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Unformatted text preview: Review Decubitus ulcers: A review of the literature
Cheryl Bansal,BA, Ron Scott,MD, David Stewart,MD, and Clay J. Cockerell,MD International Journal of Dermatology 2005,44 1/14 Introduction and Pathogenesis Constant pressure can come from lying down (“decubitus” from the Latin decumbere, “to lie down”) or from sitting.
Decubitus ulcers, also known as bedsores and pressure sores,are caused by impaired blood supply and tissue malnutrition owing to prolonged pressure over skin, soft tissue, muscle,and/or bone.
Decubitus ulcers have probably existed since the dawn of humankind.
They have been observed in unearthed human mummies and addressed in scientific writings of the19th century.
2/14 Introduction and Pathogenesis
Decubitus ulcers can develop on any part of the body where sustained pressure and compressive forces are maintained for a sufficient period of time. sacrum and hips is most often affected (67%), occiput, helices, elbows, and lower extremities (25%), including heels and ankles. 25% of decubitus ulcers start in the operating room during surgery. 83% of hospitalized patients with decubitus ulcers developed them in the first 5 days of hospitalization. The prevalence rate in nursing homes is estimated to be 17–28%. 3/14 Introduction and Pathogenesis Impaired patients decubitus ulcers occur at an annual rate of 5–8%, with lifetime risk estimated to be 25–85%.
Decubitus ulcers are listed as the direct cause of death in 7–8% of paraplegics.
Hospitalized patients have a 3–17% incidence rate, while hospitalized surgical patients have a 12–66% incidence rate. Immobilized patients in longterm care facilities have a 33% incidence rate.
Some estimates suggest that 60,000 people die from decubitus ulcers or their sequelae per year.
Present treatment costs for decubitus ulcers in the US is estimated in excess of $1 billion per year. 4/14 Morphology
Several classification systems for decubitus ulcers have been described: Daniel’s,Shea’s,and the National Pressure Ulcer Advisory Panel (NPUAP), which is a modification of Shea’s classification. The most widely accepted classification system for decubitus ulcers is the NPUAP. Stage I of the NPUAP classification represents intact skin with signs of impending ulceration: blanching and/or nonblanching erythema, warmth, and induration. Stage II ulcers present clinically as a shallow ulcer (including epidermis and possibly dermis) with pigmentation changes. 5/14 Morphology Stage II ulcers, like Stage I, can be reversible.
Stage III ulcer represents a fullthickness loss of skin with extension through subcutaneous tissue, but not underlying fascia.
Stage IV represents fullthickness skin and subcutaneous tissue loss. resulting in involvement of muscle, bone, tendon, or joint capsule. 6/14 Histopathology
Decubitus ulcers have many histologic stages. Clinically, the decubitus ulcer spectrum includes blanching erythema, nonblanching erythema, decubitus dermatitis, early ulcer, healing ulcer, chronic ulcer, and black eschar/gangrene.The progression is dynamic and multiple stages are often observed in one decubitus ulcer. 7/14 Treatment
Today, the treatment of decubitus ulcers is based on four primary modalities: (1) pressure reduction and prevention of additional ulcers, (2) wound management, (3) surgical intervention, and (4) nutrition. An additional way to reduce pressure involves turning and repositioning the patient every 2 h to reduce pressure on vulnerable areas. Current research indicates that the 2h interval may not be adequate. The key aspects of wound management to ensure effective healing are cleaning and effective drainage and absorption while protecting the skin adjacent to the wound. 8/14 Treatment Skin adjacent to the wound may be lubricated to decrease friction and be kept relatively dry.
Surgical intervention for decubitus ulcers involves debridement or flap creation for some Stage III and Stage IV ulcers.
Malnutrition should be addressed because the malnourished patient has a higher susceptibility for ulcer formation.
Other treatment modalities that can be employed as needed. 9/14 Treatment There are several risk assessment scales: Norton,Cubbin and Jackson, Braden, Douglas,and Waterlow. Current studies show these risk assessment scales may not as effective as nurses’ judgement as to which atients are at risk. 10/14 Treatment Table 1 Decubitus ulcer Do’s and Don’ts Do’s Don’ts Move the patient or encourage the Do not use donuttype patient to move every 2 h cushions and device Keep skin clean and lubricated Keep skin dry Use pressure relief devices such as pillows, foam cushions, mattresses and gel heel protectors Pay special attention to skin areas with little fat padding, such as bony prominences Put patient on a stool and urine voiding schedule Use incontinence devices as appropriate Keep incline no higher than 30 degrees to prevent sliding and friction on lower back and buttocks 11/14 Outcomes
Ferrell et al . found that no pressure ulcer healed completely or reduced in surface area greater than 50% within 30 days and only 14% of pressure ulcers completely healed within 79 days. This indicates that longterm therapy may be necessary. YaoChin et al . found 53% of pressure ulcers healed within 42 days. 12/14 Complications Osteomyelitis hypercalcemia myonecrosis necrotizing fasciitis amyloidosis sepsis gangrene death 13/14 Future Research Growth factors and hyaluronic acid have also been implicated in the process of wound healing.
Becaplermin has been given FDA approval for treatment of lower extremity diabetic neuropathic ulcers. It may also have a place in the treatment of decubitus ulcers.
Polyphenols such as catechin and black catechu have been found to have scavenger effects on oxygen radicals.
Topical vitamin E has been found to accelerate the healing of skin wounds and ulcers. 14/14 謝謝謝謝 15/14 16/14 ...
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