PATHOPHYSIOLOGY, PREVENTION, AND MANAGEMENT OF PROSTHETIC INFECTIONS IN HERNIA SURGERY

PATHOPHYSIOLOGY, PREVENTION, AND MANAGEMENT OF PROSTHETIC INFECTIONS IN HERNIA SURGERY

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PATHOPHYSIOLOGY, PREVENTION, AND MANAGEMENT OF PROSTHETIC INFECTIONS IN HERNIA SURGERY Maximo Deysine, MD

At the current infection rate of 1%to 29'0, anywhere from 7500 to 15,000 of the 750,000 patients undergoing herniorrhaphy per year in the United States may develop a wound infection.', l6 In addition, present data suggest that postherniorrhaphy infection is associated with a high recurrence rate.8 Moreover, as hernias are increasingly being repaired with meshes and plugs, surgeons should make an extended effort to prevent infection, and, when they occur, to treat them expeditiously. Despite the fact that, during surgery, bacterial entrance into the wound is unavoidable," their further adherence and colonization can be prevented by well-established operating room principles.l2?24, 25 The frequent insertion of metallic and plastic devices by orthopedists and ophthalmologists have generated a substantial amount of research geared toward the understanding of the mechanisms involved in wound and prosthetic infection, as well as in their diagnosis and treatment.9,lo Such knowledge can be advantageously applied to the field of hernia repair.

From the Department of Surgery, State University of New York at Stony Brook, Stony Brook; and Mercy Medical Centre, Rockville Centre, New York

SURGICAL CLINICS OF NORTH AMERICA VOLUME 78 * NUMBER 6 * DECEMBER 1998

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Every herniorrhaphy should be considered an exercise in infection control ruled by the following factors: (1) bacteria enter wounds from the air in the operating room, the bodies of the operating team, from errors in draping, and from perforated gloves"; (2) once in the wound, the bacteria attempt to undergo a sequence of evolutionary events leading to their survival and eventual reproduction, colonizing an$, devitalized tissue or foreign body9; and (3) the immune system recognizes and seeks to eliminate the bacteria by the process of inflammation, producing a clinical infection. This biologic sequence is being increasingly understood; thus, the operating team's first priority is to prevent bacterial wound entrance and colonization.26 BACTERIAL BINDING

After entering a wound from the previously mentioned sources, bacteria produce an adhesive substance (adhesin) designated as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs), which recognize and adhere to fibronectin-, fibrinogen-, collagen-, and heparin-related polysaccharides present in the host fluids and tissues. MSCRAMMs have an important role in bacterial binding, first to the extracellular fluid, and then to the cells or to prosthetic surfaces.20 From an atomic level, one would see that the prosthetic surfaces possess binding sites that, when interacting with live elements, acquire a film of glycoproteinaceous binding material available to host living cells and bacteria. At a distance of a few nanometers, attractive van der Waals forces counteract hydrophilic and hydrophobic forces present in the substratum and the bacteria, allowing contact of sufficient duration to permit molecular cross-linking between the glycoproteinaceous materials and the substratum, subsequently producing an almost irreversible attachment by adhesion. Under these circumstances, bacteria commence nourishing from the surrounding fluids and form an extracapsular biofilm or "polysaccharide slime," which, in association with tissue debris, allows them to remain in permanent contact with the host tissue or the prosthesis. This Darwinian survival process produces a layer in which bacteria can thrive and to which antibiotics may not reach.9 From these events, the equation necessary to produce an infection clearly requires bacteria and something inert or dead to provide for the substrate in which microorganisms can survive during the first few hours after contamination. Biomaterials and devitalized tissues are relatively passive substrates and may contribute to bacterial development. In contrast, normal healthy tissues, consisting of live cells covered by extracellular space fluid, seem to resist bacteria quite well.4 Although biomaterials seem to behave as if they were inert, they are active at their surface atomic level, integrating in different fashions with the surface

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atoms of the host, facilitating adhesion, integration, inflammation, and immune responses, which depend on a variety of factors. Ideally, a prosthesis should have at its surface particle level a morphology that allows it to integrate favorably with the cells and fluids of the ho~t.~,'O Hernia prostheses fall into two categories: (1) those that are hydrophobic, such as expanded polytetrafluoroethylene, and (2) those that are hydrophilic polyester or polypropylene. As tissues are wet, their surface tension allows them to adhere more easily to hydrophilic materials, facilitating their integration. Those repelling water take more time to become integrated'by the fibroblastic response. Likewise, hydrophobic materials may initially repel the fluids containing bacteria. BACTERIAL SURVIVAL

Bacteria survival in the wound depends on an intricate series of events related to their idiosyncratic characteristics, on the surface substratum to be colonized, and on Darwinian survival strategies. For example, Staphylococcus epidermidis, an otherwise saprophytic bacterium colonizing the skin, may turn biologically aggressive when incorporated on prosthetic devices. Pseudomonas aeruginosa, streptococci, Proteus mirabila, and many other microorganisms also participate in wound and prosthesis infections, according to a complex set of biologic determinants.l7 THE BATTLEFIELD

The initial battlefield seems to be established at the level of the slime, a loosely amorphous extracellular polysaccharide composed of low and high molecular weight polymers which has an important role in the development and persistence of prosthesis-induced infections. This complex molecule may act as an ion exchange system for improved bacterial survival, diminishing polymorphonucleocyte phagocytosis and antibody responses. It may also produce p-lactamases, actively participating in the later stages of surface adhesion, aggregation, and polybacterial interaction' 22 (Fig. 1). DEFENSE MECHANISMS COUNTERAlTACK

The biologic events associated with the surgical act alter some of the host defense mechanisms. The inflammatory cascade releases oxygen radicals and enzymes, which, together with the proteolytic bacterial toxins, add to the tissue damage produced by technical trauma. In addition, every type of bacteria releases metabolic by-products that tend to destroy tissue and thus facilitate microbial adhesion and colonization. Concomitantly, polymorphonuclear leukocytes lose some of their bacte-

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Figure 1. Relationship between the invading bacteria, prosthesis, and necrotic host tissue. Bacterial SCRAMMS recognize and adhere to those surfaces, commencing their quest for survival.

rial killing effectiveness when in contact with nylon and polytetrafluoroethylene, and their superoxide release is minimized by a preempted "burst." Moreover, bacterial contact with biomedical materials seems to increase their resistance to antibiotic^.^, 13, l4 ORDER OF BATTLE

Upon bacterial arrival on a wound, serious competition occurs between their surface macromolecules and live tissue cells for integration with receptors in the wall of the prosthesis; this interaction becomes a critical factor in the occurrence of a wound infection. Biomaterial surfaces, now wet with liquid nutrients, offer receptor sites for either healthy tissue cells or bacteria, and the possibility of infection depends on the degree of awareness by the surgeon about these events because those receptor sites will be ready to integrate with first-comers. If healthy tissue cells colonize the surface of the prosthesis, then an infection is not likely to occur, but if bacteria are allowed to adhere to it first, they

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may claim that territory and establish a strong bond, colonizing the prosthesis.

STRATEGIES FOR INFECTION REDUCTION Diminishing Bacterial Entrance

Accepting the fact that under the best of circumstances bacteria will enter the wound, tire surgeon's role is to take all possible local and systemic measures to eradicate them before they can colonize it." The whole surgical team is responsible for measures geared toward diminishing the amount of bacterial ingress in the wound by following the dictums of asepsis and antisepsis well established by pre-antibioticera surgeon^.'^ The team should recognize the fact that a foreign body will be inserted and should heighten their alertness to prevent surgical field contamination. If possible, patients in whom a large prosthesis will be inserted and those who have diminished immune responses should be operated under laminar air flow conditions. The skin should be shaved just before surgery, and antiseptic painting should well exceed the margins of the planned incision. Scrubbing, gowning, gloving, and draping should be carried under with strict supervision by all to avoid potential sources of contamination (Fig. 2).

Diminishing the Amount of Inert Material in the Wound

The surgeon should make every attempt at diminishing the volume of dead tissue present in the wound at the end of a procedure because it will become an ideal medium for bacterial colonization. This is accomplished by purposefully reducing aggressive clamping and retracting, and injudicious utilization of the electrocautery, which creates areas of coagulating necrosis. In addition, to avoid further cell death by desiccation, the wound surface should be kept moist with isotonic fluids, preferably containing a topical antibiotic. The amount of foreign matter introduced into the wound, such as catgut, polyglycols, or other suture material, should be minimized because they become a nidus for bacterial colonization. Tissue approximation by sutures should be performed with minimal tension to avoid ischemia of the involved edges. In this regard, the insertion of a prosthesis diminishes wound tension, reducing the amount of dead tissue present in the world. Finally, before the wound is closed, attention should be paid to the subcutaneous tissue, whereupon all seemingly separated dr devitalized portions should be excised (Fig. 2).

Air Bodies Perforated gloves Instruments

r

Scrubbing Gowning Painting Draping

(H Errors In

1

,,

x.

r

Coagulation Necrosis

i

L

LRetracted

Substratum

Sutures Staples Plugs Drains

Figure 2. Bacterial sources and types of substratum, which represent essential elements for a wound infection.

PREVENTION OF BACTERIAL BINDING Local Measures Accepting the fact that the wound will include bacteria, the surgeon's role is to bring about all local and systemic steps to eradicate bacteria before they can adhere to the wound surfaces and start feeding and reproducing. Perhaps the best measure to prevent bacterial adhesion is early wound irrigation with an antibiotic solution. This policy forces bacteria to land on a bactericidal terrain, inhibiting their survival. The author irrigates wounds with a solution of 80 mg of gentamicin sulfate, dissolved in 250 mL of normal saline or multiples thereof, starting with the dissection of the hernia sac and continuing intermittently until the skin is closed. During the repair of large ventral hernias, the author covers the exposed subcutaneous and fascia1 tissue flaps with towels soaked in this solution, in which he also keeps the prosthesis before it

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is inserted. This measure, which provides a highly bactericidal antibiotic concentration without known systemic effects, has eliminated wound infection in the last 3000 inguinal and ventral herniorrhaphies the author performed. Systemic Prevention

Systemic prevention should include the intravenous use of a broadspectrum antibiotic. If the patient is not allergic to penicillin, the author uses a single peroperative intravenous dose of a second-generation cephalosporin; otherwise alternative agents can be used. This measure seems to be particularly important when operating on patients with deficient immune system^.^ SYMPTOMS OF INFECTION

In the presence of a wound infection, the progressively decreasing postoperative wound pain will increase and may be associated with a throbbing sensation and perhaps fever. The wound area becomes tender, erythematous, and may exudate. TREATMENT

Upon the first suspicion of a wound infection, a broad-spectrum antibiotic should be used during an observation period of 48 to 72 hours. If this treatment ameliorates the symptoms, it should be continued for a week; however, if swelling and tenderness do not abate, the subcutaneous tissue should be widely open and appropriate cultures and sensitivity obtained from the exudate, followed by a course of a specific antibiotic.ls This therapy solves most of these events, and the wound may heal without sequelae (Fig. 3). TREATMENT OF AN INFECTED PROSTHESIS

In some patients, the aforementioned policy leads to chronicity characterized by persistent suppuration and sinus tract formation; all of which are signs of mesh or suture line infection. In the experience of some surgeons who have treated infected ventral hernias repaired with prostheses, the judicious use of systemic antibiotics and frequent wound irrigations may avoid the need for mesh replacement', 5; however, in the inguinal region, the prostheses are more deeply located, and, when infected, may not be amenable to irrigations, resulting in chronic sinus tracts. This condition requires specific systemic antibiotics and, under appropriate anesthesia, wide opening of the wound with the removal of

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Wound Infection Management Post-Op Wound Tenderness f Fever ?

4

Broad Spectrum Antibiotic

1

Imy /

Open Wound Specific Oral Antibiotic + Irrigation

1

Follow Up

4

Continuing

.

+

Suppuration Remove Foreign + Body Antibiotics

Figure 3. Course of action recommended for the treatment of a primary wound infection.

all foreign bodies, including meshes, sutures, staples, and necrotic material. This is not a simple procedure because the meshes are often intimately adherent to the elements of the cord, the protection of which demands delicate and painstaking techniques. The wound can be closed loosely over a drain, which should remain in place until the amount of exudate is minimal. It is not uncommon that some portions of the infected mesh not apparent on the first attempt may produce sinus tract recurrence depicting the presence of infected residual material, the removal of which may require repeated surgical attempts. This course of action often leaves an unprotected posterior inguinal wall, leading to a recurrence. The reoperation which requires the insertion of a new prosthesis into an area of dubious sterility. The experience of orthopedic surgeons dealing with the same problem led this author to percutaneously test those wounds for residual bacteria.” If negative, this procedure, which should be performed under sterile precautions, provides some assurance of a sterile field. If the aspirations reveal the presence of bacteria, a course of appropriate antibiotics is indicated, followed by repeated wound testing in 2 weeks. If it continues to be positive, then the wound should be open, debrided, allowed to heal, and

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Herniorrhaphy with a Prosthesis

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Wound Infection

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Prosthesis Removal Recurrent Hernia: Wound Clinically Healed

4 Indication: Prosthetic Repair

QUESTION: IS THE WOUND STERILE ??

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+ PERCUTANEOUS MICROBIOLOGICAL WOUND SAMPLING 4

4 Positive Culture

Negative Culture

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4

Specific Parenteral Antibiotics

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Repeat Percutaneous Testing 4 Negative 4 Repair with Culture New Prosthesis

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Positive Culture

4 Wound Exploration with Secondary Closure Figure 4. Course of action recommended for the treatment of a recurrent hernia occurring in a previously infected field.

the procedure should be repeated. It is recommended to establish with relative assurance that the field is sterile before attempting to insert another prosthesis. In the inguinal region, the new repair could be performed using a preperitoneal approach as described by StoppaZ3 (Fig. 4). PATIENT-DOCTOR RELATIONSHIP DURING THE CARE OF AN INFECTED WOUND

During the initial interview for the repair of a hernia, the surgeon should state in clear terms his or her infection rates, stating that the possibility of a postoperative infection cannot be completely eliminated. Before treatment of a postherniorrhaphy infection, the surgeon should delineate in understandable form the needed course of action, stressing the fact that it may be necessary to remove previously inserted prostheses and to perform several drainage and debriding procedures during a prolonged period of time before the problem is completely resolved. The fact that removal of the prosthesis may produce a late

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recurrence, as well as a recurrent infection, should be clarified. This detailed discussion, carried on over repeated sessions, preferably in the presence of a responsible member of the family, helps maintain a healthy doctor-patient relationship and diminishes the risk for litigation during a protracted therapeutic period.

References 1. Amid P K Classification of biomaterials and their related complications in abdominal wall hernia surgery. Hernia 1:15-21, 1997 2. Christensen GD, Simpson WA, Bisno AL, et al: Adherence of slime-producing strain of Staphylococcus epidevmidis to smooth surfaces. Infect Immunol 37:318-326, 1982 3. Classen DC, Scott Evans R, Pestonik SL: The timing of prophylactic administration of antibiotics and the risk of the surgical-wound infections. N Engl J Med 326:281-286, 1992 4. Dankert J, Hogt AH, Feijen J: Biomedical polymers: Bacterial adhesion, colonization and infection. CRC Crit Rev Biocompat 2:219-301, 1986 5. Flament JB, Avisse C, Palot JP, et al: Trophic ulcers in giant incisional hernias: Pathogenesis and treatment. Hernia 1:71-76, 1997 6. Ge NH, Wong CM, Lingle RL Jr, et al: Femtosecond dynamics of electron localization interfaces. Science 279:202-205, 1998 7. Gilbert AI, Felton L L Infections in inguinal hernia repair considering biomaterials and antibiotics. Surgery, Gynecology, and Obstetrics 177126-130, 1993 8. Glasow F: Is postoperative wound infection following single inguinal herniorrhaphy a predisposing cause of recurrent hernia? Can J Surg 91:870-871, 1964 9. Gristina AG, Giridhar G, Gabriel BL, et al: Cell biology and molecular mechanisms in artificial device infections. Int J Artif Organs 16:755-764, 1993 10. Gristina AG, Oga M, Webb L, et al: Adherent bacteria in the pathogenesis of osteomyelitis. Science 228:990-993, 1985 11. Howe CW Bacterial flora of clean wounds and its relation to subsequent sepsis. Am J Surg 107696-700, 1964 12. Jansen B, Peters G: Modern strategies in the prevention of polymer-associated infections. J Hosp Infect 19:83-88, 1991 13. Johnson GM, Lee DA, Regelman WE, et al: Interference with granulocyte function by SE slime. Infect Immunol 54:13-20, 1986 14. Klock JC, Baiton D Degranulation and abnormal bactericidal function of granulocytes procured by reversible adhesion to nylon wool. Blood 48:149-161, 1976 15. Kocher T (ed): Textbook of Operative Surgery. New York, Macmillan, 1911 16. Lazortes F, Chotasso P, Massip P, et al: Local antibiotic prophylaxis in inguinal hernia repair. Surgery, Gynecology, and Obstetrics 175:569-571, 1992 17. Lew DP, Waldvogel FA: Osteomyelitis. N Engl J Med 336:999-1007, 1997 18. Naber SP: Molecular pathologyand diagnogis. of infectious diseases. N Engl J Med 331:1212-1215, 1994 19. Naylor P, Jennings R, Myrvik Q, et al: Antibiotic sensitivity of biomaterial-adherent Staphylococcus epidermidis. Orthop Trans 12:524525, 1988 20. Patti JM, Allen BL, McGavin MJ, et al: MSCRAMM-mediated adherence of microorganisms to host tissues. Ann Rev Microbiol 48:585417, 1994 21. Salvati EA, Chefosky KM, Brause BD, et al: Reimplantation in infection: A twelve year experience. Clin Orthop 170:62, 1982 22. Savage D, Fletcher M (eds): Bacterial adhesion: Mechanisms and physiological significance. New York, Plenum Press, 1985 23. Stoppa RE, Warlaumont CR The preperitoneal approach and prosthetic repair of groin hernia. In Nyhus LM, Condon RE (eds): Hernia. Philadelphia, JB Lippincott, 1989, pp 199-221 24. Troy MG, Dong QS, Dobrin PB Do topical antibiotics provide improved prophylaxis

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against bacteria growth in the presence of polypropylene mesh? Am J Surg 171:391393, 1996 25. Waldvogel FA, Vadaux PE, Pittet D Perioperative antibiotic prophylaxis of wound and foreign body infection: Microbial factors affecting efficacy. Rev Infect Dis 13(~~ppl):782-789, 1991 26. Zimmerli W, Waldvogel A, Vandaux P: Pathogenesis of foreign body infections: Description and characteristics of an animal model. J Infect Dis 146487497, 1982

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