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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Burn wound infections1

, M.D., , M.D., , , M.D., , M.D., and , M.D.

US Army Institute of Surgical Research, Fort Sam Houston, Texas, U.S.A.

Introduction

The burn patient has been described as the “universal trauma model”, in which the magnitude of the physiological changes induced by injury reliably reflect, in a sigmoidal dose-response fashion, the percentage of the total body surface area burned (1). In other words, the burn wound is the central problem in the burn patient, and successful management and timely closure of the burn wound are essential to survival. The prevention of burn wound infection is certainly critical in this process. Historically, invasive burn wound infection, or “burn wound sepsis”, was the leading cause of death in burn patients. Before the introduction of effective topical antimicrobial prophylaxis in 1964 in the form of mafenide acetate (Sulfamylon®) burn cream, invasive burn wound infection was the cause of death in 60% of the patients who died at the U.S. Army Institute of Surgical Research (the US Army Burn Center) (2). Topical burn wound chemotherapy reduced the occurrence of burn wound sepsis as the cause of death to 28% of fatal burns (3). The control of microbial proliferation in burned tissue has also reduced the occurrence of bacteremia induced by wound manipulation, which permits staged and delayed burn wound excision to be performed in patients with extensive burns. Burn wound excision, in conjunction with topical antimicrobial therapy, has further reduced the occurrence of burn wound sepsis as the cause of death to once in every ten fatal burns (3).

Factors specific to both the host and the pathogen influence the pathogenesis of burn wound infection. Burn injury increases the patient's susceptibility to infection, and this susceptibility is proportional to the total extent of the burn. Loss of skin barrier function provides microorganisms with access to viable tissue over a broad area, and the protein-rich, avascular eschar provides them with an excellent culture medium (4). At the same time, burn injury causes immunologic dysfunction, manifested by impaired neutrophil function, reversal of the T-helper to T-suppressor cell ratio, decreased lymphocyte count, and decreased production of IgG and IL-2 (5, 6). There are also a variety of microbial factors - ranging from the density of organisms to antimicrobial resistance - that influence the risk of invasive infection of burn wounds. Virtually any organism can infect the wound of an extensively burned patient who is severely immunocompromised. However, multiple factors have made Pseudomonas aeruginosa the leading etiologic agent in invasive burn wound infection; these include the motility imparted by its flagellum; and the organism's production of toxins, hemolysins, and proteolytic enzymes (7).

Infections of the burn wound may be classified according to the framework provided in table I.

Table I. Classification of burn wound infections.

Table I

Classification of burn wound infections.

Invasive burn wound infection

The balance between microbial invasiveness and host resistance determines the fate of the burn wound and ultimately that of the patient. A favorable balance in which host resistance outweighs microbial invasiveness prevents the development of invasive infection. On the other hand, when microbial invasiveness outweighs host resistance an invasive burn wound infection is likely to occur. The etiologic agent in invasive burn wound infection is typically a gram-negative bacillus (most commonly, Pseudomonas) or a filamentous fungus such as Aspergillus sp., Fusarium sp., or the Phycomycetes. Rarely, Candida sp. can also invade. The relative importance of the various causative agents of invasive burn wound infection is depicted in table II.

Table II. Causative organism, invasive wound infections, 1983–98a.

Table II

Causative organism, invasive wound infections, 1983–98a.

Gram negative infection: pathophysiology

Prevention of invasive gram negative infection (fig. 1) is the primary rationale for the use of topical antimicrobial burn wound chemotherapy. In the 1950's and early 1960's, when burns were treated by exposure and without the use of topical agents, subeschar suppuration and daily debridement during hydrotherapy effected separation of the eschar and promoted the formation of granulation tissue (8). This practice was satisfactory for patients with burns of limited extent, but in those with large burns the bacterial burden of the burn wound and the degree of immunosuppression often resulted in invasive burn wound infection, primarily due to Pseudomonas aeruginosa. This syndrome was first described by Teplitz et al. in 1964 (9, 10). They developed a murine model of invasive infection, consisting of inoculation of a 20% total body surface area scald injury with a cultured suspension of Pseudomonas sp. This infection was uniformly lethal and followed a predictable and reproducible trajectory. Organisms multiplied and penetrated the eschar, particularly along and around hair follicles; proliferated at the nonviable/viable interface; caused secondary necrosis of granulation tissue if such was present; invaded viable tissue, and entered the bloodstream (9). By contrast, Pseudomonas bacteremia arising from another source typically did not precede or give rise to invasive burn wound infection (10).

Figure 1. Photomicrograph of gram negative invasive burn wound infection.

Figure 1

Photomicrograph of gram negative invasive burn wound infection. Numerous gram negative bacilli are present in viable dermis. Cultures yielded Pseudomonas aeruginosa.

Prevention

This model permitted the development of an effective topical agent, 11.1% mafenide acetate cream (Sulfamylon® burn cream) - a drug previously used in powder form during World War II for the prevention of gas gangrene in war wounds (11, 12). Whereas untreated rats with seeded burn wounds demonstrated a mortality of 95.5%, those treated with Sulfamylon® burn cream within 24 hours of injury and “seeding” all survived (13). Clinical use of the drug as the sole topical agent in burn patients began at the U.S. Army Burn Center in 1964, resulting in a reduction (comparing 1962–1963 and 1964–1966) in overall burn mortality from 38% to 20%, and a reduction in the rate of invasive burn wound infection from 22% of admissions to 2% (2).

Mafenide acetate (para-aminomethylbenzene sulphonamide) is water soluble, and rapidly penetrates full-thickness eschar (14); this is a major advantage over other antimicrobials, particularly when treating full thickness burns. Its ability to penetrate cartilage, furthermore, is advantageous in the prevention of suppurative chondritis of the burned ear (15). Mafenide does not appear to exert its antimicrobial activity by the same mechanism as the sulfonamides (16). The concentration of the drug drops to sub-therapeutic levels in eschar by 10 hours after application, mandating application twice daily if it is the sole agent used (14). It and its principal metabolite (p-carboxybenzenesulfonamide) are carbonic anhydrase inhibitors. Thus, metabolic acidosis may occur as a result of increased bicarbonate excretion. This complication is most common in patients with extensive burns treated twice daily, and in whom pulmonary dysfunction limits respiratory compensation (17).

Sulfamylon® demonstrates unparalleled efficacy against both gram positive and gram negative organisms. Between 1967 and 1992, none of the nearly 8500 strains of Pseudomonas aeruginosa isolated from burn patients at the U.S. Army Burn Center were resistant to clinically relevant concentrations of Sulfamylon® (unpublished data). By the agar-well diffusion method, Sulfamylon® demonstrated superior efficacy against Staphylococcus aureus and Pseudomonas aeruginosa when compared to povidone iodine, silver sulfadiazine, gentamicin, nitrofurazone, silver nitrate, or even hydrogen peroxide (18).

Moyer and Monafo introduced 0.5% silver nitrate (AgNO3) solution in 1964 as topical anti-infection prophylaxis for burn wounds. At this concentration, silver nitrate solution is not tissue toxic (20). The antimicrobial action of silver ion includes activities against the cell wall, essential enzymes, and certain nucleotides (19). Burn wounds are dressed with multiple layers of coarse mesh gauze, to which the silver nitrate solution is applied as often as necessary to keep the gauze continuously moist. This approach is effective if begun immediately postburn, but because silver ion precipitates on contact with chloride ion to form AgCl2, it does not penetrate the eschar and thus has no antibacterial activity within burned tissue. Another drawback of this drug is depletion of cations due to “leeching” across the open wound. This may cause hyponatremia, hypocalcemia, hypokalemia, and/or hypomagnesemia; thus, frequent monitoring and replacement as needed is performed (20).

Silver sulfadiazine (1% cream) was developed by Fox et al. in 1968 by complexing silver nitrate and sulfadiazine (21, 22). Previously, sulfadiazine alone had been used as a topical agent, but the development of resistance was problematic. The two moieties may act synergistically, and the compound may serve to provide silver ion by slow release (23). In contrast to Sulfamylon® burn cream, silver sulfadiazine burn cream is relatively painless on application and has some activity against Candida sp. Occasionally, a decrease in the neutrophil count has been observed within 72 h of initiation of therapy; this has been attributed to depression of granulocyte-macrophage progenitor cells in the marrow, and usually resolves even when use of the agent is continued (22). This phenomenon rarely requires discontinuation of therapy.

In Europe, topical therapy with a combination of cerium nitrate and silver sulfadiazine (Flammacerium, Duphar B.V. Holland) has been advocated, although evidence of increased efficacy over other available agents is limited (25).

Recently, dressings impregnated with elemental silver have been evaluated as topical therapy for burns. Silver Nylon (Swift Textile Metalizing Corporation, Hartford, CT), alone and in combination with weak direct current, has been shown to be effective in a lethal Pseudomonas murine model (26). Acticoat (Westaim Biomedical Inc., Fort Saskatchawan, Alberta, Canada) is an FDA-approved dressing containing a binary alloy of silver (97%) and oxygen (R. Swain, personal communication). Tredget et al. have reported that Acticoat is more effective than silver nitrate solution with respect to preventing heavy colonization of burn wounds (> 105 organisms per gram of tissue) (19). In both forms of treatment, conversion of silver to silver ion occurs and is necessary for efficacy (19).

In light of the above, the authors employ the following regimen of wound care. Sulfamylon® cream is applied to patients with burns in excess of 20% of the total body surface area (and to those with full thickness burns of lesser extent) in the morning following the daily cleansing and inspection of the wound. Silver sulfadiazine cream is applied twelve hours later. This regimen realizes the advantages of both drugs while minimizing their disadvantages. Critical in this process is the prevention of wound desiccation by reapplication of agent as often as necessary to maintain a uniform (approximately 0.5 cm thick) layer of agent over the wound surface. The burn unit environment may play a role in the control of infection in the burn patient. In 1983, the configuration of the burn intensive care unit at the U.S. Army Burn Center changed from an open ward to an isolation ward, in which critically ill patients and those with extensive open wounds were nursed in individual isolation rooms. Handwashing, and the donning of sterile gloves, clean gowns, masks, and caps, were required of all providers upon entry into each patient room. Cohort isolation of patients who were colonized with multiple-drug-resistant organisms was employed, in order to avoid the transmission by caregivers of such organisms to uncolonized patients. Thrice-weekly surveillance cultures were obtained to monitor the process, to identify multiple-drug-resistant organisms early, and to guide the rational choice of antibiotics when infections occurred. Comparing the 1982–1983 period prior to the remodeling and the 1983–1984 period thereafter confirmed that these nursing and environmental changes were associated with the elimination of endemic, multiple-drug resistant strains of Pseudomonas aeruginosa and Providencia stuartii, and with a reduction in bacteremia and mortality (27). These results were confirmed in a later study which compared 1974–1983 and 1984–1993 and documented a reduction in the mortality associated with gram negative bacteremia (28). Also coincident with these environmental changes, there was a marked decrease in the incidence of bacterial invasive burn wound infection from 1979–1982 (6.6%) to 1983–1989 (1.1%). The incidence of fungal invasive burn wound infection, however, remained unchanged (29).

The surgical treatment of the wound may also affect the incidence of infection and the survival of burn patients. The traditional method, in which wounds were grafted once eschar separation occurred and granulation tissue formed (2), gave way in the early 1980s to tangential excision of deep partial thickness burns and excision to fascia of extensive full thickness burns (30, 31). In some patient groups, an improvement in mortality has been observed in those who undergo excision within the first 72 hours after injury (32). In the absence of sufficient donor sites from which to obtain autologous skin grafts, biologic dressings such as cadaver allograft may be used to close the excised wound temporarily (33). Such dressings reestablish skin barrier function; in particular, they prevent desiccation-induced necrosis of the wound surface and prevent contamination of underlying tissue with exogenous bacteria. In areas of allograft adherence, wound bacteria counts decrease. However, if allograft is placed over nonviable tissue, subgraft suppuration will occur and the grafts will not adhere. Every biologic dressing should be inspected on a daily basis. If suppuration occurs beneath the grafts, they should be removed and replaced as frequently as necessary until suppuration ceases and the biologic dressing becomes adherent (34, 35). Synthetic skin substitutes, which are more likely to develop submembrane suppuration than are naturally occurring biologic dressings, can be safely applied at the time of burn wound excision but should not be applied to wounds with retained nonviable tissue.

Diagnosis

The diagnosis of invasive burn wound infection is based on careful clinical examination and histologic examination of a biopsy of the area of the wound suspected of being infected. The clinical signs of invasive burn wound infection are shown in table III. The systemic inflammatory response to severe thermal injury produces a variety of changes which mimic those seen in severe infection. This makes the diagnosis of infection somewhat more difficult and emphasizes the importance of burn wound histology in differentiating burn wound colonization (present on virtually all burns) from invasive infection. Daily inspection of the burn wound by an experienced observer is essential, to identify changes indicative of infection and to evaluate such changes by biopsy at the earliest possible time.

Table III. Clinical signs of invasive burn wound infection.

Table III

Clinical signs of invasive burn wound infection.

A burn wound biopsy is performed as follows (8). A scalpel is used to obtain a lenticular tissue sample from a suspicious area, measuring approximately 1 × 0.5 × 0.5 cm and extending into viable subcutaneous fat. This sample is divided in half; one portion is sent for microbiological determination of the identity and sensitivity pattern of the causative organism(s), and the other portion is sent in normal saline solution for histologic determination of depth of invasion. A rapid section technique permits processing and examination of the specimen within four hours (36). The scheme shown in table IV is used to report the results.

Table IV. Classification of microbial status of burn wounds.

Table IV

Classification of microbial status of burn wounds.

A frozen section technique has been developed which has 86% sensitivity and 99% specificity in comparison to the rapid section technique; thus, results of the frozen section examination are confirmed with standard tissue processing and examination used to exclude false negative cases (37). Quantitative cultures have not proven useful in the diagnosis of invasive burn wound infection, since a microbiologically positive specimen (105 organisms per gram of tissue) is sensitive (90%) but not specific (60%) for invasive infection by histopathology (38); just as importantly, histopathological results are available much more quickly. Rather, the value of wound microbiology in this setting is in guiding the selection of antibiotics against the causative organism.

Treatment

Patients with invasive burn wound infection are often critically ill and require intensive care, including invasive monitoring and correction of cardiovascular, pulmonary, or end-organ failure. Wound care is based on the identity of the infecting organism. Gram negative infections are treated by subeschar clysis with one-half the daily dose of a broadspectrum penicillin, such as piperacillin, in 150–1000 ml saline. A number 20 spinal needle is used to minimize the number of injection sites. If not already in use, mafenide acetate (Sulfamylon®) burn cream is applied to the wounds. Intravenous antibiotics are given based on the sensitivity pattern of the predominant endemic organisms, as determined by the burn center's microbial surveillance program. Eight hours later, clysis is repeated immediately before surgery. The patient is then taken to the Operating Room for excision, at the level of the investing fascia, of all involved eschar. Gauze soaked with 5% mafenide acetate solution or 0.5% silver nitrate solution is used to dress the wounds. 24–48 hours later, the patient's wounds are reexamined and, if needed, further debrided in the Operating Room; cadaver allograft or an autograft may be applied if the wound is clean. Using techniques similar to this, 53% of patients with invasive gram negative burn wound infections were cleared of such infections, of whom 50% survived; thus, invasive burn wound infection merits aggressive therapy in most patients (39). The importance of timely diagnosis and prompt treatment is indicated by the fact that in none of the survivors had the infection progressed to the point where it seeded the blood stream. The rationale for subeschar antibiotic clysis is to deliver a sufficient concentration of antibiotics to the site of infection to reduce bacterial density and to limit further proliferation, which will reduce the incidence of dissemination of viable bacteria and their metabolic products, such as endotoxin, during excision. Antibiotics other than broad spectrum penicillins have not proven useful by this route (40).

Perioperative antibiotic therapy in burn patients

Even in the absence of invasive burn wound infection, burn wound manipulation may be associated with bacteremia. For this reason, one dose each of intravenous vancomycin and amikacin are routinely given before and after excision by the authors. Sasaki et al. prospectively documented a 20.6% incidence of bacteremia following wound manipulation in 1979 (41). As a reflection of the effectiveness of current burn wound care in reducing the bacterial burden of the burned tissue, bacteremia occurred with only 12.5% of wound manipulations in a 1997 study. In the recent study, all bacteremic patients had burns exceeding 40% of the total body surface area, and bacteremia was more common after the 10th postburn day (42). In patients with extensive burns and limited donor sites, meshed split-thickness skin grafts are commonly applied following excision. These grafts are dressed with gauze soaked with a 5% aqueous Sulfamylon® solution to limit proliferation of bacteria and prevent the development of infection in the interstices of the mesh graft (43). One-half percent silver nitrate solution can be used to treat meshed grafts in similar fashion.

Fungal invasive burn wound infection

The striking reduction in gram negative invasive infection which has resulted from the use of topical antimicrobial therapy and early excision has heightened the importance of invasive fungal burn wound infections in patients with extensive burns (44).

Candida sp. are the nonbacterial organisms which most frequently colonize the burn wound, but they are seldom invasive and, therefore, rarely cause burn wound infections that require surgical excision. Invasive candidal infection may, in fact, indicate a severe collapse of host defenses and is often a preterminal event (45). Previously excised burn wounds infected with Candida species require treatment by twice-daily application of a topical antifungal agent such as clotrimazole cream or ciclopiroxolamine cream. If this treatment fails and the infection spreads to involve more tissue locally, excision may be necessary. Systemic candidiasis necessitates intravenous therapy with fluconazole or amphotericin B.

The filamentous fungi are much more aggressive invaders of the subcutaneous tissues than are Candida sp. Aspergillus sp. are the most common etiologic agents of invasive burn wound infection at the U.S. Army Burn Center at the present time. The diagnosis of invasive fungal infection is made by the histologic examination of a burn wound biopsy as previously described. Aspergillus sp. feature long filamentous hyphae which branch at a 45° angle (fig. 2). Infections caused by the Phycomycetes - which include Mucor, Absidia, and Rhizopus - are best diagnosed by identification of broad, nonseptate hyphae in unburned tissue, occasionally with wide-angle branching (fig. 3) (46).

Figure 2. Photomicrograph of Aspergillus invasive burn wound infection.

Figure 2

Photomicrograph of Aspergillus invasive burn wound infection. Note dichotomous (45° angle) medium-caliber fungal hyphae typical of Aspergillus sp. (upper left). Abundant inflammatory cells are seen around the necrosis in the subcutaneous fat. (more...)

Figure 3. Photomicrograph of Mucor invasive burn wound infection.

Figure 3

Photomicrograph of Mucor invasive burn wound infection. Note broad, direct-angular, non-septate hyphae in viable dermal capillaries. The organism was identified by culture as Mucor sp.

The treatment of burn wound infections due to the filamentous fungi is analogous to that of gram negative bacterial infections, with the following differences. Intravenous amphotericin B is mandatory for patients with extensive wound involvement, any microvascular invasion, or systemic dissemination (3). Because of the renal toxicity of this drug and the tenuous status of many of these patients, the authors often use amphotericin B lipid complex (Abelcet®), or a similar combination preparation of amphotericin B. The utility of newer triazoles such as itraconazole and voriconazole in treating this disease is unknown (4750).

There is no role for subeschar clysis in the treatment of invasive fungal infections. At surgery, wide excision of the involved tissue at the level of the investing fascia is performed. If the infection has crossed a fascial plane, the excision should be extended to include the involved fascia and subfascial tissues. Phycomycotic infections may be surrounded by a rim of edematous tissue which also must be excised. Postoperatively, all wounds are treated with clotrimazole or ciclopiroxolamine cream. Excised wounds are inspected again in 24–48 hours, and either redebrided as necessary or covered with allograft or autograft if no infected tissue remains and the wound is clean.

Following the institution of a more aggressive surgical approach, the mortality of patients with filamentous fungal infections decreased from 87% in 1973–77, to 25% in 1978 (45). In a series of patients treated at the U.S. Army Burn Center from 1954 to 1983 with infections due to the highly invasive, rapidly spreading Phycomycetes, amputation was necessary in order to encompass involved tissue in 26 of the 63 patients who underwent surgery (41%) (46).

Viral burn wound infection

Herpes simplex Type I viral infections of the burn wound are rare, and most often first appear in healing or recently healed partial thickness burns in the naso-labial area (51). The diagnosis of a herpetic burn wound infection is made by the histologic examination of a biopsy specimen or of scrapings from the cutaneous lesions. On occasion, systemic Herpes virus infections involving multiple sites such as liver, lung, spleen, adrenal glands and bone marrow occur (52), the treatment for which is intravenous acyclovir.

Tetanus

Burn wounds are tetanus-prone; even small burn wounds may lead to fatal tetanus in inadequately immunized patients (53). Thus, the immunization status of all burn patients should be determined on admission and a booster and/or tetanus immune globulin given as appropriate (5).

Invasive infection of excised wounds, donor sites, and grafted wounds

Invasive infection of excised burn wounds, donor sites, and grafted wounds may also occur (see table I). As in the case of invasive infections of the unexcised burn wound, these infections are most commonly caused by gram negative bacteria or filamentous fungi. Dessication of the wound surface exposed by excision or skin harvesting creates, in essence, a “neoeschar.” The presence of microorganisms on the surface of these wounds may represent colonization of nonviable tissue, or invasion of underlying viable tissue. Similarly, in the case of previously grafted wounds, the presence of microorganisms may represent colonization of necrotic graft, or an underlying infection which prevented engraftment. Invasive infection of excised burn wounds, donor sites, and grafted wounds is diagnosed by biopsy of suspicious areas, and treatment thereof requires immediate surgical management as described above (3).

Burn wound cellulitis

Erythema which spreads beyond the 1–2 cm immediately adjacent to the burn wound - with or without lymphangitis - most likely indicates β-hemolytic streptococcal cellulitis (see table I). This is usually responsive to penicillin therapy but occasionally broader coverage may be necessary (3).

Burn wound impetigo

Multifocal small superficial abscesses characterize burn wound impetigo (see table I). It can cause extensive destruction of previously well-engrafted skin grafts or ulceration of healed partial-thickness burns and donor sites. Staphylococcus aureus is the usual organism cultured from these lesions. Treatment includes unroofing all abscesses, twice-daily cleansing of infected areas with a detergent disinfectant, and application of a topical antibacterial ointment such as mupirocin (Bactroban®) twice a day (3, 5).

Conclusions

The development of effective antimicrobial burn creams was a major advance in the care of burn patients and was accompanied by a striking reduction in mortality. Subsequent advances which have contributed to further reductions in infection rates and mortality have included prompt burn wound excision and grafting, infection control practices, refinement of enteral nutrition techniques, prevention of stress ulcers, and improved modes of mechanical ventilation. Nevertheless, close attention to and frequent examination of the burn wound remain essential components of successful wound care in patients with extensive burns. In particular, fungal invasive burn wound infections remain a vexing problem in these patients.

Acknowledgments

The authors wish to acknowledge the assistance of Ms. Alma Griffin; Ms. Evelyn Wallsworth, ISR Librarian; and SGT Barbara Roberts-Fox.

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The opinions expressed in this article are the private views of the authors, and are not to be constued as the official views of the Department of the Army, the Department of the Air Force, or the Department of Defense.

Footnotes

1

The opinions expressed in this article are the private views of the authors, and are not to be constued as the official views of the Department of the Army, the Department of the Air Force, or the Department of Defense.

Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6970
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