) versus involuntary (reflex muscle spasm) — involuntary guarding implies true peritoneal inflammation.
  • Rigidity — board-like abdomen; a sign of established generalised peritonitis (perforated ulcer).
  • Rebound tenderness — pain on sudden release of deep palpation; tests peritoneal irritation.
• Percussion: shifting dullness and fluid thrill (ascites); lost liver dullness (free intraperitoneal gas from a perforated viscus).
• Auscultation: absent or markedly reduced bowel sounds (paralytic ileus); high-pitched tinkles suggest obstruction.
• Special manoeuvres (source-specific):
  • Murphy sign — inspiratory arrest on RUQ palpation (acute cholecystitis).
  • McBurney point tenderness (one-third between ASIS and umbilicus) — appendicitis.
  • Rovsing sign — LIF palpation causes RIF pain (peritoneal irritation).
  • Psoas sign — pain on extending the right hip (retrocaecal appendix).
  • Obturator sign — pain on internal rotation of the flexed right hip (pelvic appendix).
• Digital rectal examination: a tender, boggy, anterior mass suggests a pelvic abscess; essential in any patient with pelvic symptoms.
• Hernial orifices and genitalia — exclude strangulated hernia (a cause of small bowel obstruction and peritonitis) and testicular torsion (referred abdominal pain).[1]

Diagnostic peritoneal aspiration (DPA) — a one-off tap of ascitic fluid for cell count, Gram stain, culture and biochemistry. Diagnostic paracentesis is done in EVERY cirrhotic with ascites on admission and at any decompensation.[1]

Measurement of intra-abdominal pressure. At the bedside, bladder pressure (transvesical) approximates intra-abdominal pressure (IAP). Normal is 5 to 7 mmHg. Intra-abdominal hypertension (IAH) is a sustained IAP over 12 mmHg. Abdominal compartment syndrome (ACS) is IAP over 20 mmHg with new organ dysfunction (oliguria, high airway pressures, reduced cardiac output).[5]

The tests — bloods, the tap, and CT

First-line bloods and bedside tests:[1]

• Full blood count — leucocytosis with neutrophilia (may be normal or low in the immunocompromised or elderly); thrombocytopenia in cirrhosis.
• CRP — usually markedly raised.
• Urea and electrolytes, creatinine — AKI is common; baseline renal function in cirrhosis (HRS risk).
• Liver function tests, coagulation, albumin — gauge liver-disease severity; INR guides paracentesis risk.
• Serum lactate — marker of tissue hypoperfusion and severity; septic shock is defined by a vasopressor requirement to maintain MAP 65 mmHg or more plus serum lactate over 2 mmol per L despite adequate volume resuscitation.
• Amylase or lipase — exclude pancreatitis (lipase is more specific).
• Blood cultures (two sets) — before antibiotics where this does not delay them; positive cultures identify the organism and guide de-escalation.
• Arterial or venous blood gas — metabolic acidosis, raised lactate, hypoxaemia.
• Urinalysis and culture — exclude UTI as a source.
• ECG — exclude MI (inferior MI can present as upper abdominal pain).
• Chest X-ray erect — free gas under the diaphragm is diagnostic of a perforated viscus, but a normal erect film does not exclude perforation. Also excludes lower-lobe pneumonia.
• Point-of-care ultrasound (FAST or bedside) — ascites, intra-abdominal free fluid, AAA, biliary pathology.[10][2]

Diagnostic ascitic tap (paracentesis) — the cornerstone for SBP. Performed in the left iliac fossa (two finger-breadths cephalad and two medial to the anterior superior iliac spine), with a sterile technique and local anaesthetic; superficial infection and bleeding are the main risks; bowel injury is rare. Coagulopathy is not a contraindication to diagnostic paracentesis in cirrhosis. Send for:[1]

• Cell count and differential — PMN count over 250 cells per mm³ (0.25 x 10⁹ per L) equals SBP. Treat empirically before culture returns.
• Gram stain — usually negative in SBP (low bacterial load).
• Culture — inoculate 10 mL of ascitic fluid into blood culture bottles directly at the bedside: culture positivity rose from 42 percent to 91 percent with this technique.[15]
• Total protein, albumin — calculate the serum-to-ascites albumin gradient (SAAG) to confirm portal-hypertensive ascites; a low total protein marks the SBP-risky fluid.
• Glucose, LDH, amylase, CEA — to distinguish secondary peritonitis: total protein over 1 g per dL, glucose under 50 mg per dL and LDH above the serum upper limit flag perforation, as does CEA over 5 ng per mL.[16][17]

CT abdomen with intravenous contrast is the definitive imaging for secondary peritonitis. Look for: free intraperitoneal gas, free fluid, fat stranding, bowel wall thickening, pneumatosis intestinalis (ischaemia), abscess, mesenteric vascular occlusion, and the underlying source (perforation site, inflamed appendix, diverticulum, ischaemic segment). In the haemodynamically stable patient with suspected secondary peritonitis, CT before theatre shortens operative time and may redirect management (e.g. percutaneous drainage of a walled-off abscess instead of surgery).[5]

Severity scores (reproduced verbatim).[1]

qSOFA (use at the bedside for suspected sepsis — 2 or more predicts poor outcome):[5]

1. Respiratory rate 22 per minute or more.
2. Altered mentation (GCS under 15).
3. Systolic blood pressure 100 mmHg or less.[1]

Sepsis-3 definitions — sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection (an acute increase in SOFA score of 2 or more points); septic shock is sepsis with circulatory and cellular or metabolic abnormalities sufficient to increase mortality — clinically, hypotension requiring vasopressors to maintain MAP 65 mmHg or more AND serum lactate over 2 mmol per L despite adequate volume resuscitation (hospital mortality over 40 percent with this combination).[10]

AASLD diagnostic criteria for SBP:[1]

• Ascitic PMN count over 250 cells per mm³ (0.25 x 10⁹ per L) (regardless of culture result) — diagnostic; treat empirically.
• Ascitic culture (positive in monomicrobial form) supports but is not required.[1]

[1]

The first hour — Surviving Sepsis, antibiotics, source control

The hour-1 priorities follow the ABCDE and the Surviving Sepsis hour-1 bundle.[5]

Airway, breathing, oxygen:[1]

• Airway — secure if comatose or vomiting (aspiration risk).
• Oxygen — target SpO2 94 to 98 percent (or 88 to 92 percent in COPD at risk of CO2 retention); high-flow if shocked.
• Assess work of breathing — mechanical ventilation if fatiguing or comatose.[5]

Circulation, IV access, fluid resuscitation:[1]

• Two large-bore IV cannulae; send bloods including two sets of blood cultures before antibiotics (but do NOT delay antibiotics for cultures).
• Begin IV crystalloid resuscitation early in sepsis or septic shock, and reassess the response before repeated boluses.
• Vasopressors — required when hypotension persists despite volume resuscitation; the Sepsis-3 definition of septic shock is a vasopressor requirement to maintain MAP 65 mmHg or more with lactate over 2 mmol per L.
• Avoid over-resuscitation — excess crystalloid worsens perfusion and can drive intra-abdominal hypertension; reassess frequently.[10][5]

The first hour after recognition — bedside priorities consistent with the Sepsis-3 definitions and the sepsis-guideline framework:[10][5]

1. Measure serum lactate — a value over 2 mmol per L with vasopressor-dependent hypotension defines septic shock.
2. Take blood cultures before antibiotics whenever this does not delay them.
3. Administer broad-spectrum antibiotics immediately in septic shock and without unnecessary delay in high-risk sepsis.
4. Begin IV crystalloid resuscitation, guided by reassessment.
5. Apply vasopressors if hypotension persists during or after fluids, to maintain MAP 65 mmHg or more.
6. Measure urine output (urinary catheter) and monitor the response.[10]

Antibiotic timing targets:[5]

• Septic shock or high-risk sepsis — antibiotics immediately, with source control as soon as possible.
• Stable admitted patient with secondary peritonitis — antibiotics without unnecessary delay; early recognition, adequate source control and appropriate antimicrobial therapy are the three WSES cornerstones.[5]

Symptom control and supportive measures:[1]

• Analgesia — IV opioid titrated to comfort; avoid NSAIDs (renal risk, peptic ulcer).
• Nasogastric tube — for paralytic ileus, vomiting, bowel obstruction; decompresses the stomach.
• Urinary catheter — to monitor urine output.
• Central line and arterial line — for the shocked patient requiring vasopressors and invasive monitoring.
• Thromboprophylaxis — pharmacological prophylaxis (LMWH) unless contraindicated; antiembolism stockings.
• Stress-ulcer prophylaxis — in mechanically ventilated or coagulopathic patients.
• Glucose control — avoid both hypoglycaemia and marked hyperglycaemia.[5]

Definitive treatment — the two pillars (three for SBP)

The two pillars are antibiotics and source control; SBP additionally gets albumin. The empirical choice depends on the subtype, severity and risk of MDR organisms.[1][4]

A. Spontaneous bacterial peritonitis — the medical peritonitis

SBP does NOT need surgery. There is no intra-abdominal source to control. Treatment is medical.[1][3]

Empirical antibiotics (AASLD 2021):[1]

• First-line: a third-generation cephalosporin — cefotaxime 2 g IV every 6 hours is the dose tested head-to-head in the classic prospective randomised multicentre trial (infection resolution 77 to 79 percent; third-generation cephalosporins achieve cure in over 80 percent of SBP). De-escalate once culture returns.[11][18]
• Healthcare-acquired or quinolone-resistant infection: broaden empiric cover and watch for resistant organisms — long-term quinolone prophylaxis selects them.[18]
• Oral therapy: oral ofloxacin is an option only in non-azotaemic patients with non-advanced, uncomplicated SBP; established SBP is otherwise treated parenterally.[18]

IV albumin — the Sort 1999 NEJM trial. Adding albumin 1.5 g per kg IV at diagnosis and 1 g per kg IV on day 3 to cefotaxime reduced renal impairment (33 to 10 percent, P = 0.002), in-hospital mortality (29 to 10 percent, P = 0.01) and three-month mortality (41 to 22 percent, P = 0.03) in SBP. Give it with the first antibiotic dose.[3]

Repeat tap at 48 hours — the optimal time to assess response; on appropriate therapy the ascitic neutrophil count should fall below the baseline (to under 50 percent of the original value). A count that fails to fall suggests secondary bacterial peritonitis (search for a perforation) or a resistant organism (broaden cover).[16][14]

Duration — the classic cefotaxime trials treated for about 9 days; modern practice shortens the course with clinical and ascitic monitoring (the PMN should fall rapidly on effective therapy), stepping to an oral agent only once the patient is clearly improving.[11][14]

SBP prophylaxis (lifelong oral quinolone):[1]

• Secondary prophylaxis (after an SBP episode) — norfloxacin 400 mg daily reduces the one-year recurrence probability from 68 percent to 20 percent (selective intestinal decontamination). Refer suitable survivors for liver transplantation.[12][18]
• Primary prophylaxis — for high-risk cirrhotics: the classic indications are hospitalised patients with gastrointestinal haemorrhage or low ascitic fluid total protein; long-term use demands vigilance for quinolone-resistant organisms.[18][13]
• GI bleed prophylaxis — antibiotic prophylaxis during upper gastrointestinal bleeding in cirrhosis reduces bacterial infections (RR 0.35), mortality from bacterial infections (RR 0.43), all-cause mortality (RR 0.79) and rebleeding in a Cochrane meta-analysis of 12 randomised trials (1241 patients).[20]

B. Secondary peritonitis — antibiotics plus source control

Source control is the single most important determinant of survival in secondary peritonitis.[6]

Empirical antibiotic selection by severity (SIS or IDSA 2010; WSES 2017):[4][5]

[4] [5]

Antifungal cover — the echinocandin anidulafungin (200 mg IV loading dose, then 100 mg daily) is effective in intra-abdominal candidiasis (global response about 73 percent at the end of IV therapy in a pooled analysis of prospective studies); Candida intra-abdominal infection is increasingly recognised after abdominal surgery and with recent prolonged broad-spectrum antibiotics — add antifungal cover when Candida is isolated or risk is high.[21][4]

Source control principles (WSES 2023):[6]

1. Drainage of infected fluid — percutaneous (CT- or US-guided) for a walled-off, accessible abscess; surgical for generalised peritonitis, multiple abscesses or unsuitable anatomy.
2. Debridement of necrotic tissue — resect non-viable bowel, debride omentum.
3. Restoration of anatomy — close or resect the perforation (e.g. Graham omental patch for perforated duodenal ulcer; primary anastomosis or Hartmann's for perforated diverticulitis; appendectomy for appendicitis; resection with stoma for ischaemic bowel).
4. Repeated source control if the first fails (tertiary peritonitis).[1]

Source control by underlying cause:[2][7]

• Perforated peptic ulcer — resuscitation, antibiotics, then surgery: Graham omental patch closure (open or laparoscopic); IV PPI then H. pylori eradication; stop NSAIDs.
• Perforated appendicitis — emergency laparoscopic appendectomy; if a walled-off appendicular mass or abscess in a stable patient, percutaneous drainage plus IV antibiotics, interval appendectomy.
• Perforated diverticulitis — Hartmann's procedure (sigmoid resection with end colostomy) for the unstable or purulent or faecal peritonitis; primary anastomosis with defunctioning ileostomy in selected stable patients.
• Ischaemic bowel — resection of non-viable bowel with primary anastomosis or stoma; second-look laparotomy at 24 to 48 hours.
• Post-operative anastomotic leak — re-operation, washout, defunctioning stoma, broad-spectrum antibiotics.
• Intra-abdominal abscess — CT-guided percutaneous drainage first-line if accessible; IV antibiotics; surgery only if drainage fails or the source requires it.[1]

Duration of antibiotics:[5]

• Complicated IAI with adequate source control — a fixed course of about 4 days matched longer therapy in the STOP-IT trial: patients randomised to 4 (plus or minus 1) days had the same 30-day composite outcome (21.8 versus 22.3 percent) as those treated a median of 8 days.[9]
• Complicated IAI (no or partial source control, immunocompromise, severe sepsis) — individualise; extend if persistent fever, positive cultures, ongoing source.
• Stop antibiotics once source control is achieved AND the patient has clinically improved (afebrile, improving, tolerating diet, falling inflammatory markers).[9]

IV-to-oral step-down criteria:[4]

• Clinically improving (afebrile, falling CRP).
• Haemodynamically stable, gut function returning, tolerating oral intake.
• An oral agent with high bioavailability chosen (amoxicillin-clavulanate, moxifloxacin, or oral metronidazole with a fluoroquinolone or cephalosporin).[1]

Discharge criteria — afebrile for 24 to 48 hours, tolerating oral diet, resolving peritonism, negative or treated cultures, safe social circumstances, follow-up arranged and a safety-net given.[1]

C. Tertiary peritonitis

• Re-operation for a persistent or recurrent source.
• Broad empiric antibiotics covering Pseudomonas, Enterococcus (vancomycin or teicoplanin for MRSA or VRE), MDR Gram-negatives (carbapenem plus or minus aminoglycoside plus or minus colistin), and Candida (echinocandin).
• Antifungal cover more liberally — Candida peritonitis carries a high mortality.
• ICU support — organ failure, nutrition (preferably enteral), glucose control, thromboprophylaxis.

[1]

The complications — HRS, ACS, and the predictable clock

Local complications:[1]

• Intra-abdominal abscess — walled-off collection; CT drainage plus antibiotics.
• Fistula (enterocutaneous, entero-enteric) — from iatrogenic injury, anastomotic leak, Crohn's.
• Adhesions and small bowel obstruction — late complication of surgery.
• Wound infection or dehiscence — surgical-site infection.
• Incisional hernia — late.[1]

Systemic complications:[1]

• Sepsis, septic shock, multi-organ dysfunction syndrome (MODS).
• Acute respiratory distress syndrome (ARDS).
• Acute kidney injury (especially hepatorenal syndrome in cirrhosis).
• Disseminated intravascular coagulation (DIC).
• Venous thromboembolism (immobility, inflammation).[1]

Hepatorenal syndrome precipitated by SBP is the feared renal complication — the rationale for IV albumin in every treated episode (Sort 1999) and for albumin in cirrhotics with bacterial infections other than SBP, where a randomised trial showed improved renal and circulatory function (Guevara 2012). Treatment combines volume expansion with albumin and vasoconstrictor therapy — terlipressin with albumin increases hepatorenal-syndrome reversal and may reduce mortality (RR 0.76 in a Cochrane meta-analysis of randomised trials) — plus urgent liver transplantation assessment.[3][8][19]

Intra-abdominal hypertension and abdominal compartment syndrome:[5]

• IAH — sustained intra-abdominal pressure over 12 mmHg (transvesical bladder pressure).
• ACS — IAP over 20 mmHg with new organ dysfunction (oliguria, raised airway pressures, reduced cardiac output, metabolic acidosis).
• Treatment — decompressive laparotomy (surgical decompression, leave an open abdomen with a vacuum dressing); medical measures: nasogastric and rectal decompression, neuromuscular blockade, avoid over-resuscitation.[1]

Classic pitfalls:[1]

• Missing SBP in a cirrhotic — every cirrhotic with ascites on admission needs a diagnostic tap; relying on symptoms misses one in three.
• Delaying surgery for perforation — free gas plus peritonism equals theatre, not more imaging.
• Under-resuscitation causing shock; over-resuscitation causing ACS.
• Failing to cover anaerobes (Bacteroides) or Enterococcus in healthcare-associated IAI.
• Using an oral quinolone alone to treat established SBP — inadequate ascitic levels.
• Not giving albumin in SBP (missing the HRS-prevention benefit).
• Treating polymicrobial ascites as SBP — search for the perforation.
• Misdiagnosing pancreatitis as perforation (or vice versa) — check lipase and the erect CXR.
• Missing an atypical presentation (elderly with confusion, immunocompromised with normal exam).
• Prolonged antibiotics after adequate source control — no benefit, more resistance.[1]

Prognosis, disposition and the scores that set both

• SBP — hospital survival 69 to 79 percent in the cefotaxime randomised trials; one-year recurrence probability 68 percent without secondary prophylaxis (20 percent with norfloxacin); an episode of SBP is an indication for liver transplantation evaluation.[11][12][18]
• Secondary peritonitis — mortality depends on severity, source, delay and comorbidity; in the STOP-IT trial of complicated IAI with adequate source control, the 30-day composite of surgical-site infection, recurrent intra-abdominal infection or death was 21.8 to 22.3 percent.[9]
• Tertiary peritonitis — mortality remains high, driven by MDR organisms and organ failure.
• Predictors of poor outcome — age, comorbidity (especially cirrhosis, malignancy, immunosuppression), severity of the source, delay to source control, MDR organism, organ failure (high APACHE or SOFA), malignancy, ICU admission.
• Disposition — ICU for septic shock, organ failure, post-major surgery; surgical ward for uncomplicated source-controlled IAI; home only when discharge criteria are met with a safety-net.
• Follow-up — surgical review (wound, hernia), repeat imaging if not improving, outpatient antibiotics (OPAT) for prolonged courses, liver transplant referral for SBP.

[1] [5]

Special populations — cirrhosis, pregnancy, elderly, immunocompromised

• Cirrhosis or ascites — high SBP risk; diagnostic tap on every admission and at any decompensation; primary and secondary quinolone prophylaxis per criteria; albumin in every treated SBP.
• Pregnancy — appendicitis is the commonest non-obstetric surgical emergency; the appendix shifts superiorly and laterally with uterine enlargement; physiological leucocytosis confounds the CBC; laparoscopic appendectomy is safe in any trimester; tocolysis and left lateral tilt for venous return in late pregnancy.
• Elderly — blunted signs; perforated diverticulitis and ischaemic bowel dominate; high index of suspicion; confusion may be the only sign; aggressive resuscitation, early imaging, early source control.
• Immunocompromised or neutropenic — atypical organisms (Pseudomonas, Candida); subtle signs (no neutrophils to mount peritonism); broad empiric therapy; low threshold for CT; consider typhlitis (neutropenic enterocolitis) in the right clinical context.
• Children — appendicitis is the commonest surgical cause; perforation is common (often delayed presentation); an appendicular mass may be managed conservatively with drainage and interval appendectomy.
• Anticoagulated patient — balance bleeding versus urgent source control; reverse warfarin (vitamin K, prothrombin complex concentrate) if INR over 1.5 to 2.0 before surgery or paracentesis; DOACs held per half-life; fresh frozen plasma or PCC if emergency.
• Peritoneal dialysis patient — CAPD peritonitis managed with intraperitoneal antibiotics; catheter removal if refractory, fungal or severe Pseudomonas peritonitis.
• Asplenia or sickle cell — risk of overwhelming post-splenectomy infection; cover encapsulated organisms empirically.

[1]

Specific subtypes worth a sentence:[5]

• Tuberculous peritonitis — insidious fever, weight loss, ascites; laparoscopy with biopsy (caseating granulomas); standard anti-TB therapy (RHZE 2 months plus RH 4 months). Ascitic fluid: lymphocytic, high protein, SAAG low.
• Peritoneal dialysis (CAPD) peritonitis — cloudy effluent, abdominal pain, fever; effluent cell count over 100 WBC per mm³ (over 50 percent neutrophils); touch preparation Gram stain; intraperitoneal antibiotics (cefazolin plus ceftazidime) pending culture; catheter removal for refractory, relapsing, fungal or severe Pseudomonas peritonitis.
• Candida peritonitis — recent prolonged antibiotics, immunosuppression, post-operative leak; echinocandin (caspofungin) first-line, step down to fluconazole.
• Secondary peritonitis from trauma — hollow viscus injury (blunt or penetrating); damage-control laparotomy.[1]

Evidence, guidelines and regional differences

AASLD 2021 (US) — ascites, SBP, HRS. Biggins et al. (2021) is the current American practice guidance on ascites, SBP and hepatorenal syndrome (the MEDLINE record carries no abstract — it is a full-text guidance document). The trial evidence underpinning modern SBP care: the PMN 250 threshold (Hoefs and Runyon), cefotaxime as first-choice therapy (Rimola), albumin 1.5 g per kg day 1 and 1 g per kg day 3 (Sort), and norfloxacin prophylaxis (Gines).[1][14][11][3][12]

WSES 2017 and 2023 — intra-abdominal infections and source control. The WSES 2017 guidelines (Sartelli) classify community-acquired IAI by severity (complicated versus uncomplicated; mild to moderate versus severe) and provide empirical antibiotic ladders; the WSES 2023 source-control guidelines (Coccolini) emphasise early, effective source control as the dominant mortality determinant.[5][6]

IDSA and SIS-AAIDST 2010 — complicated IAI. Solomkin et al. provide the empirical antibiotic tables by severity and risk of resistant organisms, still widely used; they recommend anti-Enterococcus cover in healthcare-associated infection and antifungal cover in selected high-risk groups.[4]

Sort 1999 NEJM — albumin in SBP. The landmark randomised trial showing that albumin 1.5 g per kg day 1 and 1 g per kg day 3 reduced renal impairment (33 to 10 percent), in-hospital mortality (29 to 10 percent) and three-month mortality (41 to 22 percent) when added to cefotaxime in SBP.[3]

STOP-IT (Sawyer 2015). In 518 patients with complicated intra-abdominal infection and adequate source control, a fixed course of 4 (plus or minus 1) days gave the same 30-day composite outcome (21.8 versus 22.3 percent) as therapy continued until two days after fever, leucocytosis and ileus resolved (maximum 10 days; median 8 days) — stop antibiotics once source control is achieved and the patient has clinically improved.[9]

Guevara 2012 — albumin in non-SBP bacterial infections in cirrhosis. A randomised controlled study of albumin in cirrhotics with bacterial infections other than SBP, informing the broader use of albumin in cirrhotic sepsis and HRS prevention.[8]

Podda 2026 — WSES Jerusalem appendicitis guidelines. The 2025 edition of the World Society of Emergency Surgery guidelines on the diagnosis and treatment of acute appendicitis, underpinning the modern laparoscopic-first and selective-conservative approach.[7]

Regional deltas:[1]

Current controversies:[1]

• Routine Enterococcus cover — increasingly recommended in healthcare-associated infection, but not community-acquired.
• Antifungal cover — reserved for high-risk groups; over-use drives resistance.
• Optimal duration — the trend is to shorter courses (around 4 days) post-source control.
• Laparoscopy versus open — laparoscopic source control increasingly used where expertise exists.
• Peritoneal lavage volumes — extensive lavage offers no benefit over limited targeted lavage.[1]

The mantra, and the mnemonics

[1] [3] [15]

The mantra: cirrhotic plus ascites plus fever — tap before you assume; PMN over 250 — cefotaxime plus albumin; perforation — theatre, not more imaging; source control is the single determinant of survival in secondary peritonitis.[14][6]

Ward-round test — three stems, thirty seconds each

Stem 1 — the cirrhotic with encephalopathy (answer)

A 60-year-old man with alcoholic cirrhosis and ascites is brought in confused and febrile; his abdomen is soft. What is the first step, and what is the treatment if the ascitic PMN is 600 cells per mm³? Model: This is SBP until proven otherwise — a diagnostic tap is mandatory in any cirrhotic with ascites and fever, encephalopathy or renal failure; SBP may even be clinically silent. Tap the left iliac fossa, send for cell count, culture (inoculate blood culture bottles at the bedside — positivity rises from 42 to 91 percent), protein, glucose, LDH and CEA. An ascitic PMN of 600 (over 250) is SBP — treat empirically before culture returns: cefotaxime (2 g IV every 6 hours in the classic randomised trial) plus IV albumin 1.5 g per kg on day 1 and 1 g per kg on day 3 (Sort 1999 — renal impairment 33 to 10 percent, in-hospital mortality 29 to 10 percent). Repeat the tap at 48 hours — the PMN should fall below half its baseline value; if it does not, suspect secondary peritonitis or a resistant organism. Start secondary prophylaxis with norfloxacin and refer for liver transplantation.[14][15][11][3][16][12]

Stem 2 — the perforated ulcer in the small hours (answer)

A 50-year-old woman rolled over in bed, felt something tear, and now lies board-like with absent bowel sounds and free gas under the diaphragm. What do you do in the next two hours? Model: This is generalised secondary peritonitis from a perforated viscus — almost certainly a perforated peptic ulcer given the epigastric onset and free gas. Resuscitate first and run antibiotics concurrently with imaging: IV access, blood cultures before antibiotics (without delaying them), IV crystalloid resuscitation, broad-spectrum antibiotics covering enteric Gram-negatives and anaerobes, titrated opioid analgesia, an NG tube and a urinary catheter. Confirm free gas on an erect CXR or CT; if stable, a CT with contrast localises the source. Then urgent source control in theatre: operative repair of the perforation (open or laparoscopic), followed by acid suppression, H. pylori testing and eradication, and stopping NSAIDs. Free gas plus peritonism equals theatre, not more imaging — prompt recognition, resuscitation when required, appropriate antibiotic therapy and timely surgical or radiological treatment are the WSES cornerstones of complicated peptic ulcer care.[2][6]

Stem 3 — the polymicrobial ascites (answer)

A cirrhotic tapped for suspected SBP returns an ascitic PMN of 8000, multiple organisms on Gram stain including anaerobes, glucose 35 mg per dL, LDH high and CEA 8 ng per mL. The registrar wants to start cefotaxime. What is the right call? Model: This is NOT SBP — it is secondary bacterial peritonitis from a perforation. The discriminators are polymicrobial ascites with total protein over 1 g per dL, glucose under 50 mg per dL, LDH above the serum upper limit and CEA over 5 ng per mL — the validated perforation criteria, 100 percent sensitive for gut perforation — all of which imply a hollow-viscus perforation, not monomicrobial translocation. Cefotaxime alone will fail because the source is uncontrolled. Order a CT with contrast to find and localise the perforation (often appendicitis, diverticulitis or a colonic lesion), start broad-spectrum antibiotics covering enteric Gram-negatives and anaerobes, and arrange urgent surgical source control. Treating polymicrobial ascites as SBP is a classic and fatal pitfall.[16][17][4]

References

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2. [2]Tarasconi A, Coccolini F, Biffl WL, et al. Perforated and bleeding peptic ulcer: WSES guidelines World J Emerg Surg, 2020.PMID 31921329
3. [3]Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis N Engl J Med, 1999.PMID 10432325
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 Surg Infect (Larchmt), 2010.PMID 20163262
5. [5]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
6. [6]Coccolini F, Sartelli M, Sawyer R, et al. Source control in emergency general surgery: WSES, GAIS, SIS-E, SIS-A guidelines World J Emerg Surg, 2023.PMID 37480129
7. [7]Podda M, Ceresoli M, De Simone B, et al. Diagnosis and Treatment of Acute Appendicitis: 2025 Edition of the World Society of Emergency Surgery Jerusalem Guidelines JAMA Surg, 2026.PMID 41604201
8. [8]Guevara M, Terra C, Nazar A, et al. Albumin for bacterial infections other than spontaneous bacterial peritonitis in cirrhosis. A randomized, controlled study J Hepatol, 2012.PMID 22732511
9. [9]Sawyer RG, Claridge JA, Nathens AB, et al. Trial of short-course antimicrobial therapy for intraabdominal infection N Engl J Med, 2015.PMID 25992746
10. [10]Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA, 2016.PMID 26903338
11. [11]Rimola A, Salmerón JM, Clemente G, et al. Two different dosages of cefotaxime in the treatment of spontaneous bacterial peritonitis in cirrhosis: results of a prospective, randomized, multicenter study Hepatology, 1995.PMID 7875666
12. [12]Ginés P, Rimola A, Planas R, et al. Norfloxacin prevents spontaneous bacterial peritonitis recurrence in cirrhosis: results of a double-blind, placebo-controlled trial Hepatology, 1990.PMID 2210673
13. [13]Llach J, Rimola A, Navasa M, et al. Incidence and predictive factors of first episode of spontaneous bacterial peritonitis in cirrhosis with ascites: relevance of ascitic fluid protein concentration Hepatology, 1992.PMID 1505916
14. [14]Hoefs JC, Runyon BA Spontaneous bacterial peritonitis Dis Mon, 1985.PMID 3899555
15. [15]Runyon BA, Umland ET, Merlin T Inoculation of blood culture bottles with ascitic fluid. Improved detection of spontaneous bacterial peritonitis Arch Intern Med, 1987.PMID 3541825
16. [16]Akriviadis EA, Runyon BA Utility of an algorithm in differentiating spontaneous from secondary bacterial peritonitis Gastroenterology, 1990.PMID 2293571
17. [17]Wu SS, Lin OS, Chen YY, et al. Ascitic fluid carcinoembryonic antigen and alkaline phosphatase levels for the differentiation of primary from secondary bacterial peritonitis with intestinal perforation J Hepatol, 2001.PMID 11281549
18. [18]Guarner C, Soriano G Spontaneous bacterial peritonitis Semin Liver Dis, 1997.PMID 9308125
19. [19]Gluud LL, Christensen K, Christensen E, Krag A Terlipressin for hepatorenal syndrome Cochrane Database Syst Rev, 2012.PMID 22972083
20. [20]Chavez-Tapia NC, Barrientos-Gutierrez T, Tellez-Avila F, et al. Meta-analysis: antibiotic prophylaxis for cirrhotic patients with upper gastrointestinal bleeding - an updated Cochrane review Aliment Pharmacol Ther, 2011.PMID 21707680
21. [21]Sganga G, Wang M, Capparella MR, et al. Evaluation of anidulafungin in the treatment of intra-abdominal candidiasis: a pooled analysis of patient-level data from 5 prospective studies Eur J Clin Microbiol Infect Dis, 2019.PMID 31280481