A Cross-sectional Validation Study of Using NERDS and STONEES to Assess Bacterial Burden
- 1 Comments
- 8898 reads
Wound size was estimated by measuring the longest length and the widest width perpendicular to the length.30 Change in wound size at the time of the visit was recorded according to patient history or existing documentation. A sterile cotton applicator was used to determine wound depth and test whether the wound probed to bone, and a handheld infrared thermometer was used to compare the temperature of the periwound area with a similar location on the opposite extremity. The presence or absence of new areas of breakdown, including satellite lesions, was assessed and documented.
Microbiological analysis. To ensure that surface bacterial contaminants were not sampled, wounds were cleansed or irrigated with normal saline until all visible debris was washed away.14 This was followed by rotating the swab tip in a 1-cm2 area of the cleanest part of the wound, preferably in an area of granulation. Adequate pressure was used to extract tissue exudate for successful culturing. The swab then was rotated 360° and placed in the transport media (Levine technique14). The swabs were sent to a local laboratory to be processed in a timely fashion. To provide semi-quantitative culture data, the bacterial swabs were inoculated onto standard media in a Petri dish and serially diluted and streaked into four quadrants on the culture plate. Primary isolation plates were assessed after 5 days. Bacterial species isolated from the four quadrants were reported as scant (first quadrant), light (second quadrant), moderate (third quadrant), or heavy growth (fourth quadrant). Critical colonization (NERDS© variables) was evaluated by scant to light bacterial growth and STONEES© variables (deep wound infection) were evaluated by moderate to heavy growth. In a nonrandomized prospective study, Ratliff and Rodeheaver31 evaluated semi-quantitative swabs to determine bacterial burden (n = 124). Wounds where quantitative swabs revealed 105 or more bacteria/cm2 were defined as infected. Swabs that yielded moderate to heavy bacterial growth in quadrants 3 and 4 were correlated to wound infection (105 or more bacteria/cm2) with a sensitivity of 79%.
Statistical analysis. Each NERDS© and STONEES© variable was coded as a dichotomous variable based on whether the specific sign was present or absent on clinical evaluation. Data were entered into a computerized statistical program (SPSS version 16.0, Chicago, IL) and analyzed by the investigators. Odds ratios were calculated to determine the probability of bacterial growth and quantity in subjects who exhibited each individual sign and in combination of two to four signs. The accuracy of NERDS© and STONEES© to assess scant/light or moderate to heavy bacterial growth was estimated by computing the sensitivity and specificity for each clinical sign and combination of two to four signs.
A total of 112 patients with 44 leg ulcers and 68 foot ulcers were evaluated in an ambulatory wound care clinic and on community visits. Most patients were male (60.4%); average age of all subjects was 66 years (range 33 to 95). The average duration of the ulcers was 6.3 months. Leg ulcers were related to venous disease (28 patients, 63.6%), lymphedema (six, 13.6%), arterial disease (two, 4.5%), mixed venous arterial disease (five, 11.3%), and miscellaneous etiologies (three, 6.8 %).
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.