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
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)
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
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.
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
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.
29.
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
35. Damping index of HV
waveform
Minimumn velocity of downward HV
DI = ------------------------------------------------
Maximum velocity of downward HV
36.
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
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)
50.
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 .
53.
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.
56.
57.
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.
Notas del editor
For example, antegrade flow moves away from the heart in the systemic arteries and toward the heart in the systemic veins.
antegrade flow may be either toward or away from the transducer, depending on the spatial relationship of the transducer to the vessel; therefore, antegrade flow may be displayed above or below the baseline, depending on the vessel being interrogated.
Phasic is another word for cyclic; its absence or presence (and degree) may be qualified…..NOT QUANTIFIED
Phase is a stage, or portion, of a phasic process; the number of phases may be quantified
As long as there is flow, there is some form of phasicity.
If there is mild undulation (shallow slopes and a small vertical range between inflections), as in normal veins, the waveform is described as phasic. If there is marked undulation (steep slopes and a wide vertical range between inflections), as in normal arteries, the waveform is described as pulsatile
the flow pattern is described as “biphasic” if two sounds are heard during each cycle and as “triphasic” if three sounds are heard. More recently, sonologists have held that phase is defined in terms of discrete flow components in either direction
Spectral broadening is seen when the waveform is no longer traceable with a marker or pencil
In other words the spectral window starts to fill in.
1)Artificially 2)physiologically(in small vessel)
3)pathologically
From the perspective of the stenosis, transducer A is located upstream. At the position of transducer A, a downstream stenosis is detected. From the perspective of the stenosis, transducer B is located downstream. At the position of transducer B, an upstream stenosis is perceived
Sos – sinosidual obstruction syndrome
Tips – trans juglular intrahepatic porto-systemic shunt
In severe portal hypertension, there is a period of time during the disease course when flow is neither hepatopetal nor hepatofugal, but stagnant. This results in absent portal venous flow and puts the patient at increased risk for portal vein thrombosis.
The most reliable distinguishing gray-scale US feature of malignant thrombus is the combination of an echogenic filling defect with an adjacent liver mass
Arterialization (of the portal venous waveform)
Even in pathologic states, the a wave remains wider than the v wave,bwhich represents the best way to initially orient oneself on the waveform. The only time this rule breaks down is in cases of severe tricuspid regurgitation.
The position of the peak of the v wave varies from above to below the baseline in normal states
Normal value : <0.6
Severe portal hypertension : >0.6
In early systole, when the atrioventricular septum is descending and would normally create a large burst of negative right atrial pressure, creating the deepest antegrade wave (S wave), the incompetent valve instead relieves all or part of the vacuum effect. The result is an S wave that is no longer as deep as the D wave.
When severe TR, flow can switch to retrograde, resulting in an S wave that is above the baseline, merging with the a and v waves
The tall a wave is due to increased right atrial pressure toward end diastole, generated by the larger-than-normal volume contained by the RA as it contracts.
The tall v wave is due to increased right atrial pressure toward end systole, due to the larger-than-normal volume the right atrium contains while still trying to accommodate continued systemic venous return
Types OTBO obstruction: ( Obstruction d/t thrombus – hypercoagulable state)
type (I) with obstruction of the IVC (±HV), radicular type (II) with obstruction of HV, venoocclusive type (III) with obstruction of small centrilobular veins.
large intrahepatic collateral vein bypassing the occluded hepatic veins.
End stage liver disease
hepatic arterial RI is not useful for diagnosing cirrhosis or predicting its severity
inflammatory edema, arterial compression by regenerative nodules, and arterial compression by stiff noncompliant (fibrotic) parenchyma, have been thought to increase resistance
hepatic arterial buffer response” (compensatory small artery proliferation and increased numbers of arteriolar beds) and arteriovenous shunting, are thought to decrease resistance
Normal functioning TIPS . On a spectral doppler US image , the colour doppler image shows the cephalic end of a TIPS in blue
The waveform is below the baseline , a finding that corresponds to antegrade flow.
Normally functioning TIPS spectral doppler image shows the caudal end of the TIPS in red . The waveform is above the baseline (antegrade flow)
Transient dampening of the hepatic vein waveform in 51 yr old man after orthotopic liver transplantation .
Duplex doppler image obtained 1 day after surgery shows the waveform of the middle hepatic vein . The spectrum is in the correct direction , posteriorly toward the IVC : however , the waveform is blunted the pt continued to do well clinically
Duplex doppler image obtained 1 day later shows a normal waveform of the middle hepatic vein.
(a) The splenic vein can be imaged behind the body and tail of the pancreas in B-mode. Transverse section through the upper abdomen. (b) Colour Doppler of the flow in the splenic vein in a transverse section through the upper abdomen. The flow in the splenic vein (SV) along the pancreatic tail is directed towards the transducer and therefore displayed red. Close to the pancreatic head, the flow in the splenoportal confluence (SPC) is directed away from the transducer and therefore displayed blue. The aorta (DAO), the inferior vena cava (IVC), right renal artery (RA) and the superior mesenteric artery (SMA) are shown.
(c) Spectral Doppler of the flow in the splenic vein shows an antegrade flow with a time average maximal velocity (TAMAX) of 30.7 cm/s and a mean time average velocity (TAMEAN) of 16.6 cm/s. Transverse section through the upper abdomen. (d) Longitudinal section through the middle upper abdomen shows the pancreatic body (P) and the splenic vein (SV). The stomach is marked with “S”