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Basic PT Skills F10

Skin conditions

Functions of the Skin -thermoregulation -sensation -synthesis of Vitamin D
Name the layers of the skin epidermis and dermis
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)
What type of cells is the epidermis made of? -Keratinocytes= 80-90% of cells in epidermis, produce nails and hair -Melanocytes= produce melanin (pigment)
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
Dermis -thickest layer (2-4mm) -responsible for giving skin its bulk -is vascularized and innervated -major proteins are collagen and elastin
Two sub layers of the dermis -Papillary Dermis -Reticular Dermis
Papillary Dermis -outer most layer of dermis -forms dermal papillae that contain capillary loops that supply epidermis
Reticular Dermis -forms base of dermis -contains complex of cutaneous blood vessels -has thick dense collagenous fibers which give structural support
Cells in the Dermis -Macrophages -Lymphocytes -Mast cells -Fibroblasts
Macrophages phagocytosis of bacteria and damaged tissue
Lymphocytes produce antibodies which helps mediate the immune response in the skin
Mast cells secretory cells that produce chemical mediators of inflammation (histamine)
Fibroblasts secrete collagen and elastin
Dermal Proteins -collagen: major structural protein -elastin: provides skin with elastic recoil
Basement Membrane Zone -separates dermis from epidermis -anchors epidermis to dermis -layer where blisters form
Rete Ridges -basement membrane -epidermal protrusions into dermis -height of ridges decrease with age, making you more at risk for skin tears
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
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
Phases of Wound Healing 1. Inflammatory 2. Proliferative 3. Remodeling
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
Signs of Inflammatory Phase -color change in skin -increased skin temperature -increased swelling -increased pain -loss of function
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
Important Cells in the Proliferative Phase -fibroblasts -myofibroblasts -endothelial cells
Epithelialization reconstruction of injured epithelium by kerotinocytes -occurs in the proliferative phase
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
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
What to Include in a Wound Assessment -Medical History -Current and past wound history -medications -social and psychological history -Musculoskeletal assessment -Pain -Sensation
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
Tunneling -a small tight area of depth extending out from the wound base -also referred to as sinus tract or just tract
Undermining -eroded area extending under the skin beyond the visible wound edges -wider than tunneling
Granulation Tissue temporary scaffolding of vascularized connective tissue
Hypergranulation granulation tissue that has grown above the level of the surrounding skin
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
Attached Wound Edges -not very deep -wound heals faster
Unattached Wound Edges usually deeper damage or undermining
Defined Wound Edges associated with deeper wounds
Undefined Wound Edges associated with superficial wounds where epithelialization is occuring
Rolled Wound Edges -indicate chronic wound -healing can be stalled
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
Induration -abnormal firmness surrounding wound bed -can indicate infection
nonblanchable erythema can indicate ischemic damage due to pressure (important in staging pressure ulcers)
Periwound Skin color- Pale can indicate decreased blood supply
Periwound Skin color- blue or ourole can indicate severe or prolonged ischemia
Wound Drainage- Serous clear or pale yellow, watery consistency
Wound Drainage- Sanguinous red or dark brown, consistency more like blood
Wound Drainage- Serosanguinous red or brown tinted, more watery that sanguinous
Wound Drainage- Purulent -usually yellow, thicker consistency -can indicate infection or could be liquifying necrotic tissue
Wound Drainage- blue or green color -indicates Pseudomonas infection- notify physician
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
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
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
Prevalence of Pressure Ulcers over 1.3-3 million Americans
Highest pressure areas (regarding pressure ulcers) -supine= occiput, sacrum, coccyx, heels -sitting= ischial tuberosities -sidelying= trochanters
Risk Factors for PUs -shear -friction -moisture -impaired mobility -malnutrition -impaired sensation -advanced age -previous pressure ulcer
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
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
moisture -wet skin is more easily abraded, more permeable and more readily colonized by bacteria -caused by wound drainage, perspiration or incontinence
Prevention of Pressure ulcers -Identify those at risk -education -positioning -mobility -nutrition -management of incontinence
Scales for assessing PU risk -Braden Scale for Predicting Pressure Sore Risk -Norton Risk Assessment Scale
Pressure Ulcer: Stage I -nonblanchable erythema of intact skin -in those with highly pigmented skin, it may appear purple, blue or violet
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
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
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
Pressure Ulcer: Unstageable -full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough and/or eschar
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
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
Signs of PAD -thin atrophic skin -dependent rubor -pallor with elevation -absence of pedal pulses -non-healing wounds -muscle wasting -hair loss -hypertrophic nails
Pathophysiology of PAD/Arterial Ulcers -decreased delivery of oxygen -tissue ischemia -tissue loss -decreased ability to fight infection -decreased healing
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
Assessing Arterial ulcers -palpate pedal pulses -capillary refill (normal < 3 secs) -rubor of dependency -Ankle Brachial Index
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
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
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
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
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
Hemosiderin staining caused by RBCs leaked into interstitial fluid
Superficial Veins -just beneath skin -drain into deep veins through perforator veins -can form varicose veins
Perforator Veins -connect superficial and deep veins -perforate deep fascia ans they connect
Deep Veins return blood to the heart
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
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
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
Theories on Etiology of Venous Ulcers Fibrin Cuff Theory White Blood Cell Trapping Theory
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
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
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
treatment of venous ulcers *compression -check ABI before using compression -underlying arterial disease= contraindication -lifetime compression (no cure for venous insuff) -maintenance of edema
Incidence of Diabetic/Neuropathic Ulcers -caused by neuropathy (which is most often caused by diabetes) -incidence= as high as 25%
Incidence of Neuropathy in Diabetes -30-40% of people with type II -even higher percentage of people with type I
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
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
Autonomic Neuropathy -loss of sweat & oil production -skin integrity is decreased and skin can be dry and cracked, making it vulnerable to breakdown
Signs of Neuropathic feet -clawed toes -prominent metatarsal heads -small muscle wasting -dry, flaky skin
Charcot Foot -Neuropathic fracture and dislocation -results in structural change in foot; arch reverses ("rocker bottom" foot) -causes increased plantar pressures
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
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
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)
Types of burns -scalds: liquid, grease, steam -contact burns -fire: flash & flame burns -chemical -electrical -radiation
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
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
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
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
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
Indications for Debridement -necrotic tissue is impeding wound healing -epibole at wound edges -callus formation periwound -blisters
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
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
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
Mechanical Debridement use of force to remove necrotic tissue, foreign material and debris
Wound Scrubbing -type of mechanical debridement -use gauze or a sponge -non-selective so can damage and granulation tissue present
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
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
Consequences of whirlpool in debridement -may cause maceration -increase edema -can disrupt or damage healty granulation tissue -risk of cross contamination
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
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
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
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
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
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
Contraindications to NPWT -wounds with eschar -wounds with less than 70% gran tissue -untreated osteomyelitis
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
primary dressing -comes in contact with the wound bed -also known as contact layer
secondary dressing -placed over primary dressing to provide protection, cushioning, absorption or occlusion
gauze -can be used in wound scrubbing or cleansing -used to fill depth -removal can be traumatic
transparent films -primary or secondary -partial thickness wounds -stage I or II PU's -low exudating wounds -see through -promotes autolytic debridement
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
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
Created by: CWestrick



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