Chronic Liver Disease and Cirrhosis — Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Chen is a 58-year-old retired carpenter who presents with increasing abdominal distension, leg swelling and 2 days of drowsiness. He has a 25-year history of heavy alcohol use and known alcohol-related cirrhosis, diagnosed 18 months ago after a variceal bleed treated with endoscopic band ligation. He is on carvedilol 6.25 mg daily, spironolactone 100 mg daily and frusemide 40 mg daily. [1]

On examination he is drowsy with asterixis, febrile, hypotensive, with tense ascites and peripheral oedema. [1]

His main problems are:

1. Decompensated alcohol-related cirrhosis — Child-Pugh C (11), MELD-Na 26
2. Spontaneous bacterial peritonitis — ascitic PMN 420 cells/microlitre
3. Acute kidney injury — probable hepatorenal syndrome, precipitated by SBP
4. Grade 3 hepatic encephalopathy — precipitated by infection
5. Portal hypertension with varices on secondary prophylaxis
6. Alcohol dependence — needs addiction medicine input [1]

His immediate management priorities are resuscitation, treatment of SBP with cefotaxime and albumin, renal protection by withdrawing diuretics, and encephalopathy management with lactulose and rifaximin. Given his MELD-Na of 26, I would refer urgently for liver transplant assessment once the acute episode stabilises." [1]

Examiner probing questions and model answers

Q1: "What is his Child-Pugh score and what does it tell you?" [1]

"Child-Pugh 11, which is class C. It uses bilirubin, albumin, INR, ascites and encephalopathy, and gives a rough prognosis — class A 1-year survival near 100%, class C around 45%. However, Child-Pugh does not govern transplant priority; that is MELD-Na, which at 26 places him in a high-priority category. I would use Child-Pugh for prognostic framing and MELD-Na for the transplant referral." [1]

Q2: "He has an INR of 1.9. Would you give fresh frozen plasma before paracentesis?" [1]

"No. The modern understanding of haemostasis in cirrhosis is the rebalance theory — cirrhosis depletes both procoagulant and anticoagulant factors in parallel, so the net balance is roughly preserved. INR measures only the procoagulant side and overestimates bleeding risk. Routine FFP correction before low-bleeding-risk procedures such as paracentesis does not prevent bleeding and carries volume and transfusion risks. I would proceed with paracentesis without FFP, using viscoelastic testing such as ROTEM if there were specific concerns." [1]

Q3: "His creatinine rises to 210 despite antibiotics and albumin for 48 hours. What is your diagnosis and management?" [1]

"This meets the International Club of Ascites criteria for hepatorenal syndrome-AKI: cirrhosis with ascites, AKI unresponsive to 48 hours of diuretic withdrawal and albumin, no shock, no nephrotoxins, and no structural kidney disease. The mechanism is intense renal vasoconstriction driven by splanchnic vasodilation. I would start terlipressin 1 to 2 mg IV every 4 to 6 hours plus albumin, titrating to blood pressure and creatinine. The CONFIRM trial showed terlipressin achieves verified HRS reversal in 32% versus 17% with placebo, though I would monitor for respiratory failure — an 11% risk in the trial. If terlipressin were contraindicated, noradrenaline in ICU is the alternative. The definitive treatment is liver transplant." [1]

Q4: "Why does albumin reduce mortality in SBP?" [1]

"SBP triggers a systemic inflammatory response and worsens splanchnic vasodilation, which reduces effective circulating volume and drives renal vasoconstriction toward hepatorenal syndrome. Albumin expands the intravascular volume, improves renal perfusion and reduces this renal insult. The Sort trial showed albumin cut renal impairment from 33% to 10% and in-hospital mortality from 29% to 10%, using 1.5 g/kg on day 1 and 1 g/kg on day 3." [1]

Q5: "He has had recurrent encephalopathy. How do you manage it long-term?" [1]

"First, control precipitants — constipation, infection, bleeding, electrolyte disturbance, sedatives. He is on lactulose, which I would titrate to two to three soft stools daily. Because he has recurrent overt encephalopathy, I would add rifaximin 550 mg twice daily. The Bass trial showed rifaximin added to lactulose reduces breakthrough encephalopathy and HE-related hospitalisations. I would not restrict his protein intake — sarcopenia worsens outcomes. I would also reassess whether his carvedilol is causing hypotension that worsens renal perfusion, and consider a balanced approach to portal hypertension prophylaxis given his blood pressure of 96/60." [1]

Q6: "What is the role of a non-selective beta-blocker in a patient like this with decompensated cirrhosis?" [1]

"This is a nuanced area. In compensated cirrhosis with clinically significant portal hypertension, the PREDESCI trial showed NSBBs reduce the risk of first decompensation, mainly by preventing ascites — that is a paradigm shift. However, in decompensated cirrhosis with refractory ascites or hypotension, NSBBs may worsen outcomes by reducing cardiac output and renal perfusion. Mr Chen is hypotensive at 96/60 with AKI, so I would hold his carvedilol temporarily during this acute admission and reassess once his renal function and blood pressure have stabilised." [1]

Short Case Discussion

Scenario: "Examine this patient's abdominal system"

Candidate presentation (model): [1]

"I examined Mrs Patel's abdominal system. She is comfortable at rest. On general inspection she is thin, with several spider naevi over the anterior chest wall and upper back, and there is loss of axillary hair. On the hands there is palmar erythema sparing the central palm, and a Dupuytren contracture of the right ring finger. There is no asterixis. [1]

On examination of the abdomen, it is distended with shifting dullness in the flanks, consistent with ascites. There is a caput medusae with radiating veins from the umbilicus. The spleen is enlarged 4 cm below the left costal margin, and the liver edge is firm and irregular. There is no hepatic bruit. There is peripheral oedema to the mid-shin bilaterally. [1]

In summary, these findings are consistent with chronic liver disease complicated by portal hypertension, ascites and splenomegaly. The spider naevi and palmar erythema indicate chronic liver disease; the splenomegaly and caput medusae indicate portal hypertension. I would like to take a full alcohol and viral hepatitis history, perform a diagnostic ascitic tap, and organise bloods including liver function and coagulation, plus a FibroScan and screening endoscopy." [1]

Examiner: "What is the significance of the spider naevi?" [1]

"Spider naevi are vascular lesions with a central arteriole and radiating vessels that blanch with pressure. They are caused by oestrogen excess due to impaired hepatic metabolism of oestrogens. A few can be normal in pregnancy, but in the context of chronic liver disease they are a classic stigmata, distributed in the territory of the superior vena cava — face, neck, chest and upper arms." [1]

Examiner: "Why is the spleen enlarged?" [1]

"Splenomegaly in cirrhosis reflects portal hypertension. Increased portal venous pressure causes congestive splenomegaly over time. Splenomegaly is one of the most specific clinical indicators of portal hypertension — its presence, alongside ascites and caput medusae, confirms the portal-hypertensive phenotype." [1]

Examiner: "How would you grade encephalopathy if she were drowsy?" [1]

"I would use the West Haven classification. Grade 1 is mild confusion and sleep disturbance; grade 2 is lethargy with asterixis and disorientation; grade 3 is somnolent but arousable with gross disorientation; grade 4 is coma. I would test asterixis by asking her to hold the hands dorsiflexed with arms outstretched for 30 seconds and look for the irregular flapping motion. Asterixis typically appears at grade 2 to 3." [1]