Ultraviolet Light C in the Treatment of Chronic Wounds with MRSA: A Case Study
- 11/1/2002
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Outcome measures. To determine the magnitude of bacterial burden in wounds for this case study, clinicians used a standardized protocol for administering a semiquantitative swab.28-31 The lab results from the semiquantitative swab are reported as type and relative amount of bacteria present ? eg, no growth (0), occasional growth (scant), light growth (1+), moderate growth (2+), or heavy growth (3+). Other outcome measures included taking photographs and assessing changes in wound appearance using the Pressure Sore Status Tool (PSST).32 The PSST is a pen-and-paper tool consisting of 13 domains that assess the composition of wound bed; wound size, depth, and exudate; and the condition of the periulcer skin and wound edge. Scores assigned on a scale of 1 to 5 to each of the individual domains of the PSST are totaled to derive a total score ranging between 13 and 65, with 13 representing a completely healed wound. The PSST has previously been shown to produce valid and reliable assessments of wound appearance.32
Case 1
A 77-year-old man had multiple leg ulcers due to a combination of venous and arterial insufficiency related to his previous occupation that involved prolonged standing. His long history of venous insufficiency included numerous corrective surgical procedures, including vein stripping. He presented with hypertension, bilateral leg edema, and significantly impaired bilateral lower extremity blood flow with ankle brachial indices (ABI) of 0.53 and 0.61 of the left and right leg, respectively. He ambulated with a cane and had limited mobility and impaired muscle pump function in both lower extremities. The extreme pain reported by this patient not only limited his mobility, but also caused significant sleep disturbances, leading to mild depression. Current medications included: pentoxifylline (400 mg tid), enalapril maleate (2.5 mg bid), and acetaminophen (500 mg qid).
At his initial wound evaluation in July 1998, the patient presented with a total of six large superficial ulcers located in the medial and lateral lower leg region bilaterally. These ulcers ranged in size from approximately 1.54 cm2 to 30 cm2. He reported that the ulcers developed following surgery to repair an abdominal aneurysm.
After 2 years of standard wound care and many topical antimicrobial and oral antibiotic treatments, five lower extremity wounds remained in the lateral and medial aspect of the right lower leg as well as the medial aspect of the left lower leg. Before enrolling in this case study, the patient tried oral antibiotics on a recurring basis (ciprofloxacin in July 1998, November 1998, May 1999, June 1999, and August 1999; clarithromycin in June 1999 and August 1999). In addition, several different topical antimicrobials were tried, including mupirocin (Bactroban®, SmithKline Beecham Pharmaceuticals, Mississauga, Ontario, Canada), cadexomer iodine (Iodosorb®, Perstorp Pharma, Lund, Sweden), and nanocrystalline silver dressings (Acticoat™, Westaim Biomedical Corp, Exeter, NH, Fort Saskatchewan, Alberta, Canada) in combination with mechanical debridement. In general, the patient found it difficult to tolerate the application of topical antimicrobials because they exacerbated his pain.
At the time of this study, the patient's wounds were superficial with no undermining and had attached edges and loosely adherent slough. Only minimal granulation tissue was present. Examination of the dressings showed that his wounds were producing copious amounts of purulent yellow exudate. Furthermore, significant erythema surrounded the wounds. Semiquantitative bacterial cultures obtained before treatment revealed the presence of three types of bacteria: methicillin-resistant S. aureus (MRSA) in his right medial lower ulcer and a combination of Pseudomonas aeruginosa and S. aureus in his left medial ulcer.
1. McGeer A, Low D, Conly J, et al. Methicillin-resistant Staphylococcus aureus in Ontario. Can Commun Dis Rep. 1997;23:45-46.
2. Boyce JM, Causey WA. Increasing occurrence of methicillin-resistant Staphylococcus aureus in the United States. Infection Control. 1982;3:377-383.
3. Haley RW, Hightower AW, Khabbaz, RF, et al. The emergence of methicillin-resistant Staphylococcus aureus infections in United States hospitals. Possible role of the house staff-patient transfer circuit. Ann Intern Med. 1982;97:297-308.
4. Panlilio AL, Culver DG, Gaynes RP, et al. Methicillin-resistant Staphylococcus aureus in US hospitals 1975-1991. Infection Control Hospital Epidemiology. 1992;13:582-586.
5. Voss A, Milatovic D, Wallrauch-Schwarz C, et al. Methicillin-resistant Staphylococcus aureus in Europe. European Journal Clinical Microbiology Infectious Disease. 1994;13:50-55.
6. Low DE, Garcia M, Callery S, et al. Methicillin-resistant Staphylococcus aureus in Ontario. Canada Disease Weekly Report. 1981;7:249-250.
7. Dammann TA, Wiens RM, Taylor GD. Methicillin-resistant Staphylococcus aureus identification of a community outbreak by monitoring hospital isolates. Can J Public Health. 1988;79:312-315.
8. Taylor G, Kirkland T, Kowalewska-Grochowska K, et al. A multistrain cluster of methicillin-resistant Staphylococcus aureus based in a native community. Canadian Journal Infectious Disease. 1990;1:121-126.
9. Vortel JJ, Bell A, Farley JD, et al. Methicillin-resistant Staphylococcus aureus (MRSA) in a British Columbia hospital - 1990. Canada Disease Weekly Report. 1991;17:71-72.
10. Boyd N, Gidwani R. Colonization of methicillin-resistant Staphylococcus aureus in southwestern Ontario. Canada Disease Weekly Report. 1991;17:72-73.
11. Nicolle LE, Bialkowska-Hobrzanska H, Romance L, et al. Clonal diversity of methicillin-resistant Staphylococcus aureus in an acute-care institution. Infection Control Hospital Epidemiology. 1992;13:33-37.
12. Embil J, Ramotar K, Romance L, et al. Methicillin-resistant Staphylococcus aureus in tertiary care institutions on the Canadian prairies 1990-1992. Infection Control Hospital Epidemiology. 1994;15:646-651.
13. Simor AE, Augusin A, Ng J, et al. Control of MRSA in a long-term care facility. Infection Control Hospital Epidemiology. 1994;15:69-70.
14. Green K, Low DE. MRSA in Ontario - results of questionnaire survey. Laboratory Proficiency Testing Program Newsletter No. 181, June 25, 1996:1-3.
15. McGeer A, Low DE, Conly J, et al. The rapid emergence of a new strain of MRSA in Ontario: laboratory and infection control implications. Laboratory Proficiency Testing Program Newsletter No. 190, October 29, 1996:1-4.
16. Rao GG. Risk factors for the spread of antibiotic-resistant bacteria. Drugs. 1998;55(3):323-330.
17. Licht S. History of Ultraviolet Therapy in Therapeutic Electricity and Ultraviolet Radiation. Baltimore, Md.: Waverly Press;1967:191.
18. Eaglstein WH, Weinstein GD. Prostaglandin and DNA synthesis in human skin: possible relationship to ultraviolet light effects. J Invest Dermatol. 1975;64(6):386-389.
19. Agin PP, Rose AP, Lane CC, Akin FJ, Sayre RM. Changes in epidermal forward scattering absorption after UVA or UVA-UVB irradiation. J Invest Dermatol. 1981;76(3):174-177.
20. Greaves MW, Sondergaard J. Pharmacologic agents released in ultraviolet inflammation studied by continuous skin perfusion. J Invest Dermatol. 1970;54:365-367.
21. Nussbaum EL, Biemann I, Mustard B. Comparison of ultrasound/ultraviolet-C and laser for treatment of pressure ulcers in patients with spinal cord injury. Phys Ther. 1994;74 (9):812-825.
22. High A, High J. Treatment of infected skin wounds using ultra-violet radiation: an in vitro study. Physiotherapy. 1983;69:359-360.
23. Burger A, Jordaan AJ, Schoombee GE. The bactericidal effect of ultraviolet light on infected pressure sores. South African Journal of Physiotherapy. 1985;41(2):55-57.
24. Conner-Kerr TA, Sullivan PK, Gaillard J, Franklin ME, Jones RM. The effects of ultraviolet radiation on antibiotic-resistant bacteria in vitro. Ostomy/Wound Management. 1998;44 (10):50-56.
25. Sullivan PK, Conner-Kerr TA, Smith ST. The effects of UVC irradiation on group A streptococcus in vitro. Ostomy/Wound Management. 1999;45(10):50-54, 56-58.
26. Conner-Kerr TA, Sullivan PK, Keegan BS, Reynolds W, Sagemuehl T, Webb A. UVC reduces antibiotic-resistant bacterial numbers in living tissue. 1999 SAWC Selected Abstracts. Ostomy/Wound Management. 1999; 45(4):84.
27. Sibbald RG, Williamson D, Orsted HL, Campbell KE, Keast DH, Krasner D, Sibbald D. Preparing the Wound Bed - Debridement, Bacterial Balance, and Moisture Balance. Ostomy/Wound Management. 2000; 46(11):14-35.
28. Levine NS, Lindberg RB, Mason AD. The quantitative swab culture and smear: a quick simple method for determining the number of viable aerobic bacteria on open wounds. J Trauma. 1976;16:89-94.
29. Maklebust J, Sieggreen M. Pressure ulcers: Guidelines for Prevention and Nursing Management. West Dundee, Ill.: S-N Publications;1991.
30. Cuzzell JZ. The right way to culture a wound. Am J Nurs. 1993;93:48- 50.
31. Alvarez O, Rozint J, Meehan M. Principles of moist wound healing: indications for chronic wounds. In: Krasner D, ed. Chronic Wound Care: A Clinical Source Book for Health Care Professionals. King of Prussia, Pa.: Health Management Publications, Inc.; 1990:266-281.
32. Bates-Jensen BM. The Pressure Sore Status Tool a few thousand assessments later. Advances in Wound Care. 1997;10(5):65-73.
33. Wills EE, Anderson TW, Beattie BL, Scott A. A randomized placebo-controlled trial of ultraviolet light in the treatment of superficial pressure sores. J Am Geriatr Soc. 1983;31(3):130-33.
34. Dow G, Browne A, Sibbald RG. Infection in chronic wounds: controversies in diagnosis and treatment. Ostomy/Wound Management. 1999;45(8):23-40.
35. Herruzo-Cabrera R, Vizcaino-Alcaide MJ, Pinedo-Castillo C. Diagnosis of local infection of a burn by semiquantitative culture of the eschar surface. Journal of Burn Care and Rehabilitation. 1992;13:639-641.





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