Spontaneous Bacterial Peritonitis (SBP)
Summary
Spontaneous bacterial peritonitis (SBP) is an acute infection of ascitic fluid in the absence of an intra-abdominal surgically treatable source. It occurs almost exclusively in patients with cirrhosis and ascites, typically due to bacterial translocation from the gut. SBP is a serious complication with in-hospital mortality of 20-40% and triggers hepatorenal syndrome in 30% of cases. Diagnosis requires a high index of suspicion and is confirmed by ascitic fluid neutrophil count ≥250/mm³. Treatment with third-generation cephalosporins and IV albumin is life-saving. Secondary prophylaxis prevents recurrence, which has 70% annual rate without prophylaxis.
Key Facts
- Prevalence: 10-30% of hospitalised cirrhotic patients with ascites
- Cause: Bacterial translocation from gut (E. coli, Klebsiella, Streptococcus)
- Diagnosis: Ascitic fluid neutrophils ≥250/mm³
- Mortality: 20-40% in-hospital; 70% 1-year mortality post-SBP
- Hepatorenal syndrome: Develops in 30% of SBP
- Key treatment: IV cefotaxime + IV albumin (Day 1 and Day 3)
Clinical Pearls
Tap First, Ask Questions Later: Any cirrhotic patient presenting unwell should have a diagnostic paracentesis. SBP can present with fever, abdominal pain, encephalopathy, renal deterioration — or with no symptoms at all.
The Albumin Protocol: IV albumin (1.5 g/kg Day 1, 1 g/kg Day 3) prevents hepatorenal syndrome and reduces mortality. This is now standard of care.
One Episode = Prophylaxis for Life: After one episode of SBP, lifelong secondary prophylaxis (norfloxacin or ciprofloxacin) is indicated due to 70% recurrence rate.
Why This Matters Clinically
SBP is frequently under-recognised because symptoms can be subtle. Delayed treatment leads to sepsis, multi-organ failure, and death. A low threshold for paracentesis in any unwell cirrhotic patient is essential for early diagnosis.
Incidence & Prevalence
- Hospital prevalence: 10-30% of cirrhotic patients with ascites
- Community prevalence: 1-3% of outpatients with ascites
- Recurrence without prophylaxis: 70% at 1 year
Demographics
| Factor | Details |
|---|---|
| Age | Correlates with cirrhosis prevalence |
| Sex | More common in males (alcohol-related cirrhosis) |
| Underlying cause | Any cause of cirrhosis |
| Risk group | Decompensated cirrhosis, low ascitic protein |
Risk Factors for SBP
| Factor | Impact |
|---|---|
| Low ascitic protein (less than 15 g/L) | Impaired opsonic activity |
| Prior SBP | 70% recurrence without prophylaxis |
| GI bleeding | Increases bacterial translocation |
| Severe liver disease (Child-Pugh C) | Higher risk |
| Proton pump inhibitors | Possible association |
Mechanism
Step 1: Bacterial Overgrowth
- Altered gut motility and immune defects in cirrhosis
- Small intestinal bacterial overgrowth (SIBO)
- Increased intestinal permeability
Step 2: Bacterial Translocation
- Bacteria cross intestinal barrier
- Mesenteric lymph nodes and bloodstream
- Access to ascitic fluid via portal venous and lymphatic routes
Step 3: Impaired Host Defences
- Reduced ascitic fluid opsonic activity (low complement, low IgG)
- Impaired neutrophil function
- Failure to clear bacteria from ascites
Step 4: Peritoneal Infection
- Bacterial multiplication in ascitic fluid
- Inflammatory response
- Systemic inflammatory response syndrome (SIRS)
Classification
| Type | Definition | Features |
|---|---|---|
| SBP | PMN ≥250/mm³ + Positive culture | Typical SBP |
| Culture-negative neutrocytic ascites (CNNA) | PMN ≥250/mm³ + Negative culture | Treat as SBP |
| Bacterascites | PMN less than 250/mm³ + Positive culture | May resolve; repeat tap if symptomatic |
| Secondary bacterial peritonitis | Polymicrobial, surgical source | Requires surgical management |
Common Organisms:
- E. coli (40%)
- Klebsiella (15%)
- Streptococcus pneumoniae (10%)
- Enterococcus (10%)
- Others (25%)
Symptoms
Signs
Red Flags
[!CAUTION] Red Flags — Immediate paracentesis and treatment if:
- Any fever in cirrhotic patient with ascites
- New or worsening encephalopathy
- Worsening renal function
- Abdominal tenderness
- Hypotension or other signs of sepsis
- GI bleeding (high SBP risk)
Structured Approach
General:
- Vital signs (fever, tachycardia, hypotension)
- Conscious level (encephalopathy)
- Signs of sepsis
Abdominal:
- Diffuse tenderness (often mild)
- Ascites (shifting dullness)
- Peritonism (less marked than surgical causes)
Neurological:
- Asterixis (hepatic flap)
- Confusion, orientation
Special Tests
| Test | Technique | Positive Finding | Purpose |
|---|---|---|---|
| Ascitic tap | Paracentesis (bedside) | Cloudy fluid; PMN ≥250 | Diagnostic |
| Asterixis | Extended wrists | Flapping tremor | Encephalopathy |
First-Line
- Diagnostic paracentesis — Essential and urgent
- Ascitic fluid analysis — Cell count (most important), culture, albumin
Ascitic Fluid Analysis
| Test | Diagnostic Threshold | Notes |
|---|---|---|
| Neutrophil count (PMN) | ≥250/mm³ | Diagnostic of SBP |
| Gram stain | Often negative | Low sensitivity |
| Culture | inoculate at bedside | Positive in 50-80% |
| Protein | Low (less than 15 g/L) | Risk factor for SBP |
| Albumin | For SAAG calculation | Confirm portal hypertension |
| Glucose, LDH, amylase | If secondary peritonitis suspected | Rule out surgical source |
Diagnostic Criteria:
- PMN ≥250/mm³ = SBP (start treatment immediately)
Laboratory Tests
| Test | Expected Finding | Purpose |
|---|---|---|
| Blood cultures | Positive in 50% | Identify bacteraemia |
| FBC | Leukocytosis (may be absent) | Inflammatory response |
| U&Es | Raised creatinine | Hepatorenal syndrome risk |
| LFTs | Deranged | Baseline liver function |
| Lactate | Elevated if severe sepsis | Severity |
Management Algorithm
SUSPECTED SBP (Cirrhosis + Unwell)
↓
┌─────────────────────────────────────────┐
│ DIAGNOSTIC PARACENTESIS │
│ (Before or immediately after │
│ starting antibiotics) │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ ASCITIC FLUID ANALYSIS │
├─────────────────────────────────────────┤
│ PMN ≥250/mm³ → DIAGNOSE SBP │
│ PMN <250 + culture negative → Exclude │
│ PMN <250 + culture positive → Repeat │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ TREATMENT │
├─────────────────────────────────────────┤
│ 1. IV Cefotaxime 2g TDS (or │
│ Co-amoxiclav if penicillin allergy) │
│ 2. IV Albumin: │
│ Day 1: 1.5 g/kg │
│ Day 3: 1 g/kg │
│ 3. Stop diuretics, nephrotoxins │
│ 4. Repeat paracentesis at 48h if │
│ no improvement │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ SECONDARY PROPHYLAXIS │
│ Norfloxacin 400mg OD or │
│ Ciprofloxacin 500mg OD │
│ LIFELONG │
└─────────────────────────────────────────┘
Acute Treatment
Antibiotics:
- First-line: IV Cefotaxime 2g TDS for 5-7 days
- Alternative: Co-amoxiclav 1.2g TDS (if local resistance low)
- Quinolone resistance: Consider piperacillin-tazobactam if prophylaxis failure
IV Albumin (Prevents Hepatorenal Syndrome):
- Day 1: 1.5 g/kg (max 100g)
- Day 3: 1 g/kg (max 100g)
- Required if creatinine greater than 88 μmol/L or bilirubin greater than 68 μmol/L
Supportive Care:
- Stop diuretics (until infection resolved)
- Avoid nephrotoxins (NSAIDs, aminoglycosides)
- Watch for encephalopathy
Response Assessment
- Repeat paracentesis at 48 hours if poor clinical response
- Expect PMN decrease by greater than 25%
- If no response: Consider secondary peritonitis, resistant organism, or alternative diagnosis
Prophylaxis
Primary Prophylaxis (before first episode):
- Indicated if ascitic protein less than 15 g/L AND (renal impairment OR severe liver disease)
- Norfloxacin 400mg OD or Ciprofloxacin 500mg OD
Secondary Prophylaxis (after first episode):
- Lifelong unless transplanted
- Norfloxacin 400mg OD or Ciprofloxacin 500mg OD
- Alternative: Co-trimoxazole 960mg OD
Disposition
- Admit: All patients with SBP
- ICU/HDU: If septic shock, multi-organ failure, severe encephalopathy
- Follow-up: Transplant assessment, hepatology
Immediate
| Complication | Incidence | Presentation | Management |
|---|---|---|---|
| Hepatorenal syndrome | 30% | Rising creatinine, oliguria | Terlipressin + albumin |
| Septic shock | 10-20% | Hypotension, multi-organ failure | Vasopressors, ICU |
| Encephalopathy | 30% | Confusion, asterixis | Lactulose, rifaximin |
Early (Days-Weeks)
- Treatment failure: Resistant organism
- Recurrent SBP: 70% at 1 year without prophylaxis
- Worsening liver function: Acute-on-chronic liver failure
Late (Months)
- Mortality: 70% 1-year mortality post-SBP
- Need for transplant: SBP is a trigger for urgent transplant listing
Outcomes
| Variable | Outcome |
|---|---|
| In-hospital mortality | 20-40% |
| 1-year mortality | 50-70% |
| Recurrence without prophylaxis | 70% |
| HRS incidence | 30% |
Prognostic Factors
Good Prognosis:
- Low MELD score
- Good response to treatment
- Younger age
- No HRS
Poor Prognosis:
- High MELD score (greater than 20)
- Hepatorenal syndrome
- Encephalopathy
- Shock
- Nosocomial SBP (resistant organisms)
Key Guidelines
- EASL Clinical Practice Guidelines on Decompensated Cirrhosis (2018) — J Hepatol 2018
- AASLD Practice Guidance on Ascites and HRS (2021).
- BSG Guidelines on Management of Ascites and SBP (2006 — update awaited).
Key Trials
Sort et al. (1999) — Albumin + antibiotics for SBP
- 126 patients
- Key finding: IV albumin reduced HRS from 33% to 10% and mortality from 29% to 10%
- Clinical Impact: Albumin now standard of care in SBP treatment
Fernandez et al. (2007) — Primary prophylaxis for SBP
- 68 patients with low ascitic protein
- Key finding: Norfloxacin reduced SBP incidence and improved survival
- Clinical Impact: Supports primary prophylaxis in high-risk patients
Evidence Strength
| Intervention | Level | Key Evidence |
|---|---|---|
| Cefotaxime for SBP | 1b | Multiple RCTs |
| Albumin with antibiotics | 1b | Sort et al. |
| Norfloxacin prophylaxis | 1b | Fernandez et al. |
What is Spontaneous Bacterial Peritonitis?
SBP is an infection of the fluid in your tummy (ascites). It happens when bacteria from your gut get into this fluid. It is a serious complication of liver disease.
Why does it matter?
Without treatment, SBP can quickly become life-threatening. It can also damage your kidneys (hepatorenal syndrome). If treated promptly with antibiotics and albumin (a protein given through a drip), most people recover.
How is it treated?
- Antibiotics: Given through a drip immediately when SBP is suspected.
- Albumin infusion: Given on day 1 and day 3 to protect your kidneys.
- Preventing recurrence: Long-term antibiotic tablets are usually needed to stop the infection coming back.
What to expect
- You will need to stay in hospital
- Antibiotics are usually given for 5-7 days
- After recovery, you will need daily antibiotic tablets to prevent recurrence
- Your doctor may discuss liver transplant if your liver disease is advanced
When to seek help
Go to A&E or call 999 if you have liver disease and ascites, and you develop:
- Fever or chills
- Tummy pain
- Confusion or drowsiness
- Feeling very unwell
Primary Guidelines
- European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018;69(2):406-460. PMID: 29653741
Key Trials
- Sort P, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med. 1999;341(6):403-9. PMID: 10432325
- Fernandez J, et al. Primary prophylaxis of spontaneous bacterial peritonitis delays hepatorenal syndrome and improves survival in cirrhosis. Gastroenterology. 2007;133(3):818-24. PMID: 17854593
Further Resources
- British Liver Trust: britishlivertrust.org.uk
- NHS Liver Disease: nhs.uk/conditions/liver-disease
Last Reviewed: 2025-12-24 | MedVellum Editorial Team
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.