Portal Hypertension — Written Clinical Reasoning

SAQ 1 — Acute Variceal Bleeding with Multi-Complication Decompensation (20 marks, 30 minutes)

Prompt: Outline your integrated management plan for this patient, addressing the acute bleeding episode, the hepatorenal syndrome, the spontaneous bacterial peritonitis, and the hepatic encephalopathy. Justify each decision with reference to evidence and guideline recommendations. [1]

Model Answer

Problem list (4 marks): [1]

1. Acute variceal bleeding — controlled endoscopically, but high-risk bleeder (Child-Pugh B with active bleeding at endoscopy) — missed early TIPS window
2. Spontaneous bacterial peritonitis (PMN 320, above threshold of 250) — likely precipitant of further decompensation
3. Hepatorenal syndrome-AKI — creatinine doubled, on a background of cirrhosis with ascites; requires diagnostic workup and treatment
4. Hepatic encephalopathy — grade 2 to 3, likely precipitated by SBP, GI bleeding (protein load), and infection
5. Tense ascites — may require paracentesis
6. Alcohol-related cirrhosis — need withdrawal prophylaxis, thiamine, nutritional support [1]

Management of SBP (4 marks): [1]

The ascitic PMN of 320 cells/microL confirms SBP. I would: [1]

• Continue ceftriaxone 1 g IV daily (already commenced appropriately) for 5 to 7 days. Cefotaxime 2 g IV every 12 hours is an equivalent alternative.
• Give intravenous albumin: 1.5 g/kg on day 1 and 1 g/kg on day 3. The Sort trial (PMID 10432325) demonstrated that albumin reduces renal impairment from 33 percent to 10 percent and in-hospital mortality from 29 percent to 10 percent in SBP. This patient already has rising creatinine — albumin is essential.
• Repeat paracentesis at 48 hours: the PMN count should fall by at least 25 percent. If not, I would broaden antibiotic cover and search for secondary peritonitis (perform CT to exclude perforation).
• Plan secondary prophylaxis with norfloxacin 400 mg orally daily once oral intake resumes, indefinitely. [1]

Management of HRS-AKI (5 marks): [1]

The creatinine rise from 90 to 160 micromol/L over 48 hours meets ICA-AKI criteria (increase of at least 26.5 micromol/L within 48 hours). The diagnostic workup requires: [1]

• Confirm cirrhosis with ascites (present)
• Confirm AKI by ICA criteria (present)
• Stop diuretics and give albumin 1 g/kg/day for 2 consecutive days — if no response, proceed to HRS treatment
• Exclude shock (his current blood pressure is stable at 104/68 without vasopressors — acceptable)
• Exclude nephrotoxic drugs (review for NSAIDs, aminoglycosides, contrast)
• Exclude structural kidney disease (check urinalysis for proteinuria and haematuria, renal ultrasound) [1]

He is already on terlipressin — this is appropriate first-line therapy for HRS-AKI. I would: [1]

• Continue terlipressin 1 to 2 mg IV every 4 to 6 hours with albumin 20 to 40 g/day for up to 14 days.
• Monitor daily: oxygen saturation, fluid balance, blood pressure, creatinine. The CONFIRM trial (PMID 33657294) showed terlipressin reverses HRS in 32 percent vs 17 percent with placebo, but carries a significant risk of respiratory failure (11 percent vs 2 percent). I would contraindicate or reduce terlipressin if he develops hypoxia, pulmonary oedema, or volume overload.
• Target: creatinine below 133 micromol/L or a stable downward trend.
• If no response after 14 days or if he develops contra-indications to terlipressin, I would use noradrenaline in ICU as an alternative vasoconstrictor.
• Refer for liver transplant assessment — HRS-AKI is a decompensation event signalling the need for transplant evaluation. Calculate his MELD-Na (currently 19, likely rising) — this drives transplant priority. [1]

Management of hepatic encephalopathy (4 marks): [1]

He has grade 2 to 3 HE (drowsiness, confusion). I would: [1]

• Identify and treat precipitants: SBP (being treated), GI bleeding (being treated), constipation, hypokalaemia, infection at other sites.
• Continue and titrate lactulose: target 2 to 3 soft bowel motions per day. If he cannot take oral lactulose due to drowsiness, I would give 300 mL lactulose as a retention enema via rectal tube.
• Add rifaximin 550 mg orally BID: for patients with recurrent or severe HE, rifaximin plus lactulose reduces breakthrough HE (22 percent vs 46 percent with placebo, Bass PMID 20335583) and HE-related hospitalisation. Once his oral intake resumes, this should be added.
• Avoid CNS depressants: no benzodiazepines. If agitation requires management, use haloperidol in small doses with monitoring.
• Correct electrolytes: check and correct hypokalaemia, hyponatraemia, magnesium. [1]

Management of the bleeding episode and missed early TIPS (3 marks): [1]

This patient was a high-risk bleeder — Child-Pugh B with active bleeding observed at endoscopy. Per the Garcia-Pagan trial (PMID 20573925), he should have received pre-emptive TIPS within 72 hours of admission, which reduces treatment failure from 50 percent to 3 percent and improves one-year survival from 61 percent to 86 percent. Since this window may have been missed, I would: [1]

• Maintain the vasoactive agent (terlipressin or octreotide) for 2 to 5 days to reduce rebleeding risk.
• Continue prophylactic ceftriaxone for 7 days.
• Assess for ongoing bleeding or early rebleeding — if this occurs, proceed to rescue TIPS.
• Cease carvedilol temporarily during the acute bleeding episode and while hypotensive — NSBB are contraindicated in acute bleeding with haemodynamic instability. Once stable, reassess for secondary prophylaxis with NSBB plus serial EVL.
• Plan for serial EVL sessions every 2 to 4 weeks for variceal eradication once recovered. [1]

Communication and overall plan: [1]

I would discuss with the patient and family that his cirrhosis is now decompensated with multiple complications (bleeding, SBP, HRS, HE), signalling advanced disease. His prognosis without transplant is poor (one-year mortality above 30 percent for patients with multiple decompensation events). I would initiate liver transplant referral based on his MELD-Na and complication profile, assess alcohol abstinence and psychosocial support, and involve the hepatology and transplant teams early. I would also address advance care planning if transplant is not an option. [1]

SAQ 2 — Refractory Ascites Management Decision-Making (10 marks, 15 minutes)

Prompt: Six weeks later, after resolution of his acute episode, the same patient is readmitted with refractory ascites requiring large-volume paracentesis of 8 litres every 10 days. He is on maximal spironolactone (400 mg) and frusemide (160 mg). His MELD-Na is 17. He has no current hepatic encephalopathy. Discuss the management options for his refractory ascites, including the risks and benefits of each. [1]

Model Answer

Definition confirmation (1 mark): [1]

Refractory ascites is defined as ascites that cannot be mobilised or recurs rapidly despite maximal diuretic therapy and sodium restriction, or ascites that is intractable due to diuretic-induced complications (encephalopathy, renal impairment, hyponatraemia below 125). This patient meets the diuretic-refractory criterion. [1]

Management options (9 marks): [1]

1. Serial large-volume paracentesis with albumin replacement (3 marks): [1]

   This is the practical mainstay of management. LVP provides immediate symptomatic relief. For each paracentesis removing more than 5 litres, he must receive 8 g of intravenous albumin per litre removed (so for 8 litres, give 64 g albumin). Without albumin, post-paracentesis circulatory dysfunction (PPCD) occurs — causing splanchnic vasodilatation, renal vasoconstriction, and accelerated mortality. I would schedule paracentesis every 10 to 14 days as needed, with strict sodium restriction (88 mmol/day) between procedures. The main limitations are patient inconvenience, risk of infection (low with sterile technique), and that it does not treat the underlying portal hypertension. [1]

2. Transjugular intrahepatic portosystemic shunt (TIPS) (3 marks): [1]

   TIPS reduces portal pressure and improves renal sodium excretion. It is particularly effective for refractory ascites in patients with MELD below 18 (he qualifies at MELD-Na 17). Benefits include reduced ascites recurrence and improved nutritional status. However, TIPS carries significant risks:

   • New or worsened hepatic encephalopathy (20 to 40 percent) — he has no current HE, which is favourable, but prior HE (during his acute admission) increases risk.
   • Liver decompensation — risk is higher with elevated MELD; MELD-Na 17 is in the acceptable range but requires careful consideration.
   • Cardiac decompensation — screen with echocardiogram before TIPS to exclude heart failure or significant pulmonary hypertension (mPAP above 45 is a contraindication). [1]

   I would discuss TIPS with him as a reasonable option given his MELD-Na 17 and no current HE, but would counsel that it is not a cure and that transplant remains the definitive treatment. [1]

3. Liver transplant assessment (2 marks): [1]

   Refractory ascites is a decompensation event that is itself an indication for transplant assessment. His MELD-Na of 17 places him in a moderate priority range. I would urgently refer for transplant evaluation, assess alcohol abstinence history (typically 6 months required for alcohol-related cirrhosis in most centres), screen for comorbidities (cardiac, pulmonary, infection), and involve the alcohol liaison team. Transplant is the only treatment that improves survival in refractory ascites. [1]

4. Other considerations (1 mark): [1]

   • Alfapump (automated low-flow ascites pump): reinfuses ascites into the bladder via an implanted pump; considered in patients unsuitable for TIPS or transplant. Not widely available in ANZ.
   • Nutritional support: ensure adequate protein intake (1.2 to 1.5 g/kg/day) — sarcopenia worsens outcomes in refractory ascites and paracentesis accelerates protein loss.
   • Cease NSAIDs, ACE inhibitors, ARBs — they worsen renal perfusion.
   • Assess NSBB: he is on carvedilol. In refractory ascites with systolic BP below 90, NSBB should be dose-reduced or ceased (the window hypothesis). If his blood pressure is stable above 90, continue — NSBB may still be beneficial and reduce bleeding risk. [1]