Diagnosis and interventional Radiology in portal hypertension

1. Radiology in Portal Hypertension
Dr.D.Sunil Kumar

2. • Portal hypertension is a clinical syndrome that
develops when the resistance of blood flow
within the portal vein system increases.
• Portal hypertension is defined when portal
venous pressure greater than 12 mmHg.
• An actual direct measurement of portal
pressures is an invasive technique and obtained
in only in a small minority of patients.
• The non-invasive imaging modalities, in particular
ultrasound, play a crucial role in the diagnosis
and management of portal hypertension.

3. • The goals of USG are
– Make the diagnosis
– Establish the cause
– Evaluate the risk of complications
Ultrasonography

4. Portal Vein
• Portal vein diameter:
• Traditionally, enlargement of the portal vein has been considered a
sign of portal hypertension.
• Main portal vein with a dimension > 13 mm in the supine position,
has a sensitivity of 40% or less, with an accuracy of around only
60%.
• Several physiologic factors may cause size variation in the portal
vein.
– postprandial increment in splanchnic flow
– Respiratory phasic change
– Gravity
– patient positional change
Therefore this measurement is diagnostically
unreliable

5. • Relative change in size of the portal vein with
respiration is a more sensitive, rarely assessed,
finding.
• An increase of less than 20% in the diameter
of the PV with deep inspiration indicates
portal hypertension
– sensitivity 80% and specificity 100%.

6. • Portal Vein Doppler:
• Normal portal venous flow is
hepatopetal flow, throughout
systole and diastole with mild
superimposed respiratory phasicity
and cardiac periodicity.
• The degree of portal vein phasicity
is highly variable and is quantified
with a Portal vein pulsality
index(PI).
• PI =V2/V1, normal > 0.5.
• V1 = peak portal velocity,
corresponds to systole
• V2 = the trough velocity
corresponds to atrial contraction at
end diastole.
High phasicity
Low phasicity

7. • Portal hypertension
– Initially hepatopetal,
but may demonstrate
loss of respiratory
phasicity and more
pronounced cardiac
periodicity ie)
increased pulsatility
and abnormal pulsality
index.
– progresses to an
absence of end-
diastolic flow,
arterialized flow or
bidirectional “to-and-
fro” flow.

8. • Rarely, in severe portal hypertension, with increasing hepatic
parenchymal scarring and fibrosis, portal vein becomes the
pathway of least resistance for the hepatic arterial inflow,
resulting in reversed portal vein flow

9. • Portal vein velocity:
• Normal - 16–40 cm/sec
• Portal hypertension
– < 16 cm/sec diagnostic for portal hypertension
– mean PV velocity may increase in the presence of
a patent paraumbilical vein.
A slow or reversed flow are two of the most
specific findings for portal hypertension.

10. Hepatic artery (HA)
• In normal subjects the HA possesses forward flow
in diastole due to a low-resistance peripheral
vascular bed
– Normal RI = 0.5 to 0.7.
– arterial resistance index increases in cirrhosis.
• RI of HA is not specific or sensitive to allow a
diagnosis of portal hypertension, since it can fall
below 0.5 in cases of portal vein thrombosis and
cirrhosis with arteriovenous shunts.

11. Hepatic veins (HVs)
• Normal –Triphasic
• Can be biphasic with
predominantly antegrade flow
(hepatofugal)
• Waveform represents Complex
alternating antegrade-retrograde
pressure or flow variations, as a
result of transmitted cardiac
pulsations and reflux of blood
from the right atrium into the
veins during systole.
• a wave – atrial contraction
• s wave – atrial filling
• d wave – ventricular filling
• The ideal time to acquire the
spectral waveform is during a
small (incomplete) inspiratory
breath hold.

12. • Causes of decreased
phasicity and loss of
triphasicity of
hepatic veins are
– cirrhosis
– hepatic vein
thrombosis (Budd-
Chiari syndrome)
– hepatic veno-
occlusive disease
– hepatic venous
outflow obstruction
from any cause

13. • As severity of disease progresses and the veins
become more compressed by fibrotic constriction or
parenchymal edema, they lose their ability to
accommodate retrograde flow causing dampening of
the normal pulsatile flow pattern seen as decreased
phasicity (decreased pulsatility) and spectral
broadening.
• Decreased venous compliance is seen as a
waveform with a proportional loss of phasicity.
• A quick and reliable way to grade the severity of
decreased phasicity is to visually assess the
waveform, focusing on how far the a wave drops
below the baseline.

14. • normal phasicity - a wave above the baseline

15. mildly decreased phasicity - a wave goes below the
baseline, but has not crossed the halfway between the
baseline and the peak negative excursion of the wave.
Seen in 10 % normal individuals.

16. • moderately decreased phasicity - a wave is at
least halfway between the baseline and the
peak negative excursion of the waveform

17. • when waveform loses all phasic variation (ie,
becomes nonphasic) and no component
waves can be distinguished, phasicity is
severely decreased.

18. Splanchnic veins
• Enlarged splanchnic veins (superior
mesenteric vein (SMV) and splenic vein (SV)
diameter of more than 10 mm) are suggestive
of portal hypertension.
• Reversed flow may be detected in the SMV or
SV at Doppler sonography
– less than 5% of cases of portal hypertension
– classified as Child’s B and C.

19. • In portal hypertension shunting of blood away from the
liver into the systemic venous system provides a
mechanism of reducing portal venous pressure.
• The main sites of collateral pathways are :
– distal oesophagus: left gastric (coronary) vein and short
gastric veins to distal oesophageal veins
– splenorenal (lienorenal) ligament: splenic vein to left
renal vein - splenorenal shunt
– retroperitoneum: superior mesenteric veins to
retroperitoneal/lumbar veins to the inferior vena cava
– anterior abdominal wall: paraumbilical vein to
subcutaneous periumbilical veins (caput Medusae)
– anal canal: superior rectal vein (from inferior mesenteric
vein) to upper anal canal veins (haemorrhoids)
Portosystemic collateral vessels

20. • Gastro-oesophageal Junction:
– They are best visualised ultrasonically through the left
lobe of the liver. These vessels are of particular
importance as they may lead to life threatening variceal
haemorrhage.
Longitudinal sonogram in a
patient with cirrhosis and
portal hypertension. Note
the markedly enlarged and
tortuous left gastric varices
(V). These continue to
anastomose with
esophageal veins.

21. • Paraumbilical vein
• This collateral originates from
the left portal vein, runs in the
recanalised ligamentum teres
of the falciform ligament and
connects with the superior and
epigastric veins, of the
systemic circulation, around
the umbilicus.
• Hepatofugal venous flow in
the ligamentum teres with
velocity greater than 5 cm/sec
or visualised anterior to the
liver’s surface is highly specific
for presence of portal
hypertension.

22. Splenorenal and gastrorenal
collaterals• Tortuous vessels may be
seen in the hilar region of
the spleen and left
kidney.
• These are best visualised
using the enlarged
spleen as an ultrasonic
window.
• There will be associated
asymmetrical
enlargement of the left
renal vein, although this
can also be seen with
renal arteriovenous
fistula and renal tumours.

23. • Intestinal:
• These collateral pathways occur in areas where
the gastrointestinal tract is retroperitoneal (e.g.,
ascending and descending colon and duodenum)
and they connect pancreaticoduodenal,
retroperitoneal and omental veins with renal,
phrenic and lumbar veins.
• The ease with which these vessels are identified
on ultrasound depends to a large degree on the
amount of air in the bowel at the time of the
study as well as the size of the collateral vessels.

24. • Haemorrhoids:
• Collaterals in this region connect the inferior
mesenteric veins, via the superior rectal veins,
with the middle and inferior rectal veins of the
systemic circulation.
• Usually, conventional transabdominal
sonography cannot detect rectal/ pararectal
varices but these can be seen using
transvaginal scanning.

25. • Detection of abnormal collateral vessels
appears to be one of the most sensitive (70-
83%) and specific sonographic signs of portal
hypertension.
• The more severe the portal hypertension the
higher the number of portosystemic
pathways.

26. Splenomegaly
• Splenomegaly (>12 cm in longest
axis) is often seen in portal
hypertension.
• It is usually only mild to
moderate in degree and may be
the only evidence of elevated
portal pressures.
• Conversely, the absence of
splenomegaly does not rule out
portal hypertension.
• Siderotic Gamma-gandy bodies
are present in approximately
13% of cases and on ultrasound
appear as multiple hyperechoic
foci suggest that splenomegaly is
due to portal hypertension.

27. • In portal hypertension, the
splenic vein may be sclerotic
and show atheromatous
change in its intima.
• On longitudinal sonographic
section this would appear as
small echogenic parallel lines
containing blood flow on
colour doppler and are termed
as “reflective channels”.
• Their presence has been
proposed as a means of
differentiating splenomegaly
due to portal hypertension
from that due to other causes.

28. • Causes can be split in their relation to the hepatic
sinusoids:
• pre-sinusoidal
– portal vein thrombosis
– extrinsic compression of portal vein
– Schistosomiasis (S. mansoni or S. japonicum)
• sinusoidal
– cirrhosis
• post-sinusoidal
– Budd-Chiari syndrome
– hepatic veno-occlusive disease
– right heart failure or biventricular cardiac failure
Establishing the cause

29. CT Imaging
• Can demonstrate the portal venous system and
portotosystemic collaterals with minimum interference of
bowel gas, bone or fat.
• The use of multi– detector row CT combined with
postprocessing of the imaging data with a variety of three-
dimensional reformatting techniques (eg, maximum
intensity projection, shaded surface display, volume
rendering) allows creation of vascular maps whose quality
equals or exceeds that of maps created at classic
angiography for many applications.
• Three-dimensional multi– detector row CT portal
venography can help determine the extent and location of
portosystemic collateral in patients with liver cirrhosis and
is probably the optimal imaging technique in this setting.

30. Three-dimensional reformatting techniques for 3D multi–detector row CT portal
venography. MIP and SSD(shaded surface display) CT portal venograms show the
portal vein and the dilated left gastric varix

31. (a) Axial CT scan shows a dilated left gastric
vein (b) Coronal MIP CT portal venogram
shows the left gastric vein (solid arrow) and
short gastric vein (arrowhead). Esophageal
varices (open arrow) are seen to communicate
with the left gastric vein through the gastric
fundal varix.

32. Abdominal wall and paraumbilical varix. (a, b) Axial (a) and sagittal oblique (b)
MIP CT portal venograms show the paraumbilical vein (solid arrows)
as it extends superiorly and inferiorly to the anterior abdominal wall
(arrowheads in b)

33. Retroperitoneal shunt. (a) Axial CT scan shows tortuous dilated vessels (arrows) in the
medial portion of the left kidney. (b) Coronal MIP CT portal venogram demonstrates a
tortuous, dilated retroperitoneal shunt (arrows) that communicates with the inferior
vena cava (I) through the left renal vein (R).

34. MR Imaging
• MR portography
– Gadolinium enhanced breathhold MR portography
can now be achieved using fast imaging techniques
within 20-30 s.
– Higher dose (0.2 ml/kg) is required as contrast gets
diluted by the time it reaches the portal vein.
– Contrast enhanced MR is superior to doppler in
identifying collaterals.
– Pitfalls:
• Insufficient enhancement due to dilution of contrast
• Motion artifacts due to requirment of breathholding.

35. Interventional radiology in the
management of portal hypertension

36. • The primary goal in treating portal
hypertension is reduction in the portal venous
pressure itself.
• This should minimise the complications of
portal hypertension such as bleeding from
varices and congestive gastroenteropathy,
accumulation of ascites and hydrothorax, or
the hepatorenal syndrome, etc.
• When it is not possible to achieve this primary
goal, various procedures can be offered to
palliate or control the symptoms related to
portal hypertension.

37. • Interventions that reduce portal blood pressure:
a. Transjugular intrahepatic portosystemic
shunts(TIPS)
b. Recanalization of hepatic venous outflow
c. Recanalization of the occluded portal vein
and its tributaries
d. Embolization of arterioportal fistula
e. Partial splenic embolization
f. Revision of occluded surgical or radiological
portosystemic shunts

38. • Interventions to palliate symptoms related to
portal hypertension (without altering the
portal blood pressure):
a. Percutaneous transhepatic variceal
embolization
b. Balloon retrograde obliteration of gastric
varices (BRTO)
c. Percutaneous peritoneovenous shunt

39. Transjugular intrahepatic
portosystemic shunt (TIPS)
• Shunt created within the
liver parenchyma between
the hepatic vein and the
portal vein.
• Usually an 8-10 mm diameter
stent is chosen to
decompress the hypertensive
portal circulation to achieve a
final portosystemic gradient
of less than 12 mm Hg.

40. • The procedure involves many steps:
– (1) puncture of the jugular vein
– (2) cannulation of the hepatic vein
– (3) passage of a long needle from the hepatic vein,
through the liver parenchyma and into the portal vein
– (4) dilatation, with an
angioplasty balloon,
of the parenchymal
tract created by the
needle
– (5) stent deployment
to ensure patency
of the tract.

41. • Contraindications
– congestive heart failure
– severe pulmonary hypertension
– severe tricuspid regurgitation
– hepatic failure
– preexisting encephalopathy
– unrelieved biliary obstruction
– multiple hepatic cysts
– uncontrolled systemic infection
• Relative contraindications
– presence of large liver tumors
– hepatic vein thrombosis
– portal vein thrombosis
– Thrombocytopenia (<20,000/cm3)
– severe coagulopathy (INR >5)

42. TIPS performed in a patient with uncontrolled variceal
bleed. Portal venogram (A) obtained after puncture of the portal vein
shows retrograde fi lling of the left gastric vein and feeding of a large junctional
Varix.. The post-TIPS venogram (B) shows good fl ow across the TIPS. Adequate
decompression is evident from the non-fi lling of the left gastric vein and
varices and reduction of the portosystemic gradient to 4 mm Hg

43. • TIPS is successful in more than 95% of patients
and is generally safe, with a procedural mortality
of <1%.
• TIPS gives excellent short-term results by
controlling bleeding in >90% cases and controlling
ascites and hydrothorax in >70% cases.
• The poor outcome can be predicted using various
prognostic indicators
– serum bilirubin ( >3 mg/dl)
– Child-Pugh score ( >12)
– modified MELD score (>25)
– APACHE II score (>18)
– Emory risk score (>3).

44. • The long-term results of TIPS are impaired by the
high rate of shunt dysfunction from intimal
hyperplasia and the resulting recurrence of
symptoms
• Regular Doppler or angiographic surveillance of
TIPS is advised for early detection of shunt
stenosis.
Mid-shunt stenosis (arrow) in a Wallstent,
causing reappearance
of varices and ascites. This was treated by
balloon dilatation

45. • DIPS:
• Direct intrahepatic portocaval shunt (DIPS) placement
is a further modification of the TIPS procedure in which
intravascular US guidance is used for puncture from the
intrahepatic IVC to the portal vein through the caudate
lobe.
• An intravascular US probe is advanced from the right
common femoral vein to the intrahepatic IVC.
• Intravascular US is then used to guide a needle
puncture from the IVC into the PV near its bifurcation
via the caudate lobe of the liver.
• The DIPS procedure can be extremely helpful in
patients with challenging anatomy, such as inadequacy,
thrombosis, or calcification of the portal vein or
unsuitable parenchymal tract due to hepatocellular
carcinoma, and can also be used as an alternative to
occluded TIPS revision

46. Recanalization of Hepatic Venous
Outflow
• Budd-Chiari syndrome includes all obstructions to the
hepatic vein outflow at the level of the hepatic vein and/or
the inferior vena cava causing hepatic congestion which,
when left untreated, progresses to hepatic necrosis and
fibrosis.
• Recanalizing the hepatic vein or IVC by means of balloon
angioplasty or stent placement can relieve hepatic
congestion and prevent progression to irreversible liver
damage.
• This is feasible if the obstruction is over a short segment.
• Long segment hepatic vein occlusion is difficult to reopen
and even if restored the reocclusion rates are extremely
high. They require portosystemic shunt and are benefited
by TIPS.

47. Budd-Chiari syndrome secondary to hepatic vein occlusion.
The middle hepatic vein is obstructed close to its insertion into the
inferior vena cava (A); after insertion of a balloon-expandable stent at
the level of the occlusion, the hepatic venous outfl ow is restored (B)

48. Recanalization of the Portal Vein and
Its Tributaries
• Extrahepatic obstruction
of the portal vein or its
branches accounts for 5-
10% of all cases of PHT.
• Recanalization of the
blocked vein by
angioplasty and stenting
will reduce these
symptoms and can be
done either via a
transjugular or a
percutaneous
transhepatic route
Large duodenal varices due to focal occlusion of
the superior mesenteric vein (SMV. After
percutaneous transhepatic access to the portal
vein (A), a catheter is advanced into the SMV.; the
occluded segment is dilated and a stent deployed,
following which there is direct flow from the SMV
into the portal vein and no fi lling of the duodenal
varices (B)

49. Embolization of Arterioportal Fistulae
• Arterioportal fistulae (APF) are a rare cause of PHT.
• They may be congenital or secondary to trauma,
surgery, percutaneous biopsy or other liver procedures,
and liver tumors.
• Although silent most of the times, some patients with
large APFs can present with features of PHT such as
bleeding, ascites, and splenomegaly.
• The preferred treatment is transarterial embolization
of the feeding artery, using coils, detachable balloons,
or glue.
• The procedure is usually successful, provided the
fistula is not too large and is accessible.

50. Partial Splenic Embolization (PSE)
• This is done particularly when hypersplenism or
splenic vein occlusion is a prominent feature.
• The procedure involves superselective
catheterization and embolization of the
intrasplenic arterial branches, usually with
polyvinyl alcohol particles.
• This diminishes inflow of blood into the portal
vein, causing secondary reduction of the portal
venous pressure, reduction in splenic size and
improvement in hypersplenism-induced
thrombocytopenia.

51. Interventions to palliate symptoms related to
portal hypertension

52. Percutaneous Transhepatic Variceal
Embolization(PTE)
• Earliest intervention performed for portal hypertension
• In this technique, the portal vein is catheterized by a
percutaneous transhepatic approach and the gastric
vein feeding the varix is embolized with ethanol, steel
coils, or cyanoacrylate glue.
• Recurrent bleeding was seen in 10%–60% of cases,
since the underlying portal hypertension was
unaffected.
• PTE itself was responsible for inducing portal vein
thrombosis in up to 36% of patients.
• The introduction of Endoscopic therapy, TIPS and BRTO
antiquated the procedure, and PTE is now very rarely
performed.

53. Balloon-occluded Retrograde Transvenous
Obliteration of Varices (BRTO)
• Primarily for
bleeding gastric
varices
• Most isolated fundal
or fundal-cardiac
varices drain
through a developed
gastrorenal shunt.

54. • The technique involves advancing a balloon
catheter from the femoral vein into the outlet of
the gastrorenal shunt.
• Following balloon occlusion of the shunt,
sclerosant (5% ethanolamine oleate) is injected
retrogradely
to fill the gastric
varices.
• After adequate
contact of the
sclerosant with the
variceal wall, the
sclerosant is aspirated
And the balloon
catheter is withdrawn.

55. • It is as effective as TIPS in controlling gastric
variceal bleeding and has an added advantage in
that it augments portal blood flow by occluding
the natural shunt that takes blood away from the
portal vein.
• This improves liver function in cirrhotic patients
and also prevents encephalopathy, a problem
commonly associated with TIPS.
• However, occlusion of the gastrorenal shunt may
aggravate existing esophageal varices or lead to
the development of new ones, and this is one the
most significant complications of BRTO.