Identifying the presence of cirrhosis is essential in any patient with chronic liver disease. Making the diagnosis of cirrhosis will affect management and follow-up.

Key concepts

• Cirrhosis is the end stage of any chronic liver disease, such as hepatitis B, hepatitis C, alcohol-related liver disease, or metabolic dysfunction-associated steatotic liver disease
• Clinical stages of cirrhosis: compensated and decompensated
  • Patients with compensated cirrhosis may have gastroesophageal varices, but they never developed complications such as ascites, hepatic encephalopathy or variceal hemorrhage. The diagnosis of cirrhosis can usually be established without a liver biopsy, using clinical findings, imaging, lab tests and/or elastography
  • Decompensated cirrhosis is characterized by the presence or development of ascites, variceal hemorrhage, or hepatic encephalopathy; a liver biopsy is rarely needed to confirm cirrhosis

Key recommendations

• Cirrhosis should be investigated in patients with chronic (>6 months in duration) abnormalities in liver enzymes and/or in patients in whom risk factors for cirrhosis are present: alcohol use disorder, hepatitis C, hepatitis B, obesity, and metabolic syndrome (even in the absence of liver enzyme abnormalities)
• The following can help support the diagnosis of cirrhosis:
  • Careful physical exam
  • Appropriate laboratory tests
  • Appropriate imaging tests
  • Liver stiffness measurements
• However, physical exam, laboratory tests, and radiology tests (clinical findings) all may yield entirely normal results in a patient with compensated cirrhosis
• Liver biopsy (an invasive method) is required to establish (or exclude) the diagnosis of cirrhosis when there is high suspicion but absence of non-invasive findings

The diagnosis of decompensated cirrhosis is usually easy and straightforward. However, for compensated cirrhosis, a combination of clinical judgement, laboratory tests (e.g. FIB-4, imaging finding) should be used. Finally, elastography is the best non-invasive assessment of fibrosis.

Physical exam findings suggestive of decompensated cirrhosis (difficult to diagnose compensated cirrhosis with physical exam):

Exam Finding	Example
Bitemporal muscle wasting
Spider angioma Palmar erythema
Ascites Abdominal collaterals (caput medusae)
Palpation/percussion	Palpable left lobe of the liver (in the epigastrium) Splenomegaly Small liver span (right lobe: normal is ~9 cm) Shifting dullness (ascites)

Laboratory findings suggestive of cirrhosis:

• Platelet count < 150,000 (if no other explanation)
• Albumin < 3.5 mg/dL (if no albuminuria, malnutrition)
• AST > ALT
• INR > 1.2
• Bilirubin > 1.5 mg/dL (very non-specific, rule out Gilbert syndrome)
• FIB-4 or APRI scores calculated using age, AST, ALT, and/or platelet count (high negative predictive value)
• Specialized tests such as Enhanced Liver Fibrosis (not widely available)

Imaging findings (abdominal ultrasound, CT, or MRI) suggestive of cirrhosis:

• Nodular surface of the liver (subjective)
• Splenomegaly
• Collaterals or varices
• Enlarged caudate lobe/left lobe of the liver
• Shrunken right lobe of the liver
• Ascites

Elastographic findings suggestive of cirrhosis:

• Transient elastography (Fibroscan^®) is a point-of-care method to measure liver stiffness (LS)
  • Most reliable non-invasive test for diagnosis of suspected cirrhosis
  • Most useful for excluding cirrhosis
  • LS can be falsely elevated e.g., non-fasting, aminotransferases >150 IU/mL, fluid accumulation from cardiac or renal dysfunction, and pulmonary hypertension.
• Other methods to measure liver stiffness include acoustic radiation force impulse (ARFI) and magnetic resonance elastography (MRE), but they are not point-of-care and have different cutoffs
• Combination of LS measurement and platelet count can have both diagnostic and prognostic values