Review Decubitus ulcers: A review of the literature

1. ReviewDecubitus 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

2. 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.

3. 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%.

4. 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 long-term 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.

5. 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.

6. Morphology • Stage II ulcers, like Stage I, can be reversible. • Stage III ulcer represents a full-thickness loss of skin with extension through subcutaneous tissue, but not underlying fascia. • Stage IV represents full-thickness skin and subcutaneous tissue loss. resulting in involvement of muscle, bone, tendon, or joint capsule.

7. 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.

8. 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 2-h 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.

9. 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.

10. 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.

11. Treatment • Table 1 Decubitus ulcer Do’s and Don’ts • Do’s Don’ts • Move the patient or encourage the Do not use donut-type 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

12. 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 long-term therapy may be necessary. • Yao-Chin et al . found 53% of pressure ulcers healed within 42 days.

13. Complications • Osteomyelitis • hypercalcemia • myonecrosis • necrotizing fasciitis • amyloidosis • sepsis • gangrene • death

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.

15. 謝謝聆聽