Debridement as a Component of Wound Bed Preparation

Wound bed preparation is the global management of chronic wounds, which includes the goals of removing necrotic tissue from the wound, reducing the wound bacterial burden, managing the moisture content, and ensuring that the wound edges are conducive to cellular migration for resurfacing the wound (FIGURE 12-1). These components of wound bed preparation contribute to the correction of abnormal wound repair with the goal of facilitating the process of wound closure and subsequent healing. Adequate wound bed preparation is required prior to the use of advanced wound care therapies, such as cellular and tissue-based products, other biological wound interventions, collagen, and negative pressure wound therapy.¹

Debridement of necrotic tissue from a wound bed is a key component of preparing a chronic wound for closure and subsequent healing (FIGURE 12-2).^2–12 Numerous evidence-based wound care guidelines describe the importance of adequate and repeated debridement as a fundamental intervention for chronic non-healing wounds. One of these well-known international documents is the European Pressure Ulcer Advisory Panel (EPUAP) and the National Pressure Ulcer Advisory Panel (NPUAP) guideline Pressure Ulcer Prevention and Treatment: Clinical Practice, which states several reasons to debride a chronic wound (TABLE 12-1).¹³ CLINICAL CONSIDERATION

The presence of necrotic or devitalized tissue on the surface of a wound prevents accurate assessment of the extent of tissue destruction or depth of the wound.

Epibole (FIGURE 12-3) is defined as a condition in which the upper edges of the epidermis migrate down (sometimes with a rolled appearance) to envelop the basement membrane or lower edges of the epidermis. Thus, epithelial cells cannot migrate at wound edges and the wound is unable to resurface.¹⁴

During the normal cascade of events leading to wound repair, inflammatory cells such as neutrophils and macrophages are activated to remove microscopic debris, participate in microbial defense, and facilitate the beginning of the repair process. Any interruption in or impairment of the processes associated with the wound repair cascade may create an environment leading to wound chronicity and, ultimately, an environment of increasing necrotic burden.

The term necrotic burden refers to the following components:

• 
  

  Dead or devitalized tissue

  
  
• 
  

  Excess exudate

  
  
• 
  

  Levels of bacteria sufficient to interfere with wound healing.

The necrotic burden is found on the surface of many chronic, non-healing wounds. In addition, resident cells such as fibroblasts and keratinocytes may be phenotypically altered and no longer responsive to certain signals, such as those from chemical mediators, including growth factors. This state of the cell being alive but impaired by its nonresponsive condition is termed cellular senescence.^7,15

TABLE 12-2 lists processes by which necrotic or devitalized tissue impairs and impedes wound closure and healing.

There are many clinical and patient-centered factors to consider when making decisions about debridement (TABLE 12-3).

The overall condition of the patient and individual goals of care are two primary factors to be considered in the decision to debride.¹³ For example, a terminally ill patient with intact, non-infected eschar may not be a candidate for debridement because of comorbidities, medication, and poor cardiac function. The result of debridement may be a larger, potentially more painful wound requiring more extensive topical care with little or no opportunity for closure due to the patient’s severely compromised medical status. The patient’s general state of health, nutrition, hydration, medications, mobility, and activity status are other factors to be taken into consideration.¹³ Patients who take anticoagulants may need a less invasive debridement technique than sharp or surgical debridement. In addition, patients requiring more aggressive techniques are more safely debrided in a controlled setting, such as the operating room or hospital clinic, than at the bedside, in the home, or in the long-term care setting. CLINICAL CONSIDERATION

Access to adequate anesthesia (topical, regional, or general) must be considered for the patient with intact sensation in the area to be debrided.

Chronic wounds often have underlying pathogenic abnormalities that cause the necrotic burden to re-accumulate. Generally, debridement is not a singular event, but rather combines different methods and/or repeated interventions over time to achieve a clean, functional wound bed. Frequent serial debridements are often necessary to continually stimulate and refresh the surface cells, keeping the wound in a state of readiness to close.^15–17

The decision to debride requires careful consideration in certain wound etiologies. Stable, non-infected heel or lower-extremity ulcers with impaired perfusion should not be debrided unless signs of infection are present (eg, erythema, fluctuance, separation of eschar from the edge with drainage, or purulence).^13,17 Literature states that stable heel ulcers with black eschar should not be debrided¹³; however, in some instances it may be clinically appropriate to remove stable black eschar on patients who have functional goals and good blood flow. When making the decision to debride stable heel eschar, documentation to support the goals and rationale for performing the procedure are imperative. CLINICAL CONSIDERATION

• 
  

  Vascularity must be assessed prior to performing any debridement of a lower extremity wound.

  
  
• 
  

  Palpating pedal pulses only of patients with lower-extremity wounds is inadequate for assessing blood flow.

INTRODUCTION

Ms SR is a 62-year-old female resident of a long-term care facility with a past medical history of obsessive compulsive disorder, anxiety disorder, hypertension, hyperlipidemia, congestive heart failure, coronary artery disease, chronic obstructive pulmonary disease, and urinary incontinence. She presents to the wound center with an 8-week history of pressure ulcer on the sacral/coccygeal area (FIGURE 12-4).

FIGURE 12-4

Sacral pressure ulcer at the time of initial assessment, prior to debridement.

DISCUSSION QUESTIONS

1. 
   

   What other information is needed about this patient in order to make a diagnosis?

   
   
2. 
   

   What information is needed to determine the plan of care?

Patients with diabetes who have lower-extremity wounds need more extensive noninvasive vascular assessments (toe pressures [FIGURE 12-5] and wave forms, transcutaneous oxygen tension studies, skin perfusion studies, or Duplex arterial studies) to determine blood flow because of the propensity of the more proximal vessels to calcify in people with diabetes.^2,16,19,20 Guidelines for healing potential and for debridement are discussed in Chapter 4, Vascular Wounds.

Maintaining a dry, stable eschar often leads to slow eschar demarcation and separation as epithelial migration occurs from the edge, eventually closing the wound (FIGURE 12-6). This process has been reported in many cases when a patient is not a candidate for debridement. In addition, diagnoses such as pyoderma gangrenosum may result in pathergy (defined as enlarging or worsening of the wound), with sharp or surgical debridement (FIGURE 12-7).²⁰

The clinician who performs debridement must have knowledge of anatomy, understand the patient’s overall medical condition, know the wound etiology, and have the technical skills and clinical judgment for debridement, especially when using the more invasive techniques (such as sharp or surgical debridement) in order to have safe, successful outcomes. Clinicians must discriminate viable from nonviable tissue, recognize structures such as arteries and veins, recognize the difference between muscle and granulation tissue, identify fascia covering muscles, identify tendons and cartilage versus slough (which are sometimes similar in color), and identify bone and tendon (see FIGURES 12-8 to 12-17).

In addition to a thorough awareness of the patient’s clinical condition, knowledge of the different types of necrotic tissue is necessary to determine the most effective type of debridement to use. Necrotic tissue is generally categorized as slough or eschar; however, any tissue in or adjacent to the wound bed can become necrotic if it loses its blood supply (FIGURES 12-11 and 12-12). Therefore, reassessment of the wound is required at every debridement session.

Eschar may be soft or hard, depending on the amount of desiccation (extreme dryness), and is often described as leathery when completely dry. Slough (FIGURE 12-11) may be yellow, tan, gray, or brown; is generally moist; and may be loosely or firmly adhered to the wound bed. Slough is a by-product of the autolysis of necrotic tissue and as such, usually has a texture that makes it difficult to grasp with forceps.

The presence of granulation tissue is the hallmark of the proliferative phase of wound repair. Healthy granulation tissue most often appears bright or “beefy” red due to its rich vascular composition (FIGURE 12-8). Unhealthy granulation tissue, sometimes called friable or fragile granulation tissue, may be a dull, dark red or a pale, pink color.

Hypergranulation tissue (also known as “proud flesh,” exuberant granulation tissue, hypertrophic granulation tissue, and hyperplasia of granulation tissue) is a condition that is characterized by an overabundance of granulation tissue, resulting in the extension of this tissue above the level of the wound margins (FIGURE 12-9).^18–22 This condition may prevent migration of epithelial cells across the wound surface as these cells do not travel vertically, thereby delaying closure and making the wound more susceptible to infection. In addition, wounds with hypergranulation tissue have an increased risk for excessive scar formation by forcing the wound edges further apart.²² Malignancies can also present with tissue resembling hypergranulation tissue; therefore, an appropriate referral, biopsy, or both may be indicated.²² TABLE 12-4^2,18,19 provides examples of treatment to diminish or alleviate hypergranulation tissue. FIGURES 12-18 and 12-19 illustrate the use of polyvinyl alcohol foam to treat hypergranulation tissue. CLINICAL CONSIDERATION

Malignant tissue that resembles hypergranulation will bleed easily, have a darker red to purple color due to the hypervascularity, and most frequently occurs when there has been a history of hyperplasia.

Chapter 3 provides more detailed information on tissue types in chronic wounds. CASE STUDY

A review of the patient’s medical history (available through records brought to the clinic with the patient) includes the following:

• 
  

  Medications: Norvasc, Lipitor, Lasix, two antidepressants, Albuterol

  
  
• 
  

  Vital signs (taken at time of evaluation): BP—100/65; HR—78 bpm; O₂ saturation—94% on room air

  
  
• 
  

  Function: The patient arrives in a wheelchair, records indicate that she is non-ambulatory; transfers from bed to wheelchair with moderate assistance and sits in the chair 3–4 hours each morning and afternoon.

  
  
• 
  

  In addition to regular meals, patient receives protein shakes.

  
  
• 
  

  The patient’s wound measurements, using the perpendicular method, are 3.8 cm × 1.7 × 0.1 cm deep.

There is minimal serous drainage on the dressing upon removal and no odor. The patient has visible changes in facial expression and verbal complaints of pain with any tactile sensation to the wound bed.

DISCUSSION QUESTIONS

1. 
   

   What type of tissue is visible in the wound bed?

   
   
2. 
   

   Describe the edges and the periwound skin.

   
   
3. 
   

   Are any visible signs of infection present?

   
   
4. 
   

   Using the NPUAP Classification for Pressure Ulcer Staging, what stage would be appropriate for this wound?

Debridement falls into two general categories: selective and nonselective. With selective debridement, only nonviable tissue is removed; with nonselective techniques, both viable and nonviable tissue may be removed. Debridement is also classified by the method or the mechanism of action of the various techniques that are used to remove nonviable tissue.

The most common types of debridement used in clinical practice include:

• 
  

  Autolytic

  
  
• 
  

  Enzymatic

  
  
• 
  

  Mechanical (ie, scrubbing, whirlpool, pulsed lavage, and low-frequency ultrasound)

  
  
• 
  

  Instrument (sharp, surgical, and hydrosurgical)

  
  
• 
  

  Biotherapy or maggot debridement therapy

One or more types of debridement may be used over the course of the wound management to achieve and maintain a clean, functional wound bed.

Autolytic Debridement

Autolytic debridement is the process by which the body’s endogenous enzymes (eg, collagenase) loosen and liquefy necrotic tissue in the wound bed (FIGURES 12-20 and 12-21). Wound fluid contains these enzymes in addition to inflammatory cells, such as neutrophils and macrophages, that enter the wound site during the normal inflammatory process to remove bacteria and debris.^3,14 Some dressing categories customarily used to provide the optimal environment for autolytic debridement include hydrogels, hydrocolloids, transparent films, foams, alginates, medical-grade honey, and polyacrylate moist dressings (see Chapter 13, Wound Dressings).^2,18–20 CLINICAL CONSIDERATION

Clinicians working in home health or other settings where dressings are not readily available often ask, “What can I use instead?” For autolytic debridement of the dry eschar, a thin layer of KY jelly can be used instead of hydrogel, under an occlusive dressing to facilitate autolytic debridement.

The process of autolytic debridement is slower than other methods, requiring multiple dressing applications and frequently taking weeks to complete. Older or frail patients may have difficulty achieving a clean wound bed using autolytic debridement because of their impaired immune system, aging, comorbidities, and nutrition and hydration deficits. This finding suggests that older patients may need more aggressive forms of debridement than the autolytic process alone.²³ CLINICAL CONSIDERATION

An adequate immune system and local vascular supply is necessary for autolytic debridement to proceed optimally.

Autolytic debridement is frequently used in combination with other types of debridement, such as mechanical or instrument debridement. While slower, it may be the least painful type of debridement as long as the patient tolerates the dressing changes. Frequency of dressing changes depends on the amount of nonviable tissue to be removed and the amount of fluid that collects under the dressing.

Fluid collection beneath the selected dressing is monitored to prevent prolonged exposure of intact skin, which could lead to moisture-associated skin damage and ultimately create fragile skin that is at risk for further damage (FIGURE 12-22). Also, the fluid contains dead cells, cellular debris, and bacteria, frequently causing an odor that may lead to the assumption that the wound is infected, despite the absence of other clinical indicators of infection. Culture of the fluid would likely reveal bacteria that are present but not pathogenic to the wound or patient, possibly leading to unnecessary treatment with antibiotics. The wound surface should be thoroughly and safely irrigated or cleansed after each dressing removal and before assessing for clinical signs of infection.²⁰

Autolytic debridement can be employed to debride wounds of all types, regardless of etiology. However, peripheral arterial disease wounds usually have difficulty with autolytic debridement because of the impaired blood supply and consequent lack of moisture in the lower extremity skin.

Autolytic debridement is frequently the initial intervention in the home and long-term care setting where other, more aggressive forms of debridement may not be feasible or available. The only absolute contraindication to autolytic debridement is the infected wound, which needs to be debrided more urgently.¹³ Also, the moisture under the dressing is an ideal environment for bacteria to thrive. Autolytic debridement can be accomplished with minimal technical skills on the part of the caregiver; however, knowledge and skills are required to know if the process is appropriate for a particular wound and patient.

Surfactant Debridement

A unique enhancement to autolytic debridement is the use of a water-soluble Concentrated Surfactant Gel or CSG (PluroGel® Burn and Wound Dressing, Medline Industries, Inc., Northfield, IL). The surfactant, Poloxamer 188, is also often referred to as pluronic F68. Poloxamers are non-ionic synthetic surfactants comprising one central hydrophobic chain and two outer hydrophilic chains. These molecules form loose (non-covalent) cross-links with water to form a micelle matrix (Plurogel micelle matrix or PMM). The matrix is surface active, and in a dynamic system creates a “rinsing” action at a molecular level on the wound bed. This surfactant-driven activity enables the product to disrupt the non-covalent bonds which are instrumental in keeping necrotic tissue and other undesirable elements adherent to the wound bed, thus impairing healing. The product adds moisture more efficiently via the surfactant activity and essentially solubilizes dried exudate and other matter, thereby helping to soften, loosen, and trap wound debris.²⁴ These undesirable elements can then be rather easily removed at dressing changes via simple rinsing or wiping with wet gauze or similar materials.²⁵ For thermodynamic reasons specific to the polymer poloxamer, the CSG has a low viscosity appearance when at ambient conditions, particularly in cool ambient conditions (it turns into a liquid in a refrigerator for example), but forms a thick gel as it warms in contact with living tissue. This differentiates it from other common gel like preparations, which are generally viscous when cooled and “runny” when warmed to body temperature. Furthermore, because the surfactant micelles are easily water soluble, the debris-laden gel can be atraumatically washed away during dressing changes.²⁶

Lastly, laboratory and clinical studies have demonstrated the ability of the CSG to sequester planktonic microbes and disrupt wound biofilm using the mechanism of action described above.^27,28 The ability of the surfactant to salvage damaged cells has also been extensively reported in literature.^29–31

Enzymatic Debridement

Enzymatic, or chemical, debridement uses a topical pharmaceutical preparation that is specifically designed to target and break down the devitalized collagen in the wound bed.^14,23,32,33 As with autolysis, enzymatic debridement is an alternative to the more expensive and aggressive methods of debridement.

At present there is only one commercially available enzymatic debriding agent in the United States, collagenase, marketed under the trade name Santyl (Smith & Nephew, London, UK).³⁴ In wound healing, endogenous collagenases belong to a family of extracellular matrix metalloproteases (MMPs) which are naturally occurring enzymes produced by activated inflammatory cells (neutrophils and macrophages) and in certain wound cells (epithelial cells, fibroblasts, and vascular endothelial cells).^8,9,33–36

Topical collagenase is derived from the bacteria Clostridium histolyticum. Reported to be most active in a pH range of 6–8, topical collagenase is specific to native, denatured collagen.^8,15,34 Collagenase promotes debridement by selectively cleaving devitalized collagen strands anchoring necrotic cellular debris without harming viable collagen.^8,15,34 Collagenase has no known effect on viable tissue and is not associated with increased patient discomfort.^15,34 CLINICAL CONSIDERATION

A 2-mm layer of the collagenase ointment is applied directly to the tissue and covered with an appropriate dressing. The collagenase enzyme is activated by moisture, so the application of a secondary dressing that maintains a moisture balance will allow the enzyme to be released from the ointment.

Collagenase is best applied daily (FIGURES 12-23 and 12-24). Cross-hatching of dry or dense eschar is recommended to facilitate penetration of the ointment into subcutaneous tissue and to hasten the debridement process (FIGURE 12-25).^20,33 Protection of the surrounding skin with a moisture barrier can prevent maceration and denudation of the intact skin from the increased exudate that results from the enzymatic debridement process. The ointment should not be used with products that could inactivate collagenase (such as detergents or products containing iodine or heavy metals such as lead, silver, or mercury).^34,36 If a wound infection is suspected, the use of an antimicrobial agent per manufacturer’s recommendations should be considered for use on the wound surface prior to application of the collagenase ointment.³⁴