Decision support only — portal hypertension crosses clinic, endoscopy, IR and transplant care. Verify beta-blocker, anticoagulation and transplant-centre protocols; use the acute and chronic cirrhosis sheets for bedside decompensation management.
1 Identify CSPH before the first decompensation
CSPH ruled outlow short-term decompensation risk
In compensated advanced chronic liver disease, VCTE liver stiffness ≤15 kPa plus platelets ≥150 ×10⁹/L.
Treat the liver disease and reassess with labs/VCTE. Endoscopy and NSBB are not required solely for portal prophylaxis. GESA/Baveno
Grey zoneneither rule-out nor rule-in
LSM 15–25 kPa, thrombocytopenia, splenomegaly, discordant imaging or an aetiology/BMI where fixed cut-offs perform less well.
Refine risk: combine LSM and platelets; consider spleen stiffness, endoscopy or specialist review. Do not label CSPH from one noisy FibroScan.
CSPH likely / provenHVPG ≥10 mmHg or clinical surrogates
LSM ≥25 kPa in validated aetiologies, varices/collaterals, ascites, portal-hypertensive bleeding, or invasive HVPG ≥10 mmHg.
Prevent decompensation: treat cause and offer NSBB if tolerated; screen/manage HCC, nutrition and complications. GESA 2026
Decompensatedascites, HE, variceal bleed, non-obstructive jaundice
Any first decompensating event, recurrent admission, renal dysfunction, sarcopenia or HCC.
Refer for transplant evaluation now, alongside active complication treatment. Waiting for a very high MELD loses useful assessment time.
LSM ≥25 kPa is best validated in viral/alcohol-related disease and non-obese MASLD. Inflammation, congestion, cholestasis, recent food and obesity can distort the number.
2 Non-selective beta-blockers and endoscopy
CSPH: prevent decompensation
- PreferredCarvedilol 6.25 mg daily, increase after ~3 days to 12.5 mg/day if tolerated. GESA permits up to 25 mg when hypertension also requires treatment. GESA 2026
- AlternativePropranolol, commonly 20–40 mg bd and titrate; GESA target is at least 40 mg bd if tolerated, aiming HR ~60/min.
- MonitorBP, orthostasis, renal function, sodium and symptoms. Reduce/hold with SBP <90, MAP <65, AKI/HRS, severe infection or poor perfusion; restart when recovered.
When to scope
- On NSBBIf taking NSBB for proven/likely CSPH, screening endoscopy often adds no management change; individualise for gastric varices or diagnostic uncertainty.
- Cannot useEndoscopy to identify high-risk varices; use endoscopic variceal ligation for primary prophylaxis where NSBB is contraindicated or not tolerated.
- What is missedEVL treats the varix but not portal pressure and does not prevent ascites. NSBB has the broader disease-modifying aim. PREDESCI
3 Bleeding prevention, TIPS and obliteration
| Situation | Preferred strategy | Escalate / caveat |
|---|
| Primary prophylaxis | CSPH: carvedilol preferred. High-risk oesophageal varices with NSBB intolerance: serial EVL. | Do not combine NSBB + EVL routinely for primary prophylaxis. |
| After oesophageal variceal bleed | NSBB plus serial EVL after haemostasis. Address alcohol/viral/metabolic cause and transplant candidacy. | Rebleeding despite combination → TIPS assessment. Companion UGIB sheet covers the acute episode. |
| Pre-emptive TIPS | After acute bleed: Child C 10–13, Child B >7 with active bleeding, or HVPG ≥20; within 72 h, ideally 24 h. Baveno VIII | Check cardiac reserve, pulmonary pressure, infection and encephalopathy risk; early IR/transplant discussion. |
| Refractory ascites / hydrothorax | Assess for TIPS and transplant; serial paracentesis/albumin while the plan is made. | TIPS may worsen HE or heart failure. Recurrent hydrothorax is a transplant signal, not a reason for an indwelling chest tube. |
| Fundal gastric varix / ectopic varix | Map shunts with contrast imaging; expert endoscopic glue/EUS therapy, TIPS ± embolisation, or retrograde transvenous obliteration depending anatomy. | Obliteration can raise portal pressure and aggravate oesophageal varices/ascites; TIPS can aggravate HE. |
4 Portal vein thrombosis and cardiopulmonary disease
Portal vein thrombosis
- DefineContrast CT/MRI: recent vs chronic, percentage occlusion, main portal/mesenteric extension, cavernoma and HCC tumour thrombus.
- TreatRecent >50% occlusive or progressive main portal/mesenteric PVT, symptoms/ischemia, or transplant candidacy usually favours anticoagulation with specialist input.
- ChronicComplete cavernomatous occlusion may not recanalise; focus on portal complications and surgical planning rather than automatic lifelong anticoagulation.
Hepatopulmonary syndrome
- CluesPlatypnoea, orthodeoxia, clubbing; widened A–a gradient. Contrast echo shows intrapulmonary shunt.
- ActionOxygen for hypoxaemia and early transplant referral. Transplant is the only effective definitive therapy.
Portopulmonary hypertension
- ScreenEcho if symptoms, transplant/TIPS assessment or suggestive signs; confirm with right-heart catheterisation.
- ActionPulmonary-hypertension specialist therapy. Moderate/severe untreated PoPH is usually a transplant contraindication; candidacy may change if haemodynamics improve.
- TIPSAvoid until cardiopulmonary risk is defined.
5 When to refer for liver transplantation
Refer now
- DecompensationFirst ascites, variceal haemorrhage, overt HE or non-obstructive jaundice. AASLD/AST 2025
- TrajectoryMELD ≥13 is a practical Australian trigger used in HCV guidance; benefit may begin above MELD 12. Refer earlier with rapid change, frailty or recurrent admission.
- SpecificRefractory ascites/hydrothorax, HRS, recurrent SBP/HE, HPS, small HCC, severe malnutrition, selected metabolic disease.
- ALFAcute liver failure or acute severe AIH/DILI with synthetic failure → direct transplant-centre discussion, not routine outpatient referral.
MELD is not the referral gate
- UnderestimatesRefractory ascites, HE, HPS, cholestatic symptoms, recurrent sepsis and some HCC can carry major risk despite a modest score.
- Assessment takes timeCardiac/pulmonary testing, malignancy screen, infection/dental work, nutrition, substance-use care, adherence and social support all need work before listing.
- TSANZThe transplant unit determines eligibility under organ-specific criteria. Timely referral allows optimisation and, where appropriate, a second-unit opinion.
6 Transplant work-up and waiting-list care
| Domain | Registrar-level check | Why it changes candidacy or timing |
|---|
| Liver / cancer | Aetiology and reversibility; MELD/Child trend; decompensations; cross-sectional imaging, AFP and HCC staging; vascular anatomy. | HCC can qualify despite lower MELD; macrovascular invasion/extrahepatic disease may exclude. Treatable cause still matters before and after transplant. |
| Cardiopulmonary | ECG/echo ± ischaemia assessment; hypoxaemia/HPS; screen PoPH; functional capacity. | Unrecognised heart failure or pulmonary vascular disease can make TIPS or transplant lethal. |
| Infection / immunity | Dental/skin/urine focus as indicated; HBV/HCV/HIV/CMV/EBV; vaccination before immunosuppression; culture history and MDROs. | Active uncontrolled infection usually pauses listing; vaccines work better before transplant. |
| Frailty / nutrition | Weight trajectory, sarcopenia, grip/functional measures, dietitian review; protein 1.2–1.5 g/kg/day unless centre advises otherwise. | Frailty predicts wait-list and postoperative outcomes but is also a treatment target. |
| Psychosocial / substances | Understanding, adherence barriers, support, housing, mental health, alcohol and other drug treatment. | Use transparent, individual assessment. A fixed abstinence interval alone is a poor substitute for relapse-risk and engagement assessment. |
7 The transplanted patient on the ward
Call the transplant unit early
- Red flagsFever/sepsis, jaundice or rapidly rising enzymes, biliary pain, graft/vascular concern, AKI, severe diarrhoea, neurotoxicity, missed immunosuppression or any new interacting drug.
- Do not stopNever withhold tacrolimus/ciclosporin or antimetabolite casually. Sepsis, cytopenia and AKI adjustments are centre-specific.
- RejectionLiver tests are nonspecific. Exclude biliary, vascular, infectious and drug causes; biopsy often establishes the diagnosis.
Common interaction traps
- CNI level ↑Macrolides, azole antifungals, diltiazem/verapamil, protease inhibitors and grapefruit can sharply raise exposure.
- CNI level ↓Rifampicin, carbamazepine, phenytoin and St John’s wort can cause under-immunosuppression.
- AKICheck trough, volume, sepsis and nephrotoxins; do not assume tacrolimus is the sole cause.
Guidelines & reviews. GESA consensus on diagnosis and management of portal hypertension in cirrhosis 2026; Baveno VIII consensus 2026; AASLD portal-hypertension practice guidance; AASLD/AST adult liver-transplant candidate-evaluation guideline approved 2025; TSANZ current recipient-eligibility and liver guidance. Trials. PREDESCI (NSBB prevention of decompensation), Lancet 2019; García-Pagán et al. pre-emptive TIPS, NEJM 2010; carvedilol vs EVL primary prophylaxis trials. Caveats. Non-invasive thresholds are aetiology- and quality-dependent. Transplant eligibility, exception points, anticoagulation and interventional options are centre-specific. Acute decompensation details sit in the companion cirrhosis and upper-GI-bleeding sheets.