Journal of Gerontological Nursing


Impaired Skin Integrity

Martha S Iverson-Carpenter, RN, MA





Pressure sores remain a persistent dilemma for the nursing profession and its clients. While the chronically ill, the debilitated, the spinai cord injured, the aged, and the disabled client are especially prone to pressure sores, occurrence of pressure sores is not confined to these groups. Anyone who stays in one position without the relief of pressure on bony prominences can develop a pressure sore.

Studies on the effect of pressure on pressure sore formation have not yielded consistent results, leading researchers to look for other contributing factors involved in pressure sore formation.

Some factors that have been studied include activity, mobility, incontinence, nutritional state, disease states, fever, infection, mental state, stress, sex, age, race, and education. No one set or group of contributory factors has been demonstrated to be consistently associated with skin breakdown.

Responsibility for prevention and treatment of pressure sores usually falls on the nurse. Etiologies, signs, and symptoms related to pressure sore formation need to be identified so accurate nursing diagnoses can be formulated. Once clients are identified at risk for skin breakdown, preventative measures can be instituted.

In this article, a case study on impaired skin integrity and pressure sores will be presented followed by a discussion of etiologies, signs and symptoms, and appropriate nursing interventions for pressure sores.

Case Study

The client is a 71-year-old institutionalized white male with a stage II pressure sore on his coccyx. The pressure sore is approximately the size of a quarter and superficial in depth. The tissue is bright red in color; no pain or exudate are present.

This client has restricted range of motion in his extremities, ambulates with a cane, and spends the majority of his day sitting in a wheelchair taking only an afternoon break for a nap. The client is confused at times giving inappropriate responses, has nocturnal incontinence, and is overweight. He is currently on a 1600-calorie weight reduction, high-protein diet. Existing medical diagnoses include obesity, seizure disorder, organic brain syndrome, kyphoscoliosis, and a history of iron deficiency. The most recent lab results for serum electrolytes and blood chemistries were within normal limits (Hg= 14.2).

Nursing interventions listed in the client's chart for treatment of his pressure sore include a chair cushion in his wheelchair, a water mattress on his bed, application of A&D ointment to his coccyx three times a day, and a nursing order to turn every two hours when in bed. Nursing notes state the client is often found on his back despite the turning regime.

One nursing diagnosis for the client in this case study is impairment of skin integrity/related to pressure while sitting in the wheelchair, physical immobilization, nocturnal incontinence, decreased level of consciousness, and alteration in nutrition (obesity), as evidenced by the stage II pressure sore on his coccyx.

Etiologies and Defining Characteristics

The nursing diagnosis of impaired skin integrity is a general term referring to a variety of states where the skin is altered: rashes, erythema, lesions, pressure sores, and disruptions of skin layers. Etiologies for actual impairment of skin integrity have been divided into external (environmental) and internal (somatic) etiologies. Table 1 lists the etiologies and defining characteristics as noted by the North American Nursing Diagnoses Association (NANDA). ' Those etiologies with asterisks have been identified in research on pressure sores. Three defining characteristics listed are disruption of skin surface, destruction of skin layers, and invasion of body structures.

Pressure sores are one type of impaired skin integrity which result in erythema and destruction of skin layers . Pressure sores result when sufficient external pressure causes blood vessel collapse and interference with blood and fluid flow to and from the cells, resulting in ischemia. The result of ischemia is starvation and, if prolonged, cell necrosis.

The amount of pressure thought to be a factor in pressure sore formation was any pressure greater than 35 mm Hg for a period of one or two hours. 2 Recently, studies are indicating significantly higher pressures, 300 to 350 mm Hg, are required to occlude blood flow to produce ischemia.3 Pressure is most severe in body areas over bony prominences, thus these areas are at greatest risk for pressure sore formation.

Two other mechanical factors identified in pressure sore formation are shearing force and friction.4,5 Shearing force occurs when tissue layers slide on each other causing the subcutaneous blood vessels to kink or stretch, interrupting blood flow. This phenomenon can occur when the head of the bed is raised and the superficial fascia slides, but the sacral skin stays in contact with the bed due to friction, friction disrupts the skin's epithelial cells creating a superficial lesion due to mechanical forces. These mechanical forces can occur while moving a client in bed, improper lifting techniques, or improper use of the bedpan.

Nutritional conditions that have been implicated in pressure sore formation include obesity, underweight, anorexia, and hyperglycemia.6-8 A retrospective nursing study showed some evidence that alteration in nutrition was a factor in pressure sore formation.9 Fatty tissue is vulnerable to breakdown due to decreased vascularity and resiliency. In contrast, underweight people lack the adequate cushion of muscle and subcutaneous fat against pressure. Decreased body weight was identified in two nursing studies as the most effective predictor of skin breakdown.10,11

Another factor identified in pressure sore formation is decreased level of activity or decreased mobility.8,12 Conditions such as unconsciousness, anesthesia, and partial or complete paralysis result in altered mobility and activity.13 Restricting a client's activity level by imposed medical treatments or sedation places a client at risk for possible skin breakdown.

Incontinence has been identified due to the resultant skin maceration that occurs from continual contact with urine and feces.14 Disease states such as spinal cord injuries, circulatory disturbances, cancer, and orthopedic conditions have been identified in surveys of people with pressure sores.15,16 Any medical condition that decreases delivery of oxygen and nutrients to needy cells such as atherosclerosis, anemia, or edema increases the risk for skin breakdown.8 In addition, the majority of studies and surveys on pressure sores have focused on elderly populations.11,12,16,17

Other factors thought to play a role in pressure sore formation include fever and infection in a client,11,17,18 stress,18 and lack of involvement of a client in his own skin care.19 Factors that have been studied in pressure sore formation but where no relationship has been found include race, sex, and educational level.16,17,20

The initial sign of pressure on the skin is redness of the skin or erythema. This is due to a compensatory mechanism known as reactive hyperemia. When pressure is removed from an area of skin, the area is instantly flooded with blood, creating redness. With prolonged pressure, the compensatory mechanism of the body is unable to respond which can result in an irreversible condition of induration.

Classification schemes identify defining characteristics of pressure sores. One widely used system, reported by Shea,21 is a four-part classification based on soft tissue breakdown. A stage I sore is an irregular, ill-defined area of soft tissue swelling, induration, and erythema. A normally innervated client will complain of pain. A stage II pressure sore is a full thickness break in the skin involving epidermal/dermal layers.

A stage III sore is an irregular, full thickness sore extending into the subcutaneous fat tissue. And finally, a stage IV sore resembles a stage III sore except muscle and/or bone can be identified in the ulceration. Stage III and IV sores are often infected, foul-smelling, necrotic, and have undermined the surrounding tissue.

The most frequently reported locations of pressure sores on the body are the sacrum, ischial tuberosities, trochanter area of the leg, heel, and the malleolus of the ankle.22 The diagnosis of skin impairment in this case study can easily be made by the existence of the stage II pressure sore. The defining characteristics present in this case study are disruption of skin surface and destruction of skin layers, as evidenced by the classification of a stage II sore. Etiologies found in this case study include: the mechanical factor of pressure from prolonged sitting in a wheelchair and lying supine in bed; physical immobilization due to restricted range of motion in the extremities and the lack of activity in the wheelchair; nocturnal incontinence; decreased level of consciousness due to inappropriate responses; and the altered nutritional state of obesity.

Nursing Interventions

Nursing interventions for treatment of pressure sores can be divided into preventative methods, systemic methods, topical methods, and surgical methods. The most frequently used method is the application of topical creams and ointments.

Nursing interventions used in treatment of pressure sores require different approaches for the stages of pressure sores. However, there are a few basic principles in pressure sore treatment:

1) The source of pressure on the client must be removed by turning, repositioning, and redistributing the body weight of the client.22,24 Removing the pressure source allows recirculation of the blood to the -tissues. Mechanical devices (preventative aids) such as chair cushions, bed mattresses, and sheepskins do not remove the source of pressure.

2) Do not dry the surface of a pressure sore with heat lamps. Skin cells need a moist environment for their viability, epithelialization, and healing process. Winter first proposed moist wound healing from research conducted on swine.25 In a moist environment, skin cells remain viable and are able to migrate at a faster rate for skin epithelialization or epidermal healing. Winter found that skin wounds left to me open air developed scabs which hindered the healing process.

3) Be aware that solutions such as alcohol, hexachlorophene, certain soaps, and hydrogen peroxide are damaging to newly formed, fragile skin cells and should not be used.23 Povidone-iodine placed on open sores can be absorbed through the skin and it is also a drying agent on skin cells.

4) If possible, eliminate or decrease any known risk factors or etiologies.22 Increase a client's activity level or mobility by frequent body shifts of weight in a wheelchair or in bed.25 In a study by Exton-Smith and Sherwin, clients with more spontaneous body movements at night were at less risk for pressure sore formation.26

Proper nutrition and hydration are needed for skin metabolism and skin repair. Nutrients required for healthy skin are protein, zinc, sulfur, vitamins A and C, riboflavin, niacin, and linoleic acid. An existing medical condition such as anemia should be corrected. Incontinence complicates any treatment regime. Thorough cleansing of the skin after each incontinence, without rubbing, is necessary to prevent skin maceration. Clients and their families can be instructed about the risk factors of skin breakdown and the interventions to decrease risks.

5) Don't massage reddened skin areas. Redness is indicative of skin damage, a stage I pressure sore. Massaging reddened tissue may increase trauma and result in further damage.5

6) Be aware of the role the dressing plays in the treatment protocol. Dressing should not harm the normal healing process but should protect the sore from mechanical trauma and bacterial contamination.27 If the pressure sore is infected, the dressing should help absorb the exudate and help clean the wound environment.

7) Establish a method for measurement to determine if a pressure sore is healing or deteriorating. If a staging system is used in your institution, all nurses must understand the identification of each stage. Record the size of the sore by measuring the length and width of the sore or take a tracing of the sore. Remember, also, to record the depth of the sore. Note the amount and color of any exudate, the presence or the absence of pain and odor, and the color of the exposed tissue.28 Reassess the sore to determine if the sore is decreasing in size or depth after 5 to 7 days and reassess biweekly thereafter.

8) Use a consistent approach to treatment.29 Care plans should carefully state nursing interventions and steps to complete the treatment protocol. Healing a pressure sore can be a long-term, time-consuming process.

9) To determine the practicality of a chosen intervention consider the cost, ease of application, availability, and response of your client and the nurse to the intervention.

10) Pressure sore formation and the resultant treatment in normally innervated clients may result in pain and discomfort for the client. Analgesics may need to be prescribed and administered, especially before treatments.30

The goal of treatment for a stage I or II sores is to heal the sore. Interventions for stage I or II sores require a moist wound environment for healing. The use of semipermeable occlusive dressings are appropriate with these pressure sores.22,23,31 Semipermeable occlusive dressings are polyurethane films which allow water vapor and oxygen to penetrate the film and keep the wound environment moist for healing. These dressings should not be used with infected, draining wounds. On sacral and ischial sores this type of dressing often rolls up and is difficult to keep over the sore.

A second treatment method is to use wet to wet dressings with Ringer's solution or normal saline.22 These solutions are isotonic, minimizing the loss of fluid, protein, and electrolytes from the body. Wet to wet dressings keep the wound environment moist and do not harm fragile skin cells.

Interventions for stage III and IV pressure sores require a different approach. These sores are often infected, draining, and necrotic. The goal of intervention is to debride and clean the wound environment. Necrotic tissue, if present, must be removed surgically, or mechanically with wet to damp dressing using wide mesh gauze, or by using biomechanical agents which contain enzymes to liquify the necrotic tissue.22,23 Necrotic tissue is a medium for bacterial growth and inhibits granulation tissue. If exudate is present, it must be absorbed by wet to dry dressings or by use of hydrophilic beads, gel, or powder that absorb exudate. Uncontrolled infection in a stage IV sore can lead to serious complications such as osteomyletis, sepsis, and amputation.

Once the wound environment is clean, stage III and IV pressure sores will often require surgical grafts of flaps for closure. The nursing interventions listed in the case study will probably fail to heal the pressure sore because the localized pressure has not been relieved. In addition , the application of an ointment might be causing further damage if a rubbing technique is used for application.

This client would probably benefit from shifts in body weight while sitting and in bed, and decreased sitting time in the wheelchair. The use of wet to wet dressings or semipermeable occlusive dressings would also be appropriate with this client. In addition, adherence to the weight reduction diet, cleansing the skin after incontinence, and periodic evaluation of the serum hemoglobin would decrease these risk factors.

Pressure sore prevention requires the elimination of pressure or relief of pressure at frequent intervals by redistributing the body weight. An understanding of the risk factors and etiologies are essential if nurses are to select the appropriate interventions for their clients. Early detection of stage I sores, redness of the skin, is essential for successful treatment. Research on pressure sore formation and treatments is needed. Nurses must utilize relevant research findings in their nursing practice to treat pressure sores.


  • 1. Kim M, Moritz D: Classification of nursing Diagnoses: Proceedings of the Third and Fourth Conferences. New York, McGrawHill, 1982, pp 312-313.
  • 2. Kosiak M: Etiology and pathology of ischemic ulcers. Arch Phys MedRehabil 1959; 40:62-69.
  • 3. Newson T, Rolfe P: Skin surface p02 and blood flow measurements over the ischial tuberosity. Arch Phys Med Rehabil 1982; 63:553-556.
  • 4. Reiche! S: Shearing force as a factor in decubitus ulcers in paraplegics. JAMA 1958; 166:762-763.
  • 5. Dyson R: Bed Sores - the injuries hospital staff inflict on patients. Nursing Mirror 1978; 146(24):30-32.
  • 6. Bailey B: Bedsores. London, Edward Arnold, 1967.
  • 7. Natow A: Nutrition in prevention and treatment of decubitus ulcers. Topics in Clinical Nursing 1983; 5(2):39-44.
  • 8. Vasile J, Chaitin H: Prognostic factors in decubitus ulcers of the aged. Geriatrics 1972; 27(4):126-129.
  • 9. Iverson-Carpenter M: A Descriptive Study of the Etiologies and Defining Characteristics of Pressure Sore Formation, thesis. University of Iowa, 1985.
  • 10. Stetzer S: An Incidence Study of Pressure Sores, master's thesis. University of Washington, 1970.
  • 11. Williams A: A study of factors contributing to skin breakdown. Nursing Research 1972; 21:238-243.
  • 12. Norton D, McLaren R, Exton-Smith A: An Investigation of Geriatric Nursing Problems in Hospital. London, The National Corporation for the Care of Old People, 1962.
  • 13. Rudd T: The pathogenesis of decubitus ulcers. J Am GeriatrSoc 1962; 10:48-53.
  • 14. Rudd T: The Nursing of the Elderly Sick. London, Faber and Faber, 1966.
  • 15. Peterson N, Bittmann S: The epidemiology of pressure sores. Scand J Pias Reconstr Surg 1971; 5(1):62-66.
  • 16. Gerson L: The incidence of pressure sores in active treatment hospitals, lnt J Nurs Stud 1975; 12:201-204.
  • 17. Gosnell D: An assessment tool to identify pressure sores. Nurs Res 1973; 22:55-58.
  • 18. Barton A: Prevention of pressure sores. Nursing Times 1977; 73(41):1593-1595.
  • 19. Anderson T, Andberg M: Psychosocial factors associated with pressure sores. Arch Phys MedRehabil 1979; 60:341-346.
  • 20. Cull J, Smith O: A preliminary note on demographic and personality correlates of decubitus ulcer incidence. J Psychol 1973; 85:225-227.
  • 21. Shea J: Pressure sores: Classification and management. Clin Orthop 1975; 112:89-100.
  • 22. Seiler W, Stahlein H: Decubitus ulcers: Treatment through five therapeutic principles. Geriatrics 1985; 40(9):30-44.
  • 23. Morley M: 16 steps to better decubitus care. Canadian Nurse 1981; 77(4):29-33.
  • 24. Winter GD: Formation of the scab and the rate of epithelialization of superficial wounds in the skin of the young domestic pig. Nature 1962; 193:293-294.
  • 25. Horsley J, Crane J: Preventing Decubitus Ulcers. CURN Project. New York, Grane and S trattori, 1981.
  • 26. Exton-Smith A, Sherwin R: The prevention of pressure sores: Significance of spontaneous bodily movements. Lancet 1961; 2:1114-1126.
  • 27. Osmet L: The skin in wound healing. Biologic Basis of Wound Healing. Hagerstown, Maryland, Harper and Row, 1975, pp 274-289.
  • 28. Verhonick P: Decubitus ulcer observations measured objectively. Nurs Res 1961; 10:211-214.
  • 29. Tooman T, Patterson J: Decubitus ulcer warfare: Product vs. process. Geriatr Nurs 1984; 5(3): 166-167.
  • 30. Mack S: Care and management of pressure sores. Nursing (London) 1986; 3(6):218-221.
  • 31. Ahmed M: Op-Site for decubitus care. Am J Nurs 1982; 82:61-64.


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