IMAGING IN CIRRHOSIS

INTRODUCTION
DEFNITION.
cirrhosis is the generic term used to describe
chronic liver disease involving diffuse parenchymal
necrosis, active formation of connective tissue
leading to fibrosis, and nodular regeneration of the
liver resulting in dis organisation of hepatic
lobular and vascular architecture.

- It is the common end response of the liver to a

variety of insults and injuries.
CAUSES OF CIRRHOSIS
Alcoholic cirrhosis-60-70 %
Viral ,post necrotic - 10%
Biliary cirrhosis, 5-10%
Pigment cirrhosis(hemochromatosis)- 5%
Cardiac failure
Constrictive pericarditis
Hepatic vein obstruction
Malnutrition
Hereditary –wilsons, alpha 1 AT def,
Drugs- methoterxate, alpha methyl dopa,
6 MP,isoniazid
PATHOPHYSIOLOGY
Hepatocellular death
Regeneration
Progressive fibrosis

The induction of fibrosis occurs with activation of

hepatic
stellate cells, resulting in formation of increased
amounts
of collagen & other components of extracellular
matrix.

Stimuli : 1.Chr.inflammation – cytokines like TNF,

Lymphotoxin, IL-1
1.Micronodular –
-equal sized, 3 mm diameter, involve all
lobules,
2.Macronodular –
-variable sized , usually 3mm – 3cm, focal
and may not involve all lobes.

3.Mixed
1)The entire parenchymal architecture is
disorganised by interconnecting fibrous scars
formed in response to hepatocyte injury and loss.
2)Fibrous bands may be of porto-central / porto-
portal.
3)Micro /macro nodules are due to regenerating
activity.
-siderotic-more malignant potential
-non siderotic
- macronodules- more prone for malignant
transformation
4) Vascular architecture is also reorganised by
parenchymal damage and scarring with formation
of A-V interconnections
ULTRASOUND:CIRRHOSIS
-Nodular hepatic contour.
-Enlarged caudate lobe and lateral segment of left
lobe
-Atrophy of the right and quadrate lobes
-Prominence of fissures and porta hepatis
-Portal HTN
varices, ascites and splenomegaly
-Fatty infiltration
-Colonic interposition
-Altered gall bladder angle
-Regenerating nodules
3/19/2020
The senstivity of USG in
the diagnosis of cirrhosis
based upon arhitecture
is b/n 65-95%
Irregularity of liver
surface- 88 % senstivity
NODULARITY.

USG can reliably differentiate micronodular from

macronodular cirrhosis.
The presence of surface nodularity correlates
pathologically with sinusoidal obstruction to
portal flow and the development of portal HTN.
Although ultrasound has upto 98% PPV in the
diagnosis of diffuse parenchymal disease, it cannot
reliably differentiate fat from fibrosis.
On doppler ,there is flattening of the hepatic
venous waveforms due to decrease compliance of
the fibrotic liver.
 VOLUME REDISTRIBUTION.
As measured sonographically , segment IV undergoes
atrophy,
-Normal mean dia =43 +- 8mm,
-Cirrhotic liver =28+-9mm,
Right lobe/left lobe ratio
- Normal =1.44
- Cirrhotic= <1.3
(senstivity-74%, specificity-100%, accuracy-93%)
- Hepatitis related cirrhosis= 1.17
- Non hepatitis related cirrhosis=1.25
Mesenteric , omental and retroperotoneal edema can
be seen in patients with cirrosis and portal hypertension
, as the increased hydrostatic pressure cause seepage of
fluid in the mesentery.
Liver dysfunction also produce water overload due to
hypoalbunemia, and decreased aldosterone catabolism.
These features are responsible for the development of
ascites, mesenteric edema, pleural effusion .
Siderotic nodules or, Gamna Gandy bodies may rarely
be identified as hyperechoeic masses in the spleen.
Incidence of gall stones (mostly pigment stones) are
also increased in pts with cirrhosis.
CT:CIRRHOSIS
Fatty infiltration , which is the initial
feature of alcoholic liver disease is well
displayed.
Overall liver volume is diminished,
regenerating nodules infrequently
demonstrated on ct.
Nodularity of the liver contour, fibrous
scarring, non uniform lobar atrophy /
hypertrophy can be demonstrated ,
particularly in the presence of ascites.
Ct is insensitive in depicting the transformation
process of regenerating nodules to dysplastic
nodules.
Occasionally large dysplastic nodules can be
identified on unenhanced ct.

Cirrhotic liver often demonstrates less contrast

enhancement than normal liver and appears
inhomogenous due to underlying regeneration ,
fibrosis and altered portal venous blood flow.
 If the caudate lobe/ right lobe ratio exceeds 0.65,
diagnosis of cirrhosis can be made with 96 %
confidence,
The normal caudate lobe/rt lobe ratio is 0.37. and the
mean ratio in cirrhotic livers is 0.83
In patients with biliary cirrhosis in addition to
marked atrophy of the Rt lobe there is atrophy of the
lateral lobe as well along with hypertrophy of the
caudate lobe, giving it a square shaped configuration
on CT.
 There is colonic interposition b/n the liver and the
anterolateral abd wall/ diaphragm.
The gall bladder and interlobar fissure undergoes
counterclock wise rotation , and becomes more lateral
and superficial structure- more prone to injuries during
blind liver biopsy, surgery and percutaneous transhepatic
procedures.
 Normal gall bladder angle is 46 *, it is reduced to 35 *,
 Because of these parenchymal changes, it was difficult
to detect even large foci of HCC, but with the advent of
MDCT with the ability to optimally time the contrast
administration and scanning and detect arterial phase
enhancement in HCC , has substantially increased the
ability to detect small tumours in cirrhotic patients.
These tumours are visualised as small enhancing foci
during the arterial phase of contrast administration.
MRI:CIRRHOSIS
MR can often detect cirrhosis at an early stage than
ct and ultrasound.
Early in the evolution of cirrhosis , MR imaging can
demonstrate subtle changes such as fine strands of
fibrosis and enlargement of hilar and periportal
space.
The role of MR imaging in cirrhotic patients is to
assess liver size, evaluate the effects of portal HTN, to
screen for HCC and to better characterise masses
detected in the liver by other techniques.
As with CT , MR can detect nodular regeneration
only when siderotic nodules are present.
However MRI is more sensitve than CT in displaying
siderotic nodules which appear as small dark nodules
on T2 weighted, and similar appearance on T1- weighted
images.
MR imaging is also useful for differenciating
dysplastic nodules from HCC.
Large dysplastic nodules are hyperintense to adjacent
liver on T1 weighted and hypointense on T2 weighted
images.
MR imaging is useful in discrimination of alcoholic
and virus induced cirrhosis.
 The volume of caudate lobe is significantly larger
and visualization on notch in the right posterior
lobe is more common with alcoholic cirrhosis.
MR elastography can determine the degree of
liver fibrosis, pts with liver fibrosis have elevated
MR elastographic liver stiffness measurements.
PORTAL HYPERTENSION
Normal portal venous pressure is 5 to 10 mm of Hg .
PHTN defined by
1. Wedge hepatic venous pressure or direct portal
venous pressure more than 5mm Hg greater than IVC
pressure,
2. splenic vein pressure > 15mm of Hg,
3.portal venous pressure > 30cms of H2o
Presinusoidal PHTN – hepatic wedge pressure is
normal.
Cirrhosis is the M/C cause of
intrahepatic(sinusoidal) PHTN and accounts for >90%
Sonography plays a key role in the management of
patients with cirrhosis in the detection of PHTN and
portosystemic collateral circulation. Features include
ascites, splenomegaly and development of collateral
pathways.
Measuring portal vein size and observing respiratory
variation in the superior mesenteric and splenic veins
are simple and sensitive methods for detecting portal
htn.
Normal dia of pv=0.6 – 1.2 cms.
In cirrhotics mean pv = 1.2 cms
A patent pv > 1.3 cms is 100% specific for PHTN
patency of umblical vein s seen in 58% of pts with
PHTN
Splenomegaly with dialatation of splenic vein radicles -
When the resistance to flow in the portal venous
channels exceeds the resistance to blood flow in small
communicating channels between portal and systemic
circulations, porto systemic collaterals forms.
Collateral vessels can be seen sonographically in 88%
pts with P HTN.
 Various porto- systemic collaterals are-
 1.Distal oesophagus :
oesophageal tribuaries of left gastric vein (portal)
oesophageal tributaries of hemiazygous vein
(systemic)
2.Around the umbilicus:
paraumbilical vein (portal)
sup and inf epigastric veins (systemic)
3.Lower rectum and anal canal:
superior rectal vein (portal)
middle and inferior rectal veins (systemic)
4.Retrocolic:
rt and left colic veins (portal)
rt and left renal veins( systemic)
5.Retroperitoneum
tributaries of ssuperior and inferior mesenteric
veins(portal)
posterior abdominal and subdiaphragmatic
veins(systemic )
Most important varices involve the coronary veins and
their associated esophageal varices.
These are identified as circular/ tubular sonolucencies
in the region of GE junction and lesser curvature.
On doppler US- the normal portal vein demonstrates
an undulating hepatopetal flow(towards the liver), an
increase of < 20% in the diameter of portal vein in deep
inspiration indicates portal HTN, 81% senstivity and
100% specificity.
Mean portal flow velocity is approx 15-18 cms/sec and
varies with respiration and cardiac pulsations.
As portal HTN develops the flow in the portal vein
loses its undulating pattern and becomes monophasic.
As the severity of portal htn increases, flow becomes
3/19/2020
CT is also excellent in demonstrating portal htn
with its attendent varices, splenomegaly and
ascites.
On CT portosystemic collaterals appear as
tortuous, tubular, or round soft tissue masses that
may be mistaken for lymphnodes on noncontrast
scans.
Esophageal and gastric varices can be inferred
from CT scans when marked enhancement is seen
in association with mural thickening .
Ct is superior in demonstrating retroperotoneal
varices and in depicting azygous, hemiazygous,
pericardial and periesophageal varices that can
simulate mediastinal mass.
The splenic index is a good indicator of the severity
of esophageal varices and hepatic functional reserve
in cirrhotic patients.
A splenic index (=length x height x width) greater
than 963 cc is a good indicator of the presence of
esophageal varices at risk for bleeding.
Thickening of the small bowel and specifically rt
sided large bowel occur specifically due to portal htn.
The increased pressure within the superior
mesenteric vein leads to the release of inflam
.mediators such as IL-1, NO, leads to colitis which
simulate IBD.
3/19/2020
MR imaging is uniquely suited for the depiction of
large vascular collaterals because of natural contrast
between flowing blood and surrounding soft tissues.

The most successful MR imaging techniques for

delineating abdominal blood vessels are MR
angiographic techniques that can be used with or
without gadolinium injection.

Collateral pathways are demonstrated as tortuous

structures of high signal intensity on MR angiograms.

Direct sagittal scans are particularly useful for imaging

the paraumbilical vein , and coronal scans are helpful for
esophageal and mesenteric varices.
REFERENCES
TEXT BOOK OF Gastrointestinal Radiology- Gore
and Levine, vol 2
TEXT BOOK OF RADIOLOGY AND IMAGING –
DAVID SUTTON, 7TH Edition.
Text book of Diagnostic Radiology-Grainger and
Allison.
CT and MRI of the whole body-Haaga, 5th Edition.
THANK YOU