Wound Dressing

CHAPTER 44 Wound Dressing



Marisha Chilcott


Wound management is an often overlooked and undervalued aspect of patient care. Nonetheless, wounds are a source of significant patient, family, and clinician distress, causing readmission, long-term morbidity, and avoidable mortality. This brief overview of wound care and dressing selection intends to demystify basic wound management and improve patient outcomes.


There are three basic tenets to wound management:


1 To get rid of the “ick” (i.e., slough, pus, and necrotic debris)

2 To promote healthy tissue growth

3 To achieve wound closure

The key steps in attaining these goals are first to prepare the wound bed and then to manage the progressive development of the healing tissue. Selection of appropriate dressings is critical to succeed in these simple endeavors, and there is no single recipe that will work for all wounds. Dressing selection is determined by the individual wound itself, the available materials, and the psyche and physical health of the patient. For example, a wound in the perineum requires very different considerations than a wound on the scalp or back. A lower extremity wound in the exact same location is very different if the patient is diabetic, has peripheral vascular disease, or is an otherwise well patient with Hansen’s disease (with neuropathy).


In addition to the general wound types most frequently encountered (e.g., pressure ulcers, venous stasis ulcers, nonhealing infected surgical wounds), the clinician will occasionally have to address the recalcitrant and fungating malignant wound of neoplasia. These wounds may need to be addressed somewhat differently because their management objective may not be actual healing. Rather, the objective may be to maintain quality of life for the patient who must live with the open wound for the remainder of his or her life. Thus, management of odor and appearance is of greater import than achieving resolution of the wound site.


Wounds with toxins, such as those produced by brown recluse spider bites or infiltrated chemotherapeutic agents, are also treated differently in that they require aggressive, usually wide surgical débridement to remove the offending agent and limit ongoing damage to tissue.


The range of dressing choices includes a variety of materials, forms, and structures. Their individual characteristics are governed by their principal purpose, be that absorption, bacterial growth inhibition, pain relief, débridement, occlusion, compression, or simple protection. Effective management of the stages of wound healing requires an understanding of the processes and the roles potentially played by the dressings available.



Wounds 101


The word wound is defined as a break in the epithelial integrity of skin with disruption of possibly deeper tissues, including dermis, fascia, muscle, and bone. Wounds then divide neatly into acute versus chronic, and clean versus infected. The ideal wound, from the standpoint of speed of healing, cosmesis, and function, is clean and acute. An example is the classic surgical wound created in a sterile environment and approximated to maximize the probability of primary closure. The most challenging wound, from either a patient’s point of view or a clinician’s management perspective, is infected and chronic. These can be decubitus sacral ulcers exposed to feces, foot injuries on the diabetic patient with severe tinea pedis and onychomycosis, abdominal wounds that have dehisced secondary to infected seromas, or any of a number of unfortunate breakdowns in integumentary integrity.


Clean or sterile acute wounds can heal by either primary or secondary intention and are relatively straightforward to manage. The fundamentals of that process are the basis for all wound care. In fact, the goal of the management of the chronic infected wound is to modify its conditions to approximate a clean acute wound so as to follow the same uneventful healing process.


Healing of acute wounds involves a cascade of overlapping processes that includes first hemostasis, then inflammation, followed by proliferation, and culminating with remodeling. Chronic wounds become chronic when they get stuck in the stage of inflammatory processes because of infection, poor circulation, inadequate enervation, repeated trauma, or some combination of those conditions. The role of dressing selection and wound care management comes down to ameliorating those conditions that impair the progression from inflammation to proliferation.


Wound types can be generally be categorized by their cause, their depth, and their appearance. Causes are almost always multifactorial, but the underlying pathologic process that predisposes a particular patient toward wound development is relevant in the overall care of the wound and the person who hosts it.


Depth is both a physical measurement (in millimeters to centimeters) and a characterization of penetration through the skin and underlying tissues. It is generally divided into surface, partial thickness, and full thickness.


A categorization for pressure ulcers was developed in 1975 by J. D. Shea, then refined and promoted as a tool to promote clear communication between clinicians in 1989 by the National Pressure Ulcer Advisory Panel (NPUAP). In 1997 and 2007, the NPUAP updated their pressure ulcer staging system to reflect the growing understanding of the multifactorial nature of wound development. The following NPUAP definitions are directed specifically at pressure ulcers and do not apply to wounds from other causes (e.g., venous insufficiency, diabetic foot wounds):


Pressure ulcer: A localized injury to the skin and/or underlying tissue, usually over a bony prominence, as a result of pressure, or pressure in combination with shear and/or friction.

Stage I: Intact skin with nonblanching redness of a localized area, usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. Note: The area may be painful, firm, soft, warm, or cooler compared with adjacent tissues and may be difficult to detect in individuals with dark skin tones.

Stage II: Partial-thickness loss of dermis presenting as a shallow open ulcer with a red-pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister. Note: Presents as a shiny or dry shallow ulcer without slough or bruising. (Bruising may indicate deep tissue injury; see later discussion.) This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration, or denudement.

Stage III: Full-thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, or muscle is not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. Note: The actual measured depth of the stage III pressure ulcer varies by anatomic location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue, and stage III ulcers can be quite shallow. In contrast, extremely deep stage III pressure ulcers can develop in areas of significant adiposity. The key feature is that bone/tendon is neither visible nor palpable.

Stage IV: Full-thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. Often includes undermining and tunneling. Note: As with stage III ulcers, the actual depth varies by anatomic location. Areas without significant subcutaneous tissue (e.g., nose, ear, malleolus) can have very shallow stage IV ulcers, with bone/tendon that is either visible or palpable.

Unstageable: Ulcers with full-thickness tissue disruption but with the base of the wound covered by slough and/or eschar are not stageable until the base of the wound is exposed.


Types or Healing Stages of Wounds


Acute wounds heal in a relatively orderly and well-organized fashion, with “coordinated actions of both resident and migratory cell populations within the extracellular matrix environment leading to repair of injured tissues.” In contrast to this, some wounds fail to heal in a timely and orderly manner, resulting in chronic nonhealing wounds. As mentioned earlier, the usual stages of healing are hemostasis, inflammation, proliferation, and epithelialization.


Chronic wounds are those that fail to progress through the normal stages of healing. Although the most common place for a chronic wound to get “stuck” is in the inflammatory stage, a wound that is exposed to repeated trauma (because of a patient who “picks”) can also be functionally chronic. The biologic foundations for the variety of reasons a wound becomes chronic are complex, but the facts that wounds have stages of evolution and that clinical interventions play a role in their development are the obvious motivations behind wound care and dressing selections (Table 44-1).


TABLE 44-1 Chronic Wound Characteristics and Descriptions


















Wound Characteristic Features
Necrotic
Devitalized epidermis

Blackened in color

Dry and retracted
Sloughy
Containing a layer of viscous, adherent slough

Yellow in color

Wet

Potentially malodorous
Granulating
Significant amounts of highly vascularized granulation tissue

Beefy red or deep pink in color
Epithelializing
Evidence of pink margin

Isolated pink islands on the surface


Wound Bed Preparation


A clean acute wound has, by definition, a prepared wound bed. That is, the injured tissue is disrupted but not necrotic or burdened by foreign bodies or bacterial load. It is ready to start healing and needs dressings that simply protect it and keep it on its natural course by preventing it from becoming infected, necrotic, or otherwise healing impaired. This is described further later.


Whether acute or chronic, a dirty wound has a wound bed that will not heal well because the inflammatory cascade is upregulated and proliferation of the various cell lines that make up the new tissue (basal cells, fibroblasts, myofibroblasts, and epithelial cells) is inhibited. Thus, the first step in the care of a dirty wound is to prepare its bed.


Wound bed preparation means creating an optimal environment for healing with a well-vascularized foundation that is stable and has minimal exudate. This preparation requires reducing the bacterial load, removing necrotic tissue, and optimizing host systemic factors. Bacterial load reduction is achieved through both appropriate systemic antibiotics and selection of a dressing that is bactericidal or at least bacteriostatic.


Dakin’s solution and acetic acid solutions have been used for more than a century to decontaminate wounds. There is now clear clinical evidence that these solutions are toxic to fibroblasts and impair healing. However, this does not mean that they do not have a role. Both are extremely effective at reducing the bacterial burden of a wound infected with gram-negative organisms, particularly Pseudomonas. Although there is an element of toxicity to polymorphonuclear neutrophils and fibroblasts that slows healing, infection and colonization probably impair healing even more significantly. The judicious course of practice is to make staged use of these solutions as part of 1 to 2 days of wet-to-dry dressing management before converting to a more long-term, tissue-promoting (but less bactericidal) dressing choice.


Virtually all necrotic tissue requires removal to develop a healthy wound bed. The notable exception to this rule is the case of dry necrosis without infection. These cases occur under relatively special circumstances of severe frostbite, ischemic injury, and rare other circumstances. Such completely dry necrotic tissue can be allowed to autoamputate; however, if the dry necrosis is actually an eschar overlying wet necrosis, intervention is necessary. If there is any indication of infection (i.e., wet necrosis), aggressive débridement is a prerequisite to wound bed preparation and healing.


Débridement can be achieved through progressive dressing changes using a hydrogel and mechanical removal with gauze, surgical/sharp débridement, use of a vacuum device, or, if tolerable, larval therapy (i.e., medical maggots; see Chapter 45, Maggot Treatment for Chronic Ulcers). Under the appropriate conditions, larval therapy is the safest, fastest, and most efficacious method of wound débridement.


As implied earlier, wound bed preparation involves more than simply the local management of the wound. It also requires a perspective that includes the individual patient who harbors the wound. This means thinking about the patient as a whole person and recognizing that the greater milieu of the patient’s health state is hugely influential on the outcome of the healing process. Glycemic optimization and nutritional support are often at the foundation of this multidisciplinary approach. A nutritional consult can aid tight glycemic control and suggest if supplementation of key minerals (e.g., zinc) and vitamins (e.g., vitamins A, C, and E) can benefit. Note that although supplementation with zinc in patients with deficiency enhances collagen formation, supplementation with zinc in patients who are not deficient can paradoxically cause copper deficiency. Copper deficiency in turn weakens scar tissue through decreased tensile strength. Also, vitamin stores and intake can vary widely depending on individual patient circumstances. Thus, a formal nutrition consult to assess a patient’s current and impending status should guide supplementation, rather than wholesale recommendations for general replenishment. Occupational therapy consultation may aid with appropriate bed/chair fitting and selection. In addition, edema should be minimized through compression and elevation, and immunosuppressive drugs such as steroids avoided.



Dressings by Design


The general objective of all dressings is to promote rapid and cosmetically acceptable healing with minimal patient discomfort. Within this greater expectation, however, dressing types vary greatly in their material composition and primary application. Absorption, infection prevention, infection amelioration, débridement, pain management, and protection are different dressing purposes.


The following describes various dressing types and their characteristics. Each description is followed by a table that includes brand name dressings in each category (where applicable). This section is by no means meant to be an endorsement of any specific product, nor does it claim to be an exhaustive list of products currently available. Nonetheless, it is often difficult for the clinician to recognize based on name or product labeling just what category a given product might fit into. Many health care organizations do not stock the entire line of a given supplier’s products, and how to mix and match what is available at an institution to address the progressive dressing needs of a given wound can be very confusing. The purpose of the tables is to provide a basis for this sort of cross-reference.



Dressing Types and Characteristics



Antimicrobial


Antimicrobial dressings are used for locally infected or colonized wounds to reduce the microbiologic load (Table 44-2). Solutions of acetic acid or dilute bleach (Dakin’s solution) have been used for years for this purpose but except in specific and judicious applications should be replaced with the less host-toxic options now available. Dressings made with silver, in ionic or nanocrystalline form, have been demonstrated to be very effective antimicrobials with bactericidal rather than just bacteriostatic qualities. Silver dressings include both silver-infused creams and meshes (Figs. 44-1 and 44-2).


TABLE 44-2 Examples of Antimicrobial Dressings























Silver-Based Dressings Iodine-Based Dressings Other Antimicrobials
Acticoat (Smith & Nephew, St. Petersburg, Fla) Iodosorb (Smith & Nephew) Metronidazole (Metrotop Gel; Pharmacia & Upjohn, Bridgewater, NJ)
Silvadene Cream (Monarch Pharmaceuticals, Bristol, Tenn) Iodoflex (Smith & Nephew) Bacitracin zinc and polymixin B sulfate (Polysporin; Johnson & Johnson)
Actisorb Silver 2000 (Johnson & Johnson, New Brunswick, NJ)   Neomycin sulfate, polymixin B sulfate, and bacitracin (Neosporin; Johnson & Johnson)
Aquacel Ag (ConvaTec, Princeton, NJ)   Mupirocin (Bactroban; GlaxoSmithKline, London)

image

Figure 44-1 Acticoat, a silver-impregnated antimicrobial barrier dressing.


(Courtesy of Smith & Nephew, St. Petersburg, Fla.)

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May 14, 2017 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Wound Dressing

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