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Pressure Ulcers

Instructor: Sharee A. Wiggins, NP, Post-MS(N), ARNP, BC-GNP, BC-ANP
Module Revised by: Sharee A. Wiggins, NP, Post-MS(N), ARNP, BC-GNP, BC-ANP
Module Edited by: Mary McDonald, MD
Reviewed by: Anne Walling, MB, ChB

 

Specific Learning Objectives

A. Introduction

Before reviewing the learning objectives and content, please take the Pre-Test. Please review the Objectives, Content material, and Cases before our class session. We will apply the tasks in the Skills objectives to the cases, and you should think about them ahead of time.

B. Attitudes - the student will recognize that:

1. Successful treatment of pressure ulcers requires interdisciplinary care.
2. Patients at risk for pressure ulcers need active involvement in patient education.
3. Input from healthcare personnel in other disciplines - both licensed and unlicensed — who are involved in the care of the patient, or who have specific wound expertise, is essential in the prevention and management of pressure ulcers.

C. Knowledge - The student should be able to:

D. Skills

1. Identify a patient at risk for developing pressure ulcers and list preventative measures that can be taken
2. Identify a pressure ulcer, statin the grade (NPAUP/Shea classification, and listing treatment options

E. Readings

Required Readings:

• Thomas, D. R. Prevention and treatment of pressure ulcers.  JAMDA. 2006.  January; 7; 46-59.
• Sezginsoy B., & Wright, J. E.  (2007).  Pressure ulcers, 371-383. In Ham, R. J., Sloane, P. D., Warshaw, G. A., Bernard, M. A., & Flaherty, E.  Primary Care Geriatrics:  A Case Based Approach (5th ed.). Mosby:  St. Louis.

Recommended Readings:

• Thomas, D. R.  Are all pressure ulcers avoidable?  JAMDA. 2003.  March/April; 4; S44-S48.
• Takahashi, P.Y., Kiemele, L. J., & Jones, J. P. Jr. (2004).  Wound care for elderly patients: advances and clinical applications for practicing physicians. Mayo Clinic Proceedings;2004;79(2):260-7.
  

F. Module Content

1. Definition
2. Epidemiology
3. Classification
4. Etiology and Pathophysiology
5. Pressure
6. Pressure Risk Factors
7. Extrinsic Risk Factors
8. Intrinsic Risk Factors
9. Prevention
10. Evaluation
11. Complications
12. Treatment
13. Principles of Wound Care
14. Classification of wound care products and rational approach to their use
15. Skin Wound Care Products
16. Wound Care Dressing by generic classification
17. Debridement Methods
18. Wound Enhancement Therapy

G. Cases

1. Does a Broken Hip equal a Pressure Ulcer?
2. A Pressure Ulcer Than Won't Heal

 

I. PRESSURE ULCER DEFINED:

Localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear and/or friction.  (Revised:  February 2007)

• Synonyms include: pressure sores, decubitus ulcers, bed sores and ischemic ulcers. The latter three terms should not be used since they may not be accurate regarding wound pathogenesis.  Pressure ulcers or sores occur in positions other than the decubitus position or from lying in bed.  Even though there is an element of capillary ischemia present in all pressure sores, the term ischemic ulcers more commonly refers to those arising from arterial ischemic disease.
• The term pressure ulcer is most appropriate as it denotes the principle etiologic factor.
  

II. EPIDEMIOLOGY

• There are no widely accepted methods for reporting the incidence of pressure ulcers. Therefore, both the method of presenting the data and the classification of the individuals for whom the data is presented must be taken into account when reports are analyzed.
  
  
• Subgroups of hospitalized populations often cited include all hospitalized patients vs. bed bound hospitalized patients vs. post-surgical patients, etc.
  
  
• In long term care, pressure ulcers are subject to considerable regulatory scrutiny, and providers are at increased legal risk.  Controversy exists about their validity as quality of care indicators in all patients.
  
  
• Methods of quantifying incidence include percent development over time vs. number of sores per 1000 patient-days vs. number of sores per institution type, etc.
  
  
  • Prevalence among hospitalized patients:
    
    
    • 8% to 25% over 3 weeks in bed or chair-bound patients
    • 5.7 to 21.1 ulcers per 1000 patient days in adult non-ICU patients
    • 22 to 28.6 ulcers per 1000 patient-days in adult ICU patients
      
      
• Prevalence in nursing facility residents: 1 year incidence of 13.2%
  
  
  • 2 year incidence of 21.6%
  • Mortality rate of a nursing facility resident with a pressure ulcer is 2 to 6 times greater than for a resident without one.
  • Prevalence also dependent upon age.
    • 70% of lesions develop in patients older than 70 years of age
      

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III. CLASSIFICATION

The following is from the National Pressure Ulcer Advisory Panel web site.

In February 2007, following over 5 years of work, The National Pressure Ulcer Advisory Panel (NPUAP), redefined definitions of pressure ulcer and pressure ulcer stages, and added deep tissue injury.  Each stage definition is followed by “further description” commentary.

Suspected Deep Tissue Injury:   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. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue.

Further description: Deep tissue injury 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, exposing additional layers of tissue even with optimal treatment.

Stage I: Intact skin with non-blanchable 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.

Further description: The area may be painful, firm, soft, warmer or cooler as compared to adjacent tissue. Stage I may be difficult to detect in individuals with dark skin tones. May indicate "at risk" persons (a heralding sign of risk)

Stage II: 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 serum-filled blister.

Further description: Presents as a shiny or dry shallow ulcer without slough or bruising.* This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation.  *Bruising indicates suspected deep tissue injury.

Stage III: Full thickness tissue loss. Subcutaneous fat may 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.

Further description: The depth of a stage III pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue and stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage III pressure ulcers. Bone/tendon is not visible or directly palpable.

Stage IV: Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunneling.

Further description: The depth of a stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue and these ulcers can be shallow. Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis possible. Exposed bone/tendon is visible or directly palpable.

Unstageable: Full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed.

Further description: 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.

Reverse Staging:  cannot be done.  As wounds heal, the stage does not step down.  One may correctly state that a Stage III pressure ulcer is a “healing Stage III ulcer,” but it is not correct to reverse stage and note the ulcer has healed to Stage II or Stage I.  Doing so is not only an inappropriate use of staging criteria, but also does not reflect wound healing physiology.  Lost muscle, fat, and dermis are not replaced; the defect is filled in with granulation tissue then re-epithelialization occurs. Ulcer healing is described by wound assessment, rather than staging.

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IV. ETIOLOGY AND PATHOPHYSIOLOGY

“A number of contributing or confounding factors are also associated with pressure ulcers; the significance of these factors is yet to be elucidated.” (NPAUP).  Both clinical wisdom and research support the multifactorial nature of pressure ulcer development.  Conceptually, risk factors can be divided into 3 broad categories:  Pressure, Extrinsic, and Intrinsic. Both extrinsic and intrinsic factors can predispose tissues to being less tolerant of pressure.

V. PRESSURE

• When the external vertical pressure exceeds the normal capillary filling pressure of approximately 32 mm Hg, local vascular occlusion occurs sufficient to produce ischemia and subsequent necrosis of skin and subcutaneous tissues.
  
  
• Hyperemia --  pressure applied < 30 minutes.  Resolves after one hour.
  • Ischemia – occurs after 2 to 6 hours of unrelieved pressure, and may require up to 36 hours to resolved. 
  • Necrosis – develops after 6 hours of unrelieved pressure with microvasculature collapse and thrombosis.
  • Ulceration – occurs within 2 weeks after necrosis
    
    
• Studies have shown microscopic tissue damage when subjected to pressures of 60mm Hg for as little as one hour.
  
  
• Healthy persons seated on a flat board generate 300 to 500 mm Hg under their buttocks.
  
  
• Lying supine in a hospital bed generates heel-to-bed pressures of 50 to 94 mm Hg and trochanter-to-bed pressures of 50 to 94 mm Hg.
  • Thus, the amount of pressure needed to produce tissue damage and pressure ulcers is readily present in all patients confined to a bed or chair.
  • Most common sites
    • Sacrum (36%)
    • Heels (30%)
    • Other areas (6% each)  -- such as hips, buttocks, lateral ankles, shoulders, ears

VI. PRESSURE RISK FACTORS:

• Immobility - (Ulcers are very rare in ambulatory patients) Limits ability to reposition. Examples: paralysis, fractures, Parkinson's disease and other neurological disorders, and physical restraints.
  
  
• Sensory Deficit - Limited ability to sense need to reposition. Examples: neuropathies, spinal cord lesions, stroke, coma or chemical restraints.  Asensate areas are at particular risk (example:  advanced neuropathy of diabetes).
  
  
• Mental Status Changes - may not sense pressure, be able to move spontaneously, or be too confused to follow commands to move.
  
  
• Bottoming out - occurs when the pressure-relieving device is no longer preventing direct pressure on the surface the patient needs to be protected from. This is identified by the clinician being unable to slide the hand under the support surface of bony prominences.

VII. EXTRINSIC RISK FACTORS:

• Shear - Defined as the applied force that causes an opposite, parallel sliding motion in the planes of an object.
  • Described as "more disastrous" than vertical pressure as it tends to occlude larger areas of vascular supply. 
  • A common clinical situation in which a shear force occurs is on the sacrum when the head of the bed is elevated for an immobilized supine patient.  The skin and tissues remain stationary while the skeleton is forced downward by gravity and can lead to local vascular compression. 
  • Elderly persons tend to develop higher shearing forces while sitting, further predisposing them to pressure ulcers.
    
    
• Friction - Defined as superficial mechanical forces directed against the epidermis resulting in increased susceptibility to ulceration. Examples:  restraints against skin, "dragging" of patient across sheets for repositioning, and self-repositioning attempts of the supine patient with resulting friction trauma to elbows and heels.
  
  
• Moisture - increases skin friability by removing natural oils; can lead to maceration which, in turn, can lead to tissue erosion.  Shearing force and friction both increase in the presence of moisture.
  
  • Examples:
    
    
    • Incontinence of bowel or bladder – chemical damage to skin and bacterial contact with damaged skin
    • Ostomy site leakage – same as above, as well as risk of stomal maceration
    • Copious perspiration (diaphoresis

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VIII. INTRINSIC RISK FACTORS:

• Age - reduced skin cell turnover, drier skin, reduction of collagen and elastin (less pliable skin), and reduced vascularity at the dermal/epidermal junction result in: skin less resistant to shear forces, increased surface area (potential fluid loss increase), increased traumatic injury risk (e.g. skin tears), decreased homeostasis, and reduction of barrier function.
   
• Thin Body Habitus - More prone to develop pressure ulcers over bony prominences than obese or average-weight patients.
  
  
• Nutrition and Hydration - hypoalbuminemia, weight loss, cachexias, dehydration, and malnutrition are all commonly reported as risk factors predisposing persons to pressure ulcer.  Pressure ulcers can generate a stress response which further adds to nutritional demands. 
  
  
• In prospective cohorts with multivariate analysis, both lower dietary protein intake and the inability to feed oneself have been found to be predictors of pressure ulcer development. Thus, when identifying patients at risk for pressure ulcers, concentrating upon nutritional intake is recommended over other traditional markers (such as albumin and total cholesterol).
  
  
• Particular Medical Conditions - In addition to diabetes, malnutrition, altered mental status, and spinal cord injury:  orthopedic injury, depression, and vascular disease.
  
  
• Anaerobic waste products - are believed to accumulate due to pressure-induced occlusion of lymphatic vessels and contribute to tissue necrosis.

IX. PREVENTION

• Identify Patients at Risk
• Braden Scale – most researched, validated, and nationally recognized tool.  Comprehensive.  May not have the same predictive value and accuracy in LTC.  Not readily used in outpatient clinic setting. View tool at: http://www.bradenscale.com/braden.PDF
  
  
• Norton Scale – short, straightforward, easy to complete; does not address nutrition.  View tool at: http://www.woundcarehelpline.com/NortonScale.pdf

Pressure ulcer risk tools do not prevent pressure ulcers; only diligent care with attention to pressure relief will prevent pressure ulcers.  Even then, there are occasions of unavoidable occurrence when the occurrence has to do with patient morbidity factors rather than caregiver factors.  “The published data on prevention of pressure ulcers do not support an assumption that all pressure ulcers are preventable” (JAMDA 2003; 4; S44).

• In November 2004, The Centers for Medicare and Medicaid Services (CMS) published a report to guide LTC facility surveyors that, for the first time, defined unavoidable pressure ulcer:  “An unavoidable  pressure ulcer occurs when the facility staff evaluated the resident’s clinical condition and pressure ulcer risk factors, defined and implemented interventions that are consistent with resident needs, goals, and recognized standards of practice, monitored and evaluated the impact of interventions, and revised the approaches as appropriate.”
  
  
• Some pressure ulcers are actively developing with considerable tissue damage having already occurred before they can be observed externally.  Unavoidable pressure ulcers may be due to the same acute pathophysiology responsible for organ hypoperfusion or multiorgan failure.  In those cases, it is the acute illness responsible for ulcer development despite the best preventive strategies employed. 
  
  
• A particular type of pressure ulcer called the Kennedy Terminal Ulcer (KTU) has been described phenomenologically as an ulcer on the coccyx that initially presents suddenly as a pear- butterfly- or mirror-shaped Stage II ulcer that rapidly progresses in size and depth.  Color usually begins as red and then turns yellow to black.  It has been observed that such lesions frequently herald death within two weeks.  More research is needed. 

• Decrease pressure, friction and shear
  
  
  • Pressure-relieving devices (PRD)
    
    
    • Medicare Classifies PRDs according to 3 different groups; eligibility for reimbursement is tied to documentation criteria
    • The theoretic goal is to get tissue pressure reduced to below capillary closing pressure of 32 mm HG or less
    • Claims for pressure reduction in some devices may be overstated 
    • Few devices will achieve consistently decreased heel pressure below capillary pressure
    • Cushions, mattresses, or mattress overlays must not bottom-out
    • Transfer devices such as slide boards, or nylon fabric reduce friction
    • Use of two-person mobility assist if use of only one caregiver increases risk; caregiver availability issue and/or staff training issue
    • The use of “donut rings “ should not be used; they actually increase pressure in the center
    • Reposition bed bound persons at least every 2 hours
    • May increase to repositioning every 2 to 4 hours IF on PRD mattress
    • Reposition chair bound persons every hour (vertical force pressure)
    • All chair bound persons need PRD in seat (Consult with OT)
    • Limit head of bed elevation < 30 degrees (vertical force pressure)
    • Keep skin clean; clothing, linens, and disposable briefs dry;
    • Diligent skin assessment monitoring and skin care:  a) Keep moisturized, b) Do not massage bony areas, c) Treat skin infections
      
      
• Reverse, modify other risk factors
  
  
• Attend to need for adequate nutrition (see nutrition module), hydration, mobility, urinary & fecal continence
  
  • May need to consider change of diuretics, scheduled toileting, or short-term urinary catheter
    
    
• Manage pain (humane act and mobility promotion)
  
  
• Avoid over-sedation from drugs, insufficient rest periods

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X. EVALUATION 

• The Patient - Intrinsic Factors
  • Patients with pressure ulcers often have multiple comorbidities (including terminal illness status) that need to be considered and treated in concert with prescribing treatment specifically for their wounds.
    
    
  • Drug contributions: CNS-active drugs including neuroleptics, antidepressants, anxiolytics, etc. can induce somnolence, delirium, Parkinsonism, diminished mobility and exacerbate incontinence.
    
    
• The Ulcers
  • Proper assessment of the ulcer and the surrounding tissues is necessary to determine:  1) wound severity (pressure ulcer stage status), 2) biologic phase of wound healing, and 3) to establish a baseline for wound monitoring.
    
    
  • Although a variety of wound classification systems exist, the most appropriate and recognized for use with Pressure Ulcers is the National Pressure Ulcer Advisory Panel (NPAUP) Criteria. 
    • Can be used on arterial and diabetic ulcers as well, but not venous ulcers.
    •  http://www.npuap.org/pr2.htm
      
      
• Wagner Ulcer Grade Classification: 
• Dysvascular foot – Diabetes and Arterial Ulcers
• May be used on Venous Ulcers also
• Cannot be used on Pressure Ulcers
  
  
• Thickness of Skin Loss Classification
• Partial or full-thickness
• Useful with skin tears, donor sites, venous ulcers, surgical wounds, burns
  
  
• Red, Yellow, Black Classification
• Applicable to any wound type, including Pressure Ulcers
• Red = clean, healing, granulating
• Yellow = potential infection, potential necrotic tissue, need for cleaning or debridement
• Black = necrotic and in need of debridement
  
  
• Number of ulcers
  
  
• Size: acetate transparencies vs. calculation by multiplying the longest perpendiculars.
  
  
• Inspection and palpation of periwound tissue
• May also need to examine wound bed looking for undermining and tunneling which may be present in deep wounds and carry the risk of potential infection

• Inspection of ulcer bed (for tissue type), margins and wound exudate (for amount and characteristics)
  
• Ulcer bed:  Necrotic Tissue, Slough, Granulation Tissue, Epithelial Tissue, Resurfaced
  
  
• Granulation tissue presence: pink or beefy red tissue buds with moist, shiny, granular appearance heralds onset of successful wound healing.
  
  
• The Pressure Ulcer Healing Tool (PUSH) can be found online at:  http://www.npuap.org/PDF/push3.pdf
  
  
• Purulent discharge, darkened nonviable tissue appearance, periwound erythema, induration, delayed healing, and increased or new onset pain suggest local infection.
  
  
• Swab cultures are rarely helpful in directing treatment due to polymicrobial colonization and are listed as Do Not use in the AHCPR (now called AHRQ) Guideline.
• See online guideline at: http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat2.section.9173
• Cultures can be used for monitoring drug resistant bacterial presence (MRSA, VRE etc.)
• Acceptable culture methods include:
  
  
• Needle Aspiration of Fluid
• Biopsy of soft tissue
• Biopsy of bone (osteomyelitis).  Consider osteomyelitis in differential diagnosis list for refractory Stage IV and sometimes Stage III.

XI. COMPLICATIONS

• Local Infection: includes soft tissue abscesses and cellulitis. Cellulitis is identified by surrounding erythema, induration (sometimes edema), heat, and tenderness.  Cellulitis should be treated with antibiotics.  Oral or IV route depends on the severity.  CAT scans are beneficial in identifying abscesses.
  
  
• Osteomyelitis: more common complication when ulcer involves bony surface or when healing is delayed. X-rays and nuclear medicine scans often little help in diagnosis. Surgical bone pathology and cultures remains the gold standard.
  
  
• Bacteremia: among hospitalized patients, the combination of pressure ulcers and bacteremia has been associated with a mortality of 50%. When clinically suspicious of sepsis, obtain serum and deep tissue wound cultures and start empiric antibiotics to cover anaerobes, gram-negative and gram-positive bacteria.
  
  
• Marjolin's Ulcer: rare, aggressive, ulcerating squamous cell carcinoma arising from areas of previous trauma or chronic injury such as burn scars (most common), venous ulcers, osteomyelitis ulcers, or post-radiation scars.
  
  
• Mortality: patients admitted to nursing homes with a pressure ulcer have a 50% one year mortality rate compared to 27% in those without ulcers.

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XII. TREATMENT

• Pressure Ulcers are difficult to heal
• Acute Care setting:  13% heal in 2 weeks
• Long Term Care setting, healing rates depend on ulcer stage
• Stage III – possibly 59% heal at 6 months
• Some may require 1 year
  
  
• Pressure ulcers do not go through the normal wound healing process as acute wounds
• Fibroblasts and epithelial cells from normal skin tissues provide 80% covering of in vitro surfaces within 3 days
• Biopsy tissue from pressure ulcers have surface coverage of only 70% by 14 days
• Lack of hemorrhage results in reduced wound factors into the ulcer
• Release of platelets and fibrinolytic activity are decreased
• Complicated polymicrobial colonizations occur that are not well understood

XIII. PRINCIPLES OF WOUND CARE

 Optimize Local Wound Therapy

• Moist wound bed environment is essential for wound healing
  • Dry skin, but moist wound
  • In experimentally induced wounds – 40% faster resurfacing with moist environment vs. air-exposed
  • Wound exudate stimulates fibroblasts.
  • “Occlusive” dressing refers to the relative inability for moisture vapor to be transmitted from the wound to the external atmosphere.
  • MVTR = moisture vapor transmission rate
    • A measurement of how much a particular wound dressing dries a wound bed. 
    • Maintaining an adequate moist wound environment requires an MVTR of < 38 g of water vapor per square meter per hour
    • Examples: 
      • Gauze dressing MVTR = 68
      • Hydrocolloid dressing MVTR = 8
        
        
• Protect viable tissue
  
  
• Debride devitalized tissue
  • need a clean wound bed; “dirty” wound beds will not heal
    
    
• Stimulate angiogenesis
  
  
• Dealing with true bacterial infections (not colonizations)
  
  
• Maximize arterial flow when possible
  • (pressure ulcer is an ischemic injury)
    
    
• Relieve pain
  • Patient positioning
  • Systemic agent premedication
  • Perhaps topical agent prior to dressing change
    • viscous lidocaine ®
    • EMLA – eutectic mixture of local anesthetic
      • Lidocaine-prilocaine cream

XIV. CLASSIFICATION OF WOUND CARE PRODUCTS - Rational Approach to their Use

• Things that cover the wound to protect, provide moist environment
• Things that go in the wound for a specific purpose (absorb fluid, fill in dead space, debride, stimulate angiogenesis) 
• Skin care products

XV. SKIN WOUND CARE PRODUCTS

• Moisturizers  -- rehydrate dry skin.  Use around wounds, not in them.
  
  
• Moisture barrier – skin protectant for intact skin and periwound skin.  Use around wounds, not in them.
  
  
• Cleansing products – emulsify wastes, neutralize drainage on skin, and neutralize odors.  Not to be used in wounds.
  
  
• Normal Saline -- the recommended wound cleanser in national pressure ulcer guidelines.  All wounds should be cleaned with NS prior to application of new dressings.
  
  
• Cytotoxic agents -- Povidone iodine, Dakins © solution, hydrogen peroxide, sodium hypochlorite and many wound cleansers are cytotoxic to all cells and do not spare viable tissue. 

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XVI. WOUND CARE DRESSINGS by generic classification.  Multiple brands available in each category.

• Gauze   -- moistened with NS or sterile water for mechanical debridement.  Care not to allow to fully dry.  Results in indiscriminate debridement of non-viable and viable tissue. Indications:  deep necrosis; wounds covered with eschar.
  
  
• Impregnated gauze  -- used to cover (protect) surface wounds and preserve wound moisture.  [Examples:  Adaptic; Mesalt]
  
  
• Films  -- transparent semipermeable membrane films; waterproof; left in place up to 5-7 days on clean wounds.  Protection and maintenance of moist wound bed.  Large number of brand names available.  Indications:  skin tears, Stage I Ulcers (protects and reduces friction), Stage II ulcers.  They do not provide any cushioning.  [Examples:  Bioclusive; Nexcare; OpSite, Tegaderm HP]
  
  
• Hydrogels – a gel or gel sheet dressing; protect and add moisture; soften necrotic tissue. Gel sheets can provide comfort and cooling sensation.  Pliable conformity to wound surface as a  gel sheet but monitor for periwound maceration.  Can add gel alone directly into wound with moderate drainage (Stage III or Stage IV) and secondary dressing needed. [Examples:  Sheets -- Vigilon; FlexiGel; Restore / Liquid Gels -- DuoDERM hydrogel; GranuGel]
  
  
• Hydrocolloids – protects and provides autolytic debridement.  Also adds cushioning benefit.  Self-adhesive. May remain in place 5-7 days.  Can stick to bedding or clothing.  Special precuts available for heels, gluteal clefts.  Indicated for non-infected Stage II or III wound with none to lightly moderate drainage.  DO NOT use over friable skin.  [Examples:  Tegasorb; DuoDerm (also in Signal GCF and Extra Thin Versions); Granuflex; Comfeel]
  
  
• Alginates  -- nonadherent, absorbent product for heavily exudating wounds, usually Stage III and IV.  Conform to wound shape.  Needs secondary dressing.  DO NOT use on dry wound beds. [Examples:  Tegagen HG; Kaltostat; Aquacel]
  
  
• Foams – semiocclusive, cushions wound surface, maintains wound bed moisture, absorbs excess exudate in heavily draining wounds.  Secondary dressing needed.  Use in noninfected wounds. [Examples:  Allevyn; Polymen]
  
  
• Wound fillers -- variety of product forms:  pastes, granules, powders, beads, and gels. They provide a moist wound-healing environment, absorb exudate, and help debride the wound bed by softening the necrotic tissue.  Can be used in infected and non-infected wounds, deep wounds with dead space to fill, light to moderately exudating wounds.
  
  
• Composite dressings  -- have multiple layers (usually 3) and can be used as primary or secondary dressings; inner layer will not disturb new tissue growth; middle layer is absorptive and wicks away exudate; outer layer allows  moisture vapor to pass through to environment but will not allow entry of bacteria or particulate matter to enter.  Appropriate for wounds with minimal to heavy exudate, healthy granulation tissue, necrotic tissue, or a mixture.  Adhesive border requires cautious use in dehydrated or fragile skin. [Examples:  Combiderm ACD;  Alldress Absorbent Film]
  
  
• Collagens – absorbent for highly exudative wounds.  Monitor for periwound maceration. [Examples:  Promogran, Medifil, Fibracol]
  
  
• Antimicrobials  -- bactericidal to greatly reduce local wound bioburden.  Several impregnated products that deliver Ag (silver) ion into the wound. [Examples:  Acticoat; Silverlon]

XVII. DEBRIDEMENT METHODS

• Sharp 
  • scalpel and/or scissors; bedside or surgical procedure
    
    
• Mechanical
  • Gauze, whirlpool, pulsatile irrigation
• Autolytic
  • Promotes utilization of the body’s own wound fluid containing growth factors, enzymes, and immune cells to selectively debride necrotic tissue; a moist wound bed must be maintained
  • Various commercial autolytic wound dressings
    
    
• Enzymatic
  • Topical selective enzymatic debriding agents such as Collagenase or Papain-Urea
    
    
• Maggot Debridement Therapy (MDT)
  • Sterile, medical grade maggots solely for wound debridement
  • See:  http://www.medicaledu.com/maggots.htm

XVIII. WOUND ENHANCEMENT THERAPY

• Hyperbaric Oxygen Therapy (HBOT) for refractory ulcers following standard wound therapy.  Theoretically:
• improves microvascular perfusion
• promotes angiogenesis in ischemic areas
• has bacteriostatic effects
  
  
• Negative Pressure Wound Therapy
  • Vacuum Assisted Closure (V.A.C.) Dressings
    • Purported to remove fluid and wound debris, maintains moist environment, purportedly promotes perfusion, and helps draw wound edges together
    • Multiple wound types; numerous studies
    • Contraindicated in untreated osteomyelitis
      
      
• Recombinant human platelet-derived growth factor (becaplermin)
  • FDA approved for Diabetic Ulcers; efficacy not established for use in Pressure Ulcers
  • Stimulation of angiogenesis; accelerates healing time

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Case #1

Does a Broken Hip Equal a Pressure Ulcer?

An 84-year-old woman, living in the community, falls, breaking her left hip (sub-capsular). She is admitted to your service that evening, placed in traction, and the orthopedic surgeon plans to operate the following morning.

Questions:

1. What is her risk of developing a pressure sore?
2. What information do you need to better assess her risk?
3. How could you reduce her risk of developing a pressure sore?

 

Case #2

A Pressure Ulcer That Won't Heal

A 73 year old male is being followed in your clinic for the following medical problems, and medications:

Diagnosis

Medications

Type II Diabetes Mellitus	70/30 insulin bid
Hypertension	Lisinopril
Hyperlipidemia	Simvastation
Cerebrovascular accident 18 months ago	Enteric coated aspirin
Obesity
54-pack-year smoking history (quit 2 years ago)
Diabetic neuropathy
Diabetic retinopathy
Diabetic gastroparesis	Metoclopramide ac and hs

After the stroke 18 months ago, he was diagnosed with depression, and was treated for 6 months with sertraline, with improvement of mood to normal. The drug was discontinued.

The most recent functional assessment by the visiting nurse was that the patient needed assistance with bathing, but was otherwise independent. A home health aide provided assistance with bathing and light housework, and the daughter visited almost every day.

He is brought into the emergency room by ambulance, after his daughter found the patient at home lying on the floor, unconscious. The emergency room physician admits him to your service with diagnoses of pneumonia, a fall with a long lie, dehydration, and altered mental status. By the second hospital day, he has developed a new pressure ulcer over the right lateral malleolus.

The examination of the ulcer shows a round, 5 cm black eschar, that is debrided to an ulcer that extends through the dermis.

Questions

1. What information would you like about his current mobility?
2. What information would you like about his nutritional status?
3. Do you want a swab culture of the wound?
4. What would you do for initial management of the ulcer?
5. Does he need a special mattress for pressure reduction?
6. Would a growth factor be an appropriate treatment at this time?
7. Do vascular studies need to be done?
   

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