Infection Protection Burn wound protection
by Cynthia T. Crosby

Infection Protection is a monthly column dedicated to education about infection control issues. This month’s column discusses burn wound infections. Every fourth issue includes a Q&A forum to answer questions you have about the infection control information presented here. If you have a question, please submit it to jakridge@hpnonline.com or call 941-927-9345 ext. 202.

Cynthia T. Crosby
Vice President, Clinical Affairs
Medi-Flex, Inc.

Infection is the primary cause of morbidity and mortality in burn patients.¹ Damage to the barrier function of skin allows entry of microorganisms that would normally remain on the surface of skin. Once microorganisms enter the wound, suppressed immune response due to burn injury contributes to an environment that allows rapid growth of bacteria. Despite treatment, sepsis accounts for 50-60% of deaths in burn patients.²

Microbe colonization in burn wounds

Immediately after injury, burned tissue (the eschar) contains virtually no microorganisms. Without antimicrobial treatment, however, microbial colonization begins within 24 hours. Gram-positive organisms colonize first, followed by gram-negative species. Organisms commonly found in burn wounds within the first 24 hours include Staphylococcus aureus, Pseudomonas aeruginosa, Streptococcus sp, and Clostridium perfringens. Other organisms, such as Serratia marcescens, Staphylococcus epidermidis, and Candida spp, are more prevalent several days after injury.³ Most common microorganisms associated with burn wound infections migrate from other areas of the skin, although migration from the gastrointestinal and respiratory tracts is possible, as well.⁴ When rare organisms are found, the source of contamination is likely to be exogenous.⁵

Infection risk is directly correlated with the area of burn injury; the larger the injured area, the higher the risk of infection.^1,2 Other contributors to infection include poor blood flow, hypoxia, comorbid conditions, the use of invasive devices such as catheters, and poor hand hygiene among healthcare staff.^1,6,7

Treatment of burn wounds

Burn injury treatment includes the use of both systemic and topical therapies, in addition to wound debridement, immune support, and proper nutrition.⁴ Systemic antibiotics are administered to prevent development of infection; however, if sepsis occurs, antibiotics are continued until 72 hours after the infection has been eradicated.² Topical antimicrobial agents are used to prevent microbial growth within the burn wound. Silver sulfadiazine is the most commonly used topical antimicrobial agent for burn care and is generally used to treat second- and third-degree burns. It has broad-spectrum activity against gram-positive bacteria, most gram-negative bacteria, and some yeasts. It is thought to exert its effects by inhibiting microbial DNA replication and altering the cell membrane structure of microorganisms. In addition to being effective, silver sulfadiazine is painless, and it may be used with or without a dressing.² Some patients treated with silver sulfadiazine develop transient leukopenia, which must be monitored, but usually does not result in cessation of treatment. For large burn areas, additional agents are added to silver sulfadiazine. Cerium nitrate enhances the bactericidal activity of silver sulfadiazine, and chlorhexidine and norfloxacine reduce bacterial resistance.3 A summary of commonly used topical antimicrobials and their properties is presented in the table below.

Dressings

Many types of dressings are used for burn wounds, but biological dressings are the standard of care.² Biological dressings may be organic or synthetic. Their purpose is to create a wound environment that prevents moisture loss, reduces exposure to bacteria, and promotes wound healing. Moisture retention is particularly important to accelerate re-epithelization.⁴

Adequate adherence is the most important factor in the effectiveness of dressings. Examples of organic dressings include human or porcine skin grafts (allograft or xenograft) and human amnion. Several synthetic dressings are also available. The preferred wound cover for clean wounds is allograft, which may provide protection for weeks, depending on the severity of the burn. Porcine xenograft is used for temporary wound coverage. It does not adhere well, degenerates rapidly, and does not provide the same level of protection as allograft. Amnion is widely available but adheres poorly and requires additional dressing coverage.

A wide variety of synthetic dressings is available, including bi-layer products. BiobraneÒ is an example of a bi-layer dressing that consists of nylon fabric covered by a silicone membrane. This type of dressing offers good elasticity and range of movement.8 Synthetic dressings may be medicated or non-medicated. Medicated synthetic dressings generally contain antimicrobial agents such as chloramphenicol or chlorhexidine.

Regardless of the type of dressing used, changing dressings more frequently reduces wound bacterial load.³ Following strict hand hygiene protocols and aseptic technique is necessary to decrease risk of contamination during dressing changes.^1,7

Additional infection control measures

In addition to the risk of infection associated with the wound itself, catheters and other invasive devices increase risk.⁹ The use of silver-impregnated devices, including central lines and Foley catheters, may reduce catheter-related infection risk. Another cause of morbidity and mortality in patients with burn injuries are inhalation injuries and pneumonia. Precautions should be taken to reduce ventilator-associated pneumonia risk. (See the August 2005 Infection Protection column, "Fighting and Managing Ventilator-associated Pneumonia.")

Conclusion

Infection is the primary cause of morbidity and death among patients with burn injuries. Reducing infection risk involves the use of systemic antibiotics, effective topical antimicrobials, proper dressing selection, and aseptic technique. Additional measures include the selection of silver-impregnated catheters for patients who require the use of invasive devices. A wide variety of products is available to inhibit microbial colonization and the subsequent development of infection. HPN

Acknowledgement: The author wishes to acknowledge Catherine Jarrell for her assistance in developing this article.

References

1. Wibbenmeyer L, Danks R, Faucher L, et al. Prospective analysis of nosocomial infection rates, antibiotic use, and patterns of resistance in a burn population. Burn Care Res. 2006;27(2):152-160.

2. Abston S, Blakeney P, Manubhai D, et al. Post-burn infection and sepsis. Resident Orientation Manual. Galveston Shriners Burn Hospital and University of Texas Medical Branch Blocker Burn Unit. February 2000. Available at:
www.totalburncare.com/orientation_postburn_
infection.htm. Accessed on May 1, 2006.

3. Noronha C, Almeida A. Local burn treatment—topical antimicrobial agents. Annals of Burns and Fire Disasters. 2000;8(4). Available at: www.medbc.com/annals/review/vol_13/num_
4/text/vol13n4p216.htm. Accessed on April 30, 2006.

4. Bowler PG, Duerden BI, Armstrong DG. Wound microbiology and associated approaches to wound management. Clin Microbiol Rev. 2001;14(2):244-269.

5. Phillips LG, Heggers JP, Robson MC. The effect of endogenous skin bacteria on burn wound infection. Ann Plast Surg. 1989;23(1):35-38.

6. V Falanga. Wound bed preparation: science applied to practice. In: Caine S, managing ed. Wound Bed Preparation in Practice. European Wound Management Association (EWMA) position paper. London: Medical Education Partnership Ltd.; 2004:1-19.

7. Hodle AE, Richter KP, Thompson RM. Infection control practices in U.S. burn units. J Burn Care Res. 2006;27(2):142-151.

8. Martineau L, Shek PN. Evaluation of a bi-layer wound dressing for burn care. II. In vitro and in vivo bactericidal properties. Burns. 2006;32(2):172-179.

9. Church D, Elsayed S, Reid O, Winston B, Lindsay R. Burn wound infections. Clin Microbiol Rev. 2006;19(2):403-434.

June
2006