Imaging Cirrhosis and Portal Hypertension Dr.hari Edited

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.



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



?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



Anatomy







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



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



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



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



Causes of Cirrhosis

Alcohol

Viral hepatitis

Biliary obstructionVeno-occlusive disease

Hemochromatosis

Wilson’s disease

Autommune

Drugs and toxins

Metabolic diseases

Idiopathic



Classification of Cirrhosis

WHO divided cirrhosis into 3

categories based on morphologicalcharacteristics 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 liverRarely contain portal tracts or efferent

veins

Liver is of uniform size or mildlyenlarged

Reflect relatively early disease



US FEATURES

Volumeredistibution

Coarse echotexture

Noduler surface

Nodules regenerativeand dysplastic

Portal Hypertension ascites, splenomegaly

and varices



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



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



CT Liver Cirrhosis with portal hypertension



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



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



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



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



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 veinthrombosis



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. Withvarices and risk is highest in 1st yr.



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



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



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



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



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



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



THANK YOU

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Imaging Cirrhosis and Portal Hypertension Dr.hari Edited