Bedsore

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Bedsores are lesions caused by unrelieved pressure to any part of the body, especially portions over bony or cartilaginous areas. Although completely treatable if found early, without medical attention, bedsores can become life-threatening.

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Pressure ulcers may be caused by inadequate blood supply and resulting reperfusion injury when blood re-enters tissue. A simple example of a mild pressure sore may be experienced by healthy individuals while sitting in the same position for extended periods of time: the dull ache experienced is indicative of impeded blood flow to affected areas. Within hours, this shortage of blood supply, called ischemia, may lead to tissue damage and cell death. The sore will initially start as a red, painful area, which eventually turns purple. Left untreated, the skin may break open and become infected. Moist skin is more sensitive to tissue ischemia and necrosis and is also more likely to get infected.

Bedsores are accepted to be caused by three different tissue forces:

Pressure, or the compression of tissues. In most cases, this compression is caused by the force of bone against a surface. After an extended amount of time with decreased tissue perfusion, ischemia occurs and can lead to tissue necrosis if left untreated in an immunocompromised patient.

Shear force, or a force created when the skin of a patient stays in one place as the deep fascia and skeletal muscle slide down with gravity. This can also cause the pinching off of blood vessels which may lead to ischemia and tissue necrosis.

Friction, or a force resisting the shearing of skin. This may cause excess shedding through layers of epidermis.

Aggravating the situation may be other conditions such as excess moisture from incontinence, perspiration or exudate. Over time, this excess moisture may cause the bonds between epithelial cells to weaken thus resulting in the maceration of the epidermis. Other factors in the development of bedsores include age, nutrition, vascular disease, diabetes mellitus, and smoking, amongst others.

There are currently two major theories about the development of pressure ulcers. The first and most accepted is the deep tissue injury theory which claims that the ulcers begin at the deepest level, around the bone, and move outward until they reach the epidermis. The second, less popular theory is the top-to-bottom model which says that skin first begins to deteriorate at the surface and then proceeds inward.^[1]

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Within acute care, the incidence of bedsores is 0.4% to 38%; within long-term care, 2.2% to 23.9%; and in home care, 0% to 17%.

Prevalence percentages are: 10% to 18% in acute care, 2.3% to 28% in long-term care, and 0% to 29% in home care. There is a much higher rate of bedsores in intensive care units because of immunocompromised individuals, with 8% to 40% of ICU patients developing bedsores.^[1]

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People at the highest risk for developing a Bedsore include:

• Individuals who are bedridden
• Individuals bound to a wheelchair
• Malnourishment
• Risk increases with age
• Individuals with a injury or disease that may limit mobility (i.e. spinal cord injury)
• Individuals with a condition that may inhibit blood flow to certain areas of the body (i.e. diabetes)
• Individuals with urinary or bowel incontinence
• Individuals with a mental condition that may affect mobility (i.e. Alzheimer’s)

The Braden scale assesses a patient’s risk of developing a pressure ulcer by examining six criteria: ^[1]

1. Sensory Perception – This parameter measures a patient’s ability to detect and respond to discomfort or pain that is related to pressure on parts of their body. The ability to sense pain itself plays into this category, as does a the level of consciousness of a patient and therefore their ability to cognitively react to pressure-related discomfort.
2. Moisture – Excessive and continuous skin moisture can pose a risk to compromise the integrity of the skin by causing the skin tissue to become macerated and therefore be at risk for epidermal erosion. So this category assesses the degree of moisture the skin is exposed to.
3. Activity – This category looks at a clients level of physical activity since very little or no activity can encourage atrophy of muscles and breakdown of tissue. ^[2]
4. Mobility – This category looks at the capability of a client to adjust their body position independently. This assesses the physical competency to move and can involve the clients willingness to move.
5. Nutrition – The assessment of a clients nutritional status looks at their normal patterns of daily nutrition. Eating only portions of meals or having imbalanced nutrition can indicate a high risk in this category.
6. Friction and Shear – Friction and shear looks at the amount of assistance a client needs to move and the degree of sliding on beds of chairs that they experience. This category is assessed because the sliding motion can cause shear which means the skin and bone are moving in opposite directions causing breakdown of cell walls and capillaries.

Each category is rated on a scale of 1 to 4, except for the ‘friction and shear’ category which is rated on a 1-3 scale. This combines for a possible total of 23 points. A score of 23 means there is no risk for developing a pressure ulcer while the lowest possible score of 6 points represents the severest risk for developing a pressure ulcer.^[3] An adult with a score below 18 is considered to have a high risk for developing a pressure ulcer.^[4]

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The definitions of the four pressure ulcer stages are revised periodically by the National Pressure Ulcer Advisory Panel (NPUAP) in the United States. Briefly, however, they are as follows:

• Stage I is the most superficial, indicated by redness that does not subside after pressure is relieved. This stage is visually similar to reactive hyperemia (a technical term for excessive redness) seen in skin after prolonged application of pressure. Stage I pressure ulcers can be distinguished from reactive hyperemia in two ways: a) reactive hyperemia resolves itself within 3/4 of the time pressure was applied, and b) reactive hyperemia blanches when pressure is applied, whereas a Stage I pressure ulcer does not. The skin may be hotter or cooler than normal, have an odd texture, or perhaps be painful to the patient. Although easy to identify on a light-skinned patient, ulcers on darker-skinned individuals may show up as shades of purple or blue in comparison to lighter skin tones.
• Stage II is damage to the epidermis extending into, but no deeper than, the dermis. In this stage, the ulcer may be referred to as a blister or abrasion.
• Stage III involves the full thickness of the skin, extending into, but not through, the subcutaneous tissue layer. This layer has a relatively poor blood supply and can be difficult to heal. At this stage, there may be undermining that makes the wound much larger than it may seem on the surface.
• Stage IV is the deepest, extending into the muscle, tendon or even bone.
• Unstageable pressure ulcers are covered with dead cells, or eschar and wound exudate, so the depth cannot be determined.

With higher stages, healing time is prolonged. While about 75% of Stage II ulcers heal within eight weeks, only 62% of Stage IV pressure ulcers ever heal, and only 52% heal within one year.^[1] It is important to note that pressure ulcers do not regress in stage as they heal. A pressure ulcer that is becoming shallower with healing is described in terms of its original deepest depth (e.g., healing Stage II pressure ulcer).

Pressure sores can trigger other ailments, and cause patients considerable suffering and financial cost.^[2] Some complications include autonomic dysreflexia, bladder distension, osteomyelitis, pyarthroses, sepsis, amyloidosis, anemia, urethral fistula, gangrene and very rarely malignant transformation. Sores often recur because patients do not follow recommended treatment or develop seromas, hematomas, infections, or dehiscence. Paralytic patients are the most likely people to have pressure sores recur. In some cases, complications from pressure sores can be life-threatening. The most common causes of fatality stem from renal failure and amyloidosis.

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