Viral Hepatitis — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Minh Nguyen, 54 years old. [1]

Presenting complaint: Referred to hepatology clinic after a 6-month surveillance liver ultrasound showed a 2.2 cm nodule in the right hepatic lobe. He feels well and is asymptomatic. [4]

Past history: [1]

• Chronic hepatitis B, diagnosed at age 25 on migration screening (perinatally acquired). Never treated — was told he was in the immune tolerant phase.
• Type 2 diabetes (HbA1c 7.4 percent), obesity (BMI 33), hypertension.
• Small oesophageal varices found 2 years ago on screening endoscopy.

Current medications: Metformin 1000 mg BD, perindopril 5 mg daily, no antiviral therapy. [1]

Examination findings (trainee elicits): [1] [6]

• Thin, comfortable. Several spider naevi over the anterior chest. Palmar erythema. No asterixis.
• Spleen enlarged 4 cm below the left costal margin. Liver edge firm and irregular.
• No ascites. Peripheral oedema to the ankles.

Investigations: [1] [4]

• HBsAg positive, anti-HBs negative, anti-HBc positive, HBeAg negative, anti-HBe positive, HBV DNA 45,000 IU/mL. Anti-HDV negative.
• ALT 118, AST 95, platelets 110, INR 1.2, albumin 36, bilirubin 22, creatinine 80.
• FibroScan 18 kPa (consistent with cirrhosis).
• Surveillance ultrasound: 2.2 cm nodule, right lobe. AFP 45 ng/mL (mildly elevated).
• Multiphase CT: the nodule shows arterial phase hyperenhancement and washout — LI-RADS 5, compatible with hepatocellular carcinoma.

Candidate's structured presentation (model)

Opening statement: [1] [4]

"Mr Nguyen is a 54-year-old Vietnamese-born man referred after a surveillance ultrasound found a liver nodule. He has chronic hepatitis B, diagnosed at age 25 and previously untreated, type 2 diabetes and obesity. [1] [4]

His main problems are: [1] [4] [6]

1. Hepatocellular carcinoma — a 2.2 cm LI-RADS 5 nodule in the right hepatic lobe, within Milan criteria
2. Chronic hepatitis B in the HBeAg-negative immune active phase — HBV DNA 45,000 IU/mL, untreated
3. Compensated cirrhosis (Child-Pugh A) with portal hypertension — small varices, splenomegaly, platelets 110
4. Metabolic syndrome with overlapping MASLD

His immediate priorities are staging and treating the hepatocellular carcinoma, starting antiviral therapy for HBV, and planning ongoing cirrhosis surveillance." [1] [4] [6]

Management plan: [1] [4]

1. Hepatocellular carcinoma — the nodule is 2.2 cm with arterial hyperenhancement and washout [4] [5], on CT (LI-RADS 5), diagnostic of HCC in a cirrhotic liver without biopsy. It is within Milan criteria (single tumour under 5 cm, or up to 3 nodules each under 3 cm, no vascular invasion or metastasis). Given his preserved liver function (Child-Pugh A) and the small single lesion, the options are resection or ablation; he should be discussed at a multidisciplinary tumour board. Liver transplant is the gold standard for HCC in cirrhosis and is an option within Milan criteria given priority allocation (MELD exception).
2. Antiviral therapy — start tenofovir 300 mg daily immediately. He has cirrhosis with detectable HBV DNA, an absolute indication, and viral suppression reduces HCC recurrence risk after treatment.
3. Cirrhosis management — continue 6-monthly surveillance, reassess varices for primary prophylaxis, vaccinate against HAV if non-immune, address metabolic cofactors.
4. Public health — test and vaccinate family contacts.

Examiner discussion questions

Q: "The CT shows arterial hyperenhancement and washout. Why does this make biopsy unnecessary?" [4]

"In a cirrhotic liver, the hallmark of hepatocellular carcinoma is arterial phase hyperenhancement followed by washout in the portal venous or delayed phase — this reflects the tumour's arterial blood supply relative to the surrounding parenchyma. The LI-RADS classification system allows a nodule at least 1 cm with these features to be diagnosed as HCC without biopsy, with a very high positive predictive value. Biopsy carries a small but real risk of tumour seeding and bleeding, and is reserved for lesions where imaging is non-diagnostic or atypical. This lesion meets LI-RADS 5 criteria, so the diagnosis is radiological." [4]

Q: "What are the Milan criteria and why do they matter?" [5]

"Milan criteria define the transplant eligibility for HCC in cirrhosis: a single tumour up to 5 cm, or up to 3 tumours each up to 3 cm, with no macrovascular invasion or extrahepatic spread. Patients within Milan criteria have comparable post-transplant survival to patients transplanted for decompensated cirrhosis without HCC, which is the rationale for allocating donor organs. Mr Nguyen's 2.2 cm single tumour is well within Milan criteria, so transplant is a valid treatment option. The alternatives for a small tumour in preserved Child-Pugh A cirrhosis are surgical resection or radiofrequency ablation, decided at a multidisciplinary meeting." [5]

Q: "He was never treated for HBV. Was that the right decision originally?" [1]

"It depends on his phase at the time. If he was genuinely in the immune tolerant phase — HBeAg positive, DNA above one million, normal ALT — then watchful waiting was appropriate, because antivirals in that phase suppress DNA but do not reliably induce seroconversion and stopping risks flare. However, he is now HBeAg negative with a DNA of 45,000 and ALT 118, which is the immune active phase and a clear treatment indication. The concern is that the transition from immune tolerant to immune active may have been missed during years without monitoring, allowing fibrosis and ultimately cirrhosis and HCC to develop. This underscores the importance of 6-monthly ALT monitoring in immune tolerant patients." [1]

Q: "How does his metabolic syndrome affect his HCC risk?" [1]

"His type 2 diabetes and obesity represent overlapping MASLD, which is an independent risk factor for HCC — even without cirrhosis, though cirrhosis amplifies the risk. MASLD and HBV can coexist and synergise in driving fibrogenesis and carcinogenesis. Addressing his metabolic risk with weight loss and glycaemic control is part of his management, alongside viral suppression." [1]

DCE Short Case — Abdominal Examination in Chronic Viral Hepatitis

Instruction

"Examine this patient's abdominal system. You have 7 minutes for examination and 8 minutes for discussion." [1] [6]

Key signs the patient demonstrates

• General inspection: thin, spider naevi on anterior chest, loss of axillary hair, palmar erythema
• Abdomen: firm irregular liver edge, splenomegaly (4 cm), no ascites
• No asterixis (no hepatic failure signs) [1] [6]

Systematic routine

1. End of bed — cachexia, spider naevi, gynaecomastia, loss of body hair. [1]
2. Hands — palmar erythema, Dupuytren contracture, leuconychia, asterixis.
3. Face and chest — spider naevi (superior vena cava distribution), loss of axillary hair, parotid enlargement.
4. Abdomen — inspect for distension and caput medusae; palpate for hepatomegaly or shrunken liver, splenomegaly; percuss for shifting dullness; auscultate for bruit.
5. Complete — peripheral oedema, testicular atrophy. [1] [6]

Presentation template

"I examined Mr Nguyen's abdominal system. He is thin, with several spider naevi over the anterior chest wall in the superior vena cava distribution, and loss of axillary hair. On the hands there is palmar erythema sparing the central palm. There is no asterixis. [1]

The abdomen is soft. The liver edge is firm and irregular, palpable 3 cm below the costal margin. The spleen is enlarged 4 cm below the left costal margin. There is no shifting dullness. There is peripheral oedema to the ankles bilaterally. [6]

These findings are consistent with chronic liver disease complicated by portal hypertension. The spider naevi and palmar erythema indicate chronic liver disease; the splenomegaly and firm irregular liver indicate portal hypertension and parenchymal disease. I would like to take a full viral hepatitis and alcohol history, organise liver function tests, a viral hepatitis screen, a FibroScan, and screening endoscopy." [1] [6]

Discussion template

1. Summarise findings — "consistent with chronic liver disease with portal hypertension, likely viral aetiology."
2. Differential from signs — chronic HBV or HCV, alcohol-related, MASLD, haemochromatosis; the firm irregular liver and splenomegaly point to cirrhosis with portal hypertension.
3. Investigations — viral serology (HBsAg, anti-HBs, anti-HBc, anti-HCV), ferritin and transferrin saturation, autoimmune and metabolic screen, FibroScan, endoscopy.
4. Management priorities — treat the cause, screen for varices, institute HCC surveillance, vaccinate contacts. [1] [4] [6]