T.I.P.S. Imaging
This program is supported by a grant from GE Ultrasound
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The Institute for Advanced Medical Education designates this educational activity for a maximum of 1 AMA PRA Category 1 Credit(s) TM. Physicians should only claim credit commensurate with the extent of their participation in the activity. |
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These credits are accepted by the American Registry for Diagnostic Medical Sonography (ARDMS). Faculty: Myron A. Pozniak, MD Professor of Radiology University of Wisconsin Clinical Science Center Madison, Wisconsin Course: T.I.P.S. Imaging Target Audience: Physicians, sonographers and others who perform and/or interpret vascular ultrasound. System requirements: In order to complete this program you must have a computer with a recent version of Internet Explorer or Netscape, and a printer, which is configured to print from the browser. For any questions or problems concerning this program or for problems related to the printing of the certifcate, please contact IAME at 914-921-5700 or email us. Estimated Time for Completion of tutorial: approximately 50 minutes Date of Release: February 1, 2001 Date of Review: July 31, 2008 Expiration Date: July 31, 2011 Disclosure: In compliance with the Essentials and Standards of the ACCME, the author of this CME tutorial is required to disclose any significant financial or other relationships they may have with the manufacturer(s) of any commercial product(s) or provider(s) of any commercial service(s) discussed in this program. Dr. Myron A. Pozniak has indicated that no such relationships exist. IAME discloses no relevant financial relationships with commercial interests.
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T.I.P.S. Imaging Myron
A. Pozniak, MD Kevin P. Henesler, MD Objectives After completing this course, the participant should be able:
Introduction Diseases of the liver are a major cause of morbidity and mortality throughout the world. The Centers for Disease Control estimate that over 25,000 deaths and 300,000 hospitalizations are due to liver disease in the United States alone. Many causes of liver disease lead to the development of portal hypertension (PHTN) (Table 1.) The etiology of PHTN varies widely throughout the world. While cirrhosis is the major cause of PHTN in the US and Europe, schistosomiasis, a liver parasite, is a major cause in Africa, and noncirrhotic portal fibrosis is common in India. Hepatitis B and C are endemic in many parts of the world and are a major cause of PHTN in the East, and are an increasingly common etiology in Western Europe and the United States.Portal hypertension is defined as a portal venous pressure of greater than 12 mm Hg. Current theories as to the cause of the increased pressure in PHTN suggest two mechanisms: a combination of deposition of collagen between cells in the spaces of Disse and hepatocyte swelling, both of which increase the sinusoidal pressure and cause a relative resistance to blood flow into the hepatic sinusoids; and hemodynamic factors, including intrahepatic endogenous vasoconstrictors and mesenteric vasodilators, which increase blood flow and pressure in the portal venous system. Patients experiencing increased portal venous pressure can see a reversal of flow in the portal system (changing form hepatopetal [toward the liver], to hepatofugal [away from the liver]). This is thought to result from at least two types of intrahepatic arterial-portal communications. One is through the vasa-vasorum. This communication occurs through the arterioles supplying the wall of the portal veins. Another communication takes place at the portal triad. This occurs because of direct shunting of blood from the hepatic arteries, through the capillary system and into the portal vein. Since hepatic artery pressure (assume 120/80 mmHg.) exceeds portal vein pressure (normal 5-10 mmHg.) the inflow of arterial blood at the sinusoid level into the portal vein overwhelms portal inflow. Child studied the clinical course of liver disease and in 1963 described the system still used to stratify patients with end stage liver disease (ESLD) (Table 2). With progressive liver disease increasing resistance at the hepatic sinusoid level elevates portal pressure and causes the development and enlargement of portosystemic collaterals; the most clinically important of which are gastroesophageal varices (EV) (Figure 1).
Up to 30% of patients with portal hypertension undergoing endoscopy have apparent EV, and 30% of these will eventually bleeding. Bleeding from esophageal varices is a major cause of death in patients with portal hypertension. Other collaterals include paraumbilical vein recanalization and various retroperitoneal shunts including splenorenal, iliolumbar, intercostal and phrenic vein. Doctors had little to offer patients with variceal bleeding due to PHTN before the work of Whipple and others introduced surgical portosystemic shunts as a therapeutic option in the 1940¹s. Definitive treatment was first attempted in 1963, when Starzl successfully performed the first human liver transplant. Now liver transplantation is performed in over 4000 patients a year. Patients on the waiting list or those denied liver transplantation may be incapacitated by the secondary effects of PHTN such as bleeding esophageal varices or intractable ascites. In order to provide some relief from the complications of PHTN, a controlled shunt of blood from the portal system to the systemic circulation can be created. Until recently, the standard of care was a surgically created shunt. Some of the more common variations include anastomosis of the splenic vein to the renal vein, (with or without removal of the spleen) or direct anastomosis of the portal vein or superior mesenteric vein to the inferior vena cava (portocaval or mesocaval shunt). Percutaneous diversion of portal flow as a less invasive alternative to surgery was first proposed in 1969. Trans-jugular intra-hepatic porto-systemic shunt (TIPS) placement involves the percutaneous creation of a link between the high-pressure portal system of a cirrhotic patient and the low-pressure hepatic veins. A catheter placed through the patient's right jugular vein is manipulated through the heart, inferior vena cava and most commonly into the patient's right hepatic vein. A transparenchymal puncture of a portal vein branch is made and a wire passed into the main portal vein. The track along the communication between hepatic vein and portal vein is then dilated and an expandable metal stent is deployed to keep the track open. This communication allows free passage of blood from the portal system to the systemic circulation, reducing the pressure in the portal system. Although the TIPS is most often placed between the right hepatic vein and the right branch of the portal vein, the middle or left hepatic vein to left portal vein route may be chosen for technical or anatomic reasons. A successful TIPS reduces the pressure in the portal venous system. This will divert blood from the varices, and reduce the risk of life threatening hemorrhage. The reduced portal pressure also means less fluid "weeps" from the liver, and the kidneys work more efficiently to remove the ascites fluid. Patients with intractable ascites often see an improvement or resolution of their ascites. Pre-TIPS Assessment Pre-procedural assessment of the TIPS candidate is necessary to identify the vascular anatomy, rule out portal and hepatic vein thrombosis, measure vessel size and search for the presence of porto-systemic varices. This can be accomplished with conventional angiography, CTA, MRA or US and Doppler. US offers the advantage of non-invasive imaging and it provides a baseline against which to judge the hemodynamic effects of TIPS placement, changes in spleen size and the amount of ascites. Large varices should be identified prior to TIPS placement allowing occlusion by coil placement in symptomatic patients. This is best accomplished by CTA (Figure 1).
TIPS follow-up Since the TIPS device is an indwelling foreign body, TIPS complications are very common. The most common cause of TIPS malfunction is stenosis in the stent. This narrowing can be readily treated with a simple angioplasty if it can be discovered early. Clinical monitoring of TIPS patency is relatively insensitive. Sequential Doppler sonography is ideally suited to monitor the TIPS, the adjacent hepatic veins, as well as the main, right, and left portal veins, in order to ensure early detection of shunt compromise allowing timely revision. Prompt identification of a stenosis with intervention may prevent progression to thrombosis. A recently thrombosed TIPS may be recanalised successfully but if thrombus is allowed to mature the patient usually requires the placement of a second TIPS. Routine Doppler monitoring after shunt placement should include an evaluation of the TIPS within 24 hours after its creation to confirm patency and establish baseline flow directions and velocities. Subsequent evaluation is conducted just prior to discharge of the patient and periodically thereafter; the frequency varies among centres but most re-examine the shunt at 3 to 6 month intervals. Optimum scanning parameters and normal US findings following TIPS have been described by a number of investigators. Transducers of 2.25 to 3.5 MHz are usually necessary because of the frequently increased echogenicity and sound attenuating features of the cirrhotic liver, along with the fact that the shunt is usually fairly deep within the body. The Doppler gain should be set as high as possible, without encountering noise or saturation artifact (Figure 2).
The transducer is focused at the level of the shunt or vessel of interest; the sample volume is placed in the center of the shunt with an angle of insonation less than 600 when feasible. This may be difficult to accomplish, especially in the middle segment of the shunt, where the direction of flow frequently runs perpendicular to the insonating beam (Figure 3).
The pulse repetition frequency is set as low as possible, but avoiding aliasing. Optimizing the scanning parameters will help minimize the chances of making a false positive diagnosis of TIPS thrombosis. TIPS Follow-Up - Normal Findings A complete TIPS evaluation includes a survey of the abdomen to quantify ascites. The imager should also look for intrahepatic, perihepatic, or subcapsular hematomas; intraperitoneal bleeding (as indicated by increased volume or echogenicity of the ascites); biliary obstruction; and echogenic debris within the CBD or gallbladder that suggest hemobilia. The shunt is then identified, typically between the right portal and right hepatic veins (Figure 4).
The stent is highly echogenic and appears as two parallel, curvilinear lines, usually uniform in diameter in the parenchyma but may be slightly flared at the portal and hepatic venous ends (Figure 5).
The shunt diameter is easily measured but a curved TIPS that passes obliquely through the plane of insonation may appear artificially narrowed. The stent should extend from within the portal vein (Figure 3), across the parenchyma and into the hepatic vein (Figure 6).
Imaging sometimes reveals malposition of the stent as a result of inappropriate deployment, or subsequent migration down into the portal vein (Figure 7), or up into the hepatic vein and right atrium.
Flow within the stent is then evaluated by Doppler ultrasound. The presence of blood flow is easily confirmed, as the entire shunt lumen fills with color due to the relatively fast, turbulent flow. The velocity, flow direction and waveform are then checked at the portal vein end, mid-shunt, and hepatic vein end. The main portal vein and the left portal vein are assessed and the right hepatic vein is checked both proximal to and just beyond its junction with the stent (Figure 8).
Spectral Doppler evaluation should verify that the direction of flow in the shunt is from the portal vein to the hepatic vein. Flow through the average shunt is non-pulsatile but flow in a widely patent shunt may show periodicity throughout the shunt due to right atrial pressure changes being transmitted back through the shunt (Figure 9a & b).
Cardiac periodicity is most prominent near the hepatic venous end. In one study, half of the patients with patent TIPS demonstrated some periodicity at the hepatic venous end of the shunt, while the other half had high-velocity turbulent flow. Periodicity may be accentuated within the shunt in patients with tricuspid valve disease or congestive heart failure. Flow velocities in the shunt vary widely, ranging from approximately 50-270 cm/sec. Velocities can also be quite variable through the shunt itself, usually increasing from the portal venous end to the hepatic venous end of the shunt. The mean velocity of patent shunts has been reported as 95 cm/sec in the shunt near the portal venous end and 120 cm/sec in the middle segment of the shunt. Flow across the shunt is usually quite turbulent, especially when multiple stent components are used. Overriding of stent components can result in a relative narrowing of the shunt lumen (Figure 10).
Normal velocities in the main portal vein are variable. Following TIPS insertion, the mean portal vein velocity has been reported to increase from 7 cm/sec to 24 cm/sec in one study and from 20 cm/sec to 38.4 cm/sec in another. Hepatic arterial flow has also been shown to increase after TIPS, presumably because the shunt diverts the portal venous inflow away from the liver. With a properly functioning TIPS, flow direction in the entire portal system is towards the portal vein end of the stent. Therefore, flow in the main portal vein is hepatopetal and its velocity is typically quite brisk (between 20 to 50 cm/sec) (Figure 11).
It must be kept in mind that velocities measured in the stent-bearing portion of the portal vein represent flow in the portal vein, not in the shunt. Flow in the left and right portal veins usually becomes hepatofugal - flowing out of the diseased liver and towards the inflow of the shunt (Figure 12).
If the patient has a patent recanalized para-umbilical vein, it will continue to shunt blood away from the liver. Flow in the left portal vein, therefore, will continue in a hepatopetal direction despite normal TIPS function. The Doppler data are recorded and maintained in a table format for follow-up (Figure 13). TIPS FOLLOW-UP SHEET
Serial evaluation provides the best means of identifying any variations in velocity and/or flow direction over time and these changes are the best early indicator of shunt compromise. If the left portal vein changes direction over time from hepatofugal to hepatopetal, or main portal vein velocities are seen to be steadily decreasing; a significant flow-limiting lesion is assumed to be developing in the TIPS. TIPS Follow-Up - Shunt Stenosis The two most common causes of TIPS compromise are neointimal hyperplasia throughout the shunt, or a focal stenosis at the hepatic vein end. Most TIPS will have some degree of neointimal hyperplasia as the body reacts to the metal cage of the stent but this may progress to the point where it limits flow through the TIPS(Figure 14a &b).
Just beyond the point of maximum stenosis within the TIPS Doppler may perceive an increased velocity (Figure 15).
More proximally within the TIPS and throughout the portal system, however, velocities will decrease. With sufficient compromise, flow in the branch portal veins, including the left portal vein may change back to a hepatopetal direction, representing a reversion to pre-TIPS hemodynamics (Figure 16).
Eventually flow in the main portal vein may again become hepatofugal. In the patient who cannot hold their breath the Doppler sample volume may traverse the point of stenosis resulting in a sinusoidal waveform that varies with respiration (Figure 17).
Focal hepatic vein stenosis can occur where the end of the TIPS abuts the hepatic vein caused by focal irritation of the vein wall by the stent (Figure 18).
This results in decreasing velocities throughout the shunt and main portal vein. A key Doppler finding of this focal stenosis is the presence of post-stenotic flow disturbances with a high-velocity jet and turbulence in the hepatic vein or IVC. The sonologist must therefore evaluate flow beyond the end of the stent, sometimes even as far as the right atrium. Flow in all three hepatic veins is normally towards the heart but a stenosis at the junction of the TIPS and the hepatic vein can cause flow compromise peripherally in the vein with damping of periodicity, or flow reversal (Figure 19).
Several investigators have attempted to determine flow velocities which define the presence of TIPS stenosis but reported findings have varied considerably. In one study a velocity <50 cm/sec at the portal venous end was 100% sensitive and 93% specific. In another study a velocity <50 cm/sec in the middle segment of the TIPS was 78% sensitive and 99% specific, with a positive predictive value of 96%, negative predictive value of 91%, and accuracy of 92%. When these investigators used a velocity <60 cm/sec as the criterion, sensitivity increased to 84% but specificity dropped to 89% and accuracy to 87%. At <70 cm/sec, sensitivity was 89% but specificity was 83% and accuracy was 85%. In another study a velocity of 90 cm/sec was applied but the sensitivity was only 87.5% with specificity of 95%. These varied findings underscore the fact that flow velocities vary widely from patient to patient and that the best method for identifying TIPS compromise is to target variation of individual patient velocities from those baseline measurements obtained soon after TIPS placement. A change in velocity of ±50 cm/sec from baseline has been proposed as the threshold value for predicting hemodynamically significant shunt compromise. Table 3 -Doppler Criteria for compromised TIPS function
TIPS
Follow-Up - Shunt Occlusion
If no flow can be detected in the shunt and flow velocity and
direction in the portal vein is the same as it was prior to TIPS placement,
shunt occlusion must be considered. The absence of flow by color Doppler within
the TIPS is a highly specific indicator of shunt thrombosis (Figure 20a & b).
Before
concluding that the stent is occluded, however, meticulous scanning for slow
flow should be performed, since flow velocity may be extremely low in a shunt
that is tightly stenosed but still patent. Color Doppler settings (including
pulse repetition frequency, gain, and filtration) need to be optimized to differentiate
true occlusion from very slow flow. A properly functioning TIPS, however, is
not a low-flow system, so misinterpretation of thrombosis for technical reasons
is rarely a problem. Identifying low flow, however, has the same implication
as occlusion, and that is the need for TIPS revision. Indeed, repeat interventions
are the key to long-term success of TIPS.
After
TIPS thrombosis, recanalization may be attempted and/or a second TIPS may be
placed between another hepatic vein and the portal vein (Figure 21).
If
both TIPS are patent, monitoring of both stents should proceed in the same manner
with documentation of sequential velocity measurements.
TIPS - Conclusion TIPS has largely replaced surgical treatment of portal hypertension. Doppler ultrasound is an excellent noninvasive tool for the monitoring of shunt patency. The two most common patterns of shunt compromise are neointimal hyperplasia throughout the shunt or a focal stenosis at the hepatic vein end. The sequential documentation of changing velocities is the best way of identifying early stent malfunction allowing timely treatment. TIPS -References 1) Chong WK, Malisch TA, Mazer MJ, Lind CD, Worrell JA, Richards WO: Transjugular intrahepatic portosystemic shunt: US assessment with maximum flow velocity. Radiology 1993;189:789-793. 2) Coldwell DM, Ring EJ, Rees CR, et al: Multicenter investigation of the role of transjugular intrahepatic portosystemic shunt in management of portal hypertension. Radiology 1995:196:335-340. 3) Dodd GD, Zajko AB, Orons PD, Martin MS, Eichner LS, Santaguida LA: Detection of transjugular intrahepatic portosystemic shunt dysfunction: value of duplex Doppler sonography. AJR 1995;164:1119-1124. 4) Feldstein VA, Patel MD, La Berge JM: Transjugular intrahepatic portosystemic shunts: accuracy of Doppler US in determination of patency and detection of stenoses. Radiology 1996;201:141-147. 5) Foshager MC, Ferral H, Finlay DE, Castaneda-Zuniga WR, Letourneau JG: Colour Doppler sonography of transjugular intrahepatic portosystemic shunts (TIPS). AJR 1994;163:105-111. 6) Foshager MC, Finlay DE, Longley DG, Letourneau JG: Duplex and colour Doppler sonography of complications after percutaneous interventional vascular procedures. Radiographics 1994;14:239-253. 7) Furst G, Malms J, Heyer T, et al. Transjugular intrahepatic portosystemic shunts: improved evaluation with echo-enhanced color Doppler sonography, power Doppler sonography, and spectral duplex sonography. AJR 1998;170(4):1047-1054. 8) Kimura M, Sato M, Kawai N, et al. Efficacy of Doppler ultrasonography for assessment of transjugular intrahepatic portosystemic shunt patency. Cardiovasc Intervent Radiol 1996;19(6):397-400. 9) Longo JM, Bilbao JI, Rousseau HP, et al: Transjugular intrahepatic portosystemic shunt: evaluation with Doppler sonography. Radiology 1993;188:529-534. 10) Mituzani P, Saxon R, Alexander P, Barton R, Koslin D: Duplex US screening after transjugular intrahepatic portosystemic shunt placement. Radiology 1993;189(P)(suppl):254. 11) Nazarian GK, Ferral H, Castaneda-Zuniga WR, et al: Development of stenoses in transjugular intrahepatic portosystemic shunts. Radiology 1994;192:231-234. 12) Rosch J, Hanafee WN, Snow H: Transjugular portal venography and radiologic portacaval shunt: an experimental study. Radiology 1969;92:1112-1114 13) Rossle M, Siegerstetter V, Huber M, Ochs A. The first decade of the transjugular intrahepatic portosystemic shunt (TIPS): state of the art. Liver 1998;18(2):73-89. 14) Smith JM, Cox LA, Long BW. Ultrasound evaluation of TIPS placement. Radiol Technol 2000;71(4):321-325. 15) Surratt RS, Middleton WD, Darcy MD, Melson GL, Brink JA: Morphologic and haemodynamic findings at sonography before and after creation of a transjugular intrahepatic portosystemic shunt. AJR 1993;160:627-630. 15) Uggowitzer MM, Kugler C, Machan L, et al. Value of echo-enhanced Doppler sonography in evaluation of transjugular intrahepatic portosystemic shunts. AJR 1998;170(4):1041-1046. 16) Zemel G, Katzen B, Grubbs G, Moore B, Benenati J, Becker G: Sonographic indicators of unsuccessful transjugular intrahepatic portosystemic shunts. Radiology 1994;193(P)(suppl):167. 17) Zizka J, Elias P, Krajina A, et al. Value of Doppler sonography in revealing transjugular intrahepatic portosystemic shunt malfunction: a 5-year experience in 216 patients. AJR 2000;175(1):141-148. Our online courses are free of charge.
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