EXCERPT FROM NEW TEXTBOOK
Prevention and Management of Laparoendoscopic Surgical Complications, 2nd Edition
MICHAEL S. KAVIC, MD, GAYETTE F. GRIMM, MD, JOHN THOMAS, MD
A common complication of surgery is infection, which can range from minor wound infections to large, complex intraabdominal catastrophes, as well as infections distant to the site of surgery. The purpose of this chapter is to synthesize current clinical and basic science knowledge of laparoscopic infections and collate that knowledge into a set of coherent principles. This will be done by using laparoscopic hernioplasty as a conceptual framework of a sound approach to management of prosthetic infections.
Most cases of surgical infection are due to deficiencies in surgical technique (including breaks in sterile technique) or failure to control the bacterial milieu of a surgical wound. For instance, delicate handling of tissues, gentle dissection, and meticulous homeostasis are time-honored surgical principles that diminish the potential for infection . Thus, any surgical technique that minimizes the amount of contamination and decreases the amount of devitalized tissue at the operative site will decrease the incidence of surgical-site infection by decreasing the quantity of nutrients available to potential pathogens.
Distinct differences exist between laparoscopic procedures in gaining access to the operative site. In general, laparoscopic surgery has smaller skin incisions, less dissection (especially in the subcutaneous tissues), and incisions that are often distant from the operative field. This causes less traumatized tissues overall and provides fewer nutrients for pathogens as discussed above. In addition, it is thought that the smaller incisions grant fewer opportunities for introduction of bacteria into an operative site and thereby reduce the chance of infection.
Sutures or tacking materials also make a great difference in the incidence of surgical infection. As previously noted, the presence of suture material in a wound decreases the minimum bacterial concentration needed to produce clinical infection . Braided sutures compound this problem due to the presence of very small interstices between the braided strands that provide a “safe harbor” for bacteria. But even monofilament suture can have interstices, such as between the throws of a knot, that can harbor bacteria [13, 11, 12]. Thus, the use of any suture can increase the risk of infection. In some laparoscopic procedures, especially laparoscopic hernia repairs, inert, metal-anchoring tacks or clips are used. These devices are minimally reactive and have no interstices, thus providing little place for bacteria to hide and cause infection.
Finally, the presence of mesh in a surgical site also increases the chance of infections by reducing the threshold numbers of bacteria required for infection and increasing the virulence factor of bacteria . In the presence of a synthetic graft, bacteria bind to the prosthesis via microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) that are elaborated by the bacteria themselves . These adhesion molecules recognize and bind to elements of the host’s interstitial matrix. The binding process then leads to an elaboration of a glycoprotein layer that impedes the entrance of host bactericidal elements. In addition, traumatized tissues have surfaces devoid of a protective cellular layer, competent protective extracellular polysaccharide (glycocalyx), and a basement membrane, all of which promote bacterial growth [11,13].
The type of mesh chosen for hernia repair can also affect the chance of infection because macrophages and neutrophils require larger pores for admission than bacteria do. Synthetic mesh can be classified by pore size into 4 groups:
Type I—Prostheses with pores greater than 75 microns. Examples: Marlex, monofilament polypropylene meshes [8,14,15];
Type II—Prostheses with pore sizes less than 10 microns in at least 1 of their 3 dimensions. Examples: ePTFE, Dual Mesh, surgical membrane;
Type III—Macroporous prosthesis with multifilamentous or microporous components. Examples: braided Dacron, braided polypropylene;
Type IV—Biomaterial with submicron pore size. Example: silastic.
The completely macroporous materials (all pores >10 microns) will allow for admission of macrophages, fibroblasts, blood vessels, and collage fibers into the mesh, thus providing a lesser chance of infection.
In summary, current techniques of laparoscopic hernia surgery have optimized conditions to make bacterial infection of the prosthetic materials less likely. Reducing the potential inoculum with small incisions remote from the operative site minimizes bacterial contamination overall and especially to the operative site. Laparoscopic dissection is typically more meticulous than open methods due to the magnification of laparoscopic imaging, thus the amount of devitalized tissue available for bacteria to bind and utilize as nutrition is reduced. Common use of Type I biomaterials and fixation with staples or other inert tacking devices eliminates interstices less than 10 microns. The result of using the laparoscopic method and these materials is a hernia repair that is quite resistant to infection with infection rates reported as 0% to 0.1% [10,16,22,23].
DIAGNOSIS AND TREATMENT OF MESH INFECTIONS
Complications of laparoscopic hernioplasty can occur, and any deviation from normal postoperative recovery should raise suspicion of a problem. In general, the complications are similar to those of open hernioplasty, and the differential diagnosis should include hernia recurrence, hematoma, seroma, orchitis, neuralgia, “mesh inguinodynia,” and mesh infection.
Two distinct types of prosthetic infection have been described. The first type is an uncomplicated infection caused by contamination of the prosthetic material at the time of operation. This contamination may be from endogenous or exogenous sources. In uncomplicated infections, the source of sepsis is localized and not ongoing. The second type of prosthetic infection, a complicated prosthetic infection, usually results from mesh migration and erosion into adjacent viscera. In these instances, an ongoing source of sepsis is present from the eroded organ [10,16-21].
Uncomplicated infection can frequently be treated by local measures without removal of the prosthesis (particularly if a Type I mesh with large pores constructed of monofilament material has been utilized) . Graft migration, however, requires surgical intervention for removal of the mesh and management of the enteric source of sepsis [11,16,18-20]. Distinguishing between these 2 types of compilations is essential for successful management. Their clinical signs and symptoms, however, are not necessarily specific to mesh infection and may be indistinguishable from each other as well as from other postherniorrhaphy complications.
For example, hernia recurrence after laparoscopic inguinal hernia repair can present with swelling at the operative site, pain, obstructive symptoms, and skin discoloration. The presentation of recurrence may be early or delayed. Differentiating recurrence from other types of complications is important because successful treatment of mesh infections depends on the results of bacteriologic studies of fluid aspirated or drained from the operative site. Aspiration or incision and drainage of the visceral content of a recurrent hernia, however, could prove disastrous. Ultrasound and computed tomography are useful to rule out early hernia recurrence as a cause for prolonged groin swelling or pain. Radiographic evidence of recurrence does not rule out infection, but does mandate reoperation.
Once recurrence is eliminated, the differential includes infection, seroma, hematoma, and orchitis along with neuralgia. A diagnosis of postoperative neuropathy is established if the patient describes pain in the distribution of the ilioinguinal, iliohypogastric, genitofemoral, or lateral femoral cutaneous nerve that has arisen since surgery. In addition, there must be no systemic signs or symptoms of sepsis (ie, fever, leukocytosis, elevated erythrocyte sedimentation rate) and radiographic imaging is normal. Delayed presentations of postoperative neuropathy have been reported. Confirmation of neuralgia is aided when infiltration of the involved nerve with local anesthetic relieves pain. Treatment may require medication such as amitriptyline, local injection with steroid, or mesh removal with or without neurectomy of the iliohypogastric, ilioinguinal, and genitofemoral nerves.
Swelling from hematoma, seroma, and orchitis must be differentiated from swelling caused by mesh infection, as the treatment of these conditions is quite different. Seroma and hematoma can be managed expectantly with resolution expected within 6 weeks to 12 weeks. Orchitis is usually painless and associated with an indurated testicle that slowly subsides with or without antibiotics and can result in an atrophic testicle, usually within a year. Mesh infections often have the universal signs of infection: pain, redness, swelling, warmth, and possibly fever and leukocytosis.
Occasionally, persistent draining sinus tracts have been described with complicated and uncomplicated mesh infections and may herald a stitch abscess or a more severe infection [8,11,16,19,20]. Once infection is suspected and recurrence is ruled out, aspiration of fluid with appropriate bacteriologic studies should be done. Additionally, cultures of any drainage from chronic sinus tracts should be performed. Aspirations of purulent fluid should prompt open drainage and administration of broad-spectrum antibiotics . Polymicrobial infections or growth of enteric organisms should raise the suspicion of a visceral injury and prompt radiographic investigation with computed tomography or fistulography [11,18-20].
Infections that are not the result of an enteric source and involve Type I mesh are generally treatable by exposure of the prosthesis and removal of suture and unincorporated mesh, along with local wound care. Good results usually follow [11,12]. Vacuum system dressings have been used for infected wounds to reduce the effect of wound secretions and encourage tissue ingrowth. Early experience with these systems suggests that they may have utility in conservative management of open infected abdominal wall grafts (Figures 1 and 2).
Figure 1. Graft.
Figure 2. Vacuum System Dressing.
Type II prostheses typically need to be removed, as tissue incorporation is impaired in the presence of infection. A trial of conservative management with antibiotic, exposure, and local wound care, however, is warranted before removal. On the other hand, enteric fistulas will not respond well to local care and require removal of the mesh as well as repair of the fistula independent of the type of mesh used [18-20]. The operative approach for mesh removal and fistula repair may require open incision and drainage of the groin followed by laparotomy. Alternatively, a laparoscopic intervention may be attempted if the operator has sufficient skill and experience. With infection, mesh usually becomes unincorporated from the operative site and is not difficult to remove. The operator’s experience and judgment guide the choice or approach (open or laparoscopic).
As described above, it is rare for mesh to be removed because of an infectious complication. In addition, when mesh is removed after hernioplasty, recurrence seems to be infrequent . However, when mesh must be replaced because of infection, care must be taken to avoid recurrent infection. Deysine  has outlined an approach to this problem based on orthopedic experience with implantable prostheses. Essentially, this investigator advocates aspiration of any infected material to test for residual bacteria. If percutaneous microbiological wound sampling is positive, remove the prosthesis and treat the infection. Once cultures are negative, repair with a new prosthesis is possible; otherwise perform wound exploration with secondary closure (Figure 3).
Figure 3. Algorithm for Treatment of Postherniorrhaphy Infection.
In summary, infection related to laparoscopic surgery is not much different from that of conventional surgery, and all the same principles of good surgical practice hold true. The major difference is that infection seems to be much reduced with laparoscopy when compared with conventional surgery. This is likely due to a multitude of reasons, such as smaller incisions, less trauma to tissues, and use of inert foreign bodies. But, some studies suggest that physiological reasons, such as less immune system depression, may exist that account for the lower infection rates. In general, infections that do occur after a laparoscopic procedure can be treated in a similar fashion to conventional surgical infections.
Michael S. Kavic, MD, is Director of Education, General Surgery for the St. Elizabeth Health Center; Professor of Surgery and Vice Chair, Department of Surgery for the Northeastern Ohio Universities College of Medicine; and an Adjunct Professor of Surgery, Department of Surgery at the University of Pittsburgh School of Medicine. He is a founding member of the SLS and is Editor-in-Chief of JSLS, Journal of the Society of Laparoendoscopic Surgeons. Dr Kavic has written and published numerous book chapters, journal articles, and editorials and has lectured nationally and internationally on laparoscopic surgery. He is a past president of both SLS and the American Hernia Society.
Gayette F. Grimm, MD, is a general surgeon at Gundersen Lutheran Clinic in Prairie du Chien, Wisconsin. She completed her general surgery internship and residency at St. Elizabeth’s Health Center in Youngstown, Ohio. Dr Grimm is an active member of the Society of Laparoendoscopic Surgeons.
John Thomas, MD, is with the Department of General Surgery at Stonewall Jackson Memorial Hospital in Westin, West Virginia. He completed his residency at Mount Carmel Health. Dr Thomas is an active member of the Society of Laparoendoscopic Surgeons.
1. Wangensteen OH, Wangensteen SD, Klinger CF. Surgical infection and history. In: Simmons RL, Howard RJ, eds. Surgical Infectious Diseases. New York, NY: Appleton-Century-Crofts; 1982:1-10.
2. Koch R. Die aetiologie der tuberculose. Berl Klin Wschr. 1882;9:221-230.
3. Dorland’s Illustrated Medical Dictionary. 28th ed. Philadelphia, PA: WB Saunders Co; 1994:1341.
4. Lister J. On a new method of treating compound fractures, abscesses, etc., with observations on the conditions of suppuration. Lancet. 1867;1:326-329, 357-359, 507-509, 2:95-96.
5. Muscarella P, Steinberg SM. Postoperative wound infection. In: Cameron JL, ed. Current Surgical Therapy. 7th ed. St. Louis, MO: Mosby; 2001:1277-1282.
6. Elek SD, Conen PE. The virulence of Staphylococcus pyogenes for man: a study of the problems of wound infection. Brit J Exp Path. 1957;38:573-586.
7. Alexander JW, Kaplan JZ, Altemeier WA. Role of suture materials in the development of wound infection. Ann Surg. 1966;1965(2):192-199.
8. Amid PK. Classification of biomaterials and their related complications in abdominal wall hernia repair. Hernia. 1997;1:15-21.
9. Neel HB III. Implants of Gore-Tex. Comparisons with Teflon-coated polytetrafluoroethylene carbon and porous polyethylene implants. Arch Otolaryngol. 1983;109:427-433.
10. Amid Pariz, et al. The goals of modern hernia surgery. How to achieve them: open or laparoscopic repair. Probl Gen Surg. 12;2:165-171.
11. Deysine M. Pathophysiology, prevention and management of prosthetic infections in hernia surgery. Surg Clin North Am. 1998;78(6):1105-1115.
12. Gilbert A, Felton LL. Infection in inguinal hernia repair considering biomaterials and antibiotics. Surg Gynecol Obstet. 1993;177:126-130.
13. Patti JM. MSCRAMM-mediated adherence of microorganisms to host tissues. Annu Rev Microbiol. 1994;48:585-617.
14. Bobyn JD, Wilson GJ, MacGregor DC, Pilliar RM, Weathersby GC. Effect of pore size on the peel strength of attachment of fibrous tissue to porous-surfaced implants. J Biolmed Mater Res. 1982;16:571-584.
15. White RA. The effect of porosity and biomaterial on the healing and long-term mechanical properties of vascular prostheses. ASAIO. 1988;11:95-100.
16. Fitzgibbons RJ Jr, Camps J, Cornet DA, et al. Laparoscopic inguinal herniorrhaphy: results of a multicenter trial. Ann Surg. 1995;221:13-130.
17. Crist DW, Gadacz TR. Complications of laparoscopic surgery. Surg Clin North Am. 1993;73(2):265-289.
18. Hume R, Bour J. Mesh migration following laparoscopic inguinal hernia repair. J Laparoendosc Surg. 1996;6(5):333-335.
19. Kaufman Z, Engelberg M, Zager M. Fecal fistula:a late complication of Marlex mesh repair. Dis Col Rectum. 1981;24:543-44.
20. Miller K, Junger W. Ileocutaneous fistula formation following laparoscopic polypropylene mesh hernia repair. Surg Endosc. 1997;11:772-773.
21. Smith RS. The use of prosthetic materials in the repair of hernias. Surg Clin North Am. 1971;51(6):1387-1389.
22. Schultz C, Baca I, Gotzen V. Laparoscopic inguinal hernia repair. Surg Endosc. 2001;15(6):582-584.
23. Kapiris SA, Brough WA, Royston CM, O’Boyle C, Sedman PC. Laparoscopic transabdominal preperitonal (TAPP) hernia repair. A 7-year two-center experience in 3017 patients. Surg Endosc. 2001;15(9):972-975.
www.Laparoscopy.org The Laparoscopic Surgery Information Source