Advertisement

Abdominal Wall Mesh Infections

  • K. M. Coakley
  • B. T. Heniford
  • V. A. Augenstein
Chapter

Abstract

While mesh implantation significantly reduces hernia recurrence, infection of the mesh is one of the most dreaded and challenging conditions in abdominal wall reconstruction. With no available national database to track each mesh recipient’s outcome, the true incidence of mesh infection is difficult to determine and likely underestimated. With the prevalence of synthetic materials used, the number of patients who will suffer such infections is likely to increase. Currently, there is no independent database tracking mesh-related complications, no mandate to follow patients for any set amount of time, and no guidelines regarding what type of mesh to use and when. This chapter focuses on mesh infections following ventral and incisional hernia repair—incidence, presentation, risk factors, microbiome, and treatment.

Introduction

Ventral hernia repair is one of the most common operations in the world, with 765,000 repairs per year in Europe and the USA combined, as estimated by the Cochrane collaboration [1, 2]. In a recent publication in JAMA, Merkow demonstrated ventral hernia repair to be the second most common surgical procedure associated with readmissions in American College of Surgeons National Surgical Quality Improvement Program database [3]. In that particular study, 498,875 operations across six specialties were studied, and the only procedure associated with a higher percentage of readmissions than ventral hernia was lower extremity vascular bypass. One of the most common reasons for readmission were wound complications which occur in 29–66% of ventral hernia repairs [4, 5, 6, 7, 8, 9, 10]. Incidence of hernia formation after a laparotomy is 18–23% [11, 12]; the incisional hernia population is inevitably at a high risk for poor healing and wound complications as the vast majority of patients do not develop hernias.

Surgical techniques for ventral hernia repair vary, and, despite numerous studies on one of the most common surgical procedures in the world, there is little consensus regarding surgical technique, mesh type, and location of mesh placement. The benefit of using mesh, to repair ventral hernias, has been well established [13]. With 10-year follow-up, Burger et al. demonstrated a 32% recurrence rate for mesh compared to a 63% recurrence rate for suture-based repairs of singular small (<10 cm2) midline incisional hernias [14]. In that particular study, mesh was used as a bridge; there have been multiple subsequent studies showing recurrence rates as low as 6.1% when performed with midweight polypropylene mesh [15, 16]. Additionally, Finan et al. showed the overall cost effectiveness of mesh placement after considering postoperative complications and recurrences. A systematic Cochrane review and literature summary [17, 18] reported that essentially all ventral hernias should utilize mesh to reduce the rate of hernia recurrence. This research has been largely heeded: in recent years, more than 85% of ventral hernia repairs utilize prosthetic mesh [19]. However, mesh becomes controversial as mesh infection rates increase [20]. A recent Danish study by Kokotovic et al. examined 3242 elective incisional hernia repairs with 100% follow-up and found mesh repair was associated with a lower risk of reoperation for recurrence compared with nonmesh repair over a 5-year follow-up period. However, although details regarding type of mesh, mesh placement, and patient BMI are not included, the analysis reported long-term mesh-related complications can partially offset benefits, showing the incidence of complications progressively increases with time [21]. While mesh implantation significantly reduces hernia recurrence, infection of the mesh is one of the most dreaded and challenging conditions in abdominal wall reconstruction. With the prevalence of synthetic materials used, the number of patients who will suffer such infections is likely to increase. Currently, there is no independent database tracking mesh-related complications, no mandate to follow patients for any set amount of time, and no guidelines regarding what type of mesh to use and when. This chapter focuses on mesh infections following ventral and incisional hernia repair—incidence, presentation, risk factors, microbiome, and treatment.

Incidence

Seventy percent of hernia repairs are performed via an open approach through a midline abdominal incision, with slightly lower rates of laparoscopic adoption worldwide [22, 23]. Any ventral hernia repair requiring a large incision and subcutaneous dissection carries increased risk of wound infection, and wound complication rates for complex hernia repairs vary between 28 and 66% [4, 5, 6, 7, 8, 9, 10]. Wound infections are correlated with a greater incidence of mesh-related infection. The reported rate of mesh-related infection following hernia repair is between 1 and 8% [24, 25, 26, 27, 28, 29, 30, 31]. Literature shows mesh infection rates of less than 1% in laparoscopic surgery compared to 8% in open surgery [32, 33]; therefore, the laparoscopic approach is preferable in terms of risk for prosthesis infection. Two recent meta-analyses have shown the laparoscopic approach was associated with significantly lower surgical site infection rates, and there was a trend toward fewer infections requiring mesh removal [2, 34]. While a laparoscopic approach in morbidly obese patients undergoing ventral hernia repair minimizes the potential wound and mesh complications, there still exists an increased risk for recurrence with Tsereteli et al. finding recurrence following laparoscopic approach was four times higher in patients with a BMI >40 when compared to patients with lower BMI [35].

The variables involved in describing the hernia patient and technique of the hernia repair are numerous; furthermore, as shown above, there is quite a range in reporting wound and mesh infection rates. With no available national database to track each mesh recipient’s outcome, the true incidence and outcome of wound infections and mesh infection are difficult to determine and likely underestimated. For several reasons, the true mesh-related infection rate may, in fact, be substantially higher than 8%. First, patients suffering from an infection or other complication may seek assistance from someone other than the operating surgeon. Of the hernia patients surveyed at our tertiary referral center, 57% reported having a complication related to their original hernia repair, and 100% had a hernia recurrence, yet only 44% of the primary surgeons knew of the complication or recurrence [36]. Second, studies suggest that the commonly used 30-day follow-up window may be inappropriately short to rule out the possibility of surgical complications, particularly mesh infections. In a review of mesh infections treated at our Hernia Center, the patients’ mesh infection manifested itself between 6 days and 5 years after surgery, with a mean of 31 months post-implantation [37]. Thus, most mesh infections would be missed by a standard 30-day follow-up window. Ventral hernia repairs with mesh should be followed well beyond 30 days.

Presentation and Risk Factors

Mesh infections typically present with local erythema, tenderness, swelling, and warmth of the abdominal wall around the infected mesh. Generalized manifestations, such as pain, fever, malaise, chills, or rigors, are experienced by some patients [38]. Chronic mesh infections can present with a discharging sinus, enterocutaneous fistula (Fig. 40.1), and visible mesh (Fig. 40.2). Chronic mesh infections may manifest late after herniorrhaphy with skin erythema, wounds in the area of mesh, and ultrasound or CT imaging showing fistulous canals extending from skin to the infected prosthesis. Ultrasound and CT are not always helpful in determining diagnosis of mesh infection, and infection scintigraphy can be used not only to evaluate vascular and orthopedic prostheses, as commonly is done, but also to help evaluate prosthetic mesh [39]. Scintigraphy with 99mTc-antigranulocyte antibody has been utilized to differentiate between postoperative inflammation and infection following hernia repair with mesh [39].
Fig. 40.1

This patient presenting with erythema as well as an enterocutaneous fistula has an underlying mesh fistula

Fig. 40.2

Another patient with mesh fistula presenting with exposed mesh

The first step in the prevention of mesh infection is the surgeon’s recognition of the relevant risk factors. Several risk factors increase the odds of a mesh infection: wound infection, smoking, obesity, enterotomy, concomitant procedure, diabetes, and prolonged operative time [25, 40, 41, 42]. Despite well-known culprits for mesh infection, there is no standard of care for prevention or preoperative prehabilitation.

Reduction of medical comorbidities prior to surgery can have a significant effect of outcomes and medical costs. Martindale et al. clearly demonstrated that smoking cessation, diabetes management, and weight loss reduce complications and improve outcomes [43]. In a recent publication in JSR, Cox et al. demonstrated the compound effect of comorbidities; patients with comorbidities accrue more charges even without a complication when compared to patients without comorbidities and with a complication [44]. Preoperative optimization of preventable comorbidities such as diabetes, tobacco use, and obesity improves outcomes in ventral hernia repair [44]. A 2012 survey of ventral hernia surgeons revealed that surgeons are regarding morbid obesity as a relative contraindication for elective ventral hernia repair, with 43% of postponed or delayed elective ventral hernia repairs listing concomitant morbid obesity as the indication for case postponement [44, 45]. Surgeons are increasingly aware that patient’s preoperative readiness for elective hernia repair should be based on a data-driven analysis of modifiable risk factors.

In an analysis of predictors of mesh infections, Liang et al. found the Ventral Hernia Working Group (VHWG) was an independent predictor of mesh explantation. VHWG is a four-level grading system designed to predict patients at high risk for surgical sight occurrence in ventral hernia [17] incorporating a variety of patient factors including comorbidities, surgical history, operative details, and degree of contamination. By comparison, The Center for Disease Control’s four-tier classification of incisional wounds accounts for degree of contamination present in an incision [46, 47]. A Class I wound is an uninfected operative wound in which no inflammation is encountered and the respiratory, alimentary, genital, or uninfected urinary tract is not entered. Class II is an operative wound in which the respiratory, alimentary, genital, or urinary tracts are entered under controlled conditions. Class III is an open, fresh, accidental wound or an operation with major breaks in sterile technique or gross spillage from the gastrointestinal tract. And, lastly, Class IV wounds are defined as traumatic wounds with retained devitalized tissue or an existing clinical infection or perforated viscera [46]. Unlike the CDC classification, the VHWG incorporates comorbidities and patient history to define risk for wound complications. Grade 1 are low-risk patients with no history of wound infection; Grade 2 are patients who are active smokers, are obese, have diabetes, or are on immunosuppressive medications. Grade 3 are patients with previous wound infection, presence of an ostomy, or there is violation of the GI tract during the operation. Grade 4 are patients with active infection such as grossly infected mesh or septic dehiscence. It is important to keep in mind the differences in the two grading systems as, for example, an enterotomy is classified under a CDC Class II wound but a VHWG Grade 3 wound.

As hernia grade increases, the risk of mesh explantation increases. Additionally, the number of prior abdominal operations plays a role in mesh explantation as Liang et al. found that patients with four or fewer previous abdominal surgeries had 5% likelihood for an abdominal reoperation compared to those with five or more previous abdominal surgeries had 5- to 40-fold increased likelihood of needing a reoperation and mesh explantation [48]. The abdominal wall that has sustained multiple incisions is more likely to have altered vascularity, wound healing, or prior incisions that harbor latent bacteria.

Hawn et al.’s analysis of mesh explantation after ventral and incisional hernia repair found abdominal aortic aneurysm history was associated significantly with infection and explantation [26]. Similarly, Burger et al. found with 10-year follow-up risk factors for recurrence and infection included prior AAA repair [14]. Although corticosteroid use, tobacco smoking, coronary artery disease, COPD, a low preoperative serum albumin concentration, and long operative time have been shown to be independent predictors of SSI, these factors were not associated with mesh infection unlike a AAA history [26].

Carolinas Equation for Determining Associated Risk (CeDAR) is a prediction tool and a free mobile app which has been downloaded in over 140 countries around the world to estimate open ventral hernia patients’ risk of postoperative wound complications. The statistically significant variables were enterotomy or presence of stoma (OR 2.65), previous ventral hernia repair (OR 2.64), advancement flaps (OR 2.28), tobacco use (OR 2.17), active infection at surgery (OR 2.07), uncontrolled diabetes (OR 2.01), anterior component separation (OR 1.91), and BMI >26 kg/m2 (OR 1.08/unit BMI) [49]. These tools, through analysis of large databases and statistics, essentially predict high-risk patients and are specific to open ventral hernia patients. Colavita et al. found that the CeDAR equation predicts wound complications in a validation cohort of 915 open ventral hernias performed at a separate institution, Greenville Hospital System, from the 534 open ventral hernias analyzed to create the derivation cohort [50]. The model yielded an area under the curve of 0.78, demonstrating excellent statistical correlation and verifying it as a validated, effective, and user-friendly wound complication prediction tool for open ventral hernia repairs.

When predicting ventral hernia complications, the American College of Surgeons’ Surgical Risk Calculator underestimates important outcomes. While the risk calculates can accurately predicted medical complications, reoperation, and 30-day mortality in ventral hernias, SSIs, serious complications, and LOS were significantly underestimated [51]. Several hernia specific tools are available to help surgeons quantitate preoperative risk factors and guide patient optimization. Liang et al. conducted a single institutional analysis of 407 open ventral hernia repairs with mesh to determine factors that lead to mesh explantation [48] and developed a Ventral Hernia Risk Score for predicting surgical site infection based on concomitant hernia repair, skin flaps created, American Society of Anesthesiologists (ASA) score ≥3, body mass index ≥40 kg/m, and incision class [52].

In addition to the preoperative factors mentioned above, nearly one in five patients develops an incisional hernia within 5 years of an abdominal organ transplantation [53]. Immunosuppressive medications given postoperatively impair wound healing and facilitate the development of a bacterial biofilm, leading to the resistance of microorganisms to antibacterial mechanisms [54]. There exists debate in the literature with Bueno-Lledo et al. finding corticosteroids to be a predictor of mesh infection but not explantation [55] and other series finding steroids not to be an independent predictor of mesh infection nor explantation [26, 48]. Certainly, this may yet be another variable to take into consideration when repairing ventral hernias in posttransplant patients.

By nature of the re-operative field, enterotomy during incisional ventral hernia repair is often unavoidable. Many patients have had multiple previous hernia repairs, intraperitoneal mesh, or tacks making adhesiolysis challenging. Hawn et al. found patients undergoing incisional hernia repair with concomitant intra-abdominal procedures or enterotomy have a greater than sixfold increased hazard of subsequent mesh explantation [25]. In addition, enteric gram-negative bacilli, including anaerobes, are more likely to be encountered in cases of enterotomy during the repair [25]. Bueno-Lledo et al. analyzed predictive factors associated with prosthesis infection after abdominal wall hernia repair and established patients undergoing a concomitant enterotomy with prosthetic repair were five times more likely to undergo subsequent mesh explantation [55]. The rate of enterotomies during open ventral hernias has been reported around 6.7% in randomized controlled trials [34]. When evaluating 1274 ventral hernias over 38-month follow-up, the author’s data showed patients without a previous repair; the enterotomy rate was 1.4%, which increased to 3.6% if patients had even a single previous hernia repair. Mesh infection rates rose from 1.8% in those without enterotomy to 21.4% in patients with enterotomy [56]. Avoiding enterotomies and recognizing the downstream effect are important, and one should consider not using synthetic materials in high-risk patients.

The morbidity and cost associated with wound and mesh complications are significant. Colavita et al. found patients with wound or mesh complications experienced worse quality of life 6 months after surgery than those without complications [57]. Using the Carolinas Comfort Scale, patients who experienced a complication reported more discomfort (57.6 vs. 35.4%), greater limitations on activities (58.6 vs. 29.9%), and more mesh sensation (52.5 vs. 34.2%) than those without a complication. Patients who have complications required more office visits, placing a burden on the patients to travel to clinic appointments as well as additional time away from work. This increases a burden on the physician and the physician’s staff, who now must see a higher number of patients, impacting both patient and physician quality of life. Additionally, Colavita’s analysis showed that a patient who developed a mesh infection incurred inpatient hospital charges of $44,000, plus an additional $63,400 in follow-up costs, for a total average annual cost of $107,000 [57]. In comparison, a patient without hernia repair complications incurred 62% less in total charges (roughly $38,700 in hospital costs and $1400 in follow-up charges). This likely understates the actual increased expense from mesh-related infection, as this analysis does not include home nursing, antibiotic therapy, disability and rehabilitation, family-related time for care, time off work, and any charges incurred after 12 months, certainly making these underestimations [1]. Given the dramatic burden associated with mesh infection, reduction of any modifiable risk factors and avoidance of synthetic products in high-risk patients should be strongly pursued.

Microbiome

Staphylococcus aureus is the most common microorganism isolated from infected meshes [24], with over 80% of isolates displaying S. aureus [37, 55]. This is consistent with long-standing research indicating that the presence of a foreign body reduces the bacterial load required to induce Staphylococcus infection and abscess formation in healthy adults. Indeed, a single buried stitch can enhance the virulence of Staphylococcus by a factor 10,000 [58]. S. aureus can be difficult to treat, given its production of a network of exopolysaccharides, known as biofilm, that defends the bacteria from host immune response and antibiotics [54]. S. aureus is prone to attachment to surfaces and creation of biofilm. Biofilm’s hydrated polymeric matrix is the root of persistent infection; studies of biofilms have revealed differentiated, structured groups of cells with community properties creating a protective film with an inherent resistance to antimicrobial agents. Biofilms have been established to be integral in the many human infectious diseases, including prosthetic joint infection, otitis media, cystic fibrosis, and endocarditis [38]. Additionally, bacterial biofilms are important contributors to complications associated with prosthetic mesh implanted in the abdominal wall, as in the presence of biofilm, Vancomycin is 1000–1500 times less effective in eradicating S. aureus [38]. Kathju demonstrated bacterial biofilms directly on mesh from patients with mesh infections were frequently polymicrobial and underappreciated by culture alone [38]. Egelsman’s review of surgical mesh infection following abdominal wall reconstruction declared a surface biofilm is capable of resisting antimicrobial agents, and once a biofilm has formed, initiation of antibiotic treatment is too late, leaving the only option for treatment is removal of the implanted mesh [59].

Studies on the prevention of biofilm formation are mainly focused on increased mesh biocompatibility, as improved mesh tissue incorporation optimizes the host’s protection of the mesh from microorganisms [59]. Kaplan and Ragunath have demonstrated in a dental study that enzymatic detachment of biofilms from synthetic surfaces results in increased ability for infection to be cleared by antibiotics in combination with the host immune response [60]. Enzymatic application in infected mesh for the eradication of biofilm is subject to ongoing research [38]. Sadava et al. have explored in animal models presoaking mesh in vancomycin solution to reduce methicillin-resistant Staphylococcus aureus bacterial growth [61]. They concluded presoaking with vancomycin may reduce the risk of mesh infection in clean-contaminated cases, although further investigation with human trials is still necessary.

Methicillin-resistant Staphylococcus aureus, or MRSA, is widespread in patients with infected mesh, and a MRSA history predisposes patients to future increased risk of mesh infection [61, 62, 63, 64]. In the author’s series of mesh infection patients, MRSA was present in 50.3% of cultured isolates [37]. Birolini et al.’s series of 41 mesh infections from Brazil showed a similar rate of MRSA infection with 47.1% of mesh infections cultures positive for MRSA [62]. It is the author’s practice that any abdominal hernia patient who presents with signs and symptoms of a mesh infection should be placed on an antibiotic with activity against MRSA and gram-positive bacteria. While resistance of bacteria to antibiotics is a worldwide concern, it is important to consider when comparing international reports on mesh infections that MRSA incidence varies greatly internationally, with the USA showing 49% rate of MRSA isolates, compared to 10% in France, 5% in Canada, and 1% in the Netherlands [65, 66]. Bode et al. established nasal carriers of MRSA have a risk of healthcare-associated infection three to six times the risk among noncarrier and low-level carriers [67]. Blatnick et al. established in animal models that mesh types vary in ability to clear MRSA. In their study on animal models, they found monofilament unprotected polypropylene and polyester mesh can clear a large percentage of MRSA contaminants, whereas multifilament, composite anti-adhesive barrier meshes and laminar antimicrobial impregnated mesh are not able to clear bacterial contamination with MRSA [68]. Moreover, Polouse recently published data indicating that MRSA at any site increases the risk of surgical site occurrence long term [69]. Given this, it is the author’s practice to decolonize nasal and extranasal sites on hospital admission with Bactroban in combination with a 4% chlorhexidine gluconate soap such as Hibiclens.

Escherichia coli, Enterococcus, and Candida are also encountered in mesh infections [40, 55, 64], with the presence of E. coli and Enterococcus bacteria often indicating a history of surgery with enterotomy or mesh fistula presence. The variety of organisms responsible for mesh infections underscores the importance of obtaining deep fluid cultures, via image guidance when possible, to guide antibiotic choice.

Treatment

Understanding and identifications of risk factors for mesh infections play a predictive role in likelihood of mesh explantation. Predictors for mesh explantation have been supported in many studies [25, 41, 48, 55].

In our analysis of mesh infections, we have seen that predictors of mesh explantation are fistulae, smoking, MRSA, and certain types of mesh such as composite, ePTFE, and polyester meshes. Bueno-Lledo et al. showed similar mesh explantation predictors to our analysis—type of prosthesis did not affect the rate of prosthetic infection but did influence the need for mesh explantation, with ePTFE and dual meshes requiring complete removal, compared to salvage rate of 36% for polypropylene meshes [55]. Leber et al. showed higher incidences of infection, enterocutaneous fistula formation, and small bowel obstruction with the use of multifilament polyester mesh compared to meshes made by other materials [70]. In Berrevoet’s series of mesh salvage by use of topical negative pressure therapy, the only meshes that consistently had to be completely or partially removed because of ongoing infection and the lack of granulation tissue covering the mesh were multifilament polyester meshes [71]. Decreased likelihood of eradication of infection from polyester could be due to biofilm adherence, as Sadava established in animal models multifilament polyester mesh had more biofilm present on infected mesh when compared to monofilament polypropylene mesh [61]. Liang et al. showed when adjusting for covariates, ePTFE was associated with a threefold increase in the hazard of mesh explantation [48], consistent with a previous study by Hawn [25]. In a 2005 study examining FDA reported mesh complications, Robinson et al. stated mesh infections and intestinal fistulae were significantly more common with Composix-Kugel mesh, a mesh developed with both PTFE and polypropylene, when compared with meshes of polypropylene alone [72]. With more than 200 mesh types available in the USA [73, 74], mesh selection remains controversial [75, 76]. All mesh, especially synthetic, can become infected, and there is still debate in the literature in efforts to establish one material’s clear superiority. Lightweight polypropylene meshes appear more prone to salvage with drainage and antibiotics alone compared to infected ePTFE which often requires complete excision [55].

The consideration of implanting a lightweight polypropylene mesh with wide pores was first studied in animals [77], and now the once prohibited idea of synthetic mesh in contaminated cases has been explored [78, 79, 80]. In a contaminated setting, a permanent prosthesis is commonly considered contraindicated because of high rates of mesh infection and removal, directly leading to hernia recurrence. These trials utilizing synthetic mesh in a contaminated field have been pursued in hopes of lowering incidence of infection while simultaneously avoiding the cost of biologic mesh; however, these studies are limited in sample size and length of follow-up. Deerenberg et al. placed synthetic in contaminated rat abdomens and found 15 of 16 rats receiving C-Qur, a polypropylene mesh, developed a mesh infections [81]. van’t Riet et al. found when patients with postoperative wound dehiscence due to intra-abdominal infection had synthetic mesh placed, a high risk of complications resulted. Regardless of whether polypropylene or polyester was used, van’t Riet et al. concluded over 49-month follow-up, synthetic mesh in a contaminated field should be avoided [82]. The potential of lightweight mesh has previously been humbled with long-term results revealing central fracture and a recurrence rate of 22.9% [28]. This high rate of recurrence in clean cases demonstrates an appropriate concern of lightweight mesh as an alternative to biologic mesh in high-risk patients.

As guidelines for treatment of mesh infections do not exist, the authors guide their treatment by established orthopedic replacement device infection algorithms [83], which, for example, strongly recommend determining the ESR and CRP, rigorous avoidance of any potential intraoperative contamination, and fluid aspiration and subsequent microbiological workup.

After failure of antibiotic or percutaneous drainage, in many cases, physicians attempt to salvage a patient’s infected mesh through partial excision. Partial extraction of meshes has been advocated by some, driven by a belief that the remaining mesh can augment abdominal wall strength and that infection may be localized [62]. However, case reports indicate that there are significant complications with partial extraction, with over 60% of patients returning with wound complications and ongoing mesh infection [27, 84, 85]. Long-term salvage of an infected synthetic mesh is poor [55, 86], and the effects of chronic infection and inflammation have been associated with increased risks of cardiovascular disease, atherosclerosis, diabetes, and dementia [87]. Given the high ultimate failure rates and high complication rates in partial extraction, once mesh infection is identified, complete explantation should be attempted in patients who are good operative candidates and have feasible reconstruction options.

Conclusion

Increase in rates of obesity, diabetes, and resistant organisms poses further challenges for hernia surgeons. Mesh infection remains a costly and debilitating complication, and further studies are needed to confirm appropriate therapeutic strategies. Guidelines for treatment of mesh infections do not exist, but the type of bacteria, mesh, technique, and patient factors all influence outcomes and can help guide decision-making for this challenging group of patients. Incomplete removal of the mesh should be suspected in any case of persistent or recurrent signs of mesh infection, and complete excision when possible should be considered. Identifying patients at highest risk for infection, optimizing them before surgery, and making safe choices in the operating room when faced with known risk factors of mesh infection will help prevent infections. This in turn will prevent morbidity and save significant amounts of healthcare expenditures. Organized long-term follow-up for patients following a mesh implantation will help elucidate the optimal materials to use in various situations.

References

  1. 1.
    Poulose BK, et al. Epidemiology and cost of ventral hernia repair: making the case for hernia research. Hernia. 2012;16(2):179–83.CrossRefGoogle Scholar
  2. 2.
    Sauerland S, et al. Laparoscopic versus open surgical techniques for ventral or incisional hernia repair. Cochrane Database Syst Rev. 2011;3:CD007781.Google Scholar
  3. 3.
    Merkow RP, et al. Underlying reasons associated with hospital readmission following surgery in the United States. JAMA. 2015;313(5):483–95.CrossRefGoogle Scholar
  4. 4.
    Zannis J, et al. Outcome study of the surgical management of panniculitis. Ann Plast Surg. 2012;68(2):194–7.CrossRefGoogle Scholar
  5. 5.
    Itani KM, et al. Comparison of laparoscopic and open repair with mesh for the treatment of ventral incisional hernia: a randomized trial. Arch Surg. 2010;145(4):322–8; discussion 328.CrossRefGoogle Scholar
  6. 6.
    Kaafarani HM, et al. Predictors of surgical site infection in laparoscopic and open ventral incisional herniorrhaphy. J Surg Res. 2010;163(2):229–34.CrossRefGoogle Scholar
  7. 7.
    Saxe A, et al. Simultaneous panniculectomy and ventral hernia repair following weight reduction after gastric bypass surgery: is it safe? Obes Surg. 2008;18(2):192–5; discussion 196.CrossRefGoogle Scholar
  8. 8.
    Albright E, et al. The component separation technique for hernia repair: a comparison of open and endoscopic techniques. Am Surg. 2011;77(7):839–43.PubMedGoogle Scholar
  9. 9.
    Mazzocchi M, et al. Component separation technique and panniculectomy for repair of incisional hernia. Am J Surg. 2010;201:776–83.CrossRefGoogle Scholar
  10. 10.
    Zemlyak AY, et al. Comparative study of wound complications: isolated panniculectomy versus panniculectomy combined with ventral hernia repair. J Surg Res. 2012;177(2):387–91.CrossRefGoogle Scholar
  11. 11.
    Hoer J, Fischer L, Schachtrupp A. Laparotomy closure and incisional hernia prevention – what are the surgical requirements? Zentralbl Chir. 2011;136(1):42–9.CrossRefGoogle Scholar
  12. 12.
    Korenkov M, et al. Incisional hernia repair in Germany at the crossroads: a comparison of two hospital surveys in 1995 and 2001. Zentralbl Chir. 2002;127(8):700–4; discussion 704-5.CrossRefGoogle Scholar
  13. 13.
    Luijendijk RW, et al. A comparison of suture repair with mesh repair for incisional hernia. N Engl J Med. 2000;343(6):392–8.CrossRefGoogle Scholar
  14. 14.
    Burger JW, et al. Long-term follow-up of a randomized controlled trial of suture versus mesh repair of incisional hernia. Ann Surg. 2004;240(4):578–83; discussion 583-5.PubMedPubMedCentralGoogle Scholar
  15. 15.
    Mathes T, Walgenbach M, Siegel R. Suture versus mesh repair in primary and incisional ventral hernias: a systematic review and meta-analysis. World J Surg. 2016;40(4):826–35.CrossRefGoogle Scholar
  16. 16.
    Groene SA, et al. Prospective, multi-institutional surgical and quality-of-life outcomes comparison of heavyweight, midweight, and lightweight mesh in open ventral hernia repair. Am J Surg. 2016;212(6):1054–62.CrossRefGoogle Scholar
  17. 17.
    Ventral Hernia Working Group, et al. Incisional ventral hernias: review of the literature and recommendations regarding the grading and technique of repair. Surgery. 2010;148(3):544–58.CrossRefGoogle Scholar
  18. 18.
    den Hartog D, et al. Open surgical procedures for incisional hernias. Cochrane Database Syst Rev. 2008;3:CD006438.Google Scholar
  19. 19.
    Funk LM, et al. Current national practice patterns for inpatient management of ventral abdominal wall hernia in the United States. Surg Endosc. 2013;27(11):4104–12.CrossRefGoogle Scholar
  20. 20.
    Finan KR, Kilgore ML, Hawn MT. Open suture versus mesh repair of primary incisional hernias: a cost-utility analysis. Hernia. 2009;13(2):173–82.CrossRefGoogle Scholar
  21. 21.
    Kokotovic D, Bisgaard T, Helgstrand F. Long-term recurrence and complications associated with elective incisional hernia repair. JAMA. 2016;316(15):1575–82.CrossRefGoogle Scholar
  22. 22.
    Wormer BA, et al. Ventral hernia repair in the western world: prospective international study demonstrates similar surgical outcomes found in Europe and USA. J Surg Res. 2013;179(2):238–9.CrossRefGoogle Scholar
  23. 23.
    Colavita PD, et al. Laparoscopic versus open hernia repair: outcomes and sociodemographic utilization results from the nationwide inpatient sample. Surg Endosc. 2013;27(1):109–17.CrossRefGoogle Scholar
  24. 24.
    Bliziotis IA, et al. Mesh-related infection after hernia repair: case report of an emerging type of foreign-body related infection. Infection. 2006;34(1):46–8.CrossRefGoogle Scholar
  25. 25.
    Hawn MT, et al. Predictors of mesh explantation after incisional hernia repair. Am J Surg. 2011;202(1):28–33.CrossRefGoogle Scholar
  26. 26.
    Hawn MT, et al. Long-term follow-up of technical outcomes for incisional hernia repair. J Am Coll Surg. 2010;210(5):648–55, 655–7.CrossRefGoogle Scholar
  27. 27.
    Cobb WS, et al. Infection risk of open placement of intraperitoneal composite mesh. Am Surg. 2009;75(9):762–7; discussion 767-8.PubMedGoogle Scholar
  28. 28.
    Cobb WS, et al. Open retromuscular mesh repair of complex incisional hernia: predictors of wound events and recurrence. J Am Coll Surg. 2015;220(4):606–13.CrossRefGoogle Scholar
  29. 29.
    Iqbal CW, et al. Long-term outcome of 254 complex incisional hernia repairs using the modified Rives-Stoppa technique. World J Surg. 2007;31(12):2398–404.CrossRefGoogle Scholar
  30. 30.
    Samee A, Adjepong S, Pattar J. Late onset mesh infection following laparoscopic inguinal hernia repair. BMJ Case Rep. 2011;2011:bcr0920114863.CrossRefGoogle Scholar
  31. 31.
    Petersen S, et al. Deep prosthesis infection in incisional hernia repair: predictive factors and clinical outcome. Eur J Surg. 2001;167(6):453–7.CrossRefGoogle Scholar
  32. 32.
    Carlson MA, et al. Minimally invasive ventral herniorrhaphy: an analysis of 6,266 published cases. Hernia. 2008;12(1):9–22.CrossRefGoogle Scholar
  33. 33.
    Sharma A, et al. Laparoscopic ventral/incisional hernia repair: a single centre experience of 1,242 patients over a period of 13 years. Hernia. 2011;15(2):131–9.CrossRefGoogle Scholar
  34. 34.
    Forbes SS, et al. Meta-analysis of randomized controlled trials comparing open and laparoscopic ventral and incisional hernia repair with mesh. Br J Surg. 2009;96(8):851–8.CrossRefGoogle Scholar
  35. 35.
    Tsereteli Z, et al. Laparoscopic ventral hernia repair (LVHR) in morbidly obese patients. Hernia. 2008;12(3):233–8.CrossRefGoogle Scholar
  36. 36.
    Oomen B. Do patients follow-up with their original surgeon when ventral hernia repairs (VHR) fail? American Hernia Society Annual Meeting; 2014.Google Scholar
  37. 37.
    Augenstein V, et al. Treatment of 161 consecutive synthetic mesh infections: can mesh be salvaged? In Affiliated Podium presentation at the Annual Meeting of the Americas Hernia Society, Washington, DC; 2015.Google Scholar
  38. 38.
    Kathju S, et al. Direct demonstration of bacterial biofilms on prosthetic mesh after ventral herniorrhaphy. Surg Infect. 2015;16(1):45–53.CrossRefGoogle Scholar
  39. 39.
    Zuvela M, et al. (99m)Tc-antigranulocyte antibody scintiscan versus computed tomography and ultrasound in the detection of silent mesh infection of the abdominal wall. Hell J Nucl Med. 2011;14(2):181–3.PubMedGoogle Scholar
  40. 40.
    Stremitzer S, 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(7):1702–9.CrossRefGoogle Scholar
  41. 41.
    Finan KR, et al. Predictors of wound infection in ventral hernia repair. Am J Surg. 2005;190(5):676–81.CrossRefGoogle Scholar
  42. 42.
    Sanchez VM, Abi-Haidar YE, Itani KM. Mesh infection in ventral incisional hernia repair: incidence, contributing factors, and treatment. Surg Infect. 2011;12(3):205–10.CrossRefGoogle Scholar
  43. 43.
    Martindale RG, Deveney CW. Preoperative risk reduction: strategies to optimize outcomes. Surg Clin North Am. 2013;93(5):1041–55.CrossRefGoogle Scholar
  44. 44.
    Cox TC, et al. The cost of preventable comorbidities on wound complications in open ventral hernia repair. J Surg Res. 2016;206(1):214–22.CrossRefGoogle Scholar
  45. 45.
    Evans KK, et al. Survey on ventral hernias: surgeon indications, contraindications, and management of large ventral hernias. Am Surg. 2012;78(4):388–97.PubMedGoogle Scholar
  46. 46.
    Simmons BP. Guideline for prevention of surgical wound infections. Am J Infect Control. 1983;11(4):133–43.CrossRefGoogle Scholar
  47. 47.
    Alexander JW, Solomkin JS, Edwards MJ. Updated recommendations for control of surgical site infections. Ann Surg. 2011;253(6):1082–93.CrossRefGoogle Scholar
  48. 48.
    Liang MK, et al. Abdominal reoperation and mesh explantation following open ventral hernia repair with mesh. Am J Surg. 2014;208(4):670–6.CrossRefGoogle Scholar
  49. 49.
    Augenstein VA, et al. CeDAR: Carolinas equation for determining associated risks. J Am Coll Surg. 2015;221(4):S65–6.CrossRefGoogle Scholar
  50. 50.
    Colavita PD, et al. External validation of a clinical prediction tool for wound infection in open ventral hernia repair (OVHR): 39th Annual International Congress of the European Hernia Society; 2017.Google Scholar
  51. 51.
    Basta MN, et al. Assessing the predictive accuracy of the American College of Surgeons National Surgical Quality Improvement Project Surgical Risk Calculator in open ventral hernia repair. Am J Surg. 2016;212(2):272–81.CrossRefGoogle Scholar
  52. 52.
    Liang MK, et al. External validation of the ventral hernia risk score for prediction of surgical site infections. Surg Infect. 2015;16(1):36–40.CrossRefGoogle Scholar
  53. 53.
    Smith CT, et al. Incidence and risk factors of incisional hernia formation following abdominal organ transplantation. Surg Endosc. 2015;29(2):398–404.CrossRefGoogle Scholar
  54. 54.
    Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms: a common cause of persistent infections. Science. 1999;284(5418):1318–22.CrossRefGoogle Scholar
  55. 55.
    Bueno-Lledo J, et al. Predictors of mesh infection and explantation after abdominal wall hernia repair. Am J Surg. 2017;213(1):50–7.CrossRefGoogle Scholar
  56. 56.
    Huntington C, et al. Inadvertent Enterotomy: Significant Consequences for the Open Ventral Hernia Patient: 1st World Congress on Abdominal Wall Hernia Surgery; 2015.Google Scholar
  57. 57.
    Colavita PD, Zemlyak A, Burton P, et al. The expansive cost of wound complications after ventral hernia repair. Annual Meeting of the American College of Surgeons Washington, DC; 2013.Google Scholar
  58. 58.
    Elek SD, Conen PE. The virulence of Staphylococcus pyogenes for man; a study of the problems of wound infection. Br J Exp Pathol. 1957;38(6):573–86.PubMedPubMedCentralGoogle Scholar
  59. 59.
    Engelsman AF, et al. The phenomenon of infection with abdominal wall reconstruction. Biomaterials. 2007;28(14):2314–27.CrossRefGoogle Scholar
  60. 60.
    Kaplan JB, et al. Enzymatic detachment of Staphylococcus epidermidis biofilms. Antimicrob Agents Chemother. 2004;48(7):2633–6.CrossRefGoogle Scholar
  61. 61.
    Sadava EE, et al. Does presoaking synthetic mesh in antibiotic solution reduce mesh infections? An experimental study. J Gastrointest Surg. 2013;17(3):562–8.CrossRefGoogle Scholar
  62. 62.
    Birolini C, et al. A retrospective review and observations over a 16-year clinical experience on the surgical treatment of chronic mesh infection. What about replacing a synthetic mesh on the infected surgical field? Hernia. 2015;19(2):239–46.CrossRefGoogle Scholar
  63. 63.
    Hicks CW, et al. History of methicillin-resistant Staphylococcus aureus (MRSA) surgical site infection may not be a contraindication to ventral hernia repair with synthetic mesh: a preliminary report. Hernia. 2014;18(1):65–70.CrossRefGoogle Scholar
  64. 64.
    Brown RH, et al. Comparison of infectious complications with synthetic mesh in ventral hernia repair. Am J Surg. 2013;205(2):182–7.CrossRefGoogle Scholar
  65. 65.
    Jones ME, et al. Emerging resistance among bacterial pathogens in the intensive care unit–a European and North American Surveillance study (2000–2002). Ann Clin Microbiol Antimicrob. 2004;3:14.CrossRefGoogle Scholar
  66. 66.
    Huijsdens XW, et al. Methicillin-resistant Staphylococcus aureus in Dutch soccer team. Emerg Infect Dis. 2006;12(10):1584–6.CrossRefGoogle Scholar
  67. 67.
    Bode LG, et al. Preventing surgical-site infections in nasal carriers of Staphylococcus aureus. N Engl J Med. 2010;362(1):9–17.CrossRefGoogle Scholar
  68. 68.
    Blatnik JA, et al. In vivo analysis of the morphologic characteristics of synthetic mesh to resist MRSA adherence. J Gastrointest Surg. 2012;16(11):2139–44.CrossRefGoogle Scholar
  69. 69.
    Ousley J, et al. Previous methicillin-resistant Staphylococcus aureus infection independent of body site increases odds of surgical site infection after ventral hernia repair. J Am Coll Surg. 2015;221(2):470–7.CrossRefGoogle Scholar
  70. 70.
    Leber GE, et al. Long-term complications associated with prosthetic repair of incisional hernias. Arch Surg. 1998;133(4):378–82.CrossRefGoogle Scholar
  71. 71.
    Berrevoet F, et al. Infected large pore meshes may be salvaged by topical negative pressure therapy. Hernia. 2013;17(1):67–73.CrossRefGoogle Scholar
  72. 72.
    Robinson TN, et al. Major mesh-related complications following hernia repair: events reported to the Food and Drug Administration. Surg Endosc. 2005;19(12):1556–60.CrossRefGoogle Scholar
  73. 73.
    Shah BC, et al. Not all biologics are equal! Hernia. 2011;15(2):165–71.CrossRefGoogle Scholar
  74. 74.
    Kissane NA, Itani KM. A decade of ventral incisional hernia repairs with biologic acellular dermal matrix: what have we learned? Plast Reconstr Surg. 2012;130(5 Suppl 2):194S–202S.CrossRefGoogle Scholar
  75. 75.
    Le D, et al. Mesh choice in ventral hernia repair: so many choices, so little time. Am J Surg. 2013;205(5):602–7; discussion 607.CrossRefGoogle Scholar
  76. 76.
    Cevasco M, Itani KM. Ventral hernia repair with synthetic, composite, and biologic mesh: characteristics, indications, and infection profile. Surg Infect. 2012;13(4):209–15.CrossRefGoogle Scholar
  77. 77.
    Harrell AG, et al. In vitro infectability of prosthetic mesh by methicillin-resistant Staphylococcus aureus. Hernia. 2006;10(2):120–4.CrossRefGoogle Scholar
  78. 78.
    Machairas A, et al. Prosthetic repair of incisional hernia combined with elective bowel operation. Surgeon. 2008;6(5):274–7.CrossRefGoogle Scholar
  79. 79.
    Carbonell AM, et al. Outcomes of synthetic mesh in contaminated ventral hernia repairs. J Am Coll Surg. 2013;217(6):991–8.CrossRefGoogle Scholar
  80. 80.
    Slater NJ, et al. Large contaminated ventral hernia repair using component separation technique with synthetic mesh. Plast Reconstr Surg. 2015;136(6):796e–805e.CrossRefGoogle Scholar
  81. 81.
    Deerenberg EB, et al. Experimental study on synthetic and biological mesh implantation in a contaminated environment. Br J Surg. 2012;99(12):1734–41.CrossRefGoogle Scholar
  82. 82.
    van’t Riet M, et al. Mesh repair for postoperative wound dehiscence in the presence of infection: is absorbable mesh safer than non-absorbable mesh? Hernia. 2007;11(5):409–13.CrossRefGoogle Scholar
  83. 83.
    Muhlhofer HM, et al. Prosthetic joint infection development of an evidence-based diagnostic algorithm. Eur J Med Res. 2017;22(1):8.CrossRefGoogle Scholar
  84. 84.
    Tolino MJ, et al. Infections associated with prosthetic repairs of abdominal wall hernias: pathology, management and results. Hernia. 2009;13(6):631–7.CrossRefGoogle Scholar
  85. 85.
    Chung L, Tse GH, O’Dwyer PJ. Outcome of patients with chronic mesh infection following abdominal wall hernia repair. Hernia. 2014;18(5):701–4.CrossRefGoogle Scholar
  86. 86.
    Bueno-Lledo J, et al. Partial versus complete removal of the infected mesh after abdominal wall hernia repair. Am J Surg. 2016;214(1):47–52.CrossRefGoogle Scholar
  87. 87.
    Mihai MM, et al. Microbial biofilms: impact on the pathogenesis of periodontitis, cystic fibrosis, chronic wounds and medical device-related infections. Curr Top Med Chem. 2015;15(16):1552–76.CrossRefGoogle Scholar

Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  • K. M. Coakley
    • 1
  • B. T. Heniford
    • 1
  • V. A. Augenstein
    • 1
  1. 1.Carolinas Laparoscopic and Advanced Surgery Program, Carolinas Medical CenterCharlotteUSA

Personalised recommendations