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Integ 3 exam

Quiz yourself by thinking what should be in each of the black spaces below before clicking on it to display the answer.
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Question
Answer
conventional Tx for all wounds   incorporates common principles & Tx targeted to characteristics of each and the patient's clinical characteristics  
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Incorporates common principles   debridement of necroti tissue, maintainence of moist wound bed, control of infection  
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Tx targeted to characteristics of each wound and the patient's clinical characteristics   appropriate intensity of Tx delivery & no widely accepted, standardized protocols  
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Tx of chronic ulcers   based on understanding of biological and pathological events in normal wound healing (growth factor, tissue engineered skin, adjunctive physical agents)  
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Adjunctive physical agents:   dressings (moist), low level laser therapy, utrasound, ultra-violet, hyperbaric O2, electrical stimulation (hi-voltage pulsed or DC), electro -magnetic field stimulation (Diathermy)  
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contraindications to electrical stimulation   osteomyelitis, malignancies/neoplasms, carotid sinus/laryngeal muscles, pacemakers, through the thorax, phrenic nerve distribution, over topical agents containing metal ions (iodine, mercurochrome)  
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classification of Ulcers:   5P + T  
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classification of ulcers:   postion, presentation, pain, periwound, pulses, & temperature  
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Postion of the body   anatomical reference points  
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presentation   shape/drainage/color  
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pain   present/absent/severity  
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periwound   condition and structural changes of the surrounding skin  
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pulses   present/absent/dimished  
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temperature   surrounding skin  
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3 types of vascular ulcers   arterial insufficiency, chronic venous insufficiency, DM (nueuropathic)  
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Arterial insufficiency   pain=severe, position (toes/anterior or lateral leg)  
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chronic venous insufficiency   pain=mild to none, position (medial ankle and leg)  
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DM (Neuropathic)   pain=none, position(plantar surface of foot) (MET heads)  
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vascular ulcers: wound   pale wound base, atrophic skin, dry wound, red base, periwound skin staining, wet wound, periwound callous, infection  
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Background Hx for PAD   50 yr old male or older, DM, smoker, sedentary/immobile, circulatory disorders  
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circulatory disorders   (cardiac disease, CVA, PVD, HTN, Family Hx of premature ishemic heart disease, hyperhyperlipidemia/hypercholesterolemia (high levels of LDL))  
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background Hx for venous insufficiency   increasing age, DM, sedentary/immobility, cirulatory disorders (varicose veins, edema, DVT, HTN), multiple pregnancies, Trauma (previous surgery, Fx or injuries), obesity, employment requires standing  
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mortality/morbidity in arterial insufficiency   # of yrs of follow-up 5, 10, 15 mortality rates for individuals with claudication 30%, 50%, 70%  
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when does atherosclerosis occur   earlier and more often in persons with DM  
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what does complete acute ischemia cause   extensive tissue necrosis w/n 6 hrs  
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what does amputation depend upon   the number and severity of diseases affecting the peripheral vasculature (ischemia, HTN, diabetes, smoking)  
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Where does atherosclerosis occur   tunica intima; damaged and scarred by high levels of LDL (triggers biochemical changes); plaque (fat and blood by products) deposit in the arterial walls, insidious tissue ischemia  
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etilogy of arterial insufficiency   slowly progressive stenosis (>50%) and thickening of the capillary membrane (decrease blood flow)  
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Decrease blood flow: acute   intermittent claudication, thrombosis, embolus  
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decrease blood flow: chronic   ischemic rest pain, gangrene, ulcers  
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Atherosclerosis: Medical Management   balloon angioplasty, stent, endarterectomy (surgical removal of plaque)  
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Normal response of arterial system   no pain or prolonged pallor, limb elevation ~60 degrees for 1 min should not cause pallor or pain, limb dependency should cause color to return in <15-20 seconds  
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ischemic response of arterial system   limb elevation will be more painful, resting in bed will be more painful, limb dependency: standing, walking, hanging LE over the side of the bed relieves pain  
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S&S early peripheral arterial disease   skin trophic changes, pulses, wound characterisitics, ishemic pain or paresthesia  
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skin trophic changes   hair loss, dry & flaky, shiny, elevation pallor or dependent cyanosis, cool temperature, & thickened nails  
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pulses   decreased/absent  
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wound characteristics   absent granulation, gangrene, minimal drainage-dry  
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ischemic pain or paresthesia   intermittent claudication & resting limb pain  
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CLINICAL tests and measures for ischemia   capillary refill (compress 5 secs/ refill in <3 secs); Allen test (UE); intermittent claudication; pulses; elevation pallor and rubor of dependency; ABI  
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Allen test   (UE circulation)  
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Allen test:   to test the patency of the Radial (R) and ulnar (U) arteries; compress the R and U arteries at wrist (palm up), while the patient clenches his/her fist (palm should blanch), patient opens hand and either the R/U artery is released, repeat for other artery  
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Interpretation of Allen test   color of the palm should return to normal in 5-10 seconds on side released  
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intermittent claudication   local ischemia and or limb wkness with activity, c/o calf, thigh or buttock pain when walking/active, note time and distance walked before needing rest, pain usually perceived one segment distal to the obstruction  
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toe pan usually reflects   a mid-foot occlusion  
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calf pain a   knee or distal thigh occlusion  
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"cramping"   pain worse with activity or exercise  
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pain relieved with   rest in the dependent position  
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buerger's sign/elevation pallor test   supine, check for delayed and exaggerated hyperemia; increased local blood flow (supine, elevation ~60% x 1 minute) stop watch to time elevation, and recovery at rest  
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Positive test (buerger's sign)   pallor w/n 25 secs combined with dependent rubor of the feet  
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burger's sign/elevation pallor interpretation   (unlimited, no pallor, normal); (45-60, pallor, mild); (30-45, pallor, moderate); (25, pallor, severe); (unable, pallor in supine, most severe)  
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Pallor Grading from least to most severe   ~60% elevation to test  
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Rubor of Dependency   When the extremity is dependent (positive test= an ischemic extremity will slowly change color; white, to pink, to a flushed purple-red color)  
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Doppler Ultrasound- ABI   segmental pressure measurements: ABI calcualted using the highest brachial pressure.  
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characteristics of arterial ulcers: 5P + T   position, presentation, periwound, pain, pulses, pallor, temp  
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Position   dorsum of foot, interdigitial spaces, over toes, lateral leg; NWB areas of the feet (posterior aspect of the heel, Margins of the foot (especially the medial aspect of the first and lateral aspect of the fifth metatarsophalangeal joints, tips of the toes  
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Presentation and Periwound   Symmetrical, "punched out", little to no drainage, pallid, Deep (tendon or bone may be exposed if the ischemia is severe)  
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Aterial ulcers are often sloughy   (yellow base)  
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Pain/paresthesia   intermittent claudication, resting limb pain (severe, frequently at night in bed or when the LEs are elevated)  
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Pulses   diminished or absent  
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Temperature   Cold  
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Signs to look for: Arterial Ulcers: 5P+T (slide32)   e.g. poor granulation (50% pink, 50% yellow slough), cellulitis, Maceration, Trophic changes, Edema??  
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Ischemic skin changes: Pallor (slide 33)   pale, mottled, distal erythema, early ulceration of the great toe, amputated 4th digit  
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Ischemic Skin Changes (slide 34)   atherosclerosis obliterans (distal ischemia and dry gangrene with forefoot hyperemia); "blue or purple"  
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Ishemic Skin changes (slide 35)   Atheroembolism: cutaneous arterial infarctions (spontaneous or after intravascular surgery or procedures); arteries occluded atherosclerotic plaque fragments  
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Predictors of healing   ABI>0.5; ankle pressure>70mmHg, Toe pressure> 50mmHg  
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Ankle Pressure (healing)   >70mmHg  
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Toe pressure (healing)   >50mmHg  
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TCPO2   >40mmHg (supine)  
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Differential Diagnosis   intermittent claudication, painful foot, ischemic & infarctive lesions of leg/foot  
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intermittent claudication   buerger's disease (thromboangitis obliterans), arthritis, gout  
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painful foot   gout, morton's neuroma, onychomycosis with in-grown toenails, pes planus, calcanean buritis, plantar fascitis  
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ischemic and infarctive lesions of leg/foot   vasculitis, raynaud's phenomenon (vasospasm), embolization, drug induced necrosis (warfarin, heparin), external compression (popliteal entrapment)  
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raynaud's phenomenon/complex regional pain syndrome   associated with RA, SLE and scleroderma  
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PT interventions   ther ex: gait and mobility training, positoning, graded aerobic exercises, stretching (prescribe, apply or fabricate orthotic and assitive devices, physical agents)  
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Venous insufficiency S&S   edema/heaviness/tired legs:resolve at night, varicosities (incompetent valves), DVT, pain & fatigue (cramps, itching, burning, aching-worse with prolonged standing, improveswith leg elevation), dependent cyanosis, dermatitis, lipodermatosclerosis  
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venous insufficiency   hemosederin staining  
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DVT risk factors   female over 40, prior LE trauma (surgery, pregnancy, cancer), obesity, immobility (bed rest), standing for long periods, cardiac disease, varicosities (telangiectasias)  
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Surgical procedures: Venous insufficiency   none safe/effective for deep venous insufficiency, experimental, low success and high complication rates, superficial vein Tx (ablation: sclerotherapy, ligation, and stripping-outcomes equivalent, beware complications and recurrence)  
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venous insufficiency   Ablation: sclerotherapy, ligation and stripping (outcomes equivalent/beware complications and recurrence); laser and radio-frequency (non-invasive, better outcomes)  
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DVT   fatal if it is massive, can cause a pulmonary emboli (PE) (usually localized in the deep veins of the calf but can extend into the thigh and beyond)  
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Venous valve failure   retrograde blood flow dramatically increases the hydrostatic venous pressure in the LE (incompetent deep veins valves: deep venous thrombosis (DVT); No valves to prevent deep system reflux; incompetent superificial vein valves  
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venous valve failure   incompetent superficial vein valves: venous blood escapes from a normal deep system and flows backwards through dialted superficial veins in which the valves have failed  
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gravity effects on venous flow   during ambulation(normal venous pressure is ~ zero), standing(the leg veins fill slowly, venous pressure=the hydrostatic press. of a column of blood as high as the nearest competent valve), prolonged standing  
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prolonged standing   the veins fill completely (all venous valves flat open); high hydrostatic venous pressure= the unbroken column of fluid that extends from the head to the foot  
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prevention of hypertension   3 major mechanisms: Bicuspid valves, calf muscles, respiratory pump  
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Differential diagnosis: Venous insufficiency   kidney or renal failur, CHF, infection,trauma, lymphedema  
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Clinical tests and measures for venous insufficiency   observation, diagnostic imaging, Homan's sign, venous filling time, Brodie-Trendelenburg Test  
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Observation for venous insufficiency   varicosities  
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Diagnostic imaging for venous insufficiency   duplex venous ultrasound, ABI- use compression if >.7, venography,& magnetic resonance venography  
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superficial vein thrombosis:aka   phlebitis  
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superficial vein thrombosis (phlebitis)   edematous, red and painful to touch  
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Duplex imaging   duplex ultrasonography (non-invasive)  
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Venography   "GOLD STANDARD"  
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Magnetic resonance venography (MRV)   most sensitive and specific test for inaccessible areas, helps detect other nonvasular causes of pain and edema  
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Brodie-Trendelenburg (unreliable)   supine observe for distention, elevate 45deg., apply tourniquet around proximal thigh for 1 min., stand for 1 min., repeat pressure at any point along the leg until the level of the incompetence is identified, positive sign(rapid vein distention/guttering  
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Brodie-Trendelenburg test interpertation: time until distention (seconds)- possible pathology   < 10=superficial vein incompetence; <20= Deep perforator vein incompetence  
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Homan's Sign (not sensitive)   positive=calf pain elicited by: ankle DF with knee ext. OR deep palpation of gastronemius muscle; Quick and non-invasive  
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Venous Fillling Time interpretation:   same procedure as elevation pallor/rubor; sitting (dependent) position after extremity elevation  
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Seconds until color returns in superficial veins with dependency:   <5 (venous insufficiency), 5-15 (normal), >20 Arterial insufficiency  
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Characterisitcs of Venous: 5P + T   position, presentation, periwound, pain, temp  
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Position   below the knee, gaiter area, trauma sites  
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presentation   shallow, irregular shaped; pitting pedal edema  
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periwound   hemosiderin pigment (RBC lysis); brown or mottled reddish skin color; cellulitits, dermatitis  
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Lipodermato-sclerosis   "Champagne Bottle" or "piano leg" appearance(the ankle is relatively thin and the upper calf edematous); edema causes skin breakdown and infection  
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Venous Insufficiency Ulcers:   Pain-minimal, relieved by elevation or compression; Pulses-present, normal; Temperature-local warmth  
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Chronic Stasis (slide 63)   stuck in inflammatory phase  
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Normally Healing venous stasis ulcer:   overlapping healing phases: granulation tissue, reepithelialzation, wound contracting  
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Chronic Stasis   Hemosiderin pigment (RBC lysis): Brownish discoloration or hyper-pigmentation in darker-skinned individuals  
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Chronic Dermatitis   scratch marks indicate peri-wound skin itchiness (pruritis)  
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Graduated LE Compression stockings (20-30mmHg)   effectively compress superficial and deep veins in supine, not standing; varicosed legs, mid-calf stockings did not compress the long saphenous vein even when supine  
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Graduated LE compression stckings (20-30 mmHg)   upper band of the stocking constricted the long saphenous vein, perhaps why incdence of superficial venous thrombosis increases with wearing of compression stockings  
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Class 1 garment   20-30 mmHg; UE; prophylatic:varicose veins, mild edema, pregnancy  
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Class 2 garment   30-40mmHg; UE; moderate to severe varicose veins, mild edema, small ulcers, prevention  
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Class 3 garment   40-50mmHg; LE; severe varicose veins, chronic venous insufficiency, ulcers, prevention  
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Class 4 garment   60+mmHg; LE; severe  
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GOLD STANDARD Tx for venous Ulcers   External compression: graduated external compression can help to minimize or reverse skin and vascular changes, by forcing fluid from interstitial spaces back into the vascular and lymphatic compartments  
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Ulcers:   perform skin inspection and analyze wound characteristics  
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Ulcers:   Observations & Documentation  
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daibetes (DM)   the 3rd leading cause of death in the US; ~14 million people have the disease; annually~700,000 new cases develop (many cases are diagnosed only when complications occur)  
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Glucose:A systemic toxin   Normally insulin: promotes teh storage of glucose as glycogen primarily in the skeletal muscle liver; muscle mass, and good blood supply quickly remove glucose avoiding postprandial hyperglycemia  
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Glucose   attaches to proteins in the blood; microvascualture becomes weakened and damaged  
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Functional microvascular disease   glucose attaches to proteins in the blood; endothelial cells proliferate, RBCs and platelets become less deformable and more adhesive (alters cell nutrition and induces edema  
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Functional microvascular disease   basement membrane of the tunica media calcify, thicken, harden, and change function and permeability; arterioles venules, and capillaries are occluded; lumen size decrease, microvascular press. increases, fail to maximally dialte under stress  
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Fail to maximally dialte under stress   therfore, ABI values may be falsely high  
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Microvasculopathy   makes DM the leading risk factor for CAD, CVA, PAD, Retinopathy (weakened blood vessel form aneurysms that may hemorrhage), Cataracts & glaucoma, kidney failure  
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Glucose and the Immune System   elevated glucose levels impair all 3 phases of wound healing (alter the function of polymorphonuclear leukocytes; bacterial growth flourishes because of edema, hyperglycemia & or decrease insulin levels: osteomyelitis, soft tissue infections & candiasis  
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Sensory Neuropathy   begins as distal, symmetrical stocking/glove pattern of sensory loss; schwann cells exposed to glucose (lose distal myelinated and unmyelinated axons)-toes, &/or fingers, progressing up the leg or arm(abnormal pain, pressure, and proprioception)  
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Sensory Neuropathy   tingling, numbness, weakness, burning sensations, loss of sensitivity to warmth or cold  
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Distal Autonomic Neuropathy   abnormal BP, problems with bowel & bladder control, impotence, lack of sweat and sebaceous gland production (hyper-keratotic, dry (anhydrosis), and cracked (infection risk) calluses develop in wt bearing areas of the feet  
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Diabetes   decreased circulation is not the major cause of diabetic ulcers (only 5% of patients with diabetes-related ischemia require amputations); large arterial vessel, WBC, and nerve damage combined  
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Diabetic Ulcers: Peripheral Neuropathy   #1 contributing factor in the development of diabetic plantar ulcers; sensory impairment + loss of protective sensation + repetitive foot trauma (poor foot care, poor fitting shoes & smoking)  
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tissue at risk of ulceration   previous Hx; all pts with neuropatic foot ulcers are at risk of pressure (decubitis) ulcers-highest incidence of ulceration occurs at sites previous ulceration, newly healed ulcer is covered by thin skin that is likely to tear  
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tissue at risk of ulceration   scar tissue may adhere to underlying structures in completely healed areas; Distal autonomic neuropathy  
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sensory neuropathy (semmes weinstein monofilament test)   loss of protective sensation; 10 grams of force delivered with a 5.07 monofilament; negative test=senses at least 2-5 locations (met heads and great toe)  
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diabetic motor neuropathy   distal atrophy of the intrinsic and extrinsic musculature of the foot cause deformitites  
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foot deformitites increase   pressures over bony prominences, leading to callus formation (e.g. hammer/claw toes, prominent plantar surface metatarsal head, bunions on the 1st and 5th metatarsal-phalangeal (MTP) joints, high arch (pes cavus), Charcot foot  
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calluses further increase   local subcutaneous pressure and ulcers  
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multiple claw toes   similar in appearance to the claw of an animal or talon of a bird  
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callus formation at the tip of the 2nd toe and damaged (hypertropic) nail   most likely caused by friciton in a shoe with a toe box that is too short  
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Charcot Foot (arthropathy)   progressive, destructive, debilitating foot deformity and ulceration (subluxation or Fx of the midtarsal joints, osteolysis, osteophyte formation , and soft tissue edema; rocker bottom deformity (i.e. no medial arch)  
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Charcot Foot   increases pressure along the plantar surface of the midfoot and hindfoot causing ulcers to develop; is often mistaken for osteomyelitis or cellulitis  
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Charcot Foot   often mistaken for osteomyelitis or cellulitis  
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Charcot foot   edema and callus on the right; standard care (immobilization of the foot and ankle, stabilize and protect the foot, custom shoe, activity modification)  
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Summary Diabetic Ulcer Risk Factors   Male, >65, length of time w/ DM, hypergycemia-Type 1A(juvenile/IDDM)-immune mediated; Type2-heredity (asian, native americans, & hispanic americans are at greatest risk), impaired immune response, obesity, smoking, foot deformity  
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Summary Diabetic Ulcer Risk continued   Mechanical force (pressure, fricition, shear, heat or chemicals cause callous and ulcers)-reptitive moderate pressures (40+psi); tight, ill-fitted shoes; previous Hx of ulceration or amputation  
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The classic signs of preulceration inflammation   a red mark, or superficial blister on the foot caused by mechanical forces  
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Diabetic Ulcer Risk Factors   Smoking- LE gangrene occurs ~8 to 150 times more frequently in individuals with diabetes who smoke than in individuals who are not diabetic; plantar ulcers are more likely to occur if there is poor foot care, poorly fitting shoes and continued smoking  
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Diabetic Neuropathic Ulcers   5Ps + T  
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Neuropathic Ulcers: 5Ps + T   position= pressure and friction areas of the feet (most common on the sole of the foot)-under the metatarsal headsor on the plantar aspects of the toes; Presentation-(deep wounds)  
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Presentation   Deep Wound  
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Periwound and structural changes (neuropathic ulcers)   distinguishing feature; callous around the wound,; harcot deformity, clawed toes  
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Pain (sensory neuropathy)   absent (proprioception, pressure, pain & temp); autonomic involvement (intermittent claudication or rest pain, anhydrosis)  
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Pulses and Temperature   depending on the extent of microvascular damage (may be cool and pulseless, skin may be thin, shiny, and hairless, subcutamneous tissue atrophy)  
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Early ulceration (neropathic ulcers)   shallow, quickly progresses to deep  
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position   lateral border of foot-very low, prolonged, pressure (2-3 psi) causes tissue death; clawed toes  
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Stage A- Grade 0   pre/post ulcerative lesions completely epithelaized  
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Stage B- Grade 0   infected  
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Stage C- Grade 0   Ischemic  
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Stage D- Grade 0   infected and ischemic  
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Stage A- Grade 1   superficial wound not invoving tendon, capsule, or bone  
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Stage b- Grade 1   infected  
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Stage C-Grade 1   ischemic  
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Stage D- Grade 1   infected and ischemic  
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Stage A- Grade 2   wound penetrating to tendon or capsule  
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Stage B- Grade 2   infected  
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Stage C- Grade 2   ischemic  
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Stage D- Grade 2   infected and ischemic  
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Stage A- Grade 3   wound penetrating to bone or joint  
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Stage B- Grade 3   infected  
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Stage C- Grade 3   ischemic  
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Stage C- Grade 3   infected and ishemic  
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Wagner Dysvascular scale; grade 0   pre-ulcerative, healed ulcer or bony deformity  
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wagner dysvascular scale; grade 1   superficial with subcutaneous tissue involvement  
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wagner dysvascular scale; grade 2   entire subcutaneous, may have exposed bone, ligament, tendon, joint capsule  
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wagner dysvascular scale; grade 3   osteitis, abscess, osteomyelitis  
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osteomyelitis in DM   spreads to the bone via the blood when moderate force is applied (wt bearing) in the presence of infection; infection can also spread outward from the bone marrow to form abscesses (collections of pus) in adjacent soft tissues  
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diagnosis of osteomyelitits   lab values=erythrocyte sedimentation> 120mml/hr (elevated WBC); x-ray; positive bone scan (MRI, Bone Biopsy)  
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Neuropathic ulcers: GOLD STANDARD Tx   there is no single and agreed upon standard of care  
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Gold Standard Tx   Offloading-studies have nto reported a correlation b/w WB and healing rates; lack of compliance with orthotics as assessed by pedometers; total contact casting can effectively reduce pressure  
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prevention (offloading)   patella-tendon brace with custom-molded footwear  
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medicare coverage of therapeutic footwear   shoe program 1983; needs statement of need from primary physician and/or endocrinologist; Annually-1 pair custom-molded shoes +2pairs of inserts (in addition to inserts provided with the shoes) or 1 pair depth shoes per +3 add. pair of inserts  
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Qualifying conditions (DM) (medicare coverage)   peripheral neuropathy with callus; pre-ulcerative calluses, previous foot ulceration, foot deformity, foot or partial foot amputation, poor circulation  
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Customized footwear or LE orthoses   goal:enhance LE function; pressure relief, shock absorption and frction reduction; stabilize, protect structural deformities or previous plantar ulcerations(molded shoes, AFO-ankle foot orthoses)  
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growth factors in diabetic ulcers   topical application of growth factor may be of limited benefit  
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neuropathic ulcers   debridement  
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neuropathic ulcers   grafts, local flaps, or free-tissue transfers with microvascualr surgery may be needed to salvage an extremity  
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skin substitutes   some evidence that graft skin (Apligraft) may be useful  
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