Chronic Liver Disease and Cirrhosis — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr David Chen, 58 years old. [1]

Presenting complaint: Two weeks of increasing abdominal distension and leg swelling, and 2 days of progressive drowsiness. His wife reports he has been "not himself," sleeping during the day and confused at night. [1]

Past history:

• Alcohol-related cirrhosis, diagnosed 18 months ago after an upper gastrointestinal bleed from oesophageal varices (treated with endoscopic band ligation)
• Medium oesophageal varices — last OGD 6 months ago
• Hypertension
• No diabetes, no ischaemic heart disease
• 25-year history of heavy alcohol use (60 to 80 g/day), reduced to 20 g/day over the last year but not abstinent [1]

Current medications:

• Carvedilol 6.25 mg daily
• Spironolactone 100 mg daily
• Frusemide 40 mg daily
• Thiamine 100 mg daily [1]

Examination findings (trainee elicits):

• Drowsy, rousable to voice (GCS 13), asterixis present
• Temperature 37.9, blood pressure 96/60, pulse 92, respiratory rate 18, SpO2 96% on room air
• Cachectic; multiple spider naevi on chest; palmar erythema; gynaecomastia
• Abdomen: tense distension with shifting dullness and diffuse tenderness; spleen palpable 4 cm below costal margin; caput medusae
• Bilateral basal crackles; pitting oedema to the sacrum [1]

Investigations:

• Na 128, K 4.8, creatinine 145 (baseline 95), urea 14
• Bilirubin 68, ALT 45, ALP 180, albumin 24, INR 1.9
• Platelets 70, WCC 14.5, Hb 105
• Ascitic fluid: PMN 420 cells/microlitre, albumin 10 g/L, culture pending
• Child-Pugh 11 (C), MELD-Na 26 [1]

Candidate's structured presentation (model)

Opening statement: [1]

"Mr Chen is a 58-year-old retired carpenter who presents with 2 weeks of increasing abdominal distension and leg swelling, and 2 days of progressive drowsiness. He has a background of alcohol-related cirrhosis, diagnosed 18 months ago after a variceal bleed, and a 25-year history of heavy alcohol use. [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, sepsis source
3. Acute kidney injury — creatinine 145, rising, probable hepatorenal syndrome precipitated by SBP
4. Grade 3 hepatic encephalopathy — precipitated by infection
5. Tense ascites — symptomatic
6. Portal hypertension with varices on carvedilol — secondary prophylaxis
7. Alcohol dependence — needs addiction medicine
8. Hyponatraemia (Na 128) and coagulopathy (INR 1.9)" [1]

Investigation summary: [1]

"His ascitic tap confirms SBP — PMN count of 420, well above the 250 threshold. His SAAG is 15 g/L (serum albumin 24 minus ascitic albumin 10), confirming portal-hypertensive ascites. His creatinine of 145 against a baseline of 95 represents acute kidney injury. His thrombocytopenia and splenomegaly confirm portal hypertension and hypersplenism. His Child-Pugh is 11 (class C) and his MELD-Na is 26, placing him in a high-priority transplant category." [1]

Management plan: [1]

1. Resuscitate — HDU admission for grade 3 encephalopathy and sepsis; airway observation; semi-recumbent nursing.
2. Treat SBP — cefotaxime 2 g IV every 8 hours plus albumin 1.5 g/kg day 1 and 1 g/kg day 3.
3. Renal protection — cease spironolactone and frusemide; 48-hour albumin challenge; if no response, diagnose HRS-AKI and start terlipressin plus albumin.
4. Encephalopathy — lactulose titrated to two to three soft stools; add rifaximin 550 mg BID; treat the precipitant (SBP).
5. Ascites — once stable, large-volume paracentesis with albumin replacement.
6. Nutrition — high-protein, high-energy diet; thiamine; do not restrict protein.
7. Transplant referral — MELD-Na 26 is a strong indication; urgent assessment once sepsis controlled and abstinence established.
8. Withhold carvedilol temporarily given hypotension and AKI; reassess once stabilised. [1]

Examiner discussion questions

Q: "He had a variceal bleed 18 months ago. Why was he given carvedilol rather than propranolol?" [1]

"Both are non-selective beta-blockers used for secondary prophylaxis after a variceal bleed, combined with serial endoscopic band ligation. Carvedilol additionally blocks alpha-1 receptors, which lowers portal pressure more effectively than propranolol, and many units now prefer it for this reason. For secondary prophylaxis the combination of NSBB plus EVL is standard — EVL alone has a higher rebleed rate." [1]

Q: "Would you give him fresh frozen plasma before paracentesis given his INR is 1.9?" [1]

"No. The rebalance theory of haemostasis in cirrhosis recognises that cirrhosis reduces 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 paracentesis does not prevent bleeding and carries volume and transfusion risks. Paracentesis is a low-bleeding-risk procedure and I would proceed without FFP." [1]

Q: "His creatinine does not improve after 48 hours of albumin and diuretic withdrawal. What next?" [1]

"He meets the criteria for hepatorenal syndrome-AKI. 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 HRS reversal in 32% versus 17% with placebo, with a respiratory failure signal of 11% — so I would monitor oxygen saturation closely. If terlipressin were contraindicated or unavailable, noradrenaline in ICU is the alternative. The definitive treatment is liver transplant." [1]

Q: "What is his prognosis?" [1]

"His prognosis is guarded without transplant. Decompensated cirrhosis with HRS carries roughly 50% mortality at 1 month. With a MELD-Na of 26, his 90-day mortality is high. Liver transplant offers the best chance of survival, but he needs to establish alcohol abstinence and survive the acute septic episode first. I would have an honest prognostic discussion with him and his family once he is lucid, framing transplant as the path forward." [1]

DCE Short Case — Abdominal Examination

Instruction

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

Key signs the patient demonstrates

• General inspection: cachexia, spider naevi on chest, loss of axillary hair, parotid enlargement
• Hands: palmar erythema, Dupuytren contracture, clubbing, leuconychia; asterixis on wrist dorsiflexion
• Face: jaundiced sclera, fetor hepaticus
• Chest: gynaecomastia, spider naevi in superior vena cava distribution
• Abdomen: distension with shifting dullness (ascites), caput medusae, splenomegaly (4 cm), firm irregular liver edge
• Legs: peripheral oedema [1]

Systematic routine

1. End of bed — cachexia, spider naevi, gynaecomastia, loss of body hair.
2. Hands — palmar erythema, Dupuytren contracture, clubbing, leuconychia; test asterixis.
3. Face — jaundice, fetor hepaticus, Kayser-Fleischer rings (Wilson), xanthelasma (PBC).
4. Chest — spider naevi, gynaecomastia.
5. Abdomen — inspect — distension, caput medusae, surgical scars.
6. Palpate — spleen (portal hypertension), liver edge (firm, irregular in cirrhosis), ballotable organs.
7. Percuss — liver span, shifting dullness for ascites.
8. Auscultate — hepatic bruit (HCC), friction rub.
9. Complete — peripheral oedema, testicular atrophy. [1]

Presentation template

"I examined Mrs Patel's abdominal system. She is comfortable at rest but appears cachectic. There are 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, a Dupuytren contracture of the right ring finger, and leuconychia. Asterixis is present on wrist dorsiflexion. [1]

The abdomen is distended with shifting dullness in the flanks, consistent with ascites. A caput medusae is present 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]

These findings are consistent with chronic liver disease complicated by portal hypertension and hepatic failure. The spider naevi, palmar erythema and gynaecomastia indicate chronic liver disease; the splenomegaly and caput medusae indicate portal hypertension; the asterixis indicates hepatic encephalopathy. I would like to take a full alcohol and viral hepatitis history, perform a diagnostic ascitic tap, and organise bloods including liver function, coagulation and a full blood count." [1]

Discussion template

1. Summarise findings → "consistent with decompensated chronic liver disease with portal hypertension, ascites and hepatic encephalopathy."
2. Differential — the cause of cirrhosis: alcohol, viral hepatitis, MASLD, autoimmune, cholestatic (PBC, PSC), metabolic (haemochromatosis, Wilson, alpha-1-antitrypsin). Discriminate by serology and history.
3. Investigations — aetiology screen (viral, metabolic, autoimmune serology), FibroScan for fibrosis staging, CT/MRI for nodularity and HCC screening, screening endoscopy for varices, Child-Pugh and MELD-Na scoring.
4. Management — treat the cause, prevent and manage complications (portal hypertension, ascites, encephalopathy, HRS, HCC surveillance), transplant assessment. [1]