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Liver Doppler

Rebeca Lopez-Alonso MD

Department of Medical Imaging


Rambam Health Care Center and Bruce and Ruth
Rappaport Faculty of Medicine, Technion, Israel Institute
of Technology
Haifa, Israel
Learning Targets
• Portal hypertension

• Budd- Chiari syndrome

• TIPS evaluation
Portal hypertension

• Clinical suspicion: ascites, splenomegaly,


varices

• PHT is defined by direct portal vein pressure


more than 5 mm Hg greater than IVC
pressure
Portal hypertension
• Prehepatic (inflow) most common : Portal vein
and splenic vein thrombosis

• Intrahepatic (liver, sinusoids, and hepatocytes)


most common : Cirrhosis , but also hepatic
fibrosis, malignancies, veno-occlusive disease,
lymphoma, and sarcoidosis

• Posthepatic (outflow) including CHF, IVC


obstruction, and Budd-Chiari Syndrome
Portal hypertension
• Dilatation of the portal vein is a potential
indicator of elevated pressure

• There is controversy regarding the normal


value , so the parameter is not heavily relied on

• In general, an unusually large portal vein is a


good sign of PHT, but a normal size portal vein
does not exclude the diagnosis
Portal hypertension
• The PV should be less than or equal to 13
mm in quiet respiration and increase up to 50%
during deep inspiration

• Goyal et al found that the upper limit for portal


vein diameter was 16 mm within overall
sensitivity of 72% and specificity of 100%
(JUM 1990;9:45-48)
Portal hypertension
• The normal portal vein
demonstrates an
undulating hepatopedal
flow

.Normal portal venous Doppler waveform

Color Doppler of normal right portal vein, flow direction is


.hepatopedal (into the liver)
.
Portal hypertension
• In PHT the PV looses
its undulatory pattern
and becomes
monophasic, as PHT
increases the flow
becomes biphasic
and finally
hepatofugal
Portal hypertension
• Flow reversal occurs , first , in isolated peripheral
portal vein branches
• Eventually , flow in the main portal vein also reverses
, by the time this is seen PHT is severe
• Most patients with PHT maintain hepatopedal flow in
the main portal vein

• Portal vein velocities decrease


<16 cm/sec ( normal 16-40 cm/sec)
(McNaughton and Abu-Yousef . Radiographics 2011;31:161-188 )
Portal hypertension
• Slow flow that alternates between hepatopedal
and hepatofugal
How ever :
• In CHF : pulsatile high velocity flow + (dilated
IVC and hepatic veins)
Normal To and Fro Reversed
Flow flow Flow
Portal hypertension

• Hepatic artery becomes larger and tortuous


Portal hypertension
Portal systemic collaterals

• Reliable and widely used to diagnose PHT


Portal systemic collaterals
The coronary vein

• The most prevalent


collateral in PHT , its
presence implies an
increased risk for varicial
hemorrhage
• Gastroesophageal Junction
Portal systemic collaterals
The umbilical vein
• Normally is an obliterated
fibrous remnant in the
ligamentum teres.

• In PHT it recanalizes with


hepatofugal flow

• The umbilical vein travels


from the umbilical segment
of the LPV inferiorly to
communicate with the
inferior epigastric veins
Portal systemic collaterals
Splenorenal collaterals

• Multiple collaterals around the splenic


hilum and an enlarged left renal vein

• Intestinal, hemorrhoidal
Portal systemic collaterals
Gallbladder wall varices
Portal vein thrombosis
• PVT has been associated with malignancy,
hypercoagulable states, pancreatitis,
hepatitis

• Cirrhosis is a predisposing condition to


PVT due to increases portal pressure and
reduced portal flow
Portal vein thrombosis
• Thrombus within the lumen
( anechogenic material in a
widened caliber: when acute)

• Color Doppler will demonstrate


partial or complete occlusion

• Spectral Doppler will


demonstrate increased velocities
if there is partial occlusion as the
blood courses around the clot
Portal vein thrombosis
• Presence of arterial Spectral Doppler in
portal vein thrombus signifies tumor invasion.
A partially recanalized portal vein will give
portal venous signals from the vascular
channels in the clot.
Cavernous transformation
• Numerous worm-like vessels at
the porta hepatis representing
periportal collaterals
• Some works report 1-12 months
or more as the time needed for
development of Cavernous
transformation
(Diagnostic Ultrasound 2011 . C. Rumack, S. Wilson, J
Charboneau, D Levine)
(McNaughton and Abu-Yousef . Radiographics 2011;31:161-188 )
(Am J Gastro 1976;65:3-11)

• Gaetano et al reported 6-20 days


(AJR 1995;165:1151-1155 )
Cavernous transformation
• Color flow Doppler will
demonstrate flow in the
vessels and spectral
Doppler will indicate
portal venous flow;
otherwise they may be
mistaken for biliary
dilatation.
Normal To and Fro Reversed
Flow flow Flow
Budd-Chiari Syndrome

• Hepatic venous outflow obstruction


Budd-Chiari Syndrome
• Occlusion of the lumen of the hepatic
veins with or without occlusion of the IVC
lumen

There are right, middle and left hepatic


veins with a variable accessory right.

The middle and left hepatic veins


frequently share a short common trunk at
the inferior vena cava (IVC) confluence
Budd-Chiari Syndrome

Normal flow in the hepatic veins is triphasic reflecting cardiac


activity, with forward flow from the liver to the atrium during atrial
relaxation and again during tricuspid valve opening , and a small
reversal during atrial contraction

In BCS flow in hepatic veins and IVC changes from phasic


to absent, reversed, turbulent or monotonous
Budd-Chiari Syndrome
• Causes: coagulation abnormalities,
trauma, tumor extension, pregnancy ,
obstructing membranes
Budd-Chiari Syndrome
SPECIFIC SIGNS:
Non-visualization of veins
Fibrous cord
Thrombosis
Stenosis
IVC web
Budd-Chiari Syndrome
• Large liver (acute phase)

• Enlargement of caudate
lobe

• IVC may be narrowed d/ t


compression by the
enlarged caudate lobe
Budd-Chiari Syndrome

• Acute phase ( not common ):


Intraluminal
echogenicity filling a
widened lumen
Budd-Chiari Syndrome
Budd-Chiari Syndrome
• Partial or complete
inability to see the
hepatic veins

• Stenosis with proximal dilatation


• Thickened walls
• Fibrous cord replacing the vein
Budd-Chiari Syndrome
Budd-Chiari Syndrome
• Monotonous (dampened) flow is seen in
cirrhosis and even in fatty liver , and veins
may be difficult to locate due to parenchymal
compression. Color Doppler should be used
to localize veins which are invisible on
grayscale

• Is there BCS ? ?
Budd-Chiari Syndrome
Specific diagnostic
criterion:

• Abnormal intrahepatic
venous collaterals :
Turbulent vascular
structures extending to the
liver surface
Budd-Chiari Syndrome
Budd-Chiari Syndrome
Budd-Chiari Syndrome
• Portal flow may be slowed or reversed
• Portal hypertension
• Ascites

• Chronic form : Cirrhosis, irregularities of the liver


contour , regenerative nodules ,splenomegaly and
porto-systemic collaterals
Budd-Chiari Syndrome
• Budd-Chiari can be excluded only when
the patency of the major hepatic vein
branches can be confirmed without
question.
Treatment
• Thrombolysis
• Angioplasty
• Transjugular intrahepatic portosystemic
shunting –TIPS
• Liver transplantation
TIPS
Transjugular Intrahepatic
Portosystemic shunt
• Most popular technique for relief of
symptomatic PHT ( specifically GI bleeding
from varices ) and for reduction of ascites
• Treatment for Budd –Chiari Syndrome
• Performed percutaneously with insertion of
an expandable metal stent
TIPS
Transjugular Intrahepatic
Portosystemic shunt
• A transjugular puncture needle is passed
from the hepatic vein (RT) to the
intrahepatic portal vein (RT) and a shunt is
created with a bridging stent

• Doppler sonography moniters TIPS patency


– immediately after procedure , 3 month later
and as indicated clinically
TIPS
TIPS
TIPS
TIPS
• It has been reported that the patency
rate at one year without revision ranges
from 23-66%. With intervention for
occlusion or stenosis by balloon
angioplasty and thrombolysis, the
patency rate at one year is about 85%.
Sonographic evaluation-
TIPS
• Measure the angle corrected stent
velocity at three points along the stent
and in the MPV
• Evaluate the direction of flow in the
intrahepatic portal veins and the
involved hepatic vein
Normal postprocedural Doppler
• Color Doppler flow
should fill the entire
lumen of the shunt

• High velocity with


some degree of
pulsatility throughout
the stent
(mean peak velocity
135-200 cm/sec)
( Foshager MC et al ,AJR 1995 :165;1-7)
Normal postprocedural Doppler

• Increased velocity in main


portal vein (37-47 cm/sec)
(stent serves as a low
resistant conduit )

( Hazkal ZJ et al, J Vasc Interv Rad


1997:8:549-556)
(Murphy TP et al , J Vasc Interv Rad
1998:9;275-281)
Normal postprocedural Doppler

• Hepatofugal flow in intrahepatic


portal venous branches
(draining into the systemic
circulation)

• MPV remains hepatopedal

• Increased hepatic artery peak


systolic velocity
TIPS

Hepatopetal flow in MPV Monophasic pulsatile flow


Hepatofugal flow in RPV Velocity: 106 cm/sec
Diagnostic Ultrasound 2011 . C. Rumack, S. Wilson, J Charboneau, D Levine
TIPS malfunction - direct signs
• No flow
consistent with
shunt
thrombosis or
occlusion
TIPS malfunction - direct signs
• Peak shunt velocity : <90 or >190 cm/sec

• Change in peak shunt velocity : decrease of


>40 cm/sec or increase of >60 cm/sec
TIPS

Mid TIPS Mid TIPS Distal TIPS


TIPS malfunction - direct signs

• Main portal vein velocity <30 cm/sec


TIPS malfunction - direct signs
• Reversal of flow in hepatic vein away
from the IVC suggesting hepatic vein
stenosis

• Hepatopedal intrahepatic portal venous


flow
TIPS
TIPS malfunction – secondary signs

• Reaccumulation of ascites

• Reappearance of varices

• Reappearance of recanalized
paraumbilical vein
How Good is Ultrasound
? for TIPS
• The overall impression of the radiologist was reported
to have a sensitivity of 92% and specificity of 72% in
detecting abnormal shunts (Kanterman RY et al. AJR 1997 )

• A combination of criteria showed a sensitivity of 94%


for shunt stenosis ( Zizka J et al AJR 1994)
Conclusions
• Combination of grayscale sonography with Doppler
provides a valuable mean for investigating patients
with suspected vascular liver abnormalities

• Portal hypertension
• Budd – Chiari syndrome
• TIPS malfunction

• Comprehension of the hemodynamic changes and


awareness of the combination of the sonographic
expected findings is important in leading us to the
correct diagnosis.

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