Ascites, hepatomegaly and splenomegaly

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

Ascites results from portal hypertension, malignancy, cardiac congestion, infection, pancreatic disease and less common causes. Cirrhosis is common, but anchoring on it can miss ovarian or gastrointestinal malignancy, heart failure, tuberculosis or Budd-Chiari syndrome. The first questions are whether fluid is truly present, whether the patient is unstable, and what mechanism the fluid chemistry supports. Ultrasound confirms even modest fluid, identifies a safe tap site and examines liver, spleen, portal flow and masses.

Diagnostic paracentesis should usually include cell count and differential, culture with bedside inoculation into blood-culture bottles, albumin and total protein, with cytology, amylase, triglyceride or mycobacterial tests added for specific hypotheses. A high serum-ascites albumin gradient indicates portal pressure rather than cirrhosis specifically; cardiac ascites often has high gradient and relatively high protein. A low gradient raises peritoneal malignancy, tuberculosis, pancreatitis and other peritoneal processes.

Hepatomegaly and splenomegaly are anatomical findings with overlapping systemic causes. Assess texture, tenderness, pulsatility, nodularity and associated nodes, cytopenias or portal signs, but confirm with imaging. Liver disease can produce both organs through portal hypertension; congestive heart failure can cause a tender pulsatile liver and ascites; myeloproliferative or lymphoid disease may cause major splenomegaly. The management target is the cause, while urgent complications such as SBP, bleeding, rupture, infarction or respiratory compromise are treated in parallel.

Key points

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.

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

Hepatic and portal disease

Cirrhosis, portal or hepatic venous obstruction and infiltrative liver disease can cause ascites, liver enlargement and secondary congestive splenomegaly in overlapping combinations.

Cardiac and haematological disease

Right-heart congestion enlarges the liver and produces ascites, while myeloproliferative, lymphoid and haemolytic disorders commonly enlarge the spleen.

Malignancy and infection

Peritoneal cancer, hepatic metastases, abscess, granulomatous infection and systemic infection can enlarge organs or create exudative peritoneal fluid.

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

1
Peritoneal fluid accumulation
Hydrostatic pressure, reduced effective circulation, increased permeability or direct leakage overwhelms lymphatic clearance and expands the peritoneal compartment.
2
Organ enlargement
Congestion, inflammation, infiltration, storage or increased cellular turnover expands hepatic or splenic tissue and may alter consistency and tenderness.
3
Portal-system coupling
Raised portal pressure simultaneously promotes ascites, splenic congestion, thrombocytopenia and portosystemic collateral formation, linking apparently separate examination findings.

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

Decompensated cirrhosis

Ascites with jaundice, spider naevi, sarcopenia, bruising, asterixis, caput medusae or splenomegaly suggests portal hypertension, but normal enzymes and absent classic stigmata do not exclude it.

Spontaneous bacterial peritonitisRed flag

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.

Malignant ascites or organ enlargement

Weight loss, early satiety, hard nodular hepatomegaly, lymphadenopathy, a pelvic mass or low-gradient ascites raises peritoneal or solid-organ malignancy and requires a cancer pathway.

Vascular or congestive diseaseRed flag

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 emergencyRed flag

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.

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
Abdominal ultrasound with DopplerFirst step
Why
Confirm ascites, measure liver and spleen, assess contour and focal lesions, and evaluate portal and hepatic venous flow while identifying a safe paracentesis window.
Interpretation and limitations
A nodular liver, collaterals and splenomegaly support portal hypertension. Doppler abnormalities require radiology and hepatology interpretation; normal ultrasound does not exclude early fibrosis.
02
Diagnostic ascitic tap
Why
Send cell count with neutrophils, albumin, total protein and Gram stain or culture, inoculating culture bottles at the bedside; add tests driven by the differential.
Interpretation and limitations
Neutrophils at or above 250 cells/mm³ support SBP. Frank pus or polymicrobial culture raises secondary peritonitis and the need for urgent imaging and surgical review.
03
Serum-ascites albumin gradient
Why
Subtract ascitic albumin from a serum albumin taken at roughly the same time to classify portal-hypertensive versus peritoneal mechanisms.
Interpretation and limitations
A gradient of 11 g/L or greater supports portal hypertension; a lower gradient suggests peritoneal malignancy, infection or pancreatic causes. It is a mechanism test, not a final diagnosis.
04
Blood profile and cultures
Why
Check FBC, renal and liver profile, INR, CRP, glucose and blood cultures when infection is possible; add haemolysis, viral, autoimmune or haematology tests by phenotype.
Interpretation and limitations
Thrombocytopenia can reflect portal hypertension, marrow disease, sepsis or medicines. Rising creatinine in cirrhosis is prognostically important and changes diuretic and albumin decisions.
05
Contrast CT or MRI abdomen and pelvis
Why
Evaluate malignancy, peritoneum, vascular thrombosis, pancreatic disease, deep infection and organ morphology when ultrasound and fluid studies do not answer the question.
Interpretation and limitations
Choose contrast and timing with radiology, balancing emergency value against kidney, pregnancy and allergy considerations. Imaging cannot replace ascitic neutrophil count for SBP.
06
Echocardiography and cardiac assessment
Why
Investigate raised JVP, high-gradient high-protein ascites, pulsatile hepatomegaly or other signs of right-sided cardiac disease.
Interpretation and limitations
Cardiac congestion can coexist with chronic liver disease; natriuretic peptides and echo findings require whole-patient interpretation.

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

Apparent abdominal distension

Obesity, pregnancy, bowel dilatation, large ovarian cysts or urinary retention can mimic ascites; shifting dullness and ultrasound establish free fluid.

Congestive versus infiltrative liver

Raised venous pressure, pulsatility and peripheral oedema favour cardiac congestion, whereas a hard irregular liver and focal imaging lesions raise malignancy concern.

Portal versus haematological spleen

Ascites, collaterals and thrombocytopenia favour portal hypertension; profound cytopenias, lymphadenopathy or constitutional symptoms suggest primary haematological disease.

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

01TapNew or admitted ascitesFirst stepNew ascites, or cirrhosis with ascites during an acute hospital admission.

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

02SBPTreat infected ascitesAscitic neutrophils are at least 250 cells/mm³ or there is a compelling septic cirrhosis phenotype.

1Start the locally recommended intravenous antibiotic promptly after cultures, based on community or healthcare acquisition and resistance history.
2Give intravenous albumin when current BSG/BASL or local criteria are met, particularly where renal dysfunction risk is significant.
3Review culture, renal function and clinical response; repeat paracentesis when response is inadequate or secondary peritonitis is suspected.
4After recovery, involve hepatology for prophylaxis, transplant suitability and prevention of further decompensation.

03DrainTense or refractory cirrhotic ascitesPainful, respiratory-limiting, diuretic-resistant or repeatedly recurrent ascites.

1Confirm the diagnosis, exclude SBP and review precipitating medicines, sodium intake, renal function and diuretic tolerance.
2Perform ultrasound-supported large-volume paracentesis through the local protocol and give albumin replacement according to volume and current guidance.
3Monitor blood pressure, symptoms, renal function and electrolytes; restart or adjust diuretics only when safe.
4Discuss TIPS, transplantation, repeated paracentesis or palliative options in a specialist multidisciplinary setting based on goals and contraindications.

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

Aldosterone antagonism addresses sodium retention and is often first-line diuretic therapy in cirrhotic ascites.

Spironolactone

A 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.

Adds loop diuresis for recurrent or severe ascites and helps balance potassium effects.

Furosemide

Often 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.

Supports effective circulating volume after large-volume paracentesis and in selected SBP or renal-risk pathways.

Human albumin solution

After more than 5 litres is removed, BSG guidance recommends 8 g albumin per litre of ascites removed using 20% or 25% solution; other indications and smaller taps require current specialist criteria.

Fluid overload, pulmonary oedema and prescribing or formulation errors. It is a blood product and should follow local traceability and consent information processes.

Treats spontaneous bacterial peritonitis immediately while culture and source assessment proceed.

Empirical antibiotic for SBP

Use the current local cirrhosis protocol, acquisition setting, allergy and resistance data; a third-generation cephalosporin is common in susceptible community-acquired disease.

Broader healthcare-associated resistance may require another regimen. Renal adjustment, C. difficile risk and de-escalation matter; polymicrobial infection raises secondary peritonitis.

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

Decompensation and peritonitis

Cirrhotic ascites may become infected, precipitating encephalopathy, acute kidney injury, shock and a need for urgent transplant-oriented review.

Hypersplenism

Splenic sequestration can worsen thrombocytopenia, leucopenia and anaemia, complicating infection risk, bleeding assessment and invasive procedures.

Pressure and mechanical effects

Tense ascites or marked organ enlargement can impair breathing, appetite and mobility, cause hernias, and produce early satiety or abdominal discomfort.

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

Measure temperature, pulse, blood pressure, mental state, urine output and oxygen requirement closely during infection, drainage or haemodynamic instability.
Record daily weight, abdominal symptoms and fluid balance during diuresis; examine oedema and encephalopathy rather than targeting weight alone.
Repeat renal function, sodium and potassium after starting or changing diuretics and during intercurrent infection or gastrointestinal loss.
Review ascitic and blood cultures promptly, narrowing antibiotics and reassessing for secondary peritonitis if response is poor.
After large-volume paracentesis, monitor blood pressure, renal function, leakage, bleeding and respiratory improvement.
Arrange longitudinal cirrhosis care, variceal and hepatocellular-cancer surveillance, nutrition review and transplant consideration where appropriate.
For hepatosplenomegaly, trend organ size only when it changes management and follow blood counts, constitutional symptoms and the cause-specific pathway.

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

SAAG asks about pressure

A high gradient indicates portal hypertension but does not distinguish cirrhosis from cardiac congestion or hepatic venous obstruction.

Culture at the bedside

Inoculating ascitic fluid into aerobic and anaerobic blood-culture bottles immediately improves yield compared with sending only a sterile pot.

Never await pain for SBP

Encephalopathy, AKI or general decline may be the only signal. Acute admission itself is enough reason to sample ascites in cirrhosis.

The spleen moves inferomedially

A palpable splenic edge descends towards the right iliac fossa and may be notched; an enlarged left kidney is ballottable and does not behave identically, but imaging confirms.

Ascites can hide sarcopenia

Body weight and BMI may look preserved while skeletal muscle is severely depleted. Nutrition and functional assessment should accompany fluid management.

11Common pitfallsFrequent interpretation and management errors.

01
Starting diuretics for new ascites without sampling or establishing the mechanism.
02
Excluding SBP because there is no fever or abdominal tenderness.
03
Calling all cytopenias hypersplenism without considering marrow disease, haemolysis or sepsis.
04
Using SAAG as though it proves cirrhosis.
05
Removing large volumes without albumin and renal or circulatory monitoring where guidance indicates it.
06
Repeatedly draining refractory ascites without discussing TIPS, transplant or goals of care.