1. PRESSURE ULCERS & WOUND CARE
Suggestions for Lecturer
-1-hour lecture
-Use GRS slides alone or to supplement your own teaching materials.
-Refer to GRS for furtherGRS9 question #s 6, 42, 97, 118, 151, 163, and 247 for case vignettes on pressure ulcers.
-For strength of evidence (SOE) levels, please see the GRS Teaching Slides site or the GRS inside front cover.
-Refer to Geriatrics At Your Fingertips for detailed information on ulcer evaluation, management, and dressings.
-Supplement lecture with handouts, such as the Braden Scale and Norton Scale.
Topic

2. OBJECTIVES Know and understand:
The morbidity and mortality associated with pressure ulcers for older adults
The common risk factors for pressure ulcer development
Techniques for preventing pressure ulcers
The pressure ulcer staging system and treatment strategies for each stage

3. TOPICS COVERED Chronic Wound Healing
Pressure Ulcer Definition and Classification
Pressure Ulcer Assessment and Documentation
Pressure Ulcer Prevention
Principles of Pressure Ulcer Treatment
Infectious Aspects of Pressure Ulcers
Palliative Care for Chronic Wounds

4. Estimated cost of $3,500 to >$60,000 per patient
PRESSURE ULCERS
Associated with
Decreased quality of life
Longer hospital stays
Increased chance of 30-day readmission
Increased chance of admission to a long-term care facility
Increased risk of death
Estimated cost of $3,500 to >$60,000 per patient
Affect million adults in the U.S.
Are a designated quality measure and major risk management issue
Pressure ulcers are a designated quality measure in hospitals, long-term care, and home-care settings. As a result of their association with quality of care, pressure ulcers have become a major risk management issue. Pressure ulcer data for skilled nursing facilities is currently published by CMS on the Nursing Home Compare Web site, but as yet there is no federal mandate for publication of pressure ulcer statistics for hospitals and home care. In addition, pressure ulcers have been spotlighted in value-based purchasing and pay-for-performance initiatives. For example, in 2008 the CMS introduced a policy to decline payment to hospitals for certain hospital-acquired conditions that include stage III or IV pressure ulcers. These factors have resulted in an evolving standard of care that designates physicians as key players. Many hospitals and long-term care facilities require physician orders for wound care products, dressings, and devices to obtain Medicare reimbursement. Because pressure ulcers are an identified geriatric syndrome, geriatrics providers with proper training can play a pivotal role in improving quality of care for this condition.

5. UNAVOIDABLE PRESSURE ULCERS
One that develops despite the provider having
1) evaluated the individual’s clinical condition and pressure ulcer risk factors
2) defined and implemented interventions consistent with individual needs, goals, and recognized standards of practice, and
3) monitored and evaluated the impact of the interventions, revising the approaches as appropriate
Patients at high risk are those with immobility and multiple chronic conditions
These pressure ulcers may be a marker for disease severity or impending death

6. THE SPECTRUM OF CHRONIC WOUNDS
Pressure ulcers
Arterial ulcers, or wounds from PAD
Venous insufficiency ulcers
Diabetic or neuropathic ulcers
Nonhealing surgical wounds
Wounds from malignancy
Wounds from autoimmune source or vasculitis
Wounds from trauma and burns (including skin tears, lacerations, and self-induced)
PAD = peripheral arterial disease
From GRS9 Table 32.1.
Pressure ulcers are one of a diverse group of lesions classified as chronic wounds (see GRS9 Table 32.1). Chronic wounds share in common prolonged healing time and interference with normal wound healing that renders them stalled in the inflammatory and proliferative phases. The surface of a chronic wound often harbors an “antihealing environment” with elements that include biofilm, exudate that contains pro-inflammatory cytokines such as matrix metalloproteases and tumor necrosis factor alpha (TNF-α), and lack of pro-regenerative agents such as transforming growth factor (TGF-β), platelet-derived growth factor, and vascular endothelial growth factor.
Conditions leading to chronic wounds include repetitive trauma, decreased vascular perfusion, poor nutrition, poor oxygenation from anemia, diabetes or pulmonary disease, edema that interferes with nutrient delivery, pharmacologic barriers such as corticosteroids and immunosuppressants, incontinence, and biofilms.

7. Normal wound healing includes a complex but orderly sequence of:
CHRONIC WOUND HEALING
Normal wound healing includes a complex but orderly sequence of:
Hemostasis
Inflammation
Proliferation
Remodeling
Neutrophils are involved in the inflammatory phase, phagocytizing debris and microorganisms and providing a first line of defense. Macrophages play an important role in phagocytosis, debriding damaged tissue with proteases, creating granulation tissue, laying down extracellular matrix, and secreting chemotactic and growth factors. Granulation tissue consists of new blood vessels, fibroblasts, endothelial cells, myofibroblasts, and extracellular matrix. Fibroblasts produce collagen that increases the strength of the wound, plus other critical substances such as elastin, fibronectin, glycosaminoglycans, and proteases. Myofibroblasts, descended from fibroblasts, assist in contraction. Keratinocytes are the main cells responsible for epithelialization, the process of migrating across a bed of granulation tissue. Because of the disruption in normal anatomy and disorganization of new collagen, the tensile strength of a healed wound is only 50%–80% of that of undamaged skin.

8. PRESSURE ULCER DEFINITION
A localized injury to the skin and/or underlying tissue, usually over a boney prominence that results from pressure, or pressure in combination with shear.

9. STAGING OF PRESSURE ULCERS (1 of 7)
Stage
Definition
Stage 1
Nonblanchable erythema
Intact skin with nonblanchable redness of a localized area, usually over a bony prominence.
Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area.
The area may be painful, firm, soft, or warmer or cooler than adjacent tissue.
May be difficult to detect in those with dark skin tones.
May indicate “at risk” patients.
Stage 2
Partial thickness
Partial-thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough.
May also present as an intact or open/ruptured blister filled with serum or serosanguinous fluid.
Presents as a shiny or dry shallow ulcer without slough or bruising .
The stage 2 category should not be used to describe skin tears, tape burns, incontinence-associated dermatitis, maceration, or excoriation.
Staging according to the National Pressure Ulcer Advisory Panel

10. STAGING OF PRESSURE ULCERS (2 of 7)
Buttocks, Stage 1
Buttocks, Stage 2

11. STAGING OF PRESSURE ULCERS (3 of 7)
Stage
Definition
Stage 3
Full-thickness tissue loss
Subcutaneous fat can be visible but bone, tendon, or muscle are not exposed
Slough may be present but does not obscure the depth of tissue loss
May include undermining and tunneling
Depth varies by anatomical location
Stage 4
Full-thickness tissue loss with exposed bone, tendon, or muscle
Slough or eschar may be present
Often includes undermining and tunneling
Depth varies by anatomic location
The bridge of the nose, ear, occiput, and malleolus do not have (adipose) subcutaneous tissue, and Stage 3 or 4 ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep Stage 3 pressure ulcers. Stage 4 ulcers can extend into muscle and/or supporting structures (eg, fascia, tendon or joint capsule) making osteomyelitis or osteitis likely to develop.

12. STAGING OF PRESSURE ULCERS (4 of 7)
Hip, Stage 3
Sacrum, Stage 4

13. STAGING OF PRESSURE ULCERS (5 of 7)
Stage
Definition
Unstageable
Full-thickness skin or tissue loss, depth unknown
Full-thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed
Until enough slough and/or eschar is removed to expose the base of the wound, the true depth (and therefore stage) cannot be determined
Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as “the body's natural (biological) cover” and should not be removed

14. STAGING OF PRESSURE ULCERS (6 of 7)
Stage
Definition
Suspected deep tissue injury, depth unknown
Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear
May be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler than adjacent tissue
May be difficult to detect in individuals with dark skin tones
Evolution may include a thin blister over a dark wound bed
The wound may further evolve and become covered by thin eschar
Evolution may be rapid and expose additional layers of tissue, even with optimal treatment

15. STAGING OF PRESSURE ULCERS (7 of 7)
The heel, the second most common site for pressure ulcers after the sacrum, has unique anatomic features that warrant special consideration when evaluating an ulcer. These include thick skin, very little subcutaneous tissue and muscle, and vascular perfusion delivered around the large calcaneus bone that underlies the rear portion of the foot. The foot is also susceptible to circulatory impairment because of atheromatous disease of the leg, microvascular disease from diabetes mellitus, and decreased sensation from peripheral neuropathy of any etiology. Pressure ulcers of the heels often present as blisters. A clear blister over a bony prominence is considered a stage II pressure ulcer, whereas a blood-filled blister is considered DTI.
Heel, unstageable, with unstable eschar
Heel, deep tissue injury

16. Presence of odor and/or drainage Presence of undermining and tunneling
WOUND DOCUMENTATION
Diagnosis
Stage
Location
Length
Width
Depth
Presence of odor and/or drainage
Presence of undermining and tunneling
Wound bed characteristics
Margins
Surrounding skin
Supplemental information can include warmth, capillary refill, and presence of pulses, edema, anasarca, and lymphedema.
Documentation of wound progression is an important component of management and should be ongoing, systematic, and consistent. Wounds should be formally assessed at least weekly, with descriptors that include measurements, nature of the wound bed and periwound area, pressure redistribution modalities, treatments in progress, and response to healing. Some authorities recommend a validated healing scale such as the Pressure Sore Status Tool or the Pressure Ulcer Scale for Healing. No single standard exists that mandates the type and extent of information to include in a wound assessment, but the more descriptors the better. Patients with pressure ulcers frequently undergo transitions between locations within the health care continuum, and wounds should be thoroughly documented on both admission and discharge from hospitals and long-term care facilities. Similarly, initial home care visits should include thorough skin inspection. Reverse staging is not a recognized standard, because it does not accurately characterize the anatomic and physiologic process that occurs during healing.

17. Clinical judgment should also be relied on
RISK ASSESSMENT
Braden Scale
Most widely-used pressure ulcer risk assessment tool
Combines sensory perception, moisture, activity, mobility, friction, and shear
Validated in home, SNF, and hospital settings (but not ICUs)
Clinical judgment should also be relied on
SNF = skilled nursing facility, ICU = intensive care unit

18. RISK FACTORS FOR PRESSURE ULCERATION
Intrinsic Risk Factors
Extrinsic Risk Factors
Dermatitis
Friction
Edema
Immobility
Hypoperfusion
Medical devices
Moisture
Long-term corticosteroid use
Pressure
Circulatory impairment
Shear forces
Nutritional compromise
From GRS9 Table 32.3.
Patients >75 years old with malnutrition and weight loss are 3.8 times more likely to develop pressure ulcers. Medical devices are increasingly recognized as causes of pressure ulceration. These include external devices such as tubing and orthopedic splints, casts, limb immobilizers, abdominal binders, and CPAP masks. Care plans for patients with external orthopedic devices should always include periodic skin assessment. Pressure ulcers can develop over internally placed medical devices such as implantable neurostimulators and pain-control pumps that create new pressure points under the skin.

19. MOISTURE-ASSOCIATED SKIN DAMAGE (MASD) (1 OF 2)
Occurs from perspiration, urine, diarrhea, fistulas, or wound exudate
Increases susceptibility to pressure ulcers
Is a common occurrence in patients with constant loose stools from tube feeding or Clostridium difficile colitis
Strategies to avoid or treat MASD
Moisture barrier creams, absorbable undergarments, continence care, and fecal and urinary diversion devices

20. MOISTURE-ASSOCIATED SKIN DAMAGE (MASD) (2 OF 2)
Sacrum, with MASD

21. PREVENTION STRATEGIES
Strategies to minimize pressure, friction, and shear
Pillows and foam wedges to keep pressure off bony prominences
Lifting devices and draw sheets to minimize friction
Industry standard for turning and repositioning is every 2 hours, however, individualize for each patient
Patients who sit for long periods of time in chairs should be assessed for proper posture and alignment and provided pressure relief schedules and cushioning
Prevent heel wounds with local skin care, cushioning, “floating the heels”
Lifting the heels off the mattress by placing a pillow under the legs when supine is called “floating the heels.”

22. PRESSURE REDISTRIBUTION SURFACES
Group 1 support surfaces are nonpowered devices made of gel, foam, or water
Group 2 support surfaces include alternating-pressure air mattresses and pressure-reducing air mattresses of the low air loss type.
Group 3 support surfaces are complete bed systems using air-fluidized technology using pressurized silicone-coated beads that promote a flotation environment
The terms “static” and “dynamic” are also commonly applied to support surfaces, where the latter refers to powered devices. There is some evidence that a more advanced static mattress or overlay is associated with lower risk of pressure ulcers than a standard hospital mattress; however, there are little data to support the effectiveness of one type of powered device over another (SOE=C). Given the lack of evidence on efficacy of prevention devices, choices are generally made on the basis of ease of use, nursing preference, cost, availability, and reimbursement.

23. PRINCIPLES OF PRESSURE ULCER TREATMENT (1 OF 2)
Should be a holistic, patient-centered approach
Assess overall health status of the patient
Address psychosocial needs
Treat underlying comorbidities
Assess and correct causes of tissue damage
Assess and monitor the wound
Understand patient’s functional and cognitive status, home environment, family support, and other factors such as presence of depression

24. PRINCIPLES OF PRESSURE ULCER TREATMENT (2 OF 2)
Elements of pressure ulcer treatment
Offloading and pressure redistribution strategies
Removing debris and necrotic tissue
Addressing moisture balance
Clinicians must also:
Address pain
Acknowledge advance directives
Recognize wounds appropriate for a palliative approach and alter the plan accordingly

25. COMMON WOUND TREATMENT MODALITIES (1 OF 5)
Type
Content
Rationale
Best Use
Gauze
Cotton, polyester, or other fabrics
Versatile, can be absorptive or protective, primary or secondary dressing
Secondary dressing, wet to moist, or wet to dry, or as a protective to the wound and surrounding skin
Hydrocolloid
Adhesive pad with moisture-activated, gel-forming material; gelatin and pectin
Moisture retention
Superficial, clean pressure ulcers with no necrosis or infection
Semi-permeable films
Transparent polymer with acrylic adhesive
These treatments address:
Moisture balance
Bacterial balance

26. COMMON WOUND TREATMENT MODALITIES (2 OF 5)
Type
Content
Rationale
Best Use
Hydrogel
Water in a delivery vehicle such as glycerin or cross-linked polymer sheets
Promote moist wound healing and autolytic debridement
Dry wounds; wounds with some necrosis
Foam
Polyurethane with or without adhesive borders
Absorb exudate, cushioning, secondary dressing
Control exudate, protect the wound
Alginate
Seaweed derivative; can be in different forms, including sheet or rope, and combined with other materials such as silver or charcoal
Absorptive dressing
Control of exudate

27. COMMON WOUND TREATMENT MODALITIES (3 OF 5)
Type
Content
Rationale
Best Use
Collagen
Animal-derived collagen formulated into gel, powder, paste, or sheet
Deactivates matrix metalloproteases that inhibit wound healing
Partial- or full-thickness wounds with minimal necrosis
Silver-containing dressings
Silver can be impregnated into multiple types of dressings
Silver has broad-spectrum antimicrobial activity
Wounds requiring control of bacterial balance
Enzymatic debriding agent
Enzyme in a petrolatum vehicle
Selected degradation of denatured collagen
Wounds with necrosis and slough
Cadexomer iodine dressing
Iodophor in a polysaccharide polymer
Absorbent, antimicrobial
Wounds with slough, infected wounds

28. COMMON WOUND TREATMENT MODALITIES (4 OF 5)
Type
Content
Rationale
Best Use
Silicone dressings
Inert silicone polymer; sometimes has pores that allow passage of exudate
Contact layer that can be removed without causing trauma to wound or surrounding skin
When a nonadherent dressing is required, protects the wound and surrounding skin
Activated charcoal
Combined with silver or other vehicles
Control odor
Palliative wounds with odor
Honey
Medicinal grade honey can be used as a gel or impregnated into other dressing types
Antimicrobial properties, anti-inflammatory
Autolytic debriding agent on noninfected wounds

29. COMMON WOUND TREATMENT MODALITIES (5 OF 5)
Type
Content
Rationale
Best Use
Topical antiseptics
Includes hydrogen peroxide, Dakin’s solution (hypochlorite), povidone-iodine
Reduce bacterial burden of wounds
Can be cytotoxic to healing wounds; for limited use in heavily contaminated or nonhealable wounds
Petrolatum-impregnated gauze
Woven mesh; medical petrolatum and 3% bismuth tribromophenate
Bacteriostatic, nonadherent, retains moisture
Use with larger wounds with minimal necrosis and slough

30. Moisture balance Bacterial balance Management of eschar
WOUND BED PREPARATION
Moisture balance
Bacterial balance
Facilitated by cleansing, topical antibiotics, disinfectants, and debridement
Methods of debridement: autolytic, enzymatic, mechanical, biologic, surgical
Management of eschar
Moisture balance is an important component of wound healing, because a moist environment promotes autolytic debridement and encourages matrix formation. Alternatively, excess moisture inhibits wound healing through maceration that impairs both the wound bed and periwound area. Several products promote moist wound healing such as hydrocolloids, hydrogels, and other bio-occlusives. The exudate of chronic wounds contains heightened proteolytic activity, matrix metalloproteases, and macromolecules that inhibit growth factors, and products such as foams, hydrofibers, and alginates provide absorptive capabilities. Collagen-containing products inactivate harmful cytokines and factors that inhibit healing.
Bacterial balance in the wound bed is facilitated by cleansing, topical antibiotics, disinfectants, and debridement. Debridement removes necrotic tissue and bacteria, providing a clean surface that promotes healing. Debridement can be achieved by several ways, and selection should be individualized in accordance with goals of care and degree of necrosis. Autolytic debridement uses moisture retentive topical dressings to take advantage of endogenous enzymes present in the wound, whereas enzymatic debridement uses a commercially produced enzyme to digest debris and dead tissue. Mechanical debridement methods include hydrotherapy (whirlpool), irrigation (pulsed lavage), and scraping the wound base and periwound area with a blunt instrument. Wet-to-dry or wet-to-moist gauze dressings are discouraged because of their nonselective nature in removing both debris and healthy granulation tissue.

31. Electrical stimulation Therapeutic ultrasound Light therapy
ADJUNCTIVE THERAPIES
Electrical stimulation
Therapeutic ultrasound
Light therapy
Negative-pressure wound therapy (NPWT)
Hyperbaric oxygen
NPWT is the application of suction to a wound bed to facilitate healing. The wound is packed with foam and sealed with adhesive membrane, and a vacuum device delivers controlled negative pressure while collecting exudate and debris into a collection chamber or absorptive pad. Since its introduction in the 1980s, NPWT has become a multimillion dollar industry despite the limited evidence in controlled clinical trials for efficacy. NPWT is marketed for all types of wounds, including open abdominal incisions, dehisced surgical wounds, burns, preparation for skin grafts, traumatic wounds, venous stasis ulcers, diabetic foot ulcers, and pressure ulcers.
The mechanism by which NPWT promotes healing is not known but may include removal of excess fluid, improved circulation, reduced bacterial load, and the mechanical effect of negative pressure. The FDA has issued a safety communication regarding complications of NPWT, including pain, retention of foreign bodies from the dressing, bleeding, infection, death, and complications stemming from power outages. NPWT should not be used over necrotic or infected wounds and is not a substitute for good nursing care with keeping a wound clean. Patients should be carefully selected for NPWT and educated regarding use and risks of the device. NPWT initiation should be cautiously considered in a wound that is not expected to heal; and if no observable improvement is seen after 2 weeks, NPWT should be discontinued.

32. NUTRITION
Important component of pressure ulcer management
Recommendations should be individualized in response to clinical conditions and goals of care
In general the caloric requirement for wound healing is Kcal/kg/day, and the recommendation for protein is g/kg/day, but more may be required
In the absence of documented deficiencies, vitamin and mineral supplements are not useful for wound healing

33. INFECTIOUS ASPECTS OF PRESSURE ULCERS (1 OF 2)
All chronic wounds are contaminated or colonized with bacteria but may not be infected
Infectious complications
Cellulitis, abscess, osteomyelitis, pyarthrosis, necrotizing fasciitis, systemic infectious
Signs and symptoms of infection
Fever, increased drainage, pain, warmth, edema, erythema, slough, odor, cessation of healing, worsening of the wound

34. INFECTIOUS ASPECTS OF PRESSURE ULCERS (2 OF 2)
Swab cultures are best reserved for wounds with purulent drainage in the setting of high suspicion for infection
Treatment must involve
Managing underlying conditions
Protection from urine and feces
Wound infections can be treated locally, systemically, or both depending on the clinical situation
Wound cleansers include water, saline, commercial cleansers, and irrigation devices, but these do not remove deeper bacteria. Bioburden can be managed by removing devitalized tissue with debridement, which can be autolytic, enzymatic, mechanical, or surgical. Antiseptics such as povidone-iodine, betadine, peroxide, and Dakin’s solution are generally discouraged because they harm living tissue but can be useful in heavily contaminated wounds when used in limited fashion.
Local treatments include dressings containing antimicrobial compounds such as gentian violet, methylene blue, silver, and cadexomer iodine. Topical antibiotics include mupiricin, neomycin, polymixin B, and bacitracin. Multiple topical antifungals are available, including the imidazole, triazole, and thiazole compounds. Systemic treatment depends on the suspected organisms and clinical setting, and bone infection requires 6 weeks of intravenous therapy. Aggressive treatment and hospitalization should be guided by goals of care and advance directives in conjunction with education of the patient and family.

35. PALLIATIVE CARE FOR CHRONIC WOUNDS (1 OF 2)
Should be considered when it becomes clear that there is little or no realistic chance of healing within the patient’s lifetime, and when the burdens of operative procedures or advanced treatment options outweigh the benefits
Factors leading to designating a wound as palliative:
Poor nutrition, inadequate perfusion, multisystem organ failure, immunocompromise, irreversible anasarca, or a terminal prognosis that prevents the normal healing process

36. PALLIATIVE CARE FOR CHRONIC WOUNDS (2 OF 2)
THE MNEMONIC “SPECIAL” S
Stabilize the wound P
Prevent new wounds E
Eliminate odor C
Control pain I
Infection prophylaxis A
Absorbent wound dressings L
Lessen or reduce dressing changes
SOURCE: Alvarez OM, Kalinski C, Nusbaum J, et al. Incorporating wound healing strategies to improve palliation (symptom management) in patients with chronic wounds. J Pall Med. 2007;10(5):1161–1189e.

37. SUMMARY Older adults are at high risk of developing pressure ulcers
Pressure ulcers may result in serious morbidity and mortality
Risk assessment and risk factor intervention are key to pressure ulcer prevention
Many wounds have reduced or no chance of healing. For these wounds, palliative care principles may curtail suffering, improve quality of life, and decrease health care costs.

38. CASE 1 (1 of 4)
A 65-year-old man being admitted for rehabilitation after surgical repair of his left hip, fractured in a fall 1 week earlier
History: type 2 diabetes mellitus, coronary heart disease, hypertension, hyperlipidemia
50-pack-year smoking history

39. CASE 1 (2 of 4) Physical examination:
Diminished sensation in both feet (by monofilament testing)
Diminished pulses in bilateral dorsalis pedis and posterior tibialis
Crusted skin, thick toenails
Nonfluctuating, dry, black eschar on lateral left heel. Surrounding skin is intact, with no evidence of cellulitis.

40. CASE 1 (3 of 4)
Which one of the following is the most appropriate initial management of the wound?
Sharply debride the eschar.
Leave the eschar intact and elevate both heels off the bed surface.
Cover the wound with a hydrocolloid sheet; change every 3–5 days and as needed.
Apply a silver alginate dressing plus a secondary dressing over the wound; change weekly. 40

41. CASE 1 (4 of 4)
Which one of the following is the most appropriate initial management of the wound?
Sharply debride the eschar.
Leave the eschar intact and elevate both heels off the bed surface.
Cover the wound with a hydrocolloid sheet; change every 3–5 days and as needed.
Apply a silver alginate dressing plus a secondary dressing over the wound; change weekly.
ANSWER: B
When external surface pressures, friction, and shearing forces exceed the normal arterial capillary pressure of 32 mmHg, perfusion is impaired and ulceration can occur. Placing a pillow vertically under the patient’s legs will support or “float” the heels off the bed surface, thereby eliminating pressure, friction, and shearing (SOE=D).
Stable, dry eschar can act as a physiologic barrier to infection. The European Pressure Ulcer Advisory Panel and the National Pressure Ulcer Advisory Panel do not recommend its debridement, especially if there is actual or suspected vascular disease. Instead, the wound should be inspected daily for signs of infection (≥1 of the following: erythema, tenderness, edema, purulence, fluctuance, crepitus, and odor). If infection is present, the ulcer should be debrided immediately.
Hydrocolloid sheets provide a protective barrier and facilitate autolytic debridement. However, a stable dry eschar should not be debrided. When hydrocolloid sheets are indicated, they should be used with caution on patients with diabetes, because removal of the sheets may cause tissue trauma (SOE=D).
Silver-impregnated dressings are used to reduce wound bioburden if infection is evident or suspected. This patient’s wound displays no clinical signs of infection. A calcium alginate dressing, used for exudate management, is contraindicated because the wound has stable, dry eschar and no exudate (SOE=D).
Because this patient has a sign of and several risk factors for peripheral arterial disease (diminished pulses, diabetes mellitus, coronary heart disease, hypertension, hyperlipidemia, and tobacco use), he is at greater risk of poor healing and infection of open wounds. His arterial circulation should be evaluated by an ankle–brachial index; if indicated, he should be referred to a vascular surgeon as soon as possible (SOE=D). 41

42. CASE 2 (1 of 4)
An 85-year-old man with areas of redness and skin breakdown on his buttocks
History: dementia, Parkinson disease
Spends much time sitting in a recliner
Wears a diaper because of urinary and occasionally fecal incontinence
Appetite is good, weight is stable.

43. CASE 2 (2 of 4) Physical examination
Several areas on the buttocks have partial-thickness erosions with sanguineous drainage.
Tender to touch
No induration, satellite lesion, or surrounding erythema
Diaper is saturated with urine and there are traces of stool adherent to the buttocks and perirectal area.

44. Apply a petrolatum-based barrier ointment. Apply a barrier film.
CASE 2 (3 of 4)
Which one of the following is the most appropriate skin-care recommendation?
Apply a petrolatum-based barrier ointment.
Apply a barrier film.
Discontinue use of diapers and put the patient on bed rest until the areas are healed.
Apply a mild antifungal cream to the affected areas. 44

45. Apply a petrolatum-based barrier ointment. Apply a barrier film.
CASE 2 (4 of 4)
Which one of the following is the most appropriate skin-care recommendation?
Apply a petrolatum-based barrier ointment.
Apply a barrier film.
Discontinue use of diapers and put the patient on bed rest until the areas are healed.
Apply a mild antifungal cream to the affected areas.
ANSWER: B
This patient has incontinence-associated dermatitis, which results from the effects of urine and stool on skin. A flexible barrier film that coats the affected area and allows vapor transmission for up to 72 hours is an appropriate, cost-effective method of protecting the skin from the effects on incontinence. Petrolatum-based ointments, such as zinc oxide plus petrolatum, form an occlusive layer on the skin surface to support skin barrier repair, promote skin hydration, and establish a physical barrier. However, the ointment needs to be reapplied after each incontinence episode (SOE=D), requiring an effective toileting protocol. A petrolatum-based ointment provides a barrier to moisture but does not adhere well to desquamated tissue.
Extended exposure to urine can macerate the stratum corneum and increase its susceptibility to friction, leading to further skin breakdown, infection, and activation of an inflammatory response, all of which increase the likelihood that a pressure ulcer will develop. Incontinence-associated dermatitis is exacerbated by the use of containment devices, such as diapers, that reduce airflow and trap heat and moisture. Removing the diaper would be optimal and allow appropriate airflow without entrapping moisture and heat. However, limiting an older adult to bed rest, even briefly, will lead to unnecessary functional decline.
Antifungal ointments are appropriate for a fungal infection related to incontinence-associated dermatitis. An antifungal cream is not indicated at this time, because there is no evidence of a fungal infection. Use of a corticosteroid ointment is contraindicated over an area that is contained within a diaper (SOE=D).
On average, 50% of nursing-home residents are incontinent and at risk of incontinence-associated dermatitis. Unlike a pressure ulcer, dermatitis is not limited to skin over bony prominences, its areas of damage are usually profuse, and there is usually partial-thickness skin loss.
Skin products should mimic skin pH as closely as possible. Many soaps and cleansers are alkaline, with a pH around 9, and alter the skin’s acid mantle, potentially increasing susceptibility to breakdown and infection. No-rinse foam cleansers are good alternatives to soap. 45

46. Copyright © 2016 American Geriatrics Society
GRS9 Slides Editor: Tia Kostas, MD
GRS9 Chapter Author: Jeffrey M. Levine, MD, AGSF, CWSP
GRS9 Question Writer: Fran Valle, DNP, CRNP
Managing Editor: Andrea N. Sherman, MS
Copyright © 2016 American Geriatrics Society