Spontaneous bacterial peritonitis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Spontaneous bacterial peritonitis occurs mainly in advanced cirrhosis when enteric organisms translocate across the bowel and impaired hepatic and immune clearance allows infection of low-protein ascitic fluid.

Symptoms may be minimal. Fever and abdominal pain are useful when present, but encephalopathy, acute kidney injury, hypotension, ileus or otherwise unexplained decompensation may be the only clues.

The diagnostic threshold is an ascitic polymorphonuclear neutrophil count of at least 250 cells/mm³. Treatment should not await culture because culture-negative neutrocytic ascites is managed as spontaneous bacterial peritonitis.

Safe care for spontaneous bacterial peritonitis depends on separating physiological instability from diagnostic uncertainty: resuscitation and infection-control actions proceed while targeted samples, imaging and source-control decisions are arranged.

Antimicrobial decisions in spontaneous bacterial peritonitis should document indication, likely source, allergy phenotype, pregnancy possibility, renal and hepatic function, previous microbiology and the planned review or stop point.

Key points

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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Enteric bacterial translocation

Enterobacterales and streptococci cross an altered intestinal barrier, reach mesenteric lymph and blood, and seed ascitic fluid without a perforated viscus.

Impaired host defence

Advanced cirrhosis reduces complement, opsonic activity, reticuloendothelial clearance and neutrophil function, allowing low-inoculum infection to progress.

Healthcare and resistant exposure

Recent admission, invasive procedures, prophylactic antibiotics and previous resistant isolates increase the probability of organisms not covered by conventional community regimens.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Low-opsonin ascitic fluid
Low ascitic protein and complement weaken local bacterial killing, so translocated organisms can replicate within otherwise sterile portal-hypertensive fluid.
2
Vasodilatory circulatory failure
Infection amplifies splanchnic vasodilatation and inflammatory endothelial dysfunction, reducing effective arterial volume despite total-body fluid excess.
3
Kidney-liver interaction
Falling renal perfusion activates vasoconstrictor systems and can progress from acute kidney injury to hepatorenal syndrome during uncontrolled infection.
4
Systemic decompensation
Inflammation precipitates encephalopathy, coagulopathy, respiratory compromise and multiorgan failure in a patient with limited hepatic reserve.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Subtle decompensationRed flag

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

Abdominal inflammatory featuresRed flag

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

High-risk admissionRed flag

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 infectionRed flag

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

Circulatory dysfunctionRed flag

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

Context changes probability

Recent healthcare exposure, antimicrobial use, travel, procedures, devices, pregnancy, immune compromise and previous resistant isolates materially change the likely diagnosis and treatment risk in spontaneous bacterial peritonitis.

Red flags requiring action

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.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Diagnostic ascitic paracentesisFirst step
Why
Establish the neutrophil count before antibiotics and identify fluid features suggesting another source.
Interpretation and limitations
Treat when polymorphonuclear neutrophils are at least 250 cells/mm³. Routine cirrhosis-related coagulopathy or thrombocytopenia alone is not usually a reason to delay.
02
Bedside ascitic blood-culture inoculation
Why
Increase organism recovery and permit susceptibility-directed therapy.
Interpretation and limitations
Inoculate aerobic and anaerobic bottles immediately at the bedside. A negative culture does not exclude spontaneous bacterial peritonitis when the neutrophil threshold is met.
03
Blood cultures, full blood count and CRP
Why
Detect bacteraemia, inflammation and an alternative bloodstream source.
Interpretation and limitations
Obtain cultures before antibiotics if safe, but do not delay treatment in instability. Leucocytosis may be absent in hypersplenism or advanced disease.
04
Renal, liver, coagulation and electrolyte profile
Why
Stage decompensation, acute kidney injury and treatment risk.
Interpretation and limitations
Rising creatinine and bilirubin, hyponatraemia and coagulopathy indicate poor reserve; review nephrotoxins, diuretics and circulatory support with hepatology.
05
Ascitic protein, albumin, glucose and LDH
Why
Characterise portal hypertensive fluid and identify patterns concerning for secondary peritonitis.
Interpretation and limitations
Higher protein, low glucose, high LDH or multiple organisms should increase concern for a perforated or inflamed abdominal source but are not interpreted in isolation.
06
Contrast CT abdomen and pelvis
Why
Search for perforation, abscess, ischaemia or another treatable source when secondary peritonitis is plausible.
Interpretation and limitations
Arrange urgently for focal signs, polymicrobial culture or inadequate response; acute kidney injury requires risk mitigation, not automatic cancellation of essential imaging.
07
Host and prescribing assessment
Why
Identify modifiers that alter diagnostic yield, severity and safe prescribing for spontaneous bacterial peritonitis.
Interpretation and limitations
For spontaneous bacterial peritonitis, document beta-lactam allergy, renal trajectory, prophylactic antibiotic exposure, prior resistant isolates, gastrointestinal bleeding and interactions before choosing treatment.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Secondary bacterial peritonitis

Perforation, abscess, ischaemia or inflamed abdominal viscera can contaminate ascites and requires imaging and source control rather than antibiotics alone.

Malignant or tuberculous ascites

Subacute symptoms, lymphocyte-predominant fluid, high protein or constitutional decline should prompt cytology, mycobacterial and cross-sectional evaluation.

Pancreatic ascites

Pancreatic duct disruption produces high-amylase ascites and abdominal symptoms that may mimic infection while requiring a different intervention.

Non-infective decompensation

Bleeding, constipation, sedatives, dehydration, portal-vein thrombosis and medication toxicity can precipitate encephalopathy or renal dysfunction without spontaneous bacterial peritonitis.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01TAPSample before treating promptlyFirst stepA patient with cirrhosis and ascites is admitted or develops possible infection or decompensation.

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

02PROTECTReduce renal failure riskSpontaneous bacterial peritonitis is diagnosed and serum creatinine is increased or rising.

1Discuss intravenous human albumin solution promptly with hepatology, using 1.5 g/kg within six hours and 1 g/kg on day three when indicated.
2Assess perfusion, urine output, pulmonary congestion and cumulative fluid balance so albumin supports circulation without unrecognised overload.
3Stop or withhold avoidable nephrotoxins and review diuretics and vasoactive treatment according to haemodynamics and specialist advice.
4EscalationEscalate persistent renal deterioration for hepatorenal syndrome assessment, critical care and liver-transplant pathway consideration.

03RECHECKExclude a secondary abdominal sourceClinical response is poor, ascitic culture is polymicrobial or examination and chemistry are atypical.

1Repeat examination and review procedure timing, antimicrobial exposure and ascitic neutrophil trajectory at approximately 48 hours when uncertainty persists.
2Arrange urgent contrast CT and surgical discussion for focal peritonism, free gas, abscess, ischaemia or biochemical features of secondary peritonitis.
3Obtain deep cultures during drainage or operation and broaden therapy only with microbiology and surgical input appropriate to the suspected anatomy.
4Do not label persistent infection as resistant spontaneous bacterial peritonitis until inadequate source control has been actively excluded.

04REASSESSReview response and diagnosisSymptoms persist, physiology worsens or expected improvement in spontaneous bacterial peritonitis has not occurred.

1Repeat observations and examination, reconsider the anatomical source and look actively for obstruction, collection, perforation, ischaemia or another diagnosis complicating spontaneous bacterial peritonitis.
2Review ascitic and blood cultures, neutrophil trajectory, antibiotic exposure, renal function and albumin response; narrow, change or stop peritonitis treatment with hepatology and microbiology input.
3EscalationEscalate to the relevant medical, surgical, microbiology, infection or public-health team when source control, resistant infection, outbreak management or specialist follow-up is required for spontaneous bacterial peritonitis.
4Give cirrhosis-specific safety-net advice covering recurrent confusion, abdominal pain, fever, gastrointestinal bleeding, falling urine output and the route for urgent hospital reassessment.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Treats susceptible community-acquired enteric Gram-negative and streptococcal causes of spontaneous bacterial peritonitis.

Cefotaxime

Give 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.

Supports effective arterial volume and reduces renal impairment and mortality in higher-risk spontaneous bacterial peritonitis.

Human albumin solution

Give 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.

Reduces recurrence in people with previous spontaneous bacterial peritonitis while awaiting definitive liver management.

Ciprofloxacin secondary prophylaxis

Give 500 mg orally once daily for secondary prophylaxis when selected by hepatology and local antimicrobial policy after recovery.

Review susceptibility, interactions and renal function; discuss disabling tendon, neurological, vascular and glycaemic adverse effects, and stop promptly if serious toxicity develops.

Provides an alternative recurrence-prevention option when fluoroquinolone use is unsuitable or local policy differs.

Co-trimoxazole prophylaxis alternative

Give 960 mg orally once daily when specialist and local policy select it as an alternative secondary prophylaxis regimen.

Check renal function, potassium, full blood count, sulfonamide or trimethoprim allergy, pregnancy possibility and interactions with warfarin, methotrexate, ACE inhibitors or spironolactone.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Acute kidney injury

Infection-related vasodilatation and reduced effective arterial volume cause renal hypoperfusion and may progress to hepatorenal syndrome.

Septic shock

Bacteraemia and inflammatory vasoplegia can produce refractory hypotension, lactic acidosis and multiorgan failure in advanced liver disease.

Recurrent peritonitis

Previous spontaneous bacterial peritonitis strongly predicts recurrence, supporting specialist secondary prophylaxis and reassessment for liver transplantation.

Acute-on-chronic liver failure

Systemic inflammation can precipitate severe hepatic, cerebral, renal, coagulation and respiratory failure with high short-term mortality.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record observations, mental state and urine output frequently until haemodynamics and encephalopathy are clearly improving.
Repeat creatinine, sodium, potassium and acid-base assessment to identify evolving acute kidney injury or hepatorenal physiology.
Review ascitic and blood cultures daily and adjust treatment for susceptibility, healthcare exposure and clinical response.
Consider repeat paracentesis at about 48 hours when response is inadequate or secondary peritonitis remains possible.
Before discharge document prophylaxis, diuretic and nephrotoxin decisions, transplant or hepatology follow-up and urgent return symptoms.
At every review of spontaneous bacterial peritonitis, confirm that the working diagnosis still fits the trajectory and that microbiology or imaging has not revealed a source requiring a different intervention.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

The tap is an admission test

Waiting for pain or fever misses clinically silent infection; admitted cirrhotic patients with ascites need an early paracentesis strategy.

Neutrophils drive treatment

Culture-negative neutrocytic ascites is treated when the polymorphonuclear count reaches the diagnostic threshold because culture sensitivity is imperfect.

Culture technique changes yield

Immediate bedside inoculation into blood-culture bottles recovers more organisms than sending fluid only in a sterile universal container.

Albumin has a defined role

Albumin is not simply nutritional replacement; in higher-risk spontaneous bacterial peritonitis it is dosed to reduce circulatory and renal failure.

Polymicrobial means investigate

Multiple organisms or poor response should raise concern for perforation or another secondary source rather than automatic escalation of antibiotics alone.

Document the decision boundary

For spontaneous bacterial peritonitis, record why treatment, observation, admission, isolation or source control was chosen and which finding would trigger a change of plan.

11Common pitfallsFrequent interpretation and management errors.

01
Do not postpone paracentesis solely for a raised INR or thrombocytopenia typical of cirrhosis without another procedural contraindication.
02
Do not wait for an ascitic culture result before treating a neutrophil count of at least 250 cells/mm³.
03
Do not diagnose spontaneous bacterial peritonitis confidently when focal peritonism, free gas or polymicrobial culture suggests secondary disease.
04
Do not prescribe indefinite prophylaxis without reviewing resistance, adverse effects, adherence and the broader liver-management plan.
05
Do not overlook gastrointestinal bleeding, because it requires a separate evidence-based short antibiotic prophylaxis pathway.
06
Do not allow a positive colonisation-prone test, device sample or nonspecific inflammatory marker to outweigh the clinical syndrome when assessing spontaneous bacterial peritonitis.