Synopsis
Confirm cirrhosis, identify its cause and separate compensated from decompensated disease so surveillance, prevention and transplant planning begin promptly.
- 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.
Key red flags
Increasing abdominal girth, early satiety, ankle oedema, breathlessness or an umbilical hernia signals fluid retention and requires diagnostic paracentesis when new or admitted.
Sleep reversal, slowed thinking, disorientation, asterixis or coma occurs after triggers such as infection, bleeding, constipation, dehydration, sedatives or renal dysfunction.
Haematemesis, melaena, syncope or shock in cirrhosis is variceal until urgent resuscitation and endoscopy define the source.
New jaundice, kidney injury, hypotension, hypoxia or multiple organ dysfunction after infection, alcohol, bleeding or drug injury carries high short-term risk.
Investigation priorities
Assess injury, cholestasis and functional reserve.
Management branches
Clinical, laboratory or imaging features suggest advanced chronic liver disease.
- Review alcohol, metabolic, viral, autoimmune, cholestatic, vascular, inherited and medicine causes and obtain a targeted aetiology panel.
- Combine platelets, validated fibrosis score, elastography and ultrasound rather than allowing one normal or abnormal result to dominate.
- Use specialist imaging or liver biopsy when discordance would alter treatment, surveillance or the certainty communicated to the patient.
- Once cirrhosis is established, record aetiology and phase explicitly and activate surveillance immediately rather than waiting for symptoms.
The person returns to stable outpatient care after diagnosis or admission.
- Maintain six-monthly HCC surveillance and the current portal-hypertension plan, tracking every appointment through a fail-safe system.
- Review causal therapy, alcohol and smoking, weight and diabetes, vaccinations, nutrition and physical function at structured intervals.
- Monitor bilirubin, albumin, INR, sodium, creatinine and platelets and respond to trajectory, not just whether values cross the reference range.