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Preparing the Wound for Healing: The Effect of Activated Polyacrylate Dressing on Debridement
An important aspect of preparing wound beds for healing is debridement - removal of non-viable or necrotic tissue until only healthy tissue is exposed. Wounds with necrosis have high levels of bacteria and toxins1 and are more likely to have a prolonged inflammatory response and healing process with increased risk for development of acute or chronic infection.2-6
This may increase the potential for development of a slow or nonhealing, recalcitrant wound.4,5,7,8 Debriding necrotic tissue removes a large source of bacteria,1 which helps diminish the inflammatory response, decrease toxin production, and move the wound into the proliferative phase more rapidly. In addition, complete debridement allows clinicians to stage or grade the wound and evaluate the healing progress. Debridement may be completed early in wound care and/or throughout the entire wound healing process. Clean wounds without necrotic tissue create the best possible local environment for healing.
Debridement can be non-selective or selective. Non-selective methods, such as mechanical, include wet-to-dry gauze, whirlpool, and surgical debridement.7 Wet-to-dry gauze dressings are often applied incorrectly, making them less effective for debridement.9 They allow wound bed tissues to dry out, potentially prolonging the healing process. The non-selective debridement facilitated by wet-to-dry gauze dressings delays healing by adhering to and removing living tissue and is quite painful. Wet-to-dry dressings should be changed several times daily to be most effective, making the method labor intensive, costly, and complex. Thus, considering wet-to-dry gauze dressings a standard of care may be erroneous.10
Selective methods include autolytic, conservative sharp, and enzymatic debridement. To achieve a clean wound using some of these traditional methods of debridement may take weeks or even months. Autolytic debridement is accomplished by keeping wounds continually moist, allowing the host's own white blood cells and enzymes to liquify the necrotic tissue. People with ineffective inflammatory responses or large amounts of necrotic tissue will not have effective debridement with this method alone. Conservative sharp debridement is effective and rapid, but access to qualified and certified personnel may be limited. Sharp debridement methods do not remove all necrotic tissue; thus, adjunctive methods are required.
Many clinicians use enzyme agents for debridement. Enzyme preparations exert their selective debridement activity by denaturing and digesting proteins. Enzymes may have variable effectiveness based on the pH of the wound and type of necrosis.8,11 However, as a practical matter, clinicians do not test wounds for pH. The effectiveness of enzymes depends on the skill of the caregiver to appropriately apply and cleanse the enzyme and debris from the wound.5 Further, not all enzymes are indicated for infected wounds, as they are not reported to have a direct effect on bacteria.
In addition to these methods, specific types of polymers - polyacrylates - may enhance selective autolytic debridement. Moisture-activated polyacrylate dressing pads selectively debride by attracting and permanently removing proteins from necrotic tissue, as well as by attracting and retaining toxins and bacteria.12,13 Removal of these proteins breaks down the structure of the necrotic tissue. An activated polyacrylate dressing is indicated for use in any kind of wound where moist wound therapy is desired.
To apply an activated polyacrylate dressing, the clinician moistens the dressing with Ringer's solution (a physiologic solution containing sodium, chloride, calcium, and potassium). The dressing is placed on the wound and covered with an appropriate secondary dressing such as composites, foam, or bordered gauze products. The activated polyacrylate in the core of the dressing releases the Ringer's solution into the wound, supporting autolytic debridement while attracting and retaining protein molecules; thus, promoting debridement.12
Comparing the effectiveness of all of these methods is difficult because standards for effective debridement are not reported in the literature. In general, the more rapidly the wound can safely be debrided without harm to living tissue or cells, the faster the wound can move toward closure. If therapy is appropriate, the quantity of necrotic tissue in the wound should diminish, and significant progress should be noted in 1 to 2 weeks from initiation of therapy.5,6,8,9
The purpose of this study was to report the rate of debridement in a select group of patients treated with TenderWet Dressing® (Paul Hartmann AG, distributed by Medline Industries Inc., Mundelein Ill.), a new activated polyacrylate dressing. The effectiveness of the dressing, as measured by the percent reduction in necrotic tissue over time, had not previously been established in any population with chronic wounds. Rates of debridement were studied, as some literature supports the utilization of rates as clinically more useful than data obtained for a specific time interval.14,15
Methods
A retrospective, non-controlled, descriptive study16 was conducted using a convenience sample of medical records to collect data from June 1, 2001 to February 10, 2002. Consent was obtained from four wound care centers to abstract data from the medical records of patients who had completed therapy using the activated polyacrylate dressing. Medical records of patients who had wounds that required debridement were included and selected only if wound size and amount of necrosis at beginning and end of care and dates of care were documented. Wound debridement progress was followed through the medical records from the first date of treatment with activated polyacrylate dressing for debridement until clinic physician or nurse practitioner records indicated that debridement was complete.
Patients visited the clinic weekly for wound evaluation and documentation. The patients or their care providers performed daily dressing changes, which consisted of removing the old dressings and applying a new moistened activated polyacrylate dressing pad and appropriate secondary dressing. Secondary dressings were used to affix the activated polyacrylate dressing pad. No other cleansing or debridement procedures were performed.
Data collection. Nurses and physical therapists with board certification in wound care completed the wound measurements and documentation. Data abstracted from the medical records included sex, birth date, dates of the beginning and end of wound treatment with the activated polyacrylate dressing, type of necrotic tissue, percent of necrosis at the beginning and end of wound treatment, wound type (venous, diabetic, pressure, surgical, other), wound duration before treatment with the activated polyacrylate dressing, and presence or absence of a diagnosis of diabetes. The percent of necrotic tissue was estimated visually by the respective clinical caregiver.
Because not all wounds were 100% necrotic at the beginning of the study, the percentage reported is the percentage of total wound surface area that had been debrided. Not all demographic or confounding data were available from all medical records. However, all medical records included in the study contained documented wound size and amount of necrosis at recorded dates.
Statistical methods. Data were entered into electronic form with use of the SAS® Full Screen Product (SAS, Cary, NC) and analyzed with the SAS procedures, general linear models, life test, and non-parametric tests. The main outcome variable of this study was rate of debridement. The individual debridement rate was expressed in rate per week and calculated using the following formula:
% necrotic tissue at start of treatment - % necrotic tissue at end of treatment)/weeks of treatment
Preliminary analysis showed that the rate of debridement of this convenience sample was not distributed normally; therefore, tests of differences of mean rates of debridement between and among groups within confounding variables were determined using non-parametric tests. Differences in debridement rates between two groups were evaluated using the Wilcoxon two-sample test. Differences in rates of debridement among three or more groups of a confounding variable (such as wound types, duration of wound, and age groups) were evaluated using the Kruskal-Wallis test. When the Kruskal-Wallis test showed a statistical difference, but did not determine which pairs of means were different, the Bonferroni tests of differences were used. All tests of differences of means of rate of debridement used a maximum P value of 0.05 to reject the Ho of no difference of means among or between group members.
The Kaplan-Meier estimator was used to show the rate of debridement as a function of time. This non-parametric method of estimating survival functions is appropriate for this data set - survival analysis for data sets without censored data (the records showed that all patients completed the therapy period and did not drop out of therapy for any reason).17,18 The Kaplan-Meier estimator provides plots of the survival function of rate of debridement by time, plots of the survival function for each covariate of interest, the median survival function of rate of debridement with 95% confidence intervals, and the Wilcoxon chi-square test of significance differences in the plots of the survival functions.18
Results
The sample included 55 medical records that contained documentation of the percent of necrotic tissue at the beginning and end of treatment with activated polyacrylate dressing as well as the dates of the beginning and end of treatment. The 55 participants included 23 men and 30 women (the gender of two patients had not been recorded). Fourteen participants had diabetes mellitus and the following five wound types were recorded: venous ulcers, diabetic ulcers, pressure ulcers, surgical wounds, and full-thickness wounds due to various etiologies not included in the other four types. Most wounds (38) contained slough; one patient's record did not list the type of necrosis (see Table 1). At baseline, an average of 73.9% of the wound was covered with necrotic tissue while 11.5% of the wound was covered at the end of treatment; the rate of debridement per week was 37.7% (see Table 2). The mean age of the sample was 62 years and the mean treatment time was 3.9 weeks.
Participants were divided into three groups: <51 years, 51 to 80 years, and >80 years. Table 3 shows the mean rate of debridement per week per group for each of the recorded patient and wound variables. Although mean rates of debridement for the five wound types varied greatly, the differences were not statistically significant. The difference in the mean rates of debridement among the three age groups was statistically significant (P = 0.009). The Bonferroni test of differences showed that the mean rate of debridement was significantly different between the < 51 and > 80 year old patient group. Duration of the wound, patient gender, type of necrosis. or diagnosis of diabetes were not statistically significant confounders in this sample of patients (see Table 3).
Survival distribution of debridement rate for the entire sample showed that the median rate of debridement occurred at 2.86 weeks (95% confidence level: 1.7 to 3.7 weeks) (see Figure 1). Survival distribution of the debridement rates by age group was significantly different (Wilcoxon test chi-square 7.05, (df 2, P = 0.03) (see Figure 2).
Discussion
In this study sample, the mean debridement rate was 37.7% per week.
Venous and diabetic ulcers were debrided most expediently. These results are similar to the results of wound healing reported by Kantor and Margolis,14 who found that the venous ulcer debridement rate was slightly greater than twice the rate of diabetic ulcers. The wounds of younger adults took significantly less time to debride than those of the oldest group in the sample (see Table 3). Optimal host inflammatory response is an important factor in the effectiveness of autolytic debridement. The limited ability of older or frail patients to achieve autolytic debridement in this population suggests that older patients may need a more aggressive form of debridement than the autolytic method alone.
One would expect that the debridement of eschar (desiccated layers of necrotic tissue) occurs more slowly than debridement of slough (a moist composite of fibrin, bacteria, cell debris, leukocytes, and exudate). Although in this population slough-covered wounds debrided at a faster rate (38.4% per week) than eschar-covered wounds (36.3% per week), the sample size was too small to show a statistically significant difference. The fact that the men in this population were younger than the women (average age of women = 67 years, SD 18.3 years; average age of men = 55.8 years, SD 19.2 years) may explain why wounds in women took longer to debride than those in men (see Table 3). Wounds of longer duration had a slower debridement rate than those of shorter duration (see Table 3). This may be related to the down regulation of the inflammatory response in older wounds, with less ability of the hosts to facilitate autolytic debridement.2
The results of this study suggest that activated polyacrylate dressing therapy is effective for debridement of all types of necrosis and for many types of wounds. The activated polyacrylate dressing provides an effective rate of debridement. Debridement rates have not been reported. The dressing may be used for people with a variety of slow-to-heal or nonhealing wounds and does not damage healthy tissue. It is also easy for patients and caregivers to use since it eliminates some of the guesswork and complexity involved in using other methods of debridement.
Limitations
This study is not randomized, no control group was established, and the sample size is too small to adequately test the effects of known confounders of debridement. In addition, debridement rates varied widely between patients. Varying depths of necrotic tissue may help explain this variation. Because clinicians' quantification of surface area measurements of necrotic tissue were used, the depth of necrotic tissue was not measured because it is not standard practice to do so.
Multivariate analysis of the data did not uncover any other known risk factors for slow debridement - perhaps because the sample size was too small to detect significant differences. This suggests that further research is needed to determine the effect of these risk factors and others on debridement rate when the activated polyacrylate dressing or any debriding product is used in the clinical setting.
Conclusion
This study demonstrates that, in regular clinical practice, a mean debridement rate of 37.7% per week can be achieved with younger patients exhibiting the most expedient debridement of their chronic wounds. Older patients may debride more slowly, but with an effective debridement rate. Activated polyacrylate dressing may be used as an effective primary debridement or adjunctive debridement method. Further research is needed to determine the debridement rate of other available debridement methods. A standard for reporting would be useful to clinicians in deciding which debridement method is most appropriate for their patients with necrotic wounds.
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