Gastroenterology: Cirrhosis and Transplantation

• Cirrhosis: What is Cirrhosis? | Diagnosing and Staging Cirrhosis | Routine Care in Cirrhosis
• Complications: Portal Hypertension and Varices | Ascites | Chronic Hepatic Encephalopathy | Other Complications | Prescribing in Liver Disease
• Tumours and lesions: Hepatocellular Carcinoma | Benign Liver Lesions | Liver Abscess and Hydatid Disease
• Vascular and advanced: Vascular Liver Disorders | Liver Transplantation | Advanced Liver Disease and Palliative Care
• Revision: Drug Reference Table | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🧭 Cirrhosis is the end stage of chronic liver disease - scarring that distorts the liver and raises the pressure in the portal vein. People can live well for years while it is "compensated", but once complications appear (ascites, variceal bleeding, encephalopathy, jaundice) the outlook changes sharply. This chapter covers long-term care of cirrhosis, liver tumours, vascular liver disease and transplantation; acute decompensation is covered in the Gastroenterology Emergencies chapter.
Your four questions for every patient: Is the cirrhosis compensated or decompensated? Has the cause been treated (alcohol, virus, weight, iron)? Are surveillance for HCC and varices, nutrition and vaccinations up to date? Is this patient suitable for transplant, or do they need palliative care planning?

What is Cirrhosis?

What it is: Widespread liver scarring (fibrosis) with regenerating nodules, which replaces normal liver structure.

Two main consequences:

• Liver failure - low albumin, coagulopathy, jaundice, encephalopathy.
• Portal hypertension - varices, ascites, a large spleen.

Commonest UK causes:

• Alcohol.
• MASLD.
• Hepatitis C and B.
• Less often: autoimmune hepatitis, PBC, PSC, haemochromatosis, Wilson's, alpha-1 antitrypsin deficiency, drugs (methotrexate), cardiac causes (right heart failure, Fontan).

Compensated vs decompensated:

• Compensated: No complications yet. Often no symptoms; median survival over 12 years.
• Decompensated: Ascites, variceal bleeding, encephalopathy or jaundice. Median survival about 2 years without transplant.
• Treating the cause (stopping alcohol, curing hepatitis C, weight loss) can stop progression and sometimes allows "recompensation".

Signs of chronic liver disease:

• Palmar erythema; spider naevi (more than 5).
• Clubbing; leuconychia (low albumin); Dupuytren's contracture (alcohol).
• Gynaecomastia; testicular atrophy.
• Jaundice.
• Ascites; caput medusae.
• Splenomegaly.
• Asterixis (encephalopathy).
• Muscle wasting.

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Diagnosing and Staging Cirrhosis

Making the diagnosis:

• Transient elastography (FibroScan) - liver stiffness. Over about 15 kPa suggests advanced chronic liver disease; NICE uses 16 kPa or more to suggest cirrhosis in some groups.
• Blood markers: Low platelets, low albumin, raised bilirubin and INR; FIB-4, ELF.
• Ultrasound or CT: Small nodular liver, large spleen, ascites, collaterals.
• Liver biopsy - only if the diagnosis or cause is uncertain.
• NICE NG50: Offer testing for cirrhosis to people at high risk - harmful drinking, hepatitis B or C, and MASLD with advanced fibrosis.

Severity scores:

• Child–Pugh score - 5 items:
  • Bilirubin.
  • Albumin.
  • INR.
  • Ascites.
  • Encephalopathy.
• Child–Pugh classes:
  • A (5–6 points) - well compensated.
  • B (7–9).
  • C (10–15) - severe; high one-year mortality.
• MELD (bilirubin, INR, creatinine, sodium) and UKELD (bilirubin, INR, creatinine, sodium) - predict short-term survival. UKELD 49 or more is the usual threshold for liver transplant listing in the UK.

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Routine Care in Cirrhosis

• Treat the cause: Abstinence from alcohol, antivirals for hepatitis B or C, weight loss, venesection, immunosuppression for AIH.
• HCC surveillance: Ultrasound every 6 months (with or without AFP) for everyone with cirrhosis who would be fit for treatment.
• Varices:
  • Assess for portal hypertension - endoscopy, or FibroScan and platelets.
  • Baveno VII: Endoscopy can be avoided if liver stiffness is under 20 kPa and platelets are over 150 × 10⁹/L.
• Nutrition:
  • Malnutrition and sarcopenia (muscle loss) are common and predict poor outcomes.
  • Energy 30–35 kcal/kg/day; protein 1.2–1.5 g/kg/day. Do not restrict protein, even in encephalopathy.
  • Late-evening snack and avoid fasting for long periods (the cirrhotic liver can't store glycogen).
  • Dietitian review.
• Vaccinations: Hepatitis A and B (if not immune), pneumococcal, yearly influenza, COVID-19, shingles.
• Bone health: DEXA; vitamin D.
• Medication review (see Prescribing in Liver Disease).
• Exercise to maintain muscle.
• Discuss prognosis, transplant and future care plans early.

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Portal Hypertension and Varices

What it is: Scarring raises the pressure in the portal vein. Blood is diverted through collateral veins - oesophageal and gastric varices, rectal varices, and the caput medusae. Clinically significant portal hypertension (CSPH) greatly raises the risk of decompensation.

Preventing a first bleed (primary prophylaxis - BSG and Baveno VII):

• Carvedilol (a non-selective beta-blocker) - 6.25 mg once daily, increasing to 12.5 mg daily if tolerated (keep systolic BP over 90 mmHg).
• Beta-blockers are now also used for CSPH without large varices, to prevent decompensation.
• Propranolol is an alternative.
• Variceal band ligation if beta-blockers are contraindicated or not tolerated.
• Gastric varices: Specialist care (glue injection, TIPSS).

After a variceal bleed (secondary prophylaxis):

• Carvedilol (or propranolol) plus repeated band ligation every 2–4 weeks until the varices are gone, then surveillance.
• TIPSS (transjugular intrahepatic portosystemic shunt) if bleeding recurs. "Pre-emptive" TIPSS in high-risk patients improves survival.
• For the acute bleed, see the Gastroenterology Emergencies chapter.

Beta-blockers in advanced cirrhosis: Reduce or stop the dose if there is low BP (systolic under 90), AKI, hyponatraemia or refractory ascites with poor kidney function.

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Ascites

What it is: Fluid in the abdomen, the commonest complication of cirrhosis. Its onset means a poor outlook - consider transplant referral.

Diagnostic tap - for all new ascites and every admission with ascites:

• Neutrophils over 250 cells/mm³ means SBP - treat urgently (see the Gastroenterology Emergencies chapter).
• SAAG (serum minus ascitic albumin) 11 g/L or more means portal hypertension (cirrhosis, heart failure, Budd–Chiari). Under 11 g/L suggests another cause - cancer, TB, pancreatitis, nephrotic syndrome.
• Also check ascitic protein, culture (in blood culture bottles), cytology, and amylase if indicated.

Treatment (BSG 2020 guideline):

• Salt restriction - no added salt (about 5–6.5 g salt a day). Don't restrict so much that the patient stops eating.
• Spironolactone 100 mg daily, increasing every few days up to 400 mg.
• Add furosemide 40 mg daily, up to 160 mg, if the response is poor or potassium rises.
• Target weight loss: 0.5 kg/day without leg oedema, up to 1 kg/day with oedema.
• Monitor U&E, sodium and potassium closely.
• Stop diuretics if there is severe hyponatraemia (under 120–125 mmol/L), AKI, encephalopathy or severe cramps.
• Gynaecomastia with spironolactone - amiloride is an alternative.

Large-volume paracentesis:

• For tense or refractory ascites.
• Give human albumin solution (8 g of albumin per litre removed - e.g. 100 mL of 20% albumin per 2.5 L) when more than 5 L is drained, to prevent circulatory dysfunction and kidney injury.

Refractory ascites (not controlled by maximum diuretics, or diuretics not tolerated):

• Repeated paracentesis.
• TIPSS (selected patients - risk of encephalopathy).
• Transplant assessment.
• Long-term abdominal drains for palliation.

Avoid:

• NSAIDs.
• ACE inhibitors and ARBs.
• Aminoglycosides.
• Over-aggressive diuresis.

Antibiotic prophylaxis against SBP:

• After an episode of SBP.
• Consider when ascitic protein is low (15 g/L or less).
• Usually ciprofloxacin or co-trimoxazole.

Hepatic hydrothorax: A pleural effusion (usually right-sided) from ascites tracking through the diaphragm. Avoid chest drains (protein and fluid loss, infection) - treat the ascites; TIPSS.

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Chronic Hepatic Encephalopathy

What it is: Brain dysfunction caused by toxins (especially ammonia) that the failing liver can't clear and that bypass the liver through shunts.

• Overt HE: Confusion, drowsiness, asterixis, coma (graded with West Haven, 1–4). Acute management is in the Gastroenterology Emergencies chapter.
• Covert (minimal) HE: Subtle problems with attention, reaction time and sleep (reversed day–night pattern). It affects driving, work and falls risk.
• Look for triggers in every episode:
  • Infection (including SBP).
  • GI bleeding.
  • Constipation.
  • Dehydration and diuretics.
  • Low potassium or sodium; AKI.
  • Sedatives (benzodiazepines, opioids).
  • Alcohol.
  • TIPSS.
• Prevention and treatment:
  • Lactulose, titrated to 2–3 soft stools a day (e.g. 15–30 mL twice daily).
  • Rifaximin 550 mg twice daily (NICE TA337) - added after a further episode of overt HE despite lactulose. Reduces hospital admissions.
  • Don't restrict protein - malnutrition makes HE worse.
  • Avoid sedatives.
• Driving: Advise patients with HE not to drive until it is controlled, and to tell the DVLA.
• Recurrent or persistent HE is an indication for transplant assessment.

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Other Complications

• Hepatorenal syndrome and AKI - see the Gastroenterology Emergencies chapter (terlipressin and albumin).
• Hyponatraemia: Dilutional, from water retention. Stop diuretics if severe; fluid restriction (1–1.5 L) if sodium is under 125 mmol/L and the patient is overloaded. Correct slowly (risk of osmotic demyelination).
• Hepatopulmonary syndrome:
  • Dilated lung blood vessels cause hypoxia.
  • Platypnoea (breathless sitting up) and orthodeoxia (oxygen falls sitting up).
  • Diagnose with contrast ("bubble") echocardiography.
  • Cured by transplant.
• Portopulmonary hypertension:
  • Pulmonary arterial hypertension with portal hypertension.
  • Screen with echo before transplant.
  • Severe disease may prevent transplant.
• Portal vein thrombosis: Common in cirrhosis. It may worsen portal hypertension. Anticoagulation is considered, especially in transplant candidates.
• Coagulation:
  • The INR is raised, but clotting factors that prevent clotting are also low ("rebalanced haemostasis").
  • The INR does not predict bleeding - don't give FFP routinely before procedures.
  • Patients still need VTE prophylaxis in hospital.
• Low platelets: Usually from splenic pooling. Thrombopoietin agonists (e.g. avatrombopag) can be used before procedures.
• Infections: Cirrhosis weakens immunity - sepsis is a common cause of death.
• Sarcopenia and frailty; diabetes ("hepatogenous").
• Muscle cramps: Check electrolytes; reduce diuretics; consider baclofen.
• Hypogonadism; osteoporosis.

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Prescribing in Liver Disease

• Avoid NSAIDs - kidney failure, bleeding, resistant ascites.
• Paracetamol is the preferred painkiller. Usual doses are generally safe, but use a reduced maximum (e.g. 2–3 g a day) in people who weigh under 50 kg, are malnourished, or drink heavily (check local guidance).
• Opioids: Use cautiously at low doses; they can trigger encephalopathy (through constipation and sedation). Give laxatives. Avoid codeine, and avoid morphine in severe disease (oxycodone in low doses, or fentanyl, is used with specialist advice).
• Sedatives: Avoid benzodiazepines except in alcohol withdrawal.
• PPIs: Use only when needed - they increase the risk of SBP and encephalopathy.
• ACE inhibitors and ARBs: Avoid in ascites.
• Aminoglycosides: Avoid (kidney injury).
• Statins: Safe in compensated cirrhosis (lower doses in decompensated disease).
• Metformin: Avoid in decompensated disease (lactic acidosis).
• Drugs that need a working liver: Many drugs need dose reduction. Check the BNF hepatic impairment advice for every new drug.
• Anticoagulants: DOACs are used in Child–Pugh A (and some B); avoid in C. Warfarin is hard to monitor because the INR is already raised.

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Hepatocellular Carcinoma

What it is: Primary liver cancer arising from liver cells. More than 80% arise in a cirrhotic liver. It is rising in the UK, driven by alcohol and MASLD.

Risk factors:

• Cirrhosis of any cause.
• Hepatitis B (even without cirrhosis).
• Hepatitis C.
• Haemochromatosis.
• Male sex; older age.
• Smoking.
• Diabetes; obesity.
• Aflatoxin (worldwide).

Presentation:

• Most are found on surveillance ultrasound.
• Otherwise:
  • Decompensation of previously stable cirrhosis.
  • Right upper quadrant pain; weight loss.
  • A mass.
  • Haemoperitoneum (rupture).

Diagnosis:

• In cirrhosis, multiphase CT or MRI can diagnose HCC without a biopsy: arterial phase enhancement with "washout" in the later phases (LI-RADS 5).
• AFP is often raised but can be normal.
• Biopsy if the imaging is not typical, or in a non-cirrhotic liver.

Treatment - by the liver MDT, based on the BCLC staging system (tumour size and number, liver function, fitness):

• Very early or early:
  • Resection - for a good liver without significant portal hypertension.
  • Ablation - radiofrequency or microwave, for tumours under about 3 cm.
  • Liver transplant - within UK criteria (e.g. a single tumour up to 5 cm, or up to 5 tumours each 3 cm or less, with AFP limits) - treats both the cancer and the cirrhosis.
• Intermediate: TACE (transarterial chemoembolisation) or SIRT (radioembolisation).
• Advanced: Systemic treatment for Child–Pugh A:
  • Atezolizumab plus bevacizumab, or durvalumab plus tremelimumab (first line).
  • Lenvatinib or sorafenib as alternatives.
  • Check for varices before bevacizumab (bleeding risk).
• End-stage (Child–Pugh C, poor performance): Best supportive care.

Fibrolamellar carcinoma: A rare form in young people without cirrhosis; normal AFP; better prognosis with resection.

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Benign Liver Lesions

Liver lesions are often found by chance. The commonest malignant liver lesions are metastases (colon, breast, lung, pancreas, stomach, melanoma, NETs).

• Haemangioma:
  • The commonest benign liver tumour - a tangle of blood vessels.
  • Typical appearance on ultrasound and MRI (peripheral nodular enhancement filling in).
  • No follow-up needed if typical.
  • Large ones rarely cause pain or platelet consumption (Kasabach–Merritt).
• Focal nodular hyperplasia (FNH):
  • A benign overgrowth around an abnormal artery, usually in young women.
  • Central scar on imaging.
  • No malignant risk; no follow-up needed if the diagnosis is confident.
• Hepatocellular adenoma:
  • A benign tumour of liver cells.
  • Linked to the combined pill (young women), anabolic steroids (men), obesity and glycogen storage disease.
  • Risks: Bleeding and rupture; malignant change (higher in men and in β-catenin-mutated types).
  • Management:
    • Stop the pill or steroids; weight loss.
    • Resect if over 5 cm after 6 months, in men, or if β-catenin-mutated.
    • Embolise if bleeding.
• Simple liver cysts: Very common, harmless, thin-walled, fluid-filled. No follow-up unless they have complex features.
• Polycystic liver disease: Many cysts, often with autosomal dominant polycystic kidney disease. Usually no symptoms; large livers cause pressure symptoms (somatostatin analogues, surgery or transplant).
• Focal fatty change or sparing: Mimics a lesion - MRI clarifies.

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Liver Abscess and Hydatid Disease

• Pyogenic liver abscess:
  • Causes: Biliary infection, spread from the bowel (diverticulitis, appendicitis, colorectal cancer), or bloodstream.
  • Organisms: Streptococcus anginosus (milleri) group, E. coli, Klebsiella (especially in diabetes and people from East Asia - can cause eye and brain infection), anaerobes.
  • Symptoms: Fever, rigors, right upper quadrant pain, raised inflammatory markers and ALP.
  • Treatment:
    • Drainage (image-guided) for larger abscesses.
    • Prolonged antibiotics (4–6 weeks) guided by cultures.
    • Look for a source - colonoscopy for streptococcal abscesses.
• Amoebic liver abscess:
  • Entamoeba histolytica - after travel or living in the tropics, sometimes months or years later.
  • Usually a single right-lobe abscess; fever, pain.
  • Positive amoebic serology; "anchovy sauce" pus.
  • Metronidazole, then a luminal agent (e.g. paromomycin) to clear the gut. Drainage is rarely needed.
• Hydatid disease:
  • Echinococcus granulosus tapeworm - from dogs and sheep (sheep-farming areas, including Wales).
  • Slow-growing cysts with "daughter cysts"; often no symptoms.
  • Rupture can cause anaphylaxis - never aspirate without planning.
  • Diagnose with imaging and serology.
  • Albendazole plus surgery or PAIR (puncture, aspiration, injection, re-aspiration) under specialist care.

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Vascular Liver Disorders

• Budd–Chiari syndrome:
  • Blockage of the hepatic veins (outflow), usually by thrombosis.
  • Causes:
    • Myeloproliferative neoplasms (test for JAK2 even with a normal blood count).
    • Paroxysmal nocturnal haemoglobinuria.
    • Antiphospholipid syndrome; inherited thrombophilia.
    • The combined pill; pregnancy.
  • Triad: Abdominal pain, ascites and hepatomegaly. It can present acutely with liver failure.
  • Diagnosis: Doppler ultrasound, CT or MRI. The caudate lobe is often enlarged (it drains separately).
  • Treatment:
    • Anticoagulation.
    • Angioplasty or stenting.
    • TIPSS.
    • Transplant.
    • Treat the underlying cause.
• Portal vein thrombosis (without cirrhosis):
  • Causes: Abdominal infection or inflammation (pancreatitis, appendicitis), thrombophilia, myeloproliferative disease, cancer.
  • Acute: Abdominal pain - anticoagulate (risk of bowel ischaemia).
  • Chronic: A "cavernoma" with varices - bleeding with normal liver function.
• Ischaemic hepatitis ("shock liver"):
  • Very high ALT (often thousands) after hypotension, heart failure or hypoxia.
  • It rises and falls quickly; LDH is very high.
  • Treat the cause.
• Congestive hepatopathy: Right heart failure, tricuspid regurgitation, constrictive pericarditis, Fontan circulation. Causes cholestatic LFTs, hepatomegaly and eventually "cardiac cirrhosis".
• Sinusoidal obstruction syndrome (veno-occlusive disease):
  • After bone marrow (stem cell) transplant conditioning, some chemotherapy, and pyrrolizidine alkaloids (bush teas).
  • Weight gain, painful hepatomegaly, jaundice.
  • Treated with defibrotide.
• Hereditary haemorrhagic telangiectasia: Liver vascular malformations can cause high-output heart failure.

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Liver Transplantation

Who to refer:

• Decompensated cirrhosis - refer early, at the first ascites, variceal bleed or encephalopathy, or when UKELD is 49 or more.
• HCC within transplant criteria.
• Acute liver failure - "super-urgent" listing using King's College criteria (see the Gastroenterology Emergencies chapter).
• "Variant" syndromes - poor quality of life without high UKELD:
  • Intractable itch.
  • Recurrent cholangitis (PSC).
  • Hepatopulmonary syndrome.
  • Refractory encephalopathy.
  • Polycystic liver disease.

Assessment (at one of the UK transplant centres):

• Heart and lung fitness (echo, exercise testing).
• Frailty and nutrition.
• Kidney function.
• Infection screening.
• Alcohol and drug use - patients must engage with abstinence. There is no fixed rule of 6 months' abstinence in the UK; decisions are individual.
• Social support.

Contraindications:

• Ongoing alcohol or drug misuse.
• Active cancer outside the liver.
• Severe heart or lung disease (including severe portopulmonary hypertension).
• Uncontrolled sepsis.
• Severe frailty.

Outcomes: About 90% survive 1 year and about 80% survive 5 years.

After transplant:

• Immunosuppression: Tacrolimus (with mycophenolate and early steroids).
  • Side effects: kidney damage, diabetes, tremor, hypertension, high potassium, low magnesium.
  • Drug interactions - clarithromycin, erythromycin, azole antifungals and diltiazem raise levels; rifampicin and carbamazepine lower them.
• Risks:
  • Rejection.
  • Infection (CMV, PCP - prophylaxis).
  • Skin cancer (sun protection).
  • Post-transplant lymphoproliferative disorder (EBV).
  • CKD.
  • Cardiovascular disease.
  • Biliary strictures.
• Disease recurrence: PSC, PBC, AIH, MASLD and alcohol can return.
• No live vaccines.

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Advanced Liver Disease and Palliative Care

• Who: People with decompensated cirrhosis who are not transplant candidates. They have a high symptom burden and short life expectancy, but are often referred late to palliative care.
• Triggers to plan ahead:
  • Two or more unplanned admissions in 6 months.
  • Refractory ascites.
  • Recurrent encephalopathy.
  • Child–Pugh C.
  • Continued drinking with decompensation.
• Advance care planning: ReSPECT discussion, preferred place of care, ceiling of treatment (e.g. ITU, endoscopy).
• Symptoms:
  • Ascites - long-term abdominal drains at home.
  • Itch - see PBC.
  • Encephalopathy - continue lactulose and rifaximin.
  • Pain - paracetamol, cautious low-dose opioids.
  • Breathlessness; muscle cramps; low mood.
• Bleeding near the end of life: Agree a plan in advance (dark towels, midazolam).
• Palliative care can run alongside active treatment of complications.

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Drug Reference Table

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Spot the Diagnosis

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Exam-style Scenarios

1. A 58-year-old with alcohol-related cirrhosis (abstinent, Child–Pugh A) attends clinic. Endoscopy shows medium varices that have never bled.
Answer: Primary prophylaxis.

• Carvedilol 6.25 mg daily, increasing to 12.5 mg if tolerated (band ligation if beta-blockers are contraindicated).
• 6-monthly ultrasound for HCC.
• Nutrition review, vaccinations, DEXA.
• Support continued abstinence.

2. A man with cirrhosis has new moderate ascites. Ascitic neutrophils are 60/mm³ and SAAG is 15 g/L.
Answer: Portal hypertensive ascites without SBP.

• No added salt.
• Spironolactone 100 mg daily, increasing as needed; add furosemide if response is poor.
• Monitor weight, U&E and sodium.
• Avoid NSAIDs and ACE inhibitors; refer for transplant assessment.

3. A woman with cirrhosis has had two admissions with confusion despite lactulose. No other trigger was found.
Answer: Recurrent overt hepatic encephalopathy.

• Add rifaximin 550 mg twice daily to lactulose.
• Avoid sedatives; adequate protein intake.
• Advise her not to drive; consider transplant referral.

4. Surveillance ultrasound in a man with hepatitis C cirrhosis (cured) shows a new 2.5 cm nodule.
Answer: Possible HCC - multiphase CT or MRI.

• Arterial enhancement with washout confirms HCC without biopsy.
• Liver MDT. Options include ablation, resection, or transplant if within criteria.

5. A 35-year-old woman develops abdominal pain and ascites. Doppler shows no flow in the hepatic veins.
Answer: Budd–Chiari syndrome.

• Anticoagulate.
• Test for JAK2, PNH and antiphospholipid antibodies; stop the combined pill.
• Refer to a liver unit for angioplasty, TIPSS or transplant if needed.

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Key Points

• Decompensation (ascites, variceal bleed, encephalopathy, jaundice) changes the prognosis - refer for transplant assessment.
• Treating the cause can halt progression in cirrhosis.
• Everyone with cirrhosis: 6-monthly ultrasound for HCC, a variceal assessment, nutrition (protein 1.2–1.5 g/kg, late-evening snack), vaccinations and bone health.
• Carvedilol prevents first variceal bleeds and decompensation; after a bleed, give a beta-blocker plus band ligation.
• Do a diagnostic tap in all new ascites and every admission. Neutrophils over 250 means SBP; SAAG of 11 or more means portal hypertension.
• Ascites: no added salt, spironolactone with or without furosemide; albumin with large-volume paracentesis over 5 L.
• Avoid NSAIDs, ACE inhibitors, aminoglycosides and sedatives in cirrhosis; use PPIs only when needed.
• Hepatic encephalopathy: find the trigger; lactulose to 2–3 soft stools; add rifaximin for recurrence; don't restrict protein.
• INR doesn't predict bleeding in cirrhosis - patients still need VTE prophylaxis.
• HCC in cirrhosis can be diagnosed on imaging alone (arterial enhancement with washout).
• Haemangioma and FNH need no follow-up; adenomas linked to the pill or steroids may need resection.
• Budd–Chiari: pain, ascites, hepatomegaly - test for JAK2 and anticoagulate.
• After transplant: tacrolimus interactions, infection, skin cancer and disease recurrence.

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Guidelines and Further Reading

• NICE NG50: Cirrhosis in over 16s - assessment and management
• BSG guidelines on the management of ascites in cirrhosis (2020)
• BSG guidelines on the management of variceal haemorrhage in cirrhotic patients (2015)
• Baveno VII consensus on portal hypertension (2022)
• NICE TA337: Rifaximin for preventing episodes of overt hepatic encephalopathy
• EASL Clinical Practice Guidelines on hepatocellular carcinoma, nutrition in chronic liver disease, vascular diseases of the liver, and benign liver tumours
• NICE technology appraisals for HCC systemic therapies
• NHS Blood and Transplant: liver transplant selection policy
• BNF - for current doses and hepatic impairment advice

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