Porth's Essentials of Pathophysiology, 4e

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Integumentary Function

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The movements needed to shift the body weight are made unconsciously, and only when movement is restricted do people become aware of discomfort. Shearing forces are caused by the sliding of one tis- sue layer over another with stretching and angulation of blood vessels, causing injury and thrombosis. Shear occurs when the skeleton moves, but the skin remains fixed to an external surface, such as occurs with trans- fer from a stretcher to a bed or pulling a person up in bed. The same thing happens when the head of the bed is elevated, causing the torso to move toward the foot of the bed while friction and moisture cause the skin to remain fixed to the bed linens. Friction contributes to pressure ulceration by damaging the skin at the epidermal–dermal interface. It occurs as persons who are bedridden use their elbows and heels to aid in movement. Moisture contrib- utes to pressure ulcer formation by weakening the cell wall of individual skin cells and by changing the protec- tive pH of the skin. This makes the skin more susceptible to pressure, shear, and friction injury. Prevention andTreatment The prevention of pressure ulcers is preferable to their treatment. 53 Preventive measures include identifying at- risk persons and the specific factors placing them at risk, maintaining and improving tissue tolerance to prevent injury, and protecting the skin and underlying tissue against the adverse effects of external mechanical forces (i.e., pressure, friction, shear). Risk factors contributing to the development of pressure ulcers are those related to sensory perception and the ability to respond meaning- fully to pressure-related discomfort, level of skin mois- ture, urine and fecal continence, nutrition and hydration status, mobility, and circulatory status. Prevention Methods. Methods for preventing pressure ulcers include frequent position changes, meticulous skin care, and frequent and careful observation to detect early signs of skin breakdown. Moisture macerates and injures skin. Sources of moisture include sweat, wound drain- age, urine, and feces. Both urinary and fecal incontinence increase the risk of pressure ulcers. Food crumbs, intra- venous tubing, and other debris in the bed can greatly increase local skin pressure points. Adequate hydra- tion of the stratum corneum appears to protect the skin against mechanical insult. The prevention of dehydra- tion improves the circulation. It also decreases the con- centration of urine, thereby minimizing skin irritation in persons who are incontinent, and it reduces urinary problems that contribute to incontinence. Maintenance of adequate nutrition is important. Anemia and malnu- trition contribute to tissue breakdown and delay healing after tissue injury has occurred. 56 Staging and Treatment. Pressure ulcers can be staged using four categories. 57 Stage I ulcers are characterized by a defined area of persistent redness in lightly pigmented skin or an area of persistent redness with blue or purple hues in darker skin. Stage II ulcers represent a partial- thickness loss of skin involving the epidermis or dermis,

or both. The ulcer is superficial and presents clinically as an abrasion, a blister, or a shallow crater. Stage III ulcers represent a full-thickness skin loss involving dam- age and necrosis of subcutaneous tissue that may extend down to but not through underlying fascia. The ulcer manifests as a deep crater with or without undermining of adjacent tissue. Stage IV ulcers involve full-thickness skin loss and necrosis with extensive destruction or damage to the underlying subcutaneous tissues that may extend to involve muscle, bone, and supporting struc- tures (e.g., tendon or joint capsule). After skin breakdown has occurred, special treatment measures are needed to prevent further ischemic dam- age, reduce bacterial contamination and infection, and promote healing. Treatment methods are selected based on the stage of the ulcer. Stage I ulcers usually are treated with frequent turning and measures to remove pressure. Stage II or III ulcers with little exudate are treated with semipermeable or occlusive dressings. Occlusive dress- ings are credited with preventing the loss of wound fluid and maintaining a moist environment that is necessary for epithelial cell migration. Wound fluid is thought to contain a variety of growth factors that enhance wound healing. Occlusive dressings may also relieve wound pain and prevent bacterial contamination. Several types of occlusive dressings are available, and each has advan- tages and disadvantages. Finally, vasopressure infusions may be important in the healing of pressure ulcers. 54 Necrotic debris increases the possibility of bacterial infection and delays wound healing. Stage III ulcers with exudate and necrotic debris and stage IV ulcers usually require débridement (i.e., removal of necrotic tissue and eschar). This can be done surgically, with wet-to-dry dressings, or through the use of proteolytic enzymes. Stage IV wounds often require packing to obliterate dead space and are covered with nonadherent dressings. Stage IV ulcers may require surgical interventions, such as skin grafts or myocutaneous flaps. ■■ Because the skin covers the body, it is exposed to a number of potentially damaging agents in the external environment. ■■ Repeated exposure to the ultraviolet (UV) rays of the sun predisposes to sunburn, premature aging of the skin (wrinkling, degenerative changes, and irregularities in pigmentation), and skin cancer. Solar and artificial sources of UV radiation, such as from a tanning bed, contribute to the amount of radiation to which human beings are exposed. Sunburn, which is caused by excessive exposure to UV radiation, is an erythematous inflammatory reaction, ranging from mild to severe. Photosensitive drugs can also produce an exaggerated response to UV radiation when SUMMARY CONCEPTS