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Educational draft · awaiting clinical reviewUse Rapid for revision, not patient-care decisions. Check current national and local guidance and the BNF or BNFC before acting.

Spontaneous bacterial peritonitis

Infectious diseases, microbiology and sexual health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Decompensated cirrhosis with suspected peritonitis

Shock, encephalopathy, acute kidney injury, gastrointestinal bleeding or abdominal signs in a person with ascites may represent spontaneous bacterial peritonitis and rapid multiorgan deterioration.

Action: Use ABCDE, perform urgent diagnostic paracentesis without waiting for coagulopathy correction in routine circumstances, culture blood and ascites, start locally appropriate intravenous antibiotics and involve hepatology and critical care.

Synopsis

Diagnose spontaneous bacterial peritonitis promptly in cirrhosis with ascites, treat before deterioration, prevent renal failure and distinguish a surgically treatable secondary peritonitis.

  • Spontaneous bacterial peritonitis is infected ascitic fluid without a surgically treatable intra-abdominal source.
  • Perform diagnostic paracentesis promptly for admitted patients with cirrhosis and ascites, especially with pain, fever, encephalopathy, bleeding or renal deterioration.
  • An ascitic neutrophil count of at least 250 cells/mm³ supports treatment even when culture is negative.
  • Inoculate ascitic fluid into aerobic and anaerobic blood-culture bottles at the bedside to improve microbiological yield.
  • Start locally appropriate intravenous antibiotics after sampling; cefotaxime 2 g every eight hours is an established option where susceptibility supports it.
  • Consider intravenous human albumin solution at 1.5 g/kg within six hours and 1 g/kg on day three when creatinine is increased or rising.
  • Reassess at about 48 hours when response is uncertain; a poor neutrophil fall or polymicrobial result should trigger urgent secondary-source evaluation.
  • After recovery, arrange hepatology review, secondary prophylaxis assessment and liver-transplant consideration where appropriate.

Key red flags

Any hospital admission with cirrhosis and ascites requires prompt consideration of diagnostic paracentesis.

Hypotension, rising creatinine, oliguria or lactate indicates severe infection and circulatory dysfunction.

New encephalopathy, ileus or unexplained decompensation may be the only sign of spontaneous bacterial peritonitis.

Marked focal tenderness, free air, polymicrobial culture or poor response suggests secondary peritonitis requiring imaging and surgery.

Gastrointestinal bleeding increases bacterial infection risk and requires the separate cirrhosis bleeding prophylaxis pathway.

Subtle decompensation

New confusion, worsening ascites, renal dysfunction, hypotension, ileus or reduced intake may represent infection even without fever or marked abdominal tenderness.

Abdominal inflammatory features

Diffuse discomfort, tenderness, fever and vomiting support peritonitis, but examination can be deceptively mild in advanced cirrhosis.

High-risk admission

Gastrointestinal bleeding, previous spontaneous bacterial peritonitis, low ascitic protein, severe liver failure and recent healthcare exposure increase infection probability or resistance risk.

Features of secondary infection

Focal peritonism, very high neutrophils, polymicrobial culture, free gas, high ascitic protein or failure to respond should prompt urgent anatomical investigation.

Investigation priorities

01
Diagnostic ascitic paracentesisFirst step

Establish the neutrophil count before antibiotics and identify fluid features suggesting another source.

Management branches

TAPSample before treating promptly

A patient with cirrhosis and ascites is admitted or develops possible infection or decompensation.

  1. Perform focused ABCDE assessment, take blood cultures and arrange diagnostic paracentesis as early as possible without awaiting routine correction of INR or platelets.
  2. Send cell count and differential urgently and inoculate ascites into aerobic and anaerobic blood-culture bottles at the bedside.
  3. Start locally recommended intravenous treatment immediately after sampling when spontaneous bacterial peritonitis is suspected; do not wait for culture.
  4. Review diuretics, nephrotoxic medicines, fluid status, gastrointestinal bleeding and the need for higher-level monitoring with hepatology.

Key medicines

CefotaximeGive 2 g intravenously every eight hours for about five days when local susceptibility and the clinical setting support this regimen.Follow local policy for healthcare-associated or resistant-risk infection, adjust for severe renal impairment, clarify beta-lactam allergy and narrow or change therapy using cultures and response.
Human albumin solutionGive 1.5 g/kg intravenously within six hours of diagnosis and 1 g/kg intravenously on day three when creatinine is increased or rising.Confirm indication with hepatology, calculate dose from an appropriate weight, monitor respiratory status and fluid balance, and use caution with pulmonary oedema or severe cardiac dysfunction.
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Sources and review status3 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • British Society of Gastroenterology Guidelines on the management of ascites in cirrhosis
  • NICE NG50 Cirrhosis in over 16s assessment and management
  • NICE NG253 Suspected sepsis in people aged 16 or over

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateRapid draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
Circulatory dysfunction

Low mean arterial pressure, rising creatinine, hyponatraemia and oliguria reflect the interaction between infection, vasodilatation and reduced effective arterial volume.