Skin Integrity 2 Flashcards

1
Q

pressure ulcers

A

also called pressure injury
- localized injury to skin and/or underlying tissues
– usually over bony prominences
– most common on sacrum and heels
- results from prolonged pressure or pressure in combination with shearing forces
- can be injury related to medical or other devices
- will generally heal by secondary intention

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2
Q

bony prominences (pressure ulcer sites)

A
  • occipital bone
  • scapula
  • spinous processes
  • elbow
  • iliac crest
  • sacrum
  • ischium
  • achilles tendon
  • heel
  • sole
  • ear
  • shoulder
  • anterior iliac spine
  • trochanter
  • thigh
  • medial knee
  • lateral knee
  • lower leg
  • medial malleolus
  • lateral malleolus
  • lateral edge of foot
  • posterior knee
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3
Q

pathophysiology of pressure ulcer

A

(capillaries have pressure on them, are occluded, causing cell death)
pressure on body for prolonged period of time –> stops capillary flow to tissues –>
deprives tissues of oxygen and nutrients –>
cell death + tissue necrosis

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4
Q

influencing factors

A
  • pressure intensity: amount of pressure
  • pressure duration: length of time pressure is exerted on the skin
  • tissue tolerance factors: ability of tissue to tolerate the pressure, nutrition, perfusion, co-morbidities, condition of soft tissue
  • shearing forces: when skin adheres to a surface and skin layers slide in direction of body movement
  • moisture: excessive moisture that leads to skin breakdown
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5
Q

risk factors

A
  • advanced age
  • anemia: lack of oxygen to tissue bc oxygen travels on RBC and low RBC
  • diabetes
  • elevated body temperature: more sweating, moisture
  • friction
  • immobility
  • impaired circulation
  • incontinence
  • low diastolic BP (less than 60 mmHg): not getting enough perfusion so tissues aren’t getting enough oxygen
  • mental deterioration: may have restraints and bed alarm so aren’t getting up and walking
  • neurologic disorders: not getting up and walking
  • obesity
  • pain: not getting up and walking
  • prolonged surgery: laying one way for long time means reddened area
  • vascular disease
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6
Q

clinical manifestations

A
  • depends on extent of tissue involved
  • staged/categorized based on visible or palpable tissue in the ulcer bed
  • staging is based on the National Pressure Ulcer Advisory Panel (NPUAP) guidelines
  • stage 1 (minor) to stage 4 (severe)
  • presence of slough or eschar may prevent staging until it is removed
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7
Q

suspected deep tissue injury

A

INTACT SKIN
- purple or maroon localized area of discolored intact skin or blood-filled blister
- indicates damage of underlying soft tissue from pressure and/or shear
- may be preceded by tissue that is painful, firm, mushy, or boggy
- may be difficult to detect in patients with dark skin tones

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8
Q

skin assessment for patients with dark skin

A
  • darker areas of skin: look for areas of skin that are darker than surrounding skin, these may appear purple, brown or blue
  • skin temperature: use your hand to assess skin. an ulceration may feel warm initially, then become cooler with time.
  • skin/tissue consistence: apply gentle pressure to common sites of injury to feel consistency. boggy or edematous tissue may indicate a stage 1 pressure ulcer.
  • patient sensation: patients may also report pain or itchy sensation.
    (look at where edges may be and look for color difference, any differencs in temp, sensation and consistency)
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9
Q

stage 1 pressure ulcer

A
  • intact skin: non-blanchable redness of a localized area
  • common over bony prominence
  • may be painful, firm, soft, warmer, or cooler as compared to adjacent tissue
  • darkly pigmented skin may not have visible blanching, but color may differ from the surrounding area
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10
Q

stage 2 pressure ulcer

A

LOST THE EPIDERMIS (from 1 to 2)
- partial-thickness loss of dermis
- shallow open ulcer with red/pink wound bed
- may also present as an intact or ruptured serum-filled blister
- can be a shiny or dry shallow ulcer without slough or bruising
- adipose (fat) is not visible, and deeper tissues are not visible
- granulation tissue, slough, and eschar are not present

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11
Q

stage 3 pressure ulcer

A

LOST THE DERMIS, can see subq tissue
- full-thickness skin loss
- subcutaneous tissue may be visible, but bone, tendon or muscle are not
- presents as deep crater with possible undermining of adjacent tissue
- ulcer depth varies by location, depending on depth of tissue in that area

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12
Q

stage 4 pressure ulcer

A
  • full-thickness loss, extends to muscle, bone, or supporting structures
  • bone, tendon, or muscle may be visible or palpable
  • slough or eschar may be present on some parts of wound bed
  • undermining (wound goes underneath skin to the side) and tunneling (deep towards the bone it goes) may also occur
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13
Q

unstageable ulcer

A
  • full-thickness tissue loss in which actual depth or ulcer is completely obscured by slough or eschar in wound bed
  • slough may be yellow, tan, green, grey, or brown
  • eschar may be tan, brown, or black in the wound bed
  • slough or eschar may be removed to expose the base of the wound in order to stage
  • note: stable, dry eschar on heels should not be removed
    (typically not debrided bc don’t know how far down it goes)
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14
Q

complications of pressure ulcers

A

(infection is #1 complication to avoid)
- infection:
– leukocytosis: why WBCs increase count
– fever
– increased ulcer size, odor, or drainage
– necrotic tissue
– indurated, warm, painful
- untreated ulcers may lead to cellulitis, with spread of inflammation/infection to subcutaneous tissue, connective tissue, bone (osteomyelitis), can lead to sepsis and death
- most common complication is recurrence of tissue breakdown/repeat pressure ulcers.

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15
Q

complications of pressure injuries details

A
  • recurrence of tissue breakdown/repeat pressure injuries
  • infection: signs of infection include swelling, redness, and foul odor **
    – leukocytosis **
    – fever **
    – necrotic tissue **
    – increased injury size, odor, or drainage **
  • cellulitis: can lead to sepsis and death
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16
Q

nurses play a critical role in the prevention and treatment

A
  • assess skin of every patient on admission and every shift
  • assess all patients for risk for skin breakdown every 12 hours
  • stage 3 and 4 pressure injuries acquired after admission: never want to happen
17
Q

pressure ulcer prevention

A
  • pressure redistribution
  • keep skin dry: if incontinent clean with no-rinse perineal cleaner and supply barrier ointment
  • reposition:
    – drawsheet or transfer board
    – position patient at 30 degrees lateral position
    – HOB at 30 degrees or less
    – trapeze bar
  • turning schedule
  • nutrition and fluid intake
18
Q

care planning

A
  • prevent deterioration
  • reduce factors that contribute to pressure and skin breakdown
  • prevent infection
  • promote healing
  • prevent recurrence
19
Q

what to do when patient has pressure injury

A
  • document stage, size, location, exudate, infection, pain and tissue appearance
  • some facilities require pictures of pressure ulcer in EMR, have special cameras
  • wound care specialists will determine specific cleansing protocol and which types of dressings are appropriate, but general principles:
    – clean with normal saline to avoid damaging cells
    – keep slightly moist to encourage re-epithelialization
  • surgical treatment may be necessary: skin grafts, skin flaps, or musculocutaneous flaps are all surgical interventions to aid in healing
20
Q

patient and family teaching

A
  • teach prevention techniques to patient and caregivers, including early signs of skin breakdown and tissue injury
  • continued nutritional support
  • pressure ulcer care techniques, wound care at home
  • turning schedule
21
Q

lower extremity ulcers

A
  • different pathophysiology from pressure ulcers
  • in general, related to changes in blood flow to lower extremities due to chronic disease processes
22
Q

arterial ulcers

A
  • peripheral artery disease (PAD) causes problems with blood flow in arteries, becoming narrow or blocked, usually caused by atherosclerosis
  • ulcers are caused by ischemia and nutrition deprivation as a result of decreased circulation
  • skin will be thin, shiny, and dry, with loss of hair on ankles, feet
  • those with atherosclerosis, PVD, diabetes, smoking, hypertension, advanced age, obesity, and cardiovascular disease are at increased risk
23
Q

arterial ulcers details

A

(pale, even margins, deep, very painful)
- may be found between toes or on tips of toes, on phalangeal head, lateral malleolus, or areas with rubbing footwear
- even wound margins, punched-out appearance, pale, deep wound bed
- extremely painful, with minimal exudate
- must revascularize with stents to treat ischemia, then topical treatments will help with healing ulcer

24
Q

venous leg ulcers

A
  • venous insufficiency occurs when blood cannot flow upward from veins in the legs
  • chronic venous insufficiency occurs when valves are damaged, allowing blood to leak backward, resulting in venous stasis
  • those with obesity, deep vein thrombosis (DVT), pregnancy, incompetent valves, congestive heart failure (CHF), muscle weakness, decreased activity, advanced age, and family history are at increased risk
25
Q

venous leg ulcer details

A

(irregular margins, red and ruddy, not as painful)
- found in lower legs, have irregular wound margins and superficial, ruddy granular tissue
- painless to moderately painful
- surrounding skin may be red, scaly, weepy, and thin
- compression therapy promotes blood return and prevents blood from pooling

26
Q

diabetic ulcers

A
  • caused by peripheral neuropathy, fissures in skin and decreased ability to fight infection, as well as diabetic foot deformities caused by damage to ligaments and destruction of bone (neuropathy deteriorates the nerves in the foot, so can’t feel ulcers forming)
  • located on plantar aspect of foot, over metatarsal heads, under heels and on toes (bony prominences)
  • painless, even wound margins, rounded or oblong shape with surrounding callous
  • can easily turn into cellulitis or osteomyelitis
  • treatment includes removing stress/pressure from injured site, debriding wound, antibiotics if infection occurs
27
Q

cellulitis

A
  • inflammation of subq tissue, often following break in skin
  • staph and strep most often causes of infection
  • deep inflammation of subq tissue caused by enzymes produced by bacteria
  • hot, tender, erythematous, edematous area with diffuse borders
  • chills, malaise, and fever
28
Q

cellulitis treatment

A
  • moist heat, immobilization, elevation
  • systemic antibiotic therapy
  • hospitalization if IV therapy warranted (severe infections)
  • progression to gangrene if left untreated
29
Q

treatment of skin and wound infections

A

most important treatment for infection is prevention **
skin and soft tissue infections can be treated with:
- cephalosporins
- some penicillins (narrow-spectrum pen)
- carbapenems
- vancomycin
- clindamycin
- linezolid
- daptomycin
- levofloxacin

30
Q

antibiotic resistance

A
  • the emergence of resistance to antibiotics is a major concern
  • bacteria acquire resistance through conjugation, where DNA coding for drug resistance is transferred from one bacterium to another
  • antibiotics do not cause genetic changes, but they promote emergence of drug-resistant organisms by creating selection pressures that favor them.
  • broad-spectrum antibiotics promote more resistance than narrow-spectrum antibiotics.
  • prevention of resistance includes preventing infection, diagnosing and treating infection effectively, using antimicrobial drugs wisely, preventing patient-to-patient transmission of infections.
  • viral infections cannot be treated with antibiotics.
31
Q

psoriasis

A
  • common, chronic autoimmune inflammatory disorder characterized by plaque formation with varying degrees of severity
  • mild: red patches covered with silvery scales ** on scalp, elbows, knees, palms and soles
  • severe: may involve entire skin surface and mucous membranes, superficial pustules, high fever, leukocytosis, and painful fissuring of the skin
  • 2 processes: accelerated maturation of epidermal cells, excessive activity of inflammatory cells
32
Q

psoriasis treatment overview

A
  • goal is to reduce inflammation, suppress rapid turnover of epidermal cells, no cure
  • topical treatments: glucocorticoids, vitamin D3 analogs, tazarotene, salicylic acid, anthralin, tars
  • systemic treatments: methotrexate, cyclosporine, biologics (adalimumab, etanercept, others)
  • phototherapy: coal plus tar plus UVB irradiation, photochemotherapy (PUVA therapy), sunlight**
33
Q

psoriasis topical treatments

A
  • glucocorticoids: most commonly used, suppress inflammatory cells
    – high potency agents shouldn’t be used on face, groin, axilla, or genitalia
  • vitamin D3 analogs: calcipotriene, calcitriol
    – inhibit proliferation of keratinocytes
    – adverse effects mild, may include itching, irritation, and erythema
  • tars: suppress DNA synthesis, mitotic activity, and cell proliferation
    – coal tar is used most often, may be found in shampoos, lotions, creams
    – unpleasant odor, can cause irritation, stinging, burning
    – can stain skin and hair
34
Q

psoriasis systemic treatments

A

methotrexate: cytotoxic agent, given PO, IM, or IV
- helps with psoriasis by reducing proliferation of epidermal cells
- highly toxic, should be used only in patients with severe, debilitating psoriasis that has not responded to other therapy
- adverse effects: GI upset, blood dyscrasias, bone marrow suppression, must monitor hepatic function. pregnancy must be avoided.

biologic agents: adalimumab, etanercept, given subQ or IV
- most block tumor necrosis factor (TNF)
- suppress immune function, leading to decreased inflammation in psoriasis
- very effective, first line for severe psoriasis
- potential for serious opportunistic infections due to immunosuppressant activity

35
Q

psoriasis treatment (sun and phototherapy)

A
  • safe sun exposure (sunlight)
  • phototherapy
    – coal tar plus ultraviolet B irradiation
    — affected area covered with 1% coal tar ointment for 8-10 hours, washed off, area then exposed to UVB light
    — expensive and time-consuming treatment, very safe, remission in 80% of patients, up to 30 treatments necessary
    – photochemotherapy (PUVA therapy)
    — orally-administered photosensitive drug combined with UVA light therapy
    — alters DNA structure, decreases proliferation of epidermal cells
    — adverse effects: pruritus, nausea, erythema
    — may also accelerate aging of skin and increase risk of skin cancer
    — indicated for extensive, active psoriasis
36
Q

psoriasis patients should avoid

A
  • scrubbing
  • long exposures to water
  • trying to remove scales