Pressure ulcers are localized areas of tissue necrosis that typically develop when soft tissue is compressed between a bony prominence and an external surface for a long period of time. Stage 2 pressure ulcers are characterized by partial-thickness skin loss into but no deeper than the dermis. This includes intact or ruptured blisters and abrasions.
Symptoms of Stage 2 Pressure Ulcers
Stage 2 pressure ulcers are shallow with a reddish base. Intact or partially ruptured blisters that are a result of pressure can also be considered stage 2 pressure ulcers. Note that causes of erosion, ulceration, or blistering that aren't a result of pressure (skin tears, maceration, excoriation, etc.) are not included in the definition of a stage 2 pressure ulcer.
Figure 1: Superficial pressure ulcer, stage 2 developmentFigure 2: Stage 2 pressure ulcer (partial-thickness skin loss)
Pressure ulcers are accepted to be caused by three different tissue forces:
Prolonged pressure: In most cases, this pressure is caused by the force of bone against a surface, as when a patient remains in a seated or supine position for an extended period. When this pressure exceeds the tissue capillary pressure, it deprives the surrounding tissues of oxygen and can lead to tissue necrosis if left untreated.
Shear: This force is typically a result of the skin of a patient staying in one place as the deep fascia and skeletal muscle slide down, which can pinch off blood vessels and in turn lead to ischemia and tissue necrosis.
Friction: Friction is the opposing force to the shear force. This can cause microscopic and macroscopic tissue trauma, specifically when the patient is being moved across the support surface.
In addition, moisture from incontinence, perspiration or exudate can increase the coefficient of friction between the skin and the surface, making it more susceptible to friction damage. Increased moisture also can weaken the bonds between epithelial cells, resulting in skin maceration, which also makes the skin more susceptible to pressure, shear, and friction damage.
- Immobility or limited mobility
- Spinal cord injury
- Diseases that affect blood flow such as diabetes or atheroscelerosis
- Fragile skin
- Urinary or fecal incontinence
- Poor nutrition or dehydration
- Decreased mental awareness
- Neurological disease
Infection is the most common major complication of pressure ulcers. If the ulcer progresses far enough, it can lead to osteomyelitis (infection of the underlying bone) or sinus tracts, which themselves can be either superficial or connect to deeper structures.
Treatment of Stage 2 Pressure Ulcers
The goal of care for stage 2 pressure ulcers is to cover, protect, and clean the area. As always, decreasing pressure on the area is key to wound healing. With quick attention, a stage 2 pressure ulcer can heal very rapidly. Generally pressure ulcers that develop beyond stage 2 are considered to be a result of lack of aggressive intervention.
The following precautions can help minimize the risk of developing pressure ulcers in at-risk patients and to minimize complications in patients already exhibiting symptoms:
- Turn patients every two hours.
- Keep the skin clean and dry.
- Avoid massaging bony prominences.
- Provide adequate intake of protein and calories.
- Maintain current levels of activity, mobility and range of motion.
- Use positioning devices to prevent prolonged pressure bony prominences.
- Keep the head of the bed as low as possible to reduce risk of shearing.
- Keep sheets dry and wrinkle free.
Merck Sharp & Dohme Corp. Pressure Ulcers. The Merck Manual. http://www.merckmanuals.com/professional/dermatologic_disorders/pressure.... Updated July 2017. Accessed September 27, 2018.
National Pressure Ulcer Advisory Panel. Pressure Injury Prevention Points. National Pressure Ulcer Advisory Panel. http://www.npuap.org/wp-content/uploads/2016/04/Pressure-Injury-Preventi.... Accessed September 27, 2018.
Salcido R. Pressure Injuries (Pressure Ulcers) and Wound Care. Medscape Reference. http://emedicine.medscape.com/article/319284-overview#aw2aab6b2. Updated January 11, 2018. Accessed September 27, 2018.
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