Annals of Vascular Surgery
Volume 24, Issue 8 , Pages 1005-1014, November 2010

Treatment of Perigraft Seroma in Expanded Polytetrafluoroethylene Grafts by Sequential Fibrin Sealing of the Outer Graft Surface

  • Juergen Zanow

      Affiliations

    • Department of General, Visceral and Vascular Surgery, Friedrich-Schiller-University Jena, Jena, Germany
    • Corresponding Author InformationCorrespondence to: Juergen Zanow, Department of General, Visceral and Vascular Surgery, Friedrich-Schiller-University Jena, Germany, 07747 Jena, Erlanger Allee 101
  • ,
  • Ulf Kruger

      Affiliations

    • Department of Vascular Surgery, Queen Elisabeth Hospital Berlin, Berlin, Germany
  • ,
  • Utz Settmacher

      Affiliations

    • Department of General, Visceral and Vascular Surgery, Friedrich-Schiller-University Jena, Jena, Germany
  • ,
  • Hans Scholz

      Affiliations

    • Department of Vascular Surgery, Queen Elisabeth Hospital Berlin, Berlin, Germany

published online 27 August 2010.

Article Outline

Background

The recommended standard for treatment of perigraft seroma (PS) is the graft removal and the reconstruction using an alternative prosthesis. We assumed that a fibrin sealing of the outer surface of expanded polytetrafluoroethylene (ePTFE) grafts would prevent leakage and used this technique in the treatment and prevention of PS.

Methods

Over a 10-year period, 24 patients were treated for PS after subcutaneous implantation of ePTFE grafts (14 arterial bypasses and 10 arteriovenous grafts). Affected graft segments were temporarily removed and underwent sequential fibrin sealing technique before reimplantation. In addition, an in vitro experiment was carried out to demonstrate the efficacy of fibrin sealing to prevent leakage through the ePTFE graft wall, after its hydrophobic barrier was destroyed by filling with saline solution under pressure.

Results

A cure of PS was observed in 20 patients (84%) at a follow-up period of 37 ± 18 months. A later graft infection was not seen in any patient. The patency rate of reconstructed grafts appears to be unaffected. In the performed experiment we have demonstrated an elimination of leakage through the graft wall by the fibrin sealing technique.

Conclusions

Sequential fibrin sealing of the outer surface is an effective way to treat PS in ePTFE grafts. However, failure of this treatment cannot be precluded. Further studies are necessary that may provide further insights into the causes and best treatment of PS and the possibly important role of PS in the aneurysm enlargement after complete endovascular exclusion with ePTFE endografts.

 

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Introduction 

Perigraft seroma (PS) is a complication that infrequently occurs after implantation of vascular grafts and has been reported in the published data since the early 1980s. Most of these cases were because of the use of Dacron and expanded polytetrafluoroethylene (ePTFE) grafts. PS is characterized by a persistent accumulation of transparent, sterile, and ultrafiltrated fluid, confined within a fibrous pseudomembrane surrounding a vascular prosthesis.1, 2, 3 In PS, the graft is not incorporated into the surrounding tissue. Several late complications have been described for PS: graft thrombosis, skin erosion, secondary graft infection, anastomotic aneurysm formation, and anastomotic bleeding. A graft implanted as arteriovenous (AV) access for hemodialysis should not be punctured in the presence of PS.

The current knowledge about this complication is incomplete. There are neither comprehensive data about the incidence itself nor validated models that may explain the mechanisms underlying PS. It is uncertain whether PS is caused by the same mechanisms in Dacron and ePTFE grafts. Recommendations for the treatment of PS were established on the basis of studies, which included only a few cases. Indeed, they were found to be of little help because of their inconsistency.1, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20

The definition of the porosity of Dacron grafts is based on its water integral permeability, which cannot be measured reliably in hydrophobic ePTFE grafts. The latter are characterized by the internodal distance which corresponds to porosity.21 Several studies demonstrated an effective sealant to reduce leakage of Dacron.22 and high-porosity ePTFE23 grafts.

We assumed that an effective sealing at the external surface by sequential application of fibrin glue components would prevent leakage and result in a lower incident of PS in ePTFE grafts. Since 1996, we have been performing a sequential fibrin sealing of the outer surface in ePTFE grafts for AV accesses for hemodialysis immediately before the implantation. Using fibrin sealing routinely, we noticed a reduced incidence of PS and a faster first cannulation of the access, as compared with regular ePTFE grafts. Since then, fibrin sealing has been used in the treatment of PS after implantation of ePTFE grafts.

In this report, we describe our technique of fibrin sealing and report results in the treatment of PS after implantation of ePTFE E grafts. In addition, an in vitro experiment was carried out to demonstrate the efficacy of fibrin sealing to prevent leakage through the graft wall.

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Methods 

Between 1998 and 2008, a total of 24 patients with PS after implantation of an ePTFE graft were treated by the fibrin sealing technique. Data were retrospectively retrieved from the hospital charts.

The diagnosis of PS was based on the typical clinical manifestation of fluid accumulation around a subcutaneously placed ePTFE graft (Fig. 1). Inflammation of the cutis or subcutaneous tissue above the graft was not or very mildly present. The diagnosis was confirmed by ultrasound scan. A preoperative puncture of the fluid accumulation and the microbiological investigation of the fluid were not performed.

We interpreted the tissue reaction after ePTFE graft implantation as a bacterial infection in the case of marked inflammation, fever, leukocytosis, or increased levels of the C-reactive protein or in case of secondary wound infection. The complete graft was removed in these patients.

The indication for the revision of grafts was seen for acute development of PS and an ongoing drainage of serous fluid through the fresh wound. In these cases, a wound seroma or lymphatic leak was excluded intraoperatively by a typical finding of sweating at ePTFE graft surface. For chronic PS (beyond the 30th postimplantation day) with moderate fluid accumulation, patients were advised to wait for 3-4 weeks so as to promote spontaneous remission and exclude a graft infection in the clinical course. In cases of a marked fluid accumulation, we recommended an early revision after diagnosis, especially when anastomotic regions were involved.

Operative revision started with exploration of the graft in the incorporated part, 3 cm distally, at both ends of the affected segment, respectively, at the vascular anastomosis. The affected segment was identified by clinical presentation and preoperative ultrasonographic scan. The anastomosed vessel was dissected whenever an anastomotic region was involved.

The diagnosis of PS was intraoperatively confirmed by the typical morphological characteristics—a cavity surrounded the prosthesis, which was covered with shiny endothelium and filled with clear fluid and hyaline material, and an often visible sweating at the graft surface (Fig. 2). Microbiological samples were taken in all cases.

After exposure, the graft was clamped and transacted, and the involved segment was removed from the subcutaneous tunnel. In all cases of acute PS, the graft was removed completely. Periprosthetic fluid and hyaline material were removed. The outer surface of the explanted graft was dried and carefully cleared of any remaining parts of hyaline material. In case of helix or ring-supported prostheses, the helix was only partially removed, leaving the segment at the joint region intact. Thereafter, fibrin sealing of the temporarily explanted graft was performed, as described in the following paragraphs. Finally, the sealed graft was placed in a new subcutaneous tunnel and reanastomosed. A destruction of the applied fibrin layer by forced grasping and other manipulations was carefully avoided. A small volume of fibrin glue at the anastomotic region after finishing the anastomosis was applied. The wound closure was performed without placement of a drain.

The fibrin sealing technique consists of a coating of the external graft surface by sequential application of both components of fibrin glue. First, the fibrinogen was applied evenly to the outer surface and pressed into the pores of the ePTFE graft by a gentle massage. Then the graft surface was covered with the thrombin component. For treatment of PS 1-4 mL of fibrin glue was used, whereas for prevention of PS in grafts used as AV access, a volume of 0.5 mL proved to be sufficient. The Beriplast Combi Set (ZLB Behring/Nycomed Pharma, Hattersheim, Germany) was applied as fibrin glue kit, which consists of two components: component I consists of 90 mg human fibrinogen and 60 units factor XIII in 1 mL, and component II contains 500 units of human thrombin per mL. Stable fibrin nets are formed when mixing both components.

Statistical Analysis 

All statistical analysis was performed with a standard software program (SPSS Statistics 13, Chicago, IL). Values are expressed as mean ± standard error or observed range. Chi-Square test was used for data comparison. Statistical significance was assumed at p < 0.05. Survival and access patency rates were calculated with life table method (Kaplan–Meier).

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Results 

Clinical Study 

During the study period, we used ePTFE grafts as AV vascular access in 1,056 cases, in which 91% were upper arm shunts. Fibrin sealing for prevention of PS was routinely performed before implantation of ePTFE grafts as AV shunt in all these cases. An ePTFE graft was used as arterial bypass in 902 patients. The incidence of PS excluding referred cases was 0.6% for AV grafts (coated with 0.5 mL fibrin glue before subcutaneous placement) and 1.6% for arterial bypasses (untreated grafts) (p < 0.05).

The fibrin sealing technique was applied for the treatment of PS after implantation of ePTFE grafts as AV access in 10 patients (six own cases and four referred cases) and as subcutaneously placed arterial bypass in 14 patients.

The mean age of patients was 67 ± 12 (range, 28-84) years and did not differ between patients receiving an arterial bypass or an AV graft. Of the 24 patients, 11 were female and 13 were male. Specific characteristics regarding comorbid conditions, previous vascular procedures, nutrition state, routine laboratory parameters, anticoagulation regimen, or the performed operative procedure were not identified in patients with PS. The revision for PS was performed 119 ± 86 days after the primary procedure. An acute PS was treated in seven cases 11 ± 4 days after the implantation of ePTFE grafts, including two referred patients. Fourteen patients with arterial bypass and three patients with AV graft underwent fibrin sealing for chronic PS at an average of 159 ± 112 days after the primary procedure.

A previous (n = 11) or subsequent (n = 5) implantation of an ePTFE graft at different (n = 12) or the same limb (n = 4) was recorded in 14 patients without additional history of PS. Detailed information about patients, ePTFE prostheses affected by PS, and outcome after fibrin sealing are presented in Table I. An increased incidence of PS regarding different types of arterial bypasses and AV grafts was not found. In addition, an advice for a higher risk of PS in dependence of graft wall types (standard or thin wall) and brands of ePTFE grafts was not seen. However, we observed acute PS only after implantation of ePTFE grafts as AV shunts.

Table I. Characteristics of patients, grafts, and outcome after fibrin sealing
NumberTime to revision (days)Other use of ePTFE graftsGraft; manufacturerGraft positionAffected segmentCure of PSOutcome
172LaterHybrid PTFE, thin wall, 6 mm; AtriumFemoro-popliteal bypassDistal 2/3YesDead, graft patent at 41 months
2126NoFlex Thinwall, 8-5 mm; Bard-ImpraFemoro-tibial bypassDistal 1/4YesDead, graft occluded at 36 months
374EarlierHybrid PTFE, thin wall, 6 mm; AtriumFemoro-popliteal bypassDistal 1/3NoDead, graft replaced at 44 daysa
414NoVenaflo®, carbon, 4-7 mm; Bard-ImpraAxillary-axillary chest loop AV graftProximal 1/4YesDead, graft patent at 15 months
5957NoCarboflo® Flex, 8 mm; Bard-ImpraAxillo-femoral bypassProximal 1/3YesDead, graft patent at 28 months
62EarlierFlex Thinwall, 5 mm; Bard-ImpraBrachial artery-cephalic vein bridge AV graftEntire graftYesDead, graft occluded at 14 months
7144NoFlex Thinwall, 5 mm; Bard-ImpraBrachial artery-cephalic vein bridge AV graftEntire graftYesDead, graft patent at 23 months
871EarlierVenaflo®, carbon, 4-7 mm; Bard-ImpraFemoral-femoral loop AV graftProximal 2/3YesDead, graft patent at 34 months
9104NoHybrid PTFE, standard wall, 6 mm; AtriumFemoro-popliteal bypassDistal 1/2YesAlive, graft occluded at 51 months
1096LaterHybrid PTFE, standard wall, 6 mm; AtriumFemoro-popliteal bypassProximal 1/3YesDead, graft patent at 37 months
11168LaterFlex Thinwall, 8-5 mm; Bard-ImpraFemoro-tibial bypassDistal 2/3YesDead, graft patent at 8 months
1215Earlier and laterVenaflo®, carbon, 4-7 mm; Bard-ImpraAxillary-axillary looped upper arm AV graftEntire graftYesAlive, graft occluded at 32 months
13202NoFlex Thinwall, 8-5 mm; Bard-ImpraFemoro-popliteal bypassDistal 1/3NoAlive, graft replaced after 6 daysb
14139NoAvanta VS®, thin wall, 6 mm; AtriumFemoro-popliteal bypassProximal 1/2YesDead, graft patent at 17 months
152EarlierVenaflo®, carbon, 4-7 mm; Bard-ImpraFemoral-femoral loop AV graftEntire graftNoDead, graft removed immediatelyc
1658EarlierVenaflo®, carbon, 4-7 mm; Bard-ImpraAxillary-axillary loop AV graftProximal 1/3YesAlive, graft patent after thrombectomy at 46 months
175EarlierVenaflo®, carbon, 4-7 mm; Bard-ImpraAxillary-axillary loop AV graftProximal 2/3YesDead, graft patent at 14 months
1822NoVenaflo®, carbon, 4-7 mm; Bard-ImpraBrachial-axillary straight AV graftProximal 1/3YesDead, graft patent at 21 months
1989EarlierFlex Thinwall, 8-5 mm; Bard-ImpraFemoro-tibial bypassProximal 1/2YesAlive, graft patent at 37 months
208EarlierVenaflo, carbon, 4-7 mm; Bard-ImpraAxillary-axillary loop AV graftProximal 1/3YesAlive, graft patent at 32 months
21121Earlier and laterFlex EndTaper, Carbon, 8-5 mm; Bard-ImpraFemoro-popliteal bypassDistal 1/3NoAlive, graft replaced at 22 daysd
22217NoFlex EndTaper, Carbon, 8-5 mm; Bard-ImpraFemoro-popliteal bypassDistal 2/3YesAlive, graft patent at 29 months
2343NoFlex EndTaper, Carbon, 8-5 mm; Bard-ImpraFemoro-tibial bypassDistal 1/3YesAlive, graft occluded at 9 months
2467NoPropanten, thin walled stretch, 6 mm; GoreFemoro-peroneal bypassProximal 1/3YesAlive, graft patent at 14 months

aReplacement by a SEALPTFE® graft resulted in recurrent PS at the third month; repeated replacement by an ePTFE graft that was sealed with 2 mL fibrin glue and placed in the anatomical route; patent graft without PS over 62 months.

bReplacement by a SEALPTFE® graft 6 days after failed fibrin sealing; graft occlusion after 7 months with mild recurrent PS; no revision.

cA massive transudation through the AV graft was observed intraoperatively even after fibrin sealing, which immediately forced a complete removal of the graft; implantation of a SEALPTFE® graft at the contralateral leg at day 9; graft occlusion without recurrent PS after 14 months; patent after graft revision until death at 17 months.

dReplacement of the affected graft segment by arm vein as composite graft; degeneration and occlusion of the venous graft segment after 11 months without PS.

In four patients, the entire AV graft was affected by PS. The proximal (arterial) segment of the graft was involved at different lengths in the other six patients with AV graft. The graft was, segment by segment, incorporated into the subcutaneous tissue in all patients who received an arterial ePTFE bypass. The length of the segment involved in PS varied from one-fourth to two-thirds of the total graft length.

Microbiological culture of the intraoperatively obtained material was sterile in all cases and a later graft infection was not seen in any patient after fibrin sealing of the affected grafts. An early revision of a hematoma was necessary in one patient after revision procedure. Other complications did not occur.

The follow-up period after fibrin sealing for PS was 37 ± 18 months. Fourteen patients died 31 ± 19 months after the fibrin sealing procedure. None of the deaths was related to previous bypass or revision procedures. The graft was patent at the time of death in nine of the 14 cases.

A cure by the fibrin sealing technique was defined as long-term maintenance of the patent graft without recurrence of PS. Successful outcome after fibrin sealing was observed in 20 patients (84%). The cumulative patency of all grafts after a successful application of fibrin sealing technique was 94 ± 6% at 12 months and 71% ± 18% at 36 months. Here, all AV shunts were punctured for hemodialysis from 2 weeks after revision.

A failure to cure the PS was seen in four cases, which deserve a more detailed analysis as it may shed some light on the problems associated with PS treatment (Table 1). In these patients, the ePTFE graft was replaced by vein segment in one case and by a commercially available ePTFE graft with an external surface coated with gelatin (SEALPTFE®, Vascutek, Glasgow, UK) in three cases. A recurrent PS was seen in two patients, which led to removal or observation of the SEALPTFE® graft in both. The remaining SEALPTFE® grafts occluded 7 and 11 months after implantation.

Experimental Study 

An experiment was performed to evaluate the effect of the fibrin sealing technique on the hydrophobic state of ePTFE grafts, namely, prevention of fluid leakage through the graft wall.

A normal-walled ePTFE graft (Venaflo®, Bard-Impra, Tempe, AZ) was wrapped with a plastic wrap over half its length. The unwrapped segment was sealed with 0.5 mL fibrin glue by the fibrin sealing technique, as described earlier, and the wrap was removed. One end of the prosthesis was occluded and the graft was filled with isotonic saline solution under pressure. The hydrophobic barrier of the ePTFE prosthesis was destroyed in the nontreated segment and a fluid transudation with the typical wetting effect was observed. However, in the coated segment no fluid leakage was evident, even when the pressure was raised to 300 mm Hg (Fig. 3).

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  • Fig. 3 

    Fibrin-coated outer surface with penetration of applied fibrin glue into internodular spaces is demonstrated histologically in a transverse section of an ePTFE graft by hematoxylin and eosin stain.

In the second experiment, the hydrophobic barrier of an entire ePTFE graft was destroyed by filling it with saline solution at a pressure of approximately 220 mm Hg. Thereafter, half the length of the graft was dried and treated by fibrin sealing with 0.5 mL fibrin glue. A massive fluid transudation was observed in the native segment starting at a pressure of 90 mm Hg. The coated segment, however, remained without any transudation at a pressure of up to 300 mm Hg.

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Discussion 

In this study, the treatment of PS in 24 patients after the implantation of ePTFE grafts is described. To our knowledge, it represents the largest number of cases of this complication reported from a single centre.

PSs occur rarely. Therefore, most publications are case reports. Blumenberg et al.1 analyzed 279 cases of PS by analysis from submitted questionnaires. An ePTFE graft was used in 34% of the reported cases. Borrero et al.11 reported the incidence of 0.5% for 1,674 subcutaneously placed ePTFE grafts, whereas Paes et al.5 determined the incidence of PS as being 0.8% for PTFE grafts. Extra-anatomic bypasses represented 76% of the cases. The study by Dauria et al.20 is the only report about incidence of PS after AV graft placement that we could find. They observed 10 cases with PS after placement of 535 AV grafts, representing an overall incidence of 1.7%. The incidence was significantly higher for upper arm grafts (5.3%) compared with forearm grafts (0.5%).

Mediastinal PS has been described in children after modified Blalock–Taussig shunt procedures, with an ePTFE graft interposition between the subclavian and pulmonary artery.3, 24, 25 A very high incidence of 10-19% was reported.

It remains unclear from these reports whether the subcutaneous graft location represents a risk factor for PS or whether the higher incidence is due to their easy clinical recognition. The incidence of PS is likely to be underreported for deeper-sited reconstructions.26

We believe that our relatively high number of cases is the result of the level of attention paid to this problem, although other factors such as the operative procedure, graft specifics, and subcutaneous graft placement cannot be entirely excluded as causative factors. The incidence of 1.6% for subcutaneously placed arterial bypasses lies within the range reported by others.

The pathogenesis of PS involves both: failure of graft incorporation into surrounding tissue1, 27 and increased graft porosity.11, 21, 23 Different hypotheses regarding pathophysiological mechanisms of PS have been proposed and are still debated. So far, there is no conclusive evidence that PS is caused by an immunological reaction.4, 28 Several studies have demonstrated a serum-mediated inhibition of the activity and growth of fibroblasts in patients with PS.2, 6, 10, 29, 30 Other proposed mechanisms include the administration of heparin,3 lipolysis,31 damage of the graft during placement,32 or an unapparent infection.17, 33

The different assumptions about the cause of PS result in diverging recommendations for its treatment. In most reports, removal of the affected PTFE graft and the reconstruction using a Dacron prosthesis through an alternative anatomical route were recommended for treatment.1, 4, 5, 6, 7 However, similar to the study by Rhodes,16 we had two cases of recurrent seroma when replacing ePTFE by Dacron grafts. In contrast, we successfully replaced affected Dacron by ePTFE grafts in five cases, which is in accordance with the experience of others.4, 5, 9

A replacement of the involved graft with a new ePTFE graft resulted in recurrent seroma in most reports.5, 12, 31 In contrast, Dauria et al. reported a successful reconstruction without recurrence of PS in AV grafts in five cases by performing an ePTFE bypass of the affected graft segment, whereas a simple evacuation failed.20

Further observation of affected grafts without intervention.8 appears acceptable only for mild cases without affection of the anastomotic region. Despite the high rate of spontaneous resolution of PS reported in the survey of Blumenberg et al.,1 we did not observe this process in any of our patients with significant PS (larger than 2 cm in diameter) and recommend it only in mild cases. Aspiration of periprosthetic fluid and external drainage are associated with a low success rate, but a high infection rate and should be avoided1. Sladen et al.10 treated two cases with plasmapheresis aiming for an elimination of a humoral fibroblast inhibitor. Removing the fluid, surrounding material, and the pseudocapsule only does not appear to be an effective and safe method.11, 34 Replacement of the involved ePTFE grafts by an arterial homograft12 or native vein13 as alternative graft material was performed successfully in few cases. Gargiulo et al.35 treated successfully PS of AV grafts with covered stents in two cases. Intravenous fibrinogen administration,14 intraluminal injection of fibrin glue,15 insertion of microfibrillar collagen into the perigraft space,16 surgical connection between PS and the peritoneal cavity to drain the fluid,17, 18 or the wrapping of the graft with collagen fleece soaked in fibrin glue19 are other procedures that have been suggested for the treatment of PS.

PTFE grafts are chemically inert, highly electronegative, hydrophobic, and impermeable to blood. We assume that yet unknown patient-specific factors impair the hydrophobic state of ePTFE grafts leading to leakage and graft ultrafiltration, eventually resulting in PS. Several investigators have reported the efficacy of fibrin glue as a sealant for leakage in porous grafts.22, 23 We assume a sealing effect as well for normal ePTFE grafts with an internodal distance of 30 μm. A successful treatment of PS in ePTFE grafts by fibrin sealing was achieved in 84% of our patients. We observed only a partial success with respect to recurrent PS and low patency by replacement with commercially available gelatin-coated ePTFE grafts after failed fibrin sealing treatment. The long-term patency of fibrin sealed grafts appears to be equivalent to uncoated grafts. However, a fully conclusive statement cannot yet be given because of the small number of grafts used for different reconstructions.

Our clinical results regarding the treatment of PS as well as an experiment demonstrated that fibrin sealing may be an effective and safe method for the treatment and prophylaxis of PS in ePTFE grafts. The performed experiment demonstrated that the impermeability of grafts can be improved or even restored by fibrin sealing of the external graft surface if the components of the glue are applied sequentially. However, more comprehensive experiments are needed so as to study the underlying mechanisms. In particular, a structural analysis by electron microscopy of graft segments explanted for PS or modified in the aforementioned described experiment appears helpful and is in progress.

Additionally, it remains unclear to what extent the applied fibrin glue may influence the graft incorporation in vivo, for example, with respect to the decreased activity of fibroblast growth that was observed by Ahn et al.2, 29

The instillation of fibrin glue only into the space surrounding the affected graft27 does not appear to be sufficient, because a complete and stable coating of the outer graft surface cannot be achieved. Likewise, in our view the simultaneous application of both components, as recommended by the manufacturers of fibrin glue, cannot be considered as being sufficient. Sealing of pores at the PTFE graft surface with viscous and rapidly coagulating fibrin cannot be accomplished when using both components concurrently. A stable coating can be achieved only by sequential application on a dry graft surface, as illustrated in Figure 4.

  • View full-size image.
  • Fig. 4 

    Experimental demonstration of fibrin sealing. Fibrinogen is covered at the outer surface of the unwrapped PTFE graft segment A and manually introduced into internodal spaces B The thrombin component is applied C and the plastic wrap is removed. After filling the graft with isotonic saline solution under pressure, a marked transudation of water in the unsealed segment is visible D.

It may be debated whether the use of the involved graft segments and their fibrin sealing is the ideal way instead of the use of new grafts, as there is a theoretical chance of a biofilm infection. However, we have not had any negative experience with this approach.

A secondary factor of treatment of PS can be seen in the cost. The price of 2 mL fibrin glue, that is sufficient for treatment of PS in most cases, is much less than 200€. So the fibrin sealing technique is clearly cost-effective compared with the replacement of a new alloplastic graft.

A higher risk of PS for AV grafts compared with arterial bypasses as a result of higher flow rate may be suggested. Bolton and Cannon27 have demonstrated that an increased flow at a constant pressure of 181 mm Hg increases the transudation of citrated blood through segments of ePTFE grafts. Another reason for the likely important role of a high flow through the graft in the development of PS is given by the high rate of PS after modified Blalock–Taussig shunt procedures. One author of this report (H.S.) noticed a markedly higher rate of PS after use of ePTFE grafts for AV access before fibrin sealing of grafts with 0.5 mL fibrin glue was introduced as a routine. Assuming the incidence for PS in upper arm AV grafts of 5.2% from the report by Dauria et al.,20 the anticipated number of PS in our patients with PS has been 51. As compared with the observed incidence of 0.6% represented by six patients in our report, the effect of fibrin sealing of grafts for prevention of PS appears to be obvious, even though different other factors may influence this difference. Only a randomized study may provide more conclusive results.

Furthermore, we still seek an explanation why some patients had a placement of ePTFE grafts at different points in time without any occurrence of PS. A similar observation was made by Vince et al.12

A new interesting aspect of PS may arise from the observed continued expansion of aortic aneurysms after complete endovascular exclusion by stent-grafts constructed from ePTFE.36, 37, 40 The described morphological findings are very similar to PS in conventional vascular surgery.17, 34, 38, 39 The increase in aneurysm sac diameter after endovascular exclusion without apparent endoleak is attributed to endotension, which may be caused by increased graft permeability and PS.34, 37, 40 This might inspire future investigations of mechanisms, prevention, and treatment of PS.

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Conclusions 

Sequential fibrin sealing technique is an effective way to cure PS in ePTFE grafts. In 84% of patients, a long-term patent ePTFE graft was maintained without recurrent seroma. However, failure of this treatment cannot be precluded. The discussion of our results emphasizes the controversies and unanswered questions concerning importance, cause, and treatment of PS. Further investigations of this rare, but difficult to treat, complication seem necessary and may provide further insight into the possibly important role of PS in the aneurysm enlargement after endovascular repair with thin-walled ePTFE endografts.

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PII: S0890-5096(10)00182-2

doi:10.1016/j.avsg.2010.03.016

Annals of Vascular Surgery
Volume 24, Issue 8 , Pages 1005-1014, November 2010