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.
Key red flags
New ascites, encephalopathy or variceal bleeding changes prognosis and prompts transplant, precipitant and secondary-prevention assessment.
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.
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.
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.