The Effect of a Cellulose Dressing and Topical Vancomycin on Methicillin-resistant Staphylococcus aureus (MRSA) and Gram-positive Organisms in Chronic Wounds: A Case Series

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Ostomy Wound Manage. 2013;59(5):34–43.
Karen W. Albaugh, PT, DPT, MPH, CWS; Scott A. Biely, PT, PhD, DPT, OCS; and Joseph P. Cavorsi, MD

Abstract

  High levels of persistent bacteria may contribute to wound chronicity and delayed healing. A prospective study was conducted to: 1) evaluate the effect of applying vancomycin topically on appropriately cultured chronic lower leg wounds, specifically methicillin-resistant Staphylococcus aureus (MRSA) and Gram-positive bacteria, and 2) evaluate its effect in combination with a cellulose dressing on healing.

Twenty-three (23) outpatients (11 men, 12 women, average age 65 years [range 39–89 years]) with lower extremity wounds (15 venous ulcers, six chronic open wounds with a history of diabetes, and two chronic open trauma wounds) averaging 43.58 weeks’ (range 5–121 weeks) duration and swab-cultured positive for MRSA or Gram-positive bacteria were provided 1 g vancomycin delivered by a cellulose dressing and changed every 72 hours. Patients served as their own control, and all wounds were debrided once a week. Wound surface area and bacterial and exudate levels were recorded weekly during the 3-week pretreatment period and compared to 3-week treatment period levels. Patients were followed until healed. Mean change in wound surface area was +14.5% (SD 71.91) per week before and -24.6% (SD 13.59) during the vancomycin treatment period (P = 0.014), average exudate levels decreased from 2.75 (range 1–4) to 1.81 (range 0–3) (P = 0.016), and the number of patients with positive wound cultures for MRSA or Gram-positive bacteria decreased from 23 to four after the 3-week study period. All wounds healed after an average of 8.18 weeks (SD 4.76, range 2–17 weeks). The results of this study suggest topical vancomycin applied using a dressing that retains moisture reduces wound bacterial load and may facilitate healing. Randomized, controlled clinical studies to evaluate the effectiveness and efficacy of this treatment modality and explore the relationship between wound culture results and healing are warranted.

Potential Conflicts of Interest: none disclosed

Introduction

  Chronic wounds typically display signs of elevated levels of bacterial load and diversity.1 Staphylococcus aureus and Pseudomonas aeruginosa are among the most predominant pathogens seen in chronic wound infections.2,3 A spectrum of microbial involvement is believed to exist in chronic wounds, ranging from contamination to infection, including a period of time where the wound is highly contaminated but not clinically infected. Chronic wounds often display a plateau of the wound healing trajectory and changes in the wound bed appearance, which may include clinical signs such as increased exudate, friable granulation tissue, and the appearance of new areas of necrosis.4 The term critical colonization has been conceptualized to describe a wound with persistent organisms and an inflammatory state resulting in failure to heal.5,6 The normal cascade of healing is stilted until microbial burden is lessened. It is believed that microbial control will reduce the quantity of bacteria and the proteases and toxins of bacteria that further inhibit healing.4

  Animal and human studies demonstrate bacteria, such as S. aureus, have been found to further complicate the wound healing environment by forming biofilms.7 Biofilms are protective carbohydrate matrices formed by the microbes that prevent eradication by external forces such as debridement, irrigation, and topical agents.7 The relevance of biofilm and the persistence of critical colonization have prompted research into the nature of biofilms and the effectiveness of debridement and topical antibiotic use.8,9 Biofilm composition and resistance have been studied by Wolcott et al7 in four models: in vitro, porcine ex vivo, mouse wound models, and a case series of three patients.7 All four models indicated biofilm maturity contributes to its impermeability to therapeutic approaches; older bacterial biofilms were found to have slower metabolic rates and embed themselves deeper into the extracellular matrix, making them more resistant.7 In this same study, debridement was found to remove/disturb the biofilm complex; however, new biofilm formation began within 24 to 48 hours following debridement.7 The new, immature bacterial biofilms were found to have increased metabolic activity and sensitivity to antibiotics in each of the four models. These findings indicate a possible therapeutic window of opportunity to reduce bacterial colonization if topical approaches are applied within 24 hours of debridement.

  Broader literature review indicates various approaches have been used to penetrate biofilm and control bioburden in chronic wounds. Antiseptic agents, antimicrobial dressings, systemic and topical antibiotics, honey, ultraviolet C, and low-frequency ultrasound all have been utilized with varying reports of effectiveness.4,7-11 The specific use of topical antibiotics has come under much scrutiny due to the incidence of heightened sensitivities, contact dermatitis, and selection for increased resistance.4,7,11 The topical antibiotics used most often in clinical practice and described in the literature have been ointment forms such as mupirocin, bacitracin, neomycin, and nitrofurazone.12,13

  The use of systemic antibiotics in chronic wounds that do not exhibit signs of local infection has been reported as only marginally effective (25% to 32% efficacy)8,9 and is generally ill-advised. In addition to the traditional intravenous approach, systemic antibiotics have been used as washes or soaks in acute or postsurgical cases; nonsystemic lavage of the contaminated area with a topical antibiotic preparation has been reported in a clinical case series14 and an animal study.15 However, it also may be plausible that evaporation creates a potential problem, raising questions regarding the levels of antibiotic that actually reach and remain at the target tissue.

  Early documented topical use of systemic vancomycin has been noted in the field of cardiovascular surgery. Antibiotic-infused, sustained-release carriers in the form of glues have been investigated using animal models in cardiothoracic surgical procedures.16-19 In a case study,20 using a vancomycin ointment for treatment of a cranioplasty site reportedly resolved a methicillin-resistant S. aureus (MRSA) infection. In addition, three separate case series describe the use of negative pressure therapy with instillation in patients with a variety of diagnoses such as chronic osteomyelitis, wet gangrene, postoperative infections, necrotizing fasciitis, and diabetic and pressure ulcers.21-23 The case series included results such as improved wound appearance and culture results,22 reduced hospital stay, and reduced time to closure,21,23 suggesting a potential for infusing systemic antibiotics and antimicrobials in a contained environment.

  A cellulose dressing (XCell®, Medline Industries Incorporated, Mundelein, IL) purports to achieve optimal moisture balance by providing hydration or absorption based on the wound characteristics at the wound-dressing interface. The dressing is comprised of a biosynthetic cellulose material made of interconnected glucose microfibrils spun by Acetobacter xylinum and supported in a multilayer, three dimensional matrix.24 The dressing is designed to stay moist with a specifically engineered cellulose-to-fluid ratio. In vitro and preliminary human trials24 examining the hydrophilic properties of the cellulose have shown its ability to hydrate dry tissue surfaces or absorb fluids. The dressing can be left in place for up to 72 hours. Considering these properties, it was hypothesized the cellulose dressing could serve as a carrier vehicle for nonsystemic (topical) delivery of vancomycin to MRSA and Gram-positive colonized tissues in the wound bed. In theory, the antibiotic solution would be readily absorbed by the dressing and “donated” upon direct contact with the wound bed, particularly one that has been adequately prepared through debridement. In addition, the adaptogenic properties of the dressing were believed to assist in maintaining optimal moisture balance of the wound environment and allow more direct exposure of the drug to the antibiotic-sensitive bacteria. No studies examining the use of this cellulose dressing in the management of chronic or acute wounds or for delivery of vancomycin have been published. The purpose of this study was to: 1) evaluate the effect of applying vancomycin topically on wound culture results, specifically MRSA and Gram-positive bacteria, and 2) evaluate its effect in combination with a cellulose dressing on healing.

Methods

  Participants. A prospective case series was conducted among adults with chronic wounds managed between November 11, 2004 and January 24, 2006 in a hospital-based outpatient program (The Center for Advanced Wound Care, Reading, PA). Protocol approval was obtained through the St. Joseph Medical Center (SJMC) Institutional Review Board (Reading, PA) and by the hospital’s Pharmacy and Therapeutics Committee. All patients undergoing standard wound care at the Center during the above time frame were screened for study eligibility. Standard wound care consisted of weekly sharp debridement and assessment; patients were seen 2 to 3 times per week, provided appropriate moisture-retentive dressings prescribed and/or changed at that time, and assessed to determine the need for alternate or additional therapies.

  Inclusion criteria stipulated evidence of delayed healing — ie, <50% reduction in surface area over the previous 3 weeks — and at least 2 weeks’ use of an antimicrobial dressing immediately preceding the study period. Informed consent was obtained if the patient was eligible. Patients included in the study had a semiquantitative swab culture positive for MRSA or Gram-positive bacteria sensitive to vancomycin. Patients were excluded if they did not have a wound culture positive for MRSA or Gram-positive bacteria. There were no exclusions based on age, etiology, comorbidities, location, wound chronicity, or presence of other bacteria.

  Procedure. The study period comprised the 3 weeks before and the 3 weeks after provision of the vancomycin-infused dressing. The dressing was provided until closure; 3 weeks was a point of measurement. Pre-treatment variables for the 3 weeks prior were obtained retrospectively from the patient’s chart. There was no washout period. Week 0 was defined as the start of the vancomycin-infused dressing. Once started on the vancomycin-infused dressing, patients were prospectively followed until wound closure. The Center personnel — one investigator/physical therapist and two physical therapist assistants — collected and recorded the data on each patient in the medical chart. Demographic variables of age, onset of wound, onset of care at the Center, etiology, comorbidities, and location of wound were collected from the patient chart for statistical analyses. All wound measurements pretreatment and during the study period were taken after sharp debridement using a linear method of greatest length by greatest width, recorded in centimeters. Wound measurements were continued on a weekly basis on all patients until closure. A wound was deemed closed when no exudate and no measurable surface area were present.

  Wound exudate was recorded based on observation of active wound drainage as well as saturation of the dressing at the time of dressing removal on a scale where 0 = none, 1 = scant, 2 = minimal, 3 = moderate, and 4 = heavy. Semiquantitative swab cultures were taken after sharp debridement per the Levine method by one of the investigators at week 0, after 2 weeks of treatment, and every other week until closure. Samples were placed into labeled transport tubes, kept at room temperature, and sent to the SJMC microbiology laboratory for analysis. A report with complete culture and sensitivities was requested for each swab sample. Serum trough levels were taken at 1-week post initiation of the vancomycin protocol via standard blood sampling and sent to the same lab.

  Dressing preparation. The dressing was prepared in the following manner: A 1-g, single-use, standard dose vial of vancomycin was reconstituted in 30 cc of normal saline solution and prepared in a syringe by the pharmacy at SJMC, labeled for each patient, and kept refrigerated until use. The patient’s dressing was removed, and sharp debridement of necrotic tissue was performed. Wounds were measured and a digital photograph was taken. The wound then was cleansed using an antimicrobial soap (Scrub Care Surgical Hand Scrub, Cardinal Health, McGraw Park, IL) and rinsed with normal saline solution. Semiquantitative swab cultures were taken at this time per the schedule described above. A 3-inch x 5-inch sterile piece of the cellulose dressing was opened and saturated by expressing the prepared vancomycin over the dressing within the foil packaging and left to soak for 5 minutes. Once the wound was adequately debrided and cleansed, it was redressed with the saturated cellulose dressing. The dressing then was covered with a bismuth tribromophosphate gauze (Xeroform™, Tyco Healthcare/Kendall, Mansfield, MA), followed by dry gauze and appropriate additional secondary dressing if warranted. The dressing was left in place for 72 hours per the recommended application/use of the cellulose product and to allow convenience of monitoring the patient twice a week. The infused cellulose dressing was continued with each patient until full wound closure. Standard practice in this clinic is to utilize multilayer compression bandages with wounds of venous etiology; multilayer compression dressings were continued throughout the study period and until closure if the patient had a venous leg ulcer. Gradient sequential compression of 40 mm Hg was administered to patients with venous etiology for 1 hour each visit before wound redressing. Patients returned to the clinic for all dressing changes.

  Data collection and analysis. Surface area (calculated by manual linear measurement of length by width in centimeters), bacterial growth, and exudate level for each patient were recorded weekly in the medical record at the clinic by the investigators. Pretreatment surface area, bacterial growth, and exudate levels were obtained from the patient chart. Semiquantitative estimation of bacterial growth was determined by the hospital microbiology laboratory and reported using a quadrant scale of 0 to 4+, where 0 represented no growth, 1+ represented limited bacterial growth, and 4+ indicated heavy growth over the majority of the plate. The mean surface area measurement for all patients was calculated at each pretreatment interval, week 0, and each treatment interval. MRSA and Gram-positive bacterial levels for each patient were averaged the same way for each point in time of the study period.

  Patients were stratified for comparison into one of two subgroups as determined by wound surface area at start of the study period. Subgroups of wounds 20 cm2 and >20 cm2 were based on the CPT coding descriptions described in sharp debridement codes 97597 and 97598.25

  Percentage change in surface area per week for each patient was calculated using the formula: (SA1-SA2)/SA1 * 100), where SA1 was the initial surface area and SA2 was the subsequent surface area 1 week later. The mean weekly percentage changes, as recorded in the patient charts, for the 3 weeks before and the 3 weeks after the start of treatment with the vancomycin-infused dressing were calculated among all patients. Paired sample t-tests were used to compare the pre- and post treatment percentage change in surface area; significance level was set at P <0.05.

  Exudate levels were coded and recorded weekly for each patient. Exudate level and bacterial growth of MRSA and Gram-positive bacteria were plotted against time to allow for qualitative analysis. The Wilcoxin signed-rank test was used to compare differences between exudate levels 3 weeks before and 3 weeks after application of the vancomycin-infused cellulose dressing.   Data also were analyzed via Pearson’s correlation between percentage change in surface area per week and the following variables: patient age, wound chronicity, surface area of the wound, and MRSA or Gram-positive contamination at start of treatment with vancomycin. In addition, independent t-tests were performed to determine if gender, wound size, or presence of polymicrobial bacterial growth had any influence on the results.

Results

  The study cohort included 23 patients, 11 male and 12 female. All patients had lower extremity wounds: 15 had venous ulcers, six had chronic open wounds and history of diabetes mellitus, and two had chronic open wounds of traumatic origin. The average age of all patients was 65 years (SD = 16.03, range 39–89 years), and average wound duration before study treatment was 43.58 weeks (SD = 35.34, range 5–121 weeks). The mean surface area of all wounds was 13.92 cm2 (SD = 30.65, range 0.15–136.85 cm2) (see Table 1). Eighteen (18) patients had wounds with a wound surface area 20 cm2, and five wounds had a surface area >20 cm2.

  Culture results. Fourteen (14) patients had pretreatment cultures positive for MRSA; nine had cultures positive for Gram-positive bacteria, S. aureus. Bacterial levels varied from 1+ to 4+ pretreatment; 13 wounds were polymicrobial. Other organisms identified in low quantities (1+) by culture before the start of therapy included Candida parapsilos, Klebsiella oxytoca, Group G streptococcus, Haemophilus parainfluenzae, and Enterobacter cloaceae (see Table 1)

.   After 3 weeks of vancomycin treatment, MRSA and/or Gram-positive bacteria were completely eliminated in 17 of the 23 patients. Five patients experienced a reduction in MRSA levels from 3+ to 2+. In only one patient, Candida and Klebsiella persisted in low quantities (1+). Serum trough levels at 1 week post-initiation of the topical vancomycin revealed trace or barely detectable systemic absorption in all 23 patients.

  Exudate levels. A mean exudate level of 2.75 (range 1–4) was observed in patient charts at 3 weeks before topical vancomycin was applied, indicating minimal to moderate drainage levels. The mean exudate level for all patients at 3 weeks post application was 1.81 (range 0–3). A statistically significant difference (P = 0.016) was observed between exudate level at 3 weeks before and at 3 weeks post-initiation of the topical vancomycin and cellulose dressing.

  Wound healing. During the 3-week pretreatment phase, a mean percentage increase in surface area of 14.5% per week was noted. Wound surface area decreased a mean of 24.6% per week during each of the first 3 weeks of vancomycin-infused dressing treatment. The difference between pre- and post treatment change in wound surface area was significant (t[44]=-2.57, P = 0.014) (see Table 2).

  A significant difference in weekly change in wound surface area was observed pre- and post treatment in both the group with small wounds <20 cm2 (t[18] = -2.25, P = 0.038) and the group with larger wounds >20 cm2 (t[3] = -5.14, P = 0.014). All wounds healed during an average of 8.18 weeks (SD 4.76, range 2–18 weeks) (see Table 3). Table 4 reflects the mean surface area and MRSA levels from 3 weeks before starting vancomycin until closure of all wounds.

  Data also were separated and analyzed by etiology (venous ulcer, traumatic, and open wound with diabetes). The same trend was observed within each group; however, the sample size was too small to generalize results.   For all 23 patients, no significant correlation was noted between mean percentage surface area change per week and the following variables at the start of the study: age (r = -0.39, P = 0.07), chronicity of wound (r = -0.005, P = 0.98), surface area (r = -0.21, P = 0.33), or bacterial growth levels (r = 0.13, P = 0.57). No significant differences were noted between patients grouped by gender (t[21]=1.08, P = 0.29), presence of polymicrobial bacterial growth (t[21]=-0.51, P = 0.61), wound size (t[21]=1.49, P = 0.15), or percentage change in surface area.

Discussion

  This is the first study documenting the effect of using a cellulose dressing in the management of chronic or acute wounds and for delivery of vancomycin. No adverse effects occurred. After 3 weeks of treatment, MRSA or Gram-positive bacteria culture results were negative for 17 patients and reduced in the remaining five patients. All wounds went on to close, with time to heal ranging from 2 to 17 weeks from the start of antibiotic treatment. Surface area significantly decreased per week (P = 0.02) once the study topical treatment regimen started compared to changes seen in surface area during the before-treatment period.

  Figure 1a–c illustrates a 76-year-old woman with type 2 diabetes and a lower extremity wound of 15 weeks duration before start of treatment. Figure 1a shows the wound measuring 3.9 cm2 with 3+ S. aureus at 1 month before treatment. Figure 1b shows the change in wound and periwound appearance after 1 week of the cellulose and vancomycin treatment. The wound measured 1.5 cm2. By the third week, S. aureus was completely eliminated. Figure 1c depicts the healed wound at 4 weeks post start of treatment.

  As per the study inclusion criteria, all 23 enrolled patients had positive culture results. When selecting a drug, it is crucial for the organism to be sensitive to the antibiotic. Quantitative culture of wound tissue is considered the gold standard, but the semiquantitative swab cultures obtained using the Levine technique are considered valid and comparable to tissue cultures.1 In each case, Gram-positive bacteria were reduced with vancomycin use. In unpublished pilot work by this facility, topical vancomycin was discontinued when a clear culture report was obtained, usually after approximately 3 weeks of use. However, in many of the early cases, recolonization with MRSA or other Gram-positive bacteria was observed along with a regression in wound healing. Therefore, in this study, vancomycin administered via the cellulose dressing was continued until complete closure due to the chronicity of the wounds involved and the trend observed during the preliminary clinical observations.

  Despite laboratory findings that wounds were heavily colonized and/or polymicrobial, none of the patients involved exhibited classic signs of wound infection (such as advancing erythema, edema, pain, warmth, or the presence of purulent exudate)4 before the start of treatment with vancomycin. All cases involved wounds that had been receiving standard care, where edema, drainage, and necrosis were well controlled and wounds were debrided weekly. However, none of the wounds had closed. Clinical observations noted each patient had signs of increased serous exudate levels, presence of a gelatinous film between dressing changes, and/or a plateau or regression of wound healing trajectory, yet no frank signs of clinical infection.

  One of the concerns discussed in the literature is the risk of dermatitis and/or allergic reaction associated with use of topical antibiotics.10,12 This has been documented with use of topical ointments such as mupirocin or triple antibiotic ointment.10 Dermatitis or allergic reaction was not observed in any of the cases in the current study. Another concern is systemic absorption of the antibiotic. Few studies have examined systemic absorption following the administration of topical vancomycin in ointment, lavage, or powder form. The use of topical vancomycin has been cited in several cardiothoracic studies as an alternative to systemic use to offset side effects incurred with intravenous route of administration. Desmond et al26 conducted a prospective cohort study comparing seven patients randomized to the topical application of 500 mg vancomycin in powder form to seven patients randomized to 500 mg vancomycin powder mixed with 0.9% normal saline solution following coronary artery bypass surgery. Subsequent analysis of absorption results showed substantial levels of the drug present in the blood at 6 hours post surgery and in the urine at 5 days post surgery in almost all patients. They caution against the use of topical antibiotics. Extensive use of any antibiotic poses risk for selective resistance to that antibiotic; examples include the widespread use of mupirocin in wound care and the development of mupirocin-resistant strains of MRSA.23,27

  Thus, it is concerning that prolonged and repeated exposure to lower-than-therapeutic doses of vancomycin may contribute to vancomycin-resistant isolates.26 Ozcan et al15 compared the effects of topical and systemic vancomycin on deep sternal wounds with MRSA in Wistar rats and concluded that while all treatment groups demonstrated a significantly lower quantity of micro-organisms than the control group (P <0.05), the combined use of topical rinse and systemic use of vancomycin had the best response in reducing organisms. Blood levels were not measured. Although no signs of vancomycin resistance were observed in the short duration of the current study, avoidance of the empirical use of antibiotics without first obtaining a culture to identify the predominant organism and determine sensitivity to a drug is important.3

  At the time of data collection, vancomycin was the most sensitive drug for treatment of MRSA and therefore the drug of choice in the facility. The standard dose provided in single-use vials by the pharmacy is 1 g. Serum trough levels were drawn at 1 week post-initiation of the vancomycin-infused dressing. Trough blood levels at that time revealed trace or barely detectable systemic absorption, but additional studies about the penetration of the antibiotics into the tissue should be conducted. However, continued use of the topical antibiotic appears to have had a better effect on critical contamination than termination of the antibiotic-infused dressing once superficial swab cultures were negative. In earlier unpublished cases, recolonization frequently occurred, suggesting organism involvement may be deep in the tissue of these chronic wounds. This is supported by the theory that bacteria commonly seen in chronic wounds may settle into matrix biofilm communities that are increasingly resistant to various forms of antimicrobial therapies.8-10 According to a literature review by Black and Costerton,8 the presence of a biofilm might decrease the effectiveness of a topical antibiotic due to heightened resistance, senescence of the bacteria, and changes in the pH due to the chronicity of the wound. This was not observed in the current case series. Wolcott and Dowd28 theorized that targeting the predominant organism with a specific antibiotic via topical approach using gels and other such mediums may help suppress biofilm formation. This may explain why better results were seen with continued use of the vancomycin-infused dressing through closure in this study. Wolcott et al7 supports the use of concurrent sharp debridement as critical to comprehensive management of biofilm. However in this study, standard care, which included sharp debridement, did not decrease surface area as effectively as when the vancomycin-infused dressing was added to the regimen.

  The exposure to vancomycin was localized as opposed to the usual systemic delivery via intravenous dilution. The results indicate this approach may be a therapeutic alternative to systemic antibiotic administration for chronic, critically colonized wounds. In vitro, animal, and clinical research by Wolcott et al7 found an increased sensitivity to gentamicin in 1-day-old biofilms in vitro, as compared to 4-day-old biofilms. Their research demonstrated immature biofilms with highly metabolic bacteria are most susceptible to antibiotics. There is no standardized method to evaluate or measure biofilm in clinical practice, but it is hypothesized that preparing the wound bed through sharp debridement at least weekly exposed immature biofilm and antibiotic-sensitive bacteria to the vancomycin. Furthermore, the moist nature of the cellulose dressing allowed for continued contact of the vancomycin with the wound bed, which could have optimized drug delivery. In this study, the combination of regular debridement and topical antibiotic administration with a cellulose dressing resulted in a reduction of positive wound cultures and healing of chronic lower leg wounds.

  Theoretically, other appropriate aqueous preparations could be used the same way. Testing systemic absorption of topical antibiotic solutions would be prudent in future studies. This alternative does not negate or lessen the importance of surveillance and good infection control practice, which includes diligent hand-washing and avoidance of cross-contamination, as the first line of defense against endemic MRSA infection.29

Limitations

  Several limitations to this study should be discussed. Pre-vancomycin treatment data were obtained through chart review once patients were enrolled, and this may result in potential for confounding factors. As a case series, each patient served as his or her own control; therefore, there was no control group. The rate of change was the main factor compared, with the only difference in care being the addition of the vancomycin-infused cellulose dressing. A larger study would allow for comparison of a control group and a group receiving the cellulose dressing alone. Investigators were not blinded to the treatment. Measurements were recorded by three different wound clinic personnel. The physical therapist and two physical therapist assistants selected to assist with data collection had an average of 15 years experience exclusively in wound care. Although all personnel were trained to measure wounds in the same manner (greatest length by greatest width), reliability between recorders was not established specifically for this study. Two of the raters had participated in a published reliability study using the measurement technique selected, which was found to have an interclass correlation coefficient (ICC) of 0.98.30 (Standard care at this facility included wound cleansing, sharp debridement, and a redress with the above protocol and a gradient sequential compression and multilayer compression bandage [if venous in etiology]).

  For the 15 cases with venous leg ulcer, therapeutic intervention included gradient sequential compression and multilayer compression bandaging in addition to the protocol dressing during the study protocol. Although none of these therapeutic interventions was introduced during the study period, they may have contributed to healing. The data were not stratified by comorbidity because of sample size limitations.

Conclusion

  In this case series, 23 patients with chronic lower leg wounds were managed with weekly debridement and a cellulose dressing infused with topical vancomycin. All wounds had a positive culture for MRSA and/or Gram-positive organisms at baseline and had exhibited an average change in wound size of +14.54% per week (SD 71.91) during the 3 weeks before application of the study dressing. After 3 weeks of study treatment, the average change in wound size was – 24.6% (SD 13.59), a statistically significant difference. At the same time, the number of patients with positive results for MRSA and Gram-positive organism cultures was reduced from 23 to four. All wounds proceeded to heal during an average of 13.38 weeks (SD 2.87). These results suggest that when chronic wounds have stagnated in the healing process, reducing wound bacterial load may help restart healing. Adequate wound bed preparation through sharp debridement, proper identification of the highly colonized organism(s), and infusion of a dressing capable of focused administration of a therapeutic drug may present a new treatment regimen option for chronic wounds. Randomized, controlled clinical studies are needed to evaluate the efficacy of this topical treatment.

Dr. Albaugh is an Associate Professor, Neumann University, Aston, PA; and a Clinical Wound Specialist, Optimum Physical Therapy, West Chester, PA. Dr. Biely is an Associate Professor, Neumann University. Dr. Cavorsi is a Vascular Surgeon and the Medical Director, Center for Advanced Wound Care, Wyomissing, PA. Please address correspondence to: Karen W. Albaugh, PT, DPT, MPH, CWS, Neumann University, One Neumann Drive, Aston, PA 19014; email: albaughk@neumann.edu.

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