Pressure ulcers are an internationally recognised patient safety problem, estimated to affect 2.5 million people annually (House 2011). The development of pressure ulcers in any patient is a serious complication resulting in pain, decreased quality of life and significant expenditure of both time and money for the healthcare industry (VanGilder 2009). Also known as pressure injury, pressure sores, decubitus ulcers, or bedsores, pressure ulcers are a localised injury to the skin, underlying tissue, or both, usually occurring over a bony prominence, as a result of pressure, or pressure in combination with shear stress (EPUAP/NPUAP 2009).
The main factors associated with the development of pressure ulcers are exposure of the skin to excessive pressure, and a reduced tolerance of the skin to pressure. Pressure is exerted on the skin, soft tissue, muscle, and bone by the weight of an individual or a device applied against the surface. Tissue tolerance is the ability of the skin and its supporting structures to tolerate the effects of pressure by distributing it (cushioning) and by the transfer of pressure loads from the skin surface to the skeleton (AWMA 2012). Tissues are capable of withstanding enormous pressures briefly, but prolonged exposure to pressure initiates a series of events that potentially leads to necrosis and ulceration of tissue.
Factors that increase pressure on the skin include impairments in mobility, activity or sensory perception, because then the pressure is not relieved by movement or changes to body position. Intrinsic risk factors for the development of pressure ulcers include advancing age, poor nutrition, poor perfusion and oxygenation, whereas, extrinsic risk factors include increased moisture, shear and friction. Shear forces and friction aggravate the effects of pressure upon tissue and are important components of the mechanism of injury. The combination of pressure, shear forces, and friction causes microcirculatory occlusion, resulting in ischemia and tissue anoxia (lack of oxygen) and stimulation of inflammatory processes, which may lead to necrotic cell death, and ulceration. Irreversible tissue damage may occur in a vulnerable patient with as little as 30 minutes of uninterrupted pressure (Kirman 2008). In addition, excessive contact of the skin to fluids impairs its barrier function, causes maceration and an increased risk of the development of pressure ulcers.
Global prevalence rate of pressure ulcers ranges from 8% to 30%, depending on patient factors and treatment setting. Prevalence surveys in European acute care settings found an overall prevalence of 18.1%, with individual countries reporting prevalence of between 8.3% to 23% (Vanderwee 2007). A recent US study estimated pressure ulcer prevalences of approximately 13.3% in acute care settings and 29% to 30% in long‐term care settings (VanGilder 2009). Within Australia, pressure ulcer prevalence is currently estimated at between 5% to 15% in acute care settings and between 13% and 37% in aged care (DoH 2006). These international studies of prevalence illustrate the extent of the burden of all grades of pressure ulcers, however, variability in prevalence in similar settings suggests pressure ulcers are amenable to intervention, with substantial potential for improvement in patient and financial outcomes.
A number of systems for describing the amount of tissue damage exist, but pressure ulcers are generally graded 1, 2, 3 and 4, according to the depth of tissue damage, with category/stage 1 being the least severe, and category/stage 4 indicating complete tissue destruction (Moore 2005), as illustrated in Table 1 (EPUAP/NPUAP 2009). The majority of pressure ulcers occur on the sacrum or heel, but they also occur frequently over the elbow, hip, ischium, shoulder, spinous process, ankle, toe, head or face (Lahmann 2006; Shanin 2008; Vanderwee 2007).
National Pressure Ulcer Advisory Panel (NPUAP)/European Pressure Ulcer Advisory Panel (EPUAP) classification system (2009)
| Category/Stage | Definition |
| Category/Stage 1 | Intact skin with non‐blanchable redness of a localised area usually over a bony prominence.Darkly pigmented skin may not have visible blanching; its colour may differ from the surrounding area.The area may be painful, firm, soft, warmer or cooler compared to adjacent tissue.May be difficult to detect in individuals with dark skin tones. May indicate “at risk” persons. |
| Category/Stage 2 | 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 or sero‐sanguinous filled blister.Presenting as a shiny or dry shallow ulcer without slough or bruising. Stage II should not be used to describe skin tears, tape burns, incontinence associated dermatitis, maceration or excoriation. |
| Category/Stage 3 | 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 tunnelling. The depth varies according to anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue and stage III pressure ulcers (PUs) can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage III PUs. Bone or tendon is not visible or directly palpable. |
| Category/Stage 4 | Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. The depth of a stage IV pressure injury varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue and these PUs can be shallow. Stage IV PUs can extend into muscle and/or supporting structures (e.g. fascia, tendon or joint capsule) making osteomyelitis possible. Exposed bone or tendon is visible or directly palpable. |
Internationally, substantial investment has occurred over recent decades in monitoring, preventing and treating pressure ulcers. For example, it is estimated that the annual cost of treating pressure ulcers in Australia is between AUD 300‐350 million with the cost of treating a stage 4 ulcer at nearly AUD 22, 000 (AUD) (Graves 2005; Young 1997). The total annual cost for pressure ulcer management in the UK has been estimated to be approximately GBP 1.4 to 2.1 billion annually. This equates to 4% of the total UK healthcare expenditure (Bennett 2004). The main costs incurred for the treatment and management of pressure ulcers are due to prolonged hospitalisation and the extent of nursing care required. The average length of acute hospital stay for a patient with a pressure ulcer is 12 days. In comparison, the average length of stay for patients without a pressure ulcer is 4.6 days (VanGilder 2009). Furthermore, discomfort and pain, increased time spent in hospital, increased risk of mortality, altered body image and reduced quality of life, together with the potential cost associated with litigation, compounds the cost to health services and the burden upon the patient with the pressure ulcer (VQC 2004).
In spite of the level of investment in prevention and monitoring of pressure ulcers, many people continue to develop them. This is the case particularly in acute care settings where people may present with an increased number of high risk factors such as decreased mobility, impaired perfusion, poor nutrition, and fluctuating patient status. Pressure ulcer treatment strategies can be costly and complex.
Treatment of pressure ulcers is primarily two‐fold involving the relief of pressure allied with wound management. Other general strategies include patient education, pain management, optimising circulation/perfusion, optimising nutrition and the treatment of clinical infection (AWMA 2012). Wound management may involve surgical or chemical debridement (removal of dead tissue) and dressings to protect the wound and promote healing. Dressings can be divided into four main categories, namely, basic wound dressings, advanced wound dressings, anti‐microbial dressings and specialist dressings. Classification of a dressing depends on its purpose and the key material used. Key attributes of a dressing have been described (BNF 2010), and include:
the ability of the dressing to absorb and contain exudate without leakage or strike‐through (saturation);
lack of particulate contaminants left in the wound;
thermal insulation;
level of permeability to water and bacteria;
avoidance of wound trauma on dressing removal;
frequency with which the dressing needs to be changed;
provision of pain relief;
comfort.
The focus of this review is hydrocolloid dressings, the properties of which are described below. However, as hydrocolloid dressings are likely to be evaluated against one of the many wound dressings available, a description of potential comparators has been categorised, according to the British National Formulary (BNF 2010). These are listed alphabetically below, by their generic names and, where possible with their corresponding trade names and manufacturers. Dressing names, manufactures and distributors may vary between countries.
Absorbent dressings are applied directly to the wound and may be used as secondary absorbent layers in the management of heavily exuding wounds. Examples include Primapore (Smith & Nephew), Mepore (Mölnlycke) and absorbent cotton gauze (BP 1988).
Alginate dressings are highly absorbent fabrics/yarns that come in the form of calcium alginate or calcium sodium alginate and can be combined with collagen. The alginate forms a gel when in contact with the wound surface; this can be lifted off at dressing removal, or rinsed away with sterile saline. Bonding to a secondary viscose pad increases absorbency. Examples include: Curasorb (Covidien), SeaSorb (Coloplast) and Sorbsan (Unomedical).
Capillary‐action dressings consist of an absorbent core of hydrophilic fibres held between two low‐adherent contact layers. Examples include: Advadraw (Advancis) and Vacutex (Protex).
Films ‐ permeable film and membrane dressings ‐ are permeable to water vapour and oxygen, but not to water or micro‐organisms. Examples include Tegaderm (3M) and Opsite (Smith & Nephew).
Soft polymer dressings are composed of a soft silicone polymer held in a non‐adherent layer; they are moderately absorbent. Examples include: Mepitel (Mölnlycke) and Urgotul (Urgo).
Foam dressings contain hydrophilic polyurethane foam and are designed to absorb wound exudate and maintain a moist wound surface. There is a variety of versions and some include additional absorbent materials, such as viscose and acrylate fibres, or particles of superabsorbent polyacrylate, which are silicone‐coated for non‐traumatic removal. Examples include: Allevyn (Smith & Nephew), Biatain (Coloplast) and Tegaderm (3M).
Honey‐impregnated dressings contain medical‐grade honey that is purported to have antimicrobial and anti‐inflammatory properties and can be used for acute or chronic wounds. It is important to note that, when such dressings are used on patients with diabetes, the patients should be monitored for changes in blood‐glucose concentrations. Examples include: Medihoney (Medihoney) and Activon Tulle (Advancis).
Hydrocolloid dressings are usually composed of an absorbent hydrocolloid matrix on a vapour‐permeable film or foam backing. Examples include: Granuflex (ConvaTec) and NU DERM (Systagenix). Fibrous alternatives have been developed that resemble alginates and are not occlusive: Aquacel (ConvaTec).
Hydrogel dressings consist of a starch polymer and up to 96% water. These dressings can absorb wound exudate or rehydrate a wound depending on the wound moisture levels. They are supplied in either flat sheets, an amorphous hydrogel or as beads. Examples include: ActiformCool (Activa) and Aquaflo (Covidien).
Iodine‐impregnated dressings release free iodine, which is thought to act as a wound antiseptic, when exposed to wound exudate. Examples include Iodoflex (Smith & Nephew) and Iodozyme (Insense).
Low‐adherence dressings and wound contact materials usually consist of cotton pads that are placed directly in contact with the wound. They can be non‐medicated (e.g. paraffin gauze dressing) or medicated (e.g. containing povidone iodine or chlorhexidine). Examples include paraffin gauze dressing, BP 1993 and Xeroform (Covidien) dressing ‐ a non‐adherent petrolatum blend with 3% bismuth tribromophenate on fine mesh gauze.
Odour‐absorbent dressings contain charcoal and are used to absorb wound odour. Often this type of wound dressing is used in conjunction with a secondary dressing to improve absorbency. An example is CarboFLEX (ConvaTec).
Other antimicrobial dressings are composed of a gauze or low‐adherent dressing impregnated with an ointment thought to have antimicrobial properties. Examples include: chlorhexidine gauze dressing (Smith & Nephew) and Cutimed Sorbact (BSN Medical).
Protease‐modulating matrix dressings alter the activity of proteolytic enzymes in chronic wounds. Examples include: Promogran (Systagenix) and Sorbion (H & R).
Silver‐impregnated dressings are used to treat infected wounds, as silver ions are thought to have antimicrobial properties. Silver versions of most dressing types are available (e.g. silver foam, silver hydrocolloid etc). Examples include: Acticoat (Smith & Nephew) and Urgosorb Silver (Urgo).
The diversity of dressings available to clinicians (including variation within each type listed above) makes evidence‐based decision‐making difficult when determining the treatment regime for the patient. Some dressings are formulated with an 'active' ingredient such as silver that is promoted as a dressing treatment option to reduce infection and possibly to promote healing. With increasingly sophisticated technology being applied to wound care, practitioners need to know how effective these, often expensive, dressings are compared with more traditional, and usually less costly, dressings. However, far from providing critical evaluation of dressing types for clinical use, studies have shown wide variation in practice and wound (pressure ulcer) care knowledge (Maylor 1997; Pieper 1995).
The principle of moist wound healing governs wound care practice today. This is optimised through the application of occlusive or semi‐occlusive dressings and preparation of the wound bed (AWMA 2012). Animal experiments performed 50 years ago suggested that acute wounds healed more quickly when their surface was kept moist, rather than being left to dry and to scab (Winter 1962; Winter 1963a; Winter 1963b). Winter 1962 examined the rate of epithelialisation in experimental wounds cut into the skin of healthy pigs, comparing wounds with a natural scab exposed to the air against wounds that were covered with polythene film. He found that epithelialisation occurred more quickly in the latter.
Wounds exposed to the air lose water vapour, the upper dermis dries and healing takes place beneath a dry scab. Covering a wound with an occlusive dressing prevents scab formation and radically alters the pattern of epidermal wound healing. Winter’s (1962) research focused only on acute, superficial wounds, but the results have been used to generate a theory of moist wound healing for all types of wound of varying aetiologies. However, the theory of moist wound healing may not provide a basis for satisfactory management of every type of wound encountered. Whilst a moist environment at the wound site has been shown to aid the rate of epithelialisation in superficial wounds, excess moisture at the wound site can cause maceration of the peri wound (surrounding) skin (Cutting 2002). Some early studies also suggested that keeping wounds moist might predispose them to infection (Hutchinson 1991). It is not entirely clear which type(s) of wound should be kept moist, how much moisture is required, when it should be applied, and in what combination with other factors it actually confers benefit. However, Bishop and colleagues have proposed a general principle of moisture balance (Bishop 2003), that is, that dressings must absorb exudate away from the wound surface, while ensuring that the wound surface remains moist. Despite a plethora of research into wound care, the optimal level of exudate to promote wound healing has yet to be established.
The principle of moist wound healing has led to the development of several commercially available wound dressings to support optimal healing processes. These have revolutionised wound management (Benbow 2005); products include hydrogels that retain moisture in contact with the wound, hydrocolloids that absorb small amounts of excess moisture without drying the wound bed, absorbent foams, alginates, adhesive dressings, non‐adhesive dressings and silicone‐based low‐adherent dressings. Hydrocolloid dressings (the subject of this review) are composed of a layer of sodium carboxymethylcellulose (or similar material that forms a gel when wet) bonded onto a vapour‐permeable film or foam pad. These occlusive dressings absorb exudate whilst maintaining a moist wound environment. Fibrous hydrocolloids are a sub‐set of dressings that are designed for use in wounds with heavy exudate in lieu of alternate dressing types such as alginates (BNF 2010; Pan Pacific Clinical Guidelines 2011).
Pressure ulcer prevention and management is a significant burden to all healthcare systems. It is an internationally recognised patient safety problem and serves as a clinical indicator of the standard of care provided. Pressure ulcers are the second most reported incident that leads to patient harm in the health system, and are a significant source of suffering for patients and their care givers (PSC 2009; Reddy 2008). Over recent decades significant investment has been placed in strategies aimed at pressure ulcer prevention. Treatment strategies for pressure ulcers can also be costly and complex, and there is a large range of wound care products available. Despite a growing amount of literature concerned with wound care interventions, relatively few research studies have used clinical trial methodology to evaluate clinical effectiveness. The complexity of suggested interventions, and range of options available suggests that the evidence requires evaluation and presentation to the clinician to assist with effective decision making. This review is part of a suite of reviews investigating the use of individual dressing types in the treatment of pressure ulcers. Each review will focus on a particular dressing type. These reviews will then be summarised in an overview of reviews which will draw together all existing Cochrane review evidence regarding the use of dressing treatments for pressure ulcers.
There is a plethora of wound care products available, however, the evidence base to support use of some of these products remains incomplete. Thus, there is a clear need to provide clinicians with a reliable evidence base with which to make sound decisions for the treatment of pressure ulcers, if we are to reduce their prevalence and burden.