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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.

Ascites, hepatomegaly and splenomegaly

Gastroenterology and hepatology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Escalate

Fever, abdominal pain, encephalopathy, hypotension, ileus, acute kidney injury or otherwise unexplained decompensation with ascites requires urgent diagnostic paracentesis and treatment for possible spontaneous bacterial peritonitis. Sudden left-upper-quadrant pain, shock or falling haemoglobin with splenomegaly raises rupture and requires immediate resuscitation and imaging.

Synopsis

Distinguish fluid, liver and spleen enlargement at the bedside, identify decompensated cirrhosis, spontaneous bacterial peritonitis, malignancy and vascular disease promptly, and use ultrasound plus diagnostic paracentesis to establish mechanism.

  • New ascites is a diagnosis to explain, not merely a sign to diurese: confirm it with ultrasound and sample it unless a clear contraindication or specialist reason exists.
  • Any patient with cirrhosis and ascites admitted acutely should have prompt diagnostic paracentesis, including when abdominal pain or fever is absent.
  • Ascitic neutrophils at or above 250 cells/mm³ support spontaneous bacterial peritonitis and should trigger immediate treatment under the local pathway.
  • Calculate the serum-ascites albumin gradient from paired samples: 11 g/L or greater supports portal-hypertensive mechanisms, while a lower gradient redirects the differential.
  • Massive paracentesis treats tense or refractory ascites; give albumin according to current guidance and the volume removed, and monitor renal function and circulation.
  • A pulsatile tender liver suggests congestion, a hard irregular liver suggests malignancy or cirrhosis, and a smooth massive liver has a different differential; examination alone cannot settle cause.
  • Splenomegaly may reflect portal hypertension, haematological malignancy, infection, haemolysis or storage disease; cytopenias are not automatically hypersplenism.
  • Tense ascites with respiratory compromise, shock, peritonism, acute kidney injury or encephalopathy needs same-day senior and hepatology review.

Key red flags

Spontaneous bacterial peritonitis

Fever, abdominal pain, encephalopathy, hypotension, ileus, acute kidney injury or otherwise unexplained decompensation can be the presentation. A painless abdomen is common enough that routine admission taps matter.

Vascular or congestive disease

Painful hepatomegaly, rapid ascites, raised JVP, oedema or a pulsatile liver suggests cardiac congestion or hepatic venous outflow obstruction; Doppler and cardiac assessment are important.

Splenic emergency

Sudden left upper-quadrant pain, shoulder-tip pain, shock or falling haemoglobin in a person with splenomegaly raises rupture or infarction and requires immediate resuscitation and imaging.

Investigation priorities

01
Abdominal ultrasound with DopplerFirst step

Confirm ascites, measure liver and spleen, assess contour and focal lesions, and evaluate portal and hepatic venous flow while identifying a safe paracentesis window.

Management branches

TapNew or admitted ascites

New ascites, or cirrhosis with ascites during an acute hospital admission.

  1. Assess ABCDE, renal function, encephalopathy, bleeding and sepsis; use ultrasound to confirm fluid and select a safe site.
  2. Perform prompt diagnostic paracentesis and send cell count, bedside cultures, albumin and protein, adding cytology or other tests only where indicated.
  3. Calculate SAAG and combine it with protein, imaging and clinical context to separate portal-hypertensive, malignant, cardiac, pancreatic and infectious mechanisms.
  4. Assign ownership for cultures and cytology that will mature after the initial decision.

Key medicines

SpironolactoneA common specialist starting regimen for a first presentation of moderate cirrhotic ascites is 100 mg orally daily, titrated cautiously up to 400 mg daily; verify current BNF, renal function and local hepatology policy.Hyperkalaemia, renal dysfunction, hyponatraemia, gynaecomastia and hypotension. Stop or reduce during significant AKI, severe electrolyte disturbance or sepsis under specialist guidance.
FurosemideOften 40 mg orally daily when combination therapy is appropriate, titrated with spironolactone up to a specialist maximum such as 160 mg daily; use current BNF and local protocol.Hypovolaemia, hypokalaemia, hyponatraemia, AKI, ototoxicity at high exposure and precipitated encephalopathy. Daily weight loss should remain within the specialist target.
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Sources and review status4 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.

  • BSG and BASL guideline on ascites in cirrhosisDiagnostic paracentesis, SBP, diuretics, albumin, TIPS and refractory ascites.
  • BSG and BASL decompensated cirrhosis admission bundleFirst-24-hour acute assessment and complication care.
  • NICE NG50: Cirrhosis in over 16sUK cirrhosis assessment, surveillance and decompensation context.
  • BNF: DiureticsCurrent UK dose, contraindication, interaction and monitoring context.

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