Wound dressings
Gillian M. Eccleston
Chapter contents
Complications in wound healing: chronic wounds
Physical characteristics of wound dressings
Mechanical properties of dressings
Safety and acceptability specifications
Key points
Introduction
In the past, traditional fabric wound dressings were used extensively. Their primary function was considered to be to keep the wound as dry as possible by allowing evaporation of exudate. It was assumed, therefore that dressings were a passive product with only a minor role in the healing process. However, it is now realized that a wound heals faster and more successfully in a moist environment. This has led to a greater understanding of the influence that wound dressings can have on wound healing and greater attention has been given to the design of more effective dressings. Over the last two decades, a large number of new dressings has become available, based on the concept of creating an optimum environment for the treatment of wounds. However, it is emphasized that there is still no single dressing suitable for the management of all types of wounds or for the treatment of a single wound during all phases of healing.
Many of the newer dressings aim to manage chronic wounds that are difficult to treat because wound physiology is altered. Such wounds are often a problem of the elderly and bedridden. Chronic wounds, as well as compromising the quality of life of the patient, place an enormous financial burden on health services.
Some modern dressings are designed to deliver drugs or wound-healing agents directly to the affected site.
Successful design of wound dressings depends on an understanding of the healing process, the patient condition in terms of health, environment and social circumstance, and the effect that the physicochemical properties of the various dressing materials have on the wound-healing process.
Wounds and wound healing
Wounds
The protective functions of the skin are compromised by injury. A wound can be defined as a defect or a break in the skin, resulting from either mechanical or thermal damage, or as a result of the presence of an underlying medical or physiological condition. Wounds are classified according to the number of skin layers affected and the area of skin involved:
• superficial wounds involve injury to the epidermis alone
• full-thickness wounds occur when the underlying subcutaneous fat or deeper tissues are also damaged.
Wounds are described as normal (acute) if they heal rapidly with minimum scarring and chronic if they take longer than 8–12 weeks to heal.
Simple mechanical injuries such as cuts, grazes and minor burns are usually treated by the patient, whereas the more severe traumatic injuries caused by, for example, surgery, traffic accidents and fires require hospitalization. Chronic wounds require specialist nursing care. Without an understanding of all these factors, correct dressing selection is not possible; incorrect choice of dressing is potentially ineffective and wasteful in terms of nursing time.
Wound healing
Wound healing may be considered as a dynamic process in which cellular and matrix components act together to re-establish the integrity of damaged tissue and replace lost tissue. Regardless of the source or the extent of tissue damage, under normal conditions the wound-healing process occurs in a predictable fashion as four overlapping stages: inflammation, migration, proliferation and maturation (remodelling). Healing is considered to be complete when the skin surface has reformed and has regained its tensile strength.
Inflammation
Inflammation is the body’s initial response to injury and involves both cellular and vascular responses. The release of histamine and a number of other cell-mediated factors into the wound results in vasodilation, increased capillary permeation and stimulation of pain receptors. The release of a protein-rich exudate containing phagocytes and other materials from the blood capillaries onto the wound surface engulfs the debris of dead cells and bacteria (known as autolytic debridement). Fibrinogen in the exudate elicits the clotting mechanism, producing a clot or scab on the wound that causes bleeding to stop. It also gives strength and support to the injured tissue. This first stage of healing usually occurs within a few minutes to 24 hours of injury, when the wound will be red, inflamed, painful and moist.
Migration
Growth factors in the wound exudate promote the growth and migration of epithelial cells, fibroblasts and keratinocytes to the injured area to replace damaged and lost tissue. These cells regenerate from the margins, rapidly growing over the wound under the dried scab. This epithelial thickening and basal cell proliferation lasts for 2–3 days.
Proliferation
The proliferation phase involves the development of new tissue and occurs simultaneously or just after the migration phase (day 3 onwards), lasting from 5 to 20 days. Granulation tissue is formed by the infiltration of blood capillaries and lymphatic vessels into the wound, and by the supporting collagen network synthesized by fibroblasts. This process is known as granulation. The network is important for developing the tensile strength of the skin. As the proliferation continues, further epithelial cell migration across the wound takes place, providing closure and visible wound contraction. During the proliferation stage, the wound is typically beefy red in colour and moist, but not exuding.
Maturation
This final phase of wound healing (also called the ‘remodelling phase’) involves the diminution of the vasculature and enlargement of collagen fibres, which increase the tensile strength of the repair. The timescale for wound repair is from about 3 weeks to 2 years. Commonly, the tensile strength of the final scar reverts to 70–90% of that of the pre-injured tissue.
Complications in wound healing: chronic wounds
Although wound healing is a natural and predictable phenomenon and most wounds will heal uneventfully, complications can sometimes occur that lead to prolonged healing times or chronic non-healing wounds. A chronic wound fails to heal because the orderly sequence of events described above is disrupted at one or more of the wound-healing phases. A normal wound may develop into a chronic wound at any time as a result of poor primary treatment, persistent infection or disease. The most common chronic wounds include venous stasis ulcers, diabetic ulcers, ischaemic ulcers, pressure ulcers (bedsores) and ulcers due to systemic infections or malignant disease. Bacteria may gain entry to the deeper tissue of an acute or chronic wound and overcome the body’s defence mechanisms, giving rise to infection. Poor nutritional status, disease and other factors regarding the patient’s condition may reduce the ability to fight infection, as well as interfere with healing mechanisms (Table 40.1).
Table 40.1
General patient factors that delay healing
| Nutritional status | Deficiencies in protein, vitamins (especially ascorbic acid) and minerals impair the inflammatory phase and collagen synthesis and thus prolong healing times |
| Advancing age | Elderly patients have less effective immune systems, resulting in decreased resistance to pathogens. Potential problems in healing arise from skin changes, slower metabolism and chronic health conditions such as circulatory problems and diabetes |
| Disease | Poorly controlled diabetes mellitus, renal disease, malignant disease associated with hypoproteinaemia |
| Compromised circulation | Healing delayed because inadequate nutrients, blood cells and oxygen are delivered to the wound |
| Treatment | Patients receiving drugs that compromise the immune system (e.g. steroids), chemotherapy or radiotherapy |
| Mobility | Physical inactivity can result in pressure-related skin damage |
| Obesity | Excess tension placed on wound and decreased vascularity of adipose tissue delays healing. Mobility may be reduced |
| Smoking | Decreases oxygen delivery to the wound due to vasoconstriction and coagulation of small blood vessels |
Foreign bodies introduced deep into the wound at the time of injury can cause chronic inflammatory responses that delay healing, sometimes leading to granuloma or abscess formation. Keloid and other scars that are cosmetically unacceptable may result from excess collagen production during the final phases of the wound-healing process. Underlying diseases and drugs that suppress the inflammatory process, e.g. corticosteroids, also interfere with wound healing.
Wound dressings
Dressings fall into several categories, depending on their function in the wound (occlusive, absorbent, adherent), the type of material employed to produce the dressing (polyurethane, alginate, collagen, silicone) or the physical form of the dressing (film, foam, gel). Some dressings are impregnated with medicaments such as antibacterial agents or wound debridement agents. The incorporation of pharmacological agents such as growth factors into dressings is still in its infancy, although a gel containing human platelet-derived growth factor (PDGF) is now available for treating chronic diabetic ulcers.
Dressings which make physical contact with the wound surface are referred to as primary dressings while secondary dressings cover over the primary dressing. Island dressings possess a central absorbent region that is surrounded by an adhesive portion. The properties of the common dressing types in relation to the type of wound being treated are summarized in Table 40.2. The various available types of dressings are discussed in more detail below.
Table 40.2
The key properties of the common types of dressings
| Type of dressing | Key features | Uses |
| Impregnated gauze (soft paraffin or sodium chloride) | Various degrees of absorption. Inexpensive. Needs frequent changing. Dressing may stick to wound, causing pain and damage | Normal or highly exuding wounds. To apply creams or ointments to wound. Infected and necrotic wounds |
| Films | Non-absorbent. Permeable to moisture vapour, allowing some exudate to evaporate. May be transparent. Conform to contours. Adhere to wound. Impermeable to microorganisms | Later stages of wound healing where little exudate. Loss of water vapour can cause wound to dry out. Not for infected wounds and thin or fragile skin |
| Foams | Absorbent. Allow gaseous exchange. Impermeable to water and microorganisms. Can remain on wound for extended times. Thermal insulation. Some are adherent | Performance varies between dressings. Generally low to moderately exuding wounds |
| Alginates | Form hydrophilic gel on contact with wound exudate to promote moist healing. Absorbent. Physical and thermal protection. Easily washed out of the wound | Performance varies between dressings. Moderate to high exuding wounds. Haemostasis. Suitable for infected wounds. Not suitable for dry wounds |
| Gels/hydrogels | Maintain moist wound bed by balanced hydration of wound. Absorbent. Non-adherent. Require secondary dressing | Cleansing of necrotic wounds by rehydrating dead tissue and encouraging autolytic debridement |
| Hydrocolloids | Create moist environment. Absorbent. Initially impermeable to water vapour and air. Adhere to wet and dry wounds. No pain on removal. Can remain on wound for extended times. Provide insulation. Do not require secondary dressing | Performance varies between dressings. Suitable for light to moderately exuding non-infected wounds. Facilitate rehydration and autolytic debridement of sloughy or necrotic wounds |
Traditional dressings
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