Causes of TIPS Dysfunction

Va s c u l a r a n d I n t e r ve n t i o n a l R a d i o l o g y • R ev i ew Cura et al. Causes of TIPS Dysfunction

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Vascular and Interventional Radiology Review

Causes of TIPS Dysfunction Marco Cura1 Alejandro Cura2 Rajeev Suri1 Fadi El-Merhi1 Jorge Lopera1 Ghazwan Kroma1 Cura M, Cura A, Suri R, El-Merhi F, Lopera J, Kroma G

Objective. Transjugular intrahepatic portosystemic shunt (TIPS) creation is an effective method to control portal hypertension. TIPS creations with bare stents have shown limited and unpredictable patency. In nearly all cases of rebleeding or recurrent ascites after TIPS creation, there is shunt stenosis or occlusion. The purpose of this article is to review the biologic and technical factors that predispose to TIPS failure and how the use of an expandable polytetrafluoroethylene (PTFE)-covered-stent has significantly improved TIPS patency. Conclusion. Biologic and technical factors may predispose to shunt failure. The combination of improved technique and expandable PTFE has significantly improved TIPS patency. The need for follow-up venography and secondary interventions has been reduced significantly as a result of improved shunt patency.

T

Keywords: covered stent, interventional radiology, portal hypertension, transjugular intrahepatic portosystemic shunt DOI:10.2214/AJR.07.3534 Received December 11, 2007; accepted after revision June 22, 2008. 1

Cardiovascular and Special Interventions, Department of Radiology, The University of Texas Health Science Center, Mail Code 7800, 7703 Floyd Curl Dr,, San Antonio, TX 78229-3900. Address correspondence to M. Cura ([email protected]).

2 Department of Radiology, Hospital de Clinicas, Jose de San Martin, University of Buenos Aires, Buenos Aires, Argentina.

CME This article is available for CME credit. See www.arrs.org for more information. AJR 2008; 191:1751–1757 0361–803X/08/1916–1751 © American Roentgen Ray Society

AJR:191, December 2008

he transjugular intrahepatic portosystemic shunt (TIPS) is an effective method to control the complications of portal hypertension; however, shunt dysfunction is common. Some shunts may remain patent, whereas others develop stenoses and thromboses. Recurrent portal hypertension with stenoses greater than 50% develop in 25– 50% of cases 6–12 months after TIPS creation when bare stents are used [1–5]. Solving the problems of shunt dysfunction decreases the absolute rates of rebleeding and recurrent ascites after TIPS and the number of required shunt revisions. Although many lining materials have been tested as covers for TIPS stents, only expandable polytetrafluoroethylene (PTFE) grafts appear to address the biologic causes of shunt dysfunction and provide better patency rates than TIPS created with bare stents. Causes of TIPS Dysfunction Excluding early shunt failure due to technical causes such as stent shortening or migration, causes of shunt dysfunction in TIPS created with bare stents include bile-related, non-bile-related, and hepatic vein stenosis [6]. During TIPS creation, bile ducts may inadvertently be traversed during needle passes from the hepatic vein to the portal vein [7] (Fig. 1). Transected bile ducts have been associated with TIPS stenosis and occlusion

[8]. Transection of a bile duct creates communication between the bile ducts and the TIPS lumen, a biliary–TIPS fistula. The content of bile acids, salts, cholesterol, and phospholipids makes bile thrombogenic and proinflammatory [9]. Bile also appears to delay tract healing by inhibiting smooth muscle proliferation [10]. Histopathologic analysis of occluded shunts showed bile pigment in thrombus adherent to a transected bile duct associated with a granulomatous inflammatory response containing foreign-body-type giant cells [11]. Biliary–TIPS fistulas present with acute thrombosis and recurrent occlusions [12] (Fig. 2). Later, nonthrombogenic parenchymal tract stenosis or pseudointimal hyperplasia is the result of proliferation of myofibroblasts that increase in number over time [13]. The pseudointimal hyperplasia responsible for TIPS stenosis has similarities to the intimal hyperplasia responsible for arterial restenosis after vascular recanalizations [14]. The predominant cause of intimal hyperplasia after arterial stent placement is proliferation and migration of smooth muscle cells from the media. The liver parenchyma contains no smooth muscle cells; the fibroblasts of the liver stroma differentiate into myofibroblasts that migrate from the adjacent liver parenchyma into the TIPS [14, 15]. The fibrotic healing response to the trauma of shunt creation causes tissue overgrowth

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Fig. 1—45-year-old man with hepatitis C cirrhosis and variceal bleeding. Fluoroscopic image shows transjugular puncture of left bile duct during transjugular intrahepatic portosystemic shunt procedure.

Fig. 2—51-year-old man after transjugular intra hepatic portosystemic shunt (TIPS) who presented with recurrent variceal bleeding. On fluoroscopic image, contrast injection during revision of thrombosed TIPS shows opacification of biliary tree.

Fig. 3—49-year-old woman after transjugular intrahepatic portosystemic shunt (TIPS) who presented with recurrent ascites. TIPS venogram shows severe intrastent stenosis caused by myofibroblast proliferation.

Fig. 4—55-year-old man after transjugular intrahepatic portosystemic shunt (TIPS) creation who presented with variceal bleeding. TIPS venogram shows proximal hepatic vein stenosis (arrow) caused by intimal hyperplasia.

through the stent mesh into the shunt lumen [8, 16] (Fig. 3). Leaving the proximal segment of the hepatic vein unstented will predispose the patient to hepatic vein stenosis as a result of intimal hyperplasia [17]. The shear stress and turbulence from increased high-velocity blood flow cause venous intimal hyperplasia [10, 13]. Hepatic vein stenosis or intimal hyperplasia of the hepatic vein occurs months to a year after TIPS creation [16, 18] (Fig. 4). Late shortening of self-expanding stents— Wallstents (Boston Scientific)—may occur, leaving the hepatic vein at risk of subsequent intimal hyperplasia or recoiling of an unsupported parenchymal tract [19]. Therefore, extension of the stent to the junction of the hepatic vein and the inferior vena cava (IVC) is

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Fig. 5—Determining exact location of hepatocaval junction. A, Fluoroscopic image in 45-year-old man shows guidewire is placed in inferior vena cava (IVC) and a second guidewire is placed in transjugular intrahepatic portosystemic shunt (TIPS). Sheath is advanced over the two wires until its tip reaches hepatocaval junction (arrow), or simultaneous contrast injection may be performed in TIPS and IVC to define confluence of hepatic vein and IVC. B, Left anterior oblique projection (36°) of venogram in 58-year-old man and simultaneous contrast injection of shunt and IVC clearly show confluence of hepatic vein and IVC (arrow).

an important determinant of shunt patency. The optimal location of the proximal end of the stent is the hepatocaval junction; to determine the exact location of that junction, a guidewire can be placed in the IVC and a second guidewire in the TIPS. The sheath is then advanced over the two wires until its tip

reaches the hepatocaval junction. Alternatively, simultaneous contrast injection may be performed in the TIPS and the IVC to define the hepatic vein–IVC confluence (Fig. 5). Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the liver and often occurs in cirrhotic livers



Causes of TIPS Dysfunction

Fig. 6—45-year-old man with hepatitis C cirrhosis and hepatocellular carcinoma (HCC) who presented with recurrent variceal bleeding. On nonsubtracted venogram, HCC (T) invasion of portal vein end (PV) of transjugular intrahepatic portosystemic shunt (TIPS) causes decreased shunt flow.

with portal hypertension. HCC is well known to invade venous structures, including the portal and hepatic veins [20] (Fig. 6). HCC may grow through the mesh of the stent or invade the portal and hepatic veins, compromising portal vein inflow or hepatic vein outflow and resulting in subsequent TIPS occlusion [21, 22]. If TIPS thrombosis occurs in a patient with known HCC, bland thrombus should be differentiated from tumor thrombus before attempting to revise a malfunctioning shunt. CT and MRI are excellent methods to evaluate tumor extension into blood vessels. Both can display images in multiple planes and can perform multiphasic enhanced studies [23, 24]. Portal tumor thrombus shows early arterial enhancement on dynamic enhanced studies [25]. Bland thrombus may respond to mechanical thrombolysis and stenting. On the other hand, manipulation of tumor thrombus may result in the embolization of tumor cells. Other recognized causes of shunt dysfunction include iatrogenic dissection of the portal vein during TIPS creation, resulting in inflow disease and shunt thrombosis [26]. Hypercoagulability may also predispose to shunt thrombosis and occlusion, especially in patients with Budd-Chiari syndrome, in whom TIPS dysfunction of bare stents is fairly common [21, 27, 28]. Extrahepatic hemodynamic causes of TIPS dysfunction, such as flow stealing through competent varices or spontaneous


mesocaval shunts, may decrease the flow in the TIPS enough to result in flow stasis and shunt thrombosis. Mechanical causes of bare stent thrombosis may result from fractures of balloon-expandable stents deployed in the parenchymal track. The stiffness and lack of flexibility of balloon-expandable stents may preclude their use in TIPS (Fig. 7). Using the peripheral segment of any hepatic vein to start a TIPS may cause the shunt to cross the hepatic vein perpendicularly and abut the hepatic vein, thus reducing the outflow of the shunt. Kinking of the stent may be seen after peripheral punctures of the portal vein. Intrastent kinking with resultant reduction in the TIPS diameter may cause hemodynamically significant stenosis and an increased portosystemic gradient [29]. Extending the shunt with additional stents and aligning them smoothly into a shallow arch can reduce kinks. Evaluation of MRI or CT studies before TIPS creation provides useful information to determine the existence of variant anatomy or the presence of accessory veins. Detailed examination of venograms is important to direct the needle from an appropriate hepatic vein into a corresponding portal vein branch.

Graft Materials of Covered Stents Lining stents with graft material to exclude hepatic parenchyma, bile, and flow dynamic factors from the TIPS lumen ideally addresses, treats, and prevents the biologic causes of shunt failure and therefore promotes improvement in shunt patency [30]. Many graft materials have been tested in TIPS, such as silicone, polycarbonate urethane, and polyethylene terephthalate. All exhibited equal or worse shunt patency when compared with bare stents, mainly because of the development of an inflammatory reaction [6, 31–33]. On the other hand, expandable PTFE covered stents have shown improved and durable shunt patency [30]. Histologic and venographic analyses of expandable PTFE TIPS in animals and humans have shown absence of an inflammatory reaction. Expandable PTFE prevents myelofibroblasts and extracellular collagen matrix from reaching the shunt lumen [34]. In addition, TIPS created with expandable PTFE-covered stents have shown better patency rates in patients with hypercoagulopathy and Budd-Chiari syndrome [35]. The Viatorr (Gore) is the commercially available expandable PTFE-covered stent

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Fig. 7—57-year-old woman after transjugular intrahepatic portosystemic shunt (TIPS) who presented with abnormal sonographic velocities and recurrent ascites. A and B, TIPS venograms to evaluate recurrent variceal bleeding show fracture of balloon-expandable stent. After angioplasty, TIPS was revised with covered stent.

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Cura et al. Fig. 8—Commercially available expandable polytetrafluoroethylene (PTFE)covered stent designed for transjugular intrahepatic portosystemic shunt (Viatorr, Gore) consists of two portions, a 2-cm-long uncovered segment on portal side (A) allowing free blood flow to side branches of portal vein through bare nitinol stent wires. Stent-graft portion (B) is covered with expandable PTFE on inside to cover from portal vein entry to hepatic vein ostium. Radiopaque gold ring identifies junction between covered and uncovered segments (arrows), and another radiopaque gold marker identifies proximal end of device (arrowhead).

designed for TIPS. It consists of two portions. A 2-cm-long noncovered segment in the portal vein allows free blood flow to side branches of the portal vein through the bare nitinol stent wires. The expandable PTFE portion of the covered stent covers the inside of the stent and is placed from the portal vein entry site along the length of the parenchymal tract as far as the hepatic vein ostium. In general, we try to use one endoprosthesis in which the covered segment will extend from the portal vein entry to the hep atocaval junction. In those cases in which the deployed stent is short in the hepatic vein end of the shunt, an additional stent is used to extend the TIPS to the hepatic vein– IVC confluence. The expandable PTFE is composed of three layers that are designed to permit endoluminal enothelization and to minimize fibrous connective tissue cell penetration. The overlapping three expandable PTFE layers are impermeable to liquid bile. A radiopaque gold ring marks the transition from the bare to the covered segment (Fig. 8). The nitinol skeleton of the stent has considerable radial strength that prevents recoiling after insertion. Most TIPS dysfunctions in TIPS created with expandable PTFE covered stents are related to technical errors or mechanical factors. As in bare-stent TIPS, a stent short at the hepatic venous end of the TIPS will likely result in hepatic vein stenosis (Fig. 9). Stent kinking at the portal vein end of the shunt may occur in TIPS as a result of peripheral portal vein punctures [29], and in Viatorr-covered stents may be seen at the junction between the covered and uncovered

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segments of the stent (Fig. 10). Finally, we have seen mid covered-stent stenosis after TIPS revision of a Wallstent TIPS with a Viatorr stent, a finding that may be related to infolding of the graft material (Fig. 11).

TIPS Revisions TIPS patients who present with recurrent signs and symptoms of portal hypertension as well as abnormal shunt velocities during screening sonography of the TIPS are referred for TIPS venography and hemodynamic analysis of the TIPS. Careful patient examination and TIPS venographic and hemodynamic findings will determine whether the shunt should be revised. After angioplasty of the stenotic segment or recanalization of the occluded shunt, failed bare-stent shunts can be revised with Viatorr covered stents. The covered portion of the covered stent must line the entire tract from the portal vein entry to the junction between the hepatic vein and

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B

Fig. 9—43-year-old man after transjugular intrahepatic portosystemic shunt (TIPS) creation with expandable polytetrafluoroethylene covered (Viatorr, Gore) stent presents with recurrent ascites. A and B, Shunt venograms of Viatorr covered stent TIPS show TIPS ending perpendicular to hepatic vein and causing functional hepatic vein stenosis (arrow, A). Final venogram (B) after revision with a Wallstent (Boston Scientific) showed no residual stenosis.



Causes of TIPS Dysfunction [39]. Because of the improved patency in Viatorr TIPS, frequent routine sonography may not be cost-effective for long-term surveillance of expandable PTFE-covered stents [40]. The number and frequency of sonographic examinations for detection of TIPS malfunction after their creation with a cov-

ered stent are yet to be determined in prospective trials.

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Conclusion Biologic and technical factors may predispose TIPS to shunt failure. The combination of improved technique and expandable PTFE

Fig. 10—49-year-old man with transjugular intrahepatic portosystemic shunt for refractory ascites. Venogram shows peripheral puncture of portal vein system resulted in kink and angulation of Viatorr (Gore) expandable polytetrafluoroethylene covered stent at portal vein end of shunt (arrow). Measured portosystemic gradient across shunt was 13 mm Hg.

the IVC to improve patency (Fig. 12). In those cases in which an occluded TIPS cannot be recanalized, a parallel TIPS can be created to decompress the portal venous system [36]. Sonography After Covered Shunt Placement Sonography is the screening tool for detecting early shunt dysfunction. It is performed soon after TIPS creation to obtain baseline velocity values [37]. However, an acoustic barrier may prevent examination of the shunt lumen when Doppler sonography is performed during the first days after covered stent implantation. This acoustic barrier is believed to be due to the trapping of air bubbles inside the graft. This usually resolves spontaneously during the first week after TIPS creation [38]. Then TIPS hemodynamics can be analyzed as in bare stents (Fig. 13). Real-time Doppler spectral analysis is used to evaluate portal vein and stent (proximal, middle, and distal segments) blood flow velocities. Doppler results are considered abnormal on the basis of one or a combina tion of the following: an absolute stent velocity < 50 or > 200 cm/s, spatial or temporal stent gradients > 50 cm/s, a portal vein velocity < 30 cm/s, or the presence of flow reversal in the portal vein distal to the shunt


Fig. 11—56-year-old man with transjugular intrahepatic portosystemic shunt (TIPS) for variceal bleeding and refractory ascites. A and B, TIPS venograms of shunt created with a Wallstent (Boston Scientific) show mid-TIPS stenosis (arrows, A). After angioplasty, Viatorr (Gore) stentgraft was deployed, covering stenotic segment to junction of hepatic vein and inferior vena cava (asterisk, B). C and D, Shunt venograms of TIPS created with a Wallstent and revised with Viatorr show mid-stentgraft stenosis (arrows, C) likely related to oversized covered stent with infolding of graft material that responded well to angioplasty.

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Fig. 12—62-year-old woman after transjugular intrahepatic portosystemic shunt (TIPS) who presented with recurrent variceal bleeding. A–C, Fluoroscopic images and venogram show chronic TIPS occlusion preventing access to lumen by jugular approach. Therefore, access to TIPS lumen was gained percutaneously with 21-gauge needle (asterisk, A) and 0.018-inch wire. Retrograde access to inferior vena cava was regained. After angioplasty, TIPS was revised with covered stent.

has significantly improved TIPS patency. The need for follow-up venography and secondary interventions has been reduced significantly as a result of improved shunt patency,

Fig. 13—63-year-old woman with portal hypertension after creation of trans jugular intrahepatic portosystemic shunt (TIPS). A, Sonogram obtained soon after TIPS creation with covered stent fails to reveal shunt lumen (S). B, Follow-up sonogram shows lumen in covered stent.

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This article is available for CME credit. See www.arrs.org for more information.


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