Synopsis
Identify clinically significant portal hypertension, prevent first decompensation and select safe beta-blocker or endoscopic prophylaxis for variceal bleeding.
- Portal hypertension results from increased resistance to portal flow with compensatory splanchnic vasodilatation, most commonly from cirrhosis but also prehepatic and posthepatic disease.
- Clinically significant portal hypertension is the stage at which decompensation and varices become more likely and is now a treatment target before bleeding occurs.
- Direct hepatic venous pressure measurement is not routine in most UK practice; validated stiffness, platelets, imaging and endoscopy provide non-invasive and clinical evidence.
- Splenomegaly, thrombocytopenia, portosystemic collaterals, recanalised umbilical vein, ascites or varices indicate portal disease but do not identify every cause.
- Non-selective beta-blockers reduce splanchnic inflow, and carvedilol also lowers intrahepatic resistance through alpha-1 blockade.
- NICE supports low-dose carvedilol or propranolol with response-led titration in selected clinically significant portal hypertension and variceal-prevention settings.
- Endoscopic variceal band ligation is an alternative for medium or large oesophageal varices when beta-blockers are contraindicated, declined or not tolerated.
- Do not combine banding and beta-blockade routinely for primary prevention without a specialist reason; combination is commonly used after a previous bleed.
- Gastric varices have different anatomy and bleeding therapy and should enter a hepatology-interventional radiology pathway rather than standard oesophageal banding.
- The BSG position statement notes that UK evidence is evolving, so shared decisions must follow the current local hepatology pathway and not a frozen historical algorithm.
Key red flags
New ascites, encephalopathy or variceal bleeding changes prognosis and prompts transplant, precipitant and secondary-prevention assessment.
Dizziness, syncope, bradycardia, low blood pressure, rising creatinine or worsening perfusion during titration requires dose and clinical-state review.
Investigation priorities
Stratify CSPH and need for endoscopy or preventive therapy non-invasively.
Management branches
Cirrhosis or advanced chronic liver disease is diagnosed in a compensated person.
- Confirm aetiology and obtain reliable stiffness, platelets and ultrasound evidence, looking for collaterals or portal-vein thrombosis.
- Apply current NICE and BSG CSPH criteria rather than extrapolating a threshold from an unvalidated disease or poor-quality scan.
- Arrange endoscopy when non-invasive results are indeterminate, beta-blockade is unsuitable or gastric and oesophageal anatomy will change care.
- Explain haematemesis and melaena warning signs and document whether prevention follows an NSBB, banding or surveillance route.
Key medicines
CarvedilolNICE advises a low starting dose, for example 6.25 mg by mouth daily, with increase or decrease guided by heart rate, blood pressure and adverse effects under the local portal-hypertension protocol.Avoid initiation in shock or unstable decompensation. Review asthma, heart block, bradycardia, postural symptoms, falls and interacting drugs; monitor renal function, sodium and perfusion closely with ascites or acute illness.
PropranololWhere selected, NICE gives 40 mg twice daily as an example low starting regimen, but specialists use lower doses for frailty or advanced disease and titrate from pulse, pressure, renal function and tolerance.The same asthma, heart block, bradycardia, hypotension and renal-perfusion safeguards apply. Do not chase a heart-rate target through dizziness or low blood pressure, and plan temporary review and restart around sepsis or AKI.