Manufacturers of medical products have a primary focus on developing products that target underserved treatment areas, reduce the cost of care, or both. In one of the largest and most long-term treatment markets — wound management — a major focus of development is therefore the technologies to accelerate and improve the outcomes in the treatment of chronic wounds, which otherwise linger in healthcare systems, generating long-term direct and indirect costs. Among the most common types of chronic wounds are pressure ulcers.
Pressure ulcers, or bedsores, are areas of local necrosis resulting from vascular insufficiency due to the prolonged application of pressure to the tissues. There is an important relationship between the magnitude of pressure applied to the capillary bed and the duration that pressure is applied. Pressure ulcers are more likely to occur under relatively low pressures over long periods of time rather than under short episodes of high pressure. A healthy adult can develop a pressure ulcer if pressure sufficient to close capillaries (25-32 mm Hg) is applied for sufficient time, such as when undergoing a lengthy surgical procedure. In the compromised or elderly patient, significantly lower pressures may lead to pressure ulcer formation.
Pressure ulcer formation is enhanced through the additional application of shearing forces, friction, and moisture.
Shearing occurs when the skin is anchored to a surface, such as a bed or chair, and restrained from sliding over the surface while the underlying tissues are forced to move. The shearing force contributes to the destruction of deep tissue through the angulation and obstruction of blood vessels and excessive stretching of tissue. Shear occurs when a patient left sitting in a bed is pulled down into a slouch by gravity. The skin will adhere to the bed linen, while the coccyx will gradually drag the underlying tissue downward. Shearing forces may result in a disruption of the dermal-epidermal junction and produce blisters. Proper and frequent repositioning of a patient can reduce both pressure and shearing forces.
Friction occurs when the adhesion to the surface is not quite sufficient to prevent sliding, but sufficient to impart resistance to motion, that results in heat and wearing away of the outer layers of the skin. A patient who has slid down toward the bottom of the bed and is dragged back to the top will experience friction on the heels and other bony prominences. For this reason patients should be lifted back into position, and sliding over the bed surface should be avoided. Dressings that protect against friction and mattress covers with a low friction coefficient are helpful.
Moisture that is in prolonged contact with the skin produces maceration and reduction in the skin’s ability to tolerate additional stress. Macerated skin has a higher friction coefficient, increasing the likelihood of damage from friction and shear. Several sources of moisture are common in hospital and nursing home situations, including perspiration and urinary and fecal incontinence. Moisture may lead to fungal infections, and fecal incontinence can generate infections by E. coli. Thus, moisture may contribute to wound formation and present complications to wound healing.
Several pressure sore classification systems have been used since 1975, including the Shea Pressure Sore Classification (1975), and the International Association of Enterostomal Therapy (IAET) pressure ulcer classification (1987).
- Stage I ulcers are indicated by damaged friable surface skin with considerable hidden cell death caused by continuous pressure damage usually from immobilization in a single position. Identification of signs of pain and early indications of visible damage is a significant event in that it alerts caregivers of the need for interventions to prevent more serious damage.
- Stage II ulcers present as partial thickness wounds, which may heal with early intervention by regeneration under advanced wound care techniques.
- Stage III ulcers are usually full-thickness pressure sores. These are often difficult to classify due to the presence of eschar that obscures visualization of the wound bed. The presence of eschar does indicate a full thickness wound but the eschar must be debrided before classification can be established.
Early Stage III or Stage IV pressure ulcers may superficially resemble Stage I ulcers. A wound initially classified as Stage I may, therefore subsequently appear to progress to higher stages as the already damaged deeper tissues slough off or as auto-debridement occurs with moist wound healing therapy.
- Stage IV pressure ulcers are characterized by full thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (e.g., tendon, joint capsule). Undermining of healthy surrounding skin and sinus tracts may also be associated with Stage IV pressure ulcers.
Products and markets in the treatment of chronic wounds are covered in the comprehensive global report on wound management from MedMarket Diligence. See link.