Preview of "Portal Hypertension Imaging"

9/8/14 11:00 AM Portal Hypertension Imaging
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Portal Hypertension Imaging
Author: Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR; Chief Editor: Kyung J Cho, MD, FACR more...

Updated: Aug 7, 2013
Overview
In portal hypertension imaging, ultrasound techniques such as duplex ultrasonography or spectral Doppler imaging
and color Doppler imaging or power Doppler imaging are the modalities of choice, because they are noninvasive,
rapid, and highly sensitive and specific.
Portal hypertension (PH) represents an increase of the hydrostatic pressure within the portal vein or its tributaries.
It is defined as an increase in the pressure gradient between the portal vein and hepatic veins or the inferior vena
cava (IVC) (see the images below).
Barium swallow in the left lateral decubitus position shows multiple mucosal nodules in the mid to lower esophagus. In a patient with
cirrhosis, these are suggestive of esophageal varices.
Doppler sonogram at the splenic hilum reveals hepatofugal venous flow in a patient with portal hypertension.
Most patients with venous PH have intrinsic liver disease. In PH, blood that normally flows through the liver is
diverted into systemic veins because of increased resistance to portal venous flow. This diversion of portal venous
blood occurs via exiting portosystemic communications (eg, the coronary vein) and the opening of embryonic
channels (eg, paraumbilical veins). The most common portosystemic anastomosis is via the coronary-
gastroesophageal route; it occurs in 80-90% of patients and gives rise to lower esophageal and gastric varices.
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Discussion
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Hematemesis resulting from bleeding esophageal varices is the most common presentation in patients with PH,
although some patients seek medical help because of decompensated liver disease. Findings from duplex
ultrasonography (US) and color Doppler imaging (CDI), MRI, CT, and endoscopy may support the diagnosis of PH.
Preferred examination
Plain radiographs are not often obtained in cases of portal hypertension, but because most hospitalized patients
undergo chest radiography, radiologists need to be aware of abnormalities that may be found in patients with PH.
The appearance of calcification in the distribution of the portal vein on a plain abdominal radiograph may indicate
PH. An upper GI tract barium series is often performed for the detection of esophageal varices (see the images
below).
Barium swallow in a 56-year-old man with known cirrhosis who had a recent episode of hematemesis shows thickened mucosal folds
and multiple polypoid filling defects at the lower end of the esophagus. These are suggestive of varices.
Endoscopic findings in a 47-year-old man with a history of polycythemia rubra vera who had a recent episode of hematemesis.
Endoscopy showed a normal esophagus, but multiple polypoid submucosal lesions were seen in the fundus and body of the stomach).
The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.
Part of an upper gastrointestinal tract barium series (same patient as in the previous image) shows multiple polypoid filling defects
within the fundus of the stomach. The final diagnosis was a left-sided portal hypertension secondary to splenic vein thrombosis.
US techniques such as duplex US or spectral Doppler imaging and CDI or power Doppler imaging are the
modalities of choice in the evaluation of the liver and PH. These techniques are noninvasive, rapid, and highly
sensitive and specific.
Angiographic techniques such as splenosportography (SP), transhepatic portography, transumbilical
catheterization, transjugular catheterization, wedge hepatic venography, and arterial portography are invasive.
However, they are much more specific for the evaluation of PH hypertension; they are indicated when definitive
surgery or radiologic intervention is contemplated.
The use of angiographic techniques is declining because noninvasive imaging techniques such as US, CT,
computed tomographic angiography (CTA), and magnetic resonance angiography (MRA) are now available. These
techniques are quickly improving, and this will lead to further decline in the use of angiographic methods.
Splenoportography and transumbilical catheterization are rarely performed. Arterial portography (indirect
Splenoportography and transumbilical catheterization are rarely performed. Arterial portography (indirect
portography) and wedge hepatic venography with manometry is indicated before surgical portacaval shunt
placement.
Carbon dioxide wedge hepatic venography is the most commonly used method for visualizing the portal vein
before portal vein puncture for a transjugular intrahepatic portosystemic shunt (TIPS) procedure. TIPS is a
radiology-guided creation of a shunt between the portal and hepatic veins in the liver by use of a percutaneous
transjugular approach. Because of its proven safety and effectiveness, TIPS has largely replaced surgical
decompressive shunt procedures.
[1, 2, 3]
Transient elastography (TE) is a new technique used as a noninvasive method to study portal hypertension in
chronic liver disease, with variable results. Shi et al in a meta-analysis studied the performance of TE for detection
of significant portal hypertension, esophageal varices, and large esophageal varices. The analysis revealed that
TE could be used as a good screening tool for significant portal hypertension but had only moderate diagnostic
utility for the prediction of esophageal varices or large esophageal varices.
[4]
Idiopathic portal hypertension (IPH) is frequently misdiagnosed as cryptogenic cirrhosis. Seijo et al studied 39
patients retrospectively to determine whether hepatic vein catheterization and liver stiffness measurements can
differentiate IPH from noncirrhotic portal vein thrombosis. Patients with IPH frequently have hepatic vein-to-vein
communications, despite signs of portal hypertension, and lower mean hepatic venous pressure gradient and liver
stiffness values much lower than the cut-off for clinical significant portal hypertension in those with cirrhosis. Thus,
when these signs occur, it is obligatory that IPH is ruled out.
[5]
Limitations of techniques
Plain radiographs are usually not indicated for patients with portal hypertension. Most plain radiographs are
obtained for other reasons, and signs of PH are detected incidentally. Therefore, plain radiographs are of limited
value.
Duplex US is a sensitive technique for the detection of PH in addition to other important features. When respiratory
variation in the size of the portal, splenic, and superior mesenteric veins does not occur or when it is less than
20%, PH may be diagnosed with a sensitivity of 80% and a specificity of 100%.
In cases involving bleeding varices that are unresponsive to endoscopic sclerotherapy or when intractable ascites
are present, a TIPS procedure is indicated. TIPS is performed after portal vein patency is documented at duplex
US.
Radiography
Plain radiographic findings
Calcification may be seen in the portal vein after prolonged portal hypertension and may occur within a
thrombosed portal vein. The calcification is linear or strandlike, and it typically lies transversely across the upper
abdomen, or it slopes upward and obliquely toward the liver hilum.
Generalized increase in the liver opacity may be seen in patients with hemochromatosis. Although this may be
demonstrated by measuring the liver attenuation on CT scans, it rarely is demonstrable on plain abdominal
radiographs.
Esophageal varices appear as lobulated posterior mediastinal masses in 58% of patients. Silhouetting of the
descending aorta and an abnormal convex contour of the azygos-esophageal recess are further signs of portal
hypertension (PH) that may be shown on plain radiographs. Signs of underlying liver disease may be noted, such
as splenomegaly and ascites.
Portal hypertension is displayed in the radiographic images below.
Barium swallow in the left lateral decubitus position shows multiple mucosal nodules in the mid to lower esophagus. In a patient with
cirrhosis, these are suggestive of esophageal varices.
Barium swallow in a 56-year-old man with known cirrhosis who had a recent episode of hematemesis shows thickened mucosal folds
and multiple polypoid filling defects at the lower end of the esophagus. These are suggestive of varices.
Barium study findings of esophageal varices
Esophageal varices comprising dilated submucosal veins in the lower esophagus occur chiefly as a consequence
of PH, mostly in patients with cirrhosis. Varices appear as beaded or serpiginous translucent filling defects.
Barium study may depict 90% of esophageal varices; however, demonstration of esophageal varices on barium
examination is highly dependent on technique. Important factors include the intravenous administration of
anticholinergic agents, use of barium paste, and examination of the esophagus in a relaxed state.
Esophageal peristalsis milks the blood out of the varices, whereas esophageal hypotonia allows the varices to
distend with blood, making them easy to visualize.
A left anterior oblique projection with the patient recumbent or in the Trendelenburg position shows the varices to
best advantage. Images are obtained by use of the Valsalva maneuver and/or deep inspiration. The Valsalva
maneuver precludes swallowing and maintains the esophagus in a relaxed state. Exposure is made with the
esophagus slightly underdistended. Overfilling produces distention, which may obliterate the varices.
After an acute episode of bleeding from esophageal varices, varices may collapse and become difficult to detect
radiologically. Demonstration of varices in a patient with hematemesis does not necessarily establish the source as
the varices because in one third of patients, bleeding occurs from other causes, such as peptic ulcer.
Anticholinergic drugs are contraindicated in patients with a history of glaucoma, heart disease, or urinary retention.
Glucagon is not useful for demonstrating esophageal varices because it lowers esophageal sphincter pressure and
does not abolish peristalsis in the body of the esophagus.
Large esophageal varices are obvious and appear as nodular or vermiform changeable filling defects within the
esophagus. Smaller varices appear as scalloped esophageal folds that are better seen on recumbent films
because they tend to disappear on upright films.
Gastric varices are seen in 278% of patients with PH. Gastric varices that occur in the absence of esophageal
varices usually result from splenic vein thrombosis; bridging collaterals extend from the splenic hilum across the
stomach to the coronary vein and then on to the portal vein.
A higher incidence of portosystemic encephalopathy is noted in patients with gastric varices. Varices in the
stomach usually are confined to the gastric cardia and are difficult to recognize. The rate of detection on a barium
study has been reported to be 6589%.
Gastric varices usually present as a slight thickening or scalloping of the cardiac folds, but large gastric varices
presenting as large mucosal polypoid masses involving the fundus and cardia are sometimes encountered.
Angiography is occasionally necessary to exclude gastric tumor. Gastric varices bleed less frequently than
esophageal varices, but when they do bleed, the hemorrhage is more severe.
Barium study findings of varices in other parts of the gastrointestinal tract
Gastric antral and duodenal varices are sometimes seen, usually in association with gastric fundal and esophageal
varices. Duodenal varices appear as lobulated filling defects on barium study and are demonstrated best with the
patient in a prone position. Internal hemorrhoids frequently are found in patients with severe PH.
In rare cases, varices involve the colon via portosystemic collaterals through the retroperitoneal veins or through
newly formed collaterals in adhesions or scars from previous surgery. In addition, the demonstration of varices on
barium examination may include other features of PH, such as splenomegaly or ascites.
The enlarged spleen may compress the stomach and displace the splenic flexure of the colon downward. Ascites
causes a central location of the small bowel loops and separation of the colon from flank fat stripes.
Degree of confidence
Plain radiography is not sensitive in the diagnosis of portal hypertension. With good operator technique, barium
examination may depict more than 90% of varices. The rate of detection with barium study has been reported to
be 6589%.
False positives/negatives
Other causes of calcification overlying the liver may mimic portal vein calcification. One example is hepatic arterial
calcification. Esophageal varices may occur with superior vena caval obstruction and may be seen as lobulated
posterior mediastinal masses.
An enlargement of mucosal folds may be seen with esophagitis on barium swallow, but the enlarged folds are not
position dependent and are seen equally well on upright films.
A rare neoplastic process that occasionally may be confused with varices is varicoid esophageal carcinoma.
Primarily seen as a nodular fold thickening, it may be differentiated from varices by its lack of position dependence,
the fact that the involvement does not extend to the lower esophagus, and the rigidity of the involved segment.
Downhill varices may occur as a result of collateral circulation extending from the superior vena cava through the
esophageal plexus to the portal venous system. These varices are seen in patients with superior vena caval
obstruction usually distal to the entry of the azygos vein. They most commonly result from bronchogenic
carcinoma, mediastinal fibrosis, lymphoma, thymoma, or thyroid disease. Downhill varices may be seen only in the
proximal part of the esophagus, or they may involve the entire esophagus.
Differentiation of gastric varices from gastric carcinoma may be difficult at times and may require angiography.
Computed Tomography
Computed tomography has been used to assess portal hypertension (see the images below).
[6, 7, 8, 9, 10]
CT scan through the spleen of a 43-year-old man with a known history of intravenous drug abuse and hepatitis C cirrhosis. The patient
presented to the emergency department with a sudden onset of a hypotensive episode and clinical features of hepatic encephalopathy.
The scan shows splenomegaly with a dilated tortuous splenic vein/varices at the splenic hilum and free peritoneal fluid. The final
diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and
arterioportal shunting (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).
CT scan through the liver (same patient as in the previous image) was not of optimal quality because of patient movement, but the
attenuation in the left lobe of the liver was patchy, suggestive of a mass lesion. The final diagnosis was hepatitis C cirrhosis,
hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and portoarterial fistula (which had
developed inside the ruptured tumor, giving rise to severe portal hypertension).
A 52-year-old man with known hepatitis B cirrhosis was found to have a hypoechoic mass in the region of the liver hilum. CT was
performed for further characterization. Nonenhanced CT scan shows multiple polypoid masses at the splenic hilum (arrow), suggestive
of a dilated tortuous splenic vein or varices. The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein
thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.
A 52-year-old man with known hepatitis B cirrhosis was found to have a hypoechoic mass in the region of the liver hilum (same patient
as in the previous image). CT was performed for further characterization. Nonenhanced CT scan shows multiple polypoid masses at
the splenic hilum (solid arrow), suggestive of a dilated tortuous splenic vein or varices, and the origin of a large splenic vein (open
arrow). The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a
arrow). The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a
spontaneous splenorenal shunt.
Contrast-enhanced axial CT (same patient as in the previous 2 images) shows a cavernous transformation at the porta hepatis (arrows)
caused by portal vein thrombosis. The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal
hypertension complicated by a spontaneous splenorenal shunt.
Contrast-enhanced axial CT scan shows a dilated left renal vein (arrow; same patient as in the previous 3 images). The final diagnosis
was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal
shunt.
Splenomegaly and ascites are readily demonstrated. In some patients, the liver is of nonuniform attenuation. Low-
attenuating components probably represent residual foci of infiltration. Often, the attenuation of a cirrhotic liver is
homogeneous and within the reference range.
In the absence of obvious abnormality of size and shape, the liver may appear entirely normal on CT scans.
Nonenhanced CT is necessary for identification of confluent fibrosis when a cirrhotic liver is imaged. Confluent
fibrosis is characteristically of low attenuation and tends to become isoattenuating or minimally hypoattenuating
after the intravenous administration of contrast material. Thus, confluent fibrosis is frequently missed if only
contrast-enhanced CT is used.
Collateral veins are occasionally seen in the peritoneal cavity, the retroperitoneum, the abdominal wall, and the
mediastinum. In the presence of hemochromatosis, liver attenuation is increased because of excessive iron load.
As a result of poor inherent contrast between normal liver and many types of liver lesions, lesions are missed on
plain CT.
The portal vein supplies 75% of blood flow to the liver; therefore, peak liver contrast enhancement occurs during
the portal venous phase, approximately 60 seconds after the start of a bolus injection of contrast material. With
helical CT, approximately 20 seconds is required to complete a liver examination; an image usually can be
acquired in a single breath hold. The technique may be extended, and dual-phase contrast-enhanced CT scans
may be acquired. In this technique, the liver is imaged twice with a single bolus of contrast agent, first during the
arterial phase and then through the portal venous phase.
Dual-phase CT is indicated for some patients with benign and malignant lesions in which vascular characteristics
suggest the correct diagnosis. Angiographically assisted CT may be used to achieve better delineation of the
portal venous system and of the portal venous enhancement of the liver. An angiographic catheter is placed in the
common celiac axis/hepatic/superior mesenteric artery by use of a modified Seldinger technique via the femoral
artery.
CT scanning begins 35 seconds after the initiation of the contrast agent injection. The examination should be
completed as soon as possible, before the contrast material recirculates. To prevent significant artifacts related to
the contrast medium, 70 mL of dilute iodinated contrast agent (130%) is used, with an infusion rate of 2 mL/s.
Although angiographically assisted CT scanning may produce elegant images, it is invasive, it is expensive, and it
has not gained widespread acceptance.
Portal vein thrombosis (PVT) may manifest as a hypoattenuating center in the portal vein surrounded by peripheral
enhancement on contrast-enhanced CT. The attenuation of the portal vein is 2030 HU less than that of the aorta
after the administration of contrast material.
CT findings in BCS include inhomogeneous mottled-liver contrast enhancement with delayed enhancement in the
periphery of the liver and around the hepatic veins. The caudate lobe is enlarged and has increased contrast
enhancement compared with the rest of the liver. Thrombosis within the hepatic veins and the inferior vena cava
(IVC) may sometimes be identified.
CT angiography
CTA is an exciting new application of helical CT. The speed of helical CT allows the maintenance of a higher
concentration of intravenous contrast medium, particularly through the arterial enhancement phase, with the
capability of 3-dimensional reconstruction. Both peripheral intravenous injections of contrast material and CT
arterial portography have been used as a basis for CTA.
CTA has shown great promise in the evaluation of hepatic vessels before liver resection. It provides preoperative
surgical information regarding the segmental location of liver tumors, the segmental venous anatomy, and
significant arterial anomalies if present. The value of CTA for patients with PH remains unclear.
A diagnosis of portal hypertension frequently is made on the basis of the demonstration of signs of cirrhosis.
Splenomegaly and ascites are demonstrated readily on CT; however, CT findings in cases of cirrhosis are highly
variable. In some patients, the liver is of nonuniform attenuation; hypoattenuating components probably represent
residual foci of infiltration.
Often, the attenuation of a cirrhotic liver is homogeneous and within the reference range. In the absence of
obvious abnormalities of size and shape, the liver may appear entirely normal on CT scans. Nonenhanced CT is
necessary when the cirrhotic liver is imaged for the identification of confluent fibrosis. Confluent fibrosis
characteristically demonstrates low attenuation, which tends to become isoattenuating or minimally
hypoattenuating on CT following intravenous contrast enhancement. Thus, confluent fibrosis is frequently missed if
only contrast-enhanced CT is used.
Collateral veins are occasionally seen in the peritoneal cavity, retroperitoneum, abdominal wall, and mediastinum.
CT lacks the dynamic capability of angiography in demonstrating the exact sites of portosystemic shunts and the
feeding vessels.
False positives/negatives
In patients with cirrhosis, CT scans may appear entirely normal. Other causes of diffuse liver disease, such as
splenomegaly and ascites, must be considered.
Magnetic Resonance Imaging
The vascular anatomy of the liver may be outlined by use of spin-echo and gradient-recalled echo MRI, but these
techniques cannot demonstrate the direction of portal flow. Time-of-flight MRI with bolus tracking has been found
to be successful in imaging portal hypertension and its sequelae.
Phase-contrast sequences may be used to evaluate the portal vein, and phase-contrast cine MRA may show the
direction of portal venous flow and the presence of portal vein thrombus.
MRI evaluation of the portal venous system is accurate in demonstrating thrombosis and collateral circulation;
however, MRI remains an expensive tool with limited availability.
Standard MRI findings reported in BCS include hepatic vein thrombosis, hepatic vein occlusion and narrowing,
hepatomegaly, atrophy of the right lobe of the liver, and enlargement of the caudate lobe. Liver parenchyma is
inhomogeneous (64%). IVC abnormalities, as demonstrated on MRI, include diffuse narrowing or focal thrombosis.
Venous collaterals are readily shown. Liver transplantation is regarded by many as the definitive treatment for PH.
Although portal vein thrombosis is no longer considered as a contraindication to liver transplantation,
demonstration of a portal vein thrombus is necessary for patient care. MR is an ideal noninvasive method for
detection of portal vein thrombus. Although it is not critical, visualization of venous collaterals is useful for
assessing the severity of disease. All major portosystemic collaterals may be detected by using MRA.
Comma-shaped intrahepatic varices are a characteristic finding not appreciated by other modalities. These
collaterals are formed in an attempt to bypass the obstructed flow.
In patients with elevated creatinine levels who cannot undergo a CT scan with intravenous contrast enhancement,
MRI with gadolinium enhancement may often be performed. These contrast-enhanced images are typically breath-
hold fast spoiled gradient-echo sequences, which may be dynamically obtained in both the arterial and portal
venous phases.
[11, 12, 13]
Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine
[MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linked
to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). The
disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based
contrast agent to enhance MRI or MRA scans.
NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin;
burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint
stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and
muscle weakness.
MRI does not offer an advantage over CT in the diagnosis of cirrhosis; however, morphologic changes identified
on US or CT are clearly depicted on MRI. One advantage of MRI over CT is its capacity to characterize
regenerative nodules in a cirrhotic liver. MRA may offer a noninvasive, nonoperator dependent evaluation of the
portal venous system; however, the exact sensitivity and specificity still need to be determined.
Ultrasonography
Flow studies of hepatic vessels may provide important information about the hemodynamic effects of hepatic
parenchymal disease (see the images below).
[14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30]
Power Doppler sonogram through the spleen shows varices at the hilum of an enlarged spleen. The final diagnosis was hepatitis C
cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and portoarterial fistula (which had
developed inside the ruptured tumor, giving rise to severe portal hypertension).
Duplex spectral Doppler sonogram of the portal vein (same patient as in the previous image) shows a bidirectional flow within the vein.
The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum),
and portoarterial fistula (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).
Transverse sonogram of the liver in a patient with hepatitis B cirrhosis shows a coarse echo structure of the liver.
Sagittal oblique sonogram of the liver shows a small liver with an irregular surface, moderate ascites, and a dilated portal vein. Note the
thick gallbladder wall.
Sagittal oblique sonogram of the liver shows a dilated portal vein (22 mm in transverse diameter) in a patient with portal hypertension.
End-stage liver cirrhosis showing a small liver, gross ascites, and a dilated portal vein
Doppler sample volume in portal vein reveals continuous venous flow without evidence of respiratory variation, consistent with a
hypertensive portal venous system. Note the coarse liver echo structure and ascites.
Doppler sample volume in portal vein reveals bidirectional flow in the portal vein associated with portal hypertension.
Sagittal oblique sonogram of the liver shows several tubular structures at the porta hepatis resulting from cavernous transformation
secondary to portal vein thrombosis.
Duplex power Doppler sonogram shows an enlarged spleen; varices are apparent at the splenic hilum.
Doppler sonogram at the splenic hilum reveals hepatofugal venous flow in a patient with portal hypertension.
Spleen in portal hypertension, with a positive splenic interface sign.
Color Doppler ultrasound showing pericholecystic varices.
Color Doppler ultrasound showing pericholecystic varices.
Peripancreatic varices as shown on power Doppler.
Peripancreatic varices as shown on power Doppler.
Peripancreatic and perihilar varices as shown on real-time scanner.
Periportal varices on power Doppler
Periportal varices on conventional Doppler and power Doppler
Periportal varices conventional Doppler and power Doppler.
Dilatation of umbilical vein as shown on color Doppler.
Examination results are not always straightforward because the liver may move during respiration, but breath
holding may facilitate the demonstration of blood flow and hepatic waveforms, particularly in the hepatic veins.
Examination is undertaken with as small an angle as possible between the axis of the US beam and the long axis
of the vessel. This approach is usually straightforward because the hepatic veins course posteriorly to the inferior
vena cava (IVC), whereas the portal vein curves forward as it passes through the porta hepatis. The blood flow
waveform from the left hepatic vein frequently shows artifact caused by cardiac pulsation. Thus, when the hepatic
veins are examined, the middle and right hepatic veins are usually encountered. The hepatic artery is small, and
usually, it must be examined on suspended respiration.
Doppler analysis of vascular flow patterns is a valuable adjunct to real-time 2-dimensional scanning. Color-flow
analysis is a valuable means of differentiating vessels from other fluid-filled structures. Power Doppler analysis is
particularly valuable for demonstrating low flow rates in small vessels.
Vascular indices, which are used in flow analysis, include the time-averaged mean velocity and the pulsatility
Vascular indices, which are used in flow analysis, include the time-averaged mean velocity and the pulsatility
index. The pulsatility index is low if the vascular bed is of low resistance and can accommodate sudden pressure
waves. A high-resistance or low-compliance vascular bed shows a high pulsatility index.
Portal vein waveforms
The portal vein typically shows continuous forward flow with minor modulation caused by respiration and
transmitted arterial pulsation. The rate of blood flow is greatest at the center of the vessel and is least at its
margins; therefore, the average flow across a segment of the vessel is used to overcome the internal variation
resulting from respiration and transmitted cardiac pulsation. The time-averaged velocity usually is on the order of
1214 cm/s in adults.
Flow within the portal vein changes rapidly in response to eating. Blood flow to the small bowel begins to increase
within 2 minutes of taking the first mouthful of food. The time-averaged blood flow velocity in the portal vein may
increase to 25 cm/s after a meal, and with minor increase in vessel diameter, the flow volume may increase 45
times.
Most patients with mild hepatic parenchymal disease have normal portal venous blood flow. As hepatic disease
becomes more severe, the first detectable flow abnormality is a reduction in the level of increase in flow seen after
a meal. Then, the splenic and superior mesenteric veins may begin to distend, and the change in vessel caliber
that is seen normally with respiration is lost. In severe hepatic parenchymal disease, portal venous blood flow is
reduced, and a rough correlation is noted between the degree of reduction in portal flow velocity and the severity
of hepatic parenchymal disease (providing that studies are performed in strictly fasting patients).
As portal venous flow is compromised further, forward flow may be seen only during systole, with reversed flow
occurring during diastole. Eventually, flow within the portal vein may be reversed continuously, but the rate and
direction of flow may vary from day to day, particularly in patients with acute exacerbation of chronic liver disease.
Therefore, serial examinations provide a better picture than single scans. Clearly reduced portal flow velocity is
associated with an increase in the risk of thrombosis.
Portal venous shunts
Percutaneous creation of a shunt between the portal and hepatic veins with TIPS is becoming increasingly
common as a treatment for PH. Doppler US may be used to assess patency and show the direction of flow within
the portal vein and shunt. If the walls of an artificial shunt prevent direct analysis of blood flow within it, an analysis
of flow at the ends of the shunt usually allows adequate assessment of shunt function.
Surgically created shunts include portocaval (end or side of main portal vein to IVC), mesocaval, and splenorenal
shunts (Warren shunt). Mesocaval and splenorenal shunts are used more frequently to maintain portal venous
patency for transport than for other purposes. Color Doppler imaging is valuable for the evaluation of shunts.
US evaluation of PH
The diameter of the portal vein is measured with the patient in a supine position, in quiet respiration, and having
fasted for a minimum of 4 hours. Measurements are made at the point at which the portal vein crosses the IVC. In
an individual without portal hypertension (PH), the diameter of the portal vein is 13 mm or 16 mm during deep
inspiration.
Under standard conditions, measurements greater than 13 mm indicate PH with a specificity of 100% but a low
sensitivity of 4550%. Sensitivity may be increased to 81% by measuring splenic vein and superior mesenteric
vein diameters. An increase of 20100% in diameter during deep inspiration is normal. An increase of less than
20% is associated with PH.
The differential diagnosis of a dilated portal vein includes PH splenomegaly (whatever the cause), acute portal vein
thrombosis (PVT), and postprandial increase in portal vein diameter.
Portal flow direction and velocity
Usually, blood flow in the portal vein is hepatopetal (toward the liver) during the entire cardiac cycle. The mean
velocity is 1518 cm/s and varies with cardiac cycle. In PH, velocity fluctuations disappear, resulting in continuous
flow. With a further increase in portal venous pressure, the blood flow direction becomes to-and-fro (biphasic), and
finally, the direction is reversed (hepatofugal).
Differential diagnosis of hepatofugal portal venous flow includes PH, Budd-Chiari syndrome (BCS), side-to-side
portocaval shunts, surgical or spontaneous splenorenal shunts with cirrhosis, and tricuspid regurgitation (tricuspid
flow reversal). Differential diagnosis of portal venous flow reversal includes severe PH, tricuspid regurgitation, and
congestive heart failure.
The differential diagnosis of reversal of hepatofugal-to-hepatopetal portal flow includes eating and the use of drugs
that increase portal flow. Static flow without Doppler signal occurs occasionally.
Pulsatile portal vein flow
A pattern similar to that seen in patients with impaired right heart function occasionally is seen in patients with
cirrhosis and/or PH. Patients with right-sided cardiac dysfunction with pulsatile portal venous flow invariably have
abnormal liver function.
The differential diagnosis of pulsatile portal venous flow includes tricuspid regurgitation, aorticright atrial fistula,
fistula between the portal vein and hepatic vein, PH, and congestive heart failure. Rarely, it is a false-positive
finding.
Decreased volume flow in the portal vein
In mild to moderate PH, the volume of flow in the portal vein is maintained. A reduction in volume flow occurs with
advanced cirrhosis when intrahepatic obstruction to portal flow is severe, as indicated by hepatofugal flow and
extensive portosystemic collaterals.
Congestive Index
PH may be recognized by use of the congestive index, in which the ratio of the portal vein (in units of square
centimeter) is divided by the mean portal flow velocity (in units of centimeter per second). This ratio reflects the
physiologic changes that occur in PH (ie, portal vein dilatation associated with diminished flow velocity). In
individuals without PH, the ratio should not exceed 0.7.
Splenomegaly
The size of the spleen is not well correlated with the level of PH; however, if splenomegaly is absent, PH is
unlikely. The spleen is best measured in the coronal plane. In the midaxillary line, a cephalocaudal measurement
greater than 13 cm suggests enlargement.
Splenic interface sign
Linear reflective channels are observed in the splenic parenchyma in a variable number of patients with PH.
Channels may be explained by dilatation of intrasplenic venous sinuses with increased collagen in the walls and by
periarterial fibrosis. The pathologic changes are known to occur in PH. The splenic interface sign seldom is found
in patients with splenomegaly that is unrelated to PH. The vascular nature of channels is readily confirmed by
using CDI.
Ascites
Uncomplicated PH usually does not cause ascites. Usually, ascites occurs secondary to underlying liver diseases
with liver cell failure.
Arterialization of hepatic blood supply
Hepatic arteries are enlarged and usually have aliased frequency shifts compared with those of normal hepatic
arteries. The arteries also appear tortuous. As portal venous flow to the liver decreases, arterial flow increases.
Increased arterial flow occurs with the development of large collaterals and hepatopetal flow.
The differential diagnosis of an enlarged hepatic artery includes an occluded or interrupted portal vein, a surgical
portosystemic shunt, reversal of flow in the portal vein, parenteral feedings in newborns, hereditary hemorrhagic
telangiectasia, cirrhosis or hepatic diseases associated with alcohol, vascular hepatic tumors, and primary hepatic
artery dissection.
Portosystemic venous collaterals
The demonstration of portosystemic venous collaterals (PVCs) is diagnostic of PH.
Umbilical venous collateral flow is an important feature of PH because it has a specificity of 100%. Typically, an
artery or vein with a diameter of 2 mm may be present within the ligamentum teres. Thus, the demonstration of a
blood vessel in the ligamentum teres does not equate with the presence of a PVC. The diagnosis of PVCs requires
the demonstration of venous flow away from the liver. The enlarged umbilical vein is usually solitary, originating in
the left portal vein, which courses inferiorly through the falciform ligament and along the anterior abdominal wall to
the umbilicus, seen on longitudinal or transverse scans.
The diameter of a typical coronary vein is 4 mm; a diameter greater than 7 mm is evidence of an abnormal
portosystemic gradient (>10 mm Hg). Because the coronary vein may be seen in some individuals without PH, its
presence does not indicate PH. A coronary vein appears as a prominent cephalic-directed vessel that joins the
portal vein near the termination of the superior mesenteric vein.
Splenosystemic collaterals may form as a result of splenic venous occlusion as well as PH. Demonstration of
splenic venous occlusion with US is straightforward because in most patients, it is possible to trace the splenic
vein to the portal vein. With splenic vein occlusion, collaterals may be identified in the pancreatic bed or the
gastroesophageal area.
Tortuous short gastric and gastroesophageal veins near the upper pole of the spleen and gastroesophageal
junction are seen primarily on coronal images. Large portosystemic collaterals at the esophagogastric junction may
be mistaken for neoplastic masses if Doppler examination is omitted. Right gastric veins are cephalically directed
and are seen along the inferior border of the left lobe of the liver on longitudinal scans.
Splenorenal veins are demonstrated as tortuous, inferiorly directed vessels from the splenic hilum to the left
kidney; they are primarily seen on coronal images. The left renal vein may be dilated. Retroperitoneal
portosystemic collaterals (varices) may mimic other masses (eg, pancreatic carcinoma or other retroperitoneal
tumors) on both CT and US images. CDI may show the mass to be full of flow colors; other signs of PH are often
present.
Banti syndrome
Banti syndrome, or noncirrhotic idiopathic PH, is a common cause of PH in India and Japan but is rare in the
United States and Europe. The syndrome is characterized by signs of PH, but liver function test results tend to
remain normal. Hepatic wedge pressure readings are usually normal or slightly elevated. Signs of hypersplenism
are often present. US shows a normal-appearing liver; patent hepatic veins; and a patent portal vein, which may
be associated with multiple portosystemic collaterals.
Portal venous thrombosis
PVT is being recognized with increasing frequency on US images. Reduced portal blood flow resulting from
hepatic parenchymal disease and abdominal sepsis are the primary causes. Transient PVT is also being
recognized with increasing frequency, in part because of the large increase in the use of US in evaluating patients
with abdominal inflammation, such as appendicitis. Tumor within the portal vein may appear identical to
thrombosis, but it is far less common. Tumor within the portal vein is most frequently related to a hepatocellular
carcinoma, which gives rise to serpiginous filling defects in the portal venous luminal flow, but it usually persists
around the tumor without complete occlusion.
Adults with acute PVT secondary to abdominal sepsis completely recover with vessel recanalization after
successful treatment of underlying sepsis. In children, the portal vein may recanalize by developing multiple small
collateral channels, which are seen as a partly echogenic band of small vessels running to the porta hepatis.
These show reduced flow velocity of 27 cm/s. Nonvisualization of the portal vein is strongly suggestive of
occlusion. Then, the portal vein may be seen as a band of high-level echoes at the porta hepatis.
Causes of PVT include idiopathic causes, malignancy (hepatocellular carcinoma, cholangiocarcinoma, pancreatic
carcinoma, and stomach carcinoma), trauma (which may be iatrogenic, such as umbilical vein catheterization), and
abdominal sepsis (pancreatitis, perinatal sepsis, omphalitis, appendicitis, diverticulitis, cirrhosis), especially in
younger individuals.
On sonograms, clot exhibits variable echogenicity; it may be hypoechoic or anechoic if it has recently formed.
On sonograms, clot exhibits variable echogenicity; it may be hypoechoic or anechoic if it has recently formed.
Conversely, patent vessels may show increased intraluminal echogenicity because of artifact or erythrocyte
rouleaux formation. In isolation, increased or decreased echogenicity in the lumen of the portal vein is not sufficient
to make a diagnosis of PVT or to exclude PVT. In patients with PVT, the venous flow signal that is typically
obtained from the lumen of the portal vein during pulsed or color-flow Doppler imaging is absent, and flow may be
seen around a thrombus that partially occludes the vein. However, if flow is sluggish, the Doppler signal may not
be detected. Color flow may be demonstrated in other small collaterals.
Incomplete occlusion (common in neoplastic invasion) or thrombolytic recanalization may occur. These cannot be
differentiated by use of US. Hepatopetal flow may be demonstrated, and spontaneous shunts may be visualized
(splenorenal).
US may demonstrate portosystemic collaterals, and the cause may be identified, such as hepatocellular
carcinoma, metastases, cirrhosis, and pancreatic neoplasms. The incidence of PVT is reported to be low in
patients with PH, but it is associated with sclerotherapy. The string sign, or thickening of the portal vein with
narrowing of its lumen, which is interpreted as a portal phlebitis, is considered a precursor of PVT in patients with
acute pancreatitis. The portal vein thrombus may become calcified.
Cavernous transformation of the portal vein
Cavernous transformation occurs in patients with long-standing PVT (19%) when numerous multiple collateral
vessels develop around the occluded portal vein; these collateral vessels appear as vermiform tubular structures
at the porta hepatis. Application of color-pulsed Doppler imaging shows blood flow in the periportal collaterals
around the thrombosed portal vein. Cavernous transformation of the portal vein has been reported to appear as a
subhepatic spongelike mass. This appearance also has been reported in patients with pancreatic
hemangiosarcoma.
Bile duct varices, also called the pseudocholangiocarcinoma sign, are not infrequently observed during endoscopic
retrograde cholangiopancreatography. In patients with PH, they result from cavernous transformation of the portal
vein. Studies report that the sign may disappear after a TIPS procedure.
Assessment of TIPS
TIPS involves the percutaneous placement of a shunt via the jugular vein. TIPS is becoming popular as a definitive
procedure for decompressing the portal venous system or as a prelude to liver transplantation.
Doppler US is a sensitive and relatively specific means of evaluating TIPS malfunction. US evaluation of the shunt
is usually performed within 24 hours after shunt placement to establish baseline velocities within the portal vein,
hepatic vein, and shunt. Follow-up studies are usually performed at 3-month intervals unless the clinical setting
dictates a more emergent examination. The primary object of Doppler study of a TIPS is to document flow in the
shunt and to demonstrate stenosis. The accuracy of Doppler US in shunt malfunction depends on several US
parameters, which include the peak shunt velocity, distal shunt velocity, and antegrade flow in the left and right
portal veins.
Flow velocities in the portal vein may double in comparison with the preoperative velocities in a successful TIPS
placement. Direct observation of shunt thrombosis is possible with duplex or color Doppler US. Echo-enhanced
color Doppler US may also be helpful in the assessment of TIPS.
Complications of TIPS that are detectable with US include early complications and delayed complications.
Early complications
Intraperitoneal hemorrhage
Shunt thrombosis
Neck hematoma
Compromise of hepatic blood supply: PVT, hepatic artery occlusion, hepatic infarction
Failed stent deployment: inadequate stent expansion, stent migration, stent fracture
Biliary obstruction
Delayed complications
Shunt stenosis: pseudointimal hyperplasia, hepatic vein stenosis
The demonstration of portosystemic shunts is a specific sign of portal hypertension. Umbilical vein collateral flow is
an important feature of PH because it has a specificity of 100%. In individuals without PH, the caliber of portal,
splenic, and superior mesenteric veins shows significant variation during respiration. When respiratory variation
does not occur or when it is slight (< 20%), PH may be diagnosed with a sensitivity of 80% and a specificity of
100%. A portal vein diameter greater than 13 mm is specific for PH, but it is not a sensitive indicator of PH.
False positive and negatives include the following:
The differential diagnosis of a dilated portal vein includes PH splenomegaly (of any cause), acute PVT, and
postprandial increase in portal vein diameter.
The differential diagnosis of portal vein flow reversal includes severe PH, tricuspid regurgitation, and
congestive heart failure.
The differential diagnosis of reversal of hepatofugal-to-hepatopetal portal flow includes eating and the use
of drugs that increase portal flow. Static flow without Doppler signal occurs occasionally.
The differential diagnosis of pulsatile portal vein flow includes tricuspid regurgitation, aorticright atrial
fistula, fistula between the portal vein and hepatic vein, PH, and congestive heart failure. Rarely, it may be a
false-positive finding.
Uncomplicated PH usually does not cause ascites. Usually, ascites occurs secondary to underlying liver
diseases with liver cell failure.
The differential diagnosis of an enlarged hepatic artery includes an occluded or interrupted portal vein; a
surgical portosystemic shunt; reversal of flow in the portal vein; parenteral feeding in newborns; hereditary
hemorrhagic telangiectasia; cirrhosis or hepatic diseases associated with alcohol; vascular hepatic tumors;
and primary hepatic artery dissection.
Angiography
Angiographic evaluation of the portal venous system may be performed (see the images below).
Venous phase of a digital subtraction celiac-axis angiogram shows no splenic vein, but multiple collateral venous pathways are seen
through the stomach wall (straight arrows), which feed a normal portal vein (curved arrows). Several varices are noted within the body
of the stomach. The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.
Venous phase of a digital subtraction superior mesenteric angiogram (same patient as in the previous image) shows a normal portal
vein (PV) with no streaming effect from splenic venous flow (arrow), suggestive of splenic vein thrombosis. The final diagnosis was left-
sided portal hypertension secondary to splenic vein thrombosis.
Digital subtraction selective common hepatic artery angiogram shows immediate filling of the portal venous radicles in the left lobe of
the liver (straight arrow) and early filling of portal vein (curved arrow), suggestive of hepatic arterial-portal vein fistula. The final
diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and
portoarterial fistula (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).
Delayed venous phase of a selective common hepatic angiogram (same patient as in the previous image) shows the portal vein (P),
with filling of the coronary vein caused by retrograde flow feeding gastric and lower esophageal varices (arrows). Retrograde flow in
enlarged umbilical veins also is seen. The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe
(which had ruptured into the peritoneum), and portoarterial fistula (which had developed inside the ruptured tumor, giving rise to severe
portal hypertension).
Digital subtraction venous phase of a superior mesenteric artery angiogram (same patient as in the previous 2 images) shows
retrograde flow into the coronary vein (curved arrow) and the inferior mesenteric vein (straight arrow). Note the flow defect of the distal
portal vein caused by retrograde flow (open arrowhead). The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the
left hepatic lobe (which had ruptured into the peritoneum), and portoarterial fistula (which had developed inside the ruptured tumor,
giving rise to severe portal hypertension).
Conventional angiogram of the superior mesenteric artery shows a replaced hepatic artery in the right lobe of the liver in a patient with a
previous history of abdominal tuberculosis and a recent history of hematemesis. Note the multiple calcific foci in the splenic region as a
result of old healed tuberculous granulomas. Two previous liver biopsies had not revealed the changes of cirrhosis. The final diagnosis
was tuberculous calcified lymph nodes at the porta hepatis causing portal vein stenosis by extrinsic pressure, portal hypertension, and
esophageal and gastric varices.
Venous phase of a superior mesenteric angiogram shows a stenosis of the portal vein near the porta hepatis with poststenotic
aneurysmal dilatation of the portal vein. Filling of the gastric varices and the splenic vein are seen as a result of retrograde flow (same
patient as in the previous image). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal vein
stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.
Intraoperative portogram shows portal vein stenosis and a portal vein aneurysm. The splenic vein is outlined because of retrograde flow
(same patient as in the previous 2 images). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing
portal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.
Line diagram of findings on portal venous phase angiogram (same patient as in the previous 3 images). The superior mesenteric vein
has been added for anatomic clarity. The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal vein
stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.
Venous phase of digital subtraction superior mesenteric angiogram shows the portal vein to be reduced to a threadlike structure
(arrow). Retrograde flow into the splenic vein (S) is seen. The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein
thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.
Venous phase of a digital subtraction superior mesenteric angiogram shows a shunt between the splenic vein (S) and the left renal vein
(R), and the IVC (V) is outlined with contrast material. Arrows mark the tiny threadlike portal vein (same patient as in the previous
image). The final diagnosis was hepatocellular carcinoma (not shown), cirrhosis, and portal vein thrombosis/portal hypertension
complicated by a spontaneous splenorenal shunt.
Splenoportography
Because of the use of alternative imaging methods, the use of splenoportography (SP) has declined considerably
after having played a primary role in the investigation of cirrhosis and PH for several years. However, restricted
indications remain for the procedure. Even with the available methods of direct or indirect visualization of the portal
vein, much of the information necessary to evaluate cirrhosis or PH may be obtained by use of SP (see the images
below).
Splenoportogram in a patient with known alcoholic cirrhosis and two episodes of variceal bleeding in the past. The procedure was
performed as a prelude to surgical portosystemic shunt placement. The splenoportogram shows a dilated coronary vein (CV) feeding
the lower esophageal and gastric varices (arrows). Retrograde filling of the inferior mesenteric vein (I) is present, but the main portal
vein flow is hepatopetal in direction.
Digital subtraction splenoportogram in a patient with portal hypertension shows a subcapsular contrast leak (arrows), which is a known
complication of splenoportography.
Splenoportogram in a 3-year-old child with a history of serious febrile illness in infancy and recent hematemesis. Splenoportogram
shows a thrombosed distal portal vein and a cavernous malformation at the porta hepatis (C). The arrow marks gastric and esophageal
varices. The inferior mesenteric vein is outlined because of reverse flow (I).
Intraoperative portogram shows portal vein stenosis and a portal vein aneurysm. The splenic vein is outlined because of retrograde flow
(same patient as in the previous 2 images). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing
portal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.
Splenic pulp measurement provides an accurate reflection of the portal venous pressure, both in hepatic and
prehepatic causes of PH. An intravenous injection of radiographic contrast medium into the splenic pulp outlines
the portosystemic collaterals (ie, splenic and portal veins); it demonstrates well the intrahepatic portal radicles and
enables an assessment of the rapidity of washout of the vessels in a hepatopetal direction. With reversal of flow
within the portal vein resulting from severe PH, the splenic and portal veins are not visualized; the contrast outflow
tract is via gastroesophageal collaterals. With splenic thrombosis/PVT, not only is the site of the obstruction
evident but also portal-portal collateral veins, which regularly develop, are demonstrated as well.
Contraindications to SP include coagulation defects, platelet count less than 50,000, ascites, an uncooperative
patient, and splenic pathology (splenic mass lesions). To perform SP, the skin over the left side of the thorax and
abdomen overlaying the spleen is prepared with an antiseptic after the spleen is localized. Historically, the spleen
was localized by use of fluoroscopy and palpation and percussion, but currently, localization is more commonly
performed by use of US. A skin bleb is raised near the lower pole of the spleen in mid respiration, and the soft
performed by use of US. A skin bleb is raised near the lower pole of the spleen in mid respiration, and the soft
tissues are infiltrated with local anesthetic down to the peritoneum.
The entry site of the needle usually is the 9th or 10th intercostal space in the midaxillary line. The needle is
directed in a cephalic direction toward the splenic hilum. A nick is made at the site of the needle puncture, and a
track is made into the soft tissues with a 12-gauge needle, which facilitates the placement of the SP needle. The
SP needle is a 14-gauge, 6-inch-long polyethylene sheathed needle. With patient breath hold in mid respiration,
the sheathed needle is introduced toward the direction of the splenic hilum, and the stilette is withdrawn, leaving
the sheath in place. The patient is instructed to take shallow respirations during the examination.
If the spleen has been entered accurately, blood flows back via the sheath. Then, the sheath is connected to a
spinal pressure manometer filled with saline, and the splenic pulp pressure is measured. The sheath is taped to
the patient's side, and a test injection is made using 5 mL of contrast medium. When a sheath is placed correctly,
contrast medium spreads into the splenic parenchyma, providing an uneven splenogram that rapidly drains into the
splenic vein. With a subcapsular placement, the contrast agent is viewed as a homogeneous collection that
spreads slightly as the agent is injected.
With subcapsular injection, the needle is withdrawn completely, and a fresh attempt is made to place the needle
correctly. With the sheath correctly placed, a pump injection is performed using 40 mL of 75% contrast at a rate of
10 mL/s. The injection is usually painless; discomfort and shoulder pain may occur with subcapsular injection. After
the procedure is complete, the needle tract is plugged with thromboembolic material, such as Gelfoam or Ivalon.
Complications of the procedure include hemorrhage, contrast agent extravasation, puncture of other organs,
splenic hematomas, and capsular rupture. Capsular rupture may require emergency laparotomy and splenectomy.
In addition to splenectomy, splenic artery embolization may be used to stop bleeding.
Indications for SP include the following:
Patency of the splenic vein is uncertain.
Arterioportography has been unsuccessful.
Portal pressure is required and other techniques have failed.
A more accurate imaging of the intrahepatic portal veins is required (eg, when phlebosclerosis is
suggested).
In PH, the following findings may be noted with SP:
Tributary collaterals usually feed into the portal venous system and develop hepatofugal flow associated
with elongation, tortuosity, and an increase in lumen size. The coronary and short gastric veins lead to the
gastroesophageal plexus and then to the hemiazygos and azygos systems and into the superior vena cava.
The dilated veins in the esophageal submucosa that form varices may be outlined by contrast
enhancement. The inferior mesenteric vein serves as another collateral, which may be demonstrated by
reverse flow. Outflow is through the superior mesenteric vein via the retroperitoneum into the IVC.
Abdominal surgery promotes the development of portosystemic shunts via adhesions.
Embryonic collaterals are no longer used under normal conditions, but they retain a potential lumen. In
response to PH, these vessels open, dilate, and become elongated, tortuous, and beaded. They direct
portal centrifugal flow. The paraumbilical collaterals are the only vessels in this group that commonly
participate in the centrifugal flow. They communicate with the inferior or superior epigastric veins.
Watershed collaterals are usually tiny vessels that form communications between the portal and systemic
circulations. They have virtually no blood flow. With an increase in the pressure gradient on either side, as
occurs with PH or as a temporary result of the injection of contrast medium, significant flow occurs in the
direction of the pressure gradient. With prolonged PH, the channels open permanently, dilate, elongate, and
become tortuous. Splenorenal collaterals are the most common watershed collaterals; they may opacify
with left adrenal and renal vein injections. Gastrorenal collaterals that also connect the splenic vein with the
left adrenal and renal veins may opacify on rare occasions. Rarely, communications between the spleen,
inferior phrenic vein, and left adrenal and renal veins are seen. Splenoretroperitoneal collaterals feed into
the lumbar venous plexus and may communicate with intercostal veins. Unnamed collaterals frequently are
observed.
Bridging collaterals with extrahepatic portal/splenic venous obstruction occur to preserve hepatopetal flow.
With occlusion of the splenic vein, hepatopetal flow occurs via the short gastric veins into the coronary vein
and then on to the portal vein. Some flow also occurs via the gastroepiploic vein into the superior
mesenteric vein. When the portal vein is occluded close to the hilum, bridging collaterals form a cavernoma
or run parallel to the occluded portal vein. Numerous capsular vessels opacify the liver surface and feed the
peripheral portal branches.
peripheral portal branches.
Intrahepatic portal vein changes depend on the severity of the cirrhotic process. Transit time of the contrast
agent through the liver is diminished. In the early stages of cirrhosis, portal vein branches appear crowded
but later are reduced in number. Portal radicles appear tortuous with abrupt caliber changes.
Occlusion/thrombosis of the portal vein is well demonstrated. A thrombotic plaque may be seen within the
portal vein; this plaque should not be confused with nonopacified blood flowing in from the superior
mesenteric vein. Note that nonopacification of the portal vein on SP does not necessarily mean that the
portal vein is occluded; in severe hepatofugal flow, the portal vein may fail to opacify.
Carbon dioxide SP
Carbon dioxide has been employed as a contrast agent for SP; a 22- or 25-gauge needle is used (thereby
exploiting the low viscosity of the gas). This technique is less traumatic than others, and it has been effective in
visualizing the portal venous system. The hope is that the difference in the collateral venous filling patterns is
significant, because carbon dioxide fills veins in the nondependent sites, whereas contrast material flows along the
dependent sites. Contrast-enhanced SP has been infrequently used in the United States.
Transhepatic portography
With percutaneous transhepatic portography (PTP), the same technique is used as with percutaneous
cholangiography. The portal vein is punctured directly and is replaced by a guidewire/catheter, and contrast
material is injected into the splenic vein and/or the superior mesenteric vein, depending on the clinical setting. PTP
is an easy and quick procedure. As a result of the straight course of the catheter through the liver substance,
catheterization of several tributaries is possible, but the distance between the cutaneous entrance of the catheter
and the liver makes catheter manipulation difficult. The few reported complications mostly result from nontarget
organ puncture (gallbladder, pleura) and intra-abdominal hemorrhage. With US guidance, the incidence of
nontarget organ puncture is expected to decrease.
Transcatheter obliteration of esophageal varices with various embolic agents is possible via transhepatic catheter
placement, but this is not a procedure to be followed by suitable surgical procedure. Transcatheter obliteration
should not be used as an elective procedure; even in an acute setting, hemostasis is best attempted with other
methods.
Transumbilical catheterization
Transumbilical catheterization requires a surgical procedure in which a transverse incision is made 35 cm above
the umbilicus, and the umbilical vein is catheterized. Complications are few, but the procedure is difficult and time
consuming. With so many noninvasive procedures currently available, the procedure is seldom indicated.
Transjugular catheterization
The transjugular approach to the portal vein first was described by Rsch et al in 1969. Since then, the technique
has improved; currently, it is used more for therapeutic applications, such as the establishment of a TIPS.
Wedged hepatic venography
When a catheter is placed in a small hepatic vein via the inferior vena cava (IVC) or jugular vein, pressures may be
measured either with a transducer or with a saline manometer. In patients with sinusoidal or postsinusoidal portal
venous obstruction, as occurs in cases of cirrhosis, pressure measured in this way accurately reflects the total
portal pressure. The wedged hepatic venous pressure is the same as the splenic pulp pressure measured by use
of SP. Normal portal pressure levels measured in this way are 40150 mm of saline. Pressures above 150 mm of
saline indicate PH.
Two components contribute to PH. The first is intrahepatic resistance to portal venous flow, and the second is
transmitted pressure from the IVC. In addition, IVC pressures are measured, and the corrected sinusoidal pressure
is derived by subtracting the IVC pressure from the wedged hepatic pressure. The corrected sinusoidal pressure is
useful clinically because it reflects the true status of the liver disease responsible for development of portosystemic
shunts and variceal bleeding. Corrected sinusoidal pressure readings of as high as 100 mm of saline are
considered normal.
Although corrected sinusoidal pressure makes the most significant contribution to variceal bleeding in patients with
cirrhosis, the total pressure usually contributes to bleeding from esophageal varices. Thus, a patient with both
cirrhosis, the total pressure usually contributes to bleeding from esophageal varices. Thus, a patient with both
cirrhosis and congestive heart failure may bleed from esophageal varices because of a temporary increase in
central venous pressure; conversely, esophageal bleeding may cease when the central venous pressure
decreases. Typically, patients with cirrhosis do not bleed from varices with portal venous pressures of 200250
mm of saline. Patients with cirrhosis who bleed at pressures lower than 200 mm of saline almost always bleed
from an alternative source.
Arterial portography
Arterial portography (AP) is currently the preferred method of evaluating the portal venous system because it is
less invasive and has a lower complication rate. AP involves the indirect opacification of the portal venous system
with the injection of contrast material into the celiac axis (delayed images outline the splenic, gastric, and portal
veins) or into the superior mesenteric artery (outlining superior mesenteric and portal veins).
The 3 major indications for AP include the following:
To perform workup in patients with PH and its sequelae, particularly when surgical treatment is planned.
To determine the resectability of hepatic and pancreatic tumors when both arterial- and venous-phase
angiograms make significant contributions.
To perform transcatheter embolization, as in islet cell tumor metastases and carcinoid metastases, or to
perform chemoembolization, as in hepatocellular carcinoma (demonstration of a patent portal vein is a
prerequisite for these treatments).
Preparation and contraindications for AP are identical to those of standard conventional angiography. Selective
catheters are used to cannulate the appropriate artery. In a superior mesenteric artery injection, the tip of the
catheter is placed such that it opacifies all the branches with contrast medium. Before delivery of the contrast
agent, administration of a vasodilator (tolazoline, papaverine, nitroglycerin) improves opacification of the portal
vein. Manual or digital subtraction imaging improves resolution. If digital subtraction is used, administration of an
anticholinergic drug before filming reduces bowel movement. Left gastric artery injection consistently demonstrates
esophageal varices.
AP findings in PH include the following:
Arterial-phase findings: pancreatic carcinoma, hepatocellular carcinoma, pancreatitis
Venous-phase findings: splenic vein thrombosis, superior mesenteric vein thrombosis, portal vein
thrombosis, collateral channels
Splenoportography (SP) is a fairly accurate method of outlining the portal venous system and the portosystemic
communications for patients with portal hypertension; for this, SP remains the criterion standard. Diagnostic
modalities such as US, CT, and MRI have reduced the diagnostic importance of arteriography. The major role of
angiography is in mapping the vascular anatomy before surgery and in guiding the transcatheter treatment of liver
tumors. In celiac-axis and superior angiography, the venous phase provides sufficient detail to render direct
portography unnecessary in most patients.

Contributor Information and Disclosures
Author
Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR Consultant Radiologist and Honorary Professor, North
Manchester General Hospital Pennine Acute NHS Trust, UK
Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR is a member of the following medical societies: American
Association for the Advancement of Science, American Institute of Ultrasound in Medicine, British Medical
Association, British Society of Interventional Radiology, Royal College of Physicians, Royal College of
Physicians and Surgeons of the United States, Royal College of Radiologists, and Royal College of Surgeons of
England
Disclosure: Nothing to disclose.
Coauthor(s)
Murad Ali, MBBS, PhD, DTCD Consulting Radiologist, Department of Radiology, Postgraduate Medical
Institute, Lady Reading Hospital, Pakistan
Institute, Lady Reading Hospital, Pakistan
Specialty Editor Board
Eric P Weinberg, MD Associate Professor, Department of Radiology, University of Rochester Medical Center,
Strong Memorial Hospital
Eric P Weinberg, MD is a member of the following medical societies: American College of Radiology, American
Roentgen Ray Society, and Radiological Society of North America
Bernard D Coombs, MB, ChB, PhD Consulting Staff, Department of Specialist Rehabilitation Services, Hutt
Valley District Health Board, New Zealand
George Hartnell, MBChB Professor of Radiology, Tufts University School of Medicine; Director of
Cardiovascular and Interventional Radiology, Department of Radiology, Baystate Medical Center
George Hartnell, MBChB is a member of the following medical societies: American College of Cardiology,
American College of Radiology, American Heart Association, Association of University Radiologists, British
Institute of Radiology, British Medical Association, Massachusetts Medical Society, Radiological Society of
North America, Royal College of Physicians, Royal College of Radiologists, and Society of Cardiovascular and
Interventional Radiology
Robert M Krasny, MD Resolution Imaging Medical Corporation
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and
Radiological Society of North America
Chief Editor
Kyung J Cho, MD, FACR William Martel Professor of Radiology, Interventional Radiology Fellowship Director,
University of Michigan Health System
Kyung J Cho, MD, FACR is a member of the following medical societies: American College of Radiology,
American Heart Association, American Medical Association, American Roentgen Ray Society, Association of
University Radiologists, and Radiological Society of North America
Additional Contributors
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors
Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, and David Sherlock, MBBS, FRCS,to the development and
writing of this article.
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