Portal Venous Flashcards
TIPS
therapeutic porto-sytemic shunts
portal venous system
vessels involved in drainage of capillary beds of GI tract and spleen to the liver
liver receives blood from
PV- deoxygenated
HA - oxygenated
pressure of portal blood are
lower than in other organs
portal HTN most commonly due to
liver cirrhosis
liver cirrhosis can be due to
EtOH or viral
morbidity from PHTN
bleeding from GE varices
liver failure
hepatic blood flow
HVs drain into IVC
blood from PV branches pass through
cavities between hepatocellular sinusoids
blood flow from HA
mixed in sinusoids to supply hepatocytes with oxygen
mixture of blood HA and PV
percolates through sinusoids, collects in central vein, drains into HV -> IVC
PV supplies _____ blood to liver
70-75%
HA supplies _____ blood to liver
25-30%
MPV formed by confluence of
SMV, SV
MPV terminates at
porta hepatis
MPV courses
SUP, to right, behing 1st portion of duodenum
HA flow direction
hepatopedal
HA flow pattern
low resistance
HA PSV
30-40 cm/s
HA EDV
10-15 cm/s
HA RI
0.6 -0.7
PV flow
low velocity, hepatopedal
PV flow velocity
10-40 cm/s
PV flow profile
slightly phasic: increase with inspiration, decrease with expiration
measure MPV diameter where
crosses IVC
HV normal flow
pulsatile, phasic: increase with inspiration, decrease with expiration
HV normal flow pulsatile due to
transmission of RA pulsations
HV velocity
22-39 cm/s
left gastic vein aka
coronary vein
PV tributaries
left gastric vein, IMV
collateralization results in
normalization of PV flow and calibre
PHTN when portosystemic pressure gradient is
> 10 mmHg
increase in portosystemic pressure gradient due to
increase in resistance to flow within liver
increase in resistance to flow within liver can be secondary to
morphological abn, circulatory vasoconstrictors
hyperdynamic circulation
increased liver congestion, worsened portosystemic gradient
prehepatic causes of PHTN
thrombosis of PV or SV
extrinsic compression of PV
congenital atresia of PV
intrahepatic causes of PHTN
cirrhosis
hepatic fibrosis
lymphoma
post hepatic causes of PHTN
IVC obstruction
HV obstruction
PV changes with PHTN
increased MPV diameter
loss of respiratory variation (phasicity) - waveform flattens
decreased velocity - bidirectional, then reverses
HA changes with PHTN
flow increases as PV flow decreases, HA becomes dilated and tortuous with cork-screw appearance
SV and SMV changes with PHTN
diameter will not increase with deep inspiration
vascular changes with PHTN
portosystemic collaterals
normal gradient of PV
< 7 mmHg
mild pHTN
7-10 mmHg
PHTN resulting in GE varices
10-12 mmHg
PHTN with increased risk of variceal bleeding
> 12-15 mmHg
most specific US finding for PHTN
portosystemic collaterals (varices)
incidence of varices is related to
severity of liver disease
risk of bleeding in GE varices directly related to
portosystemic gradient
________ % of varices can be visualized
65-95 %
cirrhosis volume redistribution
right lobe - smaller
increased size of caudate lobe + lateral segment of Left lobe
cirrhosis appearance
coarse, nodular surface, focal masses, heterogeneous, ascites, splenomegaly, Gamna-Gandy nodules
Gamna-Gandy nodules
splenic siderotic nodules
Gamna-Gandy nodules
focal deposits of iron and calcium in spleen, echogenic, less than 1 mm
PHTN treatment
pharmocological therapy - beta blockers
endoscopic procedures - scherotherapy, variceal ligation
surgical - decompressive shunts, devascularization procedures, liver transplant
TIPS
transjugular intrahepatic portocaval shunt
TIPS - what is it
stent inserted between the hepatic inflow (portal system) and hepatic outflow (HV or IVC)
TIPS for who
pt with persistent uncontrolled bleeding from esophageal varices
TIPS contraindications
HCC - esp in right lobe polycystic liver disease - lack of adequate liver parnchyma to keep stent in stable position acute infection biliary obstruction - risk of bile leak PV thrombosis severe hepatic encephalopathy inadequate liver reserve - fulminant liver failure due to ischemia severe right heart failure
TIPS is effective for
reducing ascites, preventing hemorrhage from GE varices, improving quality of life for patients with cirrhosis
fulminant
severe and sudden onset
TIPS causes of acute morbidity
hemorrhage, cardiopulmonary failure (due to volume overload), infection, hepatic encephalopathy
hepatic encephalopathy
toxic metabolites present in blood stream due to improper liver function. (liver not removing toxins, filtering blood properly)
velocities with TIPS are
higher
TIPS flow direction
hepatopetal at portal end (into liver)
hepatofugal at hepatic end (towards IVC)
LPV and branched of RPV direction
hepatofugal - towards TIPS
normal flow velocity in TIPS
> 90 cm/s up to 200 cm/s, turbulent
normal flow velocity in PV with TIPS
> 40 cm/s
velocities in HV less than ___ suggest impending failure
30 cm/s
velocities at portal end of shunt less than ___ suggests stenosis of concern within TIPS
50 cm/s
post TIPS waveform
monophasic, slightly pulsatile, moderate turbulence- spectral broadening
PSV in shunt should be
50-60 cm/s
PSV in shunt can be up to
90-120 cm/s, can be pulsatile
new onset of ascites indicates
stenosis in shunt
recurrent varices suggests
stenosis in shunt
hepatopetal flow in LPV despite well-functioning shunt indicates
recannalized umbilical vein
reversed flow in HVs suggests
stenosis (flow directed towards TIPS)
most pts with stenoses are
asymptomatic
stenoses usually occur at ___ end of stent
hepatic end
TIPS occlusion may be indicated by
varices, ascites, pleural effusion
late TIPS stenosis or thrombosis
pseudointimal hyperplasia, turbulent blood flow
velocity at portal end should be ____ to velocity at hepatic end
similar
PV velocity post TIPS
at least 30 cm/s; 37-47 cm/s
