Doppler ultrasound is useful for assessing portal hypertension and liver cirrhosis. Key findings include increased portal vein diameter (>13mm), decreased increase in splenic or portal vein diameter with respiration, reversed or biphasic portal flow, increased hepatic artery flow and resistive index, altered hepatic vein waveforms, splenomegaly (>13cm), and presence of portosystemic collateral veins. Together these Doppler ultrasound metrics can diagnose and characterize portal hypertension noninvasively.

1. ROLE OF DOPPLER IN PORTAL
HYPERTENSION & LIVER CIRRHOSIS
DR. NISHIT VIRADIA

2. Definition
• Portal hypertension is an increase in pressure
in the portal vein which is caused by
obstructed blood flow through the liver
– Normal pressure 5-15mmHg
• Problems
– Blood will find a way to bypass (portosystemic
collaterals) the liver to reach the heart or there is
too much pressure “upstream”

3. Etiology
• Hyperkinetic
I. Arterioportal fistula or malformation
• Increased portal venous resistance
1. Intrahepatic
a. Presinusoidal: Non-cirrhotic portal fibrosis, hepatic schistosomiasis,
congenital hepatic fibrosis, sarcoidosis, and lymphoma
b. Postsinusoidal hepatic cirrhosis (alcoholic, postnecrotic) and veno-
occlusive disease
2. Extrahepatic
a. Prehepatic: Cavernous transformation (of portal vein) and splenic or
superior mesenteric vein obstruction(segmental PHT).
b. Posthepatic: Hepatic vein obstruction, suprahepatic inferior vena
caval obstruction, congestive heart failure, and constrictive
pericarditis

4. • The common feature to all the causes is an increased
resistance to portal venous flow, although in a few
cases, increased inflow into the portal venous system
is present.
• The prehepatic causes of PH include portal vein
thrombosis (PVT) and portal compression or
occlusion by biliary and pancreatic neoplasms and
metastases.
• PH may be caused by increased flow secondary to
arterioportal fistula, pancreatic arteriovenous
malformations, and massive splenomegaly.

5. •Advances in ultrasound instrumentation have
made direct, noninvasive interrogation of
portal vein flow possible.
•Ultrasound examination of the portal venous
system (portal vein, splenic vein and superior
mesenteric vein is successful in 93% to 95% of
patients.

6. Normal portal venous flow direction and waveform. Direction of flow in normal portal
veins is antegrade, or hepatopetal, which corresponds to a waveform above the baseline
at spectral Doppler US.

7. Certain ultrasound parameters have been
identified that permit sonographic diagnosis of
portal hypertension.
 portal vein diameter
response of the portal, splenic or superior
mesenteric veins to respiration
portal flow direction
portal flow velocity and waveforms
 spleen size
The presence of portosystemic collaterals.

8. Portal vein diameter
• In normal individuals the portal vein diameter
does not exceed 13 mm in quiet respiration,
measured where the portal vein crosses anterior
to the IVC.
• Respiration and patient position greatly affect the
size of the portal vein and its tributaries;
therefore, diagnostic measurements must be
standardized by examining the patient in the
supine position and in a state of quiet respiration.

9. • Under these circumstances, a portal vein
diameter exceeding 13 mm indicates portal
hypertension with a high degree of specificity
(100% reported) but with low sensitivity (45%-
50%).
• Sensitivity is increased by evaluating the
response of the splenic or superior mesenteric
veins to respiratory maneuvers.

10. The portal vein (PV) is measured where it crosses anterior to the inferior
vena cava (IVC). With the patient supine and breathing quietly, the portal
vein diameter (cursors) does not normally exceed 13 mm.

11. In the same
subject, the
diameter of the
splenic
vein (SPV)
increases more
than 70% from
quiet
respiration to
deep
inspiration

12. Features of portal hypertension, In this 48-year-old patient with alcohol-induced
liver disease, the portal vein diameter (cursors) is 18 mm with the patient supine
and breathing quietly

13. The diameter of the
splenic vein increases
only 6% from quiet
respiration to deep
inspiration

14. Portal Flow Direction
and Velocity
• In normal individuals, portal flow is
hepatopedal (toward the liver) throughout the
entire cardiac cycle.
• Mean flow velocity is about 15 to 18cm/sec.
• Portal flow velocity varies with cardiac activity
and respiration, giving the portal waveform an
undulating appearance

15. • With the development of portal hypertension, portal flow
velocity may decrease and velocity fluctuations may
disappear(flow becomes continuous).
• As portal pressure increases, portal vein flow may become
to and fro (biphasic) or the flow direction may reverse
(hepatofugal flow)
• If splenorenal collaterals are the primary mode of portal
decompression, flow may reverse in the portal vein.
• However, a large umbilical vein collateral is the primary
mode of decompression, splenic and portal vein flow may
remain normal (hepatopedal), because the diverting
collateral (the umbilical vein) originates in the left portal
system.

16. In patient with portal hypertension, splenic vein flow (arrow) is reversed (toward
the spleen). (The spleen is not visible in this view.)

17. Increased Hepatic Artery Flow
• Under normal circumstances, the liver receives about 70% of its
blood supply from the portal vein and 30% via the hepatic artery.
• When portal hypertension is caused by cirrhosis, hepatic artery flow
may increase substantially as compensation for diminished portal
vein flow.
• hepatic artery, which is visibly enlarged on color flow examination
and shows substantially increased blood flow on Doppler
interrogation.
• Unfortunately, the hepatic artery does not have the capacity to
make up for the loss of portal vein flow, and persistent hepatic
ischemia develops, representing a significant cause of ongoing
hepatocyte damage and progression of fibrotic scarring

18. • HA has a systolic velocity of approximately 30 to 40
cm/sec and diastolic velocity of 10-15 cm/sec
• Hepatic artery diastolic velocity normally is less than
the peak portal vein velocity of about 18 cm/sec.
• If hepatic arterial diastolic velocities greater than the
portal vein, we should suspect parenchymal disease
in the liver.
• Measurements of the right hepatic artery are taken
where it crosses the portal vein near the porta
hepatis.

19. • The resistive index of the hepatic artery in a fasting subject varies
from 0.55 to 0.81 (mean 0.62-0.74). RI increases in normal subjects
after a meal.
• The pulsatility index (PI) of the hepatic artery varies from 1.16 to
1.24 in normal subjects.
• The RI and PI of the hepatic artery are increased in chronic liver
disease due to an increase in intrahepatic vascular resistance.
• The most commonly used measurement is the hepatic artery RI
which is an indirect estimation of the impedance of arterial flow
into the liver. In patients with advanced hepatic cirrhosis and
chronic hepatitis the normal increase in RI after a meal is also
absent.

20. Spectral Doppler trace from a normal hepatic artery

21. Assessment of Hepatic Veins
• The hepatic veins (usually three in number) are thin walled
structures enclosed by hepatic parenchyma.
• They drain into the inferior vena cava immediately inferior to the
diaphragm.
• Doppler spectral traces from normal hepatic veins have a triphasic
appearance consisting of two large antegrade waves that represent
atrial and ventricular diastole and a small retrograde wave that
occurs in atrial systole.
• Antegrade flow direction is defined as towards the heart and
retrograde as away from the heart.
• Flow patterns in the hepatic veins depend on both cardiac
physiology and liver histology.
• Altered hepatic vein waveforms are seen in at least 50% of patients
with cirrhosis with flattening of the phasic oscillations. Similar
changes are also found in Budd-Chiari syndrome.

22. Dopper study showing the normal hepatic veins with the triphasic flow pattern

23. Splenomegaly
• It is an important manifestation of portal
hypertension.
• The size of the spleen does not correlate well
with the level of portal pressure
• splenomegaly may be caused by numerous
conditions in addition to portal hypertension.
• The spleen is best measured in a coronal plane. A
maximal cephalocaudal measurement exceeding
13 cm indicates enlargement with a high degree
of reliability.

24. PORTOSVSTEMIC VENOUS
COLLATERALS
• Porto systemic venous collaterals are important
finding. Its presence is a clear indication of portal
hypertension.
• The exception to this rule is collateralization related to
isolated splenic or mesenteric vein occlusion.
• Portosystemic collaterals develop out of necessity in
patients with portal hypertension, for blood from the
gut must have an alternative means to reach the heart
when flow through the liver is restricted.
• Ultrasound is reported to visualize 65% to 90% of
portosystemic collaterals

27. Umbilical vein collateral. A, This transverse sonogram through the ligamentum teres shows a central
vessel (arrow) that could be either normal or abnormal. B, Longitudinal color Doppler sonogram
demonstrates that flow in this vessel (arrow) is hepatopedal indicating that the umbilical vein is
functioning as a portosystemic collateral.

28. Continuous flow away from the liver is confirmed with the Doppler spectrum.

29. Coronary vein collateral. A longitudinal (parasagittal) sonogram shows a
dilated coronary vein at its attachment to the portal vein (PV), near the
portosplenic junction.

30. Gallbladder wall collateral. Longitudinal sonogram in a patient with cirrhosis
shows large varices (arrows) within the gallbladder wall. Ascites surrounds the
gallbladder.

31. Left gastric collaterals. Collateral veins are seen dorsal to the left lobe of the liver.

32. Large, tortuous collateral veins (arrows) are seen in the vicinity of the gastroesophageal
junction on this longitudinal scan through the left lobe of the liver. These collaterals arise
from the splenic hilum (not seen on this image).

33. In this patient with congenital hepatic fibrosis, large splenorenal collateral veins(arrows)
are seen to extend from the inferior end of the spleen (S) toward the left kidney (K).

34. Cirrhotic Liver Morphology
• Imaging findings that indicate the presence of cirrhosis also indicate the
presence of portal hypertension, for by the time cirrhosis is evident,
substantial sinusoidal flow obstruction is invariably present.
• Cirrhosis is the nonspecific, endstage manifestation of hepatocyte injury,
which leads, ultimately, to tissue necrosis, fibrosis, and attempted
regeneration of liver tissue. Over time, regeneration produces a nodular
liver texture, initially on a microscopic basis and eventually,
macroscopically.
• There are numerous causes of cirrhosis, but in Western nations,
alcoholism and hepatitis C infection are the principal etiologies. In Asia,
Africa, and most developing countries, viral hepatitis is the usual cause.
• Cirrhosis is classified as micronodular or macronodular, depending on the
size of regenerative nodules present.
• Macronodular cirrhosis is simply an advanced stage that has gone beyond
the micronodular form.

35. • Ultrasound is not sensitive for the presence of cirrhosis. Biopsy-definable
cirrhosis (and associated portal hypertension) is frequently present in
livers that look absolutely normal on ultrasound examination.
• Ultrasound attenuation by the cirrhotic liver is similar to that of the
normal hepatic parenchyma. The cirrhotic liver may have a slightly more
coarse texture than a normal liver, but it is not strongly echogenic and is
easily penetrated by the ultrasound beam.
• In advanced cirrhosis, the texture of the liver is more coarse than normal,
and the surface is irregular because of the presence of regenerative
nodules. Surface nodularity is most easily detected when ascites
surrounds the liver and highlights its surface. Even fine surface nodularity
is abnormal and confirms the diagnosis of cirrhosis.
• The presence of nodularity or other specific findings of cirrhosis clearly
indicates sinusoidal obstruction and the presence of portal hypertension.

36. • Large regenerative nodules may occacsionally be
visualized with ultrasound as discrete, rounded
structures within the liver parenchyma. These nodules
are either isoechoic or slightly hypoechoic relative to
the surrounding hepatic tissue.
• Regenerative nodules are extremely numerous in
cirrhotic livers, yet their visualization with ultrasound is
rare. Therefore, a regenerative nodule should not be
the first thought when a discrete lesion is seen in a
cirrhotic liver. Instead, the sonologist should think of
neoplasia and particularly of hepatocellular carcinoma.

37. • The number of visible portal or hepatic veins is reduced in cirrhotic
livers, in proportion to the severity of disease. The loss of visible
vessels appears to be a compressive phenomenon related to hepatic
fibrosis
• Portal hypertension is a frequent concomitant finding in cirrhosis. The
presence of portal hypertension confirms the diagnosis of cirrhosis,
unless there is clinical or imaging evidence for other causes of portal
hypertension.
• Severe, end-stage cirrhosis is accompanied by shrinkage of the liver in
a characteristic pattern
 The right lobe is small, with resultant widening of the fissure
between the right and left lobes (adjacent to the gall bladder)
 The caudate and left lobes are enlarged owing to regeneration.
• Cirrhosis (and portal hypertension) may be diagnosed in some patients
simply by comparing the maximum transverse dimension of the
caudate and right lobes of the liver, using a transverse ultrasound
image just below the portal bifurcation. If the caudate/right lobe ratio
exceeds 0.65, cirrhosis may be diagnosed with 90% to 100% certainty.
Unfortunately, this ratio is only 43% sensitive for cirrhosis.

38. Extrahepatic Portal Hypertension:
Prehepatic
• Portal Vein Occlusion
• Spleinic Vein Occlusion
• SMV Occlusion

39. Portal Vein Occlusion
• Sonographic manifestations of acute portal vein occlusion
include failure to visualize the portal vein and detection of
echogenic intraluminal material
• On color Doppler examination, color fill may be absent in
an occluded segment or a trickle of flow may be seen
around the thrombus. The occluding thrombus frequently
dilates the main portal vein and its branches noticeably.
• If portal vein thrombosis persists without substantial lysis,
the portal vein undergoes fibrosis and may be invisible
sonographically. Cavernous transformation is the principle
manifestation of chronic portal vein thrombosis

40. Portal vein thrombosis (acute bland thrombus). On a spectral Doppler US
image, the interrogation zone shows no color flow in the main portal vein. The
spectral waveform is aphasic, which indicates absence of flow.

41. Grey scale ultrasound showing a moderately echogenic thrombus occluding the right
branch of PV

42. Colour Doppler showing absence of MPV with a tangle of vessels at the porta
hepatis suggestive of cavernous transformation

43. Spleinic Vein Occlusion
• The most common causes of splenic vein occlusion are
pancreatitis and pancreatic carcinoma. Other less
common causes include idiopathic thrombosis,
retroperitoneal hematoma or tumor and hematological
disorders.
• The predominant collateral venous pathways that
develop, i.e. short gastric and gastroepiploic veins
return to the patient PV. Because short gastric
collaterals feed the fundus and blood can be drained
from the fundus by LGV to PV gastric varices are far
more pronounced than esophageal varices.
• Blood flow in the LGV and PV remain hepatopedal.

44. SMV Occlusion
• Regional portal hypertension from SMV
occlusion results in gastroepiploic and
peripancreatic venous collaterals which return
blood to the portal or splenic vein. Blood flow
in the portal vein remains hepatopedal.

45. Hyperkinetic Portal Hypertension
• Hyperkinetic portal hypertension is usually
caused by an intrahepatic or extrahepatic
arterioportal fistula.
• The cause of the fistula may be traumatic,
congenital, atherosclerotic or idiopathic.
• While color doppler may show the fistula in
some cases with arterialization of portal vein
flow.

46. Pitfalls of Portal Hypertension Assessment
• The absence of the findings does not exclude portal hypertension, nor
does it exclude the presence of cirrhosis.
• The direction of flow in the portal vein may be ambiguous or may
spuriously appear to be reversed for technical reasons. Abnormal flow
direction, therefore, should be confirmed with several interrogations of
the portal vein, preferably from different transducer positions.
• When flow is very sluggish, the portal vein may appear occluded on color
flow or spectral Doppler examination, even though it is patent.
• Splenic vein occlusion or splenic flow reversal may be overlooked if only
hilar branches are visualized and the splenic vein per se is not examined.
This error occurs because blood flow, of necessity, must exit the spleen,
even if subsequently channeled into collateral veins. Hence, flow in the
hilar branches is always normally directed, even if the splenic vein is
occluded.
• Portal vein dilatation may be caused by severe congestive heart failure
(CHF), because of transmission of back pressure from the right atrium
through the hepatic sinusoids to the portal circulation. Such dilation may
be attributed mistakenly to cirrhosis.

47. MEDICAL TREATMENT FOLLOW-UP
• Doppler flowmetry is an excellent noninvasive
technique to evaluate the effect of medical
treatment such as beta blockers and
vasopressin. Following treatment a reduction
in portal flow and azygos vein flow has been
reported

48. TIPS

49. • A transjugular intrahepatic portosystemic shunt
(TIPS) is a percutaneously created connection within
the liver between the portal and systemic circulations.
• A TIPS is placed to reduce portal pressure in patients
with complications related to portal hypertension.
• This procedure has emerged as a less invasive
alternative to surgery in patients with end-stage liver
disease.
• The goal of TIPS placement is to divert portal blood
flow into the hepatic vein, to reduce the pressure
gradient between portal and systemic circulations.
• Shunt patency is maintained by placing an
expandable metal stent across the intrahepatic tract.

50. Before TIPS After TIPS

51. Indications are as follows:
• Acute variceal bleeding that cannot be successfully controlled
with medical treatment, including sclerotherapy
• Recurrent and refractory variceal bleeding or recurrent variceal
bleeding in patients who cannot tolerate conventional medical
treatment.
Unproven but promising indications include the following:
• Therapy for refractory ascites
• Portal decompression in patients with hepatic venous outflow
obstruction (Budd-Chiari syndrome).
Unproven uses include the following:
• Initial therapy of acute variceal hemorrhage
• Initial therapy to prevent initial or recurrent variceal hemorrhage
• Reduction of intraoperative morbidity during liver
transplantation

52. Assessment of TIPS
• TIPS are shunts placed percutaneously via the jugular
vein. TIPS are becoming popular as a definitive
procedure for decompressing the portal venous
system or as a prelude to liver transplantation.
• Doppler US is a sensitive and relatively specific
means of evaluating TIPS malfunction.
• US evaluation of the shunt is usually performed
within 24 hours after shunt placement to establish
baseline velocities within the portal vein, hepatic
vein, and shunt.
• The primary object of Doppler study of a TIPS is to
document flow in the shunt and to demonstrate
stenosis.

53. • Complications of TIPS include thrombosis,
diffuse stenosis secondary to pseudointimal
hyperplasia, and focal stenosis, usually at the
hepatic venous end.
• Stent thrombosis is easily diagnosed if there is
complete absence of flow within the TIPS on
color or power and spectral Doppler.
• Alteration in flow velocities and turbulence
indicate stenosis

54. Normally functioning TIPS. (a) On a spectral Doppler US image, the color
Doppler image shows the cephalic end of a TIPS in blue. The waveform is
below the baseline, a finding that corresponds to antegrade flow. (b)
Spectral Doppler image shows the caudal end of the TIPS in red. The
waveform is above the baseline (antegrade flow).

55. TIPS malfunction (occlusion). Color Doppler US image obtained in the longitudinal
plane shows a TIPS with no color flow, a finding that represents direct evidence of
TIPS malfunction.

56. TIPS malfunction (hepatic vein stenosis). Spectral Doppler US image shows high-
velocity flow (282 cm/sec), which is evidence of hepatic vein stenosis. Visually
perceptible narrowing was also apparent in the color Doppler image.

57. TIPS malfunction (cephalic stenosis). In a spectral Doppler US image obtained in the
cephalic portion of a TIPS, the waveform shows a markedly increased flow velocity of 238
cm/sec.