Ascites and spontaneous bacterial peritonitis

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

Sinusoidal portal hypertension drives vasodilatation in the splanchnic bed. Effective arterial volume falls despite total-body fluid excess, activating renin-angiotensin, sympathetic and antidiuretic systems. Sodium and water are retained, lymph formation exceeds drainage and fluid enters the peritoneum. This explains why simply replacing albumin or restricting water in every patient is ineffective, and why aggressive diuresis can compromise kidney perfusion before all visible oedema disappears.

Paracentesis is diagnostic, not merely therapeutic. Cell count and differential identify neutrocytic infection; albumin paired with same-day serum albumin gives the gradient; total protein helps risk and differential; bedside culture guides later narrowing. SBP is infection without a surgically treatable intra-abdominal source and may cause only encephalopathy or renal deterioration. Secondary peritonitis from perforation or inflammation is suggested by polymicrobial culture, focal peritonism, biochemical features, imaging and failure of neutrophils or physiology to improve.

Long-term treatment aligns salt intake, diuresis and drainage with perfusion. BSG/BASL guidance supports moderate dietary salt restriction with dietetic help, not starvation or severe unpalatable restriction. Weight loss during diuresis should generally not exceed about 0.5 kg daily without peripheral oedema or 1 kg with oedema. Tense fluid is treated by one-session large-volume paracentesis and albumin replacement. Recurrence despite tolerated therapy prompts TIPS, transplant and palliative drainage discussions based on goals and candidacy.

Key points

Ascites in cirrhosis results from portal hypertension, splanchnic vasodilatation, neurohumoral sodium retention and impaired free-water handling rather than low albumin alone.
New-onset ascites requires diagnostic paracentesis to confirm portal aetiology and exclude malignancy, infection, cardiac disease, pancreatic disease or tuberculosis.
A serum-ascites albumin gradient of at least 11 g/L supports portal hypertension but does not identify the exact hepatic or cardiac cause.
All hospital admissions with cirrhosis and ascites should be tapped promptly because SBP can present without fever, pain or leucocytosis.
Ascitic neutrophils at or above 250 cells/mm³ establish the treatment threshold for SBP even when culture is negative.
Inoculating ascitic fluid into blood-culture bottles at the bedside improves organism recovery and should occur before antibiotics when it does not delay treatment.
Spironolactone is the main initial diuretic for moderate first ascites; recurrent or severe fluid often needs combined spironolactone and furosemide with close renal and electrolyte monitoring.
Large-volume paracentesis relieves tense or refractory ascites, with albumin 8 g per litre removed when more than five litres is drained.
NSAIDs, hypotension, infection, over-diuresis and nephrotoxic medicines can precipitate acute kidney injury and hepatorenal physiology.
Refractory ascites or any SBP episode should trigger transplant consideration, and selected patients may benefit from TIPS after cardiac, encephalopathy and liver-reserve review.

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

Portal-hypertensive cirrhosis

Cirrhosis is the commonest cause, combining portal pressure, splanchnic vasodilatation and renal sodium retention to accumulate low-protein peritoneal fluid.

Non-cirrhotic fluid formation

Malignancy, cardiac failure, portal or hepatic venous obstruction, pancreatitis, infection and nephrotic disease cause ascites through distinct pressure, permeability or leakage mechanisms.

Spontaneous bacterial infection

In cirrhotic ascites, intestinal bacterial translocation and impaired immune clearance can infect fluid without a surgically treatable intra-abdominal source.

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

1
Portal and splanchnic imbalance
Raised sinusoidal pressure and splanchnic vasodilatation shift fluid into the peritoneum and reduce effective arterial circulating volume.
2
Renal retention
Neurohormonal activation increases renal sodium and water retention, further expanding ascites despite overall intravascular underfilling and peripheral oedema.
3
Infection-driven circulatory failure
Bacterial translocation into ascitic fluid intensifies vasodilatation and inflammation, precipitating encephalopathy, acute kidney injury and shock.

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

Uncomplicated moderate ascites

Progressive abdominal distension, shifting dullness, ankle oedema and early satiety develop without pain, hypotension, renal injury or encephalopathy.

Tense symptomatic ascitesRed flag

Marked abdominal pressure causes pain, dyspnoea, poor intake, reflux or an umbilical hernia and usually needs therapeutic paracentesis.

Subtle spontaneous bacterial peritonitisRed flag

New confusion, kidney injury, ileus, low temperature, hypotension or unexplained decompensation occurs without classical abdominal pain or fever.

Overt peritoneal infectionRed flag

Fever, diffuse tenderness, rebound, worsening jaundice and shock accompany an ascitic neutrophil response and require immediate sepsis therapy.

Secondary peritonitis patternRed flag

Focal severe pain, rigid abdomen, free gas, multiple cultured organisms or poor antibiotic response suggests a perforated or inflamed viscus needing source control.

Diuretic complicationRed flag

Postural dizziness, cramps, confusion, rising creatinine, hyponatraemia, hypokalaemia or hyperkalaemia develops during fluid loss and requires prompt dose and cause review.

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 paracentesis cell count and differentialFirst step
Why
Identify neutrocytic ascites and establish the SBP treatment threshold.
Interpretation and limitations
Treat an absolute neutrophil count at or above 250 cells/mm³ as SBP after considering a secondary source; do not wait for culture positivity.
02
Ascitic bedside blood-culture inoculation
Why
Improve bacterial yield before antimicrobial exposure.
Interpretation and limitations
Inoculate aerobic and anaerobic bottles at the bedside and obtain blood cultures when sepsis is possible. Culture-negative neutrocytic ascites still receives SBP treatment.
03
Serum-ascites albumin gradient
Why
Separate portal-hypertensive from non-portal mechanisms.
Interpretation and limitations
A gradient at least 11 g/L supports portal pressure from cirrhosis, cardiac failure or vascular disease. A lower gradient raises malignancy, tuberculosis, pancreatic or serosal disease and prompts targeted tests.
04
Ascitic total protein
Why
Refine aetiology and future SBP risk.
Interpretation and limitations
Low protein is typical of cirrhosis and increases infection vulnerability; higher protein with a high gradient can suggest cardiac ascites. Interpret alongside cytology, amylase or microbiology when the phenotype is atypical.
05
Blood count, renal, liver, coagulation and lactate profile
Why
Assess sepsis, organ dysfunction and diuretic safety.
Interpretation and limitations
Rising creatinine or lactate, falling sodium, coagulopathy and leucocytosis increase severity, but normal inflammatory markers do not exclude SBP in immune-dysfunctional cirrhosis.
06
Abdominal ultrasonography with Doppler
Why
Confirm fluid, guide a safe tap and assess liver, portal vein and focal disease.
Interpretation and limitations
Ultrasound identifies a pocket in small-volume or loculated ascites and can detect portal thrombosis, HCC or Budd-Chiari features; it should not delay an obvious safe emergency tap.
07
Contrast-enhanced CT abdomen
Why
Find perforation, abscess, ischaemia or malignancy when secondary peritonitis is plausible.
Interpretation and limitations
Free air, focal inflammation, collection or bowel compromise redirects from SBP-only treatment to urgent surgical or radiological source control.
08
Repeat paracentesis after treatment
Why
Assess microbiological response in atypical or poorly improving SBP.
Interpretation and limitations
Failure of neutrophils and clinical state to fall appropriately prompts resistant-organism, incorrect antibiotic and secondary-source review; timing follows the specialist protocol.

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

Malignant ascites

Weight loss, peritoneal nodularity, omental disease and fluid cytology may support malignancy; the albumin gradient helps distinguish portal-pressure mechanisms.

Cardiac ascites

Raised jugular venous pressure, peripheral oedema, right-heart dysfunction and relatively protein-rich portal-hypertensive fluid favour cardiac congestion.

Secondary bacterial peritonitis

Focal peritonism, polymicrobial culture, poor response or imaging evidence of perforation or abscess suggests a source requiring surgical or radiological control.

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

01New ascitesTap before assuming the causeFirst stepAscites is newly detected or a cirrhotic patient with fluid is admitted.

1Assess haemodynamics, respiratory compromise, pain, encephalopathy, bleeding and kidney function and identify a safe paracentesis site with ultrasound when needed.
2Send cell count and differential, albumin and protein, inoculate culture bottles at the bedside and pair with same-day serum albumin.
3Add cytology, amylase, mycobacterial or other tests only when malignancy, pancreas or infection phenotype supports them.
4Use the gradient, protein, imaging and liver assessment to confirm portal ascites and treat any neutrocytic infection immediately.

02SBPTreat infection and protect the kidneysAscitic neutrophils are at least 250 cells/mm³ or SBP is strongly suspected before the count returns.

1Start empiric IV antibacterials selected for community versus hospital acquisition, allergy, renal function and local resistance and obtain cultures without delaying therapy.
2Give IV albumin under the BSG/BASL renal-risk regimen when creatinine is increased or rising and stop nephrotoxins, reviewing diuretics and NSBB against perfusion.
3Search for other infection, bleeding and organ failure and reassess physiology, renal function and mental state closely in a high-acuity setting.
4Repeat fluid assessment for inadequate response, investigate secondary peritonitis and arrange long-term secondary prophylaxis and transplant review after recovery.

03Tense fluidDrain once and replace effective volumeLarge or tense ascites causes pain, dyspnoea, poor intake or failed diuretic control.

1Perform therapeutic large-volume paracentesis using sterile technique, recording volume, blood pressure and symptoms and sending diagnostics if not already obtained.
2When more than five litres is removed, infuse 20% or 25% albumin at 8 g per litre drained after completion, using the local product and fluid protocol.
3Review kidney function, sodium, blood pressure and diuretics after drainage and avoid rapid repeated small taps when one controlled session is feasible.
4For recurrent refractory fluid assess TIPS, transplant, long-term drainage or palliative options through a multidisciplinary and patient-goal discussion.

04Diuretic careLose sodium without losing perfusionPortal-hypertensive ascites remains after acute infection and kidney injury have been excluded or treated.

1Give dietitian-supported moderate salt restriction, review NSAIDs and nephrotoxins and record baseline weight, blood pressure, sodium, potassium and creatinine.
2Use spironolactone alone for suitable first moderate ascites or combine with furosemide for recurrent or severe disease under the current BSG regimen.
3Target weight loss no faster than about 0.5 kg daily without oedema or 1 kg with oedema and recheck bloods soon after starting or changing dose.
4Reduce or stop treatment for AKI, severe sodium or potassium disturbance, symptomatic hypotension, worsening encephalopathy or disabling cramps and reassess the strategy.

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

Promotes renal sodium loss by antagonising aldosterone, with loop diuresis added to increase effect and balance potassium in recurrent or marked ascites.

Spironolactone with or without furosemide

For suitable moderate first ascites, BSG guidance starts spironolactone 100 mg daily; recurrent or severe fluid may start spironolactone 100 mg with furosemide 40 mg daily, titrated stepwise only under weight, renal and electrolyte monitoring.

Hold or reduce for AKI, severe hyponatraemia, potassium disturbance, hypotension or encephalopathy. Spironolactone can cause gynaecomastia; furosemide can cause hypokalaemia and ototoxicity. Avoid NSAIDs and monitor early after every change.

Treats spontaneous infection of ascitic fluid once neutrophils reach the diagnostic threshold or clinical suspicion is high.

Empiric intravenous antibacterial for SBP

Start the current local cirrhosis-sepsis regimen immediately, choosing the agent and dose from community versus nosocomial acquisition, recent prophylaxis or cultures, allergy, kidney function and local resistance patterns.

Culture first when this causes no delay, then narrow appropriately. Review Clostridioides difficile, renal and QT risks and investigate a resistant organism or secondary abdominal source when response is inadequate.

Reduces post-paracentesis circulatory dysfunction and, in renal-risk SBP, lowers kidney failure and mortality alongside antibiotics.

Human albumin solution

After paracentesis above five litres give 8 g albumin per litre removed. In SBP with increased or rising creatinine, BSG guidance recommends 1.5 g/kg within six hours of diagnosis followed by 1 g/kg on day three, using local maximum and fluid-safety governance.

Albumin is not a substitute for drainage, antibiotics or source control. Monitor pulmonary oedema, oxygenation and fluid balance, particularly with cardiac disease, and do not give repeated unstructured infusions for low serum albumin alone.

Reduces recurrence in a group with high repeat-infection risk while transplant suitability and definitive liver care are assessed.

Secondary SBP antibacterial prophylaxis

After recovery from confirmed SBP, hepatology and microbiology select a long-term oral prophylactic agent and BNF dose from current resistance, allergy, renal function and prior cultures; review the indication and supply regularly.

Long-term exposure selects resistant organisms and increases adverse-effect and Clostridioides difficile risk. Breakthrough infection may need broader empiric cover; primary prophylaxis requires separate high-risk assessment, not automatic treatment of all ascites.

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

Hepatorenal dysfunction

Severe vasodilatation, infection and over-diuresis can reduce renal perfusion, causing acute kidney injury or hepatorenal syndrome.

Respiratory and mechanical effects

Tense fluid restricts diaphragmatic movement, impairs eating and mobility, and promotes abdominal-wall hernias or leakage from umbilical defects.

Encephalopathy and recurrent infection

SBP commonly precipitates cognitive deterioration and has substantial recurrence risk, making secondary prevention and transplant assessment clinically important.

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

During SBP monitor blood pressure, oxygen, urine output, mental state, creatinine, sodium, lactate and inflammatory trajectory, escalating early for shock or organ failure.
After starting or increasing diuretics record daily weight and check creatinine, sodium and potassium at the local early interval and after illness or poor intake.
During large-volume drainage document volume, albumin replacement, haemodynamics and respiratory response and recheck renal function when clinically at risk.
Track recurrence of abdominal distension, hernia symptoms, nutrition and frailty and avoid severe salt restriction that reduces already inadequate intake.
Review prophylactic antibiotic adherence, adverse effects, cultures and local resistance and investigate every breakthrough decompensation rather than assuming recurrent SBP.
After refractory ascites or SBP ensure transplant, TIPS, goals-of-care and community drainage plans have named ownership and planned reassessment.

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

SBP can be painless

Immune dysfunction blunts fever and peritonism, so encephalopathy or kidney injury may be the only clue and admission itself justifies a tap.

Culture-negative still counts

Neutrocytic ascites meets the treatment threshold even when cultures remain sterile after low bacterial load or prior antibiotic exposure.

The gradient explains pressure

A high serum-ascites albumin gradient identifies portal physiology but cannot distinguish cirrhosis from cardiac or vascular causes on its own.

Albumin follows indications

Its strongest routine roles here are large-volume paracentesis replacement and selected renal-risk SBP, not correction of a laboratory concentration.

Refractory fluid is prognostic

Repeated drainage is not merely a procedural inconvenience; it should accelerate TIPS, transplant and person-centred future-care discussion.

11Common pitfallsFrequent interpretation and management errors.

01
Starting diuretics for new ascites without diagnostic paracentesis and missing infection or malignancy.
02
Reassuring from absent fever or abdominal pain in a confused cirrhotic patient with ascites.
03
Waiting for positive ascitic culture before treating a neutrophil count at or above 250 cells/mm³.
04
Giving repeated crystalloid after large-volume drainage while omitting indicated weight-based albumin replacement.
05
Continuing spironolactone and furosemide unchanged through AKI, severe hyponatraemia or hypotension.
06
Calling poor-response polymicrobial peritonitis SBP without CT and urgent surgical source-control review.