Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Diagnose hepatocellular carcinoma through risk-based imaging or tissue when required, stage tumour and liver reserve together and select resection, transplantation, ablation, transarterial, radiotherapy or systemic treatment safely.
Hepatocellular carcinoma arises from hepatocytes, usually in cirrhosis or chronic viral liver disease; prognosis and treatment are governed jointly by tumour extent, portal hypertension, liver function and performance status. Alcohol-related liver disease, metabolic dysfunction-associated steatotic liver disease, hepatitis B or C and other chronic injuries create the main carcinogenic substrate. Chronic HBV can cause HCC even without established cirrhosis through viral integration and long-term inflammatory genomic injury. Repeated hepatocyte death and regeneration in fibrotic liver selects clones with telomere, WNT, TP53 and other driver abnormalities. As nodules progress, arterial blood supply replaces portal supply, creating the characteristic arterial enhancement and later contrast washout pattern.
Alcohol-related liver disease, metabolic dysfunction-associated steatotic liver disease, hepatitis B or C and other chronic injuries create the main carcinogenic substrate.
Chronic HBV can cause HCC even without established cirrhosis through viral integration and long-term inflammatory genomic injury.
Diabetes, obesity, smoking, aflatoxin and heavy alcohol exposure interact with fibrosis and host susceptibility. In Hepatocellular carcinoma, this distinction materially changes aetiological assessment.
Haemochromatosis, alpha-1-antitrypsin deficiency, porphyria and selected metabolic disorders raise risk through chronic injury and iron or metabolite toxicity.
Repeated hepatocyte death and regeneration in fibrotic liver selects clones with telomere, WNT, TP53 and other driver abnormalities.
As nodules progress, arterial blood supply replaces portal supply, creating the characteristic arterial enhancement and later contrast washout pattern.
Tumour grows into portal or hepatic veins, worsening portal hypertension, enabling intrahepatic spread and limiting locoregional options.
Treatment can remove or injure functioning parenchyma, so an anatomically small cancer may still be untreatable without adequate hepatic reserve.
Advanced disease commonly reaches nodes, lung, bone and adrenal sites, while symptoms may still be dominated by cirrhosis.
Many potentially curable tumours are asymptomatic and found on six-monthly ultrasound in eligible people with cirrhosis.
New ascites, encephalopathy, jaundice or variceal bleeding can be the first clue and also changes treatment fitness.
Right-upper-quadrant discomfort, early satiety, weight loss and hepatomegaly suggest enlarging or advanced tumour.
Portal-vein expansion and enhancing intraluminal tissue favours malignant invasion over bland thrombosis.
Abrupt severe abdominal pain, shock and haemoglobin fall with haemoperitoneum is a life-threatening presentation.
A mass-forming biliary cancer may lack classic HCC enhancement and requires tissue because systemic and surgical pathways differ.
Multiplicity, known extrahepatic primary and target-like enhancement favour metastases, but a new lesion in cirrhosis still needs dedicated characterisation.
Cirrhotic nodules can mimic early tumour; contrast pattern, size change and expert liver radiology review guide follow-up.
A hypervascular lesion in a non-cirrhotic liver may be benign but carries haemorrhage and selected malignant-transformation risk.
Peripheral nodular enhancement with progressive fill-in is typical; biopsy of a vascular lesion should not precede expert imaging review.
Tumour thrombus worsens portal hypertension and prognosis and changes suitability for transplant, resection and embolic treatment.
Cancer progression, infection or treatment can precipitate jaundice, coagulopathy, ascites, renal injury and encephalopathy. In Hepatocellular carcinoma, this distinction materially changes complication assessment.
Portal hypertension creates life-threatening gastrointestinal haemorrhage and requires prophylaxis assessment before bevacizumab-containing therapy. In Hepatocellular carcinoma, this distinction materially changes complication assessment.
Capsular vascular HCC can bleed into the peritoneum, causing shock and need for urgent transarterial or surgical haemostasis.
Resection, ablation, embolisation and radiotherapy can decompensate marginal liver reserve even when tumour targeting is technically adequate.
A tumour stage and a liver-disease stage are both required; treating one while ignoring the other produces unsafe recommendations.
In a high-risk cirrhotic liver, the accepted arterial-enhancement and washout pattern may obviate biopsy, but atypical disease needs tissue.
A normal marker neither excludes HCC nor proves response, while hepatitis and regeneration can elevate it without tumour.
Anti-VEGF treatment can convert untreated portal-hypertensive bleeding risk into catastrophic haemorrhage.
Radiological feasibility does not justify another procedure when liver reserve declines or disease becomes extrahepatic.
Staging the tumour without documenting liver reserve and portal hypertension.
Diagnosing HCC from AFP alone.
Biopsying a vascular lesion before expert multiphase imaging review.
Starting bevacizumab without assessing significant variceal bleeding risk.
Repeating transarterial treatment despite progressive decompensation.
Assuming portal-vein thrombus is bland without assessing enhancement and expansion.
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A patient with compensated cirrhosis is eligible for hepatocellular-carcinoma surveillance and would accept treatment if an early tumour were found. What schedule is recommended?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Management is determined by physiological urgency, disease extent, treatment intent and the person's priorities. The pathway moves through move from surveillance to diagnosis, then select resection, transplant or ablation, then control unresectable liver-confined disease; each transition requires named multidisciplinary ownership. Follow-up must anticipate portal-vein invasion, liver failure, variceal bleeding while measuring function and treatment toxicity.
Assess and treat oesophageal varices before bevacizumab, and review bleeding, hypertension, proteinuria, thrombosis, wound healing and immune toxicities; avoid in uncontrolled autoimmune disease or high untreated bleeding risk.
Control blood pressure, check urine protein, ECG risk, renal, liver and thyroid function and monitor diarrhoea, appetite, weight and hand–foot toxicity.
Avoid excessive diarrhoea, dehydration, hypernatraemia and aspiration, and investigate precipitating infection, bleeding, constipation, renal injury and sedative medicines.