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MR angiography of the portal venous system
MR Angiography of the Portal Venous System Hanh Vu Nghiem, Thomas C. Winter, Udo P. Schmiedl, and Patrick C. Freeny MR angiography (MRA) has become an increasingly important and practical clinical tool for the noninvasive assessment of abdominal vessels. Both two-dimensional time-of-flight and phase contrast techniques allow accurate evaluation of the portal venous system, This article reviews these two MRA techniques and discusses their impact on the diagnosis of vascular abnormalities of the portal venous system, Copyright © 1996 by W.B. Saunders Company
HE PORTAL venous system is studied
T commonly to evaluate the patency of the portal vein, splenic vein, and superior mesenteric vein; to determine whether a tumor has invaded the veins; or to locate a thrombus. In portal hypertension, the goals of the study are the determination of the level of obstruction to flow, the presence and extent of intra-abdominal portal systemic collateral vessels, the direction of blood flow in the portal vein, and the establishment of the patency of decompressive surgical portal systemic shunts. In this article, two-dimensional (2D) time-of-flight (TOF), and phase contrast MR angiographic techniques are discussed with emphasis on their clinical applications to the diagnosis of vascular abnormalities of the portal venous system. MR ANGIOGRAPHIC TECHNIQUES
TOF MR Angiography The TOF technique is a gradient-recalled echo sequence with flow compensation. 1-4 In TOF, the signal from stationary tissue is suppressed, or "saturated," by applying radiofrequency pulses very rapidly. Blood flowing into an image section has not been pulsed and therefore does not become saturated; it thus has bright signal intensity against a dark background. This mechanism of contrast enhancement is called flow-related enhancement or, simply, inflow. Because flow enhancement on gradient-echo sequences results from the wash-in of fresh spins into the image section, the signal intensity of blood increases with thinner slices and longer repetition times as well
From the Department of Radiology, University of Washington Medical Center, Seattle, WA. Address reprint requests to Hanh Vu Nghiem, MD, Department of Radiology, University of Washington Medical Center, Box 357115, 1959 NE Pacific St, Seattle, WA 98195. Copyright © 1996 by W..B. Saunders Company 0887-2171/96/1704-000855. 00/0 360
as when flow is fast and perpendicular to the image section. On TOF images, the flowing blood appears bright independent of flow direction. The velocity and direction of blood flow may be ascertained by adding presaturation pulses. 5-7 By placing a parallel presaturation band adjacent to a single 2D TOF slice, the signal is removed from the blood that enters the slice from that side. It follows that parallel presaturation can be used to determine the direction of blood flow. Blood flow velocity and flow direction in main portal vein may be determined by use of the presaturation bolustracking technique. This technique employs a thin inplane saturation slab followed by several gradient-echo images. The displacement of the bolus over time on serial images shows the direction and velocity of blood flow. Although TOF studies can be performed as 2D or threedimensional (3D) acquisitions, 3D acquisitions are suboptimal for the study of venous structures because of the lower sensitivity to slow flow as well as saturation effects.8 The most flexible and efficient TOF technique for imaging the liver is sequential 2D TOF acquisition with breath holding. When images are acquired during suspended respiration, artifacts from respiratory motion are eliminated. This lack of artifacts is especially important in abdominal imaging. One or several 2D TOF slices can be acquired with each breath. Typical parameters for sequential 2D TOF MR angiography (MRA) of the portal venous system are a relaxation time (TR) of 28, an echo time of 8, 256 x 192 matrix, one or two excitations, 30-degree flip angle, and sections 5 mm thick with a small overlap between sections. Images are acquired routinely in the axial and coronal planes during breath holding. Once a stack of slices has been acquired, these can be postprocessed by maximum intensity projection (MIP), or another algorithm, to form projection angiograms (Fig 1).
Seminars in Ultrasound, CT, andMRI, Vo117, No 4 (August), 1996: pp 360-373
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Fig 1. Two-dimensional TOF MR angiograms of the portal vein {arrow} in {A) axial and {B) coronal projections. (Courtesy of Jorg F. Debatin, MD, University Hospital, Zurich, Switzerland.)
Administration of gadolinium chelates that shorten the T1 relaxation time of blood does not improve the depiction of blood vessels significantly in the 2D TOF techniques. In fact, many normal and pathological tissues are enhanced and appear in the TOF source images and projection images, thus potentially simulating flow signal and obscuring vessel details. Phase Contrast MRA
The contrast mechanism in phase contrast MRA is flow-induced phase shifts. 9-1a Blood is bright because it is moving, and stationary
tissue, which accumulates no phase, is dark. To make the gradient-recalled echo sequence sensitive to velocity-induced phase shifts, a bipolar flow-encoding gradient is added to the scan sequence, encoding for flow along a particular axis. It is important to note that only the motion of spins along the direction of the encoding gradient results in a change in phase. Thus, an angiogram sensitive to flow in every direction must be acquired with flow-encoding gradients along each of the three axes (slice selection, frequency-encoding, and phase-encoding directions). This process takes 2 to 3 times longer
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than encoding along one axis, because the encoding gradients must be applied on the different axes in separate acquisitions. In phase contrast, two sets of data are acquired. Bipolar flow-encoding gradients of opposite polarities are obtained and are then subtracted. The displayed pixel intensity represents phases or differences in phases rather than the amplitude of tissue magnetization. The principle reasons for performing the phase contrast angiography techniques are improvement of the detection of small or slow-flowing vessels by superior background suppression, and utilization of the velocity-phase relationships intrinsic to the phase contrast sequence to obtain direction and ve!ocity of blood flow. Before an angiogram is acquired, the appropriate maximum velocity encoded (Venc) must be chosen. A Venc that is too small results in a great deal of aliasing. A Vent that is excessively high prevents aliasing but also results in all velocities being represented by a small phase range, close to that of the stationary tissue value. Thus, the vascular contrast-tonoise ratio is decreased and the image is degraded. Because saturation effects are not as important in phase contrast imaging, venous structures can be studied with 2D or 3D acquisitions. However, 3D acquisitions require long scan
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times and preclude breath holding, thus spatial resolution is degraded by respiratory motion. In the authors' experience, sequential 2D phase contrast MRA with breath holding and gadolinium enhancement is most effective in imaging the liver. 12 Typical sequence parameters are TR of 30, TE of 8.5, 256 x 128 matrix, one excitation, a 30-degree flip angle, 5- to 7-mm-thick sections with a 2-mm overlap, and velocity encoding of 20 cm/s in all three axes. Coronal images are obtained routinely during breath holding after an intravenous injection of 0.1 mmoi/kg of gadopentetate dimeglumine. The subtraction process in phase contrast imaging provides the opportunity to use a T1shortening intravenous contrast agent. The use of such agents reduces the saturation effects on moving spins and increases the intravascular signal but does not obscure the vascular structures by enhancing overlying stationary tissues. The combination of breath holding and the use of contrast material improves overall image quality and vessel detail (Fig 2), and also improves detection and visualization of smaller and slower flowing vessels. Standard phase contrast angiographic reconstruction provides MR projection angiograms that depict blood flow as areas of high signal intensity regardless of flow direction and also
Fig 2.' Phase Contrast MR portograms (A) with and (B) without breath holding and contrast enhancement show degradation of image quality without breath holding and contrast material Overall image quality improves and vessel detail is better as noted by the clear display of the coronary vein varix (arrow) in A. P, portal vein; sp, splenic vein; ca, celiac axis. (Reprinted with permission, lz)
MRA OF THE PORTAL VENOUS SYSTEM
phase images that indicate the direction of blood flow. Limitations of phase contrast MRA include sensitivity to gradient imperfection, artifacts from turbulence of flow or pulsatile flow, and limited spatial resolution. 9 PORTAL VENOUS SYSTEM
Normal Anatomy The portal vein provides approximately 75% of the total blood flow to the liver. The main portal vein is formed from the confluences of the splenic and superior mesenteric veins. The other major tributaries of the portal vein are the short gastric, inferior mesenteric, gastroepiploic, and pancreatico-duodenal veins. At the portahepatis, the main portal vein divides into the right and left lobar branches. The right lobar branch receives the cystic vein, which drains the gallbladder, and the smaller left lobar
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branch receives the umbilical and associated paraumbilical veins. Flow in the splenic, superior mesenteric, and portal veins normally is hepatopetal (toward the liver) (Fig 3). Congenital absence or duplication of the portal vein is rare. IMAGING METHODS
Conventional angiography has been considered the gold standard for evaluation of the portal vein. However, it has limitations: (a) patients with portal vein thrombosis are less attractive candidates for this invasive procedure because of a higher incidence of coagulopathy; (b) the study requires a large amount of contrast material, which carries the risk of renal toxicity; (c) detection of varices may be difficult because of lack of adequate contrast material, dilution of contrast material on the venous side,
Fig 3. Normal anatomy of the portal venous system with hepatopetal flow. (A) Coronal phase contrast MR portogram shows flowing blood as an area of high signal intensity regardless of flow direction. Main portal vein (PV), its right (RP) and left (LP) lobar branches, superior mesenteric vein (smv), and splenic vein (sv) are shown clearly. IVC, inferior vena cava; r, renal veins; arrows, hepatic veins. (B) Phase image with flow encoding in the right-to-left direction shows blood flowing right to left in the left portal vein in white (arrow) and left-to-right flow in the main portal vein in black (arrowheads), indicating hepatopetal flow. (Reprinted with permission. 44)
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insonation limit the value of sonography for assessing the portal venous system and associated collaterals. The portal venous system also can be evalu-
Fig 4. Thombosis of the portal vein in a patient with chronic active hepatitis, hepatoma, and previous splenectomy. (A) Breath-held, gadolinium-enhanced, muitiplanar, spoiled grass image shows hypointense clots in the portal vein and its lobar branches (arrows). (B) Coronal phase contrast MR portogram does not show the portal vein, consistent with occlusion. The superior mesenteric vein is patent, HA, common hepatic artery; SA, splenic artery; SMA, superior mesenteric artery. (Reprinted with permission. 44)
and presence of overlying bowel gas and parenchymal enhancement; and (d) a patent portal vein can appear occluded when flow is present but flow direction is reversed. Color flow Doppler songoraphy is an effective and accurate study for evaluating abdominal vasculature but may be unsuccessful if a suitable acoustic window is not available at the desired angle to the vessel axis. 13-15 In addition, sonography does not display the anatomy of the portal venous system in a format familiar to many clinicians. Impediments such as bowel gas, body habitus, fatty liver, cirrhosis, ascites, and restricted angle of
Fig 5. Cavernous transformation of the portal vein. (A) Axial and (B) coronal 2D TOF MIP images show a network of collateral vessels (arrows) in the porta hepatis, typical of cavernous transformation. (Courtesy of Jorg F. Debatin, MD, University Hospital, Zurich, Switzerland.)
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Fig 6. Portal venous stenosis in a patient who had surgery for hydatid disease. (A) Coronal phase contrast MR portogram shows marked narrowing of the portal vein as a segment of flow void (long straight arrow) with poststenotic dilation (short straight arrow) and prominent coronary venous varices (curved arrow). Lack of signal in the dilated poststenotic portal vein is caused by flow phenomenon, (B) Transhepatic portal venogram shows stenosis of the portal vein (straight arrow) and coronary venous varices (curved arrow). (Reprinted with permission, 44)
ated accurately with contrast-enhanced CT. 16,17 However, sensitivity in detecting portal venous thrombosis depends on precise timing of the contrast bolus, and axial scans often do not depict the complex anatomy of the portal venous system optimally. Similar to conventional angiography, a large amount of intravenous contrast is required, and a patent portal vein may appear occluded when flow is present but flow direction is reversed, and when the portal vein is attenuated. Both TOF and phase contrast MR angiographic techniques have been shown to be accurate for evaluating the portal venous system. 6,1z,18"21MRA is a reliable and noninvasive technique that can provide crucial information
in the preoperative workup of liver transplant recipients. MRA accurately determines patency and flow direction of the portal venous system, the presence and distribution ofvarices, and the patency of surgically created shunts. The survey of abdominal venous structures may be performed faster by M R A than by conventional angiography. The projection angiogram displays the anatomic layout of the portal venous system in a single, large, field-of-view image, a format familiar to many clinicians. It is important that interpretation of abdominal angiography studies be based on both individual sections and projection images. Although the projection image is superior for showing the overall anatomic relationship and course of
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Fig 7. Reversed flow in the coronary vein in a patient with portal hypertension. (A) Coronal phase contrast MR portogram shows an enlarged, tortuous coronary vein (straight arrow) and paraesophageal varices (curved arrow). P, portal vein; ca, celiac axis; sv, splenic vein; smv, superior mesenteric vein, (B) Phase image with flow encoding in superior-to-inferior direction shows hepatofugal flow in black in the coronary vein (straight arrow). Curved arrow, superior mesenteric vein. (Reprinted with permission. 44)
vessels, the individual slices show details of specific vessels better, because vessels may be hidden by overlapping structures and may be misregistered because of variable respiration. MR imaging has the potential to replace other imaging techniques in evaluating the portal venous system, especially in the preoperative workup of liver transplant patients. It is costly, however, and may be most helpful as a complement to the sonographic examination and when contrast-enhanced CT scanning is precluded by
severe contrast allergy and suppressed renal function. CLINICAL APPLICATIONS
Portal Vein Thrombosis
The predisposing causes of portal vein thrombosis are numerous, and these often overshadow the development of venous thrombosis. In adults, major causes of portal vein thrombosis include cirrhosis and neoplastic diseases. 22-26
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Fig 8. Paraumbilical venous varix in a patient with chronic active hepatitis C and encephalopathy. Coronal phase contrast MR portogram shows an enlarged paraumbilical vein (arrowheads) as a continuation of the left portal vein and no discernible flow in the right portal vein. P, portal vein; Sp, splenic vein; arrows, hepatic veins. (Reprinted with permission. ~)
In cirrhosis, the fibrotic reaction within the liver and the distortion of the hepatic architecture result in significant resistance to blood flow from the gastrointestinal tract into the liver. Thus, the blood flow in the portal vein becomes stagnant, predisposing to thrombosis. Portal vein thrombosis associated with neoplastic diseases may result from obstruction by portahepatis lymphadenopathy; direct venous invasion and infiltration by hepatocellular carcinoma; extrinsic compression or obliteration by pancreatic carcinoma, cholangiocarcinoma, or other metastatic cancers; or periportal fibrosis secondary to surgery or radiation. Other causes of portal vein thrombosis include pancreatitis, operative injury of the vein, hypercoagulable states resulting in hyperviscocity (such as polycythemia vera and myelofibrosis), trauma, and idiopathic causes. Intraabdominal inflammatory conditions, such as diverticulitis and appendicitis, can cause septic thrombosis of the portal vein. The onset of portal vein thrombosis often is
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so gradual or indolent that no specific clinical manifestations are recognized initially. Patients may ultimately present with gastrointestinal hemorrhage from variceal bleeding, abdominal pain, and splenomegaly. Acute thrombosis of the portal vein may be detected by visualization of the clot itself or by lack of flow within the vein (Fig 4). The thrombus can extend into the splenic or superior mesenteric veins, and these tributaries thus should be evaluated to determine the extent of occlusion. Cavernous transformation of the portal vein occurs in approximately 50% of patients who have chronic portal vein thrombosis, and it can develop as early as 4 weeks after the occlusion. 27,2s The network of collateral vessels develops in the portahepatis and hepatoduodenal ligaments by enlargement of preexisting small veins that accompany the lymphatic, biliary, and vascular structures. Collaterals also develop as well as newly formed primitive venous channels. The collateral vessels bypass the occlusion and drain into the intrahepatic portal venous branches (Fig 5). Portal vein stenosis may result from a complication of liver transplantation or major abdominal surgery. The diagnosis usually is based on findings at conventional angiography, but M R A can be useful in the diagnostic evaluation (Fig 6).
Fig 9. Spontanous splenorenal shunt. Coronal 2D TOF MR angiogram shows an extensive network of collateral vessels in the splenic hilum (straight arrows) draining into the dilated left renal vein (curved arrow). (Courtesy of Jorg F. Debatin, MD, University Hospital, Zurich, Switzerland.)
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include life-threatening bleeding from gastroesophageal varices, hepatic encephalopathy, ascites, coagulopathy, splenomegaly with hypersplenism, and bacteremia. The goals of diagnostic studies when examining patients with portal hypertension are the determination of the presence of hepatic disease, the direction of portal vein flow, and the presence and extent of intraabdominal portal systemic collaterals. Any
Fig 10. Coexistent coronary, paraesophageal, splenorenal, and splenoretroperitoneal collaterals in a patient with cryptogenic cirrhosis. Coronal phase contrast MR portogram shows massive collaterals from the splenic hilum passing both medially toward the left renal vein (splenorenal collaterals, short straight arrows) and laterally and interiorly (splenoretroperitoneal collaterals, curved arrow). Additionally, note the extensive coronary and paraesophageal varices (long straight arrow). (Reprinted with permission. 44)
Portal Hypertension Portal hypertension results from either an increase in portal blood flow or an increase in resistance to flow through the portal venous system.29,3° The most common cause of portal hypertension in the United States is hepatic cirrhosis. Portal hypertension may be classified as prehepatic (eg, obstruction of the extrahepatic portal vein), intrahepatic (eg, cirrhosis), and posthepatic (eg, hepatic vein or inferior vena cava obstruction). Arterial venous fistulas can cause portal hypertension on the basis of increased portal venous flow. In the early stage of portal hypertension, the portal vein may dilate but flow is maintained. As the resistance to flow in the portal vein increases, the portal blood flow may reverse from hepatopetal (toward the liver) to hepatofugal (away from the liver), reducing the flow to the liver and the size of the portal vein. In response to elevated portal vein pressures, portal systemic collateral pathways develop to shunt portal blood into systemic veins, bypassing the hepatic parenchyma and sinusoids. The development of collateral flow does not seem to decompress the portal system, however. Complications of portal hypertension
Fig 11. Mesenteric collaterals in a patient with portal hypertension. (A) Coronal phase contrast MR portogram shows massive retroperitoneal and mesenteric venous collaterals (white arrow). The portal vein is not apparent on this image because of its small size and its overlap with the inferior vena cava. Black arrow, superior mesenteric vein. (B) Phase image with flow encoding from right to left shows a small but patent main portal vein (arrow). Flow in the main portal vein, which is displayed in white, is hepatofugal, (Reprinted with permission. 44)
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of these vessels may be the source of bleeding during liver transplantation or portal decompressive surgery, whereas spontaneous bleeding tends to occur from gastric and paraesophageal varices.
Portosystemic Venous Collaterals
Fig 12, Inferior mesenteric varices in a patient with alcoholic cirrhosis of the liver. Coronal phase contrast MR angiogram shows massive pelvic varices (curved arrows) shunting blood via the inferior mesenteric vein (small straight arrows) and enlarged left gonadal vein (large straight arrow) (Reprinted with permission, 44)
Fig 13. Thrombosis of the splenic vein in a patient with pancreatic carcinoma, Coronal phase contrast MR portogram shows occlusion of the splenic vein and partial thrombosis of the portal vein (arrow). P, portal vein.
Portosystemic collaterals can be divided into two groups according to the area of drainage. 31-35 The first group consists of portosystemic collaterals draining toward the superior vena cava. Among patients with portal hypertension, 30% to 69% have reversed flow in the coronary and short gastric veins that are shunting blood through the gastroesophageal varices and paraesophageal veins toward the azygous veins and superior vena cava (Fig 7). Gastroesophageal varices are the usual source of bleeding from the upper gastrointestinal tract. Demonstration of reversed (cephalad) flow in the coronary vein indicates increased risk for variceal bleeding, whereas a normal flow direction rules out imminent hemorrhage. 36 Treatment of esophageal varices includes vasoconstrictive drugs, endoscopic pressure tubes, endoscopic sclerotherapy, or decompression of the portal system by creation of alternative portosystemic shunts. The second group of portosystemic collaterals consists of vessels draining splanchnic blood toward the inferior vena cava. The paraumbili-
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the phrenicocolic ligament via retroperitoneal branches, and they ultimately drain into lumbar veins. The collaterals begin at the splenic hilum and pass inferiorly and laterally to the upper pole of the left kidney (Fig 10). Mesentenc Collaterals
Various collaterals can originate from the superior mesenteric and inferior mesenteric veins (Figs 11 and 12). These shunts reach the systemic veins via the retroperitoneal and rues-
Fig 14. Thrombosis of the splenic and superior mesenteric veins in a patient with cirrhosis and pancreatic carcinoma, Coronal phase contrast MR portogram shows an extensive network of peripancreatic varices (arrows). The portal vein (PV) is patent. A low-signal-intensity thrombus (T) at the portosplenic venous confluence also was seen on axial images. (Reprinted with permission. 44)
cal vein originates from the left branch of the portal vein and runs in the fissure of the ligamentum teres or through the medial segment of the left lobe (Fig 8). Outside of the liver, the paraumbilical vein courses through the falciform ligament and connects with the epigastric veins in the abdominal wall, ultimately draining into the external iliac vein. The prevalence of paraumbilical veins in portal hypertension may be as much as 33%. These shunts can become quite large and provide efficient decompression of portal hypertension. Umbilical vein collateral flow is an important feature of portal hypertension because it carries a diagnostic specificity for portal hypertension o f 100%. 37,38
Gastrorenal collaterals are tortuous vessels around the stomach that shunt blood toward the renal vein and ultimately drain into the inferior vena cava. Shunting from the splenic vein into the inferior vena cava occurs along splenorenal or splenoretroperitoneal pathways. A splenorenal shunt is seen in 10% to 20% of patients with portal hypertension?~, 39 The tortuous vessels are detected between the hilum of the spleen and the hilum of the left kidney. These enlarged veins drain into a dilated left renal vein (Fig 9). The splenoretroperitoneal collaterals connect the splenic vein and inferior vena cava through
Fig 15. Normal surgical distal splenorenal shunt. (A) Coronal phase contrast MR angiogram shows patency of surgical splenorenal shunt (S). LRV, left renal vein; SV, distal splenic vein; IVC, inferior vena cava. (B) Phase image with flow encoding from superior to inferior shows the appropriate direction of blood flow in the shunt (S); ie, from the splenic to renal vein, in white. (Reprinted with permission. 44}
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Fig 16. Surgical mesocaval shunt in a patient with chronic active hepatitis and severe portal hypertension. (A) Sagittal phase contrast MR angiogram shows patency of the shunt (straight arrow), which connects the superior mesenteric vein anteriorly (curved arrow) to the inferior vena cava posteriorly (arrowheads) just above the caval bifurcation, (B) Axial MIP image shows the anastomosis (arrow) of the shunt, IVC, inferior vena cava, (Reprinted with permission, 44)
enteric venous plexus. Pericolic collaterals also can carry hepatofugal blood flow around the colon and drain into the lumbar veins and ultimately into the inferior vena cava. The inferior mesenteric vein carries hepatofugal blood into the pelvis. Extensive collaterals may develop and connect the inferior mesenteric and iliac veins via the superior, middle, and inferior hemorroidal veins. Occasionally, blood may be shunted into the pelvis through the gonadal veins.
Occlusion of the Splenic and Superior Mesenteric Veins Acute thrombosis of the splenic vein may be detected by visualization of the clot itself or by
lack of flow (Fig 13). In chronic occlusion, collateral vessels caused by portal venous hypertension, or resulting from occlusion of the splenic vein itself, can develop along three separate pathways: (a) from the splenic hilum via the gastroepiploic vessels toward the superior mesenteric vein and into the portal vein; (b) from short gastric veins toward the venous plexus around the stomach and into the portal vein via the coronary vein; and (c) from peripancreatic collaterals into the portal vein or superior mesenteric vein, as well as to the retroperitoneal branches into the inferior vena cava (Fig 14).4° Hepatofugal shunting also can occur along the splenorenal or splenoretroperitoneal shunts. Isolated occlusion of the superior mesenteric
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vein is r a r e a n d usually occurs in c o n j u n c t i o n with occlusion o f t h e s p l e n i c vein.
Portosystemic Surgical Shunts P o r t o s y s t e m i c surgical shunts a r e effective in decompressing the hypertensive portal venous system to c o n t r o l b l e e d i n g f r o m g a s t r o e s o p h a geal varices. 41-43 T h e two types o f shunts a r e t o t a l s h u n t s a n d selective shunts. T o t a l shunts, such as t h e p o r t o c a v a l o r m e s o c a v a l shunt, d e c o m p r e s s b o t h t h e p o r t a l a n d v a r i c e a l systems. I n t h e s e shunts, b l o o d flow in all m a j o r p o r t a l vessels c o n v e r g e s t o w a r d t h e a n a s t o m o sis, a n d flow in t h e i n t r a h e p a t i c p o r t a l vein b r a n c h e s g e n e r a l l y is h e p a t o f u g a l . Selective shunts, such as t h e s p l e n o r e n a l o r c o r o n o c a v a l shunt, d e c o m p r e s s t h e varices a n d m a y n o t affect e i t h e r t h e p o r t a l v e n o u s p r e s s u r e o r flow.
T h e distal s p l e n o r e n a l , o r W a r r e n , s h u n t is t h e m o s t p o p u l a r selective shunt. T h e distal s p l e n i c vein is a n a s t o m o s e d e n d to side to t h e m i d p o r t i o n o f t h e left r e n a l vein. T h e g a s t r o e s o p h a g e a l c o l l a t e r a l s can t h e n d r a i n t h r o u g h s h o r t gastric vessels, a n d t h e s p l e n i c vein c a n d r a i n t o w a r d t h e a n a s t o m o s i s . B e c a u s e all connections between the gastrosplenic vascular area and the mesenteric portal area are interrupted at surgery, h y p e r t e n s i o n in t h e m e s e n t e r i c p o r tal a r e a r e m a i n s , p r e s e r v i n g p o r t a l inflow to t h e liver a n d p r e v e n t i n g e n c e p h a l o p a t h y . T h r e e - d i m e n s i o n a l M R i m a g e displays a r e very useful for d e t e r m i n i n g p a t e n c y o f t h e p o r t o s y s t e m i c shunt, flow d i r e c t i o n , a n d s h u n t size b e c a u s e t h e o p t i m a l s c a n n i n g p l a n e for displaying the shunt can be selected from the 3 D r e n d i t i o n (Figs 15 a n d 16).
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Value of phase contrast MR angiography. AJR Am J Roentgenol 164:871-878, 1995 13. Nelson R, Lovett K, Chezmar J, et al: Comparison of pulsed Doppler sonography and angiography in patients with portal hypertension. AJR Am J Roentgenol 149:77-81, 1987 14. Patriquin H, Lafortune B, Burns P, et al: Duplex Doppler examination in portal hypertension: Technique and anatomy. A JR Am J Roentgenol 149:71-76, 1987 15. Alpern M, Rubin J, Williams D, et al: Portal hepatis: Duplex Doppler US with angiographic correlation. Radiology 162:53-56, 1987 16. Zirinsky K, Markisz J, Ruberstine W, et al: MR imaging of portal venous thrombosis: Correlation with CT and sonography. AJR Am J Roentgenol 150:283-288, 1987 17. Mathieu D, Vasile N, Grenier P: Portal thrombosis: Dynamic CT features and course. Radiology 154:737-741, 1985 18. Finn J, Edelman R, Jenkins R, et al: Liver transplantation: MR angiography with surgical validation. Radiology 179:265-269, 1991 19. Torres W, Gaylord G, Whitmire L, et al: The correlation between MR and angiography in portal hypertension. AJR Am J Roentgenol 148:1109-1112, 1987 20. Bisset G, Strife J, Ballistreri W: Evaluation of children for liver transplantation: Value of MR imaging and sonography. AIR Am J Roentgenol 155:351-356, 1992 21. Johnson C, Ehman R, Rakela J, et al: MR angiography in portal hypertension: Detection of varices and imaging techniques. J Comput Assist Tomogr 15:578-584, 1991 22. Cohen J, Edelman R, Chopra S: Portal vein thrombosis: A review. Am J Med 92:173-182, 1992 23. Slovis T, Hailer J, Cohen H, et al: Complicated appendiceal inflammatory disease in children: Pylephlebitis and liver abscess. Radiology 171:823-825, 1989 24. Atri M, Stempel JD, Bret P, et al: Incidence of portal
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vein thrombosis complications: Liver metastasis as detected by duplex ultrasound. J Ultrasound Med 9:2854289, 1990 25. Araki T, Suda K, Sekikawa T, et al: Portal venous thrombosis associated with gastric adenocarcinoma. Radiology 174:811-814, 1990 26. JohnsonC, BaggerstossA: Mesentericvascular occlusion: Study of 99 cases of occlusion of veins. Mayo Clin Proc 24:628-636, 1952 27. Van Gansbeke D, Avni E, Delcour C, et al: Sonographic features of portal vein thrombosis. AJR Am J Roentgenol 144:749-752, 1985 28. Ohnishi K, Okuda K, Ohtsuki T, et al: Formation of hilar collaterals or cavernous transformation after portal vein obstruction by hepatocellular carcinoma. Gastroenterology 87:1150-1153, 1984 29. Schenk W, McDonald J, McDonald K, et al: Direct measurement of hepatic blood flow in surgical patients with related observations on hepatic flow dynamics in experimental animals. Ann Surg 156:463-471, 1962 30. Moreno A, Burchell A, Rousselot L, et al: Portal blood flow in cirrhosis of the liver. J Clin Invest 46:436-445, 1967 31. Burcharth F: Percutaneous transhepatic portography: I. Technique and application. AJR Am J Roentgenol 132:177-182, 1979 32. Doehner G, Ruzicka F Jr, Rousselot L, et al: The portal venous system: On its pathological roentgen anatomy. Radiology 66:206-217, 1956 33. Rousselot L, Moreno A, Panke W: The clinical and physiopathologic significance of self-established (nonsurgical) portosystemic shunts. Ann Surg 150:384-410, 1959 34. Takashi M, Igarashi M, Hino S, et al: Esophageal varices: Correlation of left gastric venography and endoscopy in patients with portal hypertension. Radiology 155:327331, 1985
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35. McCain A, Bernardino M, Sones P, et al: Varices from portal hypertension: Correlation of CT and angiography. Radiology 154:63-69, 1985 36. Wachsberg R, Simmons M: Coronary vein diameter and flow direction in patients with portal hypertension: Evaluation with duplex sonography and correlation with variceal bleeding. AJR Am J Roentgenol 162:637-641, 1994 37. Gibson R, Gibson P, Donlan J, et al: Identification of a patent paraumbilical vein by using Doppler sonography: Importance in the diagnosis of portal hypertension. AJR Am J Roentgenol 153:513-516, 1989 38. Mostbeck G, Wittich G, Herol C, et al: Hemodynamic significance of the paraumbilical vein in portal hypertension: Assessment with duplex US. Radiology 170: 339-342, 1989 39. Kane R, Katz S: The spectrum of sonographic findings in portal hypertension: A subject review and new observations. Radiology 142:453-458, 1982 40. Sherlock S: Extrahepatic portal venous hypertension in adults. Clin Gastroenterol 14:1-19, 1985 41. Warren W, Millikan W, Henderson J, et al: Ten years of portal hypertensive surgery at Emory. Ann Surg 195:530541, 1982 42. Patriquin H, Lafortune M, Weber A, et al: Surgical portosystemic shunts in children: Assessment with duplex Doppler US. Radiology 165:25-28, 1987 43. Ackroyd N, Gill R, Griffiths K: Duplex scanning of the portal vein and portosystemic shunts. Surgery 99:591597, 1986 44. Nghiem HV, Freeny PC, Winter TC III, et al: Phase-contrast MR angiography of the portal venous system: Preoperative findings in liver transplant recipients. AJR Am J Roentgenol 163:445-450, 1994
HE PORTAL venous system is studied
T commonly to evaluate the patency of the portal vein, splenic vein, and superior mesenteric vein; to determine whether a tumor has invaded the veins; or to locate a thrombus. In portal hypertension, the goals of the study are the determination of the level of obstruction to flow, the presence and extent of intra-abdominal portal systemic collateral vessels, the direction of blood flow in the portal vein, and the establishment of the patency of decompressive surgical portal systemic shunts. In this article, two-dimensional (2D) time-of-flight (TOF), and phase contrast MR angiographic techniques are discussed with emphasis on their clinical applications to the diagnosis of vascular abnormalities of the portal venous system. MR ANGIOGRAPHIC TECHNIQUES
TOF MR Angiography The TOF technique is a gradient-recalled echo sequence with flow compensation. 1-4 In TOF, the signal from stationary tissue is suppressed, or "saturated," by applying radiofrequency pulses very rapidly. Blood flowing into an image section has not been pulsed and therefore does not become saturated; it thus has bright signal intensity against a dark background. This mechanism of contrast enhancement is called flow-related enhancement or, simply, inflow. Because flow enhancement on gradient-echo sequences results from the wash-in of fresh spins into the image section, the signal intensity of blood increases with thinner slices and longer repetition times as well
From the Department of Radiology, University of Washington Medical Center, Seattle, WA. Address reprint requests to Hanh Vu Nghiem, MD, Department of Radiology, University of Washington Medical Center, Box 357115, 1959 NE Pacific St, Seattle, WA 98195. Copyright © 1996 by W..B. Saunders Company 0887-2171/96/1704-000855. 00/0 360
as when flow is fast and perpendicular to the image section. On TOF images, the flowing blood appears bright independent of flow direction. The velocity and direction of blood flow may be ascertained by adding presaturation pulses. 5-7 By placing a parallel presaturation band adjacent to a single 2D TOF slice, the signal is removed from the blood that enters the slice from that side. It follows that parallel presaturation can be used to determine the direction of blood flow. Blood flow velocity and flow direction in main portal vein may be determined by use of the presaturation bolustracking technique. This technique employs a thin inplane saturation slab followed by several gradient-echo images. The displacement of the bolus over time on serial images shows the direction and velocity of blood flow. Although TOF studies can be performed as 2D or threedimensional (3D) acquisitions, 3D acquisitions are suboptimal for the study of venous structures because of the lower sensitivity to slow flow as well as saturation effects.8 The most flexible and efficient TOF technique for imaging the liver is sequential 2D TOF acquisition with breath holding. When images are acquired during suspended respiration, artifacts from respiratory motion are eliminated. This lack of artifacts is especially important in abdominal imaging. One or several 2D TOF slices can be acquired with each breath. Typical parameters for sequential 2D TOF MR angiography (MRA) of the portal venous system are a relaxation time (TR) of 28, an echo time of 8, 256 x 192 matrix, one or two excitations, 30-degree flip angle, and sections 5 mm thick with a small overlap between sections. Images are acquired routinely in the axial and coronal planes during breath holding. Once a stack of slices has been acquired, these can be postprocessed by maximum intensity projection (MIP), or another algorithm, to form projection angiograms (Fig 1).
Seminars in Ultrasound, CT, andMRI, Vo117, No 4 (August), 1996: pp 360-373
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Fig 1. Two-dimensional TOF MR angiograms of the portal vein {arrow} in {A) axial and {B) coronal projections. (Courtesy of Jorg F. Debatin, MD, University Hospital, Zurich, Switzerland.)
Administration of gadolinium chelates that shorten the T1 relaxation time of blood does not improve the depiction of blood vessels significantly in the 2D TOF techniques. In fact, many normal and pathological tissues are enhanced and appear in the TOF source images and projection images, thus potentially simulating flow signal and obscuring vessel details. Phase Contrast MRA
The contrast mechanism in phase contrast MRA is flow-induced phase shifts. 9-1a Blood is bright because it is moving, and stationary
tissue, which accumulates no phase, is dark. To make the gradient-recalled echo sequence sensitive to velocity-induced phase shifts, a bipolar flow-encoding gradient is added to the scan sequence, encoding for flow along a particular axis. It is important to note that only the motion of spins along the direction of the encoding gradient results in a change in phase. Thus, an angiogram sensitive to flow in every direction must be acquired with flow-encoding gradients along each of the three axes (slice selection, frequency-encoding, and phase-encoding directions). This process takes 2 to 3 times longer
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than encoding along one axis, because the encoding gradients must be applied on the different axes in separate acquisitions. In phase contrast, two sets of data are acquired. Bipolar flow-encoding gradients of opposite polarities are obtained and are then subtracted. The displayed pixel intensity represents phases or differences in phases rather than the amplitude of tissue magnetization. The principle reasons for performing the phase contrast angiography techniques are improvement of the detection of small or slow-flowing vessels by superior background suppression, and utilization of the velocity-phase relationships intrinsic to the phase contrast sequence to obtain direction and ve!ocity of blood flow. Before an angiogram is acquired, the appropriate maximum velocity encoded (Venc) must be chosen. A Venc that is too small results in a great deal of aliasing. A Vent that is excessively high prevents aliasing but also results in all velocities being represented by a small phase range, close to that of the stationary tissue value. Thus, the vascular contrast-tonoise ratio is decreased and the image is degraded. Because saturation effects are not as important in phase contrast imaging, venous structures can be studied with 2D or 3D acquisitions. However, 3D acquisitions require long scan
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times and preclude breath holding, thus spatial resolution is degraded by respiratory motion. In the authors' experience, sequential 2D phase contrast MRA with breath holding and gadolinium enhancement is most effective in imaging the liver. 12 Typical sequence parameters are TR of 30, TE of 8.5, 256 x 128 matrix, one excitation, a 30-degree flip angle, 5- to 7-mm-thick sections with a 2-mm overlap, and velocity encoding of 20 cm/s in all three axes. Coronal images are obtained routinely during breath holding after an intravenous injection of 0.1 mmoi/kg of gadopentetate dimeglumine. The subtraction process in phase contrast imaging provides the opportunity to use a T1shortening intravenous contrast agent. The use of such agents reduces the saturation effects on moving spins and increases the intravascular signal but does not obscure the vascular structures by enhancing overlying stationary tissues. The combination of breath holding and the use of contrast material improves overall image quality and vessel detail (Fig 2), and also improves detection and visualization of smaller and slower flowing vessels. Standard phase contrast angiographic reconstruction provides MR projection angiograms that depict blood flow as areas of high signal intensity regardless of flow direction and also
Fig 2.' Phase Contrast MR portograms (A) with and (B) without breath holding and contrast enhancement show degradation of image quality without breath holding and contrast material Overall image quality improves and vessel detail is better as noted by the clear display of the coronary vein varix (arrow) in A. P, portal vein; sp, splenic vein; ca, celiac axis. (Reprinted with permission, lz)
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phase images that indicate the direction of blood flow. Limitations of phase contrast MRA include sensitivity to gradient imperfection, artifacts from turbulence of flow or pulsatile flow, and limited spatial resolution. 9 PORTAL VENOUS SYSTEM
Normal Anatomy The portal vein provides approximately 75% of the total blood flow to the liver. The main portal vein is formed from the confluences of the splenic and superior mesenteric veins. The other major tributaries of the portal vein are the short gastric, inferior mesenteric, gastroepiploic, and pancreatico-duodenal veins. At the portahepatis, the main portal vein divides into the right and left lobar branches. The right lobar branch receives the cystic vein, which drains the gallbladder, and the smaller left lobar
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branch receives the umbilical and associated paraumbilical veins. Flow in the splenic, superior mesenteric, and portal veins normally is hepatopetal (toward the liver) (Fig 3). Congenital absence or duplication of the portal vein is rare. IMAGING METHODS
Conventional angiography has been considered the gold standard for evaluation of the portal vein. However, it has limitations: (a) patients with portal vein thrombosis are less attractive candidates for this invasive procedure because of a higher incidence of coagulopathy; (b) the study requires a large amount of contrast material, which carries the risk of renal toxicity; (c) detection of varices may be difficult because of lack of adequate contrast material, dilution of contrast material on the venous side,
Fig 3. Normal anatomy of the portal venous system with hepatopetal flow. (A) Coronal phase contrast MR portogram shows flowing blood as an area of high signal intensity regardless of flow direction. Main portal vein (PV), its right (RP) and left (LP) lobar branches, superior mesenteric vein (smv), and splenic vein (sv) are shown clearly. IVC, inferior vena cava; r, renal veins; arrows, hepatic veins. (B) Phase image with flow encoding in the right-to-left direction shows blood flowing right to left in the left portal vein in white (arrow) and left-to-right flow in the main portal vein in black (arrowheads), indicating hepatopetal flow. (Reprinted with permission. 44)
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insonation limit the value of sonography for assessing the portal venous system and associated collaterals. The portal venous system also can be evalu-
Fig 4. Thombosis of the portal vein in a patient with chronic active hepatitis, hepatoma, and previous splenectomy. (A) Breath-held, gadolinium-enhanced, muitiplanar, spoiled grass image shows hypointense clots in the portal vein and its lobar branches (arrows). (B) Coronal phase contrast MR portogram does not show the portal vein, consistent with occlusion. The superior mesenteric vein is patent, HA, common hepatic artery; SA, splenic artery; SMA, superior mesenteric artery. (Reprinted with permission. 44)
and presence of overlying bowel gas and parenchymal enhancement; and (d) a patent portal vein can appear occluded when flow is present but flow direction is reversed. Color flow Doppler songoraphy is an effective and accurate study for evaluating abdominal vasculature but may be unsuccessful if a suitable acoustic window is not available at the desired angle to the vessel axis. 13-15 In addition, sonography does not display the anatomy of the portal venous system in a format familiar to many clinicians. Impediments such as bowel gas, body habitus, fatty liver, cirrhosis, ascites, and restricted angle of
Fig 5. Cavernous transformation of the portal vein. (A) Axial and (B) coronal 2D TOF MIP images show a network of collateral vessels (arrows) in the porta hepatis, typical of cavernous transformation. (Courtesy of Jorg F. Debatin, MD, University Hospital, Zurich, Switzerland.)
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Fig 6. Portal venous stenosis in a patient who had surgery for hydatid disease. (A) Coronal phase contrast MR portogram shows marked narrowing of the portal vein as a segment of flow void (long straight arrow) with poststenotic dilation (short straight arrow) and prominent coronary venous varices (curved arrow). Lack of signal in the dilated poststenotic portal vein is caused by flow phenomenon, (B) Transhepatic portal venogram shows stenosis of the portal vein (straight arrow) and coronary venous varices (curved arrow). (Reprinted with permission, 44)
ated accurately with contrast-enhanced CT. 16,17 However, sensitivity in detecting portal venous thrombosis depends on precise timing of the contrast bolus, and axial scans often do not depict the complex anatomy of the portal venous system optimally. Similar to conventional angiography, a large amount of intravenous contrast is required, and a patent portal vein may appear occluded when flow is present but flow direction is reversed, and when the portal vein is attenuated. Both TOF and phase contrast MR angiographic techniques have been shown to be accurate for evaluating the portal venous system. 6,1z,18"21MRA is a reliable and noninvasive technique that can provide crucial information
in the preoperative workup of liver transplant recipients. MRA accurately determines patency and flow direction of the portal venous system, the presence and distribution ofvarices, and the patency of surgically created shunts. The survey of abdominal venous structures may be performed faster by M R A than by conventional angiography. The projection angiogram displays the anatomic layout of the portal venous system in a single, large, field-of-view image, a format familiar to many clinicians. It is important that interpretation of abdominal angiography studies be based on both individual sections and projection images. Although the projection image is superior for showing the overall anatomic relationship and course of
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Fig 7. Reversed flow in the coronary vein in a patient with portal hypertension. (A) Coronal phase contrast MR portogram shows an enlarged, tortuous coronary vein (straight arrow) and paraesophageal varices (curved arrow). P, portal vein; ca, celiac axis; sv, splenic vein; smv, superior mesenteric vein, (B) Phase image with flow encoding in superior-to-inferior direction shows hepatofugal flow in black in the coronary vein (straight arrow). Curved arrow, superior mesenteric vein. (Reprinted with permission. 44)
vessels, the individual slices show details of specific vessels better, because vessels may be hidden by overlapping structures and may be misregistered because of variable respiration. MR imaging has the potential to replace other imaging techniques in evaluating the portal venous system, especially in the preoperative workup of liver transplant patients. It is costly, however, and may be most helpful as a complement to the sonographic examination and when contrast-enhanced CT scanning is precluded by
severe contrast allergy and suppressed renal function. CLINICAL APPLICATIONS
Portal Vein Thrombosis
The predisposing causes of portal vein thrombosis are numerous, and these often overshadow the development of venous thrombosis. In adults, major causes of portal vein thrombosis include cirrhosis and neoplastic diseases. 22-26
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Fig 8. Paraumbilical venous varix in a patient with chronic active hepatitis C and encephalopathy. Coronal phase contrast MR portogram shows an enlarged paraumbilical vein (arrowheads) as a continuation of the left portal vein and no discernible flow in the right portal vein. P, portal vein; Sp, splenic vein; arrows, hepatic veins. (Reprinted with permission. ~)
In cirrhosis, the fibrotic reaction within the liver and the distortion of the hepatic architecture result in significant resistance to blood flow from the gastrointestinal tract into the liver. Thus, the blood flow in the portal vein becomes stagnant, predisposing to thrombosis. Portal vein thrombosis associated with neoplastic diseases may result from obstruction by portahepatis lymphadenopathy; direct venous invasion and infiltration by hepatocellular carcinoma; extrinsic compression or obliteration by pancreatic carcinoma, cholangiocarcinoma, or other metastatic cancers; or periportal fibrosis secondary to surgery or radiation. Other causes of portal vein thrombosis include pancreatitis, operative injury of the vein, hypercoagulable states resulting in hyperviscocity (such as polycythemia vera and myelofibrosis), trauma, and idiopathic causes. Intraabdominal inflammatory conditions, such as diverticulitis and appendicitis, can cause septic thrombosis of the portal vein. The onset of portal vein thrombosis often is
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so gradual or indolent that no specific clinical manifestations are recognized initially. Patients may ultimately present with gastrointestinal hemorrhage from variceal bleeding, abdominal pain, and splenomegaly. Acute thrombosis of the portal vein may be detected by visualization of the clot itself or by lack of flow within the vein (Fig 4). The thrombus can extend into the splenic or superior mesenteric veins, and these tributaries thus should be evaluated to determine the extent of occlusion. Cavernous transformation of the portal vein occurs in approximately 50% of patients who have chronic portal vein thrombosis, and it can develop as early as 4 weeks after the occlusion. 27,2s The network of collateral vessels develops in the portahepatis and hepatoduodenal ligaments by enlargement of preexisting small veins that accompany the lymphatic, biliary, and vascular structures. Collaterals also develop as well as newly formed primitive venous channels. The collateral vessels bypass the occlusion and drain into the intrahepatic portal venous branches (Fig 5). Portal vein stenosis may result from a complication of liver transplantation or major abdominal surgery. The diagnosis usually is based on findings at conventional angiography, but M R A can be useful in the diagnostic evaluation (Fig 6).
Fig 9. Spontanous splenorenal shunt. Coronal 2D TOF MR angiogram shows an extensive network of collateral vessels in the splenic hilum (straight arrows) draining into the dilated left renal vein (curved arrow). (Courtesy of Jorg F. Debatin, MD, University Hospital, Zurich, Switzerland.)
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include life-threatening bleeding from gastroesophageal varices, hepatic encephalopathy, ascites, coagulopathy, splenomegaly with hypersplenism, and bacteremia. The goals of diagnostic studies when examining patients with portal hypertension are the determination of the presence of hepatic disease, the direction of portal vein flow, and the presence and extent of intraabdominal portal systemic collaterals. Any
Fig 10. Coexistent coronary, paraesophageal, splenorenal, and splenoretroperitoneal collaterals in a patient with cryptogenic cirrhosis. Coronal phase contrast MR portogram shows massive collaterals from the splenic hilum passing both medially toward the left renal vein (splenorenal collaterals, short straight arrows) and laterally and interiorly (splenoretroperitoneal collaterals, curved arrow). Additionally, note the extensive coronary and paraesophageal varices (long straight arrow). (Reprinted with permission. 44)
Portal Hypertension Portal hypertension results from either an increase in portal blood flow or an increase in resistance to flow through the portal venous system.29,3° The most common cause of portal hypertension in the United States is hepatic cirrhosis. Portal hypertension may be classified as prehepatic (eg, obstruction of the extrahepatic portal vein), intrahepatic (eg, cirrhosis), and posthepatic (eg, hepatic vein or inferior vena cava obstruction). Arterial venous fistulas can cause portal hypertension on the basis of increased portal venous flow. In the early stage of portal hypertension, the portal vein may dilate but flow is maintained. As the resistance to flow in the portal vein increases, the portal blood flow may reverse from hepatopetal (toward the liver) to hepatofugal (away from the liver), reducing the flow to the liver and the size of the portal vein. In response to elevated portal vein pressures, portal systemic collateral pathways develop to shunt portal blood into systemic veins, bypassing the hepatic parenchyma and sinusoids. The development of collateral flow does not seem to decompress the portal system, however. Complications of portal hypertension
Fig 11. Mesenteric collaterals in a patient with portal hypertension. (A) Coronal phase contrast MR portogram shows massive retroperitoneal and mesenteric venous collaterals (white arrow). The portal vein is not apparent on this image because of its small size and its overlap with the inferior vena cava. Black arrow, superior mesenteric vein. (B) Phase image with flow encoding from right to left shows a small but patent main portal vein (arrow). Flow in the main portal vein, which is displayed in white, is hepatofugal, (Reprinted with permission. 44)
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of these vessels may be the source of bleeding during liver transplantation or portal decompressive surgery, whereas spontaneous bleeding tends to occur from gastric and paraesophageal varices.
Portosystemic Venous Collaterals
Fig 12, Inferior mesenteric varices in a patient with alcoholic cirrhosis of the liver. Coronal phase contrast MR angiogram shows massive pelvic varices (curved arrows) shunting blood via the inferior mesenteric vein (small straight arrows) and enlarged left gonadal vein (large straight arrow) (Reprinted with permission, 44)
Fig 13. Thrombosis of the splenic vein in a patient with pancreatic carcinoma, Coronal phase contrast MR portogram shows occlusion of the splenic vein and partial thrombosis of the portal vein (arrow). P, portal vein.
Portosystemic collaterals can be divided into two groups according to the area of drainage. 31-35 The first group consists of portosystemic collaterals draining toward the superior vena cava. Among patients with portal hypertension, 30% to 69% have reversed flow in the coronary and short gastric veins that are shunting blood through the gastroesophageal varices and paraesophageal veins toward the azygous veins and superior vena cava (Fig 7). Gastroesophageal varices are the usual source of bleeding from the upper gastrointestinal tract. Demonstration of reversed (cephalad) flow in the coronary vein indicates increased risk for variceal bleeding, whereas a normal flow direction rules out imminent hemorrhage. 36 Treatment of esophageal varices includes vasoconstrictive drugs, endoscopic pressure tubes, endoscopic sclerotherapy, or decompression of the portal system by creation of alternative portosystemic shunts. The second group of portosystemic collaterals consists of vessels draining splanchnic blood toward the inferior vena cava. The paraumbili-
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the phrenicocolic ligament via retroperitoneal branches, and they ultimately drain into lumbar veins. The collaterals begin at the splenic hilum and pass inferiorly and laterally to the upper pole of the left kidney (Fig 10). Mesentenc Collaterals
Various collaterals can originate from the superior mesenteric and inferior mesenteric veins (Figs 11 and 12). These shunts reach the systemic veins via the retroperitoneal and rues-
Fig 14. Thrombosis of the splenic and superior mesenteric veins in a patient with cirrhosis and pancreatic carcinoma, Coronal phase contrast MR portogram shows an extensive network of peripancreatic varices (arrows). The portal vein (PV) is patent. A low-signal-intensity thrombus (T) at the portosplenic venous confluence also was seen on axial images. (Reprinted with permission. 44)
cal vein originates from the left branch of the portal vein and runs in the fissure of the ligamentum teres or through the medial segment of the left lobe (Fig 8). Outside of the liver, the paraumbilical vein courses through the falciform ligament and connects with the epigastric veins in the abdominal wall, ultimately draining into the external iliac vein. The prevalence of paraumbilical veins in portal hypertension may be as much as 33%. These shunts can become quite large and provide efficient decompression of portal hypertension. Umbilical vein collateral flow is an important feature of portal hypertension because it carries a diagnostic specificity for portal hypertension o f 100%. 37,38
Gastrorenal collaterals are tortuous vessels around the stomach that shunt blood toward the renal vein and ultimately drain into the inferior vena cava. Shunting from the splenic vein into the inferior vena cava occurs along splenorenal or splenoretroperitoneal pathways. A splenorenal shunt is seen in 10% to 20% of patients with portal hypertension?~, 39 The tortuous vessels are detected between the hilum of the spleen and the hilum of the left kidney. These enlarged veins drain into a dilated left renal vein (Fig 9). The splenoretroperitoneal collaterals connect the splenic vein and inferior vena cava through
Fig 15. Normal surgical distal splenorenal shunt. (A) Coronal phase contrast MR angiogram shows patency of surgical splenorenal shunt (S). LRV, left renal vein; SV, distal splenic vein; IVC, inferior vena cava. (B) Phase image with flow encoding from superior to inferior shows the appropriate direction of blood flow in the shunt (S); ie, from the splenic to renal vein, in white. (Reprinted with permission. 44}
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Fig 16. Surgical mesocaval shunt in a patient with chronic active hepatitis and severe portal hypertension. (A) Sagittal phase contrast MR angiogram shows patency of the shunt (straight arrow), which connects the superior mesenteric vein anteriorly (curved arrow) to the inferior vena cava posteriorly (arrowheads) just above the caval bifurcation, (B) Axial MIP image shows the anastomosis (arrow) of the shunt, IVC, inferior vena cava, (Reprinted with permission, 44)
enteric venous plexus. Pericolic collaterals also can carry hepatofugal blood flow around the colon and drain into the lumbar veins and ultimately into the inferior vena cava. The inferior mesenteric vein carries hepatofugal blood into the pelvis. Extensive collaterals may develop and connect the inferior mesenteric and iliac veins via the superior, middle, and inferior hemorroidal veins. Occasionally, blood may be shunted into the pelvis through the gonadal veins.
Occlusion of the Splenic and Superior Mesenteric Veins Acute thrombosis of the splenic vein may be detected by visualization of the clot itself or by
lack of flow (Fig 13). In chronic occlusion, collateral vessels caused by portal venous hypertension, or resulting from occlusion of the splenic vein itself, can develop along three separate pathways: (a) from the splenic hilum via the gastroepiploic vessels toward the superior mesenteric vein and into the portal vein; (b) from short gastric veins toward the venous plexus around the stomach and into the portal vein via the coronary vein; and (c) from peripancreatic collaterals into the portal vein or superior mesenteric vein, as well as to the retroperitoneal branches into the inferior vena cava (Fig 14).4° Hepatofugal shunting also can occur along the splenorenal or splenoretroperitoneal shunts. Isolated occlusion of the superior mesenteric
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vein is r a r e a n d usually occurs in c o n j u n c t i o n with occlusion o f t h e s p l e n i c vein.
Portosystemic Surgical Shunts P o r t o s y s t e m i c surgical shunts a r e effective in decompressing the hypertensive portal venous system to c o n t r o l b l e e d i n g f r o m g a s t r o e s o p h a geal varices. 41-43 T h e two types o f shunts a r e t o t a l s h u n t s a n d selective shunts. T o t a l shunts, such as t h e p o r t o c a v a l o r m e s o c a v a l shunt, d e c o m p r e s s b o t h t h e p o r t a l a n d v a r i c e a l systems. I n t h e s e shunts, b l o o d flow in all m a j o r p o r t a l vessels c o n v e r g e s t o w a r d t h e a n a s t o m o sis, a n d flow in t h e i n t r a h e p a t i c p o r t a l vein b r a n c h e s g e n e r a l l y is h e p a t o f u g a l . Selective shunts, such as t h e s p l e n o r e n a l o r c o r o n o c a v a l shunt, d e c o m p r e s s t h e varices a n d m a y n o t affect e i t h e r t h e p o r t a l v e n o u s p r e s s u r e o r flow.
T h e distal s p l e n o r e n a l , o r W a r r e n , s h u n t is t h e m o s t p o p u l a r selective shunt. T h e distal s p l e n i c vein is a n a s t o m o s e d e n d to side to t h e m i d p o r t i o n o f t h e left r e n a l vein. T h e g a s t r o e s o p h a g e a l c o l l a t e r a l s can t h e n d r a i n t h r o u g h s h o r t gastric vessels, a n d t h e s p l e n i c vein c a n d r a i n t o w a r d t h e a n a s t o m o s i s . B e c a u s e all connections between the gastrosplenic vascular area and the mesenteric portal area are interrupted at surgery, h y p e r t e n s i o n in t h e m e s e n t e r i c p o r tal a r e a r e m a i n s , p r e s e r v i n g p o r t a l inflow to t h e liver a n d p r e v e n t i n g e n c e p h a l o p a t h y . T h r e e - d i m e n s i o n a l M R i m a g e displays a r e very useful for d e t e r m i n i n g p a t e n c y o f t h e p o r t o s y s t e m i c shunt, flow d i r e c t i o n , a n d s h u n t size b e c a u s e t h e o p t i m a l s c a n n i n g p l a n e for displaying the shunt can be selected from the 3 D r e n d i t i o n (Figs 15 a n d 16).
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