Imaging of Cirrhosis &

Portal Hypertension

Hari Soekersi


Department of Radiology-Faculty of Medicine
Padjadjaran University/Hasan Sadikin Hospital

INTRODUCTION
All may cause change in liver echogenicity on
US but, ultimately, diagnosis relies on
history, serology, and biopsy.
The changes in cirrhosis are similar on all
imaging modalities and include a shrunken,
irregular, and nodular liver.
Portal hypertension is a common sequela of
cirrhosis and an enlarged portal vein with
abnormal.
Doppler trace is seen on US, along with coexistent
varices, splenomegaly, and ascites
Patients with cirrhosis are at risk of developing HCC,
which sould be suspected in patients with increasing
right upper quadrant pain and rising serum alpha-
feto protein
The coarse liver echogenicity on ultrasound may
make it difficult to detect small tumours and if
clinical suspicion is high, CT or MRI is more sensitive

?Liver Disease Ultrasound



Focal abnormality Diffuse abnormality or normal


Full history,
serology,
biochemistry, and
posibly biopsy

Characteristic feature,e.g. cyst,
Hemangioma or very suggestive
clinical histrory,e.g abscess


Yes

Further lesion
characterization with
CT


Stop


No


CT appearances
characteristic, eg
haemangioma, metastasis


No


Yes


Consider MRI or
Ultraound-guided
biopsy

Stop


Anatomy
CIRRHOSIS
Many definitions but common theme is
injury, repair, regeneration and scarring
NOT a localized process; involves entire
liver
Primary histologic features:
1. Marked fibrosis
2. Destruction of vascular & biliary elements
3. Regeneration
4. Nodule formation
Pathophysiology
Primary event is injury to hepatocellular
elements
Initiates inflammatory response with
cytokine release->toxic substances
Destruction of hepatocytes, bile duct cells,
vascular endothelial cells
Repair thru cellular proliferation and
regeneration
Formation of fibrous scar
Pathophysiology
Primary cell responsible for fibrosis is
stellate cell
Become activated in response to injury and
lead to ed expression of fibril-forming
collagen
Above process is influenced by Kupffer cells
which activate stellate cells by eliciting
production of cytokines
Sinusoidal fenestrations are obliterated
because of ed collagen and EC matrix
synthesis
Pathophysiology
Prevents normal flow of nutrients to
hepatocytes and increases vascular
resistance
Initially, fibrosis may be reversible if
inciting events are removed
With sustained injury, process of
fibrosis becomes irreversible and leads
to cirrhosis
Causes of Cirrhosis
Alcohol
Viral hepatitis
Biliary obstruction
Veno-occlusive disease
Hemochromatosis
Wilsons disease
Autommune
Drugs and toxins
Metabolic diseases
Idiopathic

Classification of Cirrhosis

WHO divided cirrhosis into 3
categories based on morphological
characteristics of the hepatic nodules
1. Micronodular
2. Macronodular
3. Mixed
Micronodular Cirrhosis
Nodules are <3 mm in diameter
Relatively uniform in size
Distributed throughout the liver
Rarely contain portal tracts or efferent
veins
Liver is of uniform size or mildly
enlarged
Reflect relatively early disease
US FEATURES

Volume
redistibution
Coarse echotexture
Noduler surface
Nodules regenerative
and dysplastic
Portal Hypertension
ascites, splenomegaly
and varices
US SIGN OF LIVER CIRRHOSIS ARE
Increase echogenicity of liver parenchyma (due to
associated fatty infiltration)
Irregular liver surface
Loss of normal liver architecture,i.e loss of visibility of
hepatic blood vessels
Enlarged spleen
Enlarged posrtal vein>13 mm
Decreased or reversed portal vein flow on Doppler studies
Varices may be seen in the spelnic hilum and around the
head of the pancreas, and the recanalized umbilical vein
may be seen in the falciform ligament
Ascites

CT SIGN OF LIVER CIRRHOSIS
INCLUDE
Irregular contour
Decreased density with fatty changed or
increased density with haemochromatosis
Enlarged caudate lobe
Enlarged spleen
Varices: discrete round or tubular structures
that enhance with contrast
Ascites
CT Liver Cirrhosis with portal hypertension

Portal Hypertension (PH)

Portal vein pressure above the normal range
of 5 to 8 mm Hg
Portal vein - Hepatic vein pressure gradient
greater than 5 mm Hg (>12 clinically
significant)
Represents an increase of the hydrostatic
pressure within the portal vein or its
tributaries
Pathophysiology of PH
Cirrhosis results in scarring (perisinusoidal
deposition of collagen)
Scarring narrows and compresses hepatic
sinusoids (fibrosis)
Progressive increase in resistance to portal
venous blood flow results in PH
Portal vein thrombosis, or hepatic venous
obstruction also cause PH by increasing the
resistance to portal blood flow
Pathophysiology of PH
As pressure increases, blood flow decreases
and the pressure in the portal system is
transmitted to its branches
Results in dilation of venous tributaries
Increased blood flow through collaterals and
subsequently increased venous return cause
an increase in cardiac output and total blood
volume and a decrease in systemic vascular
resistance
With progression of disease, blood pressure
usually falls
Portal Vein Collaterals
Coronary vein and short gastric veins -> veins
of the lesser curve of the stomach and the
esophagus, leading to the formation of
varices
Inferior mesenteric vein -> rectal branches
which, when distended, form hemorrhoids
Umbilical vein ->epigastric venous system
around the umbilicus (caput medusae)
Retroperitoneal collaterals ->gastrointestinal
veins through the bare areas of the liver
Etiology of PH

Causes of PH can be divided into
1. Pre-hepatic
2. Intra-hepatic
3. Post-hepatic
Pre-hepatic PH

Caused by obstruction to blood flow at
the level of portal vein
Examples: congenital atresia, extrinsic
compression, schistosomiasis, portal,
superior mesenteric, or splenic vein
thrombosis
Post-hepatic

Caused by obstruction to blood flow at
the level of hepatic vein
Examples: Budd-Chiari syndrome,
chronic heart failure, constrictive
pericarditis, vena cava webs
Complications of PH

GI bleeding due to gastric and
esophageal varices
Ascites
Hepatic encephalopathy
Varices
Most life threatening complication is
bleeding from esophageal varices
Distal 5 cm of esophagus
Usually the portal vein-hepatic vein
pressure gradient >12 mm Hg
Bleeding occurs in 25-35% of pts. With
varices and risk is highest in 1st yr.
Conclusion liver cirrhosis and
portal hypertension
Ultrasoundthe first investigation
Liver cirrhosiscommonly leads to a
shrunken irregular liver with
splenomegaly and ascites
CT/MRImore sensitive than US in
detecting HCC in patients with
cirrhosis
CT & MRIsuperior to US, both in
lession detection and characterization
Portal venous anatomy:
(a). Main portal vein is formed by the union of the right and left portal
venous branches at the porta hepatis (b). The segmental branches of the
right and left portal veins are marked. H shape of the left portal venous
bifurcation made from the ascending and horizontal left portal vein and
the segmental branches to 2,3, and 4
a
b
Caudate lobe:
(a) Sagittal and (b), tranverse views show the
caudate lobe (CL) is separated from the left lobe
by fissure for the ligamentum venosum (arrows)
anteriorly. Posterior is the inferior vena cava
(IVC)
a
b
Normal lobar anatomy.
The right lobe of the liver (RL) can be separated
from the left lobe of the liver (LL) by the main
lobar fissure that passes through the gallblader
fossa (GB) and the inferior vena cava (IVC)
Portal Hypertension

a. Recanalized
paraumbilical vein
b. Enlarged coronary
vein
c. Extensive varices
d. Extensive varices
e. Sphlenic hilar
varices
f. Sphlenic hilar
varices
a
b
c
d
e
f
Cirrhosis-spectrum of appearance:
(a) Coarse parenchyma and innumerable tiny, hyperechoic
nodules. (b) coarse parenchyma and innumerable, tiny
hypoechoic nodules. (c) coarse parenchyma and surface
nodularity.
a
b
c
Cirrhosis-spectrum of appearance:
(d) sagittal image showing an enormous caudate lobe (e)
transverse sonogram shows that the right lobe is small and the
there is enlargement of the left lateral segment (f) subcostal
oblique view showing a tiny right lobe (g to i) of the liver, which
is separated from the large left lobe by the main lobar fissure
(arrows).
d e f
Cirrhosis-spectrum of appearance:
(g) and (h) show small end-stage livers with surface nodularity,
best appreciated in patients with ascites, as here. (i) There is
great variation in liver contour as shown here where a large
nodule protrudes from the deep liver border
g h i
Hepatic vein strictures-cirrhosis:
(a). Gray-scale image of hepatic vein shows a tapered luminal
narrowing (b) Color Doppler image shows appropriately directed
flow toward the inferior vena cava in blue. There is color
aliasing from the rapid velocity flow through the points of
narrowing
Congestive-cirrhosis:
The liver still has a normal parenchymal echo pattern,
but note the curved, bulging inferior border and the tiny
breaks in the capsule (arrows). A=ascites
Hepatic-cirrhosis. Child stage A
(a) autoimmune cirrhosis: minimal changes in the echo pattern, slightly wavy contour, increased
portal vein diameter (14.2 mm. cursors) (b) Hepatic cirrhosis in GAVE syndrome:bulky,slightly
wavy hepatic border with hepatomegaly. The patient presented clinically with recurrent gastric
bleeding. A Quick PT of 60% and a history of alcohol abuse. L=liver. K=Kidney
Advanced chronic viral hepatitis, hepatic cirrhosis
(a):Severe chronic hepatitis B:patchy structural transformation with poor
delineation of the hepatic veins (b) Child stage B hepatic cirrhosis in hepatic
C: coarse, echogenic areas of fibrosis with massive enlargement of the
caudate lobe
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