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U N I T 1 3
Integumentary Function
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.
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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.
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Staging and Treatment.
Pressure ulcers can be staged
using four categories.
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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.
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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.
SUMMARY CONCEPTS
■■
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
