Commentary on ‘‘Microbial Spectrum and Primary Resistance to Rifampicin in Infectious Complications in Vascular Surgery: Limits to the Use of Rifampicin-Bonded Prosthetic Grafts’’

Abstract

In this issue of Angiology, Topel et al present a retrospective analysis of prospectively acquired data documenting the spectrum of cultured microorganisms in 48 patients with infected prosthetic grafts (n 1⁄4 46) or primary arterial infections (n 1⁄4 2). The authors conclude from their data that rifampicinbonded prosthetic grafts should be used with caution (preferring autologous reconstructions), because in 30% of cases the initiating microbial organisms were either resistant or insensitive to rifampicin. Most observers would broadly agree with this conclusion as autologous conduits are invariably superior to prosthetic material in the treatment of graft infection (whether they be antibiotic-bonded or not). However, and as is often the case, one has to be careful that one is comparing apples with apples and not with oranges. Prosthetic graft infection remains the most feared complication in vascular surgical practice as it is associated with a very high risk of death/serious morbidity. Underpinning any management strategy is the need to balance 3 (sometimes conflicting) goals; (1) eradication of infection, (2) minimization of the operative risk, and (3) prevention of recurrence. All 3 may be readily achievable in some (fortunate) patients, while a compromise may be necessary in others. Total (partial) graft excision with in situ replacement using a rifampicin-bonded prosthesis is only 1 of a number of strategies currently available to the surgeon in this difficult situation, but it was developed primarily for the treatment of aortic prosthetic infection (ie, not infrainguinal infections) and especially in those in whom autologous reconstruction was not generally possible (eg, the patient with massive hemorrhage from an acute aortoenteric fistula). In a 2002 review of the literature, the use of in situ replacement with rifampicin-bonded prostheses for the treatment of aortic graft infection was associated with a 5% mortality rate, 0% amputation, and only a 15% risk of late reinfection. It was, however, accepted that careful case selection was paramount. Unfortunately, it is not entirely clear from Topel’s paper as to the primary location of their prosthetic infections. It would seem that the majority were probably not aortic but instead involved the groin (n 1⁄4 33), thigh (n 1⁄4 6), or lower leg (n 1⁄4 6). These cases are not strictly comparable with aortic graft infection. Moreover, a significant proportion of Topel’s cases were associated with complex wound infections and chronic sinuses. It is, therefore, inevitable that this type of patient will be more likely to yield a greater spectrum of microorganisms after culture, especially the more resistant varieties. Two cases of primary arterial infection were included in Topel’s series, but these should not be considered in the same category as prosthetic infection. Virtually, no one would ever recommend in situ reconstruction, using antibiotic-bonded prostheses in this type of case. There are also issues relating to the method used for determining sensitivity to rifampicin in the current series. In an earlier study (which also challenged the role of rifampicin), the authors used a concentration of 1 mg/mL to test the ability of a graft to withstand infection. However, in ‘‘real world’’ practice, 600-mg rifampicin is dissolved in 10 mL of solvent yielding a concentration of 60 mg/mL, which is then used to bond the graft. It therefore remains unclear as to whether the concentration of rifampicin currently being used in surgical practice is comparable to that being used in routine laboratory-based in vitro sensitivity studies. If nothing else, Topel’s study reinforces a vital message that a ‘‘one size fits all’’ strategy will never work; that is, if all patients with graft infections located anywhere in the