Appropriate wound bed preparation begins with comprehensive assessment and consists of removing local barriers to healing.

W

ound bed preparation is a phrase used to describe a process essential to obtaining optimum benefits from all of the advanced wound care products on the market today, allowing the wound to progress toward healing. Dr. Vincent Falanga defines this process as “the global management of the wound to accelerate endogenous healing or to facilitate the effectiveness of other therapeutic measures.”¹ Essentially, wound bed preparation applies approved medical practices, procedures, and standards, employing a holistic approach to assess, evaluate, and remove local barriers to wound healing—allowing the process of wound repair to progress in a normal, orderly fashion.
       A 2000 article² by Sibbald et al on wound bed preparation addressed 3 major factors in chronic wound treatment:
• Identifying and treating underlying causes
• Addressing patient-centered concerns
• Applying local wound care.
       The application of local wound care in wound bed preparation relates to the removal or management of barriers to wound healing, such as excessive bacteria, dead or devitalized tissue, and the management of exudate, to achieve the overall goal of a clean, stable wound ready for the application of an appropriately chosen wound care product. An insufficiently prepared wound bed will not benefit from even the most technologically advanced wound dressings. With a prepared wound bed, the skilled clinician can apply a purposeful approach to implementing a plan of care that will advance the wound according to the goals that have been established.

A Look Back

       A brief glimpse of the history of wound healing will help explain how the process of wound bed preparation came to be. Dating back to circa 2200 BC, one of the oldest medical manuscripts known to man is a clay tablet describing the “three healing gestures.” Likely one of the first documented approaches to the healing of a wound, it included washing the wound, making plasters, and bandaging the wound. Today, these “gestures” are called interventions, in which we:
1. Cleanse the wound, removing debris and bacteria;
2. Apply dressings to achieve a moisture balance in the wound bed; and
3. Apply secondary dressings to protect the wound from injury and prevent excessive moisture from leaking onto the periwound.³
       Another milestone in history occurred in Italy, circa 1478, when Aurelius Cornelius Celsus wrote an 8-volume medical compendium entitled De Medicina. It was within this medical text that he described “the four cardinal signs of inflammation.” These included rubor, tumor, calor, and dolor or redness, swelling, heat, and pain. Today, we use those signs and symptoms to clinically diagnose inflammation.⁴

Acute and Chronic Wounds

       In order to understand why wound bed preparation is necessary, we must first understand how acute wounds differ from chronic wounds in the healing process. Applying the model of acute healing to chronic wounds will only frustrate the clinician. The phases of acute wound healing, which include hemostasis, inflammation, proliferation, and maturation (or remodeling), follow a timely, orderly, reparative process whereby the end result is sustained restoration of anatomic and functional integrity.⁵ Each phase overlaps the others, yet each remains defined

Table 1

by its own characteristics.⁶*

       In the chronic wound, these phases are interrupted, stalled, extended, or prolonged and, in general, do not proceed through the healing process in a timely, orderly fashion. Researchers have attempted to explain why the chronic wound fails to heal, coming to the growing consensus that chronic wounds are stuck in the inflammatory phase.^7,8 (See Table 1 for a comparison of the biochemical differences in acute and chronic wounds.)
       This shift in the way we think about acute versus chronic wounds and the way they heal has enabled clinicians to apply the practice of wound bed preparation, facilitating improved healing in chronic wounds. As the majority of wounds encountered by clinicians in extended care are chronic in nature (including pressure ulcers, vascular ulcers, and diabetic foot ulcers), the process of wound bed preparation becomes essential in providing expert wound care to this often physically and cognitively compromised cohort of our society.

Elements of Wound Bed Preparation: Comprehensive Assessment

       The first step in the process of wound healing begins with a comprehensive clinical assessment, entailing a holistic approach to determine which factors are present that may have inhibited a wound from healing. Especially in the long-term or extended care setting, the clinician needs to consider the following:
1. What is the etiology of the wound?

Figure 1

2. Is this patient able to heal, or is this a malignant type of wound (see Figure 1)?
3. What are the barriers to healing (ie, systemic or local barriers)?
4. What are the overall goals of treatment and care (ie, healing vs. palliative)?⁹
       Try to determine the etiology of the wound during the first patient encounter. The comprehensive assessment should include: a brief physical; vital signs; nutrition and fluid assessment (including labs); social history (eg, is the patient a smoker/former smoker?), past medical history; review of all consultations, tests, radiology reports, labs, pathology reports, and and current medications being taken (including vitamins, over-the-counter drugs, herbal preparations, and food supplements); information on whether the patient is on steroids; information on any previous treatments used on the wound and the tolerance and outcome of these treatments; and a pain assessment. Additionally, the clinician should assess the patient and family understanding of the wound(s) and determine their ability to participate in the plan of care.
       Is the patient is able to heal? Consider the chronicity of the wound. If an inflammatory vasculitic process or malignancy is the etiology and palliative care is appropriate, be honest with the patient and family regarding treatment goals. Avoid aggressive treatments that may be painful, unrealistic, expensive, and fruitless. Allow the patient and family to verbalize their overall goal for treatment, and be sure your treatment plan is in concert with theirs.
       Address underlying causes and comorbidities. It is imperative to treat the underlying etiology of a wound and eliminate any factors that may contribute to stall wound healing. Both systemic and local factors need to be evaluated. Systemic factors to be evaluated include: age (think of skin changes, including altered barrier function, cellular changes causing thinning and dry skin, and decrease in collagen with aging); tissue oxygenation (which, when decreased, interferes with the deposition of collagen and the ability to clean up the wound); chronic disease processes (such as diabetes, peripheral vascular disease, autoimmune diseases, or renal failure); medications, especially steroids (which decrease the migration of neutrophils and macrophages as well as growth factors, collagen synthesis, and contraction of tissue); body build (ie, emaciated or obese, as an obese patient can be nutritionally compromised and at risk for delayed wound healing); and stress; it has been recently been noted in the literature that couples with high levels of hostile behaviors healed their wounds with a 60% lower healing rate than non-hostile couples).^10,11
       Local factors to be addressed include: mechanical stressors (eg, pressure, shear, and friction), wound temperature (a change in this may cause capillary constriction, spurring a decrease in perfusion and altered cellular mitosis); edema (collagen cannot synthesize when there is an increase in fluid in the interstitial space); cytotoxic agents (which can have a detrimental effect on fibroblasts); heavy bioburden; a dry wound bed (desiccation of tissue inhibits division and migration of cells); excessive exudate or drainage allowed to remain in the wound bed; and the presence of necrotic tissue and infection. These factors can all impede wound healing.¹²
       Following the history and physical, assess the wound characteristics, including: anatomical location; size (measurements including undermining and/or tunneling); amount and type of exudate or drainage; signs and symptoms of infection present; odor; pain; description of wound margins or edges; periwound skin characteristics and tissue characteristics (percentage and description of granulation, slough, epithelium, eschar); and exposed structures (bone, tendon, muscle). Determine whether any adjunctive therapies are being used.
       During each subsequent encounter with the patient, assess his or her tolerance to the choice of primary and secondary dressings, follow up on requested tests or consults, and assess the patient’s pain level to see if the care plan should be altered. Interdisciplinary team members must share progress the patient makes related to each discipline. The plan of care and overall goals must be reviewed frequently and altered as the status of the patient and/or wound changes. Encouraging dialogue with the patient and family about the wound healing progress promotes buy-in to the plan of care, helping to alleviate fears and possibly eliminating any unrealistic expectations.

Wound Bed Preparation: Cleansing

       The goal of cleansing in the next step of wound bed preparation is to remove bacteria and surface contaminants or debris, allowing the wound to move more rapidly from the inflammatory phase to the proliferative phase. Proceed gently to protect the healing wound and minimize the risk of infection as well as chemical and/or mechanical trauma. There are several safe, commercially prepared wound cleansers on the market; generally, however, normal saline is sufficient for clean granulating wounds. Minimize the disruption of the wound surface, heeding the guideline of gentle flushing with noncytotoxic solutions. In 1919, Fleming stated, “It is necessary in the estimation of the value of an antiseptic to study its effect on the tissues more than its effect on the bacteria.”¹³
       For dirty, contaminated, or necrotic wounds, there are several commercial wound cleansers on the market that contain nonionic surfactants. These wounds require aggressive cleansing to remove as much necrotic tissue, exudate, debris, and bacteria as possible. This can be accomplished using a maximum irrigation pressure of 8–15 psi or with a variety of pulsed lavage systems. Hydrotherapy (which is not as popular as it once was due to the risk for nosocomial infections via cross-contamination) may be used, but this therapy is not indicated for patients with arterial insufficiency or venous hypertension. Commercial wound cleansers with quaternary ammonium compounds, such as benzalkonium chloride (BZK) and benzethonium chloride (BZC), can further address overgrowth of pathogens and be safely used for short periods of time in critically colonized or locally infected ulcers.¹⁴
       The use of antiseptics remains controversial, as they have been found to be cytotoxic to normal living tissue. For example, hydrogen peroxide, Dakin’s solution, acetic acid, or povidone iodine use is not recommended when wounds are expected to heal, since they are generally toxic to the fibroblasts; in some instances, however, an antiseptic may be warranted.¹⁵ Since the late 1960s, it has been known that disinfectants can damage blood vessels and tissue and interfere with tissue function.¹⁶ When using an antiseptic, use one at the lowest concentration toxic to bacteria and the least cytotoxic to living tissue. One can resume nonantiseptic cleansing once the bacteria are presumed to be gone.¹⁷

Wound Bed Preparation: Debridement

       Debridement is the removal of foreign material and devitalized or nonviable tissue until healthy tissue is revealed. Here, too, the patient may experience pain, and it is the duty of the clinician to pre-medicate the patient and/or provide a topical anesthetic, such as lidocaine or a lidocaine/prilocaine combination, prior to debridement.

Figure 2

       Eschar is nonviable, desiccated (dried-out), dead, compressed tissue, which appears black or brown in color and is leathery, dry, or hard, representing full-thickness destruction (see Figure 2). Once eschar is removed, a tissue deficit can be observed. A scab, on the other hand, is merely dried-out blood and exudates over a partial-thickness injury; it is not “dead” tissue. Once a scab is gone, there is no tissue deficit.
       Slough, another type of nonviable tissue is a composite of moist fibrin, living and dead bacteria and cell debris, living and dead leukocytes, and exudates. Slough is described as yellow or tan, is thin and mucus-like, and can be soft and soggy or soft and stringy. The less water content the necrotic debris has, the more adherent to the wound bed it will be (see Figure 3).¹⁸

Figure 3

       Devitalized tissue can harbor bacteria, which can increase the risk of infection and produce excessive amounts of proteases, negatively impacting healing. The removal of any necrotic tissue may contribute to the release of available growth factors in the wound, enhancing healing. Additionally, the presence of necrotic tissue in a wound will prevent the clinician from adequately assessing the wound bed and the surrounding tissues, impacting the plan of care.

       Editor’s note: The second part of this article will run in the September issue of ECPN.