Causes & symptoms
Bedsores most often happen when the most superficial blood vessels are pressed against the skin and squeezed shut, closing off the flow of blood. If the supply of blood to an area of skin is cut off for more than an hour, the tissue will began to die due to lack of oxygen and nutrients. Ordinarily, the layer of fat under the bony areas of the skin helps keep the blood vessels from being compressed in this way. Also, people have a normal impulse to change positions frequently when they are sitting or lying down, so the blood supply is usually not kept from any area of the skin for very long. Bedsores are most likely to occur in people who have lost the protective fat layer or whose movement impulse is hindered.
Physical examination of the skin, medical history, and patient and caregiver observations are the basis of diagnosis. Any sign of reddening of the skin will be closely monitored.
The use of an alternating pressure mattress to reduce pressure and increase bloodflow.
Contrasting hot and cold local applications can increase circulation to problem areas and help flush out waste products, speeding the healing process. Hot compresses should be applied for three minutes, followed by 30 seconds of cold compress application, repeating the cycle three times. The cycle should always end with the cold compress. In addition, zinc and vitamins A, C, E, and B-complex should be taken to help maintain healthy skin and repair injuries.
Friction or rubbing from poorly fitted shoes or clothing and wrinkled bedding often cause a sore to develop. Constant exposure to the moisture of urine, feces, and perspiration may also cause the skin to deteriorate. In such cases there is an increased the risk of skin infection as well as sores.
Risk factors for bedsores:
older than 60 years of age
diminished tactile sensation
paralysis or immobility
prolonged bed rest
spinal cord injury
Bedsores, more properly known as pressure ulcers or decubitus ulcers, are lesions caused by many factors such as: unrelieved pressure; friction; humidity; shearing forces; temperature; age; continence and medication; to any part of the body, especially portions over bony or cartilaginous areas such as sacrum, elbows, knees, ankles etc. Although completely treatable if found early, without medical attention, bedsores can become life-threatening, and indeed fatal. Christopher Reeve died following sepsis originating from a pressure related ulcer
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 non blanchable 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 and may extend into 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 damage that makes the wound much larger than it may seem on the surface.
Stage IV pressure ulcerStage 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. 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).
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, as when a patient remains in a single decubitus position for a lengthy period. 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.
Stage 4 decubitus displaying the Tuberosity of the ischium protruding through the tissue and possible onset of Osteomyelitis
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.
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%. There is the same wide variation in prevalence: 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.
The risk of developing bedsores can be determined by using the Braden Scale for Predicting Pressure Ulcer Risk. This scale is divided into six risk categories:
friction and shear
The best possible interpretation is a score of 23 whilst the worst is a 6. If the total score is below 11, the patient is at risk for developing bedsores.
The most important thing to keep in mind about the treatment of bedsores is that the most optimal outcomes find their roots in a multidisciplinary approach; by using a team of specialists, there is a better chance that all bases will be covered in treatment.