This document discusses non-invasive imaging techniques for evaluating portal hypertension. Ultrasound is the most widely used initial imaging modality to assess for portal vein patency, presence of collaterals, portal blood flow, and changes of cirrhosis. CT and MRI can further evaluate the portal venous system and collateral vessels. Ultrasound Doppler is used to measure portal blood flow direction, velocity, and assess for portosystemic collaterals and changes in hepatic veins. Imaging findings of various etiologies of portal hypertension are described, including cirrhosis, non-cirrhotic portal fibrosis, portal vein thrombosis, Budd-Chiari syndrome, and extrahepatic causes.
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
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.
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
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.
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
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
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.
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
.
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
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
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
Notas del editor
Two system of veins – Portal / systemic(caval)-- > Increase in pressure in portal system// Carries blood form gi tract and spleen, pancreas and gall bladder.
Hepatoduodenal ligament (cd, ha, pv ,) // Foregut mid gut and hind gut and spleen // Hepatoduodenal ligament (ha, pv ,cd)//
Valveless
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
Extrahepatic portal hypertension
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
-- 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//
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.
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).
(hyperattenuating in case of siderotic nodules)//Very advanced cirrhosis with small nodular liver with hypertrophy of the caudate lobe and extensive ascities.
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
portal hypertension occurring without hepatic cirrhosis// increase in periportal echogenicity with normal parenchymal echotexture
Notmal LFT
Portal hypertion – flow may be slow,
(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
Loss of respiratory variation in these vessels is important sign
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.
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
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
Portal vein - Exaggerated pulsatality
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
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
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.
Arises from left poratal vein runs inferiorly along falciform towards umblicusa/ Sagittal image of recanalized paraumbilical vein in patient with gross ascites.
spleen and upper pole of left kidney,
color Doppler image, show splenic hilar varices.
Pulsed Doppler waveform analysis shows loss of the normal triphasic hepatic vein pulsatility.
Normally forward flow shoud be more than reverese flow if both equeal// dilated hepatic veins
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.
increase in intrahepaticvascular resistance.
Thrombosis RI dec
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.
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
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
Contrast-enhanced fat-saturated T1-weighted MRI in a 62-year-old woman with near-occlusive thrombus in the main portal vein
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
Multiple tortuous enlarged vessels in the region oof portal vein
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
Markely narrow hepatic vein with thich wall monophasic flow
