Ascites and spontaneous bacterial peritonitis — Rapid

Synopsis

Diagnose new ascites with prompt paracentesis, treat portal fluid retention safely and recognise spontaneous bacterial peritonitis before renal failure develops.

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.

Key red flags

Tense symptomatic ascites

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

Subtle spontaneous bacterial peritonitis

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

Overt peritoneal infection

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

Secondary peritonitis pattern

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

Diuretic complication

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

Investigation priorities

Diagnostic paracentesis cell count and differentialFirst step

Identify neutrocytic ascites and establish the SBP treatment threshold.

Management branches

New ascitesTap before assuming the cause

Ascites is newly detected or a cirrhotic patient with fluid is admitted.

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

Key medicines

Spironolactone with or without furosemideFor 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.

Empiric intravenous antibacterial for SBPStart 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.

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