In helical dynamic computed tomography (CT), images are rapidly and continuously acquired during a single breath hold, resulting in improved spatial resolution and the elimination of motion artifacts (1). Multi–detector row CT is the latest advancement in CT technology and is now more readily available than in the past. Multi–detector row CT scanners are now up to four times faster than conventional single–detector row helical CT scanners. The increased speed and narrower collimation of multi–detector row CT, together with the use of intravenously administered contrast material, improves visualization of the collateral vessels in portal hypertension. Three-dimensional (3D) multi–detector row CT angiography allows improved temporal resolution, improved spatial resolution in the z axis, and longer anatomic coverage without sacrificing spatial resolution (2,3).
In cirrhotic patients with portal hypertension, some blood in the portal venous system may reverse direction and pass through the portosystemic anastomoses in the systemic venous system. As a result, a variety of major hepatofugal collateral pathways can develop in patients with portal hypertension (4). Among these collateral vessels, esophageal varices are the most important clinically because they are a frequent source of gastrointestinal bleeding. Information about collateral pathways is especially relevant when interventional procedures or surgery is contemplated because inadvertent disruption of these vessels can cause significant bleeding (5).
For many years, angiography was considered the standard for detecting collateral vessels. Single–detector row helical CT demonstrates the collateral vessels very accurately. Magnetic resonance (MR) imaging is probably as accurate as CT but is more expensive and less accessible; in addition, some of the rarest pathways (eg, pleuropericardial or thoracic wall varices) may be missed at MR imaging (6). An important advantage of multi–detector row CT over single–detector row helical CT is the increased speed of scanning, which permits routine use of very thin collimation for imaging the portosystemic collateral vessels (2). Faster scanning with multi–detector row CT, combined with the rapid intravenous administration of contrast material, allows visualization of the more distal branches of the portosystemic vessels. In multi–detector row CT, a section thickness of 0.5–1 mm is possible, thus reducing the volume averaging of small vessel branches. This thinner collimation coupled with overlapping reformatted images provides better-quality 3D angiographic images than does single–detector row helical CT.
In this article, we review the imaging technique and some of the current clinical applications of 3D multi–detector row CT portal venography. We also illustrate the portosystemic collateral vessels that can be seen with this modality in patients with cirrhosis.
CT was performed with a Lightspeed QX/I Scanner (GE Medical Systems, Milwaukee, Wis). The scanning parameters we used for multi–detector row CT portal venography are shown in the Table. The specific scanning techniques used for acquiring data with CT angiography are critical. Although specific scanning parameters vary among the various scanners and continue to evolve for the imaging of detailed vascular anatomy, we used a 2.5-mm section thickness with image data reconstructed at 1.25-mm intervals. Source images for 3D CT portal venography with reformatted images that overlap by 50% are obtained from the volumetric data obtained during the portal venous phase. Usually, a total of 250–300 reformatted images are produced. These images are then transferred to a GE Advantage Workstation (version 4.0).
A major advantage of performing multi–detector row CT in patients with liver cirrhosis is the improved quality of the 3D angiographic images. However, the choice of 3D images is crucial in this clinical setting. There are currently three main reformatting techniques available: maximum intensity projection (MIP), shaded surface display (SSD), and volume rendering.
MIP is a simple algorithm that displays the brightest voxel along computer-generated rays in a specified orientation (7). The MIP technique can depict small vessels and is helpful in clarifying both orientation and anatomic detail, thereby giving direction to a more meticulous review of the source images.
With SSD, specific attenuation thresholds are set. Voxels within the thresholds are displayed, whereas voxels outside the thresholds are excluded. Thus, only portions of the data set are being used (8). SSD is also useful for planning procedures such as transjugular portosystemic shunt placement because it allows the relative positions of various structures to be clearly displayed. However, SSD is a time-consuming process.
Unlike SSD, volume rendering incorporates all of the relevant data into the resulting image (9). Parameters can be applied to the volume set to affect the appearance of the blood vessels so that related anatomy and disease are optimally demonstrated. The soft tissues surrounding the portal venous system (eg, the liver and pancreas) are enhanced in the portal venous phase. This enhancement reduces the clarity of the edge of the portal vein or varices with the volume rendering technique, resulting in an image quality that is inferior to that possible with the MIP technique (10).
A current limitation of these techniques is that a trained individual is needed to obtain the 3D images. In particular, the SSD or volume-rendering technique is dependent on the software used and on the experience of the user with that particular software. Therefore, in daily practice (if at all) only MIP reformatted images are created, particularly because they can often be created directly on the CT console. Although a trained user creates SSD images, the time required for SSD is 20–30 minutes. MIP and volume rendering each take approximately 5–10 minutes. Soyer et al (11) found that MIP appears to be an adequate technique for 3D imaging of intrahepatic venous structures with CT data. In our clinical experience, we have not found SSD or volume rendering to be useful. MIP is our preferred 3D rendering technique for CT portal venography (Fig 1).
The major tributaries of the portal vein are the superior mesenteric vein and the splenic vein. Other tributaries include the inferior mesenteric vein and the right and left gastric veins. The portal vein is divided into the right and left lobar branches.
In portal hypertension, some blood in the portal venous system may reverse direction and pass through the portosystemic collateral vessels (4). As a result, a variety of major hepatofugal collateral pathways can develop in patients with portal hypertension (Fig 2).
On axial CT scans, varices manifest as serpentine tubular structures and represent the portosystemic collateral vessels that usually result from portal hypertension in liver cirrhosis (12). They may be classified into two groups depending on whether they drain toward the superior or inferior vena cava. The most frequently encountered collateral vessels seen at CT include the coronary and esophageal varices. Other less common types of collateral vessels can occasionally be identified (13).
The left gastric (coronary) vein is the most commonly visible varix in portal hypertension (4,13). A dilated left gastric vein is visible between the anterior wall of the stomach and the posterior surface of the left hepatic lobe (Fig 3a). Left gastric veins are frequently accompanied by esophageal or paraesophageal varices and occasionally by retrogastric varices (14).
A left gastric vein larger than 5–6 mm in diameter at Doppler ultrasonography or CT is considered abnormal and is an indicator of portal hypertension (15). When enlarged, the coronary vein is easily identified at CT as a serpiginous vessel that arises near the portal confluence and courses cephalad to the lesser curvature side of the stomach (Fig 3b).
Short gastric veins course along the lateral aspect of the gastric wall and descend along the medial aspect of the spleen (Fig 3b). The short gastric vein that communicates with the splenic vein or one of its large tributaries drains the gastric fundus and the left side of the greater curvature (16). Dilated short gastric veins appear as a complex tangle of vessels in the region of the splenic hilum, and the gastric fundus and individual vessels are often difficult to distinguish. Careful scrutiny of the source images may be necessary to detect smaller varices.
The term esophageal varices usually refers to the dilated veins located within the wall of the lower esophagus, whereas paraesophageal varices are situated outside the wall of the esophagus (Fig 4). These varices are supplied primarily by the left gastric vein (Figs 3, 5), which divides into anterior and posterior branches. The anterior branch supplies the esophageal varices, and the posterior branch forms the paraesophageal varices.
Esophageal varices usually drain into the azygos or hemiazygos system (4,13). Esophageal and gastric varices are by far the most common portosystemic pathways detected at transhepatic portography (17,18). Although esophageal and gastric varices frequently coexist, esophageal varices are more likely to be supplied by the left gastric vein, whereas gastric varices, particularly in advanced stages, are more likely to be supplied by the short gastric and posterior gastric veins (19).
Among the collateral pathways, esophageal varices are of particular clinical importance because they are a common source of upper gastrointestinal bleeding (20,21). Although endoscopy is the most reliable diagnostic procedure for detecting esophageal varices, the extent of esophageal varices and associated paraesophageal varices is better visualized at CT or MR imaging (22).
The left renal vein is frequently involved in portosystemic collateral pathways. The splenoportal vein axis and the left renal vein communicate through the coronary vein, short gastric vein (gastrorenal shunt), or other veins that normally drain into the splenic vein (splenorenal shunt) (17,18).
Splenorenal or gastrorenal shunts are seen as large, tortuous veins in the region of the splenic and left renal hila and drain into an enlarged left renal vein (Fig 6) (4). Fusiform dilatation of the inferior vena cava at the level of the left renal vein is also frequently seen (21). These shunts are so tortuous that the exact origin of the connection along the splenic vein is sometimes difficult to discern on axial images. Coronal or sagittal 3D portal venography is helpful in demonstrating the course of these shunts (Fig 6b).
The umbilical vein never opens after closure (23). Rather, patent portal veins in the ligamentum teres and falciform ligament are actually enlarged paraumbilical veins. The paraumbilical vein arises from the left portal vein (Fig 7a). Although their course and number vary, the paraumbilical veins may run through the medial segment of the liver rather than through the ligamentum teres. Paraumbilical vessels may anastomose with the superior epigastric or internal thoracic veins and drain into the superior vena cava or anastomose with the inferior epigastric vein and then drain into the inferior vena cava through the external iliac vein (Fig 7b) (24,25).
On cross-sectional images, paraumbilical and abdominal wall varices appear as circular or tubular structures more than 2 mm in diameter beebtween the medial and lateral segments of the left hepatic lobe at the anterior edge of the falciform ligament.
The paraumbilical vein can be clearly visualized at 3D CT portal venography as a tortuous, longitudinal vascular structure. Occasionally, this vein drains into the veins of the anterior abdominal wall, thereby creating a “Medusa’s head” appearance (Fig 7c). The paraumbilical vein can become quite large and function as a desirable route of natural decompression without gastroin testinal bleeding in cases of portal hypertension.
Mesenteric collateral vessels usually appear as dilated and tortuous branches of the superior mesenteric vein within the mesenteric fat (13). Mesenteric collateral vessels may arise from the superior and inferior mesenteric veins and may ultimately drain into the systemic venous system via the retroperitoneal or pelvic veins (4). As with other types of collateral vessels, it is often difficult to completely trace the drainage course for the portal system to the systemic veins due to the complex and often extensive nature of the collateral vessels. Occasionally, the drainage route can be precisely determined with postprocessing techniques.
A retroperitoneal shunt may be present between the mesenteric vessels and the renal vein or inferior vena cava (Fig 8). Retroperitoneal varices include various pathways between the intestinal or retroperitoneal tributaries of the superior or inferior mesenteric veins and systemic veins. Their communications with the inferior vena cava are known as the veins of Retzius (26) and usually appear as small, rounded or tubular areas of increased attenuation that enhance to the same degree as the vessels at contrast material–enhanced CT.
Omental collateral vessels are infrequently included in lists of common portosystemic collateral vessels, presumably because they are not well visualized with angiography or other modalities.
Cavernous transformation of the portal vein consists of formation of venous channels within and around a previously stenotic or occluded portal vein. On contrast-enhanced CT scans, the most frequent finding is a mass of veins with a characteristic beaded appearance at the porta hepatis. These vessels are well demonstrated at multi–detector row CT portal venography (Fig 9).
Patients with cirrhosis are at a much greater risk for developing portal vein thrombosis than is the general population. In these patients, the majority of portal vein thrombi occur due to the development of portal venous hypertension or venous stasis. Other causes of portal vein thrombosis include infectious disease (eg, sepsis, cholangitis, pancreatitis), neoplasms, hypercoagulable states, surgery, and embolism from thrombus located in the superior mesenteric or splenic vein (27). Evaluation of portal vein patency, particularly in patients awaiting liver transplantation, is one of the most important roles of CT. Contrast-enhanced helical CT and CT portal venography can demonstrate a filling defect that partially or totally occludes the vessel lumen (Fig 10). Indirect signs of portal vein thrombosis are the presence of cavernous transformation of the portal vein and the presence of portosystemic collateral vessels.
The development of spiral CT and subsequently of multi–detector row CT has provided unparalleled opportunities for the advancement of CT technology and the proliferation of clinical applications. Multi–detector row CT has definitely improved the capacity of CT to demonstrate collateral vessels by allowing narrower collimation and faster scanning coupled with bolus timing achieved with intravenous contrast material administration. In addition, multi–detector row CT performed with 3D angiographic techniques provides excellent vascular enhancement and enables vascular structures to be continuously traced. Three-dimensional multi–detector row CT portal venography can depict the anatomic characteristics of portosystemic collateral vessels in patients with liver cirrhosis.
Abbreviations: MIP = maximum intensity projection, SSD = shaded surface display, 3D = three-dimensional
Figure 2. Drawing illustrates the collateral vessels in portal hypertension. AWV = abdominal wall vein, GEV = gastroesophageal vein, IMV = inferior mesenteric vein, IVC = inferior vena cava, LGV = left gastric vein, LPV = left portal vein, LRV = left renal vein, MV = mesenteric vein, PDV = pancreaticoduodenal vein, PEV = paraesophageal vein, PV = portal vein, RPPV = retroperitoneal-paravertebral vein, SMV = superior mesenteric vein, SRV = splenorenal vein, SV = splenic vein, UV = umbilical vein.
Parameters for Multi-Detector Row CT Portal VenographyClick image to enlarge
We thank Bonnie Hami, MA, Department of Radiology, University Hospitals of Cleveland, Ohio, for editorial assistance in the preparation of this manuscript.
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