imaging cirrhosis and portal hypertension dr.hari edited
TRANSCRIPT
8/12/2019 Imaging Cirrhosis and Portal Hypertension Dr.hari Edited
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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.
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Doppler trace is seen on US, along with coexistentvarices, splenomegaly, and ascites
Patients with cirrhosis are at risk of developing HCC,
which sould be suspected in patients with increasingright upper quadrant pain and rising serum alpha-feto protein
The coarse liver echogenicity on ultrasound maymake it difficult to detect small tumours and ifclinical suspicion is high, CT or MRI is more sensitive
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?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 withCT
Stop
No
CT appearances
characteristic, eg
haemangioma, metastasis
No Yes
Consider MRI or
Ultraound-guided
biopsy
Stop
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Anatomy
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CIRRHOSIS
Many definitions but common theme isinjury, repair, regeneration and scarring
NOT a localized process; involves entireliver
Primary histologic features:1. Marked fibrosis
2. Destruction of vascular & biliary elements3. Regeneration
4. Nodule formation
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Pathophysiology
Primary event is injury to hepatocellularelements
Initiates inflammatory response withcytokine release->toxic substances
Destruction of hepatocytes, bile duct cells,vascular endothelial cells
Repair thru cellular proliferation andregeneration
Formation of fibrous scar
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Pathophysiology
Primary cell responsible for fibrosis isstellate cell
Become activated in response to injury andlead to ed expression of fibril-formingcollagen
Above process is influenced by Kupffer cells
which activate stellate cells by elicitingproduction of cytokines
Sinusoidal fenestrations are obliteratedbecause of ed collagen and EC matrix
synthesis
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Pathophysiology
Prevents normal flow of nutrients tohepatocytes and increases vascular
resistanceInitially, fibrosis may be reversible if
inciting events are removed
With sustained injury, process offibrosis becomes irreversible and leadsto cirrhosis
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Causes of Cirrhosis
Alcohol
Viral hepatitis
Biliary obstructionVeno-occlusive disease
Hemochromatosis
Wilson’s disease
Autommune
Drugs and toxins
Metabolic diseases
Idiopathic
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Classification of Cirrhosis
WHO divided cirrhosis into 3
categories based on morphologicalcharacteristics of the hepatic nodules
1. Micronodular
2. Macronodular
3. Mixed
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Micronodular Cirrhosis
Nodules are <3 mm in diameter
Relatively uniform in size
Distributed throughout the liverRarely contain portal tracts or efferent
veins
Liver is of uniform size or mildlyenlarged
Reflect relatively early disease
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US FEATURES
Volumeredistibution
Coarse echotexture
Noduler surface
Nodules regenerativeand dysplastic
Portal Hypertension ascites, splenomegaly
and varices
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US SIGN OF LIVER CIRRHOSIS ARE
Increase echogenicity of liver parenchyma (due toassociated fatty infiltration)
Irregular liver surface
Loss of normal liver architecture,i.e loss of visibility ofhepatic 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 thehead of the pancreas, and the recanalized umbilical veinmay be seen in the falciform ligament
Ascites
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CT SIGN OF LIVER CIRRHOSIS
INCLUDEIrregular contour
Decreased density with fatty changed or
increased density with haemochromatosisEnlarged caudate lobe
Enlarged spleen
Varices: discrete round or tubular structuresthat enhance with contrast
Ascites
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CT Liver Cirrhosis with portal hypertension
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Portal Hypertension (PH)
Portal vein pressure above the normal range
of 5 to 8 mm HgPortal vein - Hepatic vein pressure gradient
greater than 5 mm Hg (>12 clinicallysignificant)
Represents an increase of the hydrostaticpressure within the portal vein or itstributaries
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Pathophysiology of PH
Cirrhosis results in scarring (perisinusoidaldeposition of collagen)
Scarring narrows and compresses hepaticsinusoids (fibrosis)
Progressive increase in resistance to portalvenous blood flow results in PH
Portal vein thrombosis, or hepatic venousobstruction also cause PH by increasing theresistance to portal blood flow
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Pathophysiology of PH
As pressure increases, blood flow decreasesand the pressure in the portal system istransmitted to its branches
Results in dilation of venous tributaries
Increased blood flow through collaterals andsubsequently increased venous return cause
an increase in cardiac output and total bloodvolume and a decrease in systemic vascularresistance
With progression of disease, blood pressure
usually falls
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Portal Vein Collaterals
Coronary vein and short gastric veins -> veinsof the lesser curve of the stomach and theesophagus, leading to the formation ofvarices
Inferior mesenteric vein -> rectal brancheswhich, when distended, form hemorrhoids
Umbilical vein ->epigastric venous systemaround the umbilicus (caput medusae)
Retroperitoneal collaterals ->gastrointestinalveins through the bare areas of the liver
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Etiology of PH
Causes of PH can be divided into
1. Pre-hepatic
2. Intra-hepatic
3. Post-hepatic
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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 veinthrombosis
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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
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Complications of PH
GI bleeding due to gastric and
esophageal varices
Ascites
Hepatic encephalopathy
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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. Withvarices and risk is highest in 1st yr.
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Conclusion liver cirrhosis and
portal hypertensionUltrasoundthe first investigation
Liver cirrhosiscommonly leads to a
shrunken irregular liver withsplenomegaly and ascites
CT/MRImore sensitive than US in
detecting HCC in patients withcirrhosis
CT & MRIsuperior to US, both in
lession detection and characterization
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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 theright and left portal veins are marked. H shape of the left portal venous
bifurcation made from the ascending and horizontal left portal vein andthe segmental branches to 2,3, and 4
a b
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Caudate lobe:(a) Sagittal and (b), tranverse views show thecaudate lobe (CL) is separated from the left lobeby fissure for the ligamentum venosum (arrows)
anteriorly. Posterior is the inferior vena cava
(IVC)
a b
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Normal lobar anatomy.
The right lobe of the liver (RL) can be separatedfrom the left lobe of the liver (LL) by the mainlobar fissure that passes through the gallblader
fossa (GB) and the inferior vena cava (IVC)
Portal Hypertension
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Portal Hypertension
a. Recanalized
paraumbilical veinb. Enlarged coronary
vein
c. Extensive varicesd. Extensive varices
e. Sphlenic hilarvarices
f. Sphlenic hilarvarices
a
b
c
d
e
f
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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
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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
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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
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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
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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
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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
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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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