This document provides an overview of Doppler ultrasound of the normal portal system. It discusses adjusting spectral Doppler settings and interpreting normal and abnormal findings. Key points include: - Normal Doppler findings of the portal vein include a velocity of 13-23 cm/sec and antegrade flow. Increased diameter or retrograde flow indicate portal hypertension. - Hepatic vein Doppler shows a triphasic waveform. Increased pulsatility can be seen with tricuspid regurgitation or right heart failure. Loss of phasicity indicates outflow obstruction. - The hepatic artery has a resistive index over 0.7 normally. Values under 0.55 may indicate stenosis. - Transjugular intrahepatic portos

1. SPLENO-HEPATIC DOPPLER
Dr.Pradeep Patil
Radiodiagnosis Department, D.Y Patil Kolhapur

2. DOPPLER
OF
NORMAL
PORTAL
SYSTEM
•Normal US of portal system
•Principles of doppler US
•Adjusting spectral doppler US
•Normal portal vein
•Normal hepatic veins
•Normal hepatic artery

3. Antegrade- flow in the forward direction
with respect to its expected direction in the
circulatory system
Retrograde - flow in the reverse direction
with respect to its expected direction in
the circulatory system
Antegrade versus Retrograde
WRT circulatory
system
WRT transducer

4. Phasicity
versus Phase
Quantification

6. Arterial Resistance
•High-resistance arteries have an RI > 0.7 low-resistance arteries have an RI of 0.55–0.7

8. Flow Patterns and Waveform Findings

9. CAUSES OF SPECTRAL BROADENING
Artifical
• Large sample volume
• High gain
Physiologic
• Normal small vessel (hepatic arteries)
• Normal turbulence (bifurcation)
Pathologic
• Compressed vessels (eg.hepatic veins in cirrhosis)
• Turbulent flow (post stenotic flow)

10. Upstream
and
downstream
Up-stream refers to blood that has not yet passed a reference point
Downstream refers to blood that has already passed the reference point.

11. GOALS
OF
DOPPLER
• Detection flow in a vessel
• Detection direction of flow
• Detection type of flow :
-Arterial or venous
-Normal or abnormal
• Measurement of flow velocity

12. EACH
EXAMINATION
SHOULD BE
PERFORMED
WITH
•Gray – scale US
•Color Dopler
•Power Dopler
•Spectral dopler

13. Color box size/overlay
Color box should be as small and superficial as possible

14. Changing color baseline to avoid aliasing

15. Inversion of color flow

16. Obtain waveform at end of normal breath – out
• Take normal breath
• Take normal breath out
• Stop breathing
• Then obtain a waveform

17. PORTAL VEIN
 The portal vein is formed by the confluence of the splenic and superior mesenteric
veins. It provides approximately 70% of the incoming blood to the liver.
• Normal blood flow velocity is 13-23 cm/sec with an average of 18 cm/sec.
• Flow velocity is commonly somewhat phasic because rocking motion of the liver caused
by motion of the heart moves the portal vein under the Doppler sample volume.
• Slight phasicity may also be evident related to respiration.
• Normal blood flow direction is into the liver. Any reversal of blood flow direction is
abnormal and usually indicative of portal hypertension.
• The portal vein is normally <13 mm in diameter. Increased diameter suggests portal
hypertension.

18. Normal
pulsed
doppler of
portal vein

19. Interpretation
of portal vein
flow

20. Abnormal (pathologic) portal venous flow usually manifests in one of four
ways:
1. Increased pulsatility (pulsatile waveform)
2. Slow portal venous flow
3. Hepatofugal (retrograde) flow
4. Absent (aphasic) portal venous flow

21. Increased
pulsatility of
portal vein
• Portal hypertension
• Tricuspid regurtation
• Right heart failure
• Arterio-portal vein
fistula

22. Slow portal venous flow
Normal= 16-40 cm/sec
Abnormally slow flow occurs when back pressure limits
forward velocity.
Slow flow is diagnostic for portal hypertension (PSV
<16cm/sec).
Portal hypertension is caused by cirrhosis in the vast majority of
cases.
The most specific findings for portal hypertension are
development of portosystemic shunts (eg, a recanalized umbilical
vein) and slow or reversed (hepatofugal) flow.
Splenomegaly and ascites are nonspecific.

23. Hepatofugal
(retrograde) flow
•Hepatofugal flow occurs when
back pressure exceeds forward
pressure, with flow subsequently
reversing direction.
•This results in a waveform that is
below the baseline.
• As with slow flow, this finding is
diagnostic for portal hypertension
from whatever cause

24. Absent (aphasic) portal
venous flow
• Absent flow in the portal vein may be due to
stagnant flow (portal hypertension) or occlusive
disease.
• Not all cases of absent flow represent occlusive
disease-like in portal HTN.

25. • Another feature of occlusive portal vein thrombosis (especially the non acute variety) is the development of
collateral vessels in or around the occluded portal vein; this condition is referred to as cavernous transformation.
• Cavernous transformation tends to be a marker for bland thrombus, since these collateral vessels usually take a long
time to develop.

26. Congestion index of portal vein
Normal value 0.07=/- 0.03 cmm.sec
CI > o.o8 portal hypertension

27. Portal vein flow volume

28. Hepatic veins
• The bulk of hepatic venous flow is antegrade ,although there are
moments of retrograde flow Antegrade flow is away from the
liver and toward the heart; thus, it will also be away from the
transducer and, therefore, displayed below the baseline.
• Pressure changes in the RA will be transmitted directly to the
hepatic veins.

30. A wave
It is generated by increased right atrial pressure resulting from atrial
contraction.
The a wave is an upward-pointing wave with a peak that
corresponds to maximal retrograde hepatic venous flow.
In physiologic states, the peak of the a wave is above the baseline,
and the a wave is wider and taller than the v wave

31. S wave
Its initial downward-sloping portion is generated by decreasing
right atrial pressure, as a result of the “sucking” effect created by
the downward motion of the atrioventricular septum.
Note that the tricuspid valve remains closed.
The lowest point occurs in midsystole and is the point at which
negative pressure is minimally opposed and antegrade velocity is
maximal.

32. V Wave
The upward-sloping portion is generated by increasing right atrial
pressure resulting from continued systemic venous return. ( valve is
closed)
The peak of the wave marks the opening of the tricuspid
valve and the transition from systole to diastole.

33. D Wave
Its initial downward-sloping portion is generated by decreasing
right atrial pressure.
The subsequent rising portion results from increasing RA pressure
generated by the increasing right ventricular blood volume

34. Interpretation
of hepatic
vein flow

35. Damping index of HV
waveform
Minimumn velocity of downward HV
DI = ------------------------------------------------
Maximum velocity of downward HV

37. Abnormal hepatic venous flow usually manifests
in one of ways :
Increased pulsatility (pulsatile waveform)
Decreased phasicity (decreased pulsatility) and
spectral broadening.
Absent (aphasic) hepatic venous flow

38. There are two conditions that can create a pulsatile hepatic venous
waveform:
Tricuspid regurgitation
Right sided heart failure without TR
Tricuspid regurgitation
decreased S wave/ retrograde a-S-v complex
tall a and v waves
Pulsatile waveform
Increased pulsatility (pulsatile waveform)
Tricuspid regurgitation

39. There are two conditions that can create a
pulsatile hepatic venous waveform:
Tricuspid regurgitation
Right sided heart failure without TR
Right sided heart failure without TR:
The primary abnormality is too much blood volume on
the systemic venous side.
Tall a and v waves.
S and D waves – normal(tricuspid valve is
competent)
Increased pulsatility (pulsatile waveform)
Right sided heart failure without TR

40. • During late systole, when there should normally be continued systemic venous return against a closed tricuspid
valve (rising portion of the v wave), the incompetent valve allows large amounts of retrograde flow. This results in
the other finding in tricuspid regurgitation, namely, an abnormally tall v wave.
• Toward end diastole, when the right atrium contracts, there is a much higher blood volume (and thus, pressure)
than normal, resulting in a tall a wave

41. Decreased phasicity (decreased pulsatility) and spectral
broadening.
• Pathologic causes of nonphasicity - cirrhosis, hepatic vein thrombosis (Budd-Chiari syndrome), hepatic
veno-occlusive disease, and hepatic venous outflow obstruction.
• As disease severity progresses and the veins become more compressed by fibrotic constriction or
parenchymal edema, they lose their ability to accommodate retrograde flow.
• Decreased venous compliance is seen as a waveform with a proportional loss of phasicity.
• Spectral broadening is due to the narrowed caliber of compressed hepatic veins

42. This finding is diagnostic for venous outflow obstruction (Budd-Chiari
syndrome).
Absent (aphasic) hepatic venous flow

44. Normal hepatic
artery

45. Interpretation
of hepatic
artery flow

46. RI >0.7 ( usually non specific )

47. RI<0.55

48. TRANSJUGULAR INTRAHEPATIC
PORTOSYSTEMIC SHUNTS
INDICATIONS
 severe portal hypertension with refractory variceal bleding or ascites.
 Hepatorenal syndrome
 Hepatic hydrothorax
 Hepatic vein occlusion (budd-chiari syndrome)
ULTRASOUND IS A TIME TESTED TOOL FOR EVALUATION OF TIPS

49. SIGNS OF TIPS MALFUNCTION
Direct evidence
• Shunt velocity <90cm/sec or >190cm/sec.
• Temporal increase or decrease in shunt velocity >50cm/sec.
Indirect evidence
Main portal venous velocity <30cm/sec.
Collateral vessels (recurrent , new or increased )
Ascites (recurrent ,new or increased )
Right – left portal venous flow reversal (ie , hepatofugal to hepatopetal)

51. EVALUATION OF HEPATIC VEIN IN
LIVER TRANSPLANT
• Standard modality for evaluating the liver after transplantation to quickly and cost –
effectively diagnose complications and prevent graft loss.
• The presence of a triphasic waveform had a 98% negative predictive value for
hepatic vein stenosis.
• A persistent triphasic hepatic vein waveform virtually excludes hepatic vein stenosis.

52. EVALUATION OF HEPATIC VEIN IN
LIVER TRANSPLANT
Loss of a triphasic waveform was found to be nonspecific for rejection .
• Cholangitis
• Hepatitis
• Fibrosis
• Lymphoproliferative disorder
• Juxta hepatic fluid collections
Transient spectral blunting may be seen in immediate post op period because of edema .

54. MAIN INDICATIONS OF SPLENIC
DOPPLER
 Differential diagnosis of splenomegaly (acute and chronic infections, haematological and immunological
diseases, portal hypertension, storage diseases)
 Differential diagnosis of reduced splenic size (hyposplenia/asplenia)
 Diffuse alterations of the spleen (diffuse benign or malign infiltration, systemic inflammatory or infectious
diseases)
 Vascular alterations (thrombosis, infarction, aneurysm)
 Trauma
 Focal lesions of the spleen

55. SPLENIC VEIN
• The splenic vein drains the spleen and receives inflow from the inferior
mesenteric vein. The splenic vein joins the superior mesenteric vein
posterior to the neck of the pancreas to form the portal vein.
• The splenic vein shows low velocity forward flow toward the liver.
Reversal of blood flow direction is seen with advanced portal
hypertension.
• Slight respiratory variation is common.
• Normal diameter of the splenic vein is <10 mm. Increase in diameter is a
sign of portal hypertension.

58. TAKE HOME MESSAGE
• An understanding of the basic principles of vascular doppler US is required to
suuessfully perform liver doppler US
• Pathologic conditions such portal hypertension , right sided heart failure , and
tricuspid regurgitation have characteristic effects on doppler waveforms.
• Doppler US remains the “ WORKHORSE” modality for the evaluation of TIPS
patency.
• Standard modality for evaluating the liver after transplantation to quickly and cost –
effectively diagnose complications and prevent graft loss.