A Cross-sectional Validation Study of Using NERDS and STONEES to Assess Bacterial Burden
- 1 Comments
- 8910 reads
Abstract: All chronic wounds are colonized by micro-organisms. Although the presence of bacteria is not necessarily harmful, and may be beneficial in some instances, accurate evaluation of wound-related bacterial damage and infection is crucial. A cross-sectional validation study involving 112 patients was conducted to estimate the specificity and sensitivity of clinical assessment variables individually and in combination to determine the presence and quantity of bacteria in the wound. The average age of study participants was 66 years (range 33 to 95 years) and most had leg (44) and foot (68) ulcers of approximately 6 months’ duration. Wounds were evaluated using a mnemonic developed to evaluate the presence or absence of clinical signs of critical colonization (NERDS©) or infection (STONEES©) and results compared to semi-quantitative swab cultures. Wounds with debris, increased exudate, and friable tissue were found to be five times more likely to have scant or light bacterial growth; whereas, wounds with elevated temperature were eight times more likely to have moderate or heavy bacterial growth. When combining any three clinical signs, the sensitivity was 73.3% for scant or light and 90% for moderate and heavy bacterial growth and the specificity was 80.5% and 69.4%, respectively. Considering the importance of this clinical diagnosis, studies to examine the predictive validity of these assessment variables and culture results are warranted.
Key Words: wound infection, chronic wounds, assessment, bacterial swab
Potential Conflicts of Interest: Dr. Woo and/or Dr. Sibbald is a consultant, investigator, and/or speaker for one or more of the following companies/organizations: 3M (St. Paul, MN), Coloplast Corp. (Minneapolis, MN), Mölnlycke Health Care (Norcross, GA), Covidien (Mansfield, MA), Gaymar (Orchard Park, NY), KCI (San Antonio, TX), Systagenix Wound Management (Quincy, MA), Tyco International Ltd. (Mansfield, MA), ConvaTec (Skillman, NJ), Registered Nurses Association of Ontario (Canada), and the Government of Ontario.
Please address correspondence to: Kevin Y. Woo, RN, MSc, PhD, ACNP, GNC(C), FAPWCA, Wound Healing Clinic, East Room 1016, Women’s College Hospital, 76 Grenville Street, Toronto, Ontario M5S 1B2 Canada; email: firstname.lastname@example.org.
All chronic wounds are invariably colonized by a complex ecology of micro-organisms.1 More than 90% of chronic wounds have been found to host polymicrobial flora containing an average range of 1.6 to 4.4 bacterial species depending on the type of ulcer.2 The presence of nonreplicating micro-organisms on the wound surface that do not evoke clinical host response is referred to as contamination. As the micro-organisms continue to proliferate within the wound, critical colonization (ie, the presence of bacteria in the superficial wound compartment that are associated with a host inflammatory response that delays or prevents healing) and wound infection can occur, causing clinical host injury3 (see Table 1).
Although the presence of bacteria is not necessarily pathological and may actually facilitate normal healing,2 wound healing has been found to be noticeably compromised when the bacterial burden crosses a certain colonization threshold to overcome host resistance or incorporates more than four pathological bacterial species.4 Based on an analysis of wound fluid from their seminal case series, Bendy et al5 reported chronic pressure ulcer healing was significantly thwarted at a bacterial load of 1.0 x 106 or higher number of colony forming units per gram (CFU/g) of tissue.
1. Bowler PG, Davies BJ. The microbiology of infected and noninfected leg ulcers. Int J Dermatol. 1999;38:573–578.
2. Landis S, Ryan S, Woo K, et al. Infections in chronic wounds. In: Krasner DL, Rodeheaver GT, Sibbald RG. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals, 4th ed. Malvern, PA: HMP Communications;2007:99–321.
3. Frank C, Bayoumi I, Westendorp C. Approach to infected skin ulcers. Can Family Phys. 2005;51:1352–1359.
4. Davies CE, Hill KE, Newcombe RG, et al. A prospective study of the microbiology of chronic venous leg ulcers to reevaluate the clinical predictive value of tissue biopsies and swabs. Wound Rep Reg. 2007;15:17–22.
5. Bendy RH, Nuccio PA, Wolfe E, et al. Relationship of quantitative wound bacterial counts to healing of decubiti: effect of topical gentamicin. Antimicrob Agents Chemother. 1964;10:147–155.
6. Ovington LG. Bacterial toxins and wound healing. Ostomy Wound Manage. 2003;49(7a suppl):8–12.
7. Liu Y, Min D, Bolton T. Increased matrix metalloproteinase-9 predicts poor wound healing in diabetic foot ulcers. Diabet Care. 2009;32(1):117-119.
8. Muller M, Troome C, Lardy B, Morel F, Halimi S, Benhamou PY. Matrix metalloproteinases and diabetic foot ulcers: the ratio of MMP-1 to TIMP-1 is a predictor of wound healing. Diabet Med. 2008;25(4):419–426.
9. Mwaura B, Mahendran B, Hynes N. The impact of differential expression of extracellular matrix metalloproteinase inducer, matrix metalloproteinase-2, tissue inhibitor of matrix metalloproteinase-2 and PDGF-AA on the chronicity of venous leg ulcers. Eur J Vasc Endovasc Surg. 2006;31(3):306–310.
10. Woo K, Ayello EA, Sibbald RG. The edge effect: current therapeutic options to advance the wound edge. Advances Skin Wound Care. 2007;20:99–117.
11. Branom R. Is this wound infected? Wound and skin management in the ICU. Crit Care Nurs Quart. 2002;25(1):55–62.
12. Williams DT, Hilton JR, Harding KG. Diagnosing foot infection in diabetes. CID. 2004;39(2 suppl ):S83–S86.
13. Danilla S, Andrades P, Gomez ME, et al. Concordance between qualitative and quantitative cultures in burned patients analysis of 2,886 cultures. Burns. 2005;31:967–971.
14. Gardner SE, Frantz RA, Saltzman CL, et al. Diagnostic validity of three swab techniques for identifying chronic wound infection. Wound Rep Reg. 2006;14:548–557.
15. Slater RA, Lazarovitch T, Boldur I, et al. Swab cultures accurately identifying bacterial pathogens in diabetic foot wounds not involving bone. Diabet Med. 2004;21:705–709.
16. Pellizzer G, Strazzabosco M, Presi S, et al. Deep tissue biopsy vs. superficial swab culture monitoring in the microbiological assessment of limb-threatening diabetic foot infection. Diabet Med. 2001;18: 822–827.
17. Cutting KF, Harding KG. Criteria for identifying wound infection. J Wound Care. 1994;3:198–201.
18. Cutting KF. Identification of infection in granulating wounds by registered nurses. J Clin Nurs. 1998;7(6):539–546.
19. Cutting KF, White RJ. Criteria for identifying wound infection revisited. Ostomy Wound Manage. 2005;51(1):28–34.
20. Gardner SE. The validity of the clinical signs and symptoms used to identify localized chronic wound infection. Wound Rep Reg. 2001;9:178–186.
21. Prompers L, Huijberts M, Apelqvist J, et al. High prevalence of ischemia, infection and serious comorbidity in patients with diabetic foot disease in Europe. Baseline results from the Eurodiale study. Diabetologia. 2007;50:18–25.
22. Serena T, Robson MC, Cooper DM, et al. Lack of reliability of clinical/visual assessment of chronic wound infection: the incidence of biopsy proven infection in venous leg ulcers. Wounds. 2006;18(7):197–202.
23. Greenwald PW, Schaible DD, Ruzich JV, Prince SJ, Birnbaum AJ, Bijur PE. Is single observer identification of wound infection a reliable endpoint? J Emerg Med. 2002;23(4):333–335.
24. Wilson AP, Gibbons C, Reeves BC, et al. Surgical wound infection as a performance indicator: agreement of common definitions of wound infection in 4,773 patients. BMJ. 2004;329(7468):720.
25. Sheretz RJ, Garibaldi RA, Marosok RD. Consensus paper on the surveillance of surgical site infections. Am J Infect Control. 1992;20:263–270.
26. Horan TC, Gaynes RP, Martone WJ, et al. CDC definitions of nosocomial surgical site infections. Infect Control Hosp Epidemiol. 1992;13(10):606–608.
27. Wilson AP, Treasure T, Sturridge MF, Gruneberg RN. A scoring method (ASEPSIS) for postoperative wound infections for use in clinical trials of antibiotic prophylaxis. Lancet. 1986;1:311–313.
28. Lorentzen HF, Gottrup F. Clinical assessment of infection in non-healing ulcers analyzed by latent class analysis. Wound Rep Reg. 2006;14:350–353.
29. Sibbald RG, Woo K, Ayello EA. Increased bacterial burden and infection: the story of NERDS and STONES. Adv Skin Wound Care. 2006;19(8):447–461.
30. van Rijswijk L, Catanzaro J. Wound assessment and documentation. In: Krasner DL, Rodeheaver GT, Sibbald RG. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals, 4th ed. Malvern, PA: HMP Communications;2007:113-126.
31. Ratliff CR, Rodeheaver GT. Correlation of semi-quantitative swab cultures to quantitative swab cultures from chronic wounds. Wounds. 2002;14:329–333.
32. Bouza E, Burillo A, Munoz P, Cercenado E, Rodriquez-Creixems M. Semiquantitative culture of open surgical wounds for diagnosis of surgical site infection. Eur J Clin Microbiol Infect Dis. 2004;23(2):119–122.
33. Landes SJ. Chronic wound infection and antimicrobial use. Adv Skin Wound Care. 2008;21(11):531–540.
34. Sarvis CM. Calling on NERDS for critically colonized wounds. Nursing. 2007;37(5):26–27.
35. Miller R. Puzzling cases: non-healing venous leg ulcer. Wound Care Canada. 2006;4(3):38.
36. Elahi MM, Haesey AM, Graham KC, et al. Leg wound infections following cardiac surgery: a scoring system for assessment and management. J Wound Care. 2005;14:337–340.
37. Meaume S, Vallet D, Morere MN, Teot L. Evaluation of a silver-releasing hydroalginate dressing in chronic wounds with signs of local infection. J Wound Care. 2005;14(9):411–419.
38. Okan D, Woo K, Ayello EA, Sibbald RG. The role of moisture balance in wound healing. Adv Skin Wound Care. 2007;20(1):39–53.
39. Woo KY, Harding K, Price P, Sibbald RG. Minimising wound-related pain at dressing change: evidence-informed practice. Int J Wound. 2008;5(2):144–157.
40. Sen CK, Khanna S, Babior BM, Hunt TK, Ellison EC, Roy S. Oxidant-induced vascular endothelial growth factor expression in human keratinocytes and cutaneous wound healing. J Biol Chem. 2002;277(36):33284–33290.
41. Svendsen MN, Lykke J, Werther K, Bisgaard T, Christensen IJ, Nielsen HJ. Bacterial antigen induced release of soluble vascular endothelial growth factor (VEGF) and VEGFR1 before and after surgery. Scand J Clin Lab Invest. 2005;65(3):237–247.
42. Beitz JM. Wound debridement: therapeutic options and care considerations. Nurs Clin North Am. 2005;40:233–249.
43. Hapmson JP. The use of metronidazole in the treatment of malodorous wounds. J Wound Care. 1996;5(9):421–425.
44. Paul JC, Pieper BA. Topical metronidazole for the treatment of wound odor: a review of the literature. Ostomy Wound Manage. 2008;54(3):18–27.
45. Cambronne ED, Schneewind O. Bacterial invasions: molecular systems dedicated to the invasion of host tissues. Contrib Microbiol. 2005;12:181–209.
46. Armstrong DG, Lipsky BA, Polis MB, et al. Does dermal thermometry predict clinical outcome in diabetic foot infection? Analysis of data from the sidestep trial. Int Wound J. 2006;3(4):302¬–307.
47. Grayson ML, Gibbons GW, Balogh K, et al. Probing to the bone in infected pedal ulcers: a clinical sign of underlying osteomyelitis in diabetic patients. JAMA. 1995;273(9):721–723.
48. Lavery LA, Armstrong DG, Peters EJG, et al. Probe to the bone test for diagnosing diabetic foot osteomyelitis. Reliable or relic? Diabetes Care. 2007;30(2):270–274.
49. Butalia S, Palda VA, Sargeant RJ. Does this patient with diabetes have osteomyelitis of the lower extremity? JAMA. 2008;299(7):806–813.
50. Sibbald RG, Orsted H, Schultz GS, Coutts P, Keast D, International Wound Bed Preparation Advisory Board. Preparing the wound bed 2003: focus on infection and inflammation. Ostomy Wound Manage. 2003;49(11):23–51.