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.
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.
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.
The person returns to stable outpatient care after diagnosis or admission.
Key medicines
Non-selective beta-blocker in selected CSPHWhen 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.
Lactulose for overt hepatic encephalopathyUse 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.