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Vascular 1 > C7: Liver Vasculature > Flashcards

C7: Liver Vasculature Flashcards

1
Q

What is pre and post-prandial? How will it effect the spectral Doppler waveform

A

Pre: no food… waveform will be closer to the baseline

Post: w/ food… waveform will have a higher peak velocity and will be removed from the baseline b/c the arteries going to the abdo open up after eating

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2
Q

How much of the blood to the liver does the Ha supply? What type of flow pattern does it show?

A

30%

-low resistance flow pattern (tortuous vessel)

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3
Q

In what plane is the prox HA best seen? What about the distal HA?

A

Prox: trans @ level of celiac axis

Distal: intercostally @ lvl of MPV. The porta hepatis

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4
Q

Where would you measure the HA

A

Porta hepatis

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5
Q

How will the spectral tracing of the HA appear?

A
  • low resistance
  • filled in spectral window due to its small diameter
  • variable velocities due to tortuously

-RI should be 0.5-0.7

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6
Q

What’s the formula for RI and what’s it a strong indicator for

A

EDVeocity/Peak systolic volume

-strong indicator of stenosis (stronger indicator than V)

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7
Q

Is there’s a blockage in the celiac axis, and HA, how could the spectral tracing still appear norm?

A

Due to the many collaterals

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8
Q

Where to the hepatic veins empty into the IVC

A

Inferior to the diaphragm

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9
Q

Which window is best to scan the intrahepatic part of the IVC

A

Intercostal (or you can try xiphoid)

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10
Q

What value is considered dilated for the IVC

A

> 37 mm

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11
Q

How should the spectral waveform of the IVC appear? For prox and distal

A

-spontaneous waveform

Prox: pulsatile
Distal: phasic

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12
Q

Are accessory veins common with the hepatic veins? Which HV will mot commonly have collaterals?

A

Yes

RHV

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13
Q

Describe the location of the MHV

A
  • b/w the R and L lobes

- through the main lobar fissure

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14
Q

Which lobe has its own drainage directly into the IVC

A

Caudate

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15
Q

Which HV is most commonly duplicated?

A

LHV

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16
Q

Which 2 Hv commonly join before entering the IVC

A

L and M

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17
Q

If there’s agenesis of a HV which is most often not present

A

RHV, then MHV then LHV

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18
Q

How should the spectral tracing of the HV appear

A

Multiphasic and pulsatile

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19
Q

How does Budd Chiari effect distension and presence of HV?

A

-HV will be small or abscent

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20
Q

How does CHF effect distension and pulsatility of HV?

A

-HV will be distended and have increased pulsatility

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21
Q 
What are the scanning window for the:
Confluence of the HV
RHV
MHV
LHV
A

Confluence: TRX @ xiphoid

RHV: R intercostal space

LHV: anterior subcostal

MHV: midline, xiphoid or intercostally

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22
Q

Do multiphasic and pulsatile mean the same thing

A

Yes (flow in 2 directions)

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23
Q

How do portal veins (PV) course through the liver in general

A

Intrahepatic

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24
Q

What % of blood do the PV supply to the liver?

A

70%, its nutrient rich blood from the bowel, spleen

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25
Q

Which vessels form the MPV

A

Splenic vein, SMV…. IMV (drains into splenic) and coronary vein tributaries

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26
Q

with what approach is the MPV visualized

A

Subcostal or intercostally

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27
Q

What should the spectral tracing of the MPV look like?

A

-low velocity
+b/w 15-40 cm/sec…. the avg. is 15-18 cm/s

  • continuous signal
  • slightly phasic/ slight undulations
  • sounds like a windstorm
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28
Q

what is the direction of flow in the PV and does the flow increase post-prandially

A

Hepatopedal

Yes, flow will increase b/c arteries near the bowel dilate after eating

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29
Q

How will the MPV appear with thrombus

A
  • lots of collaterals (cavernous transformation)

- MPV will not be visualized but many small vessels will be

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30
Q

Which vessels do we usually look at when doing liver doppler?

A

HV
PV
Splenic vein
HA

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31
Q

What do the presence of collaterals indicate for the portal venous system?

A

Portal hypertension

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32
Q

With the liver duplex exam, do we assess with normal breathing or a breath in?

A

Norm breathing

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33
Q

Why don’t we want deep inspiration when scanning liver doppler?

For which vessel would we use a breath in?

A
  • it increases the size of the MPV
  • blunts HV pulsation
  • loss of subtle changes in PV waveform

+for HA

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34
Q

which vessels do we assess in the anterior subxiphoid window

A
  • LPV
  • LHV
  • SV
  • MPV
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35
Q

which vessels do we assess in the coronal (intercostal) window

A
  • RHV
  • MHV
  • RPV
  • MPV (if anterior window didnt work)
  • HA
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36
Q

what kind of flow do the HV have

A

hepatofugal

multiphasic/pulsatile flow

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37
Q

whats the protocol for assessing MPV

whats the norm value for MPV

A
  • measure AP diameter anterior to the IVC
  • norm respiration
  • colour and spectral tracing outside of the liver

+ < 13 mm

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38
Q

where should we be sampling the MPV for the tracing?

A

outside of the liver (usually over the IVC)

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39
Q

which approach is most accurate for sampling the MPV

at what angle are we insonating when we scan using the anterior subcostal window

A

coronal intercostal b/c we get a zero degree angle

60

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40
Q

whats the protocol for assessing SV

A
  • colour and spectral (ant. subcostal)

- long axis

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41
Q

how should your colour scale and baseline be set when scanning portal veins

A

both should be lower because the flow is slower

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42
Q

Define portal hypertension

A

Elevated pressure in portal venous system…. impedes blood flow through the liver

It means there’s a pressure gradient b/w the PV and the IVC of HV

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43
Q

List the 2 general causes of PHT

A

increased volume

Increased resistance to flow

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44
Q

What are the 3 classifications on PHT

A

Prehepatic (inflow)
Posthepatic (outflow)
Intrahepatic

Pre and post are classified as extrahepatic

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45
Q

List the prehepatic causes of PHT

A

Portal or splenic thrombosis or invasion

Extrinsic compression by a tumour

Inflammation of pancreas (compresses vessels)

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46
Q

List the intrahepatic causes of PHT

A

Hepatocellular disease

  • cirrhosis
  • hepatitis
  • fatty infiltration
  • tumours
47
Q

At what level does cirrhosis start? And how does it progress

A

At microscopic level… then the liver becomes inflamed, it starts to regenerate and scar….. this increases resistance to blood flow at the sinusoid level

48
Q

What’s the most common cause of PHT

A

Intrahepatic causes

49
Q

List the posthepatic causes of PHT

A
  • thrombosis of HV (Budd Chiari) or IVC
  • CHF
  • right sided heat disease
50
Q

Post hepatic causes of PHT involves which vessels and structures?

A

HV, IVC, or heart

51
Q

What HV waveform is indicative of PHT

A

Pulsatile

52
Q

What are the general risk factors for PHT

A
  • chronic liver disease leading to fibrosis or cirrhosis

- heart disease leading to increased right sided heart pressure

53
Q

What are the 3 causes of chronic liver disease (that can cause cirrhosis)

A

Viral hepatitis
Alcoholic liver disease
Autoimmune disorders

54
Q

List 3 processes/diseases that lead to increased R heart pressure?

A
  • TV regurgitation
  • CHF
  • constrictive pericarditis
55
Q

What are some of the clinical signs of PHT?

these symptoms are associated with what type of underlying diseases?

A
  • Ascites
  • splenomegaly
  • GI bleed
  • jaundice
  • abnormal LFTs
  • variceal hemorrhage
  • bacterial peritonitis

+ pancreatitis
+ liver disease

56
Q

What is a common sign of cirrhosis

A

Jaundice

57
Q

can a patient have PHT and have no symptoms

A

yes

58
Q

what type of signs may be found on physical examination w/ PHT

A
  • jaundice
  • splenomegaly
  • dilated abdo veins
  • hepatic encephalopathy (confusion due to poor liver function)
59
Q

what would we see sonographically is the patient had PHT

A
  • increased diameter of veins
  • portosystemic collaterals/portocaval anastomoses
  • recanalized umbilical vein
  • splenomegally
  • increased HA flow
  • ascities
60
Q

how dilated do the MPV, the coronary vein and the umbilical vein have to be to be considered PHT

A

MPV: >13 mm
CV: >7 mm
UV: >3 mm

61
Q

when might we use power doppler when assessing the liver

A

-for collaterals and tortuous vessels

62
Q

how will the spectral waveform of the PVs change with PHT?

A
  • biphasic flow (retro and ante)
  • flow reversal in sever PHT… doesnt occur often because collateral prevent this
  • loss of respiratory variation and decreased velocity
63
Q

whats the mean velocity for the PV

what might a low peak indicate?

A

15-18 cm/s

  • PHT
64
Q

pulsatile portal venous flow, a ‘W’ pattern of the HV and a dilated IVC can indicate what type of disease process

A

CHF

65
Q

what type of abnormalities/pathology can lead to portal vein thrombosis (PVT) as a primary condition

A
  • liver disease
  • hypercoagulability
  • intestinal inflammation
  • cirrhosis
  • cancer
  • trauma
66
Q

what are the US findings of a PVT

A
  • enlarged PV
  • lack of flow/decreased flow
  • periportal collateral flow
  • enlarged hepatic artery w/ increased flow
67
Q

what is periportal collateral flow or shunts (important)

another term for it

A
  • it is a cavernous transformation or shunt that occurs only in chronic PVT
  • they are made from preexisting vessels
  • portosystemic collaterals or portosystemic shunting
68
Q

is PV occlusion typically reversible?

A

no… usually permanent due to scarring/fibrotic changes which cause the vessel to basically disappear

69
Q

what are the 3 common pitfalls when looking for PVT

A
  • undetected thrombus
  • missed low velocity flow (use PW doppler)
  • bad doppler angle
70
Q

what is Budd Chiari syndrome and which vessels does it commonly effect

A

hepatic vein occlusion… involves major HV or IVC

71
Q

whats the causes of HV occlusion?

A
  • compression
  • clot
  • tumor
  • cirrhosis
  • membranous obstruction of IVC (congenital disorder with strand of tissue in the IVC impending HV flow to the IVC)
72
Q

what are 3 causes of increased hyper coagulability

A
  • BCP, HRT

- polycythemia (over production of RBCs)

73
Q

what are some signs and symptoms of HV occlusion

A
  • hepatomegaly
  • acute ascites
  • abnorm LFTs
  • splenomegaly and collaterals in chronic cases
74
Q

what are the US findings of HV occlusion

A
  • hepatomegaly
  • caudate lobe enlargement
  • clot in HV or IVC
  • no flow
  • narrow veins which lead to elevation of velocity and turbulence
  • collaterals
75
Q

where would collaterals commonly be seen in HV occlusion

A

connecting patent HV w/ portal system

76
Q

what liver ratio is used as an indicator of HV occlusion

A

Caudate lobe ratio… it willl be enlarged so will have a small ratio

77
Q

review the tables in notes…. pg 20, 21, 25

A

.

78
Q

portosystemic collaterals director flow towards which vessels (in general terms)

A

mesenteric, splenic and portal veins

79
Q

what specifically are the most common portosystemic collaterals

A
  • coronary vein/left gastric vein
  • umbilical vein
  • splenorenal vein/lienorenal
80
Q

which portosystemic collateral is the most common?
where is it located?

what can these collaterals progress to

A

coronary vein/left gastric vein

-around the celiac axis

+esophageal varices

81
Q

why are esophageal varices clinical important?

what diameter of these vessels indicates PHT?

A

these vessels are fragile and if dilated are prone to hemorrhage

> 7 mm

82
Q

what type of flow (direction) would the umbilical vein have if it became a collateral

what size and flow would it have in a norm patient?

A
  • hepatofugal and >3mm

- contain no blood flow

83
Q

what are surgical shunts (therapeutic)

when would they be used?

A

-a stent placed in the vessel in order to decompress the portal system, reduce ascities, prevent hemorrhage…

+ in sever cases of PHT or cirrhosis, can improve quality of life of the patient

84
Q

what is a Trans Jugular Intrahepatic portosystemic shunt (TIPS)

whats its success rate… what is the risk of having one?

A

-the most common type of surgical shunt made from metal

+ 90%

-subject to high rate of stenosis or occlusion

85
Q

what are the early and late complications of TIPS

where is the most common area for stenosis to occur with a TIPS

A

early:
- thrombus or stenosis

late:
- neointimal hyperplasia invading the stent

+near the HV

86
Q

in which artery would we see compensatory increased flow with a TIPS

A

HA

87
Q

when is the liver transplant (LT) used as tretment

do we assess the liver pre and post transplant

A

-end stage liver disease

+yes

88
Q

what are we looking for w/ a preoperative LT scan

A
  • assesing patency of PV, HA, HV, IVC
  • look for tumours
  • look at biliary tree
89
Q

what are we looking for w/ a postoperative LT scan

and when it is performed

A
  • 24 hrs post opt… then follow up regularly

+ confirm patency and flow direction of all major vessels
+ look at anastomoses
+ look at vessel size
+ look at liver tissue, biliary tree, perihepatic spaces

90
Q

what size is considered norm for the PV post liver transplant

A

15 mm

91
Q

which vessel is most important to confirm patency

what should the RI, PSV and accel time be?

A

HA…

+ RI: 0.5-0.8
+ PSV: <200 cm/s
+ acceleration time: <0.08 sec

92
Q

what are the postoperative transplant complications… which is the most common

A
  • HA thrombosis (most common)
  • stenosis
  • PV thrombosis
  • hematoma
  • abscess formation
  • AV fistulas
93
Q

where does stenosis often occur post transplant

A

at surgical anastomoses sites

94
Q

what will indicate clot in the HA post transplant

A
  • no flow
  • lower PSV
  • decreased diastolic flow
95
Q

viability of the liver is critical to flow in which vessel

A

HA`

96
Q

When assessing the IVC, where should we be sampling?

A

As close to the diaphragm as possible

97
Q

What’s the norm range of PSV for the HA?

A

70-150 cm/s

98
Q

What’s the norm velocity of a TIPS

Abnorm

A

90-190…. abnormal is <50

Should be similar velocities on both ends

99
Q

What’s a norm and abnormal PV peak velocity with a TIPS

A

Norm: at least 30 cm/s
Abnorm: <30 cm/s

100
Q

What can the caliper of the MPV be up to with a TIPS

A

Up to 15 mm

101
Q

With a TIPS, whats an abnormal velocity gradient at a stenosis

A

> 100 cm/s

102
Q

What quality of flow would you see with an abnormal tips? Normal?

A

Continuous flow and RPV/LPV flow away from the stent

Pulsatile flow…. RPV/LPV flow towards the stent

103
Q

A splenic vein diameter of greater than what value is indicative of PHT

A

> 10 mm

104
Q

W/ CHF or increased R sided heart pressure, will the HV and PV have increased pulsatility

A

Yes

105
Q

If the IVC is occluded can this cause primary or secondary hepatic vein occlusion?

A

secondary

106
Q

what type of HV waveform will Budd Chiari Syndrome patient show?

A
  • decreased, absent or revered flow
  • dampened HV spectral tracing
  • increased turbulence and focal increase of velocity if the veins are narrowed
107
Q

are focal areas of narrowing normal with a TIPS

A

no

108
Q

Which vessel does the coronary vein drain into?

A

Main portal vein (comes from the stomach)

109
Q

Where does the umbilical vein travel?

A

From umbilicus to tip of LPV

110
Q

intrahepatic causes of PHT refer to blood flow in the liver at what level?

A

the capillary/sinusoid level

111
Q

which intraheptatic cause of PHT is the most common

A

cirrhosis

112
Q

a TIPS shunt connects which 2 vessels

A

the MPV and a HV (usually RHV) and possess through the liver tissue

113
Q

when end of the TIPS shunt is the most common site of stenosis

A

HV end

114
Q

with a normal TIPS stent, what should the direction of flow be in the LPV/RPV

A

hepatofugal (towards the stent) instead of the normal heatopedal w/o a stent

Vascular 1 (5 decks)

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