A Cross-sectional Validation Study of Using NERDS and STONEES to Assess Bacterial Burden
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In a clinical trial, Armstrong et al46 reported a temperature difference of 2.81o F ± 5.75o F between diabetic foot ulcers of the infected limb and the corresponding site on the contralateral foot. In the present study, wounds with an elevated temperature using infrared thermometry were eight times more likely to be diagnosed with deep infection.
Using probing-to-bone tests in diabetic foot ulcer patients, Grayson et al47 demonstrated a sensitivity of 66% and a specificity of 86% for osteomyelitis confirmed by bone biopsies (n = 50). In a similar clinical trial, Lavery et al48 confirmed the probing-to-bone test was sensitive (0.87) and specific (0.91). In a recent review, Butalia et al49 concluded osteomyelitis was six times more likely to occur when diabetic ulcers were probed to bone. Considering all types of chronic wounds, the probing to bone test has a sensitivity and specificity of 40% and 81%, respectively, for wound infection in this analysis. Results were similar to findings reported in the literature.
Previous studies indicated that local erythema was difficult to detect: Greenwald et al,23 in a study of 115 chronic wounds, reported a kappa of 0.48, indicating poor inter-rater agreement. Lorentzen and Gottrup28 recruited six wound care specialists to assess 120 nonhealing wounds and documented that the sensitivity ranged from .34 to .91. In the original conceptualization (STONES), the three E’s — edema, erythema, and exudate — were combined together as one indicator. The current analysis suggests that exudate alone was a significant (odds ratio 4.13, CI = 1.72 to 9.91) indicator of increased bacterial count. However, edema and erythema individually were insignificant predictors of bacterial damage but in combination the odds ratio was 4.88 (CI = 1.79 to 13.27); associated sensitivity and specificity were 87% and 44%. Erythema and edema were also indicators of periwound inflammation (eg, from physical trauma, chemical irritation, and skin stripping) that may have affected their individual values as indicators for wound infection.
The findings indicate that some signs may be more valid than others for the evaluation of bacterial damage in chronic wounds. However, no one sign can be considered the most definitive or accurate. To determine how a combination of signs may help evaluate bacterial burden in wounds, sensitivity and specificity were calculated for wounds that exhibited any of the two, three, or four signs (see Table 4). Results suggest that the use of any three signs provides a valid and practical approach to determine the presence and level of bacterial damage.
Although infection can trigger an inflammatory response in patients with chronic wounds, the proposed signs of infection also may be observed in other inflammatory conditions such as recurrent trauma, deep structure injury, vasculitis, or pyoderma gangrenosum.50 The potential confounding effect of these inflammatory conditions on the results of this study cannot be excluded. Additional patient factors such as impaired circulation, medications, and other comorbidities that may affect healing, local temperature, exudate production and bacterial contamination were not controlled in this study. In addition, both clinicians conducting the assessments were experts and familiar with the mnemonic. Content validity and reliability studies using other expert or nonexpert clinicians have not been conducted. Finally, because patients were assessed only once, neither the predictive value of the observed bacterial counts nor that of the assessment variables can be ascertained.
The diagnosis of infection should be made clinically.
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.