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Late-onset deep prosthetic infection following mesh repair of inguinal hernia
Late-Onset Deep Prosthetic Infection following Mesh Repair of Inguinal Hernia Darren V. Mann, MS, FRCS, Jeremy Prout, MBBS, Erik Havranek, MBBS, Stuart Gould, FRCS, Ara Darzi, MD, FRCS, London, England
BACKGROUND: The use of prosthetic biomaterials for the primary repair of inguinal hernias is now commonplace. Late-onset deep-seated prosthetic infection can be an unexpected complication. METHODS: The literature from a Medline search relating to the biology of mesh in the setting of hernia repair is discussed. CONCLUSIONS: The use of a foreign body for hernia repair does not appear to alter the incidence of superficial wound infection. Late-onset deep graft infection has been rarely reported, and the true incidence is yet to be established. With the more widespread use of mesh materials, this complication may become increasingly evident. Am J Surg. 1998;176:12–14. © 1998 by Excerpta Medica, Inc.
P
rosthetic mesh biomaterials have recently enjoyed renewed popularity in the repair of inguinal hernias. The success of “tension-free” open repairs,1 and the emergence of laparoscopic mesh procedures2 has established a role for the prosthetic repair of primary and recurrent inguinal herniation. Initial concerns that the routine use of a foreign body might be attended by a higher wound infection rate have not been realized.3 An often unexpected complication, however, is the late onset of deep graft infection occurring many months after the operation.
HISTORY The use of prosthetic biomaterials to effect the repair of deficient or absent abdominal wall tissues is not a new concept. Silver mesh was initially used in Germany at the turn of the century, and introduced in the United States shortly thereafter.4 The corrosion of silver induced by contact with tissue fluids precluded widescale use, and in the 1940s mesh of inert tantalum was substituted.5 Early experience with these prosthetic materials was disappointing, however, due to an unacceptably high incidence of infection, rejection, and recurrence. The introduction of biologically tolerated synthetic polymers in the 1950s heralded a new era of mesh repairs, although these were generally restricted to incisional and recurrent hernias.6,7
From the Academic Surgical Unit, St Mary’s Hospital, London, England. Requests for reprints should be addressed to Ara Darzi, MD, Consultant Surgeon, St Mary’s Hospital, Paddington, London W2 1PG, England. Manuscript submitted June 30, 1997 and accepted in revised form March 17, 1998.
12
© 1998 by Excerpta Medica, Inc. All rights reserved.
In recent years there has been renewed interest in the use of prosthetic materials in the repair of primary inguinal hernias. Dissatisfaction with the rationale for and results of traditional sutured repair influenced Lichtenstein et al1 to explore the role of tension-free mesh repair.8 Graft repairs in the preperitoneal plane by open9 and laparoscopic10 approaches have also been advocated.
BIOLOGY OF PROSTHETIC MESH The biological response to surgically implanted prosthetic mesh materials has been extensively studied.7 The initial reaction, characterized by acute inflammatory cell infiltration, is gradually replaced by fibroblasts (which infiltrate through the interstices of porous meshes) and a variable number of giant cells.11 Uncomplicated incorporation of the mesh into the host tissues is associated with an increase in the fibroblast to inflammatory cell ratio. In animal models this is reflected in the bursting strength of the prosthesis, which increases over the first 1 to 3 months and then achieves a maximum thereafter.11,12 Experimental evidence suggests that fascial repairs with synthetic mesh display greater bursting strength than can be achieved with tissue approximation by direct suture.13 The host response to the mesh varies with the physical properties of the material used. Nonporous grafts are generally less well tolerated than porous ones, and have been shown to produce a persistent fluid collection with incomplete incorporation, and even migration.11 Similarly, the chemical composition of the mesh may have a profound effect on the local tissue reaction. Polypropylene mesh (Marlex, CR Bard) has been shown to excite a greater inflammatory reaction than polytetrafluoroethylene (GoreTex, WL Gore), resulting in greater scarring, contracture, and distortion of the graft.12,14 Under ideal circumstances, then, the implanted mesh material becomes incorporated into the surrounding tissues by means of fibrous infiltration, with the formation of a linear “neofascia.” Whether the mechanical strength relates to the subsequent scarring or the tensile characteristics of the mesh material is unclear. However, it is appreciated that biodegradable mesh materials such as polyglactin (Vicryl, Ethicon) tend to hydrolyze before fibrous tissue incorporation is complete, and are associated with a lower bursting pressure in the experimental condition.12 It would appear that scar formation is of paramount importance, but that this is to a great extent determined by the characteristics of the graft. When mesh incorporation is disordered, the result is a fluid collection (seroma) with a variable degree of surrounding fibrosis and incomplete attachment of the graft, which may even be floating free. Thus, seroma is the commonest complication of mesh insertion, occurring in 0002-9610/98/$19.00 PII S0002-9610(98)00094-4
PROSTHETIC INFECTION AFTER INGUINAL HERNIA REPAIR/MANN ET AL
45% of patients in one series following ventral herniorrhaphy (where the mesh is located deep to the subcutaneous fat).15 For the most part, these will resolve with aspiration, although repeated attempts may be required. In those cases where fluid collections persist, a mature fibrous cyst may form that ultimately requires surgical excision for cure.16
MESH-RELATED INFECTION The major source of concern regarding the use of synthetic fascial substitutes has been a perceived increase in infection risk. There is some evidence to suggest that this may be a more common occurrence when a seroma develops,11 although the influence of percutaneous aspiration will obviously be a factor. Data from published series do not support the contention that infection is more common in open mesh repair of inguinal hernia as compared with conventional sutured repair. In a review of 1,834 mesh inguinal hernia repairs, Gilbert and Felton17 reported 14 cases with infection (0.8%), compared with 659 suture repairs with 7 infections (1%). Similarly, in a comparison of prosthetic inguinal hernia repair with the Bassini operation, Thill and Hopkins18 found infection rates of 0.54% and 1.2%, respectively. The pooled “Lichtenstein” series reports an overall infection rate of 0.03% for patch repair of inguinal hernia,3 and a recent review of a series of 350 mesh repairs by a single surgeon included only one instance of infection.19 When considering bacterial invasion, a distinction must be made between superficial wound infection and deep graft infection. The former tend to occur in the early postoperative period, and do not seem to be influenced by the use of mesh. In fact, treatment of superficial wound infection may be effective using some combination of antibiotics (for cellulitis) and drainage (for subcutaneous collection), and in these circumstances removal of the prosthesis may not be necessary for complete healing.17 In contrast, deep graft infection has not been commonly reported in the literature. The presentation of deep-seated infection of the prosthesis may be a delayed one, following many months from the operation. Sporadic cases have appeared in the literature from series of open mesh20 and laparoscopic hernia repairs.2,21,22 These patients may present with signs of acute inflammation, or in a more indolent manner with a discharging sinus, occasionally with the mesh presenting through the wound.7 That bacteria may infiltrate throughout the layered mesh-fibrous reaction complex has been demonstrated by microscopic examination.19 It follows that usually the only way to ensure eradication of infection is to remove the mesh, which procedure may not necessarily result in recurrent herniation if sufficient fibrous scarring remains. The usual infecting organism in wound17 and graft19,20 infection is Staphylococcus aureus, although enteric organisms may also be found. Whether any relationship exists between early superficial wound infection and late-onset deep graft infection is unclear. The time course of these rather different infective complications suggests that while early infection relates to operative contamination, late prosthetic infection may arise as a complication of a persisting fluid collection.
INFECTION CONTROL What measures can be taken to reduce the likelihood of infection? The use of prophylactic antibiotics (systemic or topical) is still debated for the “clean” operation of herniorrhaphy.23,24 Unfortunately, there is little direct clinical evidence on which to base recommendations when implantable mesh is used. Hence, although some authors advocate the use of an antistaphylococcal agent (either parenteral25 or topical1) on empirical grounds, others contest that the benefit remains unproven.17 Work from animal models suggests that systemic and local antibiotic prophylaxis are equally effective against bacterial growth in the presence of mesh, but that their combination offers no additional advantage26 (a finding consistent with clinical experience in vascular prosthetic surgery27). Topical antiseptics (eg, povidone-iodine) applied into the wound are recommended by some, although experimental evidence suggests that their use confers additional benefit over antibiotic prophylaxis only in the case of massive bacterial inoculation.28 Probably more important than the choice of antibacterial is the observance of strict asepsis during mesh preparation and implantation (it has been suggested that the resterilization and use of previously opened meshes may predispose to microbial contamination). The diagnosis of graft sepsis is usually obvious, although occult infection may be difficult to localize, and in this context soft tissue imaging including magnetic resonance scanning may find a useful role. Whatever the mode of presentation, treatment of established infection should be prompt, as life-threatening staphylococcal toxic shock syndrome is a potentially catastrophic sequel.
CONCLUSION In summary, late onset of deep-seated graft infection is an important complication following mesh repair of inguinal hernia, whether open or laparoscopic. With the increasing use of synthetic materials for primary and recurrent hernia repair, the number of patients presenting with such infections is likely to increase.
REFERENCES 1. Lichtenstein IL, Shulman AG, Amid PK, Montllor MM. The tension-free hernioplasty. Am J Surg. 1989;157:188 –193. 2. Fitzgibbons RL, Camps J, Cornet DA, et al. Laparoscopic inguinal herniorrhaphy: results of a multicenter trial. Ann Surg. 1995; 221:3–13. 3. Shulman AG, Amid PK, Lichtenstein IL. The safety of mesh repair for primary inguinal hernias: results of 3019 operations from five diverse sources. Am Surg. 1992;58:255–257. 4. Bartlett W. An improved filigree for the repair of large defects in the abdominal wall. Ann Surg. 1903;38:47– 62. 5. Throckmorton TD. Tantalum gauze in the repair of hernias complicated by tissue deficiency. Surgery. 1948;23:32– 46. 6. Smith RS. The use of prosthetic materials in the repair of hernias. Surg Clin N Am. 1971;51:1387–1399. 7. Usher FC. Hernia repair with knitted polypropylene mesh. Surg Gynecol Obstet. 1963;117:139 –140. 8. Peacock EE. Here we are: behind again! Am J Surg. 1989;157: 187. 9. Stoppa RE. The preperitoneal approach and prosthetic repair of groin hernias. In: Nyhus LM, Condon RE, eds. Hernia. 4th ed. Philadelphia: JB Lippincott; 1995:188 –210. 10. Stoker DL, Spiegelhalter DJ, Singh R, Wellwood JM. Laparo-
THE AMERICAN JOURNAL OF SURGERY® VOLUME 176 JULY 1998
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PROSTHETIC INFECTION AFTER INGUINAL HERNIA REPAIR/MANN ET AL
scopic versus open inguinal hernia: randomised prospective trial. Lancet. 1994;343:1243–1245. 11. Arnaud JP, Eloy R, Adloff M, Grenier JF. Critical evaluation of prosthetic materials in repair of abdominal wall hernias. Am J Surg. 1977;133:338 –345. 12. Lamb JP, Vitale T, Kaminski DL. Comparative evaluation of synthetic meshes used for abdominal wall replacement. Surgery. 1983;93:643– 648. 13. Cerise EJ, Busuttil RW, Craighead CC, Ogden WW. The use of mersilene mesh in repair of abdominal wall hernias: a clinical and experimental study. Ann Surg. 1975;181:728 –734. 14. Elliot MP, Juler GL. Comparison of marlex mesh and microporous teflon sheets when used for hernia repair in the experimental animal. Am J Surg. 1979;137:342–344. 15. Jacobs E, Blaisdell FW, Hall AD. Use of knitted marlex mesh in the repair of ventral hernias. Am J Surg. 1965;110:897–902. 16. Waldrep DJ, Shabot MM, Hiatt JR. Mature fibrous cyst formation after marlex mesh ventral herniorrhaphy: a newly described pathological entity. Am Surg. 1993;59:716 –718. 17. Gilbert AI, Felton LL. Infection in inguinal hernia repair considering biomaterials and antibiotics. Surg Gynecol Obstet. 1993; 177:126 –130. 18. Thill RH, Hopkins WM. The use of mersilene mesh in adult inguinal and femoral hernia repairs: a comparison with classic techniques. Am Surg. 1994;60:553–557. 19. Berliner SD. Clinical experience with an inlay expanded poly-
14
tetrafluoroethylene soft tissue patch as an adjunct in inguinal hernia repair. Surg Gynecol Obstet. 1993;176:323–326. 20. Bauer JJ, Salky BA, Gelernt IM, Kreel I. Repair of large abdominal wall defects with expanded polytetrafluoroethylene (PTFE). Ann Surg. 1987;206:765–769. 21. Brooks DC. A prospective comparison of laparoscopic and tension-free open herniorrhaphy. Arch Surg. 1994;129:361–366. 22. Slim K, Pezet D, Le Roux S, Chipponi J. Mesh infection after laparoscopic herniorrhaphy. Eur J Surg. 1996;162:247–248. 23. Platt R, Zaleznik DF, Hopkins CC, et al. Perioperative antibiotic prophylaxis for herniorrhaphy and breast surgery. NEJM. 1990; 322:153–160. 24. Lazorthes F, Chiotasso P, Massip P, et al. Local antibiotic prophylaxis in inguinal hernia repair. Surg Gynecol Obstet. 1992; 175:569 –570. 25. Walker AP. Biomaterials in hernia repair. In: Nyhus LM, Condon RE, eds. Hernia. 4th ed. Philadelphia: JB Lippincott; 1995:534 –540. 26. Troy MG, Dong QS, Dobrin PB, Hecht D. Do topical antibiotics provide improved prophylaxis against bacterial growth in the presence of polypropylene mesh? Am J Surg. 1996;171:391–393. 27. Pitt HA, Postier RG, Macgowan WAL, et al. Prophylactic antibiotics in vascular surgery: topical, systemic or both? Ann Surg. 1980;192:356 –364. 28. Galland RB, Heine KJ, Trachtenberg LS, Polk HC. Reduction of surgical wound infection rates in contaminated wounds treated with antiseptics combined with systemic antibiotics: an experimental study. Am J Surg. 1982;97:329 –332.
THE AMERICAN JOURNAL OF SURGERY® VOLUME 176 JULY 1998
BACKGROUND: The use of prosthetic biomaterials for the primary repair of inguinal hernias is now commonplace. Late-onset deep-seated prosthetic infection can be an unexpected complication. METHODS: The literature from a Medline search relating to the biology of mesh in the setting of hernia repair is discussed. CONCLUSIONS: The use of a foreign body for hernia repair does not appear to alter the incidence of superficial wound infection. Late-onset deep graft infection has been rarely reported, and the true incidence is yet to be established. With the more widespread use of mesh materials, this complication may become increasingly evident. Am J Surg. 1998;176:12–14. © 1998 by Excerpta Medica, Inc.
P
rosthetic mesh biomaterials have recently enjoyed renewed popularity in the repair of inguinal hernias. The success of “tension-free” open repairs,1 and the emergence of laparoscopic mesh procedures2 has established a role for the prosthetic repair of primary and recurrent inguinal herniation. Initial concerns that the routine use of a foreign body might be attended by a higher wound infection rate have not been realized.3 An often unexpected complication, however, is the late onset of deep graft infection occurring many months after the operation.
HISTORY The use of prosthetic biomaterials to effect the repair of deficient or absent abdominal wall tissues is not a new concept. Silver mesh was initially used in Germany at the turn of the century, and introduced in the United States shortly thereafter.4 The corrosion of silver induced by contact with tissue fluids precluded widescale use, and in the 1940s mesh of inert tantalum was substituted.5 Early experience with these prosthetic materials was disappointing, however, due to an unacceptably high incidence of infection, rejection, and recurrence. The introduction of biologically tolerated synthetic polymers in the 1950s heralded a new era of mesh repairs, although these were generally restricted to incisional and recurrent hernias.6,7
From the Academic Surgical Unit, St Mary’s Hospital, London, England. Requests for reprints should be addressed to Ara Darzi, MD, Consultant Surgeon, St Mary’s Hospital, Paddington, London W2 1PG, England. Manuscript submitted June 30, 1997 and accepted in revised form March 17, 1998.
12
© 1998 by Excerpta Medica, Inc. All rights reserved.
In recent years there has been renewed interest in the use of prosthetic materials in the repair of primary inguinal hernias. Dissatisfaction with the rationale for and results of traditional sutured repair influenced Lichtenstein et al1 to explore the role of tension-free mesh repair.8 Graft repairs in the preperitoneal plane by open9 and laparoscopic10 approaches have also been advocated.
BIOLOGY OF PROSTHETIC MESH The biological response to surgically implanted prosthetic mesh materials has been extensively studied.7 The initial reaction, characterized by acute inflammatory cell infiltration, is gradually replaced by fibroblasts (which infiltrate through the interstices of porous meshes) and a variable number of giant cells.11 Uncomplicated incorporation of the mesh into the host tissues is associated with an increase in the fibroblast to inflammatory cell ratio. In animal models this is reflected in the bursting strength of the prosthesis, which increases over the first 1 to 3 months and then achieves a maximum thereafter.11,12 Experimental evidence suggests that fascial repairs with synthetic mesh display greater bursting strength than can be achieved with tissue approximation by direct suture.13 The host response to the mesh varies with the physical properties of the material used. Nonporous grafts are generally less well tolerated than porous ones, and have been shown to produce a persistent fluid collection with incomplete incorporation, and even migration.11 Similarly, the chemical composition of the mesh may have a profound effect on the local tissue reaction. Polypropylene mesh (Marlex, CR Bard) has been shown to excite a greater inflammatory reaction than polytetrafluoroethylene (GoreTex, WL Gore), resulting in greater scarring, contracture, and distortion of the graft.12,14 Under ideal circumstances, then, the implanted mesh material becomes incorporated into the surrounding tissues by means of fibrous infiltration, with the formation of a linear “neofascia.” Whether the mechanical strength relates to the subsequent scarring or the tensile characteristics of the mesh material is unclear. However, it is appreciated that biodegradable mesh materials such as polyglactin (Vicryl, Ethicon) tend to hydrolyze before fibrous tissue incorporation is complete, and are associated with a lower bursting pressure in the experimental condition.12 It would appear that scar formation is of paramount importance, but that this is to a great extent determined by the characteristics of the graft. When mesh incorporation is disordered, the result is a fluid collection (seroma) with a variable degree of surrounding fibrosis and incomplete attachment of the graft, which may even be floating free. Thus, seroma is the commonest complication of mesh insertion, occurring in 0002-9610/98/$19.00 PII S0002-9610(98)00094-4
PROSTHETIC INFECTION AFTER INGUINAL HERNIA REPAIR/MANN ET AL
45% of patients in one series following ventral herniorrhaphy (where the mesh is located deep to the subcutaneous fat).15 For the most part, these will resolve with aspiration, although repeated attempts may be required. In those cases where fluid collections persist, a mature fibrous cyst may form that ultimately requires surgical excision for cure.16
MESH-RELATED INFECTION The major source of concern regarding the use of synthetic fascial substitutes has been a perceived increase in infection risk. There is some evidence to suggest that this may be a more common occurrence when a seroma develops,11 although the influence of percutaneous aspiration will obviously be a factor. Data from published series do not support the contention that infection is more common in open mesh repair of inguinal hernia as compared with conventional sutured repair. In a review of 1,834 mesh inguinal hernia repairs, Gilbert and Felton17 reported 14 cases with infection (0.8%), compared with 659 suture repairs with 7 infections (1%). Similarly, in a comparison of prosthetic inguinal hernia repair with the Bassini operation, Thill and Hopkins18 found infection rates of 0.54% and 1.2%, respectively. The pooled “Lichtenstein” series reports an overall infection rate of 0.03% for patch repair of inguinal hernia,3 and a recent review of a series of 350 mesh repairs by a single surgeon included only one instance of infection.19 When considering bacterial invasion, a distinction must be made between superficial wound infection and deep graft infection. The former tend to occur in the early postoperative period, and do not seem to be influenced by the use of mesh. In fact, treatment of superficial wound infection may be effective using some combination of antibiotics (for cellulitis) and drainage (for subcutaneous collection), and in these circumstances removal of the prosthesis may not be necessary for complete healing.17 In contrast, deep graft infection has not been commonly reported in the literature. The presentation of deep-seated infection of the prosthesis may be a delayed one, following many months from the operation. Sporadic cases have appeared in the literature from series of open mesh20 and laparoscopic hernia repairs.2,21,22 These patients may present with signs of acute inflammation, or in a more indolent manner with a discharging sinus, occasionally with the mesh presenting through the wound.7 That bacteria may infiltrate throughout the layered mesh-fibrous reaction complex has been demonstrated by microscopic examination.19 It follows that usually the only way to ensure eradication of infection is to remove the mesh, which procedure may not necessarily result in recurrent herniation if sufficient fibrous scarring remains. The usual infecting organism in wound17 and graft19,20 infection is Staphylococcus aureus, although enteric organisms may also be found. Whether any relationship exists between early superficial wound infection and late-onset deep graft infection is unclear. The time course of these rather different infective complications suggests that while early infection relates to operative contamination, late prosthetic infection may arise as a complication of a persisting fluid collection.
INFECTION CONTROL What measures can be taken to reduce the likelihood of infection? The use of prophylactic antibiotics (systemic or topical) is still debated for the “clean” operation of herniorrhaphy.23,24 Unfortunately, there is little direct clinical evidence on which to base recommendations when implantable mesh is used. Hence, although some authors advocate the use of an antistaphylococcal agent (either parenteral25 or topical1) on empirical grounds, others contest that the benefit remains unproven.17 Work from animal models suggests that systemic and local antibiotic prophylaxis are equally effective against bacterial growth in the presence of mesh, but that their combination offers no additional advantage26 (a finding consistent with clinical experience in vascular prosthetic surgery27). Topical antiseptics (eg, povidone-iodine) applied into the wound are recommended by some, although experimental evidence suggests that their use confers additional benefit over antibiotic prophylaxis only in the case of massive bacterial inoculation.28 Probably more important than the choice of antibacterial is the observance of strict asepsis during mesh preparation and implantation (it has been suggested that the resterilization and use of previously opened meshes may predispose to microbial contamination). The diagnosis of graft sepsis is usually obvious, although occult infection may be difficult to localize, and in this context soft tissue imaging including magnetic resonance scanning may find a useful role. Whatever the mode of presentation, treatment of established infection should be prompt, as life-threatening staphylococcal toxic shock syndrome is a potentially catastrophic sequel.
CONCLUSION In summary, late onset of deep-seated graft infection is an important complication following mesh repair of inguinal hernia, whether open or laparoscopic. With the increasing use of synthetic materials for primary and recurrent hernia repair, the number of patients presenting with such infections is likely to increase.
REFERENCES 1. Lichtenstein IL, Shulman AG, Amid PK, Montllor MM. The tension-free hernioplasty. Am J Surg. 1989;157:188 –193. 2. Fitzgibbons RL, Camps J, Cornet DA, et al. Laparoscopic inguinal herniorrhaphy: results of a multicenter trial. Ann Surg. 1995; 221:3–13. 3. Shulman AG, Amid PK, Lichtenstein IL. The safety of mesh repair for primary inguinal hernias: results of 3019 operations from five diverse sources. Am Surg. 1992;58:255–257. 4. Bartlett W. An improved filigree for the repair of large defects in the abdominal wall. Ann Surg. 1903;38:47– 62. 5. Throckmorton TD. Tantalum gauze in the repair of hernias complicated by tissue deficiency. Surgery. 1948;23:32– 46. 6. Smith RS. The use of prosthetic materials in the repair of hernias. Surg Clin N Am. 1971;51:1387–1399. 7. Usher FC. Hernia repair with knitted polypropylene mesh. Surg Gynecol Obstet. 1963;117:139 –140. 8. Peacock EE. Here we are: behind again! Am J Surg. 1989;157: 187. 9. Stoppa RE. The preperitoneal approach and prosthetic repair of groin hernias. In: Nyhus LM, Condon RE, eds. Hernia. 4th ed. Philadelphia: JB Lippincott; 1995:188 –210. 10. Stoker DL, Spiegelhalter DJ, Singh R, Wellwood JM. Laparo-
THE AMERICAN JOURNAL OF SURGERY® VOLUME 176 JULY 1998
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PROSTHETIC INFECTION AFTER INGUINAL HERNIA REPAIR/MANN ET AL
scopic versus open inguinal hernia: randomised prospective trial. Lancet. 1994;343:1243–1245. 11. Arnaud JP, Eloy R, Adloff M, Grenier JF. Critical evaluation of prosthetic materials in repair of abdominal wall hernias. Am J Surg. 1977;133:338 –345. 12. Lamb JP, Vitale T, Kaminski DL. Comparative evaluation of synthetic meshes used for abdominal wall replacement. Surgery. 1983;93:643– 648. 13. Cerise EJ, Busuttil RW, Craighead CC, Ogden WW. The use of mersilene mesh in repair of abdominal wall hernias: a clinical and experimental study. Ann Surg. 1975;181:728 –734. 14. Elliot MP, Juler GL. Comparison of marlex mesh and microporous teflon sheets when used for hernia repair in the experimental animal. Am J Surg. 1979;137:342–344. 15. Jacobs E, Blaisdell FW, Hall AD. Use of knitted marlex mesh in the repair of ventral hernias. Am J Surg. 1965;110:897–902. 16. Waldrep DJ, Shabot MM, Hiatt JR. Mature fibrous cyst formation after marlex mesh ventral herniorrhaphy: a newly described pathological entity. Am Surg. 1993;59:716 –718. 17. Gilbert AI, Felton LL. Infection in inguinal hernia repair considering biomaterials and antibiotics. Surg Gynecol Obstet. 1993; 177:126 –130. 18. Thill RH, Hopkins WM. The use of mersilene mesh in adult inguinal and femoral hernia repairs: a comparison with classic techniques. Am Surg. 1994;60:553–557. 19. Berliner SD. Clinical experience with an inlay expanded poly-
14
tetrafluoroethylene soft tissue patch as an adjunct in inguinal hernia repair. Surg Gynecol Obstet. 1993;176:323–326. 20. Bauer JJ, Salky BA, Gelernt IM, Kreel I. Repair of large abdominal wall defects with expanded polytetrafluoroethylene (PTFE). Ann Surg. 1987;206:765–769. 21. Brooks DC. A prospective comparison of laparoscopic and tension-free open herniorrhaphy. Arch Surg. 1994;129:361–366. 22. Slim K, Pezet D, Le Roux S, Chipponi J. Mesh infection after laparoscopic herniorrhaphy. Eur J Surg. 1996;162:247–248. 23. Platt R, Zaleznik DF, Hopkins CC, et al. Perioperative antibiotic prophylaxis for herniorrhaphy and breast surgery. NEJM. 1990; 322:153–160. 24. Lazorthes F, Chiotasso P, Massip P, et al. Local antibiotic prophylaxis in inguinal hernia repair. Surg Gynecol Obstet. 1992; 175:569 –570. 25. Walker AP. Biomaterials in hernia repair. In: Nyhus LM, Condon RE, eds. Hernia. 4th ed. Philadelphia: JB Lippincott; 1995:534 –540. 26. Troy MG, Dong QS, Dobrin PB, Hecht D. Do topical antibiotics provide improved prophylaxis against bacterial growth in the presence of polypropylene mesh? Am J Surg. 1996;171:391–393. 27. Pitt HA, Postier RG, Macgowan WAL, et al. Prophylactic antibiotics in vascular surgery: topical, systemic or both? Ann Surg. 1980;192:356 –364. 28. Galland RB, Heine KJ, Trachtenberg LS, Polk HC. Reduction of surgical wound infection rates in contaminated wounds treated with antiseptics combined with systemic antibiotics: an experimental study. Am J Surg. 1982;97:329 –332.
THE AMERICAN JOURNAL OF SURGERY® VOLUME 176 JULY 1998