Pressure Ulcers and Wound Management

A key driving force in the market for wound management is the reduction of costs associated with managing chronic wounds.  Central to this is clinical challenge of dealing with pressure ulcers.  Below is an excerpt on pressure ulcers from the MedMarket Diligence report #S247, "Worldwide Wound Management, 2008-2017: Established and Emerging Products, Technologies and Markets in the U.S., Europe, Japan and Rest of World."

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.

Staging of Pressure Ulcers

  • 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 removed (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.

The success of the four-stage system of pressure ulcer classification has led to attempts to utilize it for other wound types, with varying degrees of success. The four-stage system was developed for the initial assessment of the wound by determining the depth of injury and tissues involved. As full thickness wounds heal by granulation and scar formation it is inappropriate to use the system to describe the process of healing. Stage IV wounds do not become Stage III wounds during the course of healing. Tissues destroyed during the wounding process are not regenerated in full thickness wounds.

Pressure ulcers occur most frequently over bony prominences where the padding effect provided by adipose tissue and muscle is least present. Pressure ulcers may also occur under casts, orthopedic devices and under compression bandages and stockings. The majority of pressure sores occur in the following regions:- lower spine (40%), feet (21%), trochanters 20%), scapula (5%), with upper spine, elbows, ribs, head, knees, and lower limbs making up most of the remainder.

(See further coverage of pressure ulcers and the associated products in wound management on the market and under development in MedMarket Diligence report #S247.)

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