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Bedsores, more properly known as pressure ulcers or decubitus, 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.
Additional recommended knowledge
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:
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:
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.
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:
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.
There are six major contributors to healing.
The removal of necrotic tissue is an absolute must in the treatment of pressure sores. Because dead tissue is an ideal area for bacteria growth, it has the ability to greatly compromise wound healing. There are at least seven ways to excise necrotic tissue.
Infection has one of the greatest effects on the healing of a wound. Purulent discharge provides a breeding ground for excess bacteria, a problem especially in the immunocompromised patient. Symptoms of systemic infection include fever, pain, erythema, oedema, and warmth of the area, not to mention purulent discharge. Additionally, infected wounds may have a gangrenous smell, be discoloured, and may eventually exude even more pus.
In order to eliminate this bioburden, it is imperative to apply antiseptics and antimicrobials at once. It is not recommended to use hydrogen peroxide for this task as it is difficult to balance the toxicity of the wound with this. New dressings have been developed that have cadexomer iodine and silver in them, and they are used to treat bad infections. Duoderm can be used on smaller wounds to both provide comfort and protect them from outside air and infections.
It is not recommended to use systemic antibiotics to treat infection of a bedsore, as it can lead to bacterial resistance.
Upon admission, the patient should have a consultation with a dietitian to determine the best diet to support healing, as a malnourished person does not have the ability to synthesize enough protein to repair tissue. The dietitian should conduct a nutritional assessment that includes a battery of questions and a physical examination. If malnourishment is suspected, lab tests should be run to check serum albumin and lymphocyte counts. Additionally, a bioelectric impedance analysis should be considered.
If the patient is found to be at risk for malnutrition, it is imperative to begin nutritional intervention with dietary supplements and nutrients including, but not limited to, arginine, glutamine, vitamin A, vitamin B complex, vitamin E, vitamin C, magnesium, manganese, selenium and zinc. It is very important that intake of these vitamins and minerals be overseen by a physician, as many of them can be detrimental in incorrect dosages.
How to properly care for a bedsore
The most important care for a patient with bedsores is the relief of pressure. Once a bedsore is found, pressure should immediately be lifted from the area and the patient turned at least every two hours to avoid aggravating the wound. Nursing homes and hospitals usually set programs to avoid the development of bedsores in bedridden patients such as using a standing frame to reduce pressure and ensuring dry sheets by using catheters or impermeable dressings. For individuals with paralysis, pressure shifting on a regular basis and using a cushion featuring pressure relief components can help prevent pressure wounds.
Pressure-distributive mattresses are used to reduce high values of pressure on prominent or bony areas of the body. However, methods to evaluate the efficacy of these products have only been developed in recent years.
Educating the caregiver
In the case that the patient will be returning to home care, it is very important to educate the family about how to treat their loved one's pressure ulcers. The cross-specialisation wound team should train the caregiver in the proper way to turn the patient, how to properly dress the wound, how to properly nourish the patient, and how to deal with crisis, among other things.
As this is a very difficult undertaking, the caregiver may feel overburdened and depressed, so it may be best to bring in a psychological consult.
Once the patient has reached the point that intervention is possible, there are many different options. For patients with Stages I and II ulcers, the wound care team should use guidelines established by the American Medical Directors Association (AMDA) for the treatment of these low-grade sores.
For those with Stage III or IV ulcers, most interventions will likely include surgery such as a tissue flap, skin graft or other closure methods. A more recent intervention is Negative Pressure Wound Therapy, which is the application of topical negative pressure to the wound. This technique, developed by scientists at Wake Forest University, uses foam placed into the wound cavity which is then covered in a film which creates an airtight seal. Once this seal is established, the technician is able to remove exudate and other infectious materials in addition to aiding the body produce granulation tissue, the best bed for the creation of new skin.
There are, unfortunately, contraindications to the use of negative pressure therapy. Most deal with the unprepared patient, one who has not gone through the previous steps toward recovery, but there are also wound characteristics that bar a patient from participating: a wound with inadequate circulation, a raw debridled wound, a wound with necrotised tissue and eschar, and a fibrotic wound.
After Negative Pressure Wound Therapy, the patient should be reevaluated every two weeks to determine future therapy.
Pressure sores can trigger other ailments, and cause patients considerable suffering and financial cost. 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.
Alexander's Care of the Patient in Surgery by Jane C Rothrock, Thirteenth Edition, 2007. Mosby
hair loss: Alopecia areata (Alopecia totalis, Alopecia universalis, Ophiasis) - Androgenic alopecia - Telogen effluvium - Traction alopecia - Lichen planopilaris - Trichorrhexis nodosa
other follicular disorders: Hypertrichosis (Hirsutism) - Acne vulgaris - Rosacea (Perioral dermatitis, Rhinophyma) - follicular cysts (Epidermoid cyst, Sebaceous cyst, Steatocystoma multiplex) - Pseudofolliculitis barbae - Hidradenitis suppurativasweat disorders: eccrine (Miliaria, Anhidrosis) - apocrine (Body odor, Chromhidrosis, Fox-Fordyce disease)
|Other||pigmentation (Vitiligo, Melasma, Freckle, Café au lait spot, Lentigo/Liver spot) - Seborrheic keratosis - Acanthosis nigricans - Callus - Pyoderma gangrenosum - Bedsore - Keloid - Granuloma annulare - Necrobiosis lipoidica - Granuloma faciale - Lupus erythematosus - Morphea - Calcinosis cutis - Sclerodactyly - Ainhum - Livedoid vasculitis|
|see also congenital (Q80-Q84, 757)|
Categories: Dermatology | Traumatology