C7: Liver Vasculature Flashcards
What is pre and post-prandial? How will it effect the spectral Doppler waveform
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
How much of the blood to the liver does the Ha supply? What type of flow pattern does it show?
30%
-low resistance flow pattern (tortuous vessel)
In what plane is the prox HA best seen? What about the distal HA?
Prox: trans @ level of celiac axis
Distal: intercostally @ lvl of MPV. The porta hepatis
Where would you measure the HA
Porta hepatis
How will the spectral tracing of the HA appear?
- low resistance
- filled in spectral window due to its small diameter
- variable velocities due to tortuously
-RI should be 0.5-0.7
What’s the formula for RI and what’s it a strong indicator for
EDVeocity/Peak systolic volume
-strong indicator of stenosis (stronger indicator than V)
Is there’s a blockage in the celiac axis, and HA, how could the spectral tracing still appear norm?
Due to the many collaterals
Where to the hepatic veins empty into the IVC
Inferior to the diaphragm
Which window is best to scan the intrahepatic part of the IVC
Intercostal (or you can try xiphoid)
What value is considered dilated for the IVC
> 37 mm
How should the spectral waveform of the IVC appear? For prox and distal
-spontaneous waveform
Prox: pulsatile
Distal: phasic
Are accessory veins common with the hepatic veins? Which HV will mot commonly have collaterals?
Yes
RHV
Describe the location of the MHV
- b/w the R and L lobes
- through the main lobar fissure
Which lobe has its own drainage directly into the IVC
Caudate
Which HV is most commonly duplicated?
LHV
Which 2 Hv commonly join before entering the IVC
L and M
If there’s agenesis of a HV which is most often not present
RHV, then MHV then LHV
How should the spectral tracing of the HV appear
Multiphasic and pulsatile
How does Budd Chiari effect distension and presence of HV?
-HV will be small or abscent
How does CHF effect distension and pulsatility of HV?
-HV will be distended and have increased pulsatility
What are the scanning window for the: Confluence of the HV RHV MHV LHV
Confluence: TRX @ xiphoid
RHV: R intercostal space
LHV: anterior subcostal
MHV: midline, xiphoid or intercostally
Do multiphasic and pulsatile mean the same thing
Yes (flow in 2 directions)
How do portal veins (PV) course through the liver in general
Intrahepatic
What % of blood do the PV supply to the liver?
70%, its nutrient rich blood from the bowel, spleen
Which vessels form the MPV
Splenic vein, SMV…. IMV (drains into splenic) and coronary vein tributaries
with what approach is the MPV visualized
Subcostal or intercostally
What should the spectral tracing of the MPV look like?
-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
what is the direction of flow in the PV and does the flow increase post-prandially
Hepatopedal
Yes, flow will increase b/c arteries near the bowel dilate after eating
How will the MPV appear with thrombus
- lots of collaterals (cavernous transformation)
- MPV will not be visualized but many small vessels will be
Which vessels do we usually look at when doing liver doppler?
HV
PV
Splenic vein
HA
What do the presence of collaterals indicate for the portal venous system?
Portal hypertension
With the liver duplex exam, do we assess with normal breathing or a breath in?
Norm breathing
Why don’t we want deep inspiration when scanning liver doppler?
For which vessel would we use a breath in?
- it increases the size of the MPV
- blunts HV pulsation
- loss of subtle changes in PV waveform
+for HA
which vessels do we assess in the anterior subxiphoid window
- LPV
- LHV
- SV
- MPV
which vessels do we assess in the coronal (intercostal) window
- RHV
- MHV
- RPV
- MPV (if anterior window didnt work)
- HA
what kind of flow do the HV have
hepatofugal
multiphasic/pulsatile flow
whats the protocol for assessing MPV
whats the norm value for MPV
- measure AP diameter anterior to the IVC
- norm respiration
- colour and spectral tracing outside of the liver
+ < 13 mm
where should we be sampling the MPV for the tracing?
outside of the liver (usually over the IVC)
which approach is most accurate for sampling the MPV
at what angle are we insonating when we scan using the anterior subcostal window
coronal intercostal b/c we get a zero degree angle
60
whats the protocol for assessing SV
- colour and spectral (ant. subcostal)
- long axis
how should your colour scale and baseline be set when scanning portal veins
both should be lower because the flow is slower
Define portal hypertension
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
List the 2 general causes of PHT
increased volume
Increased resistance to flow
What are the 3 classifications on PHT
Prehepatic (inflow)
Posthepatic (outflow)
Intrahepatic
Pre and post are classified as extrahepatic
List the prehepatic causes of PHT
Portal or splenic thrombosis or invasion
Extrinsic compression by a tumour
Inflammation of pancreas (compresses vessels)
List the intrahepatic causes of PHT
Hepatocellular disease
- cirrhosis
- hepatitis
- fatty infiltration
- tumours
At what level does cirrhosis start? And how does it progress
At microscopic level… then the liver becomes inflamed, it starts to regenerate and scar….. this increases resistance to blood flow at the sinusoid level
What’s the most common cause of PHT
Intrahepatic causes
List the posthepatic causes of PHT
- thrombosis of HV (Budd Chiari) or IVC
- CHF
- right sided heat disease
Post hepatic causes of PHT involves which vessels and structures?
HV, IVC, or heart
What HV waveform is indicative of PHT
Pulsatile
What are the general risk factors for PHT
- chronic liver disease leading to fibrosis or cirrhosis
- heart disease leading to increased right sided heart pressure
What are the 3 causes of chronic liver disease (that can cause cirrhosis)
Viral hepatitis
Alcoholic liver disease
Autoimmune disorders
List 3 processes/diseases that lead to increased R heart pressure?
- TV regurgitation
- CHF
- constrictive pericarditis
What are some of the clinical signs of PHT?
these symptoms are associated with what type of underlying diseases?
- Ascites
- splenomegaly
- GI bleed
- jaundice
- abnormal LFTs
- variceal hemorrhage
- bacterial peritonitis
+ pancreatitis
+ liver disease
What is a common sign of cirrhosis
Jaundice
can a patient have PHT and have no symptoms
yes
what type of signs may be found on physical examination w/ PHT
- jaundice
- splenomegaly
- dilated abdo veins
- hepatic encephalopathy (confusion due to poor liver function)
what would we see sonographically is the patient had PHT
- increased diameter of veins
- portosystemic collaterals/portocaval anastomoses
- recanalized umbilical vein
- splenomegally
- increased HA flow
- ascities
how dilated do the MPV, the coronary vein and the umbilical vein have to be to be considered PHT
MPV: >13 mm
CV: >7 mm
UV: >3 mm
when might we use power doppler when assessing the liver
-for collaterals and tortuous vessels
how will the spectral waveform of the PVs change with PHT?
- biphasic flow (retro and ante)
- flow reversal in sever PHT… doesnt occur often because collateral prevent this
- loss of respiratory variation and decreased velocity
whats the mean velocity for the PV
what might a low peak indicate?
15-18 cm/s
- PHT
pulsatile portal venous flow, a ‘W’ pattern of the HV and a dilated IVC can indicate what type of disease process
CHF
what type of abnormalities/pathology can lead to portal vein thrombosis (PVT) as a primary condition
- liver disease
- hypercoagulability
- intestinal inflammation
- cirrhosis
- cancer
- trauma
what are the US findings of a PVT
- enlarged PV
- lack of flow/decreased flow
- periportal collateral flow
- enlarged hepatic artery w/ increased flow
what is periportal collateral flow or shunts (important)
another term for it
- it is a cavernous transformation or shunt that occurs only in chronic PVT
- they are made from preexisting vessels
- portosystemic collaterals or portosystemic shunting
is PV occlusion typically reversible?
no… usually permanent due to scarring/fibrotic changes which cause the vessel to basically disappear
what are the 3 common pitfalls when looking for PVT
- undetected thrombus
- missed low velocity flow (use PW doppler)
- bad doppler angle
what is Budd Chiari syndrome and which vessels does it commonly effect
hepatic vein occlusion… involves major HV or IVC
whats the causes of HV occlusion?
- compression
- clot
- tumor
- cirrhosis
- membranous obstruction of IVC (congenital disorder with strand of tissue in the IVC impending HV flow to the IVC)
what are 3 causes of increased hyper coagulability
- BCP, HRT
- polycythemia (over production of RBCs)
what are some signs and symptoms of HV occlusion
- hepatomegaly
- acute ascites
- abnorm LFTs
- splenomegaly and collaterals in chronic cases
what are the US findings of HV occlusion
- hepatomegaly
- caudate lobe enlargement
- clot in HV or IVC
- no flow
- narrow veins which lead to elevation of velocity and turbulence
- collaterals
where would collaterals commonly be seen in HV occlusion
connecting patent HV w/ portal system
what liver ratio is used as an indicator of HV occlusion
Caudate lobe ratio… it willl be enlarged so will have a small ratio
review the tables in notes…. pg 20, 21, 25
.
portosystemic collaterals director flow towards which vessels (in general terms)
mesenteric, splenic and portal veins
what specifically are the most common portosystemic collaterals
- coronary vein/left gastric vein
- umbilical vein
- splenorenal vein/lienorenal
which portosystemic collateral is the most common?
where is it located?
what can these collaterals progress to
coronary vein/left gastric vein
-around the celiac axis
+esophageal varices
why are esophageal varices clinical important?
what diameter of these vessels indicates PHT?
these vessels are fragile and if dilated are prone to hemorrhage
> 7 mm
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?
- hepatofugal and >3mm
- contain no blood flow
what are surgical shunts (therapeutic)
when would they be used?
-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
what is a Trans Jugular Intrahepatic portosystemic shunt (TIPS)
whats its success rate… what is the risk of having one?
-the most common type of surgical shunt made from metal
+ 90%
-subject to high rate of stenosis or occlusion
what are the early and late complications of TIPS
where is the most common area for stenosis to occur with a TIPS
early:
- thrombus or stenosis
late:
- neointimal hyperplasia invading the stent
+near the HV
in which artery would we see compensatory increased flow with a TIPS
HA
when is the liver transplant (LT) used as tretment
do we assess the liver pre and post transplant
-end stage liver disease
+yes
what are we looking for w/ a preoperative LT scan
- assesing patency of PV, HA, HV, IVC
- look for tumours
- look at biliary tree
what are we looking for w/ a postoperative LT scan
and when it is performed
- 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
what size is considered norm for the PV post liver transplant
15 mm
which vessel is most important to confirm patency
what should the RI, PSV and accel time be?
HA…
+ RI: 0.5-0.8
+ PSV: <200 cm/s
+ acceleration time: <0.08 sec
what are the postoperative transplant complications… which is the most common
- HA thrombosis (most common)
- stenosis
- PV thrombosis
- hematoma
- abscess formation
- AV fistulas
where does stenosis often occur post transplant
at surgical anastomoses sites
what will indicate clot in the HA post transplant
- no flow
- lower PSV
- decreased diastolic flow
viability of the liver is critical to flow in which vessel
HA`
When assessing the IVC, where should we be sampling?
As close to the diaphragm as possible
What’s the norm range of PSV for the HA?
70-150 cm/s
What’s the norm velocity of a TIPS
Abnorm
90-190…. abnormal is <50
Should be similar velocities on both ends
What’s a norm and abnormal PV peak velocity with a TIPS
Norm: at least 30 cm/s
Abnorm: <30 cm/s
What can the caliper of the MPV be up to with a TIPS
Up to 15 mm
With a TIPS, whats an abnormal velocity gradient at a stenosis
> 100 cm/s
What quality of flow would you see with an abnormal tips? Normal?
Continuous flow and RPV/LPV flow away from the stent
Pulsatile flow…. RPV/LPV flow towards the stent
A splenic vein diameter of greater than what value is indicative of PHT
> 10 mm
W/ CHF or increased R sided heart pressure, will the HV and PV have increased pulsatility
Yes
If the IVC is occluded can this cause primary or secondary hepatic vein occlusion?
secondary
what type of HV waveform will Budd Chiari Syndrome patient show?
- decreased, absent or revered flow
- dampened HV spectral tracing
- increased turbulence and focal increase of velocity if the veins are narrowed
are focal areas of narrowing normal with a TIPS
no
Which vessel does the coronary vein drain into?
Main portal vein (comes from the stomach)
Where does the umbilical vein travel?
From umbilicus to tip of LPV
intrahepatic causes of PHT refer to blood flow in the liver at what level?
the capillary/sinusoid level
which intraheptatic cause of PHT is the most common
cirrhosis
a TIPS shunt connects which 2 vessels
the MPV and a HV (usually RHV) and possess through the liver tissue
when end of the TIPS shunt is the most common site of stenosis
HV end
with a normal TIPS stent, what should the direction of flow be in the LPV/RPV
hepatofugal (towards the stent) instead of the normal heatopedal w/o a stent
