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Cirrhosis is the common endpoint of a wide variety of chronic disease processes which cause hepatocellular necrosis.

Demographics and clinical presentation

The demographics of cirrhosis reflect that of the underlying causes, with alcoholics, IV drug users and individual from endemic hepatitis regions being the typical patients. 

The distribution of underlying aetiology will vary regionally, with viral hepatitis being much higher in the developing world, especially Asia. A typical distribution of causality in Western nations is a follows 4:

The diagnosis is made either at screening for cirrhosis due to known underlying illness, investigation of non-specific symptoms, or due to one of its complications:


Focal hepatocellular necrosis caused by a variety of insults (see above) is accompanied by the three characteristics of cirrhosis 3:

  1. fibrosis
  2. nodular regeneration
  3. distortion of hepatic architecture

Although traditionally cirrhosis has been divided into micro- and macronodular cirrhosis, many entities begin as micronodular (<3 mm) 9 and progress to macronodular (e.g. alcoholic cirrhosis) and thus it is of limited utility as a classification scheme 4.

The clinical severity of cirrhosis is often assessed by the Child-Pugh scoring system.

Radiographic features

Imaging is not reliable enough to distinguish, nor can it differentiate the various underlying etiologies.

Frequent findings in advanced cirrhosis include hypertrophy of the caudate lobe and lateral segments of left lobe (segments II & III) with concomitant atrophy of the posterior segments (VI & VII) of the right lobe. These changes are likely related to changes in blood flow. See article: caudate–right lobe ratio (C/RL).


Ultrasound is a major screening tool for cirrhosis and its complications and able to aid in biopsy. Appearances include:

  • surface nodularity: (88% sensitive, 82-95% specific 5)
  • overall coarse and heterogeneous echotexture
  • fatty change (variable)
  • segmental hypertrophy/atrophy (see above)
    • caudate width: right lobe width >0.65 (43-84% sensitive, 100% specific 5)
  • signs of portal hypertension
    • doppler flow changes
      • enlarged portal vein: >13 mm (42% sensitive, 95-100% specific 6)
      • enlarged SMV and splenic vein: >10mm
        • note: this should be measured during deep inspiration as size can vary.
      • loss of respiratory variation in SMV and splenic vein diameter
        • normal = 50-100% increase in diameter on deep inspiration
      • reversal or to-and-fro portal venous flow
      • portal vein thrombosis +/- cavernous transformation
      • portalization of hepatic vein waveform
      • re-canalisation and hepatofugal paraumbilical venous flow
      • portosystemic collaterals
    • splenomegaly
    • ascites

CT is insensitive in early cirrhosis. More established findings include:

  • surface and parenchymal nodularity
    • regenerative nodules (most) are isodense to rest of liver
    • siderotic nodules (minority) hyperdense due to accumulation of iron 6
  • fatty change (variable)
  • segmental hypertrophy/atrophy (see above)
  • parenchymal heterogeneity both on the pre and post IV contrast scans
  • isodense/hyperdense regenerative nodules
  • predominantly portal venous supply to dysplastic nodules.
  • In advanced cirrhosis, nodular margin and lobar hypertrophy/atrophy can be demonstrated.
  • signs of portal hypertension
    • portal vein enlargement
    • portal venous thrombosis +/- cavernous transformation

MRI is also insensitive in early cirrhosis, but has a significant role in assessing from small HCCs. Findings include:

  • morphologic changes (same as on CT and ultrasound)
  • regenerative nodules (or cirrhotic nodules)
    • T1
      • variable, usually isointense
      • occasionally mildly hyperintense
      • no early enhancement and washout as most supply is from the portal vein 7,9
    • T2
      • usually isointense 9
      • hypointense if siderotic
  • dysplastic nodules
    • may be of low or high grade, and thus have variable appearance
    • low-grade nodules will resemble regenerative nodules
    • high-grade nodules will resemble HCCs 9
  • small hepatocellular carcinoma (HCC)
    • T1: hyperintense, with early arterial enhancement and washout 7
    • T2: typically hyperintense 

MR angiography may also be used to asses portal vein patency and portosystemic collaterals.


Treatment and prognosis

Treatment depends on the underlying aetiology and presence of complications. Role of radiology is predominantly in treatment of portal hypertension and its complications (e.g. TIPS, ascites drainage) and chemoembolisation / radiofrequency ablation of HCC.

Differential diagnosis

There are several conditions than can potentially mimic cirrhosis on imaging 10:

The main difficulty is in distinguishing regenerative nodules, siderotic nodules and dysplasic nodules from:

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