Cirrhosis: diagnosis and staging

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

Fibrosis changes hepatic blood flow and cellular function. Portal resistance produces splenomegaly, thrombocytopenia, collaterals, varices and ascites; reduced synthesis produces coagulopathy and low albumin; impaired detoxification contributes to encephalopathy. Cirrhosis may remain compensated for years, and treating the cause can reduce decompensation risk. Once ascites, overt encephalopathy or portal bleeding occurs, systemic circulatory, immune, renal and nutritional dysfunction becomes prominent and prognosis changes sharply.

A diagnosis should be explicit and evidence-based. Nodular contour, splenomegaly, collaterals, falling platelets and high liver stiffness can establish a strong non-invasive case, while aetiology-specific pathways determine thresholds and confounders. Congestive hepatopathy, acute hepatitis, cholestasis and recent food can increase stiffness. A normal ultrasound misses early cirrhosis, and a normal aminotransferase reflects current leakage rather than architecture. Histology remains useful when competing diagnoses, infiltrative disease or treatment decisions cannot be resolved safely otherwise.

Staging has several dimensions. Compensated versus decompensated status predicts the broad clinical phase. Child-Pugh describes liver reserve and complications; MELD-Na and UKELD use objective laboratory data for short-term risk and transplant processes. Portal-hypertension severity and frailty add information not captured fully by either. The practical output is a care bundle: aetiology treatment, HCC surveillance, variceal or CSPH assessment, nutrition and sarcopenia action, bone and vaccine review, avoidance of harmful medicines, and a named escalation plan.

Key points

Cirrhosis is advanced diffuse hepatic fibrosis with architectural distortion, regenerative nodules and clinically important risks even when routine liver tests are near normal.
Diagnosis increasingly uses a concordant combination of aetiology, platelets, imaging and elastography; biopsy is reserved for uncertainty that changes management.
FIB-4 and similar scores are triage tools for advanced fibrosis, not definitive proof or exclusion in every age, disease or acute inflammatory state.
Compensated cirrhosis has no prior ascites, variceal haemorrhage or overt encephalopathy; decompensation is a prognostic watershed requiring transplant consideration.
Clinically significant portal hypertension can precede varices or ascites and is now a prevention target in current NICE and BSG pathways.
Child-Pugh uses bilirubin, albumin, INR, ascites and encephalopathy but contains subjective elements and should not be used alone.
MELD-based and UKELD scores support short-term prognosis and transplant allocation or referral; a score supplements clinical trajectory rather than replacing it.
Aetiology must remain active after the label cirrhosis: alcohol, viral hepatitis, metabolic steatosis, autoimmune, cholestatic, vascular and inherited causes may be treatable.
People with cirrhosis need six-monthly ultrasound HCC surveillance when suitable for treatment, plus portal, bone, nutrition, vaccination and medicine-safety review.
Normal ALT, albumin or an unremarkable examination cannot de-label previously established cirrhosis or remove surveillance obligations.

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

Alcohol-related liver disease

Sustained harmful alcohol exposure causes steatohepatitis, hepatocyte loss and progressive fibrosis, often interacting with metabolic or viral injury.

Metabolic steatotic liver disease

Insulin resistance, obesity and type 2 diabetes can drive steatohepatitis and fibrosis even when aminotransferase concentrations are only mildly abnormal.

Chronic viral hepatitis

Persistent hepatitis B or C infection causes repeated immune-mediated hepatic injury and can progress silently to cirrhosis over many years.

Immune, cholestatic and inherited disease

Autoimmune hepatitis, biliary disorders, haemochromatosis, Wilson disease and other less common conditions cause fibrosis through distinct but treatable pathways.

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

1
Fibrosis and nodular regeneration
Repeated injury activates fibrogenic cells, deposits extracellular matrix and partitions regenerating hepatocytes into nodules that distort normal hepatic architecture.
2
Portal vascular resistance
Scar, nodules and intrahepatic vasoconstriction impede portal flow, producing splenomegaly, collateral vessels, varices and fluid accumulation.
3
Functional hepatocyte failure
Declining effective hepatocyte mass impairs albumin and clotting-factor synthesis, bilirubin handling, glucose regulation and detoxification of ammonia and medicines.
4
Systemic decompensation
Splanchnic vasodilatation and immune dysfunction reduce effective arterial volume, promoting sodium retention, ascites, infection susceptibility, renal hypoperfusion and multiorgan deterioration.

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

Compensated occult cirrhosis

Low platelets, splenomegaly, a nodular liver or high stiffness reveals advanced disease before ascites, bleeding or overt encephalopathy has ever occurred.

Portal-hypertension phenotype

Thrombocytopenia, enlarged spleen, abdominal-wall collaterals, varices or recanalised umbilical vein indicates increased portal pressure even with preserved albumin.

Ascitic decompensationRed flag

Increasing abdominal girth, early satiety, ankle oedema, breathlessness or an umbilical hernia signals fluid retention and requires diagnostic paracentesis when new or admitted.

Overt hepatic encephalopathyRed flag

Sleep reversal, slowed thinking, disorientation, asterixis or coma occurs after triggers such as infection, bleeding, constipation, dehydration, sedatives or renal dysfunction.

Portal gastrointestinal bleedRed flag

Haematemesis, melaena, syncope or shock in cirrhosis is variceal until urgent resuscitation and endoscopy define the source.

Acute-on-chronic deteriorationRed flag

New jaundice, kidney injury, hypotension, hypoxia or multiple organ dysfunction after infection, alcohol, bleeding or drug injury carries high short-term risk.

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
Full liver and synthetic profileFirst step
Why
Assess injury, cholestasis and functional reserve.
Interpretation and limitations
Trend bilirubin, albumin and INR with aminotransferases and ALP. Normal enzymes do not exclude scar; falling albumin or rising INR may also reflect inflammation, nutrition, anticoagulants or loss and needs context.
02
Full blood count and metabolic profile
Why
Identify portal cytopenia, anaemia, renal dysfunction and sodium disturbance.
Interpretation and limitations
Falling platelets often accompany splenic sequestration, while anaemia requires bleeding and nutrition assessment. Creatinine can underestimate kidney impairment in sarcopenia, and hyponatraemia signals circulatory dysfunction.
03
Transient elastography
Why
Estimate advanced fibrosis and support non-invasive diagnosis.
Interpretation and limitations
Use disease-specific validated thresholds and technical quality. Acute inflammation, congestion, biliary obstruction, meal state and obesity can distort stiffness; repeat or escalate discordant results.
04
Hepatobiliary ultrasonography with portal Doppler
Why
Assess morphology, spleen, vessels, ascites and focal lesions.
Interpretation and limitations
Nodularity and portal collaterals support cirrhosis, but normal imaging does not exclude it. Portal thrombosis or a focal mass changes management urgently.
05
Aetiology screen
Why
Identify ongoing treatable liver injury after advanced fibrosis is recognised.
Interpretation and limitations
Select viral serology, iron studies, autoantibodies and immunoglobulins, metabolic tests, A1AT, copper studies and detailed alcohol, metabolic and medicine assessment by age and phenotype.
06
Upper gastrointestinal endoscopy or validated non-invasive portal assessment
Why
Find varices requiring prevention and evidence of clinically significant portal hypertension.
Interpretation and limitations
Apply current NICE and BSG criteria using stiffness, platelets and clinical features; patients on effective non-selective beta-blockade may follow a different endoscopy pathway.
07
Child-Pugh, MELD-Na and UKELD calculation
Why
Describe reserve, short-term mortality and transplant relevance.
Interpretation and limitations
Record input date and acute context. Ascites and encephalopathy grading adds subjectivity to Child-Pugh, while MELD-based scores may miss frailty and recurrent complications.
08
Liver biopsy
Why
Resolve uncertain aetiology or stage when non-invasive evidence is discordant.
Interpretation and limitations
An adequate specimen can show architecture and coexisting steatohepatitis, autoimmune or infiltrative disease. Sampling error remains possible; use transvenous access when ascites or haemostatic risk makes percutaneous biopsy unsuitable.

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

Advanced fibrosis without cirrhosis

Significant fibrosis can raise stiffness and future risk before established architectural nodularity or clinical portal hypertension has developed.

Congestive hepatopathy

Right-sided heart failure elevates hepatic venous pressure and liver stiffness, producing ascites and abnormal tests without primary cirrhotic architecture.

Non-cirrhotic portal hypertension

Portal-vein thrombosis, presinusoidal vascular disease or nodular regenerative hyperplasia can cause splenomegaly and varices despite relatively preserved hepatic structure and synthesis.

Acute hepatic inflammation

Acute hepatitis or cholestasis can transiently increase liver stiffness and worsen blood tests, so measurements require interpretation in their clinical context.

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

01ConfirmationDiagnose architecture and cause togetherFirst stepClinical, laboratory or imaging features suggest advanced chronic liver disease.

1Review alcohol, metabolic, viral, autoimmune, cholestatic, vascular, inherited and medicine causes and obtain a targeted aetiology panel.
2Combine platelets, validated fibrosis score, elastography and ultrasound rather than allowing one normal or abnormal result to dominate.
3Use specialist imaging or liver biopsy when discordance would alter treatment, surveillance or the certainty communicated to the patient.
4Once cirrhosis is established, record aetiology and phase explicitly and activate surveillance immediately rather than waiting for symptoms.

02Baseline stagingConvert the diagnosis into a care bundleCirrhosis has been newly confirmed without an acute emergency.

1Determine whether ascites, variceal bleeding or overt encephalopathy has ever occurred and calculate contemporaneous Child-Pugh and MELD-based scores.
2Assess CSPH or varices under current guidance, arrange six-monthly HCC ultrasound and review spleen, portal vein and renal function.
3Measure frailty, muscle, diet, bone and vaccine status and reconcile medicines for NSAIDs, sedatives, unnecessary PPI, nephrotoxins and herbals.
4Treat the cause, provide written decompensation warnings and define hepatology, primary-care and transplant referral ownership.

03Acute decompensationFind and treat the precipitant in the first dayAscites, encephalopathy, bleeding, jaundice, infection or kidney injury presents acutely.

1Admit, apply ABC assessment and the BSG/BASL bundle, review glucose and send cultures, blood count, renal, liver, coagulation and lactate tests.
2Tap ascites promptly, investigate bleeding and image for obstruction or vascular events while reviewing alcohol, constipation, dehydration and medicines.
3Treat the identified complication and precipitant in parallel, with early critical-care and specialist discussion for organ failure.
4Recalculate prognosis after initial resuscitation and initiate transplant assessment or goals-of-care planning appropriate to reversibility and patient wishes.

04Ongoing surveillancePrevent avoidable decompensationThe person returns to stable outpatient care after diagnosis or admission.

1Maintain six-monthly HCC surveillance and the current portal-hypertension plan, tracking every appointment through a fail-safe system.
2Review causal therapy, alcohol and smoking, weight and diabetes, vaccinations, nutrition and physical function at structured intervals.
3Monitor bilirubin, albumin, INR, sodium, creatinine and platelets and respond to trajectory, not just whether values cross the reference range.
4Revisit transplant suitability after first decompensation, recurrent admission, worsening frailty or a prognostic-score change rather than at a fixed terminal point.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Can lower portal pressure and reduce first decompensation or variceal bleeding risk in appropriately phenotyped compensated cirrhosis.

Non-selective beta-blocker in selected CSPH

When the current NICE and specialist portal pathway selects carvedilol, begin with a low dose such as 6.25 mg daily and titrate against pulse, blood pressure, renal function and tolerance; do not apply a universal target in unstable disease.

Review asthma, heart block, falls, hypotension and interacting rate-limiting medicines. With sepsis, acute kidney injury, severe hyponatraemia or low perfusion, seek hepatology advice about temporary reduction or withholding and planned restart.

Reduces intestinal nitrogen load while infection, bleeding, constipation, sedatives and renal or electrolyte precipitants are treated.

Lactulose for overt hepatic encephalopathy

Use the current BNF and local encephalopathy regimen, titrating oral or enteral doses to regular soft bowel motions after obstruction is excluded and adjusting promptly for diarrhoea or dehydration.

Do not use altered mental state as diagnostic proof of encephalopathy. Over-treatment causes hypovolaemia, hypernatraemia or hypokalaemia and may worsen cognition; protect the airway before enteral administration in reduced consciousness.

Reduces preventable infection and decompensation in an immune-dysfunctional chronic liver population.

Vaccination programme

Offer influenza, pneumococcal, COVID-19 and hepatitis A or B vaccination where indicated and non-immune, following the current UK Green Book and local liver schedule rather than a single fixed adult course.

Check prior records, immunosuppression, allergy and live-vaccine restrictions. Vaccination does not remove the need for early sepsis assessment because response can be reduced in advanced disease.

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

Portal hypertensive bleeding

Oesophageal or gastric varices and portal hypertensive gastropathy can cause catastrophic haemorrhage, recurrent anaemia or both.

Ascites and infection

Sodium and water retention causes ascites, which may become tense, impair breathing or develop spontaneous bacterial peritonitis.

Hepatic encephalopathy

Impaired hepatic clearance and portosystemic shunting permit neurotoxins to accumulate, causing fluctuating cognition, asterixis, reduced consciousness and aspiration risk.

Renal and circulatory failure

Infection, bleeding, overdiuresis or advanced vasodilatation can precipitate acute kidney injury, hepatorenal physiology, hypotension and multiorgan failure.

Hepatocellular carcinoma

Cirrhotic regeneration and genomic injury create a field at continuing risk of primary liver cancer, even after the original cause is controlled.

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

Record compensated or decompensated phase, current Child-Pugh and a MELD-based score at meaningful clinical transitions, including after recovery from an acute trigger.
Perform HCC ultrasound every six months when surveillance remains appropriate, with rapid diagnostic imaging for a new lesion rather than waiting for the next cycle.
Follow portal-hypertension prevention through endoscopy or a validated non-invasive and beta-blocker pathway, ensuring missed procedures are actively recalled.
Trend weight, grip strength or another frailty measure, oral intake and sarcopenia and involve a liver dietitian before severe wasting develops.
Review renal function, sodium, blood pressure, falls and medicines after every admission and after starting diuretics or portal-pressure therapy.
Check vaccination, bone health, alcohol treatment, mental wellbeing, driving advice after encephalopathy and transplant or palliative-care status at structured reviews.

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

Normal enzymes do not unscar

Aminotransferases reflect current injury and may fall as hepatocyte mass declines; they cannot reverse imaging, stiffness or histological evidence.

First decompensation is a referral moment

Ascites, overt encephalopathy or portal bleeding changes prognosis and should trigger transplant suitability review rather than merely another prescription.

Scores answer different questions

Child-Pugh, MELD-Na and UKELD weight variables differently and omit frailty, so recording the purpose and clinical context prevents false precision.

Cirrhosis has an active cause

The architectural label should never end work on alcohol, virus, metabolism, autoimmunity or obstruction that can still alter outcomes.

Surveillance needs a system

Six-monthly intention is not enough; invitations, non-attendance and abnormal scans require ownership and reliable recall.

11Common pitfallsFrequent interpretation and management errors.

01
Excluding cirrhosis because ALT, albumin or a single ultrasound report is normal.
02
Using FIB-4 as a definitive diagnosis despite acute inflammation, extreme age or disease-specific limitations.
03
Recording Child-Pugh or MELD without the date and acute context and treating it as a permanent patient property.
04
Starting complication medicines while failing to identify infection, bleeding, alcohol, obstruction or nephrotoxic precipitant.
05
Continuing NSAIDs, sedatives or an unnecessary PPI after decompensation without a documented benefit-risk review.
06
Waiting for repeated admissions before discussing transplantation after a first meaningful decompensation.