Evidence of Intensive Autolytic Debridement With a Self-adaptive Wound Dressing

Alexander M. Reyzelman, DPM; Mher Vartivarian, DPM

Disclosures

Wounds. 2015;27(8):229-235. 

In This Article

Abstract and Introduction

Abstract

Background. Chronic venous leg ulcers (VLUs) can be challenging to manage and heal. Despite the observed efficacy of surgical debridement, many patients with VLUs refuse the procedure due to the associated pain. Autolytic debridement induces no pain, but is slow or disrupted in chronic VLUs. Elucidation of the wound dressing functions that are sufficient to support autolytic debridement is needed. Materials and Methods. The authors report 2 challenging cases with large, nonresponsive VLUs. A 52-year-old female patient, Case 1, presented with a VLU of 91.4cm2 (10.5 cm x 8.7 cm); and a 58-year-old female patient, Case 2, presented with bilateral VLUs, the larger of which was 50 cm2 (10 cm x 5 cm). Both VLU cases were covered with yellow slough, and case 1 had a small area of black necrotic tissue. The patients had received standard care for more than 16 months, but their VLUs were worsening. A self-adaptive wound dressing (SAWD) with a compression wrap was applied 2 to 3 times a week. Results. Within 21 days, the VLUs of both cases had shed the yellow slough, and healthy granulation tissue was visible. Conclusion. In summary, the SAWD removed excess exudate with liquefied components of slough and nonvital tissue; provided sufficient moisture for preventing wound desiccation; sequestered microorganisms, thereby blocking their multiplication; and supported efficient autolytic debridement, clearing most of the slough and all crusted necrotic tissue within 3 weeks. The effect of SAWD on autolytic debridement is a promising mechanism for promoting healing of VLUs and warrants further study.

Introduction

The prevalence of venous leg ulcers (VLUs), the most advanced stage of chronic venous insufficiency, ranges from 0.2% to 1% in Western countries,[1] with a higher prevalence in people older than 80 years. A minor injury may initiate a skin break on the leg, and delayed healing can be aggravated by comorbidities such as diabetes, persistently high blood pressure, and chronic venous insufficiency. Chronic (VLUs) in a prospective clinical trial at one clinic ranged in size from 1.1 cm2 to 19.2 cm2, and the duration ranged from 6 weeks to 104 weeks.[2] The proportion of wounds healed within 2 years ranged from 68% for leg wounds to 51% for ankle wounds.[2] Patients with chronic bacterial infections with Pseudomonas aeruginosa, Staphylococcus aureus, Proteus mirabilis, or Enterococcus faecalis in their chronic VLU delayed healing of the wound,[3] although S. aureus and Proteus spp. did not appear to inhibit healing in a different clinic.[2] Guidelines for the management of VLUs encompass diagnosis, necessity of debridement and compression therapy, antibiotics, and adjunctive therapies such as isotonic exercise and leg elevation.[4] Despite these guidelines,[4–6] healing of chronic VLUs can be challenging, and novel approaches for restarting the healing of chronic VLUs are warranted.

Wound bed preparation for renewed healing requires attention to the healthy tissue and removal of necrotic tissue and slough; control of infection and inflammation; maintenance of correct moisture; and preservation of the growing healthy tissue at the edge of the wound during wound dressing changes, as indicated by the TIME framework for wound healing.[7,8] Wound dressings typically were designed to address 1 or more, but not all, of these critical conditions.

Debridement usually is performed before application of the dressing.[8] Debridement of chronic VLUs removes necrotic tissue, any debris, and bacteria from the wound; and it exposes the viable tissue to facilitate healing.[8] Types of wound debridement techniques include autolytic debridement, in which the body removes the necrotic tissue; enzymatic debridement, such as with collagenase-based products; biodebridement using sterilized maggots;[9] mechanical debridement; and surgical debridement.[10] Autolytic debridement usually causes no pain and leaves the wound bed at the correct moisture balance to promote granulation and growth of epithelial cells, but it can be a slow process.[10] A chronic VLU has difficulty employing adequate autolytic debridement because the wound environment is not conducive to the process, in that there is too much exudate with an increased number of matrix metalloproteinaises. Enzymatic debridement requires frequent dressing changes, and the specificity of the protein cleavage is determined by the collagenase or the collagenase/papain preparation. Mechanical debridement may involve wound cleansing at 4–14 psi, hydrosurgery at 15,000 psi, whirlpool, atomized saline, polyester fiber pad, or ultrasonic techniques. These techniques are nonspecific, can provide fast results, but can be painful and harm viable tissue.[7,10] Chemical debridement often includes the use of antimicrobials, and its short-term use can be effective; but it may be painful and may harm healthy tissues.[7] From a pain standpoint, autolytic debridement is the clear choice for patient comfort, but inadequate autolytic debridement, insufficiently controlled inflammation, and infection contribute to nonhealing VLUs. Autolytic debridement may be supported by dressings with hypertonic saline and/or honey via osmosis, and by semiocclusive dressings containing hydrocolloids or hydrogels.[7] Removal of excess exudate and cellular debris appears to assist in maintaining the process of autolytic debridement.[11] Hydration response technology, negative pressure wound therapy,[11] and a self-adaptive wound dressing (SAWD),[12] among other dressings, can remove excess exudate. The optimal moisture levels vary for the different stages of wound healing: a moist milieu is needed to promote granulation and growth of epithelial cells, whereas a drier milieu is needed on the new skin at the wound edge.

Wound bed preparation and healing involves the recurrent removal of excess exudate, microorganisms, semisolid slough debris, degraded necrotic tissue, hypertonic fluids containing toxic and/or corrosive components, and maintenance of moisture balance at the wound edge and low-exuding or nonexuding wound areas.[5,7,8,13] Minimal or no tissue damage during dressing removal maintains the progress of the healing process. The SAWD can continuously remove the exudate; sequester wound bed microorganisms from debris that may act as food sources; confine absorbed exudate and hypertonic fluids containing toxic and/or corrosive components, regardless of compression and gravity; maintain moisture balance in distinct microzones of the wound bed; adjust moisture in microzones as needed; and be removed without damage to newly formed epidermis.[14] The authors hypothesized these 6 conditions provided by the novel SAWD are not only necessary but also sufficient to support efficient autolytic debridement. These case studies examined the ability of SAWD and compression wraps to support relatively rapid autolytic debridement of 2 large VLUs that had been unresponsive to various treatments for 16.8 months and 19.2 months.

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