Skin conditions
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| Functions of the Skin | -thermoregulation
-sensation
-synthesis of Vitamin D
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| Name the layers of the skin | epidermis and dermis
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| Epidermis | -outer layer
-thin (.006 to .6 mm)
-lines hair follicles, sweat and sebaceous glands
-fingernails and toenails
-cellular, avascular- depends on dermis for blood supply
-constantly being renewed (26-42 days)
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| What type of cells is the epidermis made of? | -Keratinocytes= 80-90% of cells in epidermis, produce nails and hair
-Melanocytes= produce melanin (pigment)
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| Functions of the Epidermis | -protection from water loss
-regulates fluid
-protection from shear, friction and toxic irritants
-synthesis of Vitamin D
-pigmentation
-assists with thermoregulation
-outward appearance
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| Dermis | -thickest layer (2-4mm)
-responsible for giving skin its bulk
-is vascularized and innervated
-major proteins are collagen and elastin
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| Two sub layers of the dermis | -Papillary Dermis
-Reticular Dermis
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| Papillary Dermis | -outer most layer of dermis
-forms dermal papillae that contain capillary loops that supply epidermis
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| Reticular Dermis | -forms base of dermis
-contains complex of cutaneous blood vessels
-has thick dense collagenous fibers which give structural support
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| Cells in the Dermis | -Macrophages
-Lymphocytes
-Mast cells
-Fibroblasts
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| Macrophages | phagocytosis of bacteria and damaged tissue
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| Lymphocytes | produce antibodies which helps mediate the immune response in the skin
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| Mast cells | secretory cells that produce chemical mediators of inflammation (histamine)
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| Fibroblasts | secrete collagen and elastin
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| Dermal Proteins | -collagen: major structural protein
-elastin: provides skin with elastic recoil
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| Basement Membrane Zone | -separates dermis from epidermis
-anchors epidermis to dermis
-layer where blisters form
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| Rete Ridges | -basement membrane
-epidermal protrusions into dermis
-height of ridges decrease with age, making you more at risk for skin tears
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| Hypodermis | -subcutaneous tissue forms a layer below dermis
-attaches skin to underlying structures
-composed of loose connective tissue and fat cells
-well supplied (nn & blood)
-subcutaneous fat insulates and protects underlying structures
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| skin changes with age | decreased:
-dermal thickness
-fatty layers, therefore protection loss
-collagen and elastin fibers
-decreased Rete Ridges (easier separation of two layers)
-sensation and metabolism
-sweat glands (dry skin)
-circulation
-epidermal regulation
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| Phases of Wound Healing | 1. Inflammatory
2. Proliferative
3. Remodeling
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| Inflammatory Phase | -lasts 3 to 7 days
-provides hemostasis through platelet aggregation, formation of fibrin clot and vasocinstriction
-provides removal of cellular debris through phagocytosis
-growth factors are released (proteins that regulate and mediate cell activity
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| Signs of Inflammatory Phase | -color change in skin
-increased skin temperature
-increased swelling
-increased pain
-loss of function
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| Proliferative Phase | -3 to 5 days post injury
-overlaps and succeeds inflamm phase
-fills in wound defect through new tissue formation
-processes used are andiogenesis, collagen synthesis and wound contraction
-growth factors help mediate process
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| Important Cells in the Proliferative Phase | -fibroblasts
-myofibroblasts
-endothelial cells
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| Epithelialization | reconstruction of injured epithelium by kerotinocytes
-occurs in the proliferative phase
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| Remodeling Phase | -begins after granulation tissue forms and continues 1-2 years post injury
-increases tensile strength in the scar
-final max strength of scar will be 80% of pre-injury tissue
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| Chronic Wound Characteristics | -failure or delay of healing
-cells unresponsive or senescent
-often caused by disease or condition
-medications such as steroids or immunosuppressive drugs can affect healing
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| What to Include in a Wound Assessment | -Medical History
-Current and past wound history
-medications
-social and psychological history
-Musculoskeletal assessment
-Pain
-Sensation
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| Data About the Wound | -wound location (position on a clock; 12:00=head)
-wound size (measure and tell directions of measurements- also depth)
-tissue type and colors -include % of each
-amount, color and odor of drainage
-condition of skin surrounding
-include a photograp
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| Tunneling | -a small tight area of depth extending out from the wound base
-also referred to as sinus tract or just tract
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| Undermining | -eroded area extending under the skin beyond the visible wound edges
-wider than tunneling
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| Granulation Tissue | temporary scaffolding of vascularized connective tissue
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| Hypergranulation | granulation tissue that has grown above the level of the surrounding skin
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| Necrotic tissue | -slough
-usually yellow or tan
-stringy or soft
-leathery appearance if dry
-Eschar
-black
-can be soft or hard
-usually dry and thick
-indication that underlying damage is most likely severe
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| Attached Wound Edges | -not very deep
-wound heals faster
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| Unattached Wound Edges | usually deeper damage or undermining
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| Defined Wound Edges | associated with deeper wounds
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| Undefined Wound Edges | associated with superficial wounds where epithelialization is occuring
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| Rolled Wound Edges | -indicate chronic wound
-healing can be stalled
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| Turgor | -decreased turgor is a sign of decreased hydration
-Lightly pinch skin. if it does not quickly return to normal shape, sign of decreased turgor
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| Induration | -abnormal firmness surrounding wound bed
-can indicate infection
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| nonblanchable erythema | can indicate ischemic damage due to pressure (important in staging pressure ulcers)
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| Periwound Skin color- Pale | can indicate decreased blood supply
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| Periwound Skin color- blue or ourole | can indicate severe or prolonged ischemia
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| Wound Drainage- Serous | clear or pale yellow, watery consistency
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| Wound Drainage- Sanguinous | red or dark brown, consistency more like blood
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| Wound Drainage- Serosanguinous | red or brown tinted, more watery that sanguinous
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| Wound Drainage- Purulent | -usually yellow, thicker consistency
-can indicate infection or could be liquifying necrotic tissue
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| Wound Drainage- blue or green color | -indicates Pseudomonas infection- notify physician
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| Wound Drainage | -amt documented as minimal, mod, ma, or strike through; based on dressings
-type of dressing and frequency of dressing change can affect amt
-some dressings can alter appearance
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| Wound odor | -documented as present or absent
-can indicate infection
-so occlusive dressing will cause odor (not infection)
-assess for odor throughout treatment as odor may be present on dressings but disappear after wound bed is cleaned
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| Pressure Ulcers | -area of tissue necrosis caused when soft tissue is compressed between a bony prominence and a firm surface over a long period of time
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| Prevalence of Pressure Ulcers | over 1.3-3 million Americans
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| Highest pressure areas (regarding pressure ulcers) | -supine= occiput, sacrum, coccyx, heels
-sitting= ischial tuberosities
-sidelying= trochanters
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| Risk Factors for PUs | -shear
-friction
-moisture
-impaired mobility
-malnutrition
-impaired sensation
-advanced age
-previous pressure ulcer
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| Shear | -force parallel to soft tissue
-common cause is hospital bed with head elevated causing pt to slide down in bed
-stretch on the tissues causes ischemia
-undermining is commonly seen
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| Friction | -caused when two surfaces move across each other
-as in sliding a pt from a bed to a cart
-does not directly cause PUs but can weaken skin and put pt more at risk
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| moisture | -wet skin is more easily abraded, more permeable and more readily colonized by bacteria
-caused by wound drainage, perspiration or incontinence
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| Prevention of Pressure ulcers | -Identify those at risk
-education
-positioning
-mobility
-nutrition
-management of incontinence
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| Scales for assessing PU risk | -Braden Scale for Predicting Pressure Sore Risk
-Norton Risk Assessment Scale
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| Pressure Ulcer: Stage I | -nonblanchable erythema of intact skin
-in those with highly pigmented skin, it may appear purple, blue or violet
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| Pressure Ulcer: Stage II | -partial thickness loss of dermis
-presents as shallow, open ulcer with red/pink bed
-no slough
-may be an intact or rupture blister
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| Pressure Ulcer: Stage III | -full thickness tissue loss
-subcutaneous fat may be visible but no bone, tendon or muscle exposed
-may include undermining or tunneling
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| Pressure Ulcer: Stage IV | -full thickness tissue loss with exposed bone, tendon or muscle
-slough or eschar may be present
-often will have undermining or tunneling
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| Pressure Ulcer: Unstageable | -full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough and/or eschar
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| Pressure Ulcer: Suspected Deep Tissue Injury | -Purple or maroon area of discolored intact skin or blood filled blister
-tissue may be painful, firm, mushy, boggy, warmer or cooler as compared to adjacent skin
-likely to evolve into deeper damage
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| Lower Extremity Arterial Ulcers | -caused by a decrease in arterial blood supply, or arterial insufficiency (PVD or PAD)
-most common etiology is arteriosclerosis
-most common problem seen by vascular surgeons
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| Signs of PAD | -thin atrophic skin
-dependent rubor
-pallor with elevation
-absence of pedal pulses
-non-healing wounds
-muscle wasting
-hair loss
-hypertrophic nails
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| Pathophysiology of PAD/Arterial Ulcers | -decreased delivery of oxygen
-tissue ischemia
-tissue loss
-decreased ability to fight infection
-decreased healing
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| Risk Factors of PAD | -hyperlipidemia
-smoking
-one cigarette decreases wound &
tissue O2 saturation by 30% in
one hour in healthy indiv.
-Diabetes
-increased prevalence of calcific
arterial insufficiency, increased
prevalence of microvascular
disease
-adva
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| Assessing Arterial ulcers | -palpate pedal pulses
-capillary refill (normal < 3 secs)
-rubor of dependency
-Ankle Brachial Index
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| Ankle Brachial Index | (ABI)= non-invasive measure of peripheral tissue perfusion
-ratio of systolic blood pressure of LE to that of UE
-easily done in clinic
-just need hand held doppler and blood pressure cuff
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| Interpreting the ABI | 1.1-1.3= Vessel Calicification
0.9-1.1= Normal
0.7-0.9= Mild to mod arterial insuff.
0.5-0.7= Mod arterial insuff, intermitt claudication
>0.5= Severe areterial insuff, rest pain
>0.3= Rest pain and gangrene
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| Arterial Ulcer characteristics | -usually below the knee
-common on tips & between toes, corners of nail beds, bony prominences
-round, regular appearance w/ well marked edges
-pale, dry base
-skin can't feel cool
-high pain levels
-min to no wound drainage
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| Chronic Venous Insufficiency | -1-2% of pop is diagnosed
-venous insufficiency ulcers are most common type of leg ulcer (70-90% of all ulcers)
-up to 91% pf venous ulcers can be resolved through conservative measures
-recurrence rate ranges from 13 to 81% (often due to noncompliance
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| Signs and Symptoms of Chronic Venous Insufficiency | -pain
-spider veins
-varicose veins
-leg heaviness and fatigue
-swollen limbs
-skin changes and skin ulcers
-hemosiderin staining
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| Hemosiderin staining | caused by RBCs leaked into interstitial fluid
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| Superficial Veins | -just beneath skin
-drain into deep veins through perforator veins
-can form varicose veins
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| Perforator Veins | -connect superficial and deep veins
-perforate deep fascia ans they connect
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| Deep Veins | return blood to the heart
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| Vein Facts | -have thinner walls and increased diameter compared to arteries
-90% of venous blood moves due to the calf muscle pump
-venous insufficiency caused by incompetent valves due to thrombus or venous wall distension causing venous hypertension
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| Fibrin Cuff Theory | -vessel hypertension & distension cause incr in vasc perm
-fluids leak from vessels into interst tissues causing edema
-protein fibrinogen converts to fibrin & adheres to capillary walls
-forming a cuff thats a barrier to xchange of nutr & causes necro
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| White Blood Cell Trapping Theory | -venous hypertension & distension=> congestion
-decr BF => WBC to marginate on vessel walls impeding circulation
-WBCs become activated & begin inflamm process
-WBCs move into interstitium & release inflamm substances, further contribute to cell damage
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| Theories on Etiology of Venous Ulcers | Fibrin Cuff Theory
White Blood Cell Trapping Theory
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| Risk Factors for Venous Ulcers | -vein dysfunction
-calf muscle pump failure
-trauma
-previous venous ulcer
-advanced age
-diabetes
-multiple pregnancies
-obesity
-standing profession
-previous DVT
-family history
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| Lipodematosclerosis | -progressive replacement of skin and subcutaneous tissue by fibrous tissue
-skin will be thick, hard, contracted and tight
-ankle is narrower- "inverted champagne bottle"
-conversion to scar tissue
-sign of long standing venous insufficiency
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| Venous Ulcers | -dull pain or heaviness incr standing
-most common on med aspect of LE or med malleolus
-rarely on knee, never on plantar surface
-superf & irreg w/ mod to high amts of drain
-ruddy gran tissue or slough
-edema
-periwound w/ dermatitis & dry scaling
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| treatment of venous ulcers | *compression
-check ABI before using compression
-underlying arterial disease= contraindication
-lifetime compression (no cure for venous insuff)
-maintenance of edema
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| Incidence of Diabetic/Neuropathic Ulcers | -caused by neuropathy (which is most often caused by diabetes)
-incidence= as high as 25%
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| Incidence of Neuropathy in Diabetes | -30-40% of people with type II
-even higher percentage of people with type I
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| Sensory neuropathy | -loss of sensation (starts in ft & can progress to hands)
-gradual and painless (pt often unaware)
-pt will not detect injury to ft & ulcer can develop
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| Motor Neuropathy | -affects intrinsic mm of ft
-results in weakness & structural changes that cause increased plantar pressures & shear forces, making skin break down more easily
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| Autonomic Neuropathy | -loss of sweat & oil production
-skin integrity is decreased and skin can be dry and cracked, making it vulnerable to breakdown
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| Signs of Neuropathic feet | -clawed toes
-prominent metatarsal heads
-small muscle wasting
-dry, flaky skin
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| Charcot Foot | -Neuropathic fracture and dislocation
-results in structural change in foot; arch reverses ("rocker bottom" foot)
-causes increased plantar pressures
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| Risk Factors for Diabetic Ulceration | -vascular disease
-DM leading risk factor in PVD
-neuropathy
-structural deformity
-trauma and improperly fitted shoes
-history of previous ulcer or amputation
-limited joint mobility
-uncontrolled hyperglycemia
-poor vision (can't see ft to ch
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| Assessment for Diabetic Ulcers | -assess for signs of decreased circulation
-joint ROM & strength
-sensory assessment
-inability to perceive 10g of monofilament indicates loss of protective sensation
-assess for dry skin, foot deformities, callus formation
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| Treatment if Diabetic Ulcers | -refer to vascular surgeon if ABI warrants
-dressing management
-eliminate pressure over wound bed
-change footwear if necessary
*plantar ulcers must be offloaded (different boots/casts available- total contact casting=gold standard)
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| Types of burns | -scalds: liquid, grease, steam
-contact burns
-fire: flash & flame burns
-chemical
-electrical
-radiation
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| Superficial Burns | -compare to 1st degree
-epidermal damage only
-redness, dry skin
-painful to touch
-peeling skin
-blanch with pressure
-complete healing, no scarring
-sunburn/flash injuries
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| Superficial partial Thickness Burns | -compare to 2nd degree
-entire epidermis and upper part of dermis is affected
-blisters
-wet, pink wound beds
-good blood supply
-low risk of infection
-heals in 10-12 days w/o scarring
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| Deep Partial Thickness Burn | -compare to 2nd degree
-epidermis and almost all of dermis affected
-re-epithelialization is very slow
-grafting usually done
-lack of blister formation
-dry, white or charred skin
-minimal pain
-high risk for infection
-healing=2-3 months
-sever
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| Full Thickness Burn | -compare to 3rd and 4th degree
-desruction of entire epidermis and dermis
-absence of pain
-high risk for infetion
-4th degree involves underlying fascia, muscle, bone or other structures
-require extensive debridement and complex reconstruction
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| Debridement | -removal of necrotic tissue, foreign material & debris from wound bed
-reduces bacterial load
-stimulates production/release of growth factors
-facilitates angiogenesis
-eliminates physical barrier to wound healing
-shorten inflamm phase
-decr wound
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| Indications for Debridement | -necrotic tissue is impeding wound healing
-epibole at wound edges
-callus formation periwound
-blisters
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| Contraindications for debridement | -viable tissue
-stable heel ulcers: dry eschar need not be removed if they do not have edema, erythema, fluctuance or drainage
-muscle, tendon, ligament, capsule, fascia, bone, nerves, tendons & blood vessels (surgery)
-gangrenous tissue
-ischemic wou
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| Autolytic debridement | -uses body's own enzymes to digest necrotic tissue through use of moisture-retentive dressing; left in place for several days
-non-invasive
-doesn't destroy healthy tissue (selective)
-may be used along w/ other types of debridement
-painless & simple
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| Enzymatic Debridement | -apply topical debriding agent to devitalized tissue on wound surface
-Collegenase-Santyl: provides selective debr of collegen in necrotic tissue
-selective
-rarely painful
-cross-hatch thick eschar to allow better penetration
-prescription from phys
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| Mechanical Debridement | use of force to remove necrotic tissue, foreign material and debris
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| Wound Scrubbing | -type of mechanical debridement
-use gauze or a sponge
-non-selective so can damage and granulation tissue present
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| Wet to Dry dressings | -type of mechanical debridement
-apply moistened gauze, allow to dry & adhere to wound tissue
-when gauze is removed, tissue 'sticks' and is also removes
-non-selective
-painful
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| Whirlpool in wound debridement | -type of mechanical debridement
-softens necrotic tissue
-increases circulation
-cleanses wound of exudate
-loosens debris
-removes residual topical agents
-hydrates the wound bed
-eases ROM for burn patients
-can decrease pain
-nonselective
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| Consequences of whirlpool in debridement | -may cause maceration
-increase edema
-can disrupt or damage healty granulation tissue
-risk of cross contamination
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| Pulsed Lavage with Suction | -type of mechanical debridement
-pulsed irrigation for cleansing combined w/ suction
-good for large/multiple wound beds
-return suction assists w/ debridement
-can perform bedside
-can be used on tunneling & undermining w/ use of diff application ti
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| Sharp Debridement | -involves use of forceps,scissors,scalpel to remove devitalized tissue
-selective debridement
-fastest methos after surgical interv.
-can be painful (premidicate)
-can be used with other methods
-only certain people can perform
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| Electrical Stimulation on Wound Healing | -efficacy supported by research
-High Volt most common
-after 30 days of failed treatments, Estim is covered my medicare and medicaid
-more appropriate for chronic,nonhealing wounds or patients at risk for wound healing
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| Ultrasound in wound healing | -research not very strong
--indicated for chronic, nonhealing wounds that are clean or infected
-wound bed is covered by protective barrier- transparent film dressing or sheet hydrogel
-fill any depth with NS or hydrogel
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| Negative Pressure Wound Therapy (NPWT) | -sub-atmospheric pressure (suction) applied to wnd
-dressing usually foam w/ semiocclusive film overlay
-edema reduction
-incr in profusion
-tension-stress effect on cells; stim of gran formation w/ foam
-removal of wnd exudate
-promotes wnd contrac
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| Indications for NPWT | -chronic, acute and traumatic wounds
-partial thickness burns
-a wound that has burst open (gap)
-pressure ulcers
-neuropathic ulcers
-muscle flaps
-skin grafts
-can be used over exposed bone, tendon, muscle or hardware
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| Contraindications to NPWT | -wounds with eschar
-wounds with less than 70% gran tissue
-untreated osteomyelitis
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| General Rules for Wound Dressings | -goal is moist wound healing
-a moist wound heals 3-5 times faster than dry wound
-let amt of drainage guide frequency of dressing change but keep to a min
-can be limited by cost & availability
-always cleanse wound bed perform applying dressing
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| primary dressing | -comes in contact with the wound bed
-also known as contact layer
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| secondary dressing | -placed over primary dressing to provide protection, cushioning, absorption or occlusion
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| gauze | -can be used in wound scrubbing or cleansing
-used to fill depth
-removal can be traumatic
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| transparent films | -primary or secondary
-partial thickness wounds
-stage I or II PU's
-low exudating wounds
-see through
-promotes autolytic debridement
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| hydrocolloids | -best for partial and superficial full thickness wounds
-maintains moist environment
-helps clean wounds and promotes autolytic debridement in necrotic wounds
-not recommended for infections
-sometimes causes hypergranulation
-occlusive & can get wet
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| Effects of Estim of Wounds | -incr circulat & decr edema
-inhib bacterial growth
-incr epidermal cell prolif & migration
-incr derminal fibroblastic activity- collagen secretion
-incr phagocytosis bc attraction of macrophages & neutrophils
-lysis of necrotic tissue
-stim gran t
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