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Thursday, 5 May 2011

Portal vein, inferior vena cava...


• Portal and Hepatic System
The portal vein is formed by the junction of the splenic and superior mesenteric
vein. The portal/splenic confluence is found posterior to the neck of the pancreas. The
inferior mesenteric vein drains into the splenic vein to the left of the portal/splenic
confluence. The left gastric or coronary vein usually joins the splenic vein superiorly
near its junction with the superior mesenteric vein. It courses in a cranio-caudad
plane. From the confluence, the portal vein courses lateral and cephalad in an oblique
plane toward the porta hepatis where it enters the liver. Within the liver, the portal
vein is found posterior to the hepatic artery and common bile duct. These three
structures course together throughout the liver and are known as the portal triad.
The portal vein divides at the porta hepatis into right and left branches. The right
portal vein divides into anterior and posterior branches and the left portal vein divides
into medial and lateral branches. The left portal vein is in contact with the
ligamentum teres.
The branches of the portal vein are intrasegmental, traveling within the segments of
the liver, whereas the branches of the hepatic veins are intersegmental, traveling
between the lobes and segments of the liver.
The portal veins can be differentiated sonographically from the hepatic veins by the
bright echogenic walls that surround them. This is due to the thick collagenous tissue
in the portal vein walls. The hepatic veins do not exhibit echogenic borders.

The cystic vein, which drains the gallbladder, is a branch of the portal vein. Although
it is not usually visualized sonographically, the cystic vein has important implications
in the evaluation of portal hypertension. Impaired drainage of the cystic vein into the
portal vein can result in varices within the gallbladder wall. These are recognizable by
ultrasound imaging.

There are usually three main hepatic veins within the liver. They are the right,
middle and left hepatic veins. The hepatic veins are seen to enlarge toward the
superior aspect of the liver where they drain into the inferior vena cava.

• Function

Understanding the function of the portal venous system is key to understanding the
physiological responses manifested in disease processes.
1. The portal vein is 60% oxygen saturated and provides greater than 50% of
the oxygen requirements to the hepatocytes.
2. It brings nutrient rich blood to the liver from the bowel.
3. The portal vein is the primary collateral route for decompression of the
liver in elevated pressure.
4. In a normal state the portal venous system is a low pressure system with a
normal pressure of 5-10 mm Hg.

Portal hypertension (PV HT):

The luminal diameter of the portal veins corelate poorly to the portal pressure. Therefore to diagnose portal HT we need to analyse the spectral properties of blood flow in the PV.

- Definitive signs of PV HT are:
- ***flow reversal and abscence of flow.
- >11 mm intrahepatic, >15mm extrahepatic diameter
- Caliber variation with respiration <2mm
- Hepatic cirrhosis
- Splenomegaly
- Ascites
- Thickening of GB and stomach wall
- Dilated tributaries (left gastric vein, SMV, splenic vein)

Flow changes in PV HT:
- Flow velocity is slowd down to <10cm/s (normal 15-20 cm/s)
- Bidirectional or abscent flow in PV and its tributaries.

The causes of PV HT can be grouped in to:
- Prehepatic (PV thrombosis)
- Intrahepatic (cirrhosis)
- Posthepatic (Budd-Chiari syndrome)

Intrahepatic causes include liver cirrhosis, and hepatic fibrosis (e.g. due to Wilson's disease, hemochromatosis, or congenital fibrosis). Prehepatic causes include portal vein thrombosis or congenital atresia. Posthepatic obstruction occurs at any level between liver and right heart, including hepatic vein thrombosis, inferior vena cava thrombosis, inferior vena cava congenital malformation, and constrictive pericarditis.

Acute PV or mesenteric vein thrombosis presents with the physical signs/complaints of an acute abdomen, in US you see filling defect, vascular dilation.

Chronic PV or mesenteric vein thrombosis presents in US with little or no luminal dilation, echogenic intraluminal thrombus, no flow with collateral formation.

Signs and symptoms of PV HT:

Caused by blood being forced down alternate channels by the increased resistance to flow through the systemic venous system rather than the portal system. They include:

Congestion and the IVC:

Dilated IVC is an indication of right sided heart failiure.
Clinical presentation: dyspnoe, leg edema, in acute right heart failiure pulsatile flow in hepatic veins.

US presentation:

- >20 mm vena cava, >10 mm hepatic veins
- decreased inspiratory collapse of veins
- decreased compressibility
- abscence of soft double pulsations

Doppler Spectral Analysis

• Portal and Hepatic System

-The portal vein normally exhibits a monophasic, low velocity Doppler signal. The
normal range of flow velocity is wide, but is usually between 20-40 cm/sec. The flow
is continuous and should demonstrate little pulsatility. Flow should not cease or
reverse in the normal individual. Prominent pulsatility of the portal vein is abnormal
and may be indicative of right heart failure, tricuspid regurgitation, hepatic vein/portal
vein fistula or portal hypertension. The flow in the splenic and superior mesenteric
veins is toward the liver and both exhibit a low velocity, monophasic signal.

portal vein with a continuous hepatopetal flow in a healthy adult.

portal vein with minimal pulsatile modulation of the portal flow in a healthy adult.

portal vein with marked pulsatile modulation of the portal flow in a thin, healthy adult.

-Hepatic artery flow is in the same direction as the portal vein (hepatopetal). The
hepatic artery normally demonstrates a low resistance waveform with continuous
forward flow throughout the cardiac cycle.

-The hepatic veins (HV) drain blood from the liver into the inferior vena cava. The
normal Doppler waveform obtained from the HV’s is triphasic. This phasicity is
dependent on variations in central venous pressure during the cardiac cycle.

hepatic vein and portal vein in a patient with heart failure, New York Heart Association Calss III and tricuspid regurgitation (left), having a triphasic flow in the hepatic vein (middle) and a marked pulsatile flow of the portal vein (right)

patient with constrictive pericarditis (arrows) (left). A triphasic flow is seen in the hepatic vein (middle) and pulsatile flow in the portal vein (right). RV, right ventricle.

hepatic vein and portal vein in a patient with mediastinal haematoma. A triphasic flow is seen in the hepatic vein (left) and a pulsatile flow with a reversed component of the portal vein (right).

patient with pericardial effusion (left), and triphasic flow in the liver vein (middle) and pulsatile flow in the portal vein (right).

patient with primary cardial lymphoma with a tumour in the right atrium (left), triphasic flow in the hepatic vein (middle) and pulsatile flow in the portal vein (right).

hepatic vein (LV) and portal vein (VP) in a patient with liver cirrhosis having a monophasic flow in the hepatic vein (left) and a marked pulsatile flow of the portal vein (right).

portal vein (left and middle) in a patient with heart failure, New York Heart Association Calss III, having a marked pulsatile flow with reversed flow during deep inspiration (arrows) (right).

pericardial effusion (PE) (left) and a pulsatile flow in the portal vein with a short reversed flow during deep inspiration (arrow) (right). RV, right ventricle; LV, left ventricle.

Ultrasound Findings of Portal Hypertension

Ultrasound findings associated with portal hypertension include enlarged
diameter of the portal vein, lack of respiratory variation in the portal vein or its
tributaries, hepatofugal (away from liver) portal flow direction, decreased portal velocity (<10 cm/s) or volume, and the presence of collaterals or varices. Splenomegaly is uniformly present with portal hypertension. The spleen is enlarged when its length exceeds 13 cm. This should be measured in a cranio-caudad plane. An abnormal liver texture and ascites
are also commonly seen and are usually related to accompanying cirrhosis. A
sudden onset of ascites should prompt careful examination of the portal vein for

Enlargement of the portal vein >13 mm is indicative of portal hypertension
with a high degree of specificity (100%) but low sensitivity (45-50%). The portal vein
diameter should be measured just above the IVC with the patient in quiet respiration.
With deep inspiration, the normal diameter may increase to about 16 mm resulting in
an overestimation of portal vein diameter. It is important to recognize, however,
that the portal vein is not always enlarged with portal hypertension. In some cases,
portal flow may be primarily diverted through collateral channels resulting in a small
portal vein at the porta hepatis. This can be seen with diversion of flow through a
large coronary vein, splenorenal shunt or other similar channel. Portal vein flow velocity decreases with portal hypertension due to increased resistance to flow. However, in the presence of a recannalized paraumbilical vein, the flow velocity in the main portal vein may be increased.
As pressure increases, portal blood flow may become pulsatile. With late stages of portal hypertension, portal flow direction can reverse and course away from the liver. This is termed hepatofugal flow and is easily assessed with color Doppler. The portal flow direction can be compared with the hepatic artery. When they are in opposing directions, portal flow is reversed.
With decreasing velocity of portal flow, stagnation may lead to thrombus formation.
There are many other causes of portal vein thrombosis. Following thrombosis,
cavernous transformation of the portal vein may develop. It is seen as a tortuous
network of blood vessels located in the porta hepatis and extending into the liver.
Doppler waveforms obtained from this area will primarily show venous signals with
flow direction into the liver. Cavernous transformation most commonly occurs in
patients with otherwise healthy livers

Portal Vein Thrombosis (PVT)

Portal hypertension can cause thrombosis of the portal vein due to stagnation
of flow. Hypercoagulable states can result in thrombosis of the portal vein directly or
indirectly through thrombosis in the splenic or superior mesenteric vein. Biliary atresia/cirrhosis may cause thrombus in the main portal vein or the smaller
branches within the liver. Pancreatitis and other inflammatory processes most commonly cause thrombosis that begins in the splenic or superior mesenteric veins. Portal vein compression by
lymphadenopathy or tumor mass can also result in thrombosis. Increased flow through the hepatic artery with a decrease in resistance is associated with portal vein thrombosis. The hepatic artery may appear enlarged with prominent color Doppler signals. Use of color Doppler alone to evaluate portal flow may result in the mistaken identity of an enlarged hepatic artery for the portal vein especially when portal thrombus is isoechoic to the surrounding liver tissue. This pitfall can be avoided by always obtaining a spectral Doppler signal from the portal vein in addition to color Doppler evaluation. Partial thrombus is not associated with hepatic artery changes.


• Sonographic Window

The best scanning approach to the main portal vein is nearly always intercostal.
Although the portal vein is more easily seen with b-mode imaging in a subcostal
position, this approach commonly results in a poor Doppler angle of incidence. The
intercostal view results in Doppler angles that vary from 0º to about 60º. With color
Doppler in this view, the portal vein is seen as a red vessel adjacent to the red hepatic
artery (if color Doppler invert is not selected).

When a large amount of ascites is present, the depth to the portal and hepatic veins can be quite large. Bowel loops and gas may not allow visualization at all from the subcostal approach. Using an intercostal window will usually allow adequate imaging in these cases. If cirrhosis is severe, sound penetration through the liver will be greatly decreased. It may be necessary to use a lower frequency transducer or the lowest frequency setting on a multifrequency transducer. An anterior sagittal approach usually provides the best view to image the left portal vein, left and middle hepatic veins and ligamentum teres. It is important to image this anatomy to rule out the presence of a paraumbilical vein. A transverse or image can also be used to display the paraumbilical vein. It will be seen as a large vessel exiting the liver from the left portal vein at the level of the ligamentum teres. The right hepatic vein may be seen in this view, but is frequently best seen from an intercostal approach.

• Flow Direction

Flow direction can be very important in abdominal Doppler. Confusion about the direction of flow is a common pitfall. For this reason, it is usually best to avoid use of the color and spectral Doppler invert control. Flow away from the Doppler beam is shown as blue and below the zero baseline and flow toward the Doppler beam is shown as red and above the zero baseline. Anytime the flow direction is in question, it is helpful to check a baseline vessel in which flow direction is known. For example, to rule out hepatofugal flow in the portal vein, compare its flow direction to that of the hepatic artery. When flow direction is normal in the portal vein (toward the liver), it is the same direction as the hepatic artery. If they are on opposite sides of the spectral Doppler baseline or show opposite colors, blood flow is reversed in the portal vein.

Doppler spectrum analysis obtained with a large sample volume simultaneously demonstrates waveforms from the portal vein and hepatic artery. They are on opposite sides of the zero baseline. This finding is consistent with hepatofugal flow in the portal vein.

• Presence or Absence of Flow

Color and spectral Doppler are commonly used to determine the presence or absence of flow in a vessel. Another common pitfall is to mistakenly assume the absence of flow when in fact it is present. This most commonly occurs as a result of poor Doppler angles or inappropriate settings of the Doppler parameters.

The Dopplercontrols should be sensitized for the detection of slow flow whenever thrombosis or occlusion is suspected. This requires adjustment of the PRF and filter controls to very low levels. Additionally, if the Doppler angle is too great, the frequency shift from slow flow may be too small to detect. This may lead the sonographer to mistakenly assume that flow is absent. Since most abdominal Doppler is performed with curved linear arrays, steering of the Doppler beam cannot be performed and it is necessary to heel/toe the probe to achieve a good angle of incidence.

Commonly, the view that gives the best B-Mode image of a vessel is the poorest Doppler approach because the angle of incidence is too great. A common example of this is in evaluation of the portal vein. The portal vein is best seen with B-Mode imaging in a subcostal approach where the angle of incidence is near 90º. Color Doppler evaluation of the portal vein in this view may not demonstrate flow, especially if slow flow states are present. The best view of the portal vein for Doppler evaluation is an intercostal approach. In this view, the Doppler angle is much smaller, allowing demonstration of slower flow states.

Other related images:

IVC thrombosis patient



(Text main source:, US Thieme clinical companion, -Cindy A. Owen, RDMS, RVT-)
(Images: google images, BJR -C Görg, MD, J Riera-Knorrenschild, MD and J Dietrich, MD-, RadioGraphics-September 2003RadioGraphics, 23, 1093-1114.-)

1 comment:

  1. Varicose veins can usually be seen bulging under the skin, but symptoms can develop before the veins become visible.