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J.A. Warren and A.M. Carbonell
Fig. 49.13 Single-dock rVHR of epigastric defect. (a) Patient positioned on a split-leg table, trocars placed across the lower abdomen and the robot docked parallel to the bed. (b) Transverse
incision of the posterior rectus sheath, including the preperitoneal space along the midline. (c) Extension of dissection above the hernia defect. (d) Defect closure. (e) Placement of mesh against
the anterior abdominal wall and closure of the posterior sheath. ra rectus abdominis muscle, la linea alba, ps posterior rectus sheath, p peritoneum, hd hernia defect, m mesh
49 Robotic Ventral Hernia Repair
391
Fig. 49.14 Single-dock rVHR of suprapubic defect. (a) Transverse incision of the posterior sheath. (b) Dissection of the retromuscular space bilaterally and the preperitoneal space in the midline, preserving the linea alba. (c) Preperitoneal dissection to the Space of Retzius to
expose Coopers’ ligaments. (d) Defect closure. (e) Placement of mesh against the anterior abdominal wall. (f) Closure of the posterior rectus sheath. p peritoneum, hd hernia defect, la linea alba, ps posterior sheath, ra rectus abdominis muscle, cl Cooper’s ligament, m mesh
392
J.A. Warren and A.M. Carbonell
Table 49.1 Standard laparoscopic versus robotic retromuscular hernia repair: demographics and operative details
Laparoscopic versus robotic
Demographics Lap Robotic p Value
N
Age 60.2 ± 13.4 52.9 ± 12.3 0.001
Race 0.419
BMI, mean ± SD 35.7 ± 9.5 34.7 ± 7.4 0.468
DM 34 (33.01) 15 (28.3) 0.624
COPD 8 (7.77) 7 (13.21) 0.487
HTN 69 (66.99) 30 (56.6) 0.379
ASA 0.711
1–2 40 (38.83) 19 (35.85)
3–4 63 (61.16) 34 (64.15)
Smoking status 17 (16.5 %) 13 (24.5 %) 0.457
Converted to open 4 (3.88) 0 (0)
Wound class 0.849
1 99 (96.12) 52 (98.11)
2 4 (3.88) 1 (1.89)
Operative details
Hernia width (mean) 6.9 ± 4.1 6.5 ± 2.9 0.508
Hernia area (mean) 88.0 ± 94.0 82.5 ± 69.8 0.685
Mesh area (mean) 339.3 ± 164.1 435.0 ± 250.9 0.014
Fascial closure 52 (50.49) 51 (96.23) <0.001
Bowel injury 9 (8.74) 1 (1.89) 0.011
OR time (mean) 121.5 ± 57.2 245.6 ± 98.5 <0.001
BMI body mass index, SD standard deviation, DM diabetes mellitus, COPD chronic obstructive pulmonary disease, HTN hypertension, ASA American Society of Anesthesiology
103 53
Table 49.2 Standard laparoscopic versus robotic retromuscular hernia repair: outcomes
Laparoscopic versus robotic
Outcomes Lap Robotic p Value
N
SSI, N (%)
SSO, N (%)
Seroma 17 (16.5) 24 (45.28)
Infected seroma 0 (0) 1 (1.89)
SSO PI, N (%)
None 94.7 % 92.9 %
Percutanious drain 1 (0.97) 2 (3.77)
LOS (median; IQR) 2 (2, 4) 1 (1, 3) 0.004
SSI surgical site infection, SSO surgical site occurrence, SSO PI surgical site occurrence requiring procedural intervention, LOS length of stay, IQR interquartile range
Table 49.3 Open versus robotic retromuscular VHR: demographics
Open versus robotic
Demographics Open Robotic p Value
n
BMI (mean ± SD) 36.1 ± 6.4 35.6 ± 7.7 0.761
Wound class 1 21 21 1.000
DM (%) 7 (33.3) 3 (14.3) 0.277
Smoker (%) 3 (14.3) 7 (33.3) 0.277
COPD 9 (42.9 %) 1 (4.8 %) 0.009
Hernia width (cm) (mean ± SD) 6.5 ± 3.9 6.2 ± 3.3 0.766
BMI body mass index, SD standard deviation, DM diabetes mellitus, COPD chronic obstructive pulmonary disease
103 53
1 (0.97) 2 (3.77) 0.592
19 (18.45) 28 (52.83) <0.001
1.000
21 21
49 Robotic Ventral Hernia Repair
Table 49.4 Open versus robotic retromuscular VHR: operative details and outcomes
Open versus robotic
Demographics Open Robotic p Value
n
Surgery time (mean ± SD) 178 ± 99 229 ± 88 0.087
EBL (mL) (mean ± SD) 106 ± 122 37 ± 39 0.022
LOS (mean ± SD) 4.2 ± 3.8 2.3 ± 1.6 0.046
SSO (%) 8 (38.1) 7 (33.3) 1.000
SSI (%) 2 (9.5) 0 (0.0) .488
Recurrence (%) 3 (12.5) 1 (4.8) 0.611
SD standard deviation, EBL estimated blood loss, LOS length of stay, SSO surgical site occurrence, SSI surgical site infection
21 21
393

References

1. Snyder CW, Graham LA, Gray SH, et al. Effect of mesh type and position on subsequent abdominal operations after incisional hernia repair. J Am Coll Surg. 2011;212:496–502; discussion 502–4.
2. Liang MK, Li LT, Nguyen MT, et al. Abdominal reoperation and mesh explantation following open ventral hernia repair with mesh. Am J Surg. 2014;208:670–6.
3. Gray SH, Vick CC, Graham LA, et al. Risk of complications from enterotomy or unplanned bowel resection during elective hernia repair. Arch Surg. 2008;143:582–6.
4. Patel PP, Love MW, Ewing JA, et al. Risks of subsequent abdomi­nal operations after laparoscopic ventral hernia repair. Surg Endosc. 2016:1–6 [Epub ahead of print].
5. Warren JA, Cobb WS, Ewing JA, Carbonell AM. Standard laparo­scopic versus robotic retromuscular ventral hernia repair. Surg Endosc. 2016:1–9 [Epub ahead of print].
6. Ballantyne GH, Hourmont K, Wasielewski A. Telerobotic laparo­scopic repair of incisional ventral hernias using intraperitoneal prosthetic mesh. JSLS. 2003;7:7–14.
7. Schluender S, Conrad J, Divino CM, Gurland B. Robot-assisted laparoscopic repair of ventral hernia with intracorporeal suturing. Surg Endosc. 2003;17:1391–5.
8. Tayar C, Karoui M, Cherqui D, Fagniez PL. Robot-assisted laparo­scopic mesh repair of incisional hernias with exclusive intracorpo­real suturing: a pilot study. Surg Endosc. 2007;21:1786–9.
9. Allison N, Tieu K, Snyder B, et al. Technical feasibility of robot­assisted ventral hernia repair. World J Surg. 2012;36:447–52.
10. Gonzalez AM, Romero RJ, Seetharamaiah R, et al. Laparoscopic ventral hernia repair with primary closure versus no primary clo­sure of the defect: potential benefits of the robotic technology. Int J Med Robot. 2015;11:120–5.
11. Sugiyama G, Chivukula S, Chung PJ, Alfonso A. Robot-assisted transabdominal preperitoneal ventral hernia repair. JSLS. 2015; 19(4):1–3.
12. Abdalla RZ, Garcia RB, Costa R, Luca C. Procedimento de Rives/ Stoppa modificado robô-assistido para correção de hérnias ventrais da linha média. Arq Bras Cir Dig. 2012;25(2):129–32.
13. Warren JA, Cobb WS, Ewing J, Carbonell AM. Prospective obser­vational cohort study of robotic vs open Rives Stoppa retrorectus incisional hernia repair. Hernia. 2015;19:S177–86.

Management of Mesh Infection

Lucas R. Beffa and Jeremy A. Warren
50

50.1 Introduction

Reinforcement of the abdominal wall with mesh is a mainstay of ventral hernia repair (VHR). However, there are multiple possible surgical approaches to VHR and numerous mesh prostheses to choose from, with little consensus on the opti­mal technique. Among the most feared complications of VHR is the development of a prosthetic mesh infection, which greatly influences preoperative planning and intraop­erative decision-making. Patient comorbid conditions that increase the risk of postoperative surgical site infection (SSI), or in cases with intraoperative contamination are com­monly repaired with biologic mesh or primary suture repair, or simply not offered an operation. However, there is grow­ing recognition of the limitations of biologic constructs in the setting of contamination. There is also increasing evi­dence to suggest the safety of certain permanent synthetic meshes in these cases. Traditional teaching espouses early partial or complete removal of the mesh from the abdominal wall should a mesh infection occur, often requiring multiple operations involving sometimes complex and long-term wound care, followed finally with the inevitable hernia recurrence. This paradigm is shifting, however, and there are now numerous reports demonstrating the ability to salvage mesh infection without explantation. Technological advance­ment, coupled with the increasing interest in hernia repair as a subspecialty and renewed interest in scientific study, has led to greater understanding of the patient factors, surgical technique, and mesh material contributions to the outcomes of VHR.
L.R. Beffa • J.A. Warren (*) Department of Surgery, Greenville Health System, University of South Carolina School of Medicine - Greenville, Greenville, SC, USA e-mail: lbeffa@ghs.org; jwarrenmd@ghs.org

50.2 Epidemiology and Pathogenesis

Prosthetic mesh infection occurs in 0.7–25.6 % of VHR, but incidence varies widely across reported series depending on a number of patient factors, surgical technique, mesh selec­tion, and reporting nomenclature [14]. Recent studies put this incidence around 1 % for laparoscopic repair, and <5 % for open repairs [1, 46]. There are a number of well­recognized patient factors known to increase the risk of SSI and mesh infection, including morbid obesity, tobacco abuse, chronic obstructive pulmonary disease (COPD), diabetes mellitus (DM), and immunosuppression [5, 7, 8]. Operative factors, including operative approach, duration of surgery, degree of soft tissue disruption, intraoperative contamina­tion, size, type, and complexity of the hernia, choice of pros­thetic material and its location within the abdominal wall also impact the risk of SSI [5, 6, 8, 9].
Infection typically occurs at the time of prosthetic imp­lantation due to bacterial contamination from the patient or surgical staff skin flora, the surrounding environment, or mucosal surfaces of the patient [4]. Presentation of the infec­tion may be significantly delayed, often not clinically rele­vant for months or even years postimplantation [1013]. The ability of a prosthetic material to resist infection depends on the bacterial inoculum, virulence of the organism, adherence to the prosthetic, the architecture of the mesh material, and the host immune response, all of which can be affected by preoperative risk reduction, choice of mesh, and choice of technique [4, 6].
As expected, the most common causative organisms are skin flora, most notably Staphylococcus species, both S. aureus and S. epidermidis. Multiple other species have been reported as well, including Proteus, Klebsiella,
Enterococcus, Streptococcus, Corynebacterium, Pseudo­monas, Escheri chia, Acinetobacter, and Enterobacter spe-
cies [8, 11, 12, 14, 15]. S. aureus is the most commonly reported causative organism, occurring in up to 80 % of cases, and methicillin- resistant S. aureus (MRSA) can be particularly problematic [5]. Formation of an extracellular
W.W. Hope et al. (eds.), Textbook of Hernia, DOI 10.1007/978-3-319-43045-4_50
395© Springer International Publishing Switzerland 2017
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L.R. Beffa and J.A. Warren
polysaccharide matrix, or biofilm, can increase the virulence of adherent bacteria. Bacterial clearance in the presence of a biofilm is significantly impaired due to a phenotypic change in the bacteria, inducing a dormant phase that is not as sus­ceptible to antimicrobial therapy as the planktonic form of the organism. Additionally, the biofilm acts as a physical bar­rier, preventing accumulation of therapeutic concentration of antibiotics and inhibiting the host immune response [4, 5, 16].

50.3 Mesh Material and Structure

The three-dimensional structural architecture, chemical and biologic characteristics of the implanted material signifi­cantly impact the risk of developing and ability to clear a prosthetic infection. Generally, increasingly complex mesh architecture increases risk of bacterial adherence [4]. Smaller pore size, multifilament mesh, and laminar mesh construc­tion increase the surface area for bacterial adherence, impede leukocyte migration for bacterial clearance, and may increase the likelihood of biofilm formation [4, 5].
Several in vitro studies have evaluated the bacterial adherence to various mesh types. Sanders et al. evaluated bacterial adherence of S. aureus and S. epidermidis to eight different mesh types. Based on polymer type, expanded polytetrafluoroethylene (ePTFE) demonstrated significantly higher bacterial adherence than polypropylene (PP), poly­ethylene terephthalate (polyester, PET), or condensed PTFE (cPTFE). Multifilament, partially absorbable material (PP + polyglactin- 910) also demonstrated greater bacterial adherence compared to monofilament PP or PET. Polymer filament diameter and mesh weight similarly influenced bac­terial adherence, with increased adherence with increasing diameter and weight. Finally, pore size inversely impacted bacterial adherence, with increased adherence seen with decreasing pore size [17]. Using a different methodology, Harrell et al. compared methicillin-resistant S. aureus (MRSA) adherence to nine different commercially available meshes. Silver- impregnated ePTFE demonstrated no bacte­rial adherence and showed significant bactericidal effect. In contrast, and contradictory to previously cited study, the multifilament PP + polyglactin 910 demonstrated the greatest bacterial adherence. Other light-weight monofilament PP meshes had significantly lower bacterial adherence com­pared with the multifilament PP + polyglactin 910 [18].
In vivo models for prosthetic infection exhibit a similar pattern. Using a rat model and MRSA inoculum, Blatnik et al. showed 80–91 % bacterial clearance with monofila­ment PP and polyester (PE), while multifilament PE cleared only 36 % of the MRSA. Biologic material has demonstrated variable results. One early study comparing several bio­logic materials demonstrated 58–92 % bacterial clearance
compared to control multifilament PET [19]. A more recent study contradicts this finding, demonstrating that monofila­ment PET cleared both E. coli and S. aureus 88 and 75 % of the time, respectively, compared to just 17 and 50 % clear­ance with porcine acellular dermal matrix (PADM) [20].

50.4 Management of Mesh Infections

For patients who develop an SSI after VHR, the first step is to determine if the infection actually involves the prosthetic material. Ultrasound and CT imaging is useful in determin­ing the extent of any abdominal wall fluid collections and if there is direct connection with the space in which the mesh was placed. If a prosthetic mesh infection is present, the various options for management must be considered, rang­ing from antibiotic therapy alone to complete mesh exci­sion, and must be tailored to the clinical condition of the patient. The operative technique, particularly the position of the mesh within the abdominal wall, the prosthesis involved, and the bacteriology of the SSI are all critically important factors that determine the ultimate success or failure of mesh salvage. A multidisciplinary approach is often helpful, including the surgeon, wound care, and infec­tious disease. Perhaps most importantly, the expectations of the patient must be managed. Prolonged wound care, repeated operations, and a high risk of hernia recurrence require patience and perseverance from both patient and surgeon.

50.4.1 Mesh Salvage

Most patients presenting with prosthetic mesh infection should have an initial attempt at mesh salvage due to the morbidity associated with mesh removal and the invariably recurrent incisional hernia. Traditional wound opening and local wound care with wet-to-dry dressings remains an important measure, but is not required for every patient and has been largely supplanted by percutaneous drainage with or without antibiotic irrigation, or negative pressure wound therapy (NPWT). The success of these techniques is signifi­cantly impacted by the bacteriology of the SSI, the mesh material, and mesh location. It is important to recognize that long-term management is typically necessary; complete wound healing when mesh salvage is successful can take several months [21]. The patient must be prepared to deal with the social, psychological, and physical impact of deal­ing with chronic wound therapy, and frequent office visits, counseling, and reassurance are required. A general algo­rithm to guide the management of infected mesh is shown in Fig. 50.1.
50 Management of Mesh Infection
397
Fig. 50.1 Algorithm for the management of prosthetic mesh infection
Fig. 50.2 Operatively placed drains after colostomy reversal and VHR
with midweight, large-pore polypropylene in the retromuscular space with serous output in bulb 1 and enteric contents in 2. Management with antibiotics and parenteral nutrition with complete resolution and no further mesh or wound complications at 2 years

50.4.2 Mesh Type

The mesh material and construct impacts the outcome of any attempt at mesh salvage. Polypropylene mesh is typically better suited for mesh preservation, with salvage rates as high as 100 % in some series [13, 22, 23]. This is likely due to the monofilament nature of the mesh construct, and more recently the larger interstices of the light- and midweight meshes. Our experience with large-pore polypropylene mesh in the retromuscular space is excellent, and mesh explanta­tion is almost universally a result of intraabdominal compli­cations, such as anastomotic leak, requiring reoperation, rather than direct mesh-related infection [24, 25]. Even with significant contamination, such as concurrent ostomy rever­sal, mesh explantation is rare, even in the event of deep space SSI (Fig. 50.2) [26]. Multifilament mesh has been shown to develop a greater density biofilm, inhibiting host and antibi­otic effectiveness of bacterial clearance [16]. Clinically, mul­tifilament polyester infection has a higher rate of salvage
398
Fig. 50.3 (a) Infected intraperitoneal multifilament, barrier coated polyester requiring complete excision. (b) Explant of multiple pieces of intraperitoneal barrier coated multifilament polyester mesh fistulized to small bowel, colon, and vagina
L.R. Beffa and J.A. Warren
Fig. 50.4 (a) Infected retromuscular microporous polypropylene mesh associated with colocutaneous fistula requiring explantation of all unin­corporated mesh. (b) Exposed infected ePTFE mesh requiring complete
failure reported in several series (Fig. 50.3) [22, 27]. Leber reported a three times higher rate of long-term complications with the use of polyester mesh, including a 15.7 % rate of enterocutaneous fistula formation [27]. In our experience with this construct, complete explantation is required almost universally if infection occurs, though it doesn’t appear that the incidence of infection overall is any higher than other mesh materials. These outcomes are consistent with the animal studies discussed above demonstrating poor bacterial clearance with multifilament materials. However, other series report successful salvage of polyester mesh with ade­quate drainage, antimicrobials, and local wound care [13,
28]. Microporous, heavy-weight polypropylene mesh is also
more difficulty to salvage, as is PTFE, due to its micropo­rous, laminar structure, and each portends mesh removal in most cases [23], particularly if placed during an open VHR (Fig. 50.4) [22, 23, 29]. Composite mesh constructs are also
excision. (c) Heavyweight, microporous polypropylene fistulized into small bowel
poorly salvageable in the event of infection [8, 14], though explantation can sometimes be avoided with aggressive con­servative therapy [21].
A variety of biologic matrices, derived from porcine, bovine, or human tissue, are also available. Theoretically, these materials serve as a biologic scaffold to facilitate native tissue in growth, new collagen deposition, and remodeling, though the true biologic activity of these materials in vivo is largely unknown. In the largest study of biologic mesh explants, no evidence of remodeling was seen, with little or no neovascularization, and the mesh induced significant for­eign body reaction and even encapsulation, particularly with cross-linked porcine [30]. Use of biologic mesh for abdomi­nal wall reconstruction is widely promulgated in high-risk patients and in the repair of hernias in a contaminated field. There is a paucity of literature to support this practice, how­ever. It should also be noted that biologic mesh is not
50 Management of Mesh Infection
Fig. 50.5 (a) Explanation of infected, degraded porcine mesh
approved for use in contaminated fields by the Food and Drug Administration (FDA) [31]. Harth et al. compared four commercially available biologic products using a rat model of contaminated hernia repair, and demonstrated decreasing bacterial clearance and tensile strength across wound classi­fication for all materials except the non-crosslinked porcine. Additionally, multiple material failures were seen with bio­mechanical testing in class II–IV wounds, while no material failure was seen in the synthetic mesh used as the control [32]. Clinically, heavily cross-linked porcine results in high rates of infection, mesh explantation, and hernia recurrence in contaminated hernia repairs [3, 33]. Non-crosslinked por­cine appears to perform better than cross-linked, however rates of SSI are comparable to most series using synthetic mesh, and recurrence rates are typically higher [3438]. Even considering studies that compare favorably with syn­thetic mesh [3942], cost should be considered. Biologic grafts typically cost as much as ten times that of synthetic mesh [36].
Regarding salvageability of biologic materials, there is little data to guide decision-making. As with synthetic mate­rials, attempt at salvage is appropriate providing the clinical stability of the patient. Cross-linked porcine was poorly sal­vageable in long-term analysis by Abdelfatah et al. with 25 % rate of mesh explantation with a mean follow-up of >5 years [3]. Removal of biologic implants for infection has been reported elsewhere as well (Fig. 50.5) [30, 41, 43, 44]. There is insufficient data to determine the particular benefit of percutaneous drainage, local wound care, or NPWT in biologic mesh infections.
Newer absorbable synthetic mesh may have a role in reconstruction in high-risk and contaminated cases, though current data is limited. The COBRA trial [45], in which a bio­absorbable construct of polyglycolide-trimethylene carbonate
399
was used in the repair of contaminated hernias, demonstrated comparable results to previous studies published from the same group using porcine [34] and synthetic mesh [25]. Of 21 SSIs in this series, no patient required complete mesh removal, indicating the suitability of this material for mesh salvage. Cost of these materials is significantly lower than biologic and may present an alternative for use in this complex patient population.

50.4.3 Mesh Position

As already alluded to, the position of the mesh within the abdominal wall plays a significant role in the ability to salvage mesh. Retromuscular mesh position provides a well- vascularized compartment for mesh placement that is separate from the viscera, with musculocutaneous tissue coverage of the mesh, making this space ideal for decreasing the risk of infection and salvaging prosthetic mesh in the event of infection [13, 22, 24, 25]. This is our preferred tech- nique for open VHR, using large pore PP mesh, and we very rarely remove mesh for infection in this space. Mesh onlay has been shown to have a higher rate of SSO and SSI in many studies [9, 46, 47], but local wound care, including partial mesh excision, can be successful. Mesh infection of intraperitoneal mesh is more difficult to preserve. This may be in part due to differing mesh properties, as mesh placed in an intraperitoneal position typically has some barrier coating designed to prevent visceral adhesions. The effect of these various tissue-separating layers on bacterial adherence and infection is unknown. Additionally, mesh placed over the peritoneum does not necessarily truly incorporate into the abdominal wall; rather, a neoperitoneum forms over the vis­ceral mesh surface and the mesh is held to the abdominal wall by this thin layer and whatever fixation was used to secure the mesh. This is evidenced clinically in our experi­ence with mesh removal, which typically peels off of the abdominal wall quite easily, leaving the posterior rectus sheath and even native peritoneum intact. In our experience with over 10 years of infected mesh management, we have found intraperitoneal mesh infection to be rarely salvage­able, while large pore PP mesh placed in the retromuscular space was preserved 100 % of the time [14, 23].
Any attempt at mesh salvage should be accompanied by appropriate antibiotic therapy. Whenever possible, cultures should be obtained and therapy tailored to the organism grown. In the absence of speciation of the causative organ­ism, empiric antibiosis should be directed toward the most common associated bacteria as noted above. There is cur­rently no data to guide duration of therapy, or the most appropriate route of treatment, whether oral or parenteral. In the event of complete mesh explantation, once the offending
400
L.R. Beffa and J.A. Warren
Fig. 50.6 (a) CT demonstrating periprosthetic SSI (arrow) after retromuscular repair with large-pore PP. (b) Percutaneous drainage of deep SSI. (c) Resolution of mesh infection at 3 months. (d) CT demon-
prosthetic is removed, there should be relatively little need for continued antibiosis. These decisions are left to the judgment of the treating surgeon, guided by microbiologic data and local antibiograms.

50.4.4 Percutaneous Drainage

Percutaneous drainage of periprosthetic fluid collections after VHR is an excellent initial intervention for confirmed or suspected infection. Kuo et al. were able to successfully salvage 16 of 21 mesh infections with percutaneous drainage and antibiotic therapy. Greater success was seen with PP mesh than ePTFE, with 40 % of the ePTFE requiring even­tual explantation, compared to just 14 % of PP meshes [48]. Similar poor salvageability was seen with infected ePTFE in other series, ranging from 36 to 100 % rates of explantation [13, 14, 21, 29]. The addition of antibiotic irrigation of the
strating periprosthetic infection (large arrow) after LVHR with IPOM (arrows). (e) Percutaneous drainage of fluid collection. (f) Daily antibi­otic irrigation via percutaneously placed drains
mesh via the drain may increase the likelihood of successful percutaneous treatment [15]. Aguilar et al. reported three cases of successfully salvaged intraperitoneal PTFE mesh using percutaneous drainage, long-term parenteral antibiot­ics, and thrice daily gentamycin irrigation through the drain [49]. Figure 50.6 shows successful mesh salvage with percu­taneous drainage.

50.4.5 Negative Pressure Wound Therapy

Negative pressure wound therapy can be employed for mesh preservation as well, with excellent reported results (Fig. 50.7). Berrevoet et al. applied NPWT to a total of 63 patients with infection following VHR. Of 30 patients repaired with PP mesh in a retromuscular position who devel­oped a deep SSI, none required mesh explantation. Conversely, three of nine patients with mesh in the intraperitoneal position