Cirrhosis

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

 surface nodularity: 88% sensitive, 82-95% specific 5

 overall coarse and heterogeneous echotexture
 segmental hypertrophy/atrophy (see above)
o caudate width: right lobe width >0.65 (43-84% sensitive, 100% specific 5)
o reduction of the transverse diameter (<30 mm) of the medial segment of the left
lobe (segment 4) 11
 signs of portal hypertension
o Doppler flow changes
 portal venous system
 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 venous thrombosis +/- cavernous transformation
 enlarged superior mesenteric vein and splenic vein: >10
mm
 NB: this should be measured during deep
inspiration as size can vary
 loss of respiratory variation in superior mesenteric vein
and splenic vein spectral Doppler waveforms
 enlarged paraumbilical vein with hepatofugal flow 17
 portosystemic collaterals
 hepatic veins
 portalisation of hepatic vein waveform
 hepatic arteries
 "corkscrew" appearance
 increased velocity (compensating for decreased portal vein
flow)
o splenomegaly
o ascites
 o fatty change (variable)

Sonoelastography may also be useful to assess the amount of liver fibrosis 12. Suggested values for
diagnosis are:

 >7 kPa: advanced fibrosis

 12.5-15 kPa: cirrhosis

Contrast-enhanced ultrasound may have a role in the diagnosis of cirrhosis, as diminished mean

hepatic venous transit time is similar to that of perfusion CT 13.

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

 surface and parenchymal nodularity

o regenerative nodules (majority): isodense/hyperdense to the rest of liver
o siderotic nodules (minority): hyperdense due to accumulation of iron 6
 fatty change (variable)
 parenchymal heterogeneity both on the pre and post intravenous contrast scans
 predominantly portal venous supply to dysplastic nodules
 in advanced cirrhosis, nodular margin and lobar hypertrophy/atrophy may be demonstrated
 signs of portal hypertension
o portal vein enlargement
o portal venous thrombosis +/- cavernous transformation
o splenomegaly
o portosystemic collaterals
 upper abdominal lymphadenopathy in end-stage disease 16

MRI
MRI is also insensitive in early cirrhosis but has a significant role in screening cirrhotic livers for small
hepatocellular carcinomas (see LI-RADS). MRI findings include:

 morphologic changes (same as on CT and ultrasound)

 regenerative nodules (or cirrhotic nodules)
o T1
 variable, usually isointense
 occasionally mildly hyperintense
 no early enhancement and washout as most supply is from the portal
vein 7,9
o T2
 usually isointense 9
 hypointense if siderotic
  dysplastic nodules
o maybe of low or high grade, and thus have a variable appearance
o low-grade nodules will resemble regenerative nodules
o high-grade nodules will resemble hepatocellular carcinomas 9
 small hepatocellular carcinoma (HCC)
o T1 C+ (Gd)
 arterial phase enhancement and washout 7
 late enhancing capsule
 growth in the interval between studies
o T2: typically mildly or moderately hyperintense

MR angiography or a balanced steady-state free precession sequence may also be used to assess
portal vein patency and portosystemic collaterals.

Treatment and prognosis

Treatment depends on the underlying etiology and presence of complications. One of the key roles of
diagnostic radiology is the detection of hepatocellular carcinoma (six-monthly ultrasound should be
done for surveillance as per 2018 AASLD (American Association for the Study of Liver Diseases)
guidelines in cirrhotic patients to screen for hepatocellular carcinoma development) 15. Interventional
radiology can be very helpful for the treatment of portal hypertension and its complications (e.g. TIPS,
ascites drainage), as well as chemoembolisation or radiofrequency ablation of hepatocellular
carcinoma.

Complications
 pulmonary complications of cirrhosis
 musculoskeletal complications of cirrhosis
 central nervous system (CNS) complications of cirrhosis

History and etymology

The word cirrhosis derives from the Ancient Greek word "κιρρόειν", meaning "to turn reddish-yellow"
or "tawny". The French physician René Laennec (1781-1826) was first to use the term to describe the
macroscopic appearance of fibrotic changes in a liver with alcoholic cirrhosis.

Differential diagnosis
There are several conditions that can potentially mimic cirrhosis on imaging 10:

 pseudocirrhosis
 widespread (miliary type) liver metastases
 Budd-Chiari syndrome (particularly chronic)
  fulminant hepatic failure
 hepatic sarcoidosis
 congenital hepatic fibrosis
 idiopathic portal hypertension
 early primary biliary cholangitis (PBC)
 chronic portal vein thrombosis
 nodular regenerative hyperplasia of the liver

Severity scoring
 clinical scoring: Child-Pugh scoring system
 biochemical scoring: hepascore
METAVIR score
 Hepatopulmonary syndrome (HPS)
is a clinical syndrome defined by the presence of the following:

 liver disease
 dilation of pulmonary vasculature
o may involve pulmonary capillaries, pulmonary arteriovenous malformations, or
pleural AVMs
 abnormalities in oxygenation
o elevation in the alveolar-arterial (A-a) oxygen gradient with or without hypoxemia
on room air

Radiographic features
The radiologic manifestations of this disease include distal vascular dilatation associated with an
abnormally large number of visible terminal vessel branches, which are always concentrated in the
lower lung zones.

Plain radiograph
Chest x-ray may include bibasal medium-sized (1.5-3 mm) nodular or reticulonodular opacities 2,4

CT
May show peripheral arteriolar dilatation on CT with an increased number of terminal branches
extending towards the pleura.

Two patterns have been described on CTPA 6:

 type I
o most common (~85%) 
o manifests as distal vascular dilatation with subpleural telangiectasia
o features include multiple, slightly dilated subpleural vessels that do not taper
normally and therefore extend to the pleural surface
 type II
o less common (~15%) 
o seen as individual arteriovenous malformations on angiograms and nodular
dilatation of peripheral pulmonary vessels
 Hepatorenal syndrome
refers to a form of acute kidney injury caused by changes in renal blood flow regulation due to liver
pathology 1. Although the syndrome occurs mainly in cirrhotic livers it has been reported in patients
with acute fulminant liver failure as well 1.

The incidence of hepatorenal syndrome in patients with end-stage liver disease is up to 7.6% 2.

Clinical presentation

The patient usually has chronic liver disease with cirrhosis. Symptoms may include reduced urine
output, and there may or not be a precipitant (e.g. spontaneous bacterial peritonitis). The signs and
symptoms of underlying chronic liver disease may also be present.

The main laboratory finding of hepatorenal syndrome is an acutely elevated serum creatinine level.
However, it is difficult to diagnose hepatorenal syndrome based on these non-specific findings alone,
instead it is a diagnosis of exclusion after other causes of acute kidney injury have been ruled out 2.

Pathology

Hepatorenal syndrome is thought to develop from a number of pathological processes occurring in

the diseased liver. One of these processes is portal hypertension causing bacterial translocation from
the gut into the portal system, as well as causing splanchnic and systemic blood vessel dilatation, and
the activation of liver chemoreceptors and baroreceptors. The summative effect of these lead to the
activation of neurohumoral pathways (e.g. sympathetic nervous system, renin-angiotensin-
aldosterone system) which stimulate renal vasoconstriction and reduce blood flow to the kidneys
leading to injury 2,3.

Classification

Two types have been identified, based upon how rapid the decline in renal function is:

 type 1 hepatorenal syndrome: rapidly progressive with a doubling of creatinine in two weeks
or less 
 type 2: defined as simply less acute than type 1

Radiographic features

Ultrasound 

In cases of hepatorenal syndrome where there is no pre-existing intrinsic renal disease the kidneys
should show a normal size and no evidence of atrophy 2. Normal appearing kidneys on ultrasound is
required for the diagnosis of hepatorenal syndrome according to the Hepatorenal Syndrome-AKI
Guidelines produced by the International Club of Ascites 2.
Benign Hepatic Tumors and Iatrogenic Pseudotumors

Angiomyolipoma
Hepatic angiomyolipoma are a rare benign tumour of the liver composed of smooth muscle, blood
vessels, and a variable amount of adipose tissue. Although they are more commonly sporadic, there
is a known association of hepatic angiomyolipoma with tuberous sclerosis .

At US, these lesions appear as circumscribed hyperechoic lesions and may be mistaken for a
haemangioma given similar imaging appearances . Angiomyolipoma may show some at attenuation
and subtle shadowing as well as relative hypervascularity at US (haemangiomas are hypo vascular) .
At CT, areas of macroscopic fat with corresponding attenuation values may be identified, depending
on the amount of adipose tissue within the lesion. On contrast-enhanced CT images, hepatic
angiomyolipoma typically demonstrate marked enhancement during the arterial phase, often with
visualization of large central vessels .

At MR imaging, macroscopic fat may be detected by using fat suppression techniques (Fig 18),
depending on the distribution and degree of adipose tissue; microscopic fat may be identified by
using in-phase and opposed phase gradient-echo T1-weighted sequences . Again, intense
enhancement is seen on arterial phase MR images
 Lipoma
Hepatic lipomas are even less common than hepatic angiomyolipoma but typically do not represent
a diagnostic dilemma, since they have characteristic features at CT and MR imaging .

At US, hepatic lipomas are seen as a well circumscribed echogenic lesion, a nonspecific appearance
similar to that of haemangiomas and angiomyolipoma, as described earlier. Lipomas may or may not
show acoustic shadowing at US. At CT, lipomas in the liver, as elsewhere in the body, are
homogeneously hypoattenuating and do not enhance after contrast material administration. At MR
imaging, hepatic lipomas are hyper intense on T1-weighted images and demonstrate signal
suppression on fat-suppressed images.

Peliosis Hepatis
Peliosis hepatis is a rare benign vascular lesion characterized by sinusoidal dilatation and blood filled
hepatic spaces. Myriad causes of peliosis hepatis have been described, including toxins such as
arsenic and polyvinyl chloride; drugs such as oral contraceptives, anabolic steroids, and
corticosteroids; and infectious agents such as Bartonella and the tuberculosis bacillus

Other causes of peliosis that have been described include various malignancies (especially HCC),
renal and cardiac transplantation, and diabetes; it is idiopathic in up to 50% of patients.

At US, peliosis hepatis demonstrates variable echogenicity relative to the surrounding liver and may
have internal vascularity on colour Doppler images .

In patients with normal livers, peliosis is typically hyperechoic; however, it may appear hypoechoic
in patients with abnormally echogenic liver parenchyma, such as in steatosis. At unenhanced CT,
peliosis is commonly seen as a focal hypoattenuating area; however, areas of haemorrhage may
increase the attenuation .

At contrast-enhanced CT, early globular enhancement is typically identified with a centripetal

increase in enhancement during later phases of imaging, although brisk early enhancement may be
seen (Fig 19). Also, areas of central enhancement, termed the target sign, may be identified. On
delayed phase images, peliosis hepatis typically appears homogeneously hyperintense to
surrounding liver parenchyma (44). Central areas of thrombosis or areas of internal calcification may
also be seen. At MR imaging, peliotic lesions are typically hypointense on T1-weighted images owing
to subacute blood products, but the signal intensity may be variable. On T2-weighted images, the
lesions are commonly hyperintense with smaller foci of increased signal intensity centrally, which
are possibly related to necrosis . Enhancement characteristics at MR imaging are similar to those at
CT.
 Paraganglioma

Paragangliomas represent rare tumours of neural crest origin, the majority of which are benign.
These tumours are typically seen along the sympathetic chain; however, numerous intraabdominal
locations have been described, including the liver (46). As with many of the mesenchymal tumours,
nonspecific imaging characteristics are seen. At CT, paragangliomas typically appear as smooth, well-
circumscribed lesions with avid contrast enhancement (Fig 20) (47). Cystic areas and punctate
calcifications are described (48). MR imaging descriptions typically include high signal intensity to
surrounding liver on T2-weighted images with possible visualization of hypointense internal septa
(49). As at CT, avid enhancement is also seen at MR imaging.
 Inflammatory Pseudotumor
Inflammatory pseudotumor is a benign hepatic tumor consisting of inflammatory cells and fibrous
stroma .

The cause of these lesions is unknown, although they have been speculated to be secondary to an
inciting hepatic infection .

At US, inflammatory pseudotumor have been described as hypo- as well as hyperechoic masses with
increased through transmission and visualization of multiple septa .

Nonspecific imaging characteristics are seen at CT. Commonly, the tumours are hypoattenuating to
liver parenchyma on unenhanced images, and variable patterns of enhancement are seen after
contrast material administration, including peripheral enhancement or enhancement of multiple
internal septa (Fig 21).

Variable appearances of inflammatory pseudotumor of the liver have been described at MR imaging
as well. The lesions are typically hypointense on T1-weighted images and hyperintense on T2-
weighted images with variable enhancement patterns .

Effects of Transcatheter Chemoembolization

In patients treated with transcatheter chemoembolization, posttreatment CT scans may reveal a
variety of unusual appearances. After chemoembolization, the treated tumors may undergo
significant necrosis, with release of nitrogen forming visible gas collections in the liver parenchyma
at CT (57). With significant areas of tumor lysis, tumor lysis syndrome may occur, which is of
significant clinical importance given the associated morbidity and mortality (58). Although these
areas may mimic a hepatic abscess and patients may be febrile and experience right upper quadrant
pain, the lack of fluid associated with tumoral necrosis is useful in making the distinction at imaging
In patients who recently underwent chemoembolization, diffuse heterogeneous areas of high
attenuation are seen in the treated portions of the liver parenchyma with focal areas of relatively
increased attenuation, which correspond to the lesions that were treated (Fig 22) (59). The high
attenuation evident at CT immediately after chemoembolization is due to the ethiodized oil
component of the chemoembolization agent. The iodine content of this component, which is
combined with the ethyl esters of the fatty acids of poppy seed oil, yields the attenuation
characteristics seen at CT. Tumours demonstrate increased attenuation relative to that of adjacent
normal liver parenchyma because of the differences in vascular supply, with tumours predominantly
receiving arterial vascular supply.

In those patients who underwent chemoembolization further back in time, the residual areas of high
attenuation may simulate focal lesions, possibly mimicking the appearance of psammomatous
calcifications related to mucinous hepatic metastases (Fig 22). In these cases, knowledge of prior
imaging results and the patient history allows one to avoid the diagnostic dilemma
Effects of Percutaneous Intervention

Percutaneous interventional procedures including image-guided liver biopsy as well as

percutaneous tumour therapies including radiofrequency ablation may yield focal post procedure
liver abnormality. Although uncommon, significant haemorrhage may follow routine nontargeted or
targeted liver biopsies (Fig 24). If this results in focal areas of high attenuation, the findings may be
mistaken for a focal hepatic lesion. Because the hematoma represents haemorrhage within viable
liver parenchyma, enhancement may be identified after contrast material administration. In these
cases, follow-up imaging documenting a serial decrease in the intraparenchymal hematoma size as
well as the clinical history may be used to distinguish a hematoma from the consideration of a solid
liver lesion.

In patients who undergo radiofrequency ablation to treat malignant hepatic tumors, nonenhancing
postprocedure areas of relative low attenuation are typically identified (Fig 25). The lack of
enhancement is useful in differentiating these postprocedure areas from solid hepatic mass lesions.
Successfully treated tumors remain nonenhancing, with the development of peripheral nodular
enhancement being suggestive of tumor recurrence (61).
Malignant liver lesions
Hepatocellular carcinoma (HCC)
 

Epidemiology
Hepatocellular carcinoma is the fifth most common cancer in the world and is the third most common
cause of cancer-related death (after lung and stomach cancer). The incidence of hepatocellular
carcinoma is rising, largely attributable to a rise in hepatitis C infection .

The highest prevalence occurs in Asia, in regions where chronic hepatitis B infection is endemic, and
this accounts for >80% of hepatocellular carcinoma cases worldwide. In Western countries, the rate of
hepatitis B infection is lower and alcohol accounts for the majority of cases.

Hepatocellular carcinoma is typically diagnosed in late middle-aged or elderly adults (average 65

years) and is more common in males (75% of cases) 7. In regions where chronic hepatitis B infection is
endemic, young adults aged 20 to 40 (who had contracted the virus via maternal-fetal transmission)
have the highest risk of developing hepatocellular carcinoma.

Hepatocellular carcinoma also occurs in the paediatric population, and is the second most common
paediatric primary liver tumour after hepatoblastoma.

Fibrolamellar hepatocellular carcinoma is a distinct variant of hepatocellular carcinoma not associated

with cirrhosis and has different demographics and risk factors.

Risk factors

Risk factors include 1:

 hepatitis B (HBV) infection: 10% 5-year cumulative risk 3

 hepatitis C (HCV) infection: 30% 5-year cumulative risk
 alcoholism: 8% 5-year cumulative risk
 biliary cholangitis: 5% 5-year cumulative risk
 food toxins, e.g. aflatoxins
 congenital biliary atresia
 inborn errors of metabolism
Radiographic features
Hepatocellular carcinomas can have a variety of appearances:

 massive (focal)
o large mass
o may have necrosis, fat and /or calcification
 nodular (multifocal)
o multiple masses of variable attenuation
o may also have central necrosis
 infiltrative (diffuse) 10
o may be difficult to distinguish from associated cirrhosis: also called
cirrhotomimetic-type hepatocellular carcinoma or cirrhosis-like hepatocellular
carcinoma

Hepatocellular carcinoma receives most of its blood supply from branches of the hepatic artery,
accounting for its characteristic enhancement pattern: early arterial enhancement with early
"washout." Hence, small foci of hepatocellular carcinoma may be seen within a regenerative liver
nodule as foci of arterial enhancement (nodule-in-nodule appearance) 11.

Rim enhancement on delayed post-contrast images causing a capsule-appearance is considered

relatively specific for hepatocellular carcinoma . 

Additionally, these tumors have the propensity to invade vascular structures, most commonly the
portal vein, but also the hepatic veins, IVC, and right atrium. One should remember that a large
number of patients will have concomitant cirrhosis, and thus also be at risk for bland portal vein
thrombosis from synthetic dysfunction of clotting factors.

Ultrasound
Variable appearance depending on the individual lesion, size, and echogenicity of background liver.
Typically:

 small focal hepatocellular carcinoma appears hypoechoic compared with normal liver
 larger lesions are heterogeneous due to fibrosis, fatty change, necrosis and calcification 12
 a peripheral halo of hypoechogenicity may be seen with focal fatty sparing (see the discussion
below on the CT session)
 diffuse hepatocellular carcinoma may be difficult to identify or distinguish from background
cirrhosis
 contrast-enhanced ultrasound 13
o arterial phase
 arterial enhancement from neovascularity
o portal venous phase
 decreased echogenicity relative to background liver ("washout")
 tumor thrombus may be visible
o variants have been described with arterial phase hypovascularity with no
enhancement or arterial enhancement with no "washout"
CT
Several patterns can be seen, depending on the subtype of hepatocellular carcinoma. Enhancement
pattern is the key to the correct assessment of hepatocellular carcinomas.

Usually, the mass enhances vividly during late arterial (~35 seconds) and then washes out rapidly,
becoming indistinct or hypoattenuating in the portal venous phase, compared to the rest of the liver.

Additionally, they may be associated with a wedge-shaped perfusion abnormality due to arterioportal
shunts (APS), and this, in turn, can result in a focal fatty change in the normal liver or focal fatty
sparing in the diffusely fatty liver 14. A halo of focal fatty sparing may also be seen around a
hepatocellular carcinoma in an otherwise fatty liver 15.

Portal vein tumor thrombus can be distinguished from bland thrombus by demonstrating
enhancement.

MRI
When seen in the setting of cirrhosis, small hepatocellular carcinomas need to be distinguished from
regenerative and dysplastic nodules 16.

In general, MRI signal is:

 T1
o variable
o iso- or hypointense cf. surrounding liver 17
o hyperintensity may be due to
 intratumoral fat 3
 decreased intensity in the surrounding liver
 T1 C+ (Gd)
o enhancement is usually arterial ("hypervascularity")
o rapid "washout", becoming hypointense to the remainder of the liver (96%
specific) 3
 this is because the supply to hepatocellular carcinoma is
predominantly from the hepatic artery rather than the portal vein
o rim enhancement may persist ("capsule")
 T1 C+ (Eovist/Primovist)
o similar to assessment with extracellular gadolinium, but evaluation of the
hepatobiliary phase requires care
 arterial hyperenhancement
 washout assessed on the portal venous phase
 washout on transitional phase (3 minutes delayed) is less reliable
 T2: variable, typically moderately hyperintense
 C+ post-SPIO (iron oxide): increases sensitivity in diagnosing small hepatocellular
carcinomas
 DWI: intratumoral high signal; increases sensitivity and specificity

Angiography (DSA)

 hypervascular tumor
 threads and streaks pattern: sign of tumor thrombus in the portal vein
Major criteria for HCC:

• Arterial enhancement.

• Non-peripheral washout on portal venous and delayed phases.

• Enhancing capsule/pseudo capsule seen in portal venous or delayed phases.

• Threshold growth with diameter increase of >50% in < 6 months

Ancillary findings favouring HCC include non-enhancing capsule, nodule-in-nodule architecture,

mosaic architecture, fat in mass, blood products in mass.
Liver transplant Surgical candidates

• The Milan criteria is used to assess appropriateness of liver transplantation in those with HCC or
cirrhosis. To be considered for orthotopic liver transplantation, one must have:

Single tumour <5 cm or 3 tumours less than 3 cm.

No extrahepatic involvement.

No major vascular involvement.

Post-operative appearance :

• Normal findings may include periportal oedema, minimal ascites, right-sided pleural effusion, and a
small perihepatic hematoma.

Complications

• Vascular: Hepatic artery thrombosis is the most common vascular complication. Others include
hepatic artery stenosis and pseudoaneurysm, IVC or hepatic vein stenosis or thrombosis and portal
vein stenosis or thrombosis.

• Biliary: Ductal stricture is the most common biliary complication. Leaks and obstruction due to
choledocholithiasis are also possible.

• Other complications include hematoma, abscess, hepatitis, splenic infarct, recurrent malignancy or
primary sclerosing cholangitis (depending on the indication for transplant) and post-transplant
lymphoproliferative disorder (PTLD).

PTLD is a type of lymphoma caused by Epstein-Barr virus which can arise after solid organ or bone
marrow transplant. Patients with renal transplants are at particular risk. PTLD may occur anywhere,
regardless of which organ was transplanted.

Treatment is reduction/withdrawal of immunosuppression. PTLD appears as a mass with a variable

and nonspecific appearance