GC026 Abdominal Distension: Ascites And Cirrhosis
Abdominal distension resulting from ascites, the pathological accumulation of fluid in the peritoneal cavity, most commonly caused by hepatic cirrhosis with portal hypertension and splanchnic vasodilation.
Cirrhosis, Ascites & Portal Hypertension — Comprehensive Exam-Ready Notes
This lecture (GC 026, Prof. Wai-Kay Seto) is the single most important source for understanding decompensated chronic liver disease from a medical perspective. It covers the pathogenesis, clinical features, investigation, and management of the major complications of cirrhosis — all of which are heavy exam topics at HKUMed.
Big Idea: Cirrhosis → Portal Hypertension → a cascade of life-threatening complications (varices, ascites, SBP, hepatic hydrothorax, portal vein thrombosis, hepatorenal syndrome). Treatment of the underlying cause can stabilise or even reverse early cirrhosis. When decompensation occurs, every complication must be anticipated, screened for, and managed proactively.
How it fits into the curriculum:
- Connects backward to GC 025 (Liver Failure / Hepatic Encephalopathy), GC 240 (MASLD / Alcoholic Liver Disease), Hepatitis B/C lectures.
- Connects forward to HCC (surgical lecture, Prof. TT Cheung), Liver Transplant, and GI Data Interpretation sessions.
- Overlaps with Upper GI Bleeding lecture (variceal bleeding), Splenomegaly lecture (GC 086), and Abdominal Examination CFB.
Covered in this lecture (per slide 2) [1]:
- Cirrhosis: aetiology and terminology
- Portal hypertension: pathogenesis → variceal disease
- Ascites: pathogenesis → ascites management, SBP, hepatic hydrothorax, portal vein thrombosis
- AKI / hepatorenal syndrome
Stated as covered elsewhere [1]: Liver failure, hepatic encephalopathy, HCC, liver transplant.
1. Cirrhosis: Definition, Aetiology & Terminology
Cirrhosis is the late stage of liver fibrosis with distortion of liver architecture and formation of regenerative nodules. [1]
Why does this matter from first principles?
- The liver normally has an elegant lobular architecture that allows blood to flow from the portal triad through sinusoids to the central vein. Hepatocytes sit along these sinusoids and perform metabolic, synthetic, and detoxification functions.
- Chronic injury (viral, toxic, metabolic, immune) triggers hepatic stellate cells to produce collagen → fibrosis. Over time, fibrosis distorts the normal vascular channels and creates regenerative nodules (hepatocytes trying to regenerate but enclosed by fibrotic bands).
- This structural distortion increases resistance to portal blood flow → portal hypertension. It also reduces functioning hepatocyte mass → liver insufficiency (↓ albumin, ↓ clotting factors, ↓ bilirubin clearance).
Compensated = Child's A. Decompensated = Child's B/C. [1]
| Feature | Compensated (Child A) | Decompensated (Child B/C) |
|---|---|---|
| Symptoms | Often asymptomatic | Ascites, variceal bleeding, HE, jaundice |
| Liver function | Relatively preserved | Impaired synthetic function |
| Prognosis | Better; treating aetiology can improve | Worse; treating aetiology has less impact (Child C) |
| Complications | Varices, PVT, HCC can still occur | All complications: varices, PVT, ascites, SBP, hydrothorax, HRS, HE, HCC, liver failure |
High Yield — Lecture Slide 34
The one-slide overview from the lecture [1] is a favourite exam framework. Compensated cirrhosis can still have variceal disease, PVT, and HCC. Decompensated adds ascites, SBP, hepatic hydrothorax, and hepatorenal syndrome. Additionally, infections and bleeding tendency cut across both.
In Hong Kong: HBV 64%, HCV 10%, heavy alcohol 5%, MAFLD 18%. [1]
| Aetiology | HK | Mainland China | Global |
|---|---|---|---|
| HBV | 64% | 68% | 42% |
| HCV | 10% | 7% | 21% |
| Heavy alcohol | 5% | 11% | Variable |
| MAFLD | 18% | 5% | Variable |
Why HBV dominates in HK: Vertical transmission (mother-to-child) was extremely common before universal neonatal vaccination (1988). Chronic HBV → ongoing immune-mediated hepatocyte destruction → fibrosis → cirrhosis.
Other causes to know (from senior notes and past papers [2][3]):
- Autoimmune hepatitis, PBC (Primary Biliary Cholangitis), PSC (Primary Sclerosing Cholangitis)
- Wilson's disease, haemochromatosis
- Drug-induced (e.g., methotrexate)
- Alpha-1 antitrypsin deficiency
Past Paper Trap
In the 2022 Minicase [3], students were asked to name three causes of cirrhosis apart from chronic viral hepatitis. Common mistakes: forgetting MASLD/NAFLD (now called MASLD), autoimmune hepatitis, or Wilson's disease. Don't just write "alcohol" — think systematically.
1.4 Prognostic Models for Cirrhosis
Five parameters: Bilirubin, Albumin, INR, Ascites, Encephalopathy. [1]
| Parameter | 1 point | 2 points | 3 points |
|---|---|---|---|
| Bilirubin (μmol/L) | < 34 | 34–51 | > 51 |
| Albumin (g/L) | > 35 | 28–35 | < 28 |
| INR | < 1.7 | 1.7–2.3 | > 2.3 |
| Ascites | None | Mild | Refractory |
| Encephalopathy | None | Grade 1–2 | Grade 3–4 |
| Class | Score | Interpretation |
|---|---|---|
| A | 5–6 | Compensated |
| B | 7–9 | Significant functional compromise |
| C | 10–15 | Decompensated |
Note: 1 mg/dL bilirubin = 17.1 μmol/L [1]
Why Child-Pugh? It grades severity and guides management decisions (e.g., operability for HCC, suitability for TIPSS). It's clinically intuitive — it captures synthetic function (albumin, INR), excretory function (bilirubin), and complications (ascites, encephalopathy).
- Uses Bilirubin, INR, Creatinine (3 parameters)
- Higher score = worse short-term survival
- Used for transplant prioritisation — not first-come-first-served [2][4]
- Also useful in prognosticating ACLF (acute-on-chronic liver failure) [5]
2021 SAQ (Q5c) [6]: "Name two prognostic models that can be used to grade the severity of cirrhosis." → Child-Pugh score and MELD score.
Treating the underlying disease can lead to some degree of fibrosis regression. [1]
| Aetiology | Reversibility | Treatment |
|---|---|---|
| HBV | Majority (but not all) | Long-term nucleoside analogue (entecavir/tenofovir) |
| HCV | Some (but not all) | Direct-acting antivirals (DAAs) |
| Alcohol | Uncertain | Alcohol abstinence → ↓ inflammation, ↓ fat, ? fibrosis |
Key point from lecture: Treating underlying disease in Child's A/B → ↓ complications/hospitalisation. In Child's C → less impact. [1]
Why? In early cirrhosis the fibrotic scaffolding can be partially remodelled by matrix metalloproteinases once the injurious stimulus is removed. In advanced cirrhosis (Child C), the degree of architectural distortion, vascular remodelling, and hepatocyte loss is so extensive that reversal is minimal → liver transplant becomes the definitive option.
2. Portal Hypertension
Portal hypertension = resistance to portal blood flow. [1]
Gold standard measurement:
HVPG (Hepatic Venous Pressure Gradient) = WHVP − FHVP [1]
- HVPG ≥ 10 mmHg = clinically significant portal hypertension (CSPH)
- HVPG ≥ 12 mmHg = risk of variceal bleeding
Normal HVPG is ≤ 5 mmHg [7]. The measurement involves catheterising a hepatic vein and comparing the wedged (occluded) pressure with the free (unoccluded) pressure. Not widely performed in practice.
Why does portal hypertension develop in cirrhosis?
- Structural changes: Fibrosis, regenerative nodules, and angiogenesis physically compress and distort sinusoids → ↑ intrahepatic vascular resistance.
- Dynamic changes: Imbalance of vasoactive substances within the liver — ↑ endothelin (vasoconstrictor), ↓ nitric oxide (vasodilator) in hepatic sinusoids → further vasoconstriction.
- Splanchnic vasodilation: Paradoxically, in the splanchnic (gut) circulation, there is ↑ NO production → vasodilation → ↑ portal blood inflow → worsens portal hypertension further.
Pre-hepatic, Hepatic (most common = cirrhosis), Post-hepatic. [1]
| Level | Causes | Key Points |
|---|---|---|
| Pre-hepatic (A) | Portal vein thrombosis | No liver disease; normal LFTs initially |
| Hepatic | Cirrhosis (C) — most common | See above |
| Schistosomiasis, congenital hepatic fibrosis, veno-occlusive disease (B, D) | Uncommon causes | |
| Post-hepatic (E) | Cardiac failure, Budd-Chiari syndrome (hepatic vein thrombosis) | Budd-Chiari: sudden ascites + tender hepatomegaly |
OSCE/Clinical Tip
"Think of portal hypertension first, not cirrhosis" [8] — When you see splenomegaly + ascites, the unifying pathophysiology is portal hypertension. Then determine the level (pre-hepatic, hepatic, post-hepatic).
3. Variceal Disease
When portal pressure rises (HVPG ≥ 10), blood seeks alternative routes back to the systemic circulation via portosystemic collaterals:
- Oesophageal varices (left gastric vein → oesophageal veins → azygos) — most clinically significant
- Gastric varices (short gastric veins / left gastric vein → fundus)
- Caput medusae (paraumbilical veins → superficial epigastric veins)
- Rectal varices (inferior mesenteric vein → rectal veins)
- Retroperitoneal collaterals
3.3 Management of Acute Oesophageal Variceal Bleeding
Pre-endoscopy [1]:
- As per upper GI bleeding protocol
- Correct coagulopathy / ↓ platelet
- Restrictive transfusion strategy: Transfuse only when Hb < 7 g/dL, aim 7–9 g/dL
- Antibiotic prophylaxis (cephalosporin)
Why restrictive transfusion? Over-transfusion in cirrhotics increases portal pressure (more intravascular volume → more splanchnic flow → ↑ portal pressure) and worsens bleeding. The landmark Villanueva 2013 NEJM trial showed improved survival with restrictive strategy [1].
Why antibiotics? Cirrhotic patients with GI bleeding have extremely high rates of bacterial infection (up to 50%) due to bacterial translocation from the gut. Prophylactic antibiotics reduce mortality [1].
Endoscopy [1]:
- Band ligation (preferred) or sclerotherapy injection
Vasoconstrictor [1]:
- IV terlipressin (synthetic vasopressin analogue; reduces mortality; side effects: hyponatraemia, ischaemic injury)
- IV somatostatin / octreotide (inhibits release of vasodilator hormones → splanchnic vasoconstriction)
Manage cirrhotic complications (e.g., hepatic encephalopathy) [1]
Pre-Endoscopy Drug Checklist — Exam Favourite
The 2022 Minicase Section 3 [3] asked: "Name three drugs you would give before upper endoscopy." Answer: IV terlipressin (vasoconstrictor), IV cephalosporin (antibiotic prophylaxis), IV PPI (often given empirically for UGIB before cause is known). Some mark schemes also accept IV erythromycin (prokinetic to clear stomach of blood for better endoscopic view).
- Complications are few: transient oesophageal pain, ulceration (rarely bleeds), sloughing of bands, mediastinitis/infection (rare)
- Reassessment scope a few weeks later → consider further banding if residual varices
- Synthetic analogue of vasopressin
- Reduces mortality
- Side effects: hyponatraemia, ischaemic injury (coronary, peripheral, mesenteric)
- Inhibits release of vasodilator hormones
- Causes splanchnic vasoconstriction → ↓ portal inflow
TIPSS (Transjugular Intrahepatic Portosystemic Shunt) [1]:
- Creates a shunt between hepatic vein and portal vein within the liver
- Other indications: refractory ascites, refractory hydrothorax
- Contraindications: right heart failure, pulmonary hypertension, hepatic encephalopathy (relative)
- Complications: acute (infection/bleeding/rupture), HE, stent occlusion/migration
- Limited availability in HK
Why does TIPSS work? It decompresses the portal system by creating a low-resistance channel directly from the portal vein to the hepatic vein (systemic circulation). This dramatically lowers portal pressure and stops variceal bleeding. The trade-off: more blood bypasses the liver → ↑ risk of hepatic encephalopathy (ammonia not being cleared).
Balloon tamponade — Sengstaken-Blakemore Tube [1]:
- Temporary measure only (bridge to definitive treatment)
- Requires intubation to prevent aspiration
- Complications: aspiration, rebleeding, oesophageal rupture
- "Try to avoid!" [1]
Other options (rarely used): Oesophageal stent (experimental), Shunt surgery (seldom needed) [1].
Treated with cyanoacrylate (tissue glue) injection. [1] Other management similar to oesophageal variceal bleeding. [1]
Why tissue glue not banding? Gastric varices (especially fundal) are larger, higher-flow, and in a location where band ligation is technically difficult and less effective. Cyanoacrylate polymerises on contact with blood, physically occluding the varix.
Clinical pearl from senior notes [9]: Isolated gastric varices without oesophageal varices → think splenic vein thrombosis (e.g., from pancreatitis) causing localised portal hypertension → "sinistral/left-sided portal hypertension."
Screening OGD [1]:
- Indicated for all patients with cirrhosis
- NOT needed if liver stiffness ≤ 15 kPa AND platelet count > 150 × 10⁹/L (indicates no CSPH)
- If high-risk lesions present (red-wale signs) → prophylactic banding
Prevention — Non-selective beta-blocker (NSBB) [1]:
- Oral carvedilol / propranolol / nadolol
- Side effects: hypotension, bradycardia
- Used for both primary and recurrence prevention
- Survival benefit
Why non-selective beta-blockers?
- β1 blockade → ↓ cardiac output → ↓ portal inflow
- β2 blockade → unopposed α1 activity in splanchnic vessels → splanchnic vasoconstriction → ↓ portal inflow
- Net effect: ↓ portal pressure
2024 MCQ Q11
"Indicated for beta-blocker use" → Answer: Oesophageal varices. [10] This tests whether you know that NSBBs are specifically used for variceal prophylaxis.
4. Ascites
The pathogenesis of ascites links portal hypertension, splanchnic vasodilation, and neurohormonal activation. [1]
The forward flow / peripheral arterial vasodilation hypothesis:
- Portal hypertension → ↑ NO and other vasodilators in splanchnic circulation → splanchnic vasodilation
- Splanchnic vasodilation → ↓ effective arterial blood volume (arterial underfilling)
- Baroreceptors detect underfilling → activate RAAS, AVP (arginine vasopressin), SNS (sympathetic nervous system)
- Result: Na+ and water retention → ↑ plasma volume
- Simultaneously: ↑ hydrostatic pressure in hepatic sinusoids (portal HTN) + ↓ oncotic pressure (hypoalbuminaemia from poor synthetic function) → fluid weeps into peritoneal cavity
- Lymphatic drainage capacity is overwhelmed → ascites accumulates
Ascites is the MOST common complication of cirrhosis. [11]
Generally indicated for all new-onset ascites. [1]
Tests to order on ascitic fluid:
| Test | Purpose | Key Thresholds |
|---|---|---|
| WCC + PMN (neutrophil) count | Screen for SBP | PMN ≥ 250/mm³ = SBP |
| Total protein | Distinguish aetiology | |
| Albumin → calculate SAAG | Determine portal HTN vs other | SAAG > 11 g/L = portal hypertension (cirrhosis, HF, PVT); SAAG < 11 g/L = other (TB peritonitis, nephrotic syndrome, malignancy, pancreatitis) |
| Gram stain + culture | Identify organism in SBP | Often culture-negative |
| Cytology | Screen for malignancy | Low sensitivity (~10%) |
| Others | Amylase (pancreatitis), Triglyceride (chylous), ADA / adenosine deaminase (TB) |
SAAG — The Critical Test
SAAG = Serum Albumin − Ascitic Fluid Albumin. A SAAG > 11 g/L (or 1.1 g/dL) means the ascites is driven by portal hypertension. This is because portal hypertension creates a hydrostatic gradient that "pushes" protein-poor fluid into the peritoneum, keeping the albumin concentration in ascites low relative to serum. In exudative causes (infection, malignancy), the peritoneal membrane is inflamed and protein-rich fluid leaks out, narrowing the gradient.
Where to tap: Always LLQ (left lower quadrant). The sigmoid colon is mobile on its mesentery and moves out of the way. The caecum is fixed → right-sided puncture risks caecal perforation [1][11].
Low salt diet (½–2 g/day) [1] Fluid restriction ( < 1 L/day) [1] — Senior notes clarify: fluid restriction only strictly necessary if dilutional hyponatraemia < 125 mmol/L [7] Diuretics: Potassium-sparing diuretics +/− Loop diuretics [1]
| Drug | Class | Notes |
|---|---|---|
| Spironolactone | Aldosterone antagonist (K⁺-sparing) | First-line; side effect: gynaecomastia [1] |
| Amiloride | K⁺-sparing | Alternative if gynaecomastia intolerable |
| Eplerenone | Selective aldosterone antagonist | Alternative |
| Furosemide | Loop diuretic | Added if spironolactone alone insufficient |
| Bumetanide | Loop diuretic | Alternative |
DO NOT give loop diuretics alone! [1]
Why not? Loop diuretics alone cause avid potassium loss and can worsen the hyperaldosteronism already present in cirrhotic ascites. This leads to hypokalaemia and metabolic alkalosis, which promotes renal ammonia production and can precipitate hepatic encephalopathy. Spironolactone counteracts aldosterone directly at the collecting duct, which is the primary mechanism driving sodium retention in cirrhotic ascites.
Typical dosing ratio: Spironolactone 100 mg : Furosemide 40 mg (maintain ~100:40 ratio) [7]. Start low (spironolactone 50 mg, furosemide 20 mg) and titrate up weekly.
Be aware of overdiuresis / acute kidney injury. [1] Aim weight loss ≤ 0.5 kg/day [7].
Monitoring: Daily weights, strict I/O chart, urine sodium (target > 30 mmol/day indicates adequate diuresis), regular RFT.
Therapeutic paracentesis [1]:
- For diuretic-refractory TENSE ascites
- 4–5 L (up to 8 L)
- IV albumin (colloid) replacement, especially if paracentesis > 5 L
- Complications (rare): AKI (inadequate albumin replacement), HE, perforation of caecum (R-sided puncture)
Why IV albumin? Large-volume paracentesis rapidly removes protein-rich fluid from the peritoneum. Without volume replacement, the already underfilled arterial circulation worsens → exaggerated neurohormonal activation → renal vasoconstriction → post-paracentesis circulatory dysfunction → AKI. Albumin is the preferred colloid because it stays intravascular and expands effective circulating volume.
Dose: 6–8 g albumin per litre removed if > 5 L drained [11].
Other options for refractory ascites [1]:
- TIPSS
- Experimental: long-term intermittent albumin administration, low-flow ascitic pump
5. Spontaneous Bacterial Peritonitis (SBP)
Bacterial translocation from the gut lumen across the intestinal wall into ascitic fluid. [1]
In cirrhosis:
- Gut mucosal oedema (portal HTN) → ↑ intestinal permeability
- Impaired gut motility → bacterial overgrowth
- Reduced opsonin activity in ascitic fluid (low protein ascites)
- Impaired reticuloendothelial function (liver not clearing bacteria)
- Result: bacteria (usually a single Gram-negative organism, e.g., E. coli, Klebsiella) seed the ascitic fluid
Typical: Fever, abdominal pain, new-onset ascites [1] Can have atypical symptoms or be asymptomatic [1] Need HIGH INDEX OF SUSPICION! [1]
Mortality: 90% (untreated); < 20% (early treatment) [1]
Why high index of suspicion? Cirrhotic patients may not mount a typical inflammatory response (impaired immune function, low complement, impaired opsonisation). They may present only with worsening encephalopathy, worsening renal function, or unexplained clinical deterioration without classic peritoneal signs. Any cirrhotic patient admitted to hospital with ascites should have a diagnostic paracentesis — this is the standard of care.
Ascitic PMN (neutrophil) count ≥ 250 cells/mm³ [1] Often culture-negative [1]
2025 MCQ Q30 — Directly Tests This
"Which test would suggest SBP?" → Answer: Polymorph (neutrophil) count ≥ 250/mm³. [12]
- Abnormal cells on cytology → malignancy, not SBP
- Polymicrobial culture → secondary bacterial peritonitis (bowel perforation)
- Milky ascitic fluid → chylous ascites
Important differentials: other causes of acute abdomen, bowel perforation. [1] Look out for: surgical signs, atypical presentation, polymicrobial culture growth, lack of treatment response. [1]
| Feature | SBP | Secondary Peritonitis |
|---|---|---|
| Organism | Usually monomicrobial | Polymicrobial |
| PMN | ≥ 250/mm³ | Often very high |
| Ascitic glucose | Normal | Low |
| Ascitic LDH | Normal | High |
| Clinical | Subtle signs | Peritoneal signs, may need surgical Rx |
| Response to antibiotics | Yes (PMN ↓ after 5 days) | Poor |
Why is this distinction critical? Missing secondary peritonitis (e.g., from a perforated viscus) and treating as SBP alone can be fatal — the patient needs surgical intervention, not just antibiotics.
Treatment [1]:
- Empirical antibiotics — do not wait!
- IV 3rd-generation cephalosporin (cefotaxime/ceftriaxone) for 5–7 days
- Consider carbapenem if severe disease
- IV albumin (prevent progression to AKI)
Reassessment diagnostic paracentesis after ~5 days [1]:
- If PMN ↓ → stop antibiotics
- If PMN not ↓ → consider alternative diagnosis (secondary peritonitis?)
Prophylaxis to prevent recurrence [1]:
- Fluoroquinolones (levofloxacin / ciprofloxacin)
Why IV albumin in SBP? SBP triggers a massive inflammatory response → further splanchnic vasodilation → ↓ effective circulating volume → renal hypoperfusion → AKI. Albumin acts as a plasma volume expander to prevent this circulatory collapse. Studies show albumin reduces renal impairment and mortality in SBP.
Small diaphragmatic defects allow peritoneal fluid to enter the pleural space. [1] Right-sided > Left-sided [1] (because the right hemidiaphragm has more congenital micro-defects and the liver sits directly underneath) Negative intrathoracic pressure draws fluid from peritoneum to pleura [1] Transudative pleural fluid biochemistry [1]
Must EXCLUDE OTHER CAUSES of pleural effusion [1]
Management [1]:
- Ascites management (salt restriction, diuretics) — if you control the ascites, you control the hydrothorax
- Thoracocentesis / pleurodesis / thoracoscopic repair
Key point: Hepatic hydrothorax can occur even when ascites is minimal or clinically undetectable, because the negative intrathoracic pressure sucks fluid from the peritoneum.
7. Portal Vein Thrombosis (PVT) Related to Cirrhosis
Majority: clinically silent [1] Minority: abdominal pain when new-onset [1] When chronic (cavernous transformation): ↑ variceal bleeding, ↑ ascites, ↓ treatment options if HCC develops [1]
Cavernous transformation = the body forms a network of small collateral veins around the thrombosed portal vein. This restores some portal flow but is disorganised and maintains portal hypertension.
Diagnosis: Ultrasound Doppler or CT with contrast [1]
Consider other causes of PVT [1]:
- Malignancy (pancreatic, cholangiocarcinoma)
- Venous thrombosis / hypercoagulability causes
- Septic (e.g., alcoholic pancreatitis)
Management [1]:
- Acute stage: Anticoagulation (Warfarin vs NOAC)
- Chronic (cavernous transformation): Anticoagulation is controversial
- Balance bleeding risk (↑ INR, ↓ platelet)
Why is PVT management tricky in cirrhotics? These patients already have coagulopathy (↑ INR from impaired synthetic function) and thrombocytopenia (hypersplenism). Adding anticoagulation increases bleeding risk, especially variceal bleeding. Yet untreated PVT worsens portal hypertension and can make the patient ineligible for liver transplant (if the portal vein is completely occluded, transplant is technically very challenging).
8. Acute Kidney Injury (AKI) in Liver Disease
AKI: ↑ ≥ 50% creatinine in 7 days OR ↑ ≥ 26.5 μmol/L creatinine in 48 hours [1]
Causes of AKI in liver disease [1] — Hepatorenal syndrome is NOT the most common cause!
- Hypovolaemia — diuretics, GI bleeding
- Sepsis
- Nephrotoxic drugs/herbs
- Parenchymal renal disease
- Obstructive uropathy
- Hepatorenal syndrome
Always exclude other causes of AKI! [1]
Common Exam Trap
Students jump to "hepatorenal syndrome" whenever they see AKI + cirrhosis. The lecture explicitly states HRS is not the most common cause. Pre-renal causes (overdiuresis, bleeding, sepsis) and nephrotoxins (NSAIDs, aminoglycosides, contrast) are far more common and must be excluded first.
Same underlying mechanism as ascites, taken to the extreme [1]:
- Splanchnic vasodilation → arterial underfilling → neurohormonal activation (RAAS, AVP, SNS)
- Intense renal vasoconstriction → ↓ renal perfusion → functional renal failure
- The kidneys are structurally normal — if you transplant them into a healthy recipient, they work fine
HRS-AKI (formerly Type 1 HRS): Rapid deterioration, often precipitated by SBP or GI bleeding. Very high mortality. HRS-CKD (formerly Type 2 HRS): Gradual decline, usually in the context of refractory ascites.
Simultaneous management [1]:
- Exclude other causes
- Discontinue potential culprit drugs (diuretics, NSBB, NSAIDs, etc.)
- Treat infection
- IV Albumin (volume expansion)
- IV Terlipressin (splanchnic vasoconstriction → redirects blood to kidneys)
Spot urine sodium < 10 mmol/L suggestive of HRS [1] Can recur after treatment discontinuation [1] RRT (renal replacement therapy) / LT (liver transplant) may be needed [1]
Why terlipressin? It is a V1 receptor agonist → causes splanchnic vasoconstriction → reverses the arterial underfilling → less compensatory renal vasoconstriction → improved renal perfusion.
Why spot urine sodium < 10? In HRS, the kidneys are avidly retaining sodium because they are being "told" (by RAAS and SNS) that the body is volume-depleted. Very low urine sodium with normal urine sediment (no casts, no proteinuria) supports a functional cause (HRS) rather than intrinsic renal disease (ATN, which would show urine Na > 20 and muddy brown casts).
9. Clinical Approach: History and Examination of the Cirrhotic Patient
- Aetiology: HBV/HCV status, alcohol history (amount, duration, pattern), obesity/metabolic syndrome (MASLD), autoimmune symptoms, drugs, family history (Wilson's, haemochromatosis, alpha-1 AT deficiency)
- Symptoms of CLD: Jaundice, pruritus, dark urine, bruising, ↓ libido (males), amenorrhoea (females) [11]
- Symptoms of complications: Abdominal distension (ascites), haematemesis/melaena (varices), fever/abdominal pain (SBP), confusion/sleep disturbance (HE), oedema
- Constitutional: Weight loss, fatigue, anorexia, muscle cramps [11]
- Red flags: Rapid deterioration, acute confusion, GI bleeding, oliguria
From CFB abdominal examination [13] and past papers [3]:
| Region | Signs |
|---|---|
| Hands | Clubbing, leuconychia (hypoalbuminaemia), palmar erythema, Dupuytren's contracture, asterixis (hepatic flap) |
| Arms | Bruising, muscle wasting, spider naevi (> 5 = significant, SVC territory) |
| Face/Trunk | Jaundice, scleral icterus, parotid swelling (alcohol), spider naevi |
| Chest (males) | Gynaecomastia, loss of body hair |
| Abdomen | Hepatomegaly (early) / shrunken liver (late), splenomegaly, ascites (shifting dullness, fluid thrill), caput medusae, abdominal striae, umbilical hernia |
| Lower limbs | Peripheral oedema |
From 2021 SAQ Q5(e) [6]: "Suggest additional investigations which will aid further management."
| Category | Tests | Why |
|---|---|---|
| Bloods | CBC (anaemia, thrombocytopenia), LRFT (bilirubin, albumin, ALT/AST, ALP/GGT), INR/PT | Assess severity, calculate Child-Pugh/MELD |
| Aetiology screen | HBsAg, anti-HCV, HBV DNA, HCV RNA, autoimmune markers (ANA, ASMA, anti-LKM), caeruloplasmin, ferritin/transferrin saturation, immunoglobulins | Treat the underlying cause |
| Imaging | USG abdomen (liver size/texture, spleen, portal vein, ascites, HCC screening) | First-line; cheap, non-invasive |
| AFP | Q6 monthly with USG for HCC surveillance | HCC screening in all cirrhotics |
| Diagnostic paracentesis | SAAG, PMN count, culture, cytology, protein, +/− ADA, amylase | Evaluate ascites aetiology, exclude SBP |
| OGD | Variceal screening | Unless LSM ≤ 15 kPa and plt > 150 |
| Liver stiffness (Fibroscan) | Quantify fibrosis non-invasively | Guides need for OGD screening |
Slide 34 [1] is the ultimate summary slide:
| Compensated (Child A) | Decompensated (Child B/C) | Both | |
|---|---|---|---|
| Complications | Variceal disease, PVT, HCC | Variceal disease, PVT, Ascites, SBP, Hepatic hydrothorax, HRS | HE, HCC, Liver failure, Infections, Bleeding tendency |
Management principle: Treat the underlying cause first. Then screen for and manage each complication systematically. Consider liver transplant referral for decompensated disease.
11. Integration with Related Material
"Known alcoholic cirrhosis admitted for increased confusion. Arterial ammonia 120. Which MOST LIKELY precipitates confusion?"
- A. Diagnostic paracentesis → Unlikely
- B. Duodenal ulcer bleeding → CORRECT (GI bleeding → ↑ protein load in gut → ↑ ammonia production → HE)
- C. Failure of alcohol abstinence → Less acute
- D. Recent HCC diagnosis → Less direct
2024 MCQ Q9 [10]: "Can occur after GI bleeding" → Answer: Hepatic Encephalopathy. 2024 MCQ Q10 [10]: "Can occur in non-cirrhotic chronic HBV" → Answer: HCC (HBV is directly carcinogenic even without cirrhosis).
- Splenomegaly in cirrhosis → congestive (portal hypertension) → leads to hypersplenism (↑ destruction of all cell lines → pancytopenia)
- 2022 Minicase Section 3 [3]: "Most likely cause for pancytopenia?" → Answer: Hypersplenism (secondary to portal hypertension/cirrhosis).
- MASLD is the rising cause of cirrhosis globally and in HK (18%)
- Alcohol: ↓ inflammation and ↓ fat with abstinence, but fibrosis reversal uncertain [1]
Based on lecture content and past paper patterns:
-
SAQ: "A 60-year-old man with HBV cirrhosis presents with new abdominal distension. Shifting dullness is positive. (a) What does the examination finding suggest? (b) Name the investigations you would perform on the ascitic fluid and their significance."
- Markscheme: Ascites. Investigations: WCC + PMN count (SBP if ≥ 250), total protein, albumin for SAAG ( > 11 = portal HTN), Gram stain + culture, cytology, +/− ADA/amylase/triglyceride.
-
SAQ: "Explain the pathogenesis of ascites in liver cirrhosis."
- Markscheme: Portal HTN → splanchnic vasodilation → ↓ effective arterial volume → activation of RAAS/AVP/SNS → Na and H₂O retention. Portal HTN + hypoalbuminaemia → ↑ transudation into peritoneal cavity. Lymphatic drainage overwhelmed.
-
MCQ: "What is the diagnostic criterion for SBP?" → Ascitic PMN ≥ 250 cells/mm³
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MCQ/SAQ: "A cirrhotic patient on diuretics develops AKI. What is your approach?"
- Exclude hypovolaemia (overdiuresis, GI bleed), sepsis, nephrotoxins, obstructive uropathy FIRST. Stop diuretics. If HRS suspected: IV albumin + IV terlipressin.
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Minicase: "Name 3 drugs to give before OGD for variceal bleeding."
- IV terlipressin, IV cephalosporin (antibiotic prophylaxis), IV PPI.
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SAQ: "What are the complications of TIPSS?"
- Hepatic encephalopathy, stent occlusion/migration, acute complications (infection, bleeding, rupture).
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MCQ: "SAAG > 11 g/L suggests what?" → Portal hypertension (cirrhosis, heart failure, PVT)
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SAQ: "Name 2 prognostic scoring systems for cirrhosis and their components."
- Child-Pugh (bilirubin, albumin, INR, ascites, encephalopathy); MELD (bilirubin, INR, creatinine).
High Yield Summary
• Cirrhosis = end-stage fibrosis with regenerative nodules and distorted architecture. In HK, HBV is the #1 cause (64%).
• Child-Pugh (5 parameters: bilirubin, albumin, INR, ascites, encephalopathy) and MELD (3 parameters: bilirubin, INR, creatinine) grade severity.
• Portal hypertension: HVPG ≥ 10 = clinically significant; ≥ 12 = risk of variceal bleeding. Classification: pre-hepatic (PVT), hepatic (cirrhosis), post-hepatic (HF, Budd-Chiari).
• Variceal bleeding management: Restrictive transfusion (Hb target 7–9), IV terlipressin, IV cephalosporin prophylaxis, endoscopic band ligation. TIPSS / balloon tamponade for refractory cases. Prevention: NSBB (carvedilol/propranolol) + screening OGD.
• Ascites: SAAG > 11 g/L = portal hypertension. Management: salt restriction, spironolactone +/− furosemide (never loop diuretics alone!), therapeutic paracentesis with IV albumin for refractory cases.
• SBP: PMN ≥ 250/mm³. High index of suspicion (can be asymptomatic). Treat immediately with IV cephalosporin + IV albumin. Prophylaxis: fluoroquinolones.
• Hepatic hydrothorax: R > L, transudative. Manage ascites first.
• PVT: > 10% of cirrhotics. Anticoagulation in acute stage; controversial in chronic.
• AKI in cirrhosis: HRS is NOT the most common cause — exclude hypovolaemia, sepsis, nephrotoxins first. HRS management: IV terlipressin + IV albumin. Spot urine Na < 10 suggestive of HRS.
• Always treat the underlying cause — this can reverse fibrosis in early disease (especially HBV, HCV).
Active Recall - Lecture Notes
[1] Lecture slides: GC 026. Abdominal distension_ascites and cirrhosis.pdf (all pages) [2] Senior notes: Block A - Gastrointestinal Data Interpretation.pdf (p5) [3] Past papers: 2022 Fourth Summative Minicase.pdf (p2, p5) [4] Senior notes: Maksim Medicine Notes.pdf (p137) [5] Senior notes: Block A - A jaundiced and incoherent patient_ liver failure.pdf (p12) [6] Past papers: 2021 Fourth Summative SAQ.pdf (p6) [7] Senior notes: Ryan Ho GI.pdf (p316–317, p323) [8] Medicine lecture slides: abdominal exam (MBBS IV) (student version).pdf (p34) [9] Senior notes: Block A - Coffee ground vomitus tarry stool upper GI bleeding.pdf (p23) [10] Past papers: 2024 Fourth Summative MCQ.pdf (p39) [11] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p787, p793) [12] Past papers: 2025 Fourth Summative MCQ.pdf (p13) [13] Lecture slides: CFB (MED07) Examination of the Abdomen.pdf (p33) [14] Past papers: 2022 Fourth Summative MCQ.pdf (p14) [15] Lecture slides: GC 086. Splenomegaly.pdf (p18) [16] Lecture slides: GC 240. MASLD and Alcoholic Liver Disease.pdf (p2)
GC025 A Jaundiced And Incoherent Patient Liver Failure
Liver failure is a severe deterioration of hepatic function resulting in jaundice, hepatic encephalopathy (manifesting as confusion and incoherence), coagulopathy, and potential multiorgan dysfunction due to the liver's inability to perform its synthetic, metabolic, and detoxification functions.
GC027 Abnormal Bleeding After Tooth Extraction
Prolonged or excessive hemorrhage following tooth extraction, often indicating a local complication such as disrupted clot (dry socket) or an underlying coagulopathy.