Cirrhosis

Published on 19/07/2015 by admin

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Last modified 22/04/2025

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 Hyperdense on NECT, isodense on CECT

image Hypointense on T2 and GRE MR
image 3-10 mm in size
• Vascular derangements

image Arterioportal and portovenous shunts
image Varices (gastroesophageal, caput medusae, etc.)
• Fibrosis: Diffuse, lace-like, thick, or confluent foci

image Hypointense on T1W; hyperintense on T2W MR
• Cirrhosis-induced hepatocellular carcinoma (HCC)

image Heterogeneous enhancement on arterial phase; usually hypodense on venous and delayed phase CT + MR
image Hyperintense on T2W MR
image Bright on DWI MR
image ± capsule, fat, venous invasion, metastases

TOP DIFFERENTIAL DIAGNOSES

• Treated liver metastases or lymphoma
• Budd-Chiari syndrome
• Hepatic sarcoidosis
• Primary portal vein thrombosis
• Nodular regenerative hyperplasia

DIAGNOSTIC CHECKLIST

• MR has advantage in detection and characterization of focal nodules within cirrhotic liver
image
(Left) Graphic shows a cirrhotic liver with a nodular surface contour and an increase in the caudate to right lobe ratio, measured from the branch point of the right portal vein image to the edges of the caudate and right lobes, respectively. Note the bands of fibrosis image and ascites.

image
(Right) Axial CECT shows a cirrhotic liver and large varices image. Note the enlarged caudate lobe image, which is as wide as the right lobe, although the caudate lobe is normally no more than 60% of the width of the right lobe.
image
(Left) Axial NECT in this 50-year-old woman with primary biliary cirrhosis shows innumerable small hyperdense regenerative nodules image, surrounded by lace-like fibrosis.

image
(Right) The nodules disappear into the background cirrhotic liver on this CECT from the same patient. Prominent porta hepatis lymphadenopathy image, another typical feature of primary biliary cirrhosis, is also noted. Primary biliary cirrhosis is an autoimmune disease that typically affects women in their 5th or 6th decade.

TERMINOLOGY

Definitions

• Chronic liver disease characterized by diffuse parenchymal injury, extensive fibrosis, and conversion of liver architecture into structurally abnormal nodules

IMAGING

General Features

• Best diagnostic clue

image Nodular contour, widened fissures, and enlarged caudate lobe with ascites, splenomegaly, and varices
• Size

image Moderate to advanced cirrhosis: Decreased size

– Earlier disease: May be enlarged
– Especially in primary biliary cirrhosis
• Key concepts

image Common end response of liver to variety of insults and injuries
image Classification by morphology (not very useful)

– Micronodular (Laennec) cirrhosis

image Usually due to alcoholism
– Macronodular (postnecrotic) cirrhosis

image Usually viral hepatitis
image Classification by etiology and severity more useful

CT Findings

• Atrophy of right lobe and medial segment of left lobe
• Enlarged caudate lobe and lateral segment of left lobe

image Caudate: Right lobe ratio often > 1.0 in cirrhosis
image Caudate is normally < 60% width of right lobe
• Widened fissures between segments/lobes
• Deep gallbladder (GB) fossa

image GB often lies against anterolateral abdominal wall
• Vascular derangements

image Varices (gastroesophageal, caput medusae, etc.)
image Arterioportal and portovenous shunts

– Arterioportal (AP) shunts are usually peripheral, wedge-shaped, small; seen only on arterial phase
– Small AP shunt difficult to distinguish from very small hepatocellular carcinoma (HCC)

image Follow-up imaging (CT or MR) in 3-6 months is sufficient for surveillance
image “Corkscrew” hepatic arterial branches

– Enlarged and displaced around regenerative nodules
• Splenomegaly
• Nodular liver contour (not apparent in all)
• Siderotic regenerative nodules

image Hyperdense on NECT, isodense on CECT
image Most regenerative nodules are not detected by CT
• Fibrotic and fatty changes

image Fibrosis: Diffuse, lace-like, thick bands or confluent “masses”

– More apparent on NECT (hypodense)
– May show persistent enhancement on delayed CECT (or contrast-enhanced MR)

image Distinguishes from HCC, which shows washout on delayed imaging
image Fatty changes: Diffuse or geographic areas of low attenuation

– Usually limited to alcoholic hepatitis with early cirrhosis
• Peribiliary cysts

image Cystic dilation of peribiliary gland in wall of large bile ducts
image Range in size from 2 mm to 2 cm
image Resemble string of pearls or grapes on a stem
• Cirrhosis-induced HCC

image NECT: Hypodense or heterogeneous, ± fat
image CECT

– Heterogeneous enhancement on arterial phase; usually iso- to hypodense on venous and delayed phase scans
– ± capsule, portal or hepatic venous invasion, metastases

MR Findings

• Siderotic regenerative nodules: Paramagnetic effect of iron within nodules

image T1WI: Hypointense
image T2WI: Increased conspicuity of low signal intensity
image T2 gradient-echo and fast low-angle shot (FLASH) images

– Markedly hypointense (best sequence for detection)
image Gamna-Gandy bodies (siderotic nodules in spleen)

– T1WI and T2WI: Hypointense
• Dysplastic regenerative nodules

image T1WI: Hyperintense; T2WI: Hypointense

– Opposite to usual pattern for HCC
image Minimal vascularity
image Take up and retain hepatobiliary MR contrast agents on delayed phase

– Most specific test to distinguish from HCC
• HCC nodule

image T1WI: Iso-, hypo-, or hyperintense
image T2WI: Hyperintense
image T1 C+: Increased enhancement on arterial phase

– Washes out to hypointense on venous and delayed phases
image Diffusion-weighted imaging

– Restricted diffusion (bright signal) within HCC
image Rarely take up or retain hepatobiliary MR contrast agents
• Fibrotic and fatty changes

image T1WI: Fibrosis = hypointense; fat = hyperintense
image T2WI: Fibrosis = hyperintense; fat = hypointense
• MR elastography

image Shows promise in noninvasive evaluation of extent of liver fibrosis

Ultrasonographic Findings

• Grayscale ultrasound

image Nodular liver contour and parenchyma
image Increased and coarsened liver echogenicity

– Decreased visualization of deep liver
image Atrophy of right lobe and medial segment of left lobe
image Features of portal hypertension

– Increased pulsatility of portal vein Doppler tracing
– Dilated hepatic and splenic arteries with increased flow
• Color Doppler

image Used to determine portal vein patency and direction of flow

– Hepatopetal is normal
– Hepatofugal is sign of severe portal hypertension
• Ultrasound is of most value and accuracy in screening patients with less advanced chronic liver disease

image Less accurate in detecting or characterizing nodules within cirrhotic liver
image Presence of fibrosis, fat, regenerative nodules makes detection of HCC very difficult

Imaging Recommendations

• Best imaging tool

image Multiphasic CT or MR
• Protocol advice

image US is suitable for screening until cirrhosis is established
image CECT is preferable in acutely ill patients or those with ascites
image MR is preferable in alcoholic cirrhosis and for detection/distinction of hepatic nodules

– Include delayed phase MR or CT (5-10 minutes)
– Hepatobiliary MR contrast agents may aid in detection of HCC

image Gadoxetate (Eovist, Primovist) is retained in normal liver, variably in cirrhotic liver, rarely in HCC

DIFFERENTIAL DIAGNOSIS

Treated Liver Metastases or Lymphoma

• Simulates nodules, fibrosis, volume loss of cirrhotic liver
• Breast carcinoma metastases to liver

image May result in “pseudocirrhosis,” especially after treatment

Budd-Chiari Syndrome

• Liver damaged but usually no bridging fibrosis

image Therefore, no true cirrhosis
• Occluded or narrowed IVC ± hepatic veins
• Chronic phase: “Large regenerative nodules”

image Hypervascular foci mimic HCC

– But no washout on delayed imaging
– Retain gadoxetate, unlike most HCC
image Focal form of nodular regenerative hyperplasia
• Central hypertrophy, peripheral atrophy

Hepatic Sarcoidosis

• May simulate or cause cirrhosis
• Hypodense nodules and lymphadenopathy
• Look for thoracic and clinical correlation

image Including peribronchial nodularity and lymphadenopathy

Primary Portal Vein Thrombosis

• May be result of hypercoagulable state
• Chronic → hepatic ischemia with peripheral atrophy, central hypertrophy, varices
• Clue: Cavernous transformation of portal vein; infarcts or ischemia of other organs

Nodular Regenerative Hyperplasia

• By definition lacks fibrosis
• Can cause portal hypertension and nodules

PATHOLOGY

General Features

• Etiology

image Alcohol: No longer most common cause of cirrhosis in USA and Europe
image Etiology of cirrhosis in USA

– Hepatitis C (∼ 25%)
– Alcoholic liver disease (∼ 20%)
– “Cryptogenic” (believed to be due to nonalcoholic steatohepatitis [NASH] in most cases) (∼ 20%)
– Hepatitis C and alcohol (∼ 15%)
– Hepatitis B (± hepatitis D) (∼ 15%)
– Miscellaneous (∼ 5%)

image Autoimmune hepatitis
image Primary biliary cirrhosis
image Secondary biliary cirrhosis (obstruction)
image Primary sclerosing cholangitis
image Hemochromatosis
image Wilson disease
image α-1 antitrypsin deficiency
image Granulomatous disease (e.g., sarcoidosis)
image Type IV glycogen storage disease
image Drug-induced liver disease (e.g., methotrexate, amiodarone)
image Venous outflow obstruction (Budd-Chiari and venoocclusive disease)
image Chronic right-sided heart failure
image Tricuspid insufficiency
• Due to combination of cell death, fibrosis, and regeneration

image Deposition of extracellular matrix and fibrous tissue in parenchyma
image Separation of hepatocytes into islands or nodules

Staging, Grading, & Classification

• Grading of severity: Child-Pugh  classification

image “Points” assigned for ascites, encephalopathy, ↑ serum bilirubin, ↓ serum albumin, ↑ prothrombin time
image Correlates well with survival (1 year)

– Child-Pugh A = 100%
– Child-Pugh B = 80%
– Child-Pugh C = 45%
• Model for End – Stage Liver Disease (MELD)

image Based on assessment of etiology of cirrhosis, serum creatinine and bilirubin level, and international normalized ratio (INR)

Gross Pathologic & Surgical Features

• Alcoholic and other causes of micronodular cirrhosis → macronodular cirrhosis with progression

image End-stage cirrhotic livers have similar gross morphologic changes
image Small, hard, nodular liver with linear and confluent fibrosis

Microscopic Features

• Fibrosis

image Present in all cirrhotic livers
image Collagen and other extracellular matrix deposited around portal tracts
• Vascular derangements

image Occlusion of fenestrations in sinusoids

– Converts sinusoids into capillaries
image Sclerosis and thrombosis of portal tracts

– Increases resistance (portal hypertension)
– Found at microscopic level in most cases, less commonly in large vessels
image Arteriovenous and portovenous shunts

– Important in imaging (may simulate HCC)
– Contributes to hepatocyte death (ischemia and loss of portal vein nutrients)
• Regeneration

image Occurs in almost all cases
image Results in regenerative nodules, often surrounded by fibrous bands
image May compress bile ducts and blood vessels, contributing to damage

CLINICAL ISSUES

Presentation

• Most common signs/symptoms

image Signs of portal hypertension

– Splenomegaly, varices, ascites
image Fatigue, jaundice, ascites, encephalopathy
image Gynecomastia and testicular atrophy in males
image Umbilical hernia
• Other signs/symptoms

image Hepatorenal and hepatopulmonary syndromes
image Coagulopathy (due to decreased hepatic synthetic function)
image Hepatic encephalopathy
image Hepatic hydrothorax

– Usually right sided
– Due to ascites traversing diaphragm into chest
image Cardiomyopathy
image Portal hypertensive colopathy and gastropathy

– Due to portal hypertension and hypoproteinemia
– Results in submucosal edema of wall of colon ± stomach
image Hepatocellular carcinoma (HCC)

– All patients with cirrhosis have markedly ↑ risk of developing HCC
– Patients with most forms of chronic liver disease are not at ↑ risk of HCC until cirrhosis develops

image Exception is chronic hepatitis B (may develop HCC before cirrhosis)

Demographics

• Age

image Many patients die in 5th or 6th decade

– Highly variable depending on etiology and severity of underlying etiology
• Gender

image M > F
• Epidemiology

image 3rd leading cause of death for men age 34-54 years in USA

– 35,000 deaths per year
image 10th leading cause of mortality worldwide

Natural History & Prognosis

• Mortality due to complications

image Progressive liver failure
image Complication related to portal hypertension

– Variceal hemorrhage, infected ascites
image HCC
• Prognosis

image Advanced cirrhosis is irreversible
image Prognosis depends on etiology and severity

– 10-year survival from diagnosis ∼ 50%

Treatment

• Advanced stage: Liver transplantation

DIAGNOSTIC CHECKLIST

Consider

• Rule out other causes of nodular dysmorphic liver

image Imaging can strongly suggest cirrhosis
image Biopsy is necessary for establishing presence, etiology, and severity

Image Interpretation Pearls

• Nodular liver contour; lobar atrophy and hypertrophy
• Regenerative nodules, ascites, splenomegaly, varices
• Ultrasound is excellent for surveillance patients with chronic liver disease

image Especially in thin patients who have not yet developed cirrhosis
image Once cirrhosis has developed, US screening is less effective
image Difficult to distinguish HCC from other types of nodules within cirrhotic liver
• Multiphasic CECT and MR are accurate in detecting HCC > 2 cm in size

image MR has advantage in detection and characterization of focal nodules within cirrhotic liver

Reporting Tips

• Evaluate extent of cirrhosis and portal hypertension

image Comment on extent of ascites, size of varices
• Specifically evaluate all hepatic vessels

image Hepatic and portal veins (for thrombosis, tumor invasion)
image Presence and type of varices and collaterals

– e.g., spontaneous splenorenal shunt
image Hepatic artery for congenital variations (e.g., replaced origin from SMA)
image Median arcuate ligament compression of celiac axis

– May decrease flow to liver allograft
– Can easily be relieved if known prior to transplantation
image
(Left) MR shows obvious signs of cirrhosis with widening of the fissures, right lobe atrophy, and large varices image. Within the spleen are innumerable small lesions that are especially evident as hypointense foci on this GRE T1WI contrast-enhanced image image, representing Gamna-Gandy bodies.

image
(Right) Sagittal US shows a coarse echotexture of the liver that is typical, but not diagnostic, of cirrhosis.
image
(Left) Axial CECT in a patient with autoimmune hepatitis and primary sclerosing cholangitis (PSC) shows a nodular, cirrhotic liver with splenomegaly, ascites, and varices image. The intrahepatic ducts image are dilated with an abnormal arborization, suggestive of PSC.

image
(Right) Axial CECT in the same patient shows the lobular contour of the liver and the hypertrophy of the caudate lobe with atrophy of the entire peripheral liver, all characteristic of cirrhosis due to PSC.
image
(Left) Arterial phase CECT shows a small hypervascular lesion image that was isodense to the liver on all other phases. This lesion was not evident on repeat CT or MR over the next 2 years and presumably represents a small arterioportal shunt.

image
(Right) The small vascular lesion is not evident on this portal venous phase image in the same patient nor was it visible on delayed phase imaging (not shown).
image
(Left) This patient had cirrhosis due to PSC. NECT shows a lobulated contour of the liver with relatively lower density atrophic peripheral liver, and hypertrophied and hyperdense, large, nodular segments of the deep right and caudate segments image.

image
(Right) On CECT (same patient) the liver becomes more homogeneous in attenuation. Note the prominent nodes image in cardiophrenic regions. The intrahepatic ducts are not dilated but were found to be beaded and strictured on ERCP.
image
(Left) Axial CECT (same patient) shows marked caudate hypertrophy and rounded contours of the liver. PSC tends to result in disproportionate atrophy of the peripheral segments of liver, whereas the more central hepatic segments hypertrophy, presumably due to preserved biliary drainage of those segments that drain more directly into the central bile ducts.

image
(Right) Axial CT (same patient) shows the peculiar rounded contours of the liver due to chronic PSC. Note the prominent porta hepatis nodes image.
image
(Left) Axial T2WI MR shows innumerable subcentimeter hypointense nodules that are typical of cirrhotic regenerative nodules.

image
(Right) Axial CECT in a patient with cardiac cirrhosis shows a mottled enhancement of the hepatic parenchyma and massive distention of the inferior vena cava and hepatic veins image. Unrecognized or untreated right heart failure or constrictive pericarditis can lead to acute or irreversible hepatic damage.
image
(Left) Axial arterial phase CECT shows arterioportal (AP) shunts as multiple, small, wedge-shaped, peripheral hypervascular lesions image.

image
(Right) More caudal arterial phase CT of the same patient shows an additional peripheral hypervascular lesion image. Also note the “corkscrew” enlarged hepatic arterial branch image and the widened fissures, all typical of cirrhosis.
image
(Left) Portal venous phase CT of same patient shows that all the peripheral hypervascular lesions have become isodense to background liver, typical of arterioportal shunts.

image
(Right) Delayed phase CT of the same patient shows there is no sign of washout from the sites of shunts. AP shunts are common within the cirrhotic liver. Imaging features that favor AP shunt over hepatocellular carcinoma (HCC) include peripheral and subcapsular location, small size, wedge shape, and no corresponding lesion on venous or delayed phase imaging.
image
(Left) Axial T2WI FS MR shows a small cirrhotic liver and ascites. Also shown are water-intensity lesions in the portal triads image that do not arborize (branch) as bile ducts and are spherical in shape, representing peribiliary cysts.

image
(Right) CT of a patient with cirrhosis shows that the portal vein branches image are surrounded by a collar of low density, some of which probably represent periportal edema. However, there are also discrete low-density focal lesions image that represent periportal cysts.
image
(Left) Axial NECT of a 78-year-old woman with chronic hepatitis C and cirrhosis shows a mass in the lateral segment that has 2 distinct components, including a fat-density left half image and a soft tissue-density right half image.

image
(Right) Axial T1WI fat-suppressed MR in the same patient shows low signal within the fatty component of the mass image and only relatively hyperintensity within the right lateral component image.
image
(Left) Axial T2WI of the same patient shows that the right component has MR characteristics of a dysplastic nodule, hypointense on T2WI image, while the other portion of the lesion shows relatively bright signal image on this non-fat-suppressed T2WI.

image
(Right) On this T2WI without fat suppression, the fatty component of the mass image is hyperintense and represents HCC, while the other half of the nodule is hypointense and is a dysplastic nodule image.
image
(Left) Fat-suppressed T2WI of the same patient shows signal loss from the fat-containing part of the mass image, which is strongly suggestive of HCC in a cirrhotic liver.

image
(Right) Axial T1WI GRE MR shows signal dropout from the HCC image. At resection, this was an HCC with fatty components within a larger dysplastic nodule. In addition, there are innumerable tiny cirrhotic regenerative nodules that are most evident as tiny hypointense foci on this GRE image.
image
(Left) On this arterial phase CECT in a patient with cirrhosis and HCC, the mass is heterogeneously hyperdense and hypervascular image.

image
(Right) On portal venous (hepatic) phase CECT in the same patient, the mass image is iso- to hypodense to the liver. These are typical features of HCC, particularly for a tumor detected as part of a surveillance program for patients with known cirrhosis who are at risk for developing HCC.
image
(Left) Arterial phase CECT of a 56-year-old man with chronic viral hepatitis shows a subtle hypervascular mass image. This proved to be HCC.

image
(Right) A more caudal CECT section in the same patient shows signs of cirrhosis, including widened fissures, a big caudate lobe, and an enlarged “corkscrew” hepatic artery image.
image
(Left) Portal venous (hepatic) phase image in the same patient shows the mass image, an HCC, much more clearly due to washout of contrast medium from the lesion.

image
(Right) In the same patient, the tumor was treated with intraarterial chemotherapy mixed with Ethiodol, an oily iodinated contrast medium that results in dense, very persistent enhancement of the tumor image. The tumor responded well to treatment, but liver function deteriorated, as evidenced by volume loss and development of ascites.
image
(Left) NECT shows a low-attenuation hepatic lesion image within the anterior and medial segments; the overlying hepatic capsule is retracted. These findings are characteristic of confluent hepatic fibrosis, which is common in advanced cirrhosis.

image
(Right) The focal confluent fibrotic lesion image in the same patient becomes almost isodense to the liver on this portal venous phase CECT. Also evident are varices image, splenomegaly, and ascites, typical manifestations of portal hypertension.
image
(Left) Axial CT of the same patient shows a massive paraumbilical collateral vein image and a thick-walled stomach image that might represent portal hypertensive gastropathy.

image
(Right) More caudal CT section of the same patient shows periumbilical varices (caput medusae) image, ascites, and mesenteric edema image that accentuates the mesenteric vessels and their enveloping fat.
image
(Left) Axial CECT shows typical signs of cirrhosis (wide fissures; increased caudate:right lobe ratio) and portal hypertension, including splenomegaly and ascites.

image
(Right) In the same patient, note the thickened wall of the ascending colon image, which simulates findings seen with colitis. On colonoscopy, there was no mucosal inflammation, only venous engorgement, known as portal hypertensive colopathy.
image
Axial CECT shows the nodular surface of a scarred liver with a fibrotic, small right lobe and enlarged caudate lobe and lateral segment. Splenomegaly, varices, and ascites are also noted.

image
Axial CECT shows a shrunken dysmorphic liver, ascites, and large varices.
image
Axial CECT shows large periumbilical varices (“caput medusae”), ascites, and mesenteric edema, all manifestations of portal venous hypertension.
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Axial NECT shows dysmorphic liver and ascites, along with dozens of hyperdense nodules, 0.5-2 cm in diameter, representing siderotic regenerative nodules.
image
Axial T2WI MR shows innumerable subcentimeter hypointense lesions throughout a cirrhotic liver, representing siderotic nodules.
image
Axial CECT in arterial phase shows a dysmorphic liver with widened fissures. The heterogeneous hypervascular lesion image is hepatocellular carcinoma.
image
Axial CECT shows a dysmorphic liver with atrophy of the right lobe and medial segment, hypertrophy of caudate, and irregular dilatation of intrahepatic bile ducts. This patient’s cirrhosis was due to primary sclerosing cholangitis.

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