spontaneous bacterial peritonitis
Contents
Infection of ascitic fluid without a surgically treatable intra-abdominal source. Diagnosed by ascitic fluid PMN ≥250 cells/mm³ — do not wait for cultures. Treat empirically with a third-generation cephalosporin plus albumin (1.5 g/kg day 1, 1 g/kg day 3). SBP is the single most common precipitant of hepatorenal syndrome, and albumin at diagnosis is one of the few interventions proven to prevent it. Every patient who survives an episode needs lifelong secondary prophylaxis.
SBP develops through bacterial translocation across a gut wall made permeable by portal hypertension and mucosal oedema, into ascitic fluid with impaired opsonic activity. It complicates roughly 10–30% of hospitalisations in patients with cirrhosis and ascites, and in-hospital mortality sits at 20–30% even with treatment. The two things that have most improved outcomes are albumin co-administration and antibiotic prophylaxis in high-risk groups — both are underused.
pathophysiology
The gut barrier in portal hypertension is leaky. Intestinal bacterial overgrowth (driven by reduced motility and mucosal congestion) plus increased mucosal permeability allows viable organisms to cross into mesenteric lymph nodes and then the systemic circulation — bacterial translocation. Ascitic fluid with a low protein concentration (below 15 g/L) has reduced complement and opsonic activity, so bacteria that reach the peritoneum survive and proliferate rather than being cleared.
The organisms are overwhelmingly enteric gram-negatives (E. coli, Klebsiella) and gram-positive cocci (Streptococcus, Enterococcus). Single-organism infection is the rule; polymicrobial growth should raise suspicion for secondary peritonitis.
SBP triggers a systemic inflammatory response that worsens the haemodynamic derangement of cirrhosis — arterial vasodilation deepens, effective circulating volume falls further, and the kidney bears the cost. This is the pathophysiological bridge between SBP and hepatorenal syndrome.
diagnosis
when to tap
Every patient with cirrhosis and ascites admitted to hospital should have a diagnostic paracentesis, regardless of the reason for admission. Also tap for any new symptom — fever, abdominal pain, encephalopathy, ileus, unexplained deterioration, GI bleeding, or rising creatinine. There is no threshold below which the pre-test probability is low enough to skip the tap.
SBP is clinically silent in up to a third of cases. Fever, abdominal pain, and peritoneal signs are absent more often than they are present. The diagnosis is made by the lab, not the bedside. Waiting for symptoms before tapping is the single most common error.
diagnostic criteria
| entity | ascitic fluid PMN | culture | action |
|---|---|---|---|
| SBP | ≥250 cells/mm³ | positive (usually monomicrobial) | treat |
| culture-negative neutrocytic ascites (CNNA) | ≥250 cells/mm³ | negative | treat as SBP |
| monomicrobial non-neutrocytic bacterascites | <250 cells/mm³ | positive (single organism) | repeat tap in 48h; treat if symptomatic or PMN rise |
| secondary bacterial peritonitis | usually very high (often >1000) | polymicrobial | surgical evaluation |
The threshold is 250 PMN/mm³ (equivalent to 0.25 × 10⁹/L). This is PMNs specifically, not total WBC — the lab must provide a differential. If only a total nucleated cell count is available, a rough rule is that PMN fraction in infected ascites is typically above 50%.
culture technique
Inoculate blood culture bottles at the bedside — 10 mL into aerobic and 10 mL into anaerobic bottles. This raises sensitivity from roughly 50% (lab-sent fluid) to about 80%. Culture-negative neutrocytic ascites is still SBP and receives the same treatment.
ruling out secondary peritonitis
Secondary peritonitis (perforated viscus, abscess) requires surgery and will not respond to antibiotics alone. Suspect it when:
- ascitic fluid shows two or more of Runyon’s criteria: glucose <2.8 mmol/L, protein >10 g/L, LDH above the upper limit of normal for serum
- polymicrobial culture (especially anaerobes or fungi)
- PMN count is extremely high (often >5000 cells/mm³)
- patient does not improve on appropriate antibiotics within 48 hours
Get CT abdomen and involve surgery early. Missing secondary peritonitis is fatal.
management
empiric antibiotics
Start antibiotics immediately after the diagnostic tap — do not wait for culture results. The choice depends on where the infection was acquired.
| setting | first-line | alternatives | notes |
|---|---|---|---|
| community-acquired, no quinolone prophylaxis | ceftriaxone 2 g IV daily or cefotaxime 2 g IV q8h | amoxicillin-clavulanate IV | 3rd-gen cephalosporins remain reliable here |
| community-acquired, on quinolone prophylaxis | ceftriaxone 2 g IV daily or cefotaxime 2 g IV q8h | — | quinolone resistance is expected |
| nosocomial or healthcare-associated | piperacillin-tazobactam or meropenem | — | local resistance patterns should guide choice; MRSA/VRE cover if prevalence is high |
In patients already on quinolone prophylaxis, the organisms causing SBP are predictably quinolone-resistant and increasingly resistant to third-generation cephalosporins as well. Nosocomial SBP carries a substantially different microbiological profile — gram-positives (including MRSA and Enterococcus) and resistant gram-negatives are more common, and empiric coverage must be broader.
Duration: 5 days is standard. Longer courses have not shown benefit and increase the risk of fungal superinfection.
repeat paracentesis
Repeat the tap at 48 hours. A fall in PMN count of at least 25% from baseline confirms response. If the PMN count has not fallen — or has risen — reconsider the diagnosis (secondary peritonitis? resistant organism? wrong antibiotic?) and broaden coverage.
albumin
Albumin co-administration with antibiotics reduces the incidence of hepatorenal syndrome and mortality. This is one of the best-supported interventions in hepatology, based on Sort (NEJM 1999).
- Day 1: 1.5 g/kg IV (max 100 g)
- Day 3: 1 g/kg IV (max 100 g)
The benefit is clearest in patients with bilirubin above 68 µmol/L or creatinine above 88 µmol/L — these are the patients at highest risk of developing HRS. In a patient with normal renal function, normal bilirubin, and no haemodynamic compromise, the absolute benefit is smaller, but the standard of care is to give it to all SBP patients.
The albumin must be given at the time of SBP diagnosis, not after renal function deteriorates. By the time creatinine is rising, the window for prevention is closing. This is pre-emptive, not reactive.
what not to do
- Do not use aminoglycosides — nephrotoxicity in cirrhosis is severe and alternatives exist
- Do not use quinolones empirically if the patient is already on quinolone prophylaxis
- Do not delay antibiotics for culture results
- Do not give albumin for non-SBP infections — this does not generalise; trials of albumin in non-SBP infections have not shown a mortality benefit and carry a risk of pulmonary oedema
prophylaxis
secondary prophylaxis (after first episode)
Every patient who survives an episode of SBP should receive lifelong antibiotic prophylaxis until transplant, death, or resolution of ascites.
- First-line: norfloxacin 400 mg PO daily
- Alternatives: ciprofloxacin 500 mg PO daily, or TMP-SMX DS daily (where norfloxacin is unavailable — and norfloxacin availability in Canada is intermittent)
Without secondary prophylaxis, the one-year recurrence rate is roughly 70%.
primary prophylaxis
Primary prophylaxis is indicated in two high-risk groups:
-
Low ascitic fluid protein (<15 g/L) with at least one of:
- Child-Pugh score ≥9 with bilirubin ≥51 µmol/L
- renal dysfunction (creatinine ≥106 µmol/L, BUN ≥8.9 mmol/L, or Na ≤130 mmol/L)
-
Acute GI bleeding in cirrhosis — short-course prophylaxis (ceftriaxone 1 g IV daily for up to 7 days) reduces infection, rebleeding, and mortality. This is one of the highest-yield interventions in variceal bleeding management.
Every cirrhotic patient admitted with GI bleeding gets antibiotic prophylaxis — ceftriaxone 1 g IV daily is preferred over oral quinolones, particularly in patients with advanced liver disease (Child-Pugh B/C) or on quinolone prophylaxis already.
the resistance problem
Long-term quinolone prophylaxis selects for resistant organisms. The infections that break through prophylaxis — both SBP and non-SBP — tend to be quinolone-resistant gram-negatives and gram-positive organisms that are harder to treat. This is the trade-off: prophylaxis reduces recurrence and mortality, but it shifts the microbiology of breakthrough episodes toward more resistant and more dangerous organisms. There is no good solution to this yet. Rifaximin has been studied as an alternative, but evidence is insufficient to recommend it as a replacement for quinolone prophylaxis.
complications
hepatorenal syndrome
SBP is the most common precipitant of hepatorenal syndrome. The mechanism is straightforward: systemic inflammation from peritoneal infection amplifies the splanchnic vasodilation and haemodynamic compromise that are already present in decompensated cirrhosis, tipping the kidney into failure. Albumin at diagnosis is the primary preventive measure. Monitor creatinine daily during and after SBP treatment — a rise should prompt assessment for HRS-AKI and consideration of vasoconstrictors.
ACLF
SBP can precipitate acute-on-chronic liver failure. In patients who develop multi-organ failure during an SBP episode, mortality exceeds 50% despite treatment. Early recognition and ICU transfer for patients with haemodynamic instability or rising lactate is appropriate.
prognosis
SBP carries roughly 20–30% in-hospital mortality, and one-year survival after a first episode is approximately 30–50% without transplant. The development of SBP is itself a marker of advanced decompensation and should trigger transplant evaluation in every eligible patient — it signals a liver that can no longer maintain the gut barrier and immune function that prevent peritoneal infection.
Recurrence without prophylaxis is high (~70% at one year), which is why secondary prophylaxis is non-negotiable. Even with prophylaxis, these patients remain at high risk for other infections and progressive liver failure.
related: hepatorenal syndrome · cirrhosis · ascites · acute kidney injury · ceftriaxone · norepinephrine