Applied Radiology

Dr. Jeffrey is a Professor of Radiology and Chief of Abdominal Imaging; and Dr. Dresser is an Assistant Professor of Radiology, Stanford University School of Medicine, Stanford, CA.

In the past decade, there has been considerable improvement in color Doppler sensitivity with an expanding array of transducer options and capabilities for hepatic imaging. Color Doppler imaging is often the initial technique of choice for the noninvasive assessment of abnormalities of the portal veins. ^1-10 It is important to remember, however, that most hepatic vascular disorders are often not suspected clinically and are only diagnosed by imaging studies. This is due to the nonspecific clinical and laboratory abnormalities associated with most hepatic vascular lesions. Gray-scale imaging alone is inadequate for hepatic vascular diagnosis. Therefore, the routine use of color and spectral Doppler is essential in all hepatic sonograms. This article will address common abnormalities of the portal veins that can be detected readily with a combination of color and spectral Doppler.

Technique Optimization

In general, the greatest color Doppler sensitivity for imaging of the portal veins can be obtained by using the highest frequency transducer, which provides sufficient penetration to visualize the portal veins. In patients without cirrhosis, a 5- to 6-MHz curved array transducer is often the transducer of choice. Imaging the portal veins in cirrhotic patients may be quite challenging, and a 2.5-MHz transducer using 1.75 MHz Doppler frequency may be essential for adequate color Doppler sensitivity. In patients who are able to perform a 15 to 20 second breathhold, power Doppler imaging may also be quite useful. All potential abnormalities detected with color Doppler should be confirmed with spectral Doppler tracings with an angle correction <60º.

Portal Veins

Normal Anatomy, Physiology, and Anatomic Variants

In normal patients, the extrahepatic portal vein may range in size from 6 to 20 mm; however, in the vast majority of patients it is <13 mm. The portal vein may dilate in patients with cirrhosis or arterioportal fistulas, but rarely exceeds 2 cm in diameter. Patients with portal veins >2 cm, particularly if the dilatation is focal or fusiform in nature, may be thought to have portal venous aneurysms (Figure 1). ¹

Normal antegrade flow in the portal veins is toward the liver (hepatopetal) and demonstrates a slightly undulating spectral tracing due to cardiac and respiratory motion (Figure 2). Angle-corrected spectral Doppler tracings of the main portal vein in normal fasting patients demonstrate mean flow typically ranging from 15 to 18 cm per second. ¹ Experimental studies have shown that the right lobe of the liver is preferentially supplied by mesenteric flow and the left lobe of the liver by splenic flow. ⁷ Following a standard meal, there is a greater increase in portal flow to the left lobe than to the the right lobe. Postprandially the main portal vein velocity increases significantly. The diameter of the portal vein during quiet breathing in normal patients typically increases >20% with deep inspiration. This increase is typically dampened in patients with cirrhosis and portal hypertension. ¹

Congenital Anomalies of the Portal Veins

Congenital anomalies of the portal veins include agenesis of the right or left branches, variations in the branching patterns of the main portal vein, congenital portal to hepatic venous communications, and aneurysms of the intra- or extrahepatic portal vein. ⁶ Awareness of the range of anatomic variants of the portal venous system is important when considering surgery or invasive procedures of the liver, including split liver transplantation in living related donors and TIPS procedures (transjugular intrahepatic portosystemic shunts). The most common congenital anomaly of the portal vein is agenesis of either the right or left main branches. In normal patients, the main portal vein divides into a right and left branch in the porta hepatis. The most common branching abnormality is a trifurcation, in which there is no normal right portal vein. The main portal vein trifurcates into the right anterior, right posterior, and left portal branches at the same level. Other branching anomalies include the right anterior branch arising from the left portal vein, or the right posterior branch arising from the main portal vein. Failure to recognize this anomaly may lead to inadvertent ligation of the left portal vein during liver donor surgery and/or surgical resection and result in extensive liver necrosis and hepatic insufficiency.

Portal venous aneurysms may be either congenital or acquired. Although in most instances they are of little clinical significance, rarely they may result in thrombosis and/or rupture.

Anatomic Variants in Portal Venous Flow

In approximately 2% of patients, portal venous flow is nonlaminar and appears in a swirled or helical fashion (Figure 3). ² Helical flow may be seen relatively frequently as a transient finding following liver transplantation or TIPS procedure. ² Many patients with helical flow in the portal vein have underlying portal hypertension, and this finding should prompt further evaluation in portosystemic shunts. ²

Abnormalities of the Portal Vein

Portal vein occlusion

There are numerous causes of portal vein occlusion, but the most common in clinical practice include in situ thrombosis and tumor invasion. ³ Thrombosis is often related to hypercoagulable states, pancreatitis, septic thrombosis (pyelephlebitis), or stagnant flow within the portal vein due to cirrhosis. In order to avoid misdiagnosis due to technical factors, portal vein occlusion suspected on the basis of color Doppler sonography should be confirmed with both power Doppler and spectral Doppler tracings, using low MHz transducers (2.5 MHz) for optimal penetration. In cirrhotic patients with stagnant portal venous flow, ultrasound may produce a false-positive finding of portal vein thrombosis, which can be demonstrated to be patent using contrast-enhanced MRI. Acute thrombosis may be relatively anechoic and, therefore, can be difficult to detect with confidence using gray-scale imaging alone (Figure 4).

Neoplastic invasion of the portal veins is seen most commonly in hepatocellular carcinoma (HCC), but may be due to other neoplasms, such as cholangiocarcinoma or pancreatic carcinoma. In patients with HCC, tumor invasion can be differentiated from bland thrombus by detection of arterial tracings with a retrograde flow pattern (Figures 5 and 6), ⁵ indicating tumor neovascularity extending caudally down the portal vein. Tumor invasion typically causes significant enlargement of the portal vein segment. In fact, any flow detected within the thrombus should indicate tumor invasion. Extension of intrahepatic tumor thrombus into the main portal vein carries a very poor prognosis, generally precluding surgical resection for cure. In addition, main portal vein involvement from HCC may influence the use of chemoembolization as a palliative maneuver.

Chronic occlusion of the portal vein may result in its fibrous obliteration, making it impossible to identify. The detection of numerous periportal collaterals has been termed cavernous transformation, which has a typical color Doppler appearance with a tangle of venous structures seen along the course of the hepatoduodenal and gastrohepatic ligaments (Figure 7). Venous collaterals may directly involve the wall of the gallbladder or bile duct. ¹

The pulsatile portal vein

Markedly phasic or pulsatile flow in the portal vein may be seen in a variety of pathologic states, but it may also be a normal finding in very thin patients (Figure 8). Pulsatility of the portal vein has been reported in right heart failure, tricuspid regurgitation, constrictive pericarditis, cirrhosis, and hepatic arterioportovenous fistulas. There are numerous etiologies of arterioportal shunts including neoplasms, such as hepatomas; cirrhosis; trauma; congenital vascular malformations; and iatrogenic causes due to invasive procedures (Figure 9).

Portal hypertension

In patients with cirrhosis a variety of complex flow patterns in the portal vein may be seen in various stages of portal hypertension. Flow patterns in the portal vein are influenced by the degree of hepatic fibrosis, development of portosystemic collaterals, arterioportal shunts, and therapeutic intervention, such as TIPS and/or drug therapy with beta blockers to lower portal hypertension. Large paraumbilical collaterals in patients with cirrhosis may produce hyperdynamic flow states. Patients without paraumbilical collaterals may demonstrate markedly diminished or reversed (hepatofugal) flow or bi-directional flow. Because the gray-scale imaging features of cirrhosis are often subtle, demonstration of hepatofugal flow may be the only convincing sign of portal hypertension.

Reversal of Portal Venous Flow (Hepatofugal Flow)

Ralls ³ noted that, in patients with portal hypertension, reversal of flow within intrahepatic portal venous branches is actually more common than hepatofugal flow in the main portal vein. Reversal of flow in the right portal vein is noted in patients with large paraumbilical collaterals. Flow reversal in the left portal vein is associated both with reversal of flow in the coronary vein and with TIPS placement in the right portal vein. In some patients, hepatofugal flow in the portal vein may transiently reverse to hepatopetal flow postprandially, presumably due to significant increase in splanchnic flow.

Direct arterial communications with the portal veins via the arterioportal fistulas cause reversal of portal flow with a phasic waveform. Arterioportal fistulas may be due to tumors, invasive procedures, or congenital causes.

Conclusion

Color and spectral Doppler imaging of the portal veins offers a unique diagnostic opportunity to detect abnormalities of the portal veins. Because hepatic vascular disorders are infrequently suspected clinically and because of the limitations of gray-scale evaluation, color and spectral Doppler of the portal veins should be a routine component of hepatic sonography. *