Background Information

Definition

Cirrhosis is defined as the end stage of chronic liver disease, characterised by diffuse hepatic fibrosis and the formation of regenerative nodules that disrupt normal liver architecture

Complications and Manifestations

Complications of decompensated cirrhosis include:

Pathophysiology mechanism	Manifestations
Portal hypertension	Varices (most common: oesophageal varices) Splenomegaly Ascites +/– SBP Caput medusae (visible dilated abdominal veins)
Impaired liver synthetic / detoxification function	Hepatic encephalopathy (from ammonia and other toxins) Coagulopathy (→ easy bruising) Hypoalbuminaemia (→ oedema, ascites) Hyperbilirubinaemia
Other	Increased risk of hepatocellular carcinoma Hepatorenal syndrome (advanced liver disease → renal vasoconstriction → AKI)

Diagnosis

Cirrhosis Diagnosis

Transient elastography (e.g. FibroScan) should be offered to the following to diagnose cirrhosis:

• Hepatitis C virus infection
• People who drink excess alcohol (men >50 units and women>35 units per week)
• Alcohol-related liver disease
• NAFLD only if there is advanced liver fibrosis (defined by ELF score ≥10.51) – see this article for more information on NAFLD

Screening and Monitoring for Complications

Calculate MELD score every 6 months:

• ≥12 indicates high risk of complications

 

In patients with cirrhosis, routine monitoring for the following complications is recommended:

Complication	Test
Hepatocellular carcinoma	Ultrasound +/- AFP every 6 months
Oesophageal varices	Perform upper GI endoscopy after diagnosis (unless planning to take carvedilol or propranolol) For subsequent actions and monitoring, see below

Management

Compensated Cirrhosis

No specific management, with the aim of preventing progression of liver disease and complications:

• Complete alcohol abstinence (in patients who drink)
• Weight loss (in overweight / obesity / NAFLD patients)
• Routine vaccinations (for all chronic liver disease patients)
  • Annual influenza
  • Pneumococcal
  • Hepatitis A and B
  • SARS-CoV-2
• Ensure adequate nutrition
• Screening and monitoring for complications (see above)

Decompensated Cirrhosis

Portal Hypertension

Primary prevention of decompensation:

• 1st line: carvedilol
• 2nd line: propranolol

Variceal Bleeding

Primary Prevention

Screening upper GI endoscopy should be offered if the patient is NOT taking carvedilol or propranolol:

• No varices → annual surveillance
• Small varices → annual surveillance or primary prophylaxis with carvedilol (if Child Pugh class C)
• Medium / large varices → primary prophylaxis
  • 1st line: NSBB (carvedilol / propranolol)
  • 2nd line: endoscopic variceal band ligation

 

No further surveillance needed if on NSBB for primary prophylaxis.

Acute Bleed Management

Pre-endoscopic management (in addition to resuscitation) for ALL patients:

• Terlipressin (stop after 5 days or after definitive haemostasis), and
• Prophylactic antibiotic

Definitive management: endoscopic interventions:

• Oesophageal varices → band ligation
• Gastric varices → cyanoacrylate glue injection (chemical ligation)

If endoscopic interventions failed → TIPS

Post-Acute Variceal Bleed (Secondary Prevention)

Offer all the following:

• Carvedilol
• Variceal band ligation every 4 weeks until eradication
• Surveillance upper GI endoscopy

Hepatic Encephalopathy

Acute Management ^[Ref]

• Identify & treat precipitants
• Pharmacological therapy
  • Step 1: lactulose (aiming for 2-3 soft stools/day)
    • Alternative: if unsafe swallow (impending coma/coma) → phosphate enema
  • Step 2: add rifaximin

 

Secondary prophylaxis (post-encephalopathy episode)

• Step 1: lactulose (continued indefinitely after 1st episode)
• Step 2 (if ≥ 1 recurrence within 6 months): add rifaximin 

Ascites

All patients:

• Dietary salt restriction (but no routine fluid restriction)
• Stop exacerbating medications (e.g. NSAIDs, ACE inhibitors)
• Spironolactone 
  • If inadequate or severe ascites: add furosemide to spironolactone

 

Other procedures:

• Consider therapeutic large-volume paracentesis for tense or refractory ascites
  • Followed by IV albumin (20 / 25%) infusion if >5 L is drained to prevent paracentesis-induced circulatory dysfunction
• Last resort: TIPS

Spontaneous Bacterial Peritonitis (SBP)

Management

Empirical antibiotic therapy for SBP:

• IV ceftriaxone, or
• Oral co-amoxiclav (for outpatient management)

Prophylaxis

Do not routinely offer antibiotics to prevent SBP

 

Consider prophylactic antibiotic (ciprofloxacin / norfloxacin / co-trimoxazole) if:

• Previous episode of SBP (secondary prevention), or
• Severe liver disease (ascitic protein ≤15 / Child-Pugh score >9 / MELD score >16), or
• Consequences of SBP could seriously impact the patient’s care (e.g. affect their wait for TIPS)

Hepatorenal Syndrome

HRS-AKI (formerly, type 1 HRS)^[Ref]

• 1st line: IV vasoconstrictor (terlipressin is preferred, noradrenaline) + IV human albumin solution

 

HRS-NAKI (formerly, type 2 HRS)^[Ref]

• The mainstay of treatment is managing the underlying ascites & portal hypertension
  • Includes repeated large-volume paracentesis with albumin replacement, sodium restriction, and consideration of TIPS in selected patients
  • Medical therapy with vasoconstrictor / albumin is less effective and not routine in HRS-NAKI

 

Definitive treatment (both HRS-AKI/HRS-NAKI): liver transplantation

Symptoms in Advanced Liver Disease

Selected recommendations from BSG guidelines:

Symptom	Recommendation
Pain	1st line: paracetamol If opioids are needed, 1st line is morphine if eGFR >30, hydromorphone if eGFR <30 (monitor for constipation and encephalopathy) Avoid the following if possible: NSAIDs (bleeding risk and nephrotoxic) Tramadol (lowers seizure threshold) Codeine
Nausea and vomiting	1st line: GI causes: metoclopramide / domperidone CNS causes / opioid induced: haloperidol 2nd line: Ondansetron Levomepromazine

References