Pressure Ulcers: Prevention and Treatment
A continuing education supplement to The Journal
of Care Management, provided by Derma Sciences, Inc.

By Sharon Cassidy, RN, MS, CETN,
Director of Clinical Education, Derma Sciences, Inc.

After studying this material, the reader will:

1. Understand the structure and function of the skin, as well as the phases of normal wound healing.
2. Recognize the pathophysiology and clinical presentation of pressure ulcers.
3. Be able to choose an appropriate dressing based on the characteristics of a wound

INTRODUCTION

The number of chronic wounds treated in the United States is 5.6 million annually.(1) The treatment of pressure ulcers alone costs $ 1.3 billion dollars a year. In order to preserve increasingly scarce healthcare dollars, caregivers need to decrease the expenditures on chronic wounds for progressively greater returns. The AHCPR Guidelines report that a 3% savings or $40 million(2) of the total cost of treating pressure ulcers could be realized by adopting consistent and effective guidelines for treatment. One way to accomplish this is to prevent pressure ulcers from forming in the first place. Another way to decrease expenditures is through the correct assessment of wounds and the choice of appropriate dressings.

STRUCTURE AND FUNCTION OF THE SKIN

To better understand wound assessment and dressing options, it is important to understand the skin and its functions.

The skin is divided into two layers--the epidermis or outermost layer, and the dermis or innermost layer.(3) The epidermis consists of five layers. The outermost layer is abraded daily and replaced by cells that migrate from deeper layers. The dermis, the thicker of the two layers, is composed of both proteins and cells. Collagen and elastin are the principal proteins. Collagen gives the skin its tensile strength. Elastin makes the skin elastic. Fibroblasts--the cells present in the dermis--synthesize and secrete these proteins.(3) Beneath the dermis is subcutaneous tissue that provides a reservoir for fat and thus a cushion that enables the skin to withstand pressure without injury. Fascia and muscle under the subcutaneous tissue provides another cushion, especially over bony prominences .3

The epidermis shields the underlying tissue against water loss, mechanical injury and environmental trauma.(3) The epidermis is avascular and can regenerate when injured. This regeneration is referred to as epithelialization. In contrast, when the dermis is injured it heals by collagen substitution, or granulation tissue formation. (4) 

The skin also provides a barrier against bacterial invasion. Sebum, which is secreted by the sebaceous glands, provides an acid mantle whose pH on the skin ranges from 4 to 6.8 with a mean of 5.5. This acidic coating retards the growth of microorganisms .3 The skin also regulates body temperature, mediates pain, temperature and pressure, and in the presence of sunlight, synthesizes Vitamin D.(3)

WOUND HEALING

Partial-thickness wounds penetrate the epidermis and involve the dermis. These wounds heal by reepithelialization, which is the horizontal movement of epidermal cells across the surface of a wound until a sheet of epithelium covers the wound bed.(4,5) If the dermis is injured, healing requires collagen synthesis. Full-thickness wounds involve the epidermis and dermis, and may include subcutaneous tissue, muscle, and bone. Full-thickness wounds normally heal by means of hemostasis, inflammation, proliferation and maturation.

The body's normal early response to injury is hemostasis and inflammation.(4,6) During hemostasis, the body responds by reducing blood flow, isolating the injury from the rest of the body, and preventing or reducing bacterial contamination.(6) Inflammation begins soon after the initial injury and can last four to six days.(6) Tissue injury and the activation of clotting factors during hemostasis stimulate the release of vasoactive substances that cause the blood vessels to dilate and become more permeable .(4) Vasocongestion results and with it the leakage of serous fluid into the wound bed. The wound becomes erythematous, edematous, warm, and exudative.(4) Leukocytes are attracted to the wound bed. These are subsequently replaced by macrophages, which debride the wound and stimulate the formation of fibroblasts.(6) If inflammation is inhibited, then wound healing is compromised.(6,7) Steroids and anti-inflammatory drugs can deter this phase of wound healing.(6,8)

Proliferation occurs four to twenty one days after injury.(6) During this phase, granulation tissue formation, contraction and epithelialization occur.(7) Granulation is the formation of new connective tissue that fills the wound. This involves angiogenesis, which refers to the formation of new blood vessels, and the synthesis of collagen.(6) Fibroblasts are responsible for collagen synthesis and are therefore critical to wound repair.(4) Granulation tissue is red and vascular due to the newly formed blood vessels. It is granular and has a cobblestone appearance. This newly formed granulation tissue is delicate and care should be taken to protect it from trauma.(7) Dressings that provide a moist wound bed promote angiogenesis and connective tissue synthesis.(4,5) Contraction occurs in large wounds that are healing by secondary intention.(4) Contraction decreases the amount of granulation tissue needed to fill the wound bed. The final component of the proliferative phase is epithelialization. If the wound bed is dry or if necrotic tissue is present, it will take longer for epithelialization to occur.(4,5,8)

The final phase of wound healing is maturation, which can take up to a year or longer to occur.(4,7) During this time, collagen lysis and synthesis are still ongoing as the collagen is reorganizing and strengthening.(8) The healed wound will only gain about 80% of the skin's original tensile strength .(4)

FACTORS AFFECTING WOUND HEALING

Both systemic and local factors can affect wound healing.

Systemic Factors:

• With aging there is a reduced local inflammatory response, decreased ability to repair epidermal damage, decreased sensory loss and decreased collagen synthesis.(3,9)
• The diabetic patient with insulin deficiency has suppressed collagen formation. Angiopathic changes in blood vessels result in impaired perfusion leading to a delay in wound repair.(4)
• Steroids attenuate or eliminate the inflammatory phase, and interfere with epidermal migration and collagen synthesis.(4)
• Poor tissue perfusion leads to decreased collagen synthesis, and a decreased resistance to infection.(4,7)
• Malnutrition creates myriad problems. Consider the normal function of these nutrients:

1. Protein is needed for collagen synthesis, epidermal migration and prevention of infection.(4,7)
2. Calories provide energy for tissue defense and wound repair.(4)
3. Vitamin C is needed for collagen synthesis. (4,6 4)
4. Vitamin A counters the effects of steroids, restores local inflammatory responses, and stimulates  epithelialization.(4)
5. Zinc is a cofactor for collagen synthesis.(4,7)
6. Iron is required for transporting oxygen and is a cofactor for collagen synthesis.(7)

Local Factors:

• The presence of necrotic tissue, dressing residue and excessive exudate impedes wound healing and increases the potential for infection.
• Infection prolongs the inflammatory phase of wound healing, creates additional tissue destruction, delays collagen synthesis, and prevents epithelialization. (4)
• A dry wound decreases epidermal migration.

PRESSURE ULCERS

The prevalence of pressure ulcers in acute-care settings is 3.5% to 29.5%, in long-term care settings 2.4% to 23% and in home-care settings 12.9%.(2) The treatment cost of one pressure ulcer can range from $5,000 to $27,000.(11) One method for managing pressure ulcers is to understand their causes and to utilize care plans that eliminate them.

Pressure ulcers are caused by unrelieved forces that damage underlying tissues.(2) These forces include pressure, friction, shearing and maceration. Pressure closes the capillaries. As a result, nutrients and oxygen cannot be transported to the tissues and wastes cannot be eliminated. Cell death then ensues. Tissue damage associated with pressure is greatest in the skin overlying bony prominences.

Shearing occurs when two surfaces move against one another. This occurs when the skin is held in place relative to the movement of underlying muscle and bone. Blood vessels then become angulated and stretched. This leads to the equivalent of small-vessel thrombosis and therefore in tissue death.(12) For example, when the head of a bed is elevated, the body slides toward the foot of the bed. This shears the posterior sacral tissues.(10)

Friction is often described as "sheet burn" and occurs when the skin moves across a coarse surface.(12) The resulting irritation is superficial and will heal quickly, but the injured tissue becomes more susceptible to further tissue damage.

Maceration caused by incontinence or perspiration waterlogs the skin, decreases its tensile strength, and loosens the connective tissue between the dermis and epidermis. This can make the skin more vulnerable to external forces.

WOUND MANAGEMENT

Following is the staging system for pressure ulcers utilized by the AHCPR Guidelines to define the degree of tissue destruction caused by the forces just described.(2)

• Stage I: Nonblanchable erythema of intact skin. This is the heralding lesion  of skin ulceration. In individuals with darker skin, discoloration, warmth, edema, induration, or hardness may also be indicators.
• Stage II: Partial-thickness skin loss involving epidermis, dermis or both. the ulcer is superficial and presents clinically as an abrasion, blister or shallow crater.
• Stage III: Full-thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia. The ulcer presents clinically as a deep ulcer with or without undermining of adjacent tissue.
• Stage IV: Full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (e.g., tendon, joint capsule). Undermining and sinus tracts may also be associated with Stage IV pressure ulcers.

Management begins with prevention. This can start with the use of a risk assessment tool when a patient is admitted to a health care facility or a home care program. The 1992 AHCPR Guidelines identify at-risk individuals and the specific factors placing them at risk. These factors include immobility, incontinence, nutritional deficits, advanced age, impaired perception or sensation, predisposing health problems and altered levels of consciousness.(12) Criteria for selecting an effective assessment tool include: ease of use, minimal completion time, inclusion of all pertinent risk factors, and utility as a guide for patient care plans. Two widely used risk assessment tools are the Braden and Norton scales.

Prophylaxis

According to the AHCPR Guidelines, tissue loads must be managed. The goal should be to create an environment that will enhance tissue viability and promote the healing of pressure ulcers.(2) To this end prevention protocols should address relieving pressure, decreasing shear and friction, and keeping the skin dry, and otherwise maintaining its integrity. This can be accomplished by repositioning bedridden patients every two hours and chair- bound patients every hour. Positioning devices should be used to keep bony prominences from direct contact with one another and to keep the heels off the bed. The use of pressure reducing devices should be considered for individuals who are at risk for developing pressure ulcers while lying in bed or for individuals who are chairbound. Donut-type devices are not appropriate.(12) In selecting support surfaces, certain characteristics should be considered: increased support area, shear and pressure reduction, low moisture retention, reduced heat accumulation, dynamic properties, and cost per day.(2)

Shear and friction can be decreased by using lifting devices for patients who cannot assist during transfer or position changes. This includes the use of draw sheets and trapezes. The head of the bed should be kept at the lowest degree of elevation consistent with a patient's condition.(2)

Patients should be kept free of bodily wastes to prevent maceration. This includes cleaning the patient at the time of soiling with a mild cleanser, applying a moisture barrier ointment, using products that wick moisture away from the skin and using external collecting devices. Care should be utilized when cleaning a patient to avoid massaging over bony prominences, as this may lead to further tissue trauma.

Debridement

When eschar is present, a pressure ulcer cannot be staged adequately until the eschar is removed.2 Necrotic tissue also needs to be removed because it supports growth of pathogens, provokes inflammation, places phagocytic demand on the wound and retards wound healing.(4,10,13) There are four methods of debridement: surgical, autolytic, chemical and mechanical. The choice of debridement will depend on assessment of both the patient and wound, the desired outcome, as well as social and environmental issues.(13)

Surgical debridement utilizes sharp instruments to remove necrotic tissue. This method is the most rapid and is the preferred method of debridement for infected wounds.(2) The procedure should be performed by a qualified clinician. when extensive necrosis is present, a surgical procedure is generally warranted. Debridement of small wounds can be done at the bedside, provided that resources are available to manage complications. However, if the patient is not a surgical candidate then alternative means of debridement should be considered.

Autolytic debridement is the breakdown of devitalized tissue by the body's own enzymes and white blood cells.(4) By using moisture retentive dressings, the devitalized tissue is hydrated. The wound fluid so produced will contain enzymes and white blood cells that digest the devitalized tissue.(4) Autolysis is non-invasive and will not disrupt healthy tissue.(13)

Chemical debridement is done with topical enzymatic agents that are placed directly on the devitalized tissue. These require a prescription, are not rapid and may not be the treatment of choice in patients with an increased risk of infection.(13) The enzymes are activated by a moist environment and are not meant for use on dry eschar. This type of wound should be crosshatched prior to the use of the enzyme.(4,13) when the wound becomes free of necrotic tissue the enzyme should be discontinued.

Mechanical debridement can be accomplished by the use of wet- to-dry dressings, whirlpools, and irrigations. This is a non-selective form of debridement, in which healthy tissue may be removed along with devitalized tissue. Once devitalized tissue has been removed, a non-traumatic dressing should be used to protect the granulation tissue.(13)

Wound Cleansing

The AHCPR Guidelines suggest that a wound be cleansed with every dressing change. The goal is to remove necrotic tissue, exudate and metabolic wastes, all of which impair wound healing. A balance must be maintained so enough mechanical force is utilized to remove this dead material without harming healthy tissue. Safe and effective cleansings occur when the solution is applied with forces ranging from 4 psi to 15psi (pounds per square inch).(2) One method that is suggested in the AHCPR Guidelines, is to use a 35cc syringe with a 19 gauge needle. This will deliver cleansing agents with a force of about 8psi. This is effective enough to cleanse the wound, and reduces the risk of infection and trauma.(2) Cytotoxic agents should not be used for cleansing wounds. The AHCPR Guidelines specify that povidone iodine, iodophor, sodium hypochlorite solution, hydrogen peroxide and acetic acid are toxic to fibroblasts.(2)

WOUND ASSESSMENT & DRESSING CHOICES

All wounds should be assessed weekly or more often if changes occur. (2,14) Concurrently, the treatment plan should be monitored if the ulcer is healing and reassessed if the ulcer is not healing. The following should be documented when a pressure ulcer is assessed: stage, anatomic location, size (length, width and depth), wound bed characteristics, presence of necrotic tissue, type and amount of exudate, duration of the wound, presence of undermining or tunneling, condition of the periulcer skin and wound edges, and the presence or absence of infection. Proper wound assessment can suggest treatments and appropriate dressings.(14)

When selecting dressings the following should be addressed:

• Removal of necrotic tissue and elimination of infection (4,14)
• Obliteration of dead-space (4,14)
• Maintenance of both a moist wound bed (4,14) and dry intact periulcer skin.
• Protection of the wound bed from trauma and bacterial invasion. (4,14)
• Absorption of excessive exudate. (4,14)
• Use of non-toxic substances. (14)
• Appreciation of time and cost expenditures.

Dressing Selection

Clinicians should familiarize themselves with the properties, indications and contraindications of the wound care products in which they are interested.

Vapor permeable/transparent adhesive dressings (4,15).

• allow gas exchange between the wound bed and environment.
• are impervious to external contaminants and bacteria.
• create a fluid environment that supports autolytic debridement.
• are non-traumatic to the wound bed, adhere to periulcer skin and can damage fragile skin.
• maintain moist wound environments.
• are not absorptive.
• can be used on Stage I pressure ulcers to decrease surface friction, on Stage II ulcers, and on dry necrotic pressure ulcers that need debridement.
• allow a 1- to -2 inch margin of healthy tissue around the wound bed.
• are changed according to wound drainage, usually every two to four days.

Hydrocolloid dressings(4,15):

• generally are occlusive and do not allow gas exchange between the wound bed and environment.
• are impervious to external contaminants and bacteria.
• support autolytic debridement.
• are non-traumatic to the wound bed: they adhere to periulcer skin and can damage fragile skin.
• maintain moist wound environments.
• are minimally to moderately absorptive.
• can be used on Stage I ulcers to decrease surface friction.
• can be used on Stage II to IV pressure ulcers, but are not suitable for wounds with undermined skin or sinus tracts, unless used with some form of packing.
• may not always be appropriate for Stage IV ulcers with exposed bones or tendons that may need close monitoring.
• allow a 1-1/4 inch margin of healthy tissue around the wound bed.
• are changed according to wound drainage, usually every' three to seven days.

Nonadhesive semipermeable polyurethane foam dressings(4,15):

• support autolytic debridement in moist wounds.
• may be impervious to external fluid, depending on the product.
• are non-traumatic to the wound bed.
• maintain moist wound environments, but may macerate wound edges.
• are minimally to moderately absorptive.
• can be used on draining Stage III and Stage IV ulcers, provided that the dead space is obliterated.
• are not recommended for use on wounds with no exudate or dry eschar.
• are changed according to wound drainage, usually every two to five days.
•  

Alginates (4,15)

• support autolytic debridement in moist wounds.
• absorb up to 20 times their weight.
• maintain moist wound environments, if not allowed to dry out.
• are non-traumatic to the wound bed.
• can be used on moderately to heavily draining Stage III and IV ulcers.
• can be used in wounds that have tunneling or undermining.
• are not recommended for wounds with dry eschar or minimal drainage.
• are changed according to wound drainage, usually every one to four days.

Hydrogel dressings (4-15):

• support autolytic debridement.
• are non-traumatic to the wound bed.
• maintain moist wound environments.
• are useful on wounds with minimal to moderate drainage.
• are best used in sheet form on Stage II ulcers.
• are best used in granulate and impregnated gauze forms on Stage III and IV ulcers.
• can eliminate dead space when used in granulate and impregnated gauze forms.
• are changed according to wound drainage, usually every one to three days.
•  

Gauze dressings(4):

• support autolytic debridement, if they are kept moist.
• need to be used with appropriate solutions or gels to keep wound beds moist.
• absorb exudate.
• obliterate dead space.
• can be used on Stage II ulcers, if used with topical agents to keep the wound bed moist.
• can be used with Stage III and IV ulcers if they are moistened and packed lightly into the wound bed, and not in contact with the periulcer skin.
• are changed according to wound drainage.

SUMMARY

Pressure ulcer treatment is costly, but the problem can be minimized by identifying the causative factors and preventing them. By understanding wound healing and the criteria for wound assessment, and by relating both to dressing options, it is possible to decrease inappropriate dressing use. While this article only addresses conservative wound management, the clinician should be aware of aggressive treatment modalities for the management chronic pressure ulcers. These include the use of hyperbaric oxygen, electrical stimulation, wound healing (growth) factors and surgery.(4)

REFERENCES

1. Brookens TJ Fishman TD Freedline AD. Wound care specialization will build your practice. Podiatry Today 1995;8(7): 33-4, 40. 42, 44.
2. Treatment of Pressure Ulcers Guideline Panel. Treatment of Pressure Ulcers. Clinical Practice Guideline, Number 15. Rockville, MD, U.S. Department of Health and Human Services. Public Health Service. Agency for Health Care Policy and Research. AHCPR Publication No. 95-0652. December 1994.
3. Wysocki AB, Bryant RA. Skin. In: Acute and Chronic Wounds: Nursing Management (RA Bryant ed.). St. Louis: Mosby-Year Book, 1992;1-10.
4. Doughty DB. Principles of wound healing and wound management. In: Acute and Chronic Wounds: Nursing Management (RA Bryant, ed.). St. Louis: Mosby-Year Book 1992; 31-61.
5. Kerstein MD. Moist wound healing: the clinical perspective. Ostomy/Wound Management 1995; 41(7a suppl): 37S-44S: discussion 45S.
6. Cooper DM. The physiology of wound healing: an overview. In: Chronic Wound Care (Krasner D. ed.). King of Prussia: Health Management Publications, Inc. 1990:1-11.
7. Gogia PP. The biology of wound healing. stomy/Wound Management 1992;38(9): 12, 14-6, 18-20.
8. Ennis WJ, Menes P. Leg ulcers: a practical approach to the leg ulcer patient. Ostomy/Wound Management 1995;41(7a suppl): 52S-60S.
9. Levine JM, Simpson M. McDonald RJ. Pressure sores: a plan for primary care prevention. Geriatrics 1989 44(4): 75-6 83-7. 90.
10. Barr JE. Principles of wound cleansing. Ostomy/ Wound Management 1995:41(7a suppl): 15S-22S.
11. Bryant RA. Shannon ML Pieper B, et al. Pressure ulcers. In: Acute and Chronic Wounds: Nursing Management (RA Bryant, ed.). St. Louis: Mosby-Year Book, 1992: 105-63.
12. Panel for the Prediction and Prevention of Pressure Ulcers in Adults. Pressure Ulcers in Adults: Prediction and Prevention. Clinical Practice Guideline. Number 3. AHCPR Publication No. 92- 0047. Rockville MD: Agency for Heafth Care Policy and Research. Public Health Service. U.S. Department of Health and Human Senices. May 1992.
13. Fowler E, van Rijswijk L. Using wound debridement to help achieve the goals of care. Ostomy/Wound Management 1995;41(7a suppl): 23S-35S.
14. Baranoski S. Wound assessment and dressing selection. Ostomy/Wound Management 1995:41(7a suppl): 7S-12S.
15. Halpin-Landry J Loehner D. Cofone E et al. Dressed for successful healing: understanding wound care products. Advances in Wound Care 1995: 8(5):4-13.

An educational supplement to the Journal of Care Management, volume 2, number 3