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Cirrhosis

Cirrhosis is the common endpoint of a wide variety of chronic liver disease processes which cause hepatocellular necrosis. Cirrhosis can be diagnosed with ultrasound, CT, and MRI, and these imaging modalities can also be used to evaluate for possible sequelae of cirrhosis, such as portal hypertension or hepatocellular carcinoma.

Epidemiology

The demographics of cirrhosis reflect the underlying causes. Alcoholism, viral hepatitis from IV drug use, or viral hepatitis from and endemic region are common causes.

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:

Clinical presentation

The diagnosis is made either at screening for cirrhosis due to known risk factors, elevated liver enyzmes, or discovered incidentally in an examination for nonspecific symptoms (e.g. right upper quadrant pain). It may also present due to one of its complications:

Pathology

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

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 between the segments. See article: caudate–right lobe ratio (C/RL).

Imaging is not reliable enough to differentiate between various underlying etiologies.

The main imaging challenge is distinguishing regenerative nodules, siderotic nodules and dysplasic nodules from:

Ultrasound

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

  • surface nodularity: (88% sensitive, 82-95% specific 5)
  • overall coarse and heterogeneous echotexture
  • 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)
      • slow portal venous flow <15 cm/sec
      • reversal or to-and-fro portal venous flow
      • portal vein thrombosis +/- cavernous transformation
      • 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 spectral Doppler waveforms
      • portalization of hepatic vein waveform
      • re-canalisation and hepatofugal paraumbilical venous flow
      • portosystemic collaterals
    • splenomegaly
    • ascites
    • fatty change (variable)
CT

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 may be demonstrated.
  • signs of portal hypertension
    • portal vein enlargement
    • portal venous thrombosis +/- cavernous transformation
MRI

MRI is also insensitive in early cirrhosis, but has a significant role in screening cirrhotic livers for small HCCs (see LI-RADS). MRI 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 + C: 
      • arterial phase enhancement and washout 7
      • late enhancing capsule
      • growth in the interval between studies
    • T2: typically mildly or moderately hyperintense 

MR angiography or a balanced steady state free precession sequence 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. One of the key roles of diagnostic radiology is detection of hepatocellular carcinoma. Interventional radiology can be very helpful for treatment of portal hypertension and its complications (e.g. TIPS, ascites drainage), as well as chemoembolisation or radiofrequency ablation of HCC.

Differential diagnosis

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

Practical points


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Ultrasound

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