cirrhosis

This note covers compensated cirrhosis — the stage before ascites, variceal bleeding, encephalopathy, or jaundice. The key modern concept is compensated advanced chronic liver disease (cACLD), diagnosed non-invasively with liver stiffness measurement. Clinically significant portal hypertension (CSPH) is the prognostic watershed: HVPG ≥10 mmHg, or LSM ≥25 kPa as a non-invasive rule-in. All cirrhotic patients need HCC surveillance (q6-month US ± AFP) and variceal screening. For decompensated disease, see decompensated cirrhosis.

new cirrhosis diagnosis workup

aetiology — core: HBsAg, anti-HBc, anti-HCV, ANA, ASMA, IgG, AMA, ferritin, Tsat
if Tsat >45% → HFE genotyping
if age <40 or unexplained → ceruloplasmin, alpha-1 antitrypsin level
LSM (FibroScan) if not done — confirm cACLD (≥15 kPa)
portal hypertension assessment: LSM + platelet count → Baveno VII criteria
if portal hypertension present or indeterminate → screening OGD
HCC surveillance: abdominal US ± AFP q6 months
if clinically significant portal hypertension → NSBB: carvedilol 6.25–12.5 mg daily
vaccinations: HAV, HBV (check titres), pneumococcal, influenza
stop hepatotoxins: NSAIDs, limit acetaminophen ≤2 g/day, review supplements
nutrition: protein 1.2–1.5 g/kg/day, late evening snack; DEXA if cholestatic

aetiology workup

Order guided by clinical context, not as a reflex panel. The first three causes account for >80% of cases in Canada.

cause	key tests
alcohol	history (AUDIT-C), AST:ALT ≥2:1, GGT
MASLD / MetALD	metabolic syndrome, US steatosis, exclude other causes
HBV / HCV	HBsAg, anti-HBc, anti-HCV → HCV RNA if positive
autoimmune hepatitis	ANA, ASMA, IgG
PBC	AMA (or anti-sp100/gp210 if AMA negative)
PSC	MRCP (AMA negative, cholestatic pattern, often with IBD)
hereditary hemochromatosis	transferrin saturation, ferritin → HFE if Tsat >45%
Wilson’s disease	ceruloplasmin (age <40), 24-hour urine copper
alpha-1 antitrypsin deficiency	alpha-1 antitrypsin level

more than one cause

Dual aetiology is common — alcohol + MASLD, alcohol + HCV, MASLD + autoimmune overlap. Do not stop at the first positive result.

diagnosis

non-invasive assessment (Baveno VII criteria)

Liver biopsy is no longer the default. Liver stiffness measurement (LSM) by transient elastography (FibroScan) is the primary tool.

LSM (kPa)	interpretation
<10	cACLD excluded (rule-out)
10–15	grey zone — correlate with clinical context, consider repeat or second modality
≥15	cACLD confirmed (rule-in)

FIB-4 is the recommended first-line screening test in primary care and general medicine:

FIB-4	interpretation
<1.3	advanced fibrosis unlikely — repeat in 1–3 years if risk factor persists
1.3–2.67	indeterminate → proceed to LSM
>2.67	advanced fibrosis likely → proceed to LSM

LSM pitfalls

Falsely elevated by: acute hepatitis/flare (ALT >5× ULN), obstructive cholestasis, congestion (right heart failure), recent food intake (fast 2 hours), heavy alcohol intake in the preceding days. Always check ALT alongside LSM.

when to biopsy

Discordant non-invasive results
Suspected overlap syndrome (e.g. AIH + PBC)
Unexplained cirrhosis after full workup
Staging needed before specific therapy (e.g. autoimmune hepatitis)

clinically significant portal hypertension

CSPH is the threshold at which complications become likely. Defined as hepatic venous pressure gradient (HVPG) ≥10 mmHg, but measured non-invasively in most patients.

non-invasive rule-in (Baveno VII criteria)

LSM ≥25 kPa → CSPH can be ruled in without HVPG measurement
LSM 20–25 kPa → CSPH likely if platelet count <150 × 10⁹/L
LSM ≥20 kPa + platelets <150 → sufficient to rule in CSPH
LSM <20 kPa + platelets ≥150 → CSPH unlikely; can avoid screening endoscopy (Baveno VII expanded criteria)

variceal screening

No CSPH by Baveno VII criteria → defer endoscopy; repeat LSM + platelets annually
CSPH present or indeterminate → screening OGD
Compensated patients with no varices and no CSPH by Baveno criteria can safely skip endoscopy — this is the major practice change from Baveno VII

HCC surveillance

Every patient with cirrhosis, regardless of aetiology or treatment status.

Modality: abdominal US ± AFP q6 months
Certain HBV populations qualify for surveillance even without cirrhosis — see viral hepatitis
Continue surveillance even after HCV cure (SVR12) if cirrhosis was present before treatment
CT or MRI for patients with inadequate US windows (obesity, nodular liver)

do not use AFP alone

AFP has poor sensitivity (~60%) as a standalone screening test. US is the backbone; AFP adds incremental value. A normal AFP does not exclude HCC.

management of compensated cirrhosis

The goal is to prevent decompensation. Once a patient decompensates, median survival drops from >12 years to ~2 years (D’Amico, J Hepatol. 2006).

Treat the underlying cause — this is the single most effective intervention. HCV cure, HBV suppression, alcohol abstinence, and weight loss (MASLD) can all reverse early cirrhosis and reduce CSPH.
Non-selective beta-blockers — carvedilol 6.25–12.5 mg daily (or propranolol/nadolol) for patients with CSPH to prevent first variceal bleeding and first decompensation. Carvedilol is preferred over propranolol in compensated disease based on the PREDESCI trial extension data showing reduced decompensation.
Avoid hepatotoxins — no NSAIDs, minimise acetaminophen to ≤2 g/day, avoid unnecessary antibiotics, review all supplements
Vaccinations — HAV, HBV (if non-immune), pneumococcal, influenza, COVID-19. Immune response may be blunted; check titres.
Bone health — osteoporosis screening (DEXA), especially in cholestatic liver disease (PBC, PSC)
Nutrition — sarcopenia is universal and undertreated. Protein intake 1.2–1.5 g/kg/day; late evening snack to reduce overnight catabolism.

common traps

Assuming normal ALT means no cirrhosis — transaminases can normalise as fibrosis progresses and hepatocyte mass declines. A “burnt-out” liver may have normal ALT with advanced disease.
Using LSM during a flare — an ALT >5× ULN can double the stiffness reading. Repeat after the flare settles.
Skipping HCC surveillance after HCV cure — SVR12 eliminates the virus, not the fibrosis-driven cancer risk. Surveillance continues indefinitely if cirrhosis was present.
Restricting protein for encephalopathy prevention — worsens sarcopenia without evidence of benefit. Protein restriction is never appropriate in compensated cirrhosis.
Starting NSAIDs — removes the prostaglandin-dependent renal perfusion that cirrhotic kidneys rely on. Precipitates AKI and hepatorenal syndrome.
Forgetting the second aetiology — alcohol + MASLD, alcohol + HCV, and MASLD + AIH overlap are common and change management.