Treatment of Hemodialysis Access Rupture during PTA with Wallstent Implantation

Treatment of Hemodialysis Access Rupture during PTA with Wallstent Implantation

Treatment of Hemodialysis Access Rupture during PTA with Wallstent implantationi Alain C. Raynaud, MD Claude Y. Angel, MD Marc R. Sapoval, MD Bernar...

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Treatment of Hemodialysis Access Rupture during PTA with Wallstent

implantationi

Alain C. Raynaud, MD Claude Y. Angel, MD Marc R. Sapoval, MD Bernard Beyssen, MD Jean-Yves Pagny, MD Mario Auguste, MD

Index terms: Angioplasty, complications. Dialysis, shunt. Stents and pros. theses

JVIR 1998; 9:437-442 Abbreviation: PTA = percutaneous transluminal angioplasty

PURPOSE: To report the authors' experience in treatment of ruptures complicating percutaneous transluminal angioplasty (PTA) of hemodialysis access with implantation of a Wallstent. MATERIALS AND METHODS: Between January 1,1990, and October 1,1995, the authors performed 2,414 PTAs of angioaccesses. A severe rupture occurred in 40 (1.7%) of these procedures and was treated by means of stent placement. Wallstents were implanted in 37 of these ruptures. The angioaccesses comprised 22 grafts and 15 fistulas. The indications for stent placement were four isolated pseudoaneurysms and 33 cases of bleeding: 15 major leaks, five moderate leaks that persisted despite prolonged inflation at low pressure, seven leaks associated with greater than 50% residual stenosis, four leaks associated with pseudoaneurysm, and two leaks associated with both greater than 50%residual stenosis and pseudoaneurysm. Seventeen ruptures were located on a vein, 19 on the venous anastomosis of a graft, and one on a graft itself. RESULTS: Stent placement stopped the bleeding immediately in 28 cases and after prolonged inflation within the stent in four cases. Residual bleeding required implantation of a covered Cragg stent within the Wallstent in one case. A pseudoaneurysm was still visible at the end of the intervention in 11cases. Two complications occurred; one hematoma was drained surgically and one access occluded on day 2. Follow-up angiography showed a small pseudoaneurysm in only one patient with impaired platelet function. The primary and secondary patency of the angioaccesses were 48% and 86%at 1year, respectively. CONCLUSION: Wallstent implantation is very effective for both immediate and long-term treatment of rupture of angioaccess during PTA.

PERCUTANEOUS transluminal

IFrom the Alleray-Labrouste Clinic (A.C.R., C.Y.A., J.Y.P.), 64 m e Labrouste, 75015 Paris, France; and the Broussais Hospital (A.C.R., M.R.P., B.B., J.Y.P., M.A.), Paris, France. Received JUIY 25, 1997; revision requested September 4; revision received November 11; accepted November 14. Address correspondence to A.C.R.

o SCVIR,

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angioplasty (PTA) is an accepted method for the treatment of failing hemodialysis access. In our experience, rupture is the most frequent significant complication during such a procedure. Minor rupturesare frequent; they spontaneously close 01. are easily treated with prolonged low-pressure inflation of the balloon (1) and do not have any consequences. In cases of moderate rupture, the leakage is similar to minor

ruptures but has consequences: (a) either the bleeding cannot be stopped and jeopardizes the access life or (b) it can be stopped but may lead to the development of a pseudoaneurysm (2) or the persistence of an extrinsic stenosis due to compression by the hematoma, causing failure of the angioplast~. Larger ruptures have a poor prognosis. They require immediate stoppage of the bleeding by manual compression or prolonged inflation

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of the balloon until complete thrombosis of the access occurs. In case of persistent major rupture, salvage by surgical revision is very difficult and often not attempted because of the hematoma surrounding the access and because of the access thrombosis resulting from prolonged balloon inflation. Therefore, such ruptures frequently lead to access loss (2-4). We report the immediate and long-term results of Wallstent placement for treatment of venous and graft rupture after balloon angioplasty of hemodialysis access.

las. In the latter case, six ruptures were located on the cephalic arch. Our technique for PTA of hemodialysis access includes the use of a 5-7-F sheath according to balloon catheter size. The balloon used was of the same diameter or 1 mm larger than the access. Balloon catheters used were Ultrathin and BlueMax (Medi-tech/Boston Scientific, Watertown, MA) and Smash (Schneider, Bulach, Switzerland). Stenoses located at the venous anastomosis of grafts were dilated with a 7-mm, noncompliant balloon. However, for stenoses located immediately downstream from the anastomosis, wider balloons may be used according to vein diameter. MATERIALS AND METHODS Balloons were progressively inflated under pressure gauge monitoring to Between January 1, 1990, and the pressure required to obtain the October 1, 1995, we performed 2,414 PTAs of angioaccesses (50.3% complete disappearance of the waist on the balloon. When necessary, in men and 49.7% in women), compressure as high as 25 atm could be prising 2,066 simple PTAs and 348 reached. We did not routinely give performed during declotting (289 any heparin to the patient during after local fibrinolysis with or withsuch a procedure. Immediately after out thromboaspiration and 59 after the deflation of the balloon, an anthromboaspiration alone). Severe giogram was obtained through the ruptures occurred in 40 (1.7%)of side port of the sheath, with a guide these procedures and were treated wire remaining in place through the by means of stent placement. The lesion. The diagnosis of rupture was stents implanted were Wallstents made based on the angiogram. In (Schneider, Bulach, Switzerland) in cases of active bleeding, it showed 37 cases, covered Cragg (Mintech, extravasation of contrast material La Ciotat, France) stents in two spreading into the soft tissues. In cases, and a Palmaz (Johnson & cases of pseudoaneurysm, this exJohnson), stent in one case. travasation was confined within the This report is focused only on the aneurysm. We have never at37 patients treated with Wallstent tempted PTA on infected angioacimplantation. Thirty-two ruptures cess or within 4 weeks of surgical occurred during simple PTA and access creation or revision. Therethe other five occurred during perfore, these were never the reason cutaneous declotting. Ruptures ocfor rupture. curred in 22 arteriovenous grafts The maximal inflation pressure and in 15 arteriovenous fistulas in of the balloon before rupture was 12 men and 25 women (mean age, lower than 10 bars in 15 cases and 58 years 2 11). equal to or higher in 22 cases. In 10 In the graft group, 19 ruptures cases, the pressure reached during were located at the venous anastoPTA was very high, ranging from mosis, one on the graft itself, and 15 to 23 bars. two downstream of it. Three of the Four ruptures were isolated 22 arteriovenous graft were loop at pseudoaneurysms not associated the elbow; the remaining 19 were with active bleeding. In these four straight (three at the forearm, 16 at cases, stents were implanted at the same time as the PTA to avoid furthe upper arm). ther enlargement of the pseudoanIn the fistula group, six ruptures occurred in Brescia-Cimino, three in eurysm. A greater than 50% residual stenosis was another reason for basilic, and nine in cephalic fistu-

I

stent placement in one of these four cases. In the other 33 cases, ruptures were associated with bleeding into the surrounding soft tissue. Major leaks were characterized by very fast enlargement of the hematoma with rapid tissue swelling. Nearly all the contrast material injected during angiography passed through the leak, and the access beyond the rupture site was not, or was poorly, opacified. Such major leaks requiring emergency treatment occurred in 15 of our cases (Fig 1). When such a major leakage was identified, the balloon catheter was immediately slid over the guide wire and the balloon was inflated at low pressure, either upstream of the rupture or at the same level to stop the bleeding. Afterward, the stent was prepared. The balloon was then deflated and the arterial anastomosis manually compressed, and the stent was implanted as quickly as possible. When the leak of contrast material was moderate, the balloon was repositioned at the rupture site and then inflated at low pressure for 3-10 minutes. Such a maneuver was often sufficient to stop the bleeding and could be repeated in case of failure. Eighteen stents were implanted in such moderate leaks: five leaks continued to bleed despite repeated prolonged inflation, seven leaks were associated with greater than 50% residual stenosis due to localized dissection or to compression by the hematoma, four leaks were associated with pseudoaneurysm, and two leaks were associated with both greater than 50% residual stenosis and pseudoaneurysm. Forty stents were implanted. Their mean unconstrained diameter was 8 mm ? 0.78 (from 7 to 10 mm). A single Wallstent was implanted in 35 accesses. In one patient, three Wallstents were necessary to cover the lesion entirely. In the last patient, a covered Cragg stent was implanted through a Wallstent. Only one stent was implanted at the elbow crease. An angiogram was obtained after the procedure to evaluate the pa-

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Figure 1. (a)Stenosis of the venous anastomosis of a straight hemodialysis access graft. (b)Major rupture identified on the angiogram obtained immediately after PTA with a 7-mm balloon. ( c )After implantation of a Wallstent (10 mm in diameter) and 5-minute balloon inflation within the stent a t low pressure, the access appears normally patent without any residual leak. (dl Follow-up angiogram 4 months after stent placement shows moderate hyperplasia within the stent and immediately downstream of it. The access is patent, without stenosis and without pseudoaneurysm. Note the expansion of the Wallstent to its nominal diameter (10 mm) within the venous part of the stented zone.

tency of the access by measuring the residual stenosis, to detect any residual pseudoaneurysm, and to establish the disappearance of any residual leaking. All procedures were performed on an outpatient basis. Patients were discharged approximately 2 hours after the examination after careful clinical examination of the access and of the upper limb. However, one patient was admitted on the day after the procedure for surgical evacuation of a hematoma. Follow-up was accomplished ac-

cording to dialysis records. A follow-up angiogram was obtained in 26 of 36 patients with an access patent 1 month after the procedure. Life-time analysis was performed with use of the Kaplan-Meier method. Primary patency was defined as the time during which the access was used for hemodialysis until the access required a further intervention (surgical or radiological). Secondary patency was defined as the time during which the access was used after the procedure without requiring any surgical intervention.

Patients were considered as lost to follow-up in cases of renal transplantation and in cases of death (not linked to a procedure) with a patent access.

RESULTS Thirty-three patients had bleeding at the time of stent placement. Wallstent implantation immediately stopped the leakage in 28 patients (85%),and prolonged inflation at low pressure was necessary in four patients (12%). In one patient (3%),

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Primary and Secondary Patency Following Stent Placement for Ruptures Interval (mo) Primary Patency 0-3 3 4 6-12 12+18 Secondary Patency 0+3 3 4 6+12 12-18

-

Patients

Access Failure

37 32 24 11

5 7 6 7

37 36 32 19

1 3 1 3

End of Follow-up*

Patency Rate (%) Interval

Cumulative

SE (%)

0 1 7 0

86 78 71 36

100 86 67 47

0 5 7 10

0 1 12 6

97 92 96 81

100 97 89 86

0 3 5 7

Note.-SE = standard error. * Including short-term participation, renal transplantation and patient death. No patients were lost to follow-up.

a major leak decreased, but remained, after stent placement and prolonged inflations were ineffective. A covered Cragg stent was implanted within the Wallstent. One prolonged inflation into the Cragg stent was necessary to close the breach. In patients with acute pseudoaneurysm, stent placement immediately decreased the size of the pseudoaneurysm, which was reduced to less than a 3-mm-thick stain of contrast material. However, stent placement completely closed the aneurysm in only one of 10 patients. In two of the 15 patients with major rupture, a small pseudoaneurysm appeared outside the endoprosthesis after stoppage of the bleeding by stent placement. Therefore, a small pseudoaneurysm was still visible at the end of the procedure in 11patients. Two com~licationsoccurred: one was acute thrombosis of a poorquality cephalic fistula on day 2, leading to the loss of the access; and another patient had a large hematoma that required surgical drainage. Among the 11patients with a pseudoaneurysm still visible a t the end of the procedure, the first follow-up angiograms, performed a t 7.6 months + 7.8, showed complete disappearance of the pseudoaneurysm in nine patients. In a 10th patient with severe impairment of

Figure 2. Primary and secondary patency following stent placement for ruptures.

platelet function, the pseudoaneurysm remained patent but did not increase in size within 9 months of follow-up. In the 11th patient, the fistula occluded 2 days after stent placement. Primary patency of the angioaccess after stent placement for rupture (Table, Fig 2) was 67% 2 8% at 6 months and 48% + 10% a t 12 months. Secondary patency (Table, Fig 2) was 89% + 5% a t 6 months and 86% + 7.5% a t 12 months.

1 DISCUSSION The most frequent complication of angioaccess for hemodialysis is the development of stenosis, which leads to thrombosis and the loss of the access when not treated. PTA has become the treatment of choice

for most of these stenoses (2-8). thereby, increasing their life-time. Ruptures are one of the most frequent significant complications of PTA of angioaccess. In our series, this complication occurred in 1.7% of PTA of angioaccess, compared to the 8% incidence reported by Quinn et a1 (l), 20% reported by TurmelRodrigues et a1 (2), and 2.1% reported by Beathard et al (3). However. all three included some minor ruptures in their series. In our experience, ruptures never occurred during a dilation when the encroachment on the balloon d i s a ~ peared progressively with inflation pressure rise. However, ruptures should be suspected when the waist on the balloon disappeared more suddenlv than is usual. and when the p a i i worsened with balloon de-

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flation (4). In our experience, ruptures occurred more frequently in women (68%) than in men (32%), while 49.7% of the PTAs of angioaccess were performed in women. Certain sites, especially the cephalic arch, appeared more proneto rupture. Sixteen percent of the severe ruptures occurred a t the cephalic arch, whereas the percentage of PTA performed on the cephalic arch was far lower. Most ruptures in our series were minor, with a small leak of contrast material. Ruptures may close very quickly and spontaneously (1,3). When ruptures remain unidentified, they may be responsible for some failures of PTA (compression by a small localized hematoma being responsible for a recoiling stenosis) and. in some cases. the delayed appearance of a pseudoaneurysm a t the site of the dilatation. When the leak is identified, these small ruptures are usually easily treated by prolonged, low-pressure inflation of the balloon, possibly associated, in the infrequent cases in which we had administered heparin, with injection of protamin. Complementary treatment is needed in a few cases: for examole. when ruptures do not close after repeated prolonged inflation, despite their small size; when they are associated with a pseudoaneurysm (prolonged inflation is ineffective in such lesions, which frequently will gradually grow when a stent has not been placed and then will require specific treatment); and when they are associated with obstructive localized dissection. Prolonged inflation may treat the leak but the dissection and the residual stenosis usually remain, leading to failure of the PTA. Major ruptures are less frequent and require immediate stoppage of the bleeding. This is very easily achieved when a guide wire is still in place through the lesion. It is very quick and simple to replace the balloon catheter upstream or at the leak site, and to inflate it a t low pressure. When the guide wire has been withdrawn, it can be very difficult, and L

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sometimes impossible, to reposition it through the lesion. We, therefore, strongly recommend leaving the guide wire in place for the angiogram obtained immediately after deflation of the balloon. The stent is prepared for implantation once the balloon is inflated. The smallest implanted stent was 7 mm in diameter and we never had to place a stent in very small vessels. However, in such cases, we would not have contraindicated stent placement because ruptures require urgent treatment. In our experience, use of uncovered self-expandable Wallstents is a very effective method to stop bleeding at angioaccess rupture sites. The mechanisms by which stent placement successfully treats the rupture remain speculative, but we believe that the following factors may be involved: (i) Ruptures are associated with a stenosis created by the hematoma itself. Stent placement immediately removes the stenosis and, therefore, decreases the pressure into the angioaccess. This is clearly felt by palpation during such events; the access immediately flattens after stent release. The drop in pressure immediately decreases the leak and facilitates thrombosis. (ii) An intimal flap floating into the lumen of the access may, during stent deployment, be flattened against the vessel wall and form a fortuitous plug. (iii) The breach in the access wall can be oblique or tortuous. In such cases, stent placement reapplies both sides of the breach closing the leak. (iv) Wallstents are somewhat thrombogenic, as are all metallic foreign bodies. This favors occlusion of the breach. Effectiveness of Wallstent implantation to prevent pseudoaneurysm expansion is difficult to assess. In our experience, before January 1990, we did not implant stents, and the development of subsequent pseudoaneurysms after ruptures was frequent. In this series, after treatment of ruptures by stent placement, a pseudoaneurysm was identified only once on a follow-up angiogram, and it occurred in a patient with severe impairment

of platelet function, which had probably facilitated its development. However, efficiency of Wallstent implantation in that indication needs to be confirmed. Wallstents have been reported to be effective in the treatment of stenoses that cannot be adequately treated by PTA alone (9). This is confirmed by our experience. Our series includes 59.5% grafts, 16.2% Brescia-Cimino fistulas, and 24% proximal fistulas. The 1-year primary and secondary patency rates were 48% -t 10% and 86% + 7.5%, respectively. Such primary and secondary patencies are consistent with data of the literature, which are variable, ranging from approximately 10% (1)to more than 40% (2,101 and from approximately 70% (1)to more than 90% (I), respectively. Many factors may explain such discrepancies: the type of access (2,11), the policy of access thrombosis prevention ( l l ) , the sites of stenoses (3), the technique of dilation and especially the location of stents (21, the number of PTAs performed on the same site (101, and so forth. Among the bare stents, the Wallstent is one of the most appropriate in cases of rupture: (i) It is self-expandable and can be implanted without having to inflate a balloon at the rupture site; this is probably an advantage. If prolonged lowpressure balloon inflation may stop moderate leaks, to inflate a balloon at the pressure required to expand a stent can widen the breach. (ii) It is flexible and can, therefore, easily be applied against the access wall, even in the case of a tortuous course or of disparities of caliber. (iii) It is a narrow meshed stent that favors thrombosis of the breach. In cases of rupture, the use of a covered stent seems better. However, such stents are not currently available and their use in angioaccess has been somewhat disappointing (12). Nevertheless, in one of our patients, the leak persisted after Wallstent implantation, despite two prolonged inflations. Placement of a covered Cragg stent in the Wallstent eventually stopped the bleed-

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ing. The use of a covered stent probably saved the access in this patient.

I CONCLUSION We recommend having self-expandable Wallstents available when PTA is attempted on hemodialysis access because, when severe rupture occurs during such a procedure, implantation of a self-expandable stent usually saves the access. It stops the bleeding in most cases, successfully treats the residual stenosis due to parietal damage and to compression by the hematoma, and avoids the appearance and development of pseudoaneurysms. References 1. Quinn SF, Schuman ES, Demlow TA, et al. Percutaneous transluminal angioplasty versus endovascular stent placement in the treatment of venous stenoses in patients undergoing hemodialysis: intermediate results. JVIR 1995; 6:851-855. 2. Turmel-Rodrigues L, Pengloan J , Blanchier D, et al. Insufficient dial-

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ysis shunts: improved long-term patency rates with close hemodynamic monitoring, repeated percutaneous balloon angioplasty and stent placement. Radiology 1993; 187:273-278. Beathard GA. Percutaneous transvenous angioplasty in the treatment of vascular access stenosis. Kidney Int 1992; 42:1390-1397. Melki PS, Pelage J-P, Boyer J-C, Legendre C, Lacombe M, Moreau J-F. Vascular rupture complicating transluminal angioplasty applied on a failed dialysis vascular access in a patient under chronic steroid therapy. Eur J Radiol 1997; 7:313-315. Cada E, Karnel F, Mayer G, Langle F, Schurawitzki H, Graft H. Percutaneous transluminal angioplasty of failing arteriovenous dialysis fistulae. Nephrol Dial Transplant 1989; 4:57-61. Gaux JC, Bourquelot P, Raynaud A, Seurot M, Cattan S. Percutaneous transluminal angioplasty of stenotic lesions in dialysis vascular accesses. Eur J Radiol 1983; 3:189-193. Glanz S, Gordon DH, Butt KM, Hong J , Lipkowitz GS. The role of percutaneous angioplasty in the management of chronic hemodialysis fistulas. Ann Surg 1987; 206:777-781.

8. Gmelin E, Winterhoff R, Rinast E. Insufficient hemodialysis access fistulas: late results of treatment with percutaneous balloon angioplasty. Radiology 1989; 171:657660. 9. Vonverk D, Guenther RW, Mann H, et al. Venous stenosis and occlusion in hemodialysis shunts: follow-up results of stent placement in 65 patients. Radiology 1995; 195: 140-146. 10. Kanterman RY, Vesely TM, Pilgram TK, Guy BW, Windus DW, Picus D. Dialysis access grafts: anatomic location of venous stenosis and results of angioplasty. Radiology 1995; 195:135-139. 11. Safa AA, Valji K, Roberts AC, Ziegler TW, Hye RJ, Oglevie SB. Detection and treatment of dysfunctional hemodialysis access grafts: effect of a surveillance program on graft patency and the incidence of thrombosis. Radiology 1996; 199: 653-657. 12. Sapoval MR, Turmel-Rodrigues LA, Raynaud AC, Bourquelot P, Rodrigue H, G a w JC. Cragg covered stents in hemodialysis access: initial and midterm results. JVIR 1996; 7:335-342.