Portal hypertension and variceal prevention

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

Normal portal venous pressure depends on low-resistance flow through hepatic sinusoids. Cirrhotic scar, nodules, endothelial dysfunction and active vasoconstriction raise resistance, while splanchnic vasodilatation increases flow. The resulting collaterals decompress the portal system but create oesophageal, gastric, rectal and abdominal-wall varices. Portal hypertensive gastropathy, hypersplenism, ascites, hepatorenal physiology and encephalopathy are related consequences. Portal vein thrombosis, schistosomiasis, Budd-Chiari syndrome and right-heart disease require different causal treatment despite similar signs.

A hepatic venous pressure gradient of at least 10 mmHg defines CSPH in sinusoidal cirrhosis, but invasive measurement is usually confined to specialist indications or research. Transient elastography with platelet count can rule in or rule out risk in selected aetiologies, while grey-zone results need imaging, endoscopy or expert review. Collaterals or varices themselves are conclusive clinical evidence. Cut-offs depend on technique, obesity, inflammation and disease, so the BSG position statement adds UK caveats to international thresholds.

Prevention operates at two levels. In compensated CSPH, a tolerated non-selective beta-blocker can reduce first decompensation, not only bleeding. Once medium or large oesophageal varices exist, carvedilol, propranolol or band ligation is selected through NICE guidance, haemodynamics and preference. Banding removes visible columns but does not lower portal pressure or prevent ascites, and it needs repeated sessions and surveillance. Beta-blockers can cause hypotension, bradycardia and renal hypoperfusion, so safe titration and temporary review during acute illness are part of efficacy.

Key points

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.

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

Cirrhotic intrahepatic resistance

Cirrhosis is the commonest cause, with scar, regenerative nodules, endothelial dysfunction and vasoconstriction obstructing portal flow through hepatic sinusoids.

Prehepatic obstruction

Portal or splenic vein thrombosis obstructs inflow before blood reaches the liver and may produce varices with preserved hepatic synthesis.

Presinusoidal disease

Schistosomiasis, infiltrative disorders and porto-sinusoidal vascular disease raise resistance before the sinusoids and can mimic cirrhotic portal hypertension.

Posthepatic outflow obstruction

Budd-Chiari syndrome, inferior vena cava obstruction and severe right-sided cardiac disease impede hepatic drainage and raise portal pressure upstream.

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

1
Increased portal resistance
Structural obstruction and dynamic intrahepatic vasoconstriction increase the pressure needed to move splanchnic venous blood through the liver.
2
Hyperdynamic splanchnic flow
Splanchnic vasodilatation increases portal inflow while lowering effective arterial volume, amplifying pressure and activating sodium-retaining neurohormonal systems.
3
Portosystemic collateral formation
Venous channels enlarge to bypass resistance, creating oesophageal, gastric and other varices that remain thin-walled and vulnerable to rupture.
4
Fluid and renal consequences
Reduced effective perfusion activates sympathetic, renin-angiotensin and antidiuretic pathways, promoting ascites, dilutional hyponatraemia and progressive renal vasoconstriction.

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

Non-invasive CSPH phenotype

High liver stiffness with falling platelets and splenomegaly suggests portal pressure significant enough to consider preventive treatment under validated current criteria.

Established collaterals

Oesophageal or gastric varices, recanalised paraumbilical vein or spontaneous portosystemic shunts directly demonstrate clinically important portal hypertension.

Hypersplenic pattern

Progressive thrombocytopenia with an enlarged spleen can precede symptoms, although marrow disease, alcohol, infection and medicines remain alternative explanations.

First decompensationRed flag

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

Beta-blocker intoleranceRed flag

Dizziness, syncope, bradycardia, low blood pressure, rising creatinine or worsening perfusion during titration requires dose and clinical-state review.

Non-cirrhotic portal pattern

Varices or splenomegaly with relatively preserved liver stiffness and synthesis raises portal-vein, vascular, infiltrative or presinusoidal causes requiring targeted imaging.

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
Transient elastography with platelet countFirst step
Why
Stratify CSPH and need for endoscopy or preventive therapy non-invasively.
Interpretation and limitations
Apply current BSG-endorsed criteria only in validated populations and with a technically reliable scan. Inflammation, congestion, cholestasis and obesity can create a grey zone requiring further assessment.
02
Doppler ultrasonography
Why
Assess portal-vein patency, direction of flow, spleen, ascites and collaterals.
Interpretation and limitations
Thrombosis, cavernous transformation or abnormal hepatic veins redirects the causal pathway. Normal flow direction does not exclude sinusoidal portal hypertension.
03
Upper gastrointestinal endoscopy
Why
Detect and size oesophageal or gastric varices and portal hypertensive mucosal change.
Interpretation and limitations
Record location, size and high-risk stigmata and distinguish gastric anatomy. Endoscopy may be unnecessary in selected patients already receiving effective NSBB or meeting validated low-risk non-invasive criteria.
04
Cross-sectional portal-phase imaging
Why
Map thrombosis, shunts, collaterals, tumour and anatomy before intervention.
Interpretation and limitations
CT or MRI clarifies portal and splenic vein obstruction and TIPS feasibility. A new thrombosis needs duration, extension, bleeding and transplant implications reviewed by hepatology.
05
Cardiac evaluation
Why
Identify posthepatic pressure and beta-blocker or TIPS constraints.
Interpretation and limitations
Echocardiography and natriuretic or clinical assessment are selected for right-heart failure, pulmonary hypertension or planned shunt; treating cardiac disease may be the key portal intervention.
06
Hepatic venous pressure gradient
Why
Measure sinusoidal portal pressure directly in selected specialist settings.
Interpretation and limitations
A gradient at or above 10 mmHg defines CSPH in appropriate cirrhosis, but presinusoidal disorders can have a misleadingly normal measurement. It is not required before routine prophylaxis when other evidence is decisive.
07
Baseline beta-blocker safety profile
Why
Identify contraindications and establish titration observations.
Interpretation and limitations
Record sitting and standing blood pressure, pulse, ECG where conduction disease is possible, creatinine, sodium, asthma, falls and interacting medicines before treatment.

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

Cirrhotic portal hypertension

A nodular liver, high stiffness, impaired synthesis and chronic liver-disease features support sinusoidal resistance from cirrhosis.

Portal-vein thrombosis

Acute abdominal pain or chronic cavernous transformation with relatively preserved liver function suggests prehepatic obstruction and requires vascular imaging.

Hepatic venous outflow disease

Painful hepatomegaly, ascites and abnormal hepatic veins raise Budd-Chiari syndrome, while cardiac signs suggest congestive hepatopathy.

Alternative cytopenia or splenomegaly

Marrow disease, infection, haematological malignancy and medicine effects can cause thrombocytopenia or splenic enlargement without raised portal pressure.

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

01Risk identificationClassify portal hypertension before varices bleedFirst stepCirrhosis or advanced chronic liver disease is diagnosed in a compensated person.

1Confirm aetiology and obtain reliable stiffness, platelets and ultrasound evidence, looking for collaterals or portal-vein thrombosis.
2Apply current NICE and BSG CSPH criteria rather than extrapolating a threshold from an unvalidated disease or poor-quality scan.
3Arrange endoscopy when non-invasive results are indeterminate, beta-blockade is unsuitable or gastric and oesophageal anatomy will change care.
4Explain haematemesis and melaena warning signs and document whether prevention follows an NSBB, banding or surveillance route.

02NSBB preventionStart low and titrate to perfusionCSPH or varices merit beta-blockade and no overriding contraindication is present.

1Review asthma, conduction disease, blood pressure, pulse, falls, sodium, renal function, ascites and interacting medicines and obtain informed agreement.
2Begin low-dose carvedilol or propranolol according to NICE and local hepatology guidance and increase only with preserved pressure, renal function and tolerability.
3Recheck observations and bloods after each titration and teach the patient to report fainting, wheeze, poor intake, sepsis or reduced urine output.
4During hypotension, severe infection or AKI seek specialist advice about a temporary pause, then record who will reassess and restart after recovery.

03Banding preventionEradicate high-risk oesophageal varices endoscopicallyMedium or large oesophageal varices need primary prevention and NSBB is unsuitable or declined.

1Confirm the varices are oesophageal and discuss band ulceration, bleeding, dysphagia, repeated procedures and the absence of protection from non-bleeding decompensation.
2Perform elective band ligation in an experienced service and repeat at the current local interval until eradication.
3Arrange surveillance for recurrence and provide urgent return advice for chest pain, haematemesis, melaena or swallowing difficulty.
4If bleeding occurs despite prophylaxis, move to the acute and then secondary-prevention pathway rather than merely scheduling another routine banding list.

04Special anatomyEscalate gastric and non-cirrhotic portal diseaseEscalationGastric varices, portal-vein thrombosis or preserved liver architecture makes standard oesophageal prevention inappropriate.

1Obtain high-quality portal-phase imaging and classify gastric varix and shunt anatomy with hepatology and interventional radiology.
2Review anticoagulation, glue or coil therapy, TIPS or retrograde obliteration under the current regional pathway rather than routine oesophageal bands.
3Investigate myeloproliferative, thrombotic, vascular and infiltrative causes when portal hypertension is not explained by cirrhosis.
4Coordinate long-term bleeding prevention with treatment of the causal vascular disorder and any transplant strategy.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Preferred NSBB in many compensated CSPH pathways because beta and alpha-1 effects reduce splanchnic inflow and intrahepatic resistance.

Carvedilol

NICE 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.

Established non-selective beta-blocker alternative for primary or secondary variceal prevention when carvedilol is unsuitable or local practice favours it.

Propranolol

Where 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.

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

Variceal haemorrhage

Rupture of oesophageal or gastric varices causes haematemesis, melaena, shock and a substantial risk of early infection and rebleeding.

Ascites and peritonitis

Portal pressure and renal sodium retention produce ascites, which can become infected spontaneously or cause hernias and respiratory restriction.

Portosystemic encephalopathy

Collateral shunting bypasses hepatic detoxification, increasing susceptibility to cognitive change, asterixis and coma when infection, bleeding or constipation intervenes.

Hypersplenism

Congestive splenic enlargement sequesters platelets and other blood cells, producing cytopenias that may complicate bleeding assessment and procedures.

Hepatorenal physiology

Advanced splanchnic vasodilatation and renal vasoconstriction can cause progressive kidney dysfunction, particularly during infection, bleeding or excessive volume removal.

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

During NSBB titration measure sitting and standing blood pressure, pulse, creatinine, sodium, weight, falls and symptoms at the local early-review interval.
Reassess the dose after infection, acute kidney injury, new refractory ascites, poor oral intake or hospital discharge and document any temporary withholding and restart.
Track banding sessions through eradication and subsequent surveillance with a fail-safe recall system, including pathology or imaging when anatomy changes.
Repeat liver stiffness, platelets and imaging only at evidence-based intervals and recognise that effective NSBB may change the need for screening endoscopy.
Monitor for first decompensation, portal thrombosis, HCC and frailty and reconsider transplant referral after any event rather than focusing solely on varix size.
Give written emergency advice for haematemesis, melaena, fainting, confusion, fever or falling urine output and identify the acute hospital route.

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

Prevent pressure, not just veins

NSBB can reduce ascites and broader decompensation risk in CSPH, while banding treats visible oesophageal columns only.

Thresholds need validation

A stiffness value developed in viral or metabolic cirrhosis may not transfer reliably to cholestatic, congestive or presinusoidal disease.

Blood pressure sets the ceiling

A lower pulse is not beneficial if the patient becomes hypotensive, dizzy or renally hypoperfused; titration is a whole-patient decision.

Gastric is different anatomy

Fundal varices and spontaneous shunts often need glue, radiological obliteration or TIPS planning, not routine oesophageal bands.

Guidance is deliberately interim

BSG endorses current international principles with UK caveats while new trial data mature, making shared and locally governed decisions essential.

11Common pitfallsFrequent interpretation and management errors.

01
Treating one elevated stiffness measurement as CSPH despite inflammation, congestion or poor technical quality.
02
Starting carvedilol during septic shock or acute kidney injury because portal prevention is on the clinic plan.
03
Increasing NSBB solely to reach a pulse number despite postural hypotension or worsening renal function.
04
Banding gastric fundal varices as though their anatomy and definitive options match oesophageal varices.
05
Assuming successful oesophageal eradication removes portal pressure or the risk of ascites and encephalopathy.
06
Failing to arrange active restart review after an appropriate temporary beta-blocker pause during acute illness.