This presentation is prepared by Dr Parikha Rampal, Senior Resident, Department of Radiology, ABVIMS & Dr RML Hospital, New Delhi

1. IMAGINGINPORTAL
HYPERTENSION

2. ANATOMY
• Portal vein formed by the joining of
the splenic vein and the superior
mesenteric vein behind the neck of
the pancreas at the level of L1-L2
vertebrae.
• Other tributaries are
 Inferior mesenteric vein (IMV)
 Coronary vein (left gastric vein)
 Right gastric vein
 Pancreaticoduodenal vein
 Cystic vein

3. PORTAL VEIN PARAMETERS
• LENGTH – 6-8cm
• CALIBRE – 9-13mm
• DIRECTION OF FLOW – Hepatopetal
• VELOCITY OF BLOOD FLOW – 15-18cm/sec
• PRESSURE – 5-10mm Hg
• NORMAL WAVEFORM – undulating pattern

4. DEFINITION OF PORTAL HYPERTENSION
Portal Hypertension is defined by
• Wedge hepatic venous pressure or direct portal vein
pressure more than 5mmHg greater than IVC pressure.
• Splenic vein pressure greater than 15mmHg, or
• Portal vein pressure(measured surgically) greater than 30cm
of water

5. CAUSES
PREHEPATIC
Caused by obstruction of
the portal, splenic or
superior mesenteric veins.
• Portal vein thrombosis,
extrahepatic portal vein
obstruction.
• Congenital origin such as
aplasia or hypoplasia
• Infection such as
pyelophlebitis
• Splanchnic arteriovenous
fistula
INTRAHEPATIC
Caused by intrinsic causes
of the parenchyma
• Cirrhosis due to various
causes
• Congenital hepatic
fibrosis
• Noncirrhotic portal
fibrosis/idiopathic portal
hypertension
POSTHEPATIC
Caused by diseases
obstructing the blood
outflow from the liver
• Budd chiari syndrome
• Veno-occlusive disorder

6. hjj
Increased arterial
resistance
Increased arterial flow
from hepatic artery to PV
Increased intrahepatic
resistance due to various
causes
Obstruction of blood flow into the distal
sinusoids
Reduction of blood flow from PV & hepatic artery
into the hepatic veins
Increase in PV pressure
Collateral pathways open directing
blood away from liver
Increased sinusoidal
pressure
Liver cell
failure
ascites
Increased
fluid in space
of disse
Congestion of SPA
PATHOPHYSIOLOGY

7. APPROACH

8. PATIENT PRESENTATION
Abdominal pain
Abdominal distension (due to ascites)
Haematemesis, melena due to variceal bleed
Dilated veins seen around the umbilicus (caput medusae)
Altered sensorium/ confusion due to hepatic encephalopathy

9. PATIENT WORK UP
Laboratory studies –aimed at identifying the cause of portal
hypertension
• LFT
• PT
• Serum albumin
• Hepatitis serology
• Platelet count
• Presence of ANA, Alpha 1 Antitrypsin levels
• Ceruloplasmin levels

10. AIM OF ULTRASONOGRAPHY
• To establish the diagnosis
• To look for the cause of portal hypertension
• To evaluate the complications
This is the first imaging modality to be used.

11. ULTRASONOGRAPHY & DOPPLER FINDINGS
Things to look for -
Liver size and echotexture, margins, focal SOL’s
Patency of the Splenoportal axis (Main Portal vein/ splenic vein/
SMV)
Diameter of the Splenoportal axis
Direction of flow( hepatopetal/ hepatofugal)
Respiratory variation of the portal blood flow
Spleen size
Presence of free fluid in the peritoneal cavity
Presence of porto-systemic collaterals

12. the image shows Portal
vein bifurcation with an
intraluminal thrombosis
extending into its
Subchondral sonographic view of
liver depicting coarsened
echotexture with irregular margins
and ascites.
The image shows a
dilated portal vein
with its calibre 17mm
1cm before
GRAY SCALE USG FINDINGS IN PORTAL HTN

13. CHANGES IN PORTAL VEIN IN PORTAL HTN
• The normal portal vein - undulating hepatopetal flow
• Mean portal vein velocity 15-18cm/sec, varies with respiration and
cardiac pulsation.
• As portal htn. develops, the flow in portal vein loses its undulating
pattern and becomes monophasic. As the severity of portal hypertension
increases, flow becomes biphasic and finally hepatofugal.
• Portal vein diameter >13mm indicated portal Htn, however this finding
lacks sensitivity due to the collateral pathways which partially
decompress the system.
• The loss of variation in portal vein diameter with respiration is a more
sensitive and specific measure of portal hypertension.
• Reversal of portal blood flow is also indicative of portal hypertension,

14. NORMAL PORTAL VEIN WAVEFORM
• A-The vein shows moderate
pulsatility. The velocity does not
touch zero and does not
reverse.
• B- The waveform shows a flat
monophasic flow.
• Congestion Index = PV cross
sectional area/PV velocity-
higher in patients with cirrhosis
& portal htn than in normal
subjects

15. COLOR & SPECTRAL DOPPLER FINDINGS IN
PORTAL HTN
• Color doppler view of right lobe of liver
shows two parallel vessels red being
the hepatic artery showing hepatopetal
flow and blue being the portal vein
with hepatofugal flow.
• Pulsed doppler waveform from the
same 2 vessels shows hepatic arterial
flow above the baseline and portal vein
flow below the baseline implying the
direction of flow to be opposite in the

16. CAVERNOUS TRANSFORMATION OF PORTAL
VEIN

17. HEPATIC ARTERY
• In normal subjects, the hepatic
artery possesses forward flow in
diastole due to a low resistance
peripheral vascular bed.
• Normal RI= 0.5-0.7
• Arterial resistance increases in
cirrhosis.
• In portal hypertension, the EDV of
the hepatic artery becomes greater
than the PSV of the portal vein.

18. Hepatic vein strictures in
cirrhosis
GRAY SCALE & COLOR DOPPLER FINDINGS IN HEPATIC
VEINS
Grey scale image of hepatic veins shows
a tapered luminal narrowing of the
visualised hepatic veins
Color doppler image shows appropriately
directed blood flow towards the IVC in blue and
color aliasing indicates rapid velocity flow
through the points of narrowing

19. SPECTRAL DOPPLER OF HEPATIC VEINS
• NORMAL SUBJECT PORTAL HYPERTENSION
INVERSION OF SYSTOLIC VEIN IS
SEEN

20. TRENDS OF DOPPLER PARAMETERS IN PORTAL
HTN.
HEMODYNAMIC PARAMETER TENDENCY IN PORTAL
HTN.
CLINICAL RELEVANCE
MEAN PORTAL VEIN VELOCITY DECREASE Cut off 15cm/sec
PORTAL VEIN CONGESTION
INDEX
INCREASE >0.1 s/o portal htn.
HEPATIC ARTERY PI INCREASE OR NO CHANGE >0.15 s/o severe portal
htn.
SPLENIC ARTERY RI INCREASE OR NO
CHANGE
>0.60 s/o portal htn
(gastroesophageal
varices)

21. PORTOSYSTEMIC COLLATERALS
• In order to decompress the portal system, there is diversion of
blood away from it into its tributaries causing congestion of
the Splenoportal axis.
• There is dilatation of the existing anastomoses between the
portal and systemic circulation so that the blood ultimately
reaches the heart.
LOCATION PORTAL CIRCULATION SYSTEMIC CIRCULATION
• Rectum and anal canal
• Umbilicus
• Bare area of liver
• Retroperitoneum
Superior rectal vein
Paraumbilical veins
Portal vein branches
Tributaries of splenic,
pancreatic and colic veins
Middle and inferior rectal
vein
Superior and inferior
epigastric veins
Inferior phrenic vein
Renal, suprarenal, gonadal
and paravertebral veins

22. TYPES OF VARICES

23. SPONTANEOUS SHUNTS
INTRAHEPATIC TRANSHEPATIC EXTRAHEPATIC
Rare Recanalised
paraumbilical vein
Gastrorenal
Splenorenal
Gastrocaval

24. MAJOR SITES IDENTIFIED ON USG
1.Gastroesophageal
junction
2.Paraumbilical vein
3.Splenorenal and
gastrorenal
4.Intestinal
5.Hemorrhoidal

25. IMAGES DEPICTING PORTOSYSTEMIC
COLLATERALS
• Sagittal image of a recanalised paraumbilical vein
with gross ascites
• Sagittal image of a large coronary vein running
cephalad from the splenic vein

26. Grey scale and color doppler image
showing varices in the distribution of the
coronary vein

27. Grey scale and color doppler image
shows splenic hilar varices

28. COMPUTED TOMOGRAPHY
•It is not a prime diagnostic tool for diagnosis
but its main indications are
• To demonstrate the collateral pathways
• To identify the possible cause of portal
hypertension
• To identify and characterize focal lesions like HCC

29. ESOPHAGEAL AND PARAESOPHAGEAL
VARICES
• These are the most common to occur in cirrhotic patients and also
the most common to bleed owing to the large volume of blood they
carry.
• These are supplied by the left gastric vein or the coronary vein which
arises at the portal confluence, traverses the gastric fundus and
drains into the veins of the lower esophageal plexus.
• Its anterior branch supplies the esophageal varices while its
posterior branch supplies the paraesophageal varices.

31. CRUVEILHEIR BAUMGARTER SYNDROME
• This sign refers to the venous hum heard over the umbilicus
or caput medusae due to the hepatofugal flow from the
recanalized paraumbilical vein.
• On CT, it is characterised by the presence of dilated tortuous
paraumbilical vein in patients with cirrhosis, which arises from
the left branch of portal vein, traverses along the falciform
ligament towards the umbilicus, forming a network of dilated
periumbilical veins, giving a ‘caput medusae’ appearance. The
blood eventually drains into the systemic circulation to finally

32. RECANALISED PARAUMBILICAL VEIN

34. SONOGRAPHIC CAPUT MEDUSAE SIGN
The grey scale image shows enlarged
tortuous vessels in the periumbilical
region.
The doppler image shows abundant
flow within these collaterals.
These collaterals arise from the
recanalized paraumbilical vein which
ultimately drains into the iliofemoral
system to return blood back to the
systemic circulation.

35. ECTOPIC VARICES

36. ROLE OF MRI
• Provides morphologic information comparable to CT scan when
USG findings are inadequate.
• MRI angiography helps in localizing and defining the presence
& extent of portosytemic collaterals.
• Phase contrast MRI - non invasive technique to measure flow in
a blood vessel without the use of iv contrast agents.

37. MR MARKERS OF HEPATIC ARCHITECTURE AND
SPLANCHNIC HEMODYNAMICS
• These have the advantage of estimating the HVPG accurately.
• Various markers such as
• T1 relaxation time is associated with the degree of fibrosis and
inflammation in the liver.
• The increase in splenic artery velocity measured using PC MRI is
likely to represent the hyperdynamic state of portal
hypertension.

38. CONTRAST ENHANCED US IN PORTAL
HYPERTENSION
• Second generation microbubble contrast agents for abdomen in use are
• Sonovue
• Sonazoid
• Definity

39. PHASES OF CONTRAST ENHANCEMENT
• Arterial enhancement (10-20 to 30-45sec)
• Portal venous phase(30-45 to 120sec)
• Late phase (after 120 sec to the time of microbubble
appearance)

40. CEUS of the liver showed enhancement of the hepatic artery in the arterial phase, right portal
vein in the Portovenous phase. In the post vascular phase, there is homogenous enhancement
of the liver parenchyma with the disappearance of enhancement in the portal and hepatic veins.

41. ROLE OF CEUS IN PORTAL HYPERTENSION
• The major advantage of contrast enhanced ultrasound is in
differentiating cirrhosis from idiopathic portal hypertension or non
cirrhotic portal hypertension (NCPH).
• This is essential as their prognosis and management is completely
different.
• Various studies have been done which show the unique architecture
of portal vein characteristic of NCPH, others showed a delayed
arterial hepatic periportal enhancement, also considered a
characteristic of NCPH.
• Studies have also reported a higher microbubble contrast
accumulation in IPH livers than in cirrhosis.

42. SPECIAL CONDITIONS
• EXTRAHEPATIC PORTAL VEIN OBSTRUCTION (EHPVO)
Causes : neonatal sepsis,
dehydration, umbilical vein
catheterisation,
hypercoagulable states
Large thrombus MPV Portal
cavernoma
Presinusoidal
resistance
EHPVO

43. IMAGING FINDINGS IN EHPVO
MPV is replaced by echogenic
fibrosis and multiple collateral
channels
around the porta i.e. cavernoma
formation.

44. BUDD CHIARI SYNDROME
• It is a disorder of hepatic venous outflow obstruction which
may involve the hepatic veins, IVC or both and is characterised
by the structural and functional abnormalities of the liver.
• Types-
Obstruction is at the level of IVC
Obstruction is at the level of hepatic veins
Mixed type

45. PRESENTATION
ACUTE
Due to large and sudden
blockage
Presents with sudden
abdominal pain, ascites,
tender hepatomegaly,
jaundice.
SUBACUTE
Insidious onset
So collaterals can
develop
CHRONIC
Presents with
postsinusoidal portal
hypertension, upper GI
bleed, pedal edema,
large nodular liver,
develops over a period
of several months.

46. CAUSES
Primary Secondary
When the obstruction is due
to a primary cause such as a
thrombosis, stenosis or web.
When the obstruction is due
to extrinsic compression by a
cyst, tumor or abscess.

47. IMAGING FINDINGS
• USG is the modality of choice for diagnosis, however it may be
suboptimal in cases of scarred or shrunken liver.
• Look for
Hepatic veins and their diameter (upto 10mm is normal)
Presence of intraluminal webs, thrombosis, membranes, within
the hepatic veins and IVC
Caudate lobe hypertrophy (>3mm in diameter is strongly
suggestive)
Hepatomegaly or shrunken liver +/-cirrhotic changes,
hypoechoic in echotexture( in acute settings)

48. COLOR DOPPLER FINDINGS
• Normal hepatic veins show a triphasic pattern with 2 negative
and 1 positive wave.
• In BCS, there is a loss of normal triphasic pattern of waves
• Presence of a flat waveform(uniphasic flow) without flutter or
absent or reversed flow in hepatic veins are the most reliable
signs of hepatic vein thrombosis.

49. IVC & HEPATIC VEIN THROMBOSIS

50. TAKE HOME MESSAGE
Portal hypertension is not the disease, rather the
manifestation of an underlying disease, so look for the cause!!!
Portosystemic collaterals are the most definite sign of portal
hypertension.
 Diagnostic modalities include
 Ultrasonography with color doppler study
 Computed tomography
Upcoming modalities include MRI, contrast enhanced

51. THANK YOU