Info
A. Definition
- Localized area of soft-tissue injury
- Resulting from compression between a bony prominence and an external surface
- Normal Stages of Wound Healing [3]
- Inflammation
- Tissue Formation
- Tissue Remodelling
- Pressure ulcers appear to arrested in inflammatory / proliferative phases
B. Staging [1]
- Useful for selecting therapy and reporting prevalence
- Before Stage 1, tissue subject to pressure will exhibit blanching erythema
- This is due to capillary congestion
- This will resolve within 2 to 24 hours after pressure is relieved
- Stage 1
- Nonblanchable erythema with intact skin
- Caused by extravasation of blood with tissue damage
- Stage 2
- Partial-thickness skin loss
- Epidermis is interrupted by an abrasion, blister, or shallow crater
- Stage 3
- Full-thickness skin loss with damage and/or necrosis
- May extend to the fascia but not beyond
- Stage 4
- Full thickness skin loss with damage and/or necrosis
- Extends to muscle, bone, or supporting structures (tendons, joint capsule)
C. Epidemiology
- 17-37% of patients have ulcers when transferred from an acute hospital to a nursing home
- Prevalence among nursing home residents is 7 to 23%
- Prevalence has doubled over the past 10 years
- Number of discharges for older persons is decreasing
- Prevalence at each stage among nursing home residents with ulcers
- Stage 1: 24%
- Stage 2: 41%
- Stage 3: 22%
- Stage 4: 13%
- Common Ulcer Sites/Percent of ulcers at site among patients with ulcers
- sacrum or coccyx/36%
- hips (over trochanter)/17%
- buttocks (over ischium)/15%
- heels/12%
- ankles (over malleolus)/7%
- other/13%
D. Causes
- Pressure
- In canine trials, levels as low as 60 mm Hg applied for 1 hour were capable of producing reversible tissue changes
- Supine humans generate heel to bed pressure of 50 to 94 mm Hg.
- Friction - rubbing of one body against another, resulting in tissue abrasions or tears
- Shear
- stress from applied pressure causing one body to slide on another
- May occur when a patient is brought to a seated position
- Skin stays stationary but body moves
- May result in bent or torn blood vessels and subsequent tissue ischemia
E. Risk Factors
- Immobility
- Limited ability to sense the need to reposition self
- Sensation may be impaired because of disease or chemical restraints
- Limited ability to reposition self because of disease or mechanical restraints
- Combination of a and c above
- Malnutrition
- Manifested by poor dietary intake, especially low protein intake.
- Manifested by inability to feed oneself
- If a or b are present, then biochemical markers of malnutrition may be unreliable
- These markers include serum albumin, vitamin C levels, transferrin level
- Fecal Incontinence
- Older patients are at higher risk than younger patients
- Nonwhite patients are at risk because pre-Stage 1 and Stage 1 ulcers may be less visible
- When multiple risk factors exist, patients are at greater risk for developing pressure ulcers
F. Prevention [5]
- Prevention is strongly preferred over need for treatment
- Prevention is based on modification of risk factors
- Reduce pressure - most important risk factor
- Patient or caregiver should reposition patient every 15 minutes
- Static pressure reducers (support surfaces) include 4-6 inch solid foam mattresses: thicker is better,solid is better than convoluted
- Water bed may be best but is impractical in many settings
- Dynamic pressure reducers include low air loss beds, oscillating and kinetic beds
- Foam mattresses are least expensive and may be more effective for may patients
- Oscillating and kinetic beds are useful for patients with spinal cord injuries
- Cushions are available for chairbound patients - selection should be customized
- Reduce shear and friction
- Maintain bed at lowest elevation possible given patient's medical condition
- Install trapeze or use a bed sheet for repositioning and moving patient
- Skin moisturizers may reduce friction
- Maintain adequate nutrition - add supplements if patient borderline
- Fecal Incontinence
- Manage fecal incontinence aggressively
- This avoids seeding ulcers with fecal bacteria
G. Treatment
- Stage 1
- Aggressive management is critical to prevent progression
- Minimize pressure, shear and friction as above
- Correct malnutrition, increase protein consumption, supplement vitamin C
- Manage fecal incontinence
- Polyurethane dressing may be applied to further reduce friction and protect ulcer from bacterial contamination but permit gas exchange and water vapor escape
- Stage 2
- As for Stage 1, but polyurethane dressing applied
- Avoid saline wet-to-dry dressings because of cost and may remove healing tissue
- Assess patient discomfort and provide pain management if necessary
- Stage 3
- Reduce pressure, shear and friction, and add the following
- Debride necrotic tissue or eschar
- Small areas may be debrided by primary care physician; larger areas should be debrided by a surgeon
- Debridement may produce bacteremia - consider prophylactic antibiotics for patients with implanted prosthetic devices and for immunocompromised patients
- Wet-to-dry saline dressings may be used to debride loose material but are not recommended for use after debridement is complete - may remove healing tissue
- Use polyurethane or hydrocolloid dressings for shallow wounds
- For deeper wounds, pack with absorbent material - hydrophilic foam, alginates, saline- impregnated gauze. Change material daily, ensuring it is moist when changed to avoid removing healing tissue
- Consider using a low-air-loss bed , especially if patient is expected to recover
- Low-air-loss beds are probably not beneficial or cost-effective for terminal patients and patients with poor prognoses
- Pressure ulcers may be very painful - provide adequate pain management
- Stage 4
- As above for Stage 3, and consider the following
- Debridement should be performed by a surgeon
- Consider grafting procedures in context of patient's preferences and expected outcome
- Nerve Growth Factor (NGF) [4]
- Topical NGF for severe, noninfected pressure ulcers of the foot
- NGF group had reduced ulcer area 738mm2 versus 485mm2 at 6 weeks
References
- Lyder CH. 2003. JAMA. 289(2):223

- De Araujo T, Valencia I, Federman DG, Kirsner RS. 2003. Ann Intern Med. 138(4):326

- Bello YM and Phillips TJ. 2000. JAMA. 283(6):716

- Landi F, Aloe L, Russo A, et al. 2003. Ann Intern Med. 139(8):635

- Reddy M, Gill SS, Rochon PA, et al. 2006. JAMA. 296(8):974
