Mesh Infection in Ventral Incisional Hernia Repair: Incidence,Contributing Factors,and Treatment

Abstract

Background:

Prosthetic mesh infection is a catastrophic complication of ventral incisional hernia (VIH) repair.

Methods:

The current surgical literature was reviewed to determine the incidence, microbiology, risk factors, and treatment of mesh infections.

Results:

Mesh infections tend to present late. Diagnosis depends on high clinical suspicion and relies on culture of the fluid surrounding the mesh or of the mesh itself. Risk factors may include a high body mass index (obesity); chronic obstructive pulmonary disease; abdominal aortic aneurysm repair; prior surgical site infection; use of larger, microporous, or expanded polytetrafluoroethylene mesh; performance of other procedures via the same incision at the time of repair; longer operative time; lack of tissue coverage of the mesh; enterotomy; and enterocutaneous fistula. The best treatment is prevention. Treatment of mesh infection is evolving on a case-by-case basis from explantation toward mesh salvage, to prevent complications such as hernia recurrence.

Conclusion:

Higher-quality reporting on mesh infection in VIH repair must be achieved through better classification and quantification of these infections. Tactics to avoid mesh infection should be based on best evidence and high-quality prospective trials and observational studies.

Mesh infection is the number one cause of major device-related complications reported in the U.S. Food and Drug Administration (FDA) database [1]. Although resistance to infection would be an ideal characteristic of any implantable mesh, unfortunately, that ideal property does not exist. The diagnosis of mesh infection can be challenging to make, because of a lack of consensus on diagnostic criteria. Although many reports discuss surgical site infection (SSI) following ventral incisional hernia (VIH) repair, data on mesh infections in the setting of VIH repairs are scarce. Critical review of the literature is complicated by erroneous out-comes classification, whereby VIH mesh infections often are grouped with superficial SSIs or re-operations. A meta-analysis of studies involving more than 6,000 patients suggested that the literature was rife with inconsistent definitions and classification criteria [2]. As a result, the literature may underestimate the true incidence of mesh infections, and, therefore, the results require cautious interpretation. In addition, the U.S. Centers for Disease Control and Prevention (CDC) definition of SSIs is rarely taken into consideration when classifying mesh infections. With placement of a prosthesis, SSIs are defined as occurring as late as one year after operation, as opposed to within 30 post-operative days when no prosthesis is used [3]. Furthermore, although mesh can be associated with either superficial, deep, or organ/space SSIs, it is more likely to be linked to deep and organ/space infections; reports in the literature fail to differentiate cases on this crucial point.

Mesh infections are deleterious to both patients and the healthcare system, as they prolong hospitalization and increase re-operations, morbidity, and the cost of care [4]. In the analysis of VIH mesh infections in 21 patients by Cobb et al., re-operations accounted for 44 additional procedures, averaging 2.1 procedures/patient (range 1–5) [5].

Incidence

Mesh infection can follow either open or laparoscopic VIH repair. The reported incidence after open repair ranges from 6%–10% [5 –7], whereas that after laparoscopic repairs is lower, from 0–3.6% [8]. A mesh infection rate as low as 0.78% (45/6,266) after laparoscopic VIH repair was published in a systematic review by Carlson et al. Twenty-eight of the 45 patients (56%) with mesh infection required re-operation, and such infections were the third leading cause of re-operation [2]. In 2001, experts from the European Hernia Association published a report on the classification and treatment of VIH, suggesting a higher mesh removal rate after laparoscopic repair (0–7%) than after open repair (0–4%) [9]. This difference could be related to the more-prevalent use of expanded polytetrafluoroethylene (ePTFE) mesh in laparoscopic repair, which often requires removal once infected. A more recent review of 1,346 open and laparoscopic cases in the Veterans Affairs (VA) Hospital System revealed a 4.5% rate of mesh explantation for infection [10].

Diagnosis

The presentation of a mesh infection can range from erythema overlying the incision to signs of systemic sepsis. Early mesh infection must be distinguished primarily from superficial SSI. Unlike mesh infections, superficial incisional SSIs sometimes can be cured with antibiotics alone, when the sole manifestation is cellulitis. Additionally, mesh infections can present as infected fluid collections, which must be distinguished from non-infected seromas, which occur commonly after VIH. Therefore, any true diagnosis of mesh infection should be associated with either a positive deep culture from the fluid surrounding the mesh (not a superficial swab) or a positive culture of the mesh itself.

Diagnostic clues to mesh infection depend on the technique of VIH repair; for instance, purulent drainage occurs at the incision site after open repair, but emanates from one or more trocar sites after laparoscopic repair. Signs and symptoms common to open and laparoscopic repair include fever, pain, cellulitis, infected fluid collections adjacent to the mesh or the incision/trocar site, leukocytosis, elevated erythrocyte sedimentation rate, and systemic signs of sepsis. Some patients present late, especially in cases of formation of an abscess without sepsis [11], whereas other patients present with persistent suppuration and sinus formation [12].

Although radiographic imaging is of some assistance with diagnosis, fluid surrounding the mesh can be a normal, benign finding. When flecks of gas are identified on imaging, either an anaerobic infection or a communication with a gastrointestinal tract hollow viscus is possible. In any case, the definitive diagnosis of a mesh infection relies on positive deep cultures of either the fluid surrounding the mesh or the mesh itself. If a mesh infection is suspected, fluid should be aspirated promptly from the surgical site and sent for gram stain and culture if re-opening of the incision is believed to be avoidable.

Timeline in Mesh Infections

The onset of mesh infections has a bimodal distribution. Infections that occur early in the post-operative period are more likely to be associated with an enterocutaneous fistula (ECF) or a superficial incisional SSI. However, most infections present months after the original hernia repair even in the absence of bowel injury. Studies such as those of Jezupovs and Cobbs, on open VIH repairs with polypropylene mesh, reported presentations of infection at an average of 11.3 months (range 2.5–18 months) and 10.9 months, respectively. This has been substantiated by a recent VA study of 55 mesh removals, revealing a median time to explantation of 224 days. Infection (69%), followed by small bowel obstruction (10.9%) and ECF (9.1%), were the primary indications for explantation [13]. It is not clear why mesh infections tend to present so long after the repair. According to the VA study, mesh infections associated with ECF tended to present much earlier than those of other etiologies, within a median of 27 days; additionally, ePTFE meshes were explanted earlier than PP meshes by 331 days [13].

Microbiology

Staphylococcus aureus has been implicated in most cases of mesh infection, but other organisms, such as S. epidermidis, Streptococcus pyogenes, Enterococcus spp., Acinetobacter spp., Klebsiella spp., and even Aspergillus spp. [14] have been documented. In a large retrospective review of open VIH repairs with mesh, 81% of the infections were caused by S. aureus and 17% by gram-negative organisms, such as Klebsiella spp. and Proteus spp. Methicillin-resistant S. aureus (MRSA) was the culprit in 52% of the S. aureus infections [5]. Enteric gram-negative bacilli, including anaerobes, are more likely to be encountered in cases of enterotomy during the repair, with concomitant gastrointestinal procedures, and with formation of an ECF after repair.

In general, bacterial adherence to the mesh is required to produce an infection. The microbiology of mesh infections is unique in that bacteria adhere to the structural matrix of any indwelling medical device, including meshes, by creating a microenvironment called a “biofilm” or “polysaccharide slime.” Different constructs of prosthetic mesh have differing abilities to withstand biofilm formation, with monofilament construction (e.g., polypropylene (PP) mesh) being relatively impervious [15]. Biofilm formation has serious consequences, as biofilm-dwelling bacteria behave differently from their free (planktonic) counterparts, being shielded within the coating of extracellular polymers, which confer protection against antimicrobial treatment in two ways [12,16]. First, whereas planktonic bacteria divide rapidly and thus are susceptible to antibacterial agents, bacteria in biofilms are dormant and thus non-susceptible. Second, high antibiotic concentrations cannot be achieved, because biofilms create a physical barrier to antibiotic penetration. In fact, bacteria in biofilms can survive in a tissue antibiotic concentration as high as 1,000–1,500 times that tolerated by planktonic bacteria [17].

Etiology of Mesh Infection: Patient- and Hernia-Related Factors

Evidence of the association of mesh infections with given patient-related factors is inconsistent. One study analyzed risk factors for mesh infection after open VIH repair in 751 patients, and failed to demonstrate any association of infection with patient factors [5]. A review of 31 mesh infections demonstrated only high body mass index (BMI) as a factor significantly associated with mesh infection by univariable analysis [18]. Another study of 121 patients undergoing open VIH repair found chronic obstructive pulmonary disease (COPD) to be associated with deep prosthetic mesh infection [7]. In an analysis of mesh explantation after VIH repair, abdominal aortic aneurysm was the only co-morbidity associated significantly with infection [10]. Although corticosteroid use, tobacco smoking, coronary artery disease, COPD, a low pre-operative serum albumin concentration, long operative time, and use of absorbable mesh (likely a surrogate for more complex procedures) are significant independent predictors of SSI [19,20], these factors have not been associated with mesh infection.

A post-hoc analysis of data from the randomized, controlled trial (RCT) of open vs. laparoscopic VIH repair with mesh by Itani at al. attempted to determine the predictors of SSI, including mesh infections [21]. Seven patients, of whom five had undergone open repair and two laparoscopic repair, required mesh removal. Two additional patients required re-operation for debridement and drainage without mesh removal. In a multivariable analysis within that study, the open surgical technique and the medical center, rather than patient co-morbidities or hernia characteristics, were associated with the formation of SSI after VIH.

It is unclear whether a history of SSI translates into a higher risk of mesh infection. Houck et al. demonstrated a higher incidence of infection (41%) among patients with a history of SSI than in patients with no documented prior infection (12%) [22]. The study of Jezupovs and Mihelsons on VIH of all types reported only patients with a history of deep incisional SSI were at risk for developing mesh infections (p < 0.0001) [11]. In the recent study by Hawn et al. of 55 patients who required mesh explantation, a statistically significant correlation was found between SSI and explantation, with a history of SSI conferring a more than seven-fold increase in the risk of explantation by Cox regression analysis. Recurrent VIH repair with prior mesh implantation also was a risk factor [13].

Etiology of Mesh Infection: Mesh Factors

In an analysis of mesh infection after open repair of VIH, lighter meshes appeared to carry a lower risk of infection (7.3%) than heavier meshes (14.5%) [5]. Although this study also showed a trend toward a higher rate of infection with larger meshes, another study has clearly implicated larger meshes (300 cm² vs. 200 cm²) as a risk factor for infection [18]. Furthermore, in open VIH, PP carries a lower rate of mesh removal at 0.7%, as opposed to ePTFE at 1.7% [23]. The recent analysis of Hawn et al. also found a statistically significant three-fold higher incidence of explantation with ePTFE mesh than with PP mesh [13].

Need for removal of PP mesh is infrequent after infection [23,24]. In one study, despite a 4.8% incidence of infection after open VIH repairs, only 0.7% of PP meshes required removal [23]. The use of PP mesh in contaminated and clean-contaminated operative fields was described in 23 patients. Twenty-one percent (n = 5) of these patients experienced incision-related complications, but none required mesh removal [25]. This could be attributed to the fact that a PP mesh becomes incorporated into the anterior abdominal wall with neovascularization within two weeks of implantation, allowing leukocytes and macrophages to gain access to the local microenvironment [23].

In a report where non-absorbable synthetic polyethylene terephthalate mesh (Mersilene®; Ethicon, Somerville, NJ) was placed in the retromuscular rectus sheath, there were no differences in outcome among clean, clean-contaminated, contaminated, and dirty incisions [6].

A greater total surface area of mesh, such as in multi-filament-based products, carries a theoretically higher risk of bacterial adherence than does monofilament-based mesh, as suggested by studies comparing multi-filament with mono-filament sutures [26]. However, no differences in infection rates between mono-filament- and multi-filament-based intraperitoneal meshes were found in rats after inoculation of the mesh with S. aureus [27]. On the other hand, micropore material has been associated with higher infection rates than macropore material; this is attributed to bacterial penetration of pores that are too small to enable leukocyte migration and bacterial clearance [8,28].

Etiology of Mesh Infection: Technical Factors

Mesh infection can occur after either open or laparoscopic VIH repair. However, studies suggest that a laparoscopic repair carries a lower risk of mesh infection. The reported incidence of mesh infection after open VIH repair ranges from 6%–10% [5 –7], whereas that after laparoscopic repair ranges from 0–3.6% [8].

Additional procedures performed with VIH repair via the same incision increase the incidence of mesh infection. In a study by Hawn et al., the performance of concomitant procedures through the same incision as VIH repair with mesh resulted in a six-fold increase in the need for mesh explantation [13]. Hernia recurrence, mesh explantation, or both were identified in 52% of same-site concomitant-procedure repairs, in 29.3% of other-site concomitant-procedure repairs, and in 32.8% of single-procedure VIH repairs. Wound status (e.g., clean vs. contaminated) did not account for the difference in the rates of recurrence and mesh explantation.

Longer operative times may be associated with a higher incidence of mesh infection, but this is controversial. Cobb et al. found no significant association of operative time or drain utilization with mesh infection after open incisional VIH repair [5]. Stremitzer et al. noted a statistically significant 42-min difference in operative time by univariable analysis (p = 0.0005) among the 31/476 VIH repair patients who developed mesh infection [18].

Although the site of mesh placement (underlay vs. overlay) has not been linked to the likelihood of mesh removal [13], tissue coverage decreases the risk of mesh infection. In a retrospective study, ventral rectus fascial closure over the mesh was associated with lower infection rates (2%) than non-coverage (26%). Additionally, technical factors such as enterotomy and ECF formation are significantly associated with mesh explantation [13].

The association of seroma formation with mesh infection is unclear. Because seromas are common after VIH repair, the overall SSI infection rate in seroma patients is higher than that of patients without seromas (29.1% vs. 11.6%; p = 0.0499) [30]. The infection rate tended to be higher after drainage of seromas (57.1%; n = 4) than for non-drained seromas (17.6%; n = 3), although this study is underpowered.

Treatment

If a mesh infection is suspected early after a procedure, especially if it is associated with an SSI, the SSI should be treated; the value of culture data to inform therapy of an uncomplicated superficial incisional SSI is dubious. If it is determined that the SSI is not resolving after appropriate local normal care and antibiotic therapy (for a period not clearly documented in the literature), if indicated, fluid surrounding the mesh should be aspirated aseptically for culture.

Treatment of mesh infection depends first and foremost on the patient's clinical status. Patients who are unstable as a result of severe sepsis secondary to presumed mesh infection should be operated on urgently for drainage of the infection, possibly deferring explantation (which can require protracted, tedious dissection) until the patient has stabilized. Historically, for stable patients, operative treatment generally consisted of mesh explantation, especially if ePTFE mesh was in place [7,31,32]. Mesh explantation consists of opening the prior incision and extirpating the mesh, sutures, and tacks, with closure of the fascia, if possible. More recently, there has been a trend toward mesh salvage, as explantation is plagued by hernia recurrence, loss of domain, and risk of enterotomy or ECF formation [33].

Hernia recurrence can be a consequence of mesh removal. Preventive measures for recurrence involve leaving the mesh in situ or replacement of the explant with a biologic mesh, as has been successful in small series [7,18,31]. In cases where a thickened rind of tissue (capsule or scar plate or neofascia) is noted beneath the infected mesh, the rind should remain intact, and the wound should be left open, followed by dressing changes or application of a vacuum-assisted closure device (V.A.C.®; Kinetic Concepts, Inc., San Antonio, TX). Although this approach is suitable for controlling the infection, explantation alone does not prevent recurrence of the hernia. In a single-center retrospective analysis of 22 patients with ePTFE mesh infections, mesh removal was performed for all patients; the hernia recurred universally despite fascial closure [34]. With addition of autologous flap reconstruction to removal of infected mesh, a hernia recurrence rate of less than 10% was obtained [35].

Mesh removal with primary skin closure has been practiced, particularly for patients who are critically ill, or who have little or no tissue coverage of their abdominal organs. LeBlanc [31] advocates waiting 6–9 months before implanting another mesh, and performing a preoperative biopsy of subcutaneous tissue for culture to ensure that no residual bacteria are present. At the time of explantation, appropriate antibiotic prophylaxis should be given to cover the original causative pathogen.

In carefully selected patients who do not have sepsis, some authors have advocated mesh excision, followed by sequential temporary closure, along with dressing changes and intravenous (IV) antibiotics, until the defect can be closed primarily [31]. Other patients, in whom the mesh is infected partially, have been treated with debridement of infected tissue, partial excision of the involved mesh, re-approximation, drains, a V.A.C. dressing, and IV antibiotics for four weeks, with acceptable results [34]. Infections after open placement of PP-based meshes have been treated similarly, with no hernia recurrences or infections at three years' follow-up [33]. Most of the patients had resolution of their mesh infection within 6.3 mos (range 1–12 mos).

Percutaneous drainage of mesh infections, along with irrigation with gentamicin by catheter and parenteral administration of antibiotics, has also been used in small series of patients without sepsis, with acceptable results on short-term follow-up [36,37]. One patient infected with MRSA was maintained on long-term oral doxycycline as suppressive therapy [37].

Prevention of Mesh Infection

Preoperative techniques to minimize mesh infections should include proper adherence to the guidelines set by the Surgical Care Improvement Project (SCIP). This includes appropriate choice of antibiotic, proper dosing of antibiotic, clipping the hair of the patient only insofar as necessary and immediately prior to the surgical procedure, and prevention of hypothermia [38]. Additionally, prophylaxis against organisms implicated in a prior episode of SSI should be considered. The procedure should be postponed if there is evidence of active bacterial infection at any other site [39].

Intraoperative techniques, which may minimize bacterial contamination of the mesh include avoidance of mesh contact with the skin, placement of the mesh intraperitoneally by means of a trocar and not directly through the abdominal wall (if performed laparoscopically), and changing surgical gloves prior to handling the mesh [31,39]. In potentially contaminated VIH repairs, such as in patients with previous SSI, in infected cases, in cases of violation of the gastrointestinal tract, and in the presence of a stoma, consideration should be given to the use of a biologic mesh (see below) [40].

Other Considerations

Because of the paucity of high-quality studies, evidence to support antibiotic prophylaxis against infections at a VIH repair site is lacking. A study by Rios et al. of 216 patients undergoing VIH repairs with mesh showed that antibiotic prophylaxis was significantly associated with a lower incidence of infections by both univariable and multivariable analyses [41]. However, there has been only one RCT of antibiotic prophylaxis in abdominal wall hernia repair (35 patients) [42]. Of the 16 patients undergoing incisional repair, 25% developed SSIs, all of whom had been randomized to placebo (p = 0.08). However, if incisional and umbilical hernia repairs were categorized together, 44% of patients not given antibiotics developed SSIs, compared with only 6% given cefonicid (p = 0.02). Major criticisms of this study include its small size, as well as the fact that only 23% of the patients had mesh placed at the time of repair.

One group of authors advocated utilization of post-operative antibiotics for one week to decrease the incidence of cellulitis associated with seromas in VIH repair [43], but this practice has not been accepted widely.

If the value of antibiotic prophylaxis for abdominal wall repair is extrapolated from inguinal hernia studies, it should not be given. A Cochrane database review did not show that prophylactic antibiotics are beneficial in elective inguinal hernia repairs with mesh [44]. A meta-analysis by Aufenacker et al. of six RCTs evaluating antibiotic prophylaxis in mesh repairs (inguinal and femoral) did not favor the routine utilization of prophylactic antibiotics, although the odds ratio of 0.54 suggested a benefit [45].

At present, data are non-existent regarding the utilization of prophylactic antibiotics in mesh VIH repairs. It is difficult to extrapolate the wisdom imparted by trials in inguinal hernias, as ventral hernias often involve tissue infected previously or contaminated with skin and bowel flora. Given that mesh infections can be catastrophic, it is reasonable to administer an antibiotic efficient against gram-positive cocci, perhaps with special attention to the patient's MRSA status [46].

Mesh Impregnated with Antibiotic

The use of ePTFE mesh impregnated with silver/chlorhexidine (ePTFE Plus) may be more advantageous than ePTFE mesh alone. One study found lower bacterial counts five days after implantation of ePTFE Plus compared with PP mesh, biologic mesh, and no mesh [47]. An in vitro experiment in which nine types of mesh were inoculated with MRSA revealed that only ePTFE Plus was bactericidal [48,49]. Whether these data can be extrapolated to cases of true mesh infection in human beings is yet to be ascertained.

Lysostaphin, a novel antimicrobial agent active against S. aureus, is being used to coat meshes. It is a peptide created by a different Staphylococcus sp. and specifically targets S. aureus, creating pores in the bacterial wall, leading to cell death. In a study of lysostaphin coating of a porcine xenographic mesh (Strattice; LifeCell Corp., Branchburg, NJ) inoculated with S. aureus before implantation in rats, all animals receiving lysostaphin-coated mesh survived, whereas all rats with non-coated mesh died. Clinical studies on synthetic mesh coated with lysostaphin are under way [17].

Biologic Mesh in an Infected Field

Biologic prostheses comprise a broad and expanding class. Biologic mesh is for the most part absorbable and ultimately leaves no foreign body. Some biologic repair materials do not inhibit the body's ability to fight infection, and do not require removal when exposed or infected. That biologic mesh is not impervious to infection is well-established [50]. No comparative trials have been performed to distinguish among the different materials or to compare them with non-absorbable mesh [51]. In the only large prospective multi-institutional study of patients in whom porcine-derived dermal matrix (Strattice®) was used for VIH repair in contaminated fields, the incidence of incision-related complications was 33.8% at six months, but none of the patients required mesh removal [52]. Biologic materials may be advantageous in view of their availability and the fact that they do not require removal after infection, but they are undeniably costly. Moreover, the long-term durability of biologic mesh after infection or debridement is unknown.

Conclusion

Mesh infections are morbid complications of VIH repairs. They should be distinguished from superficial incisional SSIs, which can be treated with local wound care with or without antibiotic. Definitive diagnosis relies on a positive bacterial culture from fluid obtained aseptically from the area that surrounds the mesh or from the mesh itself. Oftentimes, mesh infections present months after implantation. Risk factors include obesity, abdominal aortic aneurysm, COPD, SSI, and prior hernia repair with mesh. Expanded PTFE mesh may be more prone to infection and is less likely to be salvaged, despite lower rates of infection. Polypropylene mesh is more likely to be salvaged despite infection. Increasingly, mesh infections are being treated with more conservative measures to avoid explantation, such as drainage, antibiotics, antibiotic irrigation, mesh debridement, and V.A.C. utilization. Mesh explantation has been associated with a high morbidity rate resulting from recurrent hernia and damage to surrounding structures, and should therefore be avoided if possible. Every attempt should be made to prevent mesh infection both pre-operatively and intra-operatively, including possibly utilization of biologic mesh in a contaminated field. Higher-quality literature on mesh infection in VIH repair must be attained through better quantification and classification of mesh infections and by prospective studies.

Footnotes

Author Disclosure Statement

The authors have no financial conflicts of interest in connection with this paper.

References

Robinson

, Clarke

, Schoen

et al. Major mesh-related complications following hernia repair. Surg Endosc, 2005; 19:1556–1560.

Carlson

, Frantzides

, Shostrom

et al. Minimally invasive ventral herniorrhaphy: An analysis of 6,266 published cases. Hernia, 2008; 12:9–22.

Mangram

, Horan

, Pearson

et al. Guidelines for prevention of surgical site infection. Am J Infect Control, 1999; 27:97–132.

Collage

, Rosengart

. Abdominal wall infections with in situ mesh. Surg Infect, 2010; 11:299–305.

Cobb

, Carbonell

, Kalbaugh

et al. Infection risk of open placement of intraperitoneal composite mesh. Am Surg, 2009; 75:762–768.

Vix

, Meyer

, Rohr

et al. The treatment of incisional and abdominal hernia with a prosthesis in potentially infected tissues: A series of 47 cases. Hernia, 1997; 1:157–161.

Petersen

, Henke

, Freitag

et al. Deep prosthesis infection in incisional hernia repair: Predictive factors and clinical outcome. Eur J Surg, 2001; 167:453–457.

Eriksen

, Gogenur

, Rosenberg

. Choice of mesh for laparoscopic ventral hernia repair. Hernia, 2007; 11:481–492.

Korenkov

, Paul

, Sauerland

et al. Classification and surgical treatment of incisional hernia: Results of an experts' meeting. Langenbecks Arch Surg, 2001; 386:65–73.

10.

Hawn

, Snyder

, Graham

et al. Long-term follow-up of technical outcomes for incisional hernia repair. J Am Coll Surg, 2010; 210:648–657.

11.

Jezupovs

, Mihelsons

. The analysis of infection after polypropylene mesh repairs of abdominal wall hernia. World J Surg, 2006; 30:2270–2278

12.

Deysine

. Pathophysiology, prevention, and management of prosthetic infections in hernia surgery. Surg Clin North Am, 1998; 78:1105–1115.

13.

Hawn

, Gray

, Snyder

et al. Predictors of mesh explantation following incisional hernia repair. J Am Coll Surg (in press).

14.

Woodward

, Wright

. Aspergillus infection of abdominal wall biologic mesh. Surg Infect, 2010; 11:405–406.

15.

Halaweish

, Harth

, Broome

et al. Novel in vitro model for assessing susceptibility of synthetic hernia repair meshes to Staphylococcus aureus infection using green fluorescent protein-labeled bacteria and modern imaging techniques. Surg Infect, 2010; 11:449–454.

16.

Donlan

. Biofilms and device-associated infections. Emerg Infect Dis, 2001; 7:277–281.

17.

Miller

. Promising agent emerging to battle mesh infections. Gen Surg News, 2010; 37,6:1, 16–17.

18.

Stremitzer

, Bachleitner-Hofmann

, Gradl

et al. Mesh graft infection following abdominal hernia repair: Risk factor evaluation and strategies of mesh graft preservation. A retrospective analysis of 476 operations. World J Surg, 2010; 34:1702–1709.

19.

Dunne

, Malone

, Tracy

. Abdominal wall hernias: Risk factors for infection and resource utilization. J Surg Res, 2003; 111:78–84.

20.

Finan

, Vick

, Kiefe

et al. Predictors of wound infection in ventral hernia repair. Am J Surg, 2005; 190:676–681.

21.

Kaafarani

, Kaufman

, Reda

et al. Predictors of surgical site infection in laparoscopic and open ventral incisional herniorrhaphy. J Surg Res, 2010; 16:229–234.

22.

Houck

, Rypins

, Sarfeh

. Repair of incisional hernia. Surg Gynecol Obstet, 1989; 169:397–399.

23.

Morriss-Stiff

, Hughes

. The outcomes of nonabsorbable mesh placed within the abdominal cavity: Literature review and clinical experience. J Am Coll Surg, 1998; 186:352–367.

24.

Luijendijk

, Hop

WCJ

, van den Tol

et al. A comparison of suture repair with mesh repair for incisional hernia. N Engl J Med, 2000; 343:392–398.

25.

Kelly

, Behrman

. The safety and efficacy of prosthetic hernia repair in clean-contaminated and contaminated wounds. Am Surg, 2002; 68:524–529.

26.

Merritt

, Hitchins

, Neale

. Tissue colonization from implantable biomaterials with low numbers of bacteria. J Biomed Mater Res, 1999; 44:261–265.

27.

Klinge

, Junge

, Spellerberg

et al. Do multifilament alloplastic meshes increase the infection rate? Analysis of the polymeric surface, the bacteria adherence, and the in vivo consequences in a rat model. J Biomed Mater Res, 2002; 63:765–771.

28.

Amid

. Classification of biomaterials and their related complications in abdominal wall hernia surgery. Hernia, 1997; 1:15–21.

29.

Petersen

, Henke

, Zimmermann

et al. Ventral rectus fascia closure on top of mesh hernia repair in the sublay technique. Plast Reconstr Surg, 2004; 114:1754–1760.

30.

Kaafarani

, Hur

, Hirter

et al. Seroma in ventral incisional herniorrhaphy: Incidence, predictors and outcome. Am J Surg, 2009; 198:639–644.

31.

LeBlanc

. Laparoscopic incisional and ventral hernia repair: Complications—how to avoid and handle. Hernia, 2004; 8:323–331.

32.

Heniford

, Park

, Ramshaw

et al. Laparoscopic ventral and incisional hernia repair in 407 patients. J Am Coll Surg, 2000; 190:645–650.

33.

Greenberg

. Can infected composite mesh be salvaged? Hernia, 2010; 14:589–592.

34.

Paton

, Novitsky

, Zerey

et al. Management of infections of polytetrafluoroethylene-based mesh. Surg Infect, 2007; 8:337–341.

35.

Szczerba

, Dumanian

. Definitive surgical treatment of infected or exposed ventral hernia mesh. Ann Surg, 2003; 237:437–441.

36.

Aguilar

, Chapital

, Madura JA

et al. Conservative management of mesh-site infection in hernia repair. J Laparoendosc Adv Surg, 2010; 20:249–252.

37.

Trunzo

, Ponsky

, Williams

et al. A novel approach for salvaging infected prosthetic mesh after ventral hernia repair. Hernia, 2009; 13:545–549.

38.

Surgical Care Improvement Project (SCIP) Module 1: Infection Prevention. Medscape General Surgery 2006. http://cme.medscape.com/viewarticle/531895_2

39.

Carlson

, Frantzides

, Shostrom

et al. Minimally invasive ventral herniorrhaphy: An analysis of 6,266 published cases. Hernia, 2008; 12:9–22.

40.

Breuing

, Butler

, Ferzoco

et al. Incisional ventral hernias: Review of the literature and recommendations regarding the grading and technique of repair. Surgery, 2010; 148:544–558.

41.

Rios

, Rodriguez

, Munitiz

et al. Antibiotic prophylaxis in incisional hernia repair using a prosthesis. Hernia, 2001; 5:148–152.

42.

Abramov

, Jeroukhimov

, Yinnon

et al. Antibiotic prophylaxis in umbilical and incisional hernia repair: A prospective randomized study. Eur J Surg, 1996; 162:945–948.

43.

Edwards

, Angstadt

, Whipple

et al. Laparoscopic ventral hernia repair: Postoperative antibiotics decrease incidence of seroma related cellulitis. Am Surg, 2005; 71:931–936.

44.

Sanchez-Manuel

, Lozano-Garcia

, Seco-Gil

. Antibiotic prophylaxis for hernia repair. Cochrane Database Syst Rev, 2007; 3:CD003769.

45.

Aufenacker

, Koelemay

MJW

, Gouma

et al. Systematic review and meta-analysis of the effectiveness of antibiotic prophylaxis in prevention of wound infection after mesh repair of abdominal wall hernia. Br J Surg, 2006; 93:5–10.

46.

Kollef

, Barie

. Methicillin-resistant Staphylococcus aureus (MRSA) nasal colonization predicts intensive care unit-acquired MRSA infections: True or false? Surg Infect, 2010; 11:497–499.

47.

Carbonell

, Kercher

, Sing

et al. Susceptibility of prosthetic biomaterials to infection. Surg Endosc, 2006; 20:174–175.

48.

Harrell

, Novitsky

, Kercher

et al. In vitro infectability of prosthetic mesh by methicillin-resistant Staphylococcus aureus. Hernia, 2006; 10:120–124.

49.

Penttinen

, Gronroos

. Mesh repair of common abdominal hernias: A review on experimental and clinical studies. Hernia, 2008; 12:337–344.

50.

Awad

, Rao

, Berger

et al. Microbiology of infected acellular dermal matrix (AlloDerm) in patients receiving complex abdominal closure after emergency surgery. Surg Infect, 2009; 10:79–84.

51.

Rosen

. Biologic mesh for abdominal wall reconstruction: A critical appraisal. Am Surg, 2010; 76:1–6.

52.

Itani

KMF

, Awad

, Baumann

et al. Prospective clinical study: Evidence of safe, single stage repair of infected/contaminated abdominal incisional hernias using Strattice reconstructive tissue matrix. Hernia, 2009; 13,supp 1:S28.