Viral Hepatitis — DCE Clinical Case

The instruction decoded

"Examine the abdomen" in a viral hepatitis patient is really three tasks: demonstrate the stigmata of chronic liver disease, demonstrate the signs of portal hypertension, and then — the physician's flourish — examine for the complications and the cause, and land on a management synthesis, not a sign list [1] [2].

Systematic examination routine

From the end of the bed. Comfort at rest, nutritional state (muscle wasting of chronic disease), jaundice in the sclerae, and the exposed skin: spider naevi on the upper trunk and arms, scratch marks, bruising, and gynaecomastia in a male patient [1].

Hands. Palmar erythema, clubbing (uncommon but described in cirrhosis), Dupuytren's contracture (alcohol and association), asterixis — ask the patient to cock the wrists back and hold: a hepatic flap declares decompensation and encephalopathy risk [5].

Face and chest. Parotid fullness (alcohol cofactor), scleral icterus, foetor hepaticus; spider naevi in the superior vena cava distribution; loss of body hair and gynaecomastia of altered hormone metabolism [1].

Abdomen — inspect, then the sequence. Distension and flank fullness of ascites; a caput medusae of portosystemic shunting (flow away from the umbilicus); scars (transplant, paracentesis); prominent veins. Palpate: a firm, possibly nodular liver edge — in cirrhosis the left lobe may be palpable while the right shrinks; splenomegaly — the key portal hypertension sign; ballot the kidneys briefly. Percuss: liver span, splenic percussion, and shifting dullness for ascites — the most reliable bedside ascites sign. Auscultate: a hepatic bruit raises hepatocellular carcinoma or alcoholic hepatitis; a venous hum at the umbilicus (Cruveilhier-Baumgarten) is rare but golden [1] [2].

Complete the circuit. Ankle oedema of hypoalbuminaemia; ask about pruritus, haematemesis, confusion, and weight change — the decompensation and HCC questions [2].

Presentation template (deliver this to the examiner)

"Mr Doyle is comfortable at rest with mild temporal wasting and no icterus. He has palmar erythema and three spider naevi on the upper chest; there is no asterixis. His abdomen is soft and non-tender with no distension or shifting dullness. The liver edge is palpable 2 cm below the costal margin, firm, with a palpable left lobe; the spleen is palpable 3 cm below the costal margin. There is no caput medusae and no bruit. In summary: stigmata of chronic liver disease with splenomegaly indicating portal hypertension, clinically compensated, in a man with HCV cirrhosis cured by antiviral therapy two years ago. My concerns going forward are his ongoing HCC surveillance, his variceal screening status, and his metabolic and alcohol risk factors." [2] [4].

Discussion — where the examiner takes it next

"He is cured of hepatitis C. Why is he still in your clinic?" — "Because SVR eradicated the virus, not the scar. Established cirrhosis retains its risk of hepatocellular carcinoma and decompensation after cure, so he continues 6-monthly ultrasound HCC surveillance for life, and his variceal screening continues per endoscopy schedules. Cure changed his prognosis; it did not discharge him." [2] [4].

"Which single examination finding matters most today?" — "The spleen. Splenomegaly tells me portal hypertension persists after cure — it is the bedside marker that keeps him in the variceal and HCC risk frame, and a newly RISING spleen or new ascites would make me hunt for a complication: HCC, portal vein thrombosis, or decompensation." [2].

"How would your examination change if he were encephalopathic?" — "I would move asterixis, foetor and the confusion assessment to the front, look for the precipitant rather than the diagnosis — gastrointestinal bleeding, infection, constipation, sedatives — and treat this as decompensated disease. In acute liver failure the encephalopathy plus coagulopathy defines the emergency and the transplant-centre conversation." [5].

"If this were chronic hepatitis B instead, what differs?" — "The examination is identical; the frame differs. In HBV I would be asking about disease phase and fluctuating ALT, whether he is on tenofovir or entecavir and his adherence, his HDV screening status, and family testing — and I would remember that HBV drives HCC even without cirrhosis in defined risk groups, so surveillance can precede the stigmata." [1] [3].

"What red flags would you voice unprompted?" — "Three: new weight loss, a hepatic bruit or a rising spleen suggesting HCC; any haematemesis suggesting variceal bleeding in a portal-hypertensive patient; and confusion suggesting decompensation. Each one converts a surveillance patient into an admission." [2] [5].