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NON- INVASIVE IMAGING OF PORTAL
HYPERTENSION
DR. DEVKANT LAKHERA
Portal hypertension
Increase in portal pressure above 6-
10 mm Hg
Gradient - of more than 5 mm Hg
between hepatic veins and portal vein
Carries blood form GIT and spleen,
pancreas and gall bladder
PORTAL VEIN - Anatomy
Length - 6-8 cm
Caliber - 9-12 mm
Location:-
NECK OF PANCREAS
L1 –L2 vertebral level
Venules hepatic sinusoids
Terminal hepatic veins IVC heart
Hepatoduodenal ligament
Blood is not pumped  Driven via gradient
Pressure = Flow x Resistance
Gradient
Portal system
Caval venous
system
Valveless
Portocaval anastomosis
Distal esophagus
(Left gastric vein – oesophageal vein azygous  SVC)
Rectum
(Superior rectal– Middle and inferior rectal Internal
iliac)
Umbilicus
(Superficial epigastric  femoral  External iliac –
Paraumblical) (developed collaterals)
Tributary collaterals
Developed Collaterals (Hepatofugal)
gastrorenal// splenorenal// splenoretroperitoneal//
Paraumbilical vein: Runs in the falciform ligament and
connects the left portal vein to the systemic epigastric veins
near the umbilicus (close during development and reopen later
Pre-sinusoidal
(MC in India)
Sinusoidal Post-sinusoidal
Portal vein
thrombosis
Cirrhosis
(Hepatitis>
Alcoholic)
Budd-Chiari syndrome
Extrinsic
compression
of portal vein
Hepatic veno-occlusive
disease
Schistosomiasis Right heart failure
Causes of
cirrhosis
Hepatic
Intrahepatic
Non invasive imaging modalities
 Ultrasound and CDFI – Most widely used
Vascular patency
Presence of collaterals
Portal flow
Distinguish between extra and intrahepatic portal hypertension
Changes of cirrhosis
 Computed tomography and MRI – Portal venous system and collateral assessment.
INTRAHEPTIC PORTAL HYPERTENSION
USG evaluation of liver – Cirrhosis
-- Altered size
-- surface nodularity of with coarsened
echo texture
-- reduction in the number of visible portal
or hepatic veins
-- segmental hypertrophy/atrophy
◦ Transverse diameter segment IV - (<30 mm)
-- Splenomegaly and ascites.
Increased nodularity in liver undersurface enlargement of the caudate lobe
CT scan
Early - fatty infiltration (alcoholic liver disease)
Diminished volume
Nodularity of the liver, parenchymal
heterogeneity
Nonuniform lobar atrophy or hypertrophy may be
demonstrated
widening of the gallbladder fossa
enlargement of the lateral segment (LS) of the left lobe and
caudate lobe (C) of the liver, ascites, varices (red arrow), and
splenomegaly (S).
Prominent porta hepatis and intrahepatic
fissures - Hepatic atrophy
Regenerative nodules – Isoattenuating .
Very advanced cirrhosis with small nodular liver with
hypertrophy of the caudate lobe and extensive ascities
Hepatic C/RL ratio
line 1: Right lateral border of the portal vein
line 2: Left lateral border of the caudate lobe
line 3: Midway between the portal vein and the
IVC extended to the right liver edge
RL measurement: C measurement
caudate-right lobe ratio: C/RL
C/RL >0.65 = 96% likely to be cirrhotic//C/RL >0.73 = 99% likely
to be cirrhotic
: axial slice immediately below the bifurcation of the main
portal vein
Non cirrhotic portal fibrosis (Pre-sinusoidal portal hypertension
Smooth liver surface
Marked dilation of portal vein (selectively
left branch)
Thickening of portal vein wall
Increase in periportal echogenicity
increase in periportal echogenicity with normal parenchymal echotexture
CT
Normal sized liver
Splenomegaly
Dilated portal and splenic veins
1. Portal vein diameter
2. Portal flow direction
3. Portal velocity and waveforms
4. Presence of portosystemic collaterals
5. Hepatic vein evaluation
6. Hepatic artery changes.
VASCULAR EVALUATION IN PORTAL HYPERTENSION
Portal vein diameter –> 9-12 mm in quiet respiration
>13 mm indicates portal hypertension
(>17mm –Large varices)
Portal vein diameter
(1-2 cm proximal to bifurcation)
Splenic vein and
Superior mesenteric vein
Splenic vein and superior mesenteric
vein - Diameter > 10mm
increase of diameter <20% during
inspiration
Loss of respiratory variation in these vessels is important sign
Normal portal vein
flow and velocity
Undulating hepatopetal flow.
Remain above baseline
Mean portal venous flow velocity
- 12 to 18 cm/sec
Average portal flow – 500-900
ml/min
Normal portal venous flow direction and waveform.
Normal portal vein flow
May become accentuated in portal hypertension
Portal hypertension
Portal vein loses its undulatory pattern and
becomes monophasic.
Later flow becomes biphasic and finally
hepatofugal
Flow velocity < 12cm /sec
US image shows slow flow in the main portal vein
Reversal of flow –Hepatofugal flow
Interpretation of flow
Normal flow To and Fro flow Reversed flow
Portal hypertension Advanced PHTN
Cardiac failure
Other causes of portal vein dilatation
Portal vein dilatation and flow reversal can CHF.
--- portal flow is markedly pulsatile
--- dilated IVC
Cardiac failure
Tricuspid regurgitation
Portal vein - Exaggerated pulsatality
Vascular indices
Liver Vascular Index
(LVI = PVVel/ Hepatic Artery PI) - < 12 cm/sec
Congestive index :
Cross-sectional area mean flow velocity of the portal trunk - > 0.13 cm/sec
Effective liver perfusion
Both the volume flow and velocity – decrease
may increase - large paraumbilical collateral
is lower as calculated from flow volume in portal trunk minus portal flow volume in the
umbilical vein.
Important indicators of portal hypertension.
Left gastric
Short gastric
Paraumblical
Splenorenal
Splenoretroperitoneal
Splenocaval
Splenoportal
Portosystemic Venous
Collaterals
Left gastric (coronary vein) – Normally <4mm  > 7mm
Associate with esophageal and gastric varices
Short gastric veins-- spleen and gastric wall.
Left gastric (coronary vein)
Paraumbilical vein
Paraumbilical vein
Ligamentum teres in the left lobe of liver
Recanalized visible as a channel greater
than 3 mm in diameter
Hepatofugal flow
Recanalization of umbilical vein is a highly
specific sign of portal hypertension
Splenorenal shunts --Splenic hilar
Splenoretroperitoneal
Spenocalval
Splenoportal
Hepatic vein assessment
Doppler spectral traces from normal
hepatic veins have a triphasic appearance
two waves that represent atrial and ventricular
diastole and a small wave that occurs in atrial systole
Altered hepatic vein waveforms
50% of patients with cirrhosis  flattening of the
phasic oscillations
Loss of pattern
Monophasic flow
Cirrhosis (Poor prognosis)
Infiltrative liver disease
Budd Chiari (Hepatic vein thrombosis)
Pulsed Doppler waveform analysis shows loss of the normal
triphasic hepatic vein pulsatility.
Exaggerated phasicity
Congestive heart failure
Tricuspid incompetence
Hepatic artery
normal hepatic artery (HA)
-- 4-6 mm
-- 25 to 30% of blood to the liver.
-- anterior to the portal vein
systolic velocity - 30 to 40 cm/sec and
diastolic velocity - 10-15 cm/sec
.
HEPATIC ARTERY
Resistivity Index -0.55 to 0.81
Pulsatility index (PI) - 1.16 to 1.24
Increased in chronic liver disease
CT
Splenoportal axis – Best visualized on portal phase
images
Retroperitoneal and mesenteric collaterals are better
visualized on CT
Axial CT scan showing esophageal (white arrow) and
paraesophageal (red arrow) varices. Superficial collateral
vessels are also present (yellow arrows
Coronal reformatted MDCT image shows short gastric and
perigastric varices (arrow).//Axial CECT in portal phase showing
recanalized paraumbilical vein.
Extrahepatic portal hypertension
Portal vein occlusion –Thrombosis, Tumor
invasion or compression.
Causes
◦ Sepsis.
◦ Acute Pancreatitis
◦ Tumor invasion – Pancreatic / HCC
◦ Hypercoagulable states
Non visualization of portal vein to thrombus occluding the of
PV (echogenic intraluminal material(arrow) or absent color flow
CT
Presents
Low attenuation filling defect
Lack of portal vein enhancement
Portal vein thrombosis
Contrast-enhanced fat-saturated T1-weighted
MRI in a 62-year-old woman with near-
occlusive thrombus in the main portal vein
Cavernous transformation
Tortuous vessels in the porta
hepatis
periportal collateral circulation
Cavernous transformation of liver
Splenic vein thrombosis
Regional portal hypertension
Pancreatitis and pancreatic carcinoma
short gastric and gastroepiploic veins return blood to the patient PV
Budd-Chiari Syndrome
Hepatic vein thrombosis
Rare
Acute : Result of thrombosis of main hepatic vein of IVC
Chronic: due to intrahepatic venous fibrosis
USG
No flow in hepatic vein or discontinuity between
the main hepatic vein and the inferior vena cava
Reversed flow in hepatic veins and intra-and
extrahepatic collaterals
increased resistive index within the hepatic
artery: >0.75
CT
Inhomogeneous mottled apperance (nutmeg
liver)
Delayed enhancement of the peripheral liver
with accompanying central low density areas
Inability to identify hepatic veins
Chronic phase, there is caudate lobe
enlargement and atrophy of the peripheral
liver in affected areas
THANK YOU
sample volume should be placed in the midportion of the lumen
An angle indicator line is subjectively placed parallel to the vessel
direction, velocity, and acceleration
Factors which affect imaging
Focal zone at the level of portal vein
Inc sensitivity
◦ Slow velocity range
◦ Small angle
◦ Patient positioning
◦ Small color box
Aliasing

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Imaging of portal hypertension

  • 1. NON- INVASIVE IMAGING OF PORTAL HYPERTENSION DR. DEVKANT LAKHERA
  • 2. Portal hypertension Increase in portal pressure above 6- 10 mm Hg Gradient - of more than 5 mm Hg between hepatic veins and portal vein Carries blood form GIT and spleen, pancreas and gall bladder
  • 3. PORTAL VEIN - Anatomy Length - 6-8 cm Caliber - 9-12 mm Location:- NECK OF PANCREAS L1 –L2 vertebral level Venules hepatic sinusoids Terminal hepatic veins IVC heart Hepatoduodenal ligament
  • 4. Blood is not pumped  Driven via gradient Pressure = Flow x Resistance Gradient Portal system Caval venous system Valveless
  • 5. Portocaval anastomosis Distal esophagus (Left gastric vein – oesophageal vein azygous  SVC) Rectum (Superior rectal– Middle and inferior rectal Internal iliac) Umbilicus (Superficial epigastric  femoral  External iliac – Paraumblical) (developed collaterals) Tributary collaterals Developed Collaterals (Hepatofugal) gastrorenal// splenorenal// splenoretroperitoneal// Paraumbilical vein: Runs in the falciform ligament and connects the left portal vein to the systemic epigastric veins near the umbilicus (close during development and reopen later
  • 6. Pre-sinusoidal (MC in India) Sinusoidal Post-sinusoidal Portal vein thrombosis Cirrhosis (Hepatitis> Alcoholic) Budd-Chiari syndrome Extrinsic compression of portal vein Hepatic veno-occlusive disease Schistosomiasis Right heart failure Causes of cirrhosis Hepatic Intrahepatic
  • 7. Non invasive imaging modalities  Ultrasound and CDFI – Most widely used Vascular patency Presence of collaterals Portal flow Distinguish between extra and intrahepatic portal hypertension Changes of cirrhosis  Computed tomography and MRI – Portal venous system and collateral assessment.
  • 8. INTRAHEPTIC PORTAL HYPERTENSION USG evaluation of liver – Cirrhosis -- Altered size -- surface nodularity of with coarsened echo texture -- reduction in the number of visible portal or hepatic veins -- segmental hypertrophy/atrophy ◦ Transverse diameter segment IV - (<30 mm) -- Splenomegaly and ascites.
  • 9. Increased nodularity in liver undersurface enlargement of the caudate lobe
  • 10. CT scan Early - fatty infiltration (alcoholic liver disease) Diminished volume Nodularity of the liver, parenchymal heterogeneity Nonuniform lobar atrophy or hypertrophy may be demonstrated widening of the gallbladder fossa enlargement of the lateral segment (LS) of the left lobe and caudate lobe (C) of the liver, ascites, varices (red arrow), and splenomegaly (S).
  • 11. Prominent porta hepatis and intrahepatic fissures - Hepatic atrophy Regenerative nodules – Isoattenuating . Very advanced cirrhosis with small nodular liver with hypertrophy of the caudate lobe and extensive ascities
  • 12. Hepatic C/RL ratio line 1: Right lateral border of the portal vein line 2: Left lateral border of the caudate lobe line 3: Midway between the portal vein and the IVC extended to the right liver edge RL measurement: C measurement caudate-right lobe ratio: C/RL C/RL >0.65 = 96% likely to be cirrhotic//C/RL >0.73 = 99% likely to be cirrhotic : axial slice immediately below the bifurcation of the main portal vein
  • 13. Non cirrhotic portal fibrosis (Pre-sinusoidal portal hypertension Smooth liver surface Marked dilation of portal vein (selectively left branch) Thickening of portal vein wall Increase in periportal echogenicity increase in periportal echogenicity with normal parenchymal echotexture
  • 14. CT Normal sized liver Splenomegaly Dilated portal and splenic veins
  • 15. 1. Portal vein diameter 2. Portal flow direction 3. Portal velocity and waveforms 4. Presence of portosystemic collaterals 5. Hepatic vein evaluation 6. Hepatic artery changes. VASCULAR EVALUATION IN PORTAL HYPERTENSION
  • 16. Portal vein diameter –> 9-12 mm in quiet respiration >13 mm indicates portal hypertension (>17mm –Large varices) Portal vein diameter (1-2 cm proximal to bifurcation)
  • 17. Splenic vein and Superior mesenteric vein Splenic vein and superior mesenteric vein - Diameter > 10mm increase of diameter <20% during inspiration Loss of respiratory variation in these vessels is important sign
  • 18. Normal portal vein flow and velocity Undulating hepatopetal flow. Remain above baseline Mean portal venous flow velocity - 12 to 18 cm/sec Average portal flow – 500-900 ml/min Normal portal venous flow direction and waveform.
  • 19. Normal portal vein flow May become accentuated in portal hypertension
  • 20. Portal hypertension Portal vein loses its undulatory pattern and becomes monophasic. Later flow becomes biphasic and finally hepatofugal Flow velocity < 12cm /sec US image shows slow flow in the main portal vein
  • 21. Reversal of flow –Hepatofugal flow
  • 22. Interpretation of flow Normal flow To and Fro flow Reversed flow Portal hypertension Advanced PHTN Cardiac failure
  • 23. Other causes of portal vein dilatation Portal vein dilatation and flow reversal can CHF. --- portal flow is markedly pulsatile --- dilated IVC Cardiac failure Tricuspid regurgitation Portal vein - Exaggerated pulsatality
  • 24. Vascular indices Liver Vascular Index (LVI = PVVel/ Hepatic Artery PI) - < 12 cm/sec Congestive index : Cross-sectional area mean flow velocity of the portal trunk - > 0.13 cm/sec
  • 25. Effective liver perfusion Both the volume flow and velocity – decrease may increase - large paraumbilical collateral is lower as calculated from flow volume in portal trunk minus portal flow volume in the umbilical vein.
  • 26. Important indicators of portal hypertension. Left gastric Short gastric Paraumblical Splenorenal Splenoretroperitoneal Splenocaval Splenoportal Portosystemic Venous Collaterals
  • 27. Left gastric (coronary vein) – Normally <4mm  > 7mm Associate with esophageal and gastric varices Short gastric veins-- spleen and gastric wall. Left gastric (coronary vein)
  • 29. Paraumbilical vein Ligamentum teres in the left lobe of liver Recanalized visible as a channel greater than 3 mm in diameter Hepatofugal flow Recanalization of umbilical vein is a highly specific sign of portal hypertension
  • 30. Splenorenal shunts --Splenic hilar Splenoretroperitoneal Spenocalval Splenoportal
  • 31. Hepatic vein assessment Doppler spectral traces from normal hepatic veins have a triphasic appearance two waves that represent atrial and ventricular diastole and a small wave that occurs in atrial systole Altered hepatic vein waveforms 50% of patients with cirrhosis  flattening of the phasic oscillations
  • 32. Loss of pattern Monophasic flow Cirrhosis (Poor prognosis) Infiltrative liver disease Budd Chiari (Hepatic vein thrombosis) Pulsed Doppler waveform analysis shows loss of the normal triphasic hepatic vein pulsatility.
  • 33. Exaggerated phasicity Congestive heart failure Tricuspid incompetence
  • 34. Hepatic artery normal hepatic artery (HA) -- 4-6 mm -- 25 to 30% of blood to the liver. -- anterior to the portal vein systolic velocity - 30 to 40 cm/sec and diastolic velocity - 10-15 cm/sec .
  • 35. HEPATIC ARTERY Resistivity Index -0.55 to 0.81 Pulsatility index (PI) - 1.16 to 1.24 Increased in chronic liver disease
  • 36. CT Splenoportal axis – Best visualized on portal phase images Retroperitoneal and mesenteric collaterals are better visualized on CT Axial CT scan showing esophageal (white arrow) and paraesophageal (red arrow) varices. Superficial collateral vessels are also present (yellow arrows
  • 37. Coronal reformatted MDCT image shows short gastric and perigastric varices (arrow).//Axial CECT in portal phase showing recanalized paraumbilical vein.
  • 38. Extrahepatic portal hypertension Portal vein occlusion –Thrombosis, Tumor invasion or compression. Causes ◦ Sepsis. ◦ Acute Pancreatitis ◦ Tumor invasion – Pancreatic / HCC ◦ Hypercoagulable states Non visualization of portal vein to thrombus occluding the of PV (echogenic intraluminal material(arrow) or absent color flow
  • 39. CT Presents Low attenuation filling defect Lack of portal vein enhancement
  • 40. Portal vein thrombosis Contrast-enhanced fat-saturated T1-weighted MRI in a 62-year-old woman with near- occlusive thrombus in the main portal vein
  • 41. Cavernous transformation Tortuous vessels in the porta hepatis periportal collateral circulation
  • 43. Splenic vein thrombosis Regional portal hypertension Pancreatitis and pancreatic carcinoma short gastric and gastroepiploic veins return blood to the patient PV
  • 44. Budd-Chiari Syndrome Hepatic vein thrombosis Rare Acute : Result of thrombosis of main hepatic vein of IVC Chronic: due to intrahepatic venous fibrosis
  • 45. USG No flow in hepatic vein or discontinuity between the main hepatic vein and the inferior vena cava Reversed flow in hepatic veins and intra-and extrahepatic collaterals increased resistive index within the hepatic artery: >0.75
  • 46.
  • 47. CT Inhomogeneous mottled apperance (nutmeg liver) Delayed enhancement of the peripheral liver with accompanying central low density areas Inability to identify hepatic veins Chronic phase, there is caudate lobe enlargement and atrophy of the peripheral liver in affected areas
  • 49.
  • 50. sample volume should be placed in the midportion of the lumen An angle indicator line is subjectively placed parallel to the vessel direction, velocity, and acceleration
  • 51. Factors which affect imaging Focal zone at the level of portal vein Inc sensitivity ◦ Slow velocity range ◦ Small angle ◦ Patient positioning ◦ Small color box Aliasing

Editor's Notes

  1. Two system of veins – Portal / systemic(caval)-- > Increase in pressure in portal system// Carries blood form gi tract and spleen, pancreas and gall bladder.
  2. Hepatoduodenal ligament (cd, ha, pv ,) // Foregut mid gut and hind gut and spleen // Hepatoduodenal ligament (ha, pv ,cd)//
  3. Valveless
  4. Sites of venous communication// Mc sites of flow reversal// SMV  retroperitoneal IVC//gastrorenal// splenorenal// splenoretroperitoneal// Paraumbilical vein: Runs in the falciform ligament and connects the left portal vein to the systemic epigastric veins near the umbilicus (close during development and reopen later//This facilitates shunting of blood away from the liver into the systemic venous system in portal hypertension, as a means for reducing portal venous pressur
  5. Extrahepatic portal hypertension
  6. As well as other findings associated with portal hypertension like – cirrhosis, ascites splenomegaly//Portal venous system and collaterals without any interference form bowel gas, fat, bone// gadolinium enhanced..higher dose
  7. -- presence of regenerating nodules // // Contour nodularity of undersurface of liver has more sensitivity Echogenitcity-Ability to reflect and produce an echo- Homogenous/ inhomogenous Echotexture is the changes in the echoes produced due to chang in the consistency of the organ pparenchyma– Coarsened echotexture Surface nodularity  suggests sinusoidal involvement – portal hypertension// Sono-elastography may also be useful to assess the amount of liver fibrosis 12. Suggested values for diagnosis // >7 kPa: advanced fibrosis//12.5-15 kPa: cirrhosis//
  8. Increased nodularity in liver undersurface// D. Sagittal sonogram showing enlargement of the caudate lobe (C) in a patient with cirrhosis. Arrows, Fissure for the ligamentum venosum.
  9. Contrast-enhanced CT scan demonstrates widening of the gallbladder fossa (white arrow), enlargement of the lateral segment (LS) of the left lobe and caudate lobe (C) of the liver, ascites, varices (red arrow), and splenomegaly (S).
  10. (hyperattenuating in case of siderotic nodules)//Very advanced cirrhosis with small nodular liver with hypertrophy of the caudate lobe and extensive ascities.
  11. image: axial slice immediately below the bifurcation of the main portal vein //C/RL >0.65 = 96% likely to be cirrhotic//C/RL >0.73 = 99% likely to be cirrhotic
  12.  portal hypertension occurring without hepatic cirrhosis// increase in periportal echogenicity with normal parenchymal echotexture
  13. Notmal LFT
  14. Portal hypertion – flow may be slow,
  15. (1-2 cm proximal to bifurcation)/ crossing with hepatic artery // normal diameter does not exclude// image shows enlargement of the main portal vein of 1.5 cm compatible with portal hypertension
  16. Loss of respiratory variation in these vessels is important sign
  17. Towards the liver and shows mild phasicity -due to respiration and cardiac activity. Cross sectional area is measured at mid portal vein with angle of insonaton <60 degThe PI is used to quantify pulsatility. Normal phasicity results in a PI greater than 0.5.
  18. Hepatopeta flow with mild phasicity. Mid potal vein has laminar flow // but as it reaches porta (intrahepatic .. Mild helical flow) // May become accentuated in portal hypertension
  19. Hepatofugal flow is due to severe portal hypertension from any cause //peak velocity - 9.0 cm/sec//US image shows slow flow in the main portal vein. Slow portal venous flow is a consequence of portal hypertension
  20. Portal vein - Exaggerated pulsatality
  21. Portosystemic collateral pathways (also called varices) develop spontaneously via dilatation of pre-existing anastomoses between the portal and systemic venous systems.  //USG- 65 -95% of collaterals can be visualized. Clear indiacation of portal hypertension
  22. located between medial wall of gastric body and posterior margin of left hepatic lobe in lesser omentum Important indicator of portal hypertension//Volume and flow velocity vary depending upoun collateral development/ scale image, and D, color Doppler image, show extensive varices in the distribution of the coronary vein
  23. Paraumblical veinligamentum teres hepatis) is a degenerative string of tissue that exists in the free edge of the falciform ligament of the liver. //The round ligament represents the remnant of the fetal umbilical vein.
  24. Arises from left poratal vein runs inferiorly along falciform towards umblicusa/ Sagittal image of recanalized paraumbilical vein in patient with gross ascites.
  25. spleen and upper pole of left kidney, color Doppler image, show splenic hilar varices.
  26. Pulsed Doppler waveform analysis shows loss of the normal triphasic hepatic vein pulsatility.
  27. Normally forward flow shoud be more than reverese flow if both equeal// dilated hepatic veins
  28. right hepatic artery are taken where it crosses the portal vein near the porta hepatis// resistive index of the hepatic artery in a fasting subject varies from 0.55 to 0.81 (mean 0.62-0.74) RI increases in normal subjects after a meal.
  29. increase in intrahepaticvascular resistance. Thrombosis RI dec
  30. Axial CT scan showing esophageal (white arrow) and paraesophageal (red arrow) varices. Superficial collateral vessels are also present (yellow arrows
  31. Coronal reformatted MDCT image shows short gastric and perigastric varices (arrow).//Axial CECT in portal phase showing recanalized paraumbilical vein. 
  32. Due to stagnant flow in phtn/Initially – Thrombus may be anechoic// Non visualization of portal vein to thrombus occluding the of PV (echogenic intraluminal material(arrow) or absent color flow
  33. The portal vein (with its right and left main branches) and splenic vein are distended with luminal thrombosis. The superior mesenteric vein and the inferior mesenteric vein as well as their branches are completely thrombosed (mesenteric vascular occlusion). The spleen is markedly enlarged (measuring 22 cm) showing multiple wedge shaped non enhanced areas representing splenic infarcts
  34. Contrast-enhanced fat-saturated T1-weighted MRI in a 62-year-old woman with near-occlusive thrombus in the main portal vein
  35. Instead of a single anechoic poratal vein multiple tubular structure are seen at porta hepatis// prmary manifestation which occurs following long standing portal vein thrombosis //Difffernece between malignant thorombus is that it is expansive Normally portal vein lies posterior to hepatic artery// if channel is seen anterior to hepatic artery
  36. Multiple tortuous enlarged vessels in the region oof portal vein
  37. Filing defect within the hepatic vein suggestive of thrombus// low or absent flow in the inferior vena cava or balanced bidirectional flow bland thrombus or tumour thrombus within the inferior vena cava
  38. Markely narrow hepatic vein with thich wall  monophasic flow
  39. Aliasing