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Chronic Ulcers

Integ 3 exam

QuestionAnswer
conventional Tx for all wounds incorporates common principles & Tx targeted to characteristics of each and the patient's clinical characteristics
Incorporates common principles debridement of necroti tissue, maintainence of moist wound bed, control of infection
Tx targeted to characteristics of each wound and the patient's clinical characteristics appropriate intensity of Tx delivery & no widely accepted, standardized protocols
Tx of chronic ulcers based on understanding of biological and pathological events in normal wound healing (growth factor, tissue engineered skin, adjunctive physical agents)
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)
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)
classification of Ulcers: 5P + T
classification of ulcers: postion, presentation, pain, periwound, pulses, & temperature
Postion of the body anatomical reference points
presentation shape/drainage/color
pain present/absent/severity
periwound condition and structural changes of the surrounding skin
pulses present/absent/dimished
temperature surrounding skin
3 types of vascular ulcers arterial insufficiency, chronic venous insufficiency, DM (nueuropathic)
Arterial insufficiency pain=severe, position (toes/anterior or lateral leg)
chronic venous insufficiency pain=mild to none, position (medial ankle and leg)
DM (Neuropathic) pain=none, position(plantar surface of foot) (MET heads)
vascular ulcers: wound pale wound base, atrophic skin, dry wound, red base, periwound skin staining, wet wound, periwound callous, infection
Background Hx for PAD 50 yr old male or older, DM, smoker, sedentary/immobile, circulatory disorders
circulatory disorders (cardiac disease, CVA, PVD, HTN, Family Hx of premature ishemic heart disease, hyperhyperlipidemia/hypercholesterolemia (high levels of LDL))
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
mortality/morbidity in arterial insufficiency # of yrs of follow-up 5, 10, 15 mortality rates for individuals with claudication 30%, 50%, 70%
when does atherosclerosis occur earlier and more often in persons with DM
what does complete acute ischemia cause extensive tissue necrosis w/n 6 hrs
what does amputation depend upon the number and severity of diseases affecting the peripheral vasculature (ischemia, HTN, diabetes, smoking)
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
etilogy of arterial insufficiency slowly progressive stenosis (>50%) and thickening of the capillary membrane (decrease blood flow)
Decrease blood flow: acute intermittent claudication, thrombosis, embolus
decrease blood flow: chronic ischemic rest pain, gangrene, ulcers
Atherosclerosis: Medical Management balloon angioplasty, stent, endarterectomy (surgical removal of plaque)
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
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
S&S early peripheral arterial disease skin trophic changes, pulses, wound characterisitics, ishemic pain or paresthesia
skin trophic changes hair loss, dry & flaky, shiny, elevation pallor or dependent cyanosis, cool temperature, & thickened nails
pulses decreased/absent
wound characteristics absent granulation, gangrene, minimal drainage-dry
ischemic pain or paresthesia intermittent claudication & resting limb pain
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
Allen test (UE circulation)
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
Interpretation of Allen test color of the palm should return to normal in 5-10 seconds on side released
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
toe pan usually reflects a mid-foot occlusion
calf pain a knee or distal thigh occlusion
"cramping" pain worse with activity or exercise
pain relieved with rest in the dependent position
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
Positive test (buerger's sign) pallor w/n 25 secs combined with dependent rubor of the feet
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)
Pallor Grading from least to most severe ~60% elevation to test
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)
Doppler Ultrasound- ABI segmental pressure measurements: ABI calcualted using the highest brachial pressure.
characteristics of arterial ulcers: 5P + T position, presentation, periwound, pain, pulses, pallor, temp
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
Presentation and Periwound Symmetrical, "punched out", little to no drainage, pallid, Deep (tendon or bone may be exposed if the ischemia is severe)
Aterial ulcers are often sloughy (yellow base)
Pain/paresthesia intermittent claudication, resting limb pain (severe, frequently at night in bed or when the LEs are elevated)
Pulses diminished or absent
Temperature Cold
Signs to look for: Arterial Ulcers: 5P+T (slide32) e.g. poor granulation (50% pink, 50% yellow slough), cellulitis, Maceration, Trophic changes, Edema??
Ischemic skin changes: Pallor (slide 33) pale, mottled, distal erythema, early ulceration of the great toe, amputated 4th digit
Ischemic Skin Changes (slide 34) atherosclerosis obliterans (distal ischemia and dry gangrene with forefoot hyperemia); "blue or purple"
Ishemic Skin changes (slide 35) Atheroembolism: cutaneous arterial infarctions (spontaneous or after intravascular surgery or procedures); arteries occluded atherosclerotic plaque fragments
Predictors of healing ABI>0.5; ankle pressure>70mmHg, Toe pressure> 50mmHg
Ankle Pressure (healing) >70mmHg
Toe pressure (healing) >50mmHg
TCPO2 >40mmHg (supine)
Differential Diagnosis intermittent claudication, painful foot, ischemic & infarctive lesions of leg/foot
intermittent claudication buerger's disease (thromboangitis obliterans), arthritis, gout
painful foot gout, morton's neuroma, onychomycosis with in-grown toenails, pes planus, calcanean buritis, plantar fascitis
ischemic and infarctive lesions of leg/foot vasculitis, raynaud's phenomenon (vasospasm), embolization, drug induced necrosis (warfarin, heparin), external compression (popliteal entrapment)
raynaud's phenomenon/complex regional pain syndrome associated with RA, SLE and scleroderma
PT interventions ther ex: gait and mobility training, positoning, graded aerobic exercises, stretching (prescribe, apply or fabricate orthotic and assitive devices, physical agents)
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
venous insufficiency hemosederin staining
DVT risk factors female over 40, prior LE trauma (surgery, pregnancy, cancer), obesity, immobility (bed rest), standing for long periods, cardiac disease, varicosities (telangiectasias)
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)
venous insufficiency Ablation: sclerotherapy, ligation and stripping (outcomes equivalent/beware complications and recurrence); laser and radio-frequency (non-invasive, better outcomes)
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)
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
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
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
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
prevention of hypertension 3 major mechanisms: Bicuspid valves, calf muscles, respiratory pump
Differential diagnosis: Venous insufficiency kidney or renal failur, CHF, infection,trauma, lymphedema
Clinical tests and measures for venous insufficiency observation, diagnostic imaging, Homan's sign, venous filling time, Brodie-Trendelenburg Test
Observation for venous insufficiency varicosities
Diagnostic imaging for venous insufficiency duplex venous ultrasound, ABI- use compression if >.7, venography,& magnetic resonance venography
superficial vein thrombosis:aka phlebitis
superficial vein thrombosis (phlebitis) edematous, red and painful to touch
Duplex imaging duplex ultrasonography (non-invasive)
Venography "GOLD STANDARD"
Magnetic resonance venography (MRV) most sensitive and specific test for inaccessible areas, helps detect other nonvasular causes of pain and edema
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
Brodie-Trendelenburg test interpertation: time until distention (seconds)- possible pathology < 10=superficial vein incompetence; <20= Deep perforator vein incompetence
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
Venous Fillling Time interpretation: same procedure as elevation pallor/rubor; sitting (dependent) position after extremity elevation
Seconds until color returns in superficial veins with dependency: <5 (venous insufficiency), 5-15 (normal), >20 Arterial insufficiency
Characterisitcs of Venous: 5P + T position, presentation, periwound, pain, temp
Position below the knee, gaiter area, trauma sites
presentation shallow, irregular shaped; pitting pedal edema
periwound hemosiderin pigment (RBC lysis); brown or mottled reddish skin color; cellulitits, dermatitis
Lipodermato-sclerosis "Champagne Bottle" or "piano leg" appearance(the ankle is relatively thin and the upper calf edematous); edema causes skin breakdown and infection
Venous Insufficiency Ulcers: Pain-minimal, relieved by elevation or compression; Pulses-present, normal; Temperature-local warmth
Chronic Stasis (slide 63) stuck in inflammatory phase
Normally Healing venous stasis ulcer: overlapping healing phases: granulation tissue, reepithelialzation, wound contracting
Chronic Stasis Hemosiderin pigment (RBC lysis): Brownish discoloration or hyper-pigmentation in darker-skinned individuals
Chronic Dermatitis scratch marks indicate peri-wound skin itchiness (pruritis)
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
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
Class 1 garment 20-30 mmHg; UE; prophylatic:varicose veins, mild edema, pregnancy
Class 2 garment 30-40mmHg; UE; moderate to severe varicose veins, mild edema, small ulcers, prevention
Class 3 garment 40-50mmHg; LE; severe varicose veins, chronic venous insufficiency, ulcers, prevention
Class 4 garment 60+mmHg; LE; severe
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
Ulcers: perform skin inspection and analyze wound characteristics
Ulcers: Observations & Documentation
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)
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
Glucose attaches to proteins in the blood; microvascualture becomes weakened and damaged
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
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
Fail to maximally dialte under stress therfore, ABI values may be falsely high
Microvasculopathy makes DM the leading risk factor for CAD, CVA, PAD, Retinopathy (weakened blood vessel form aneurysms that may hemorrhage), Cataracts & glaucoma, kidney failure
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
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)
Sensory Neuropathy tingling, numbness, weakness, burning sensations, loss of sensitivity to warmth or cold
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
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
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)
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
tissue at risk of ulceration scar tissue may adhere to underlying structures in completely healed areas; Distal autonomic neuropathy
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)
diabetic motor neuropathy distal atrophy of the intrinsic and extrinsic musculature of the foot cause deformitites
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
calluses further increase local subcutaneous pressure and ulcers
multiple claw toes similar in appearance to the claw of an animal or talon of a bird
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
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)
Charcot Foot increases pressure along the plantar surface of the midfoot and hindfoot causing ulcers to develop; is often mistaken for osteomyelitis or cellulitis
Charcot Foot often mistaken for osteomyelitis or cellulitis
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)
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
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
The classic signs of preulceration inflammation a red mark, or superficial blister on the foot caused by mechanical forces
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
Diabetic Neuropathic Ulcers 5Ps + T
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)
Presentation Deep Wound
Periwound and structural changes (neuropathic ulcers) distinguishing feature; callous around the wound,; harcot deformity, clawed toes
Pain (sensory neuropathy) absent (proprioception, pressure, pain & temp); autonomic involvement (intermittent claudication or rest pain, anhydrosis)
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)
Early ulceration (neropathic ulcers) shallow, quickly progresses to deep
position lateral border of foot-very low, prolonged, pressure (2-3 psi) causes tissue death; clawed toes
Stage A- Grade 0 pre/post ulcerative lesions completely epithelaized
Stage B- Grade 0 infected
Stage C- Grade 0 Ischemic
Stage D- Grade 0 infected and ischemic
Stage A- Grade 1 superficial wound not invoving tendon, capsule, or bone
Stage b- Grade 1 infected
Stage C-Grade 1 ischemic
Stage D- Grade 1 infected and ischemic
Stage A- Grade 2 wound penetrating to tendon or capsule
Stage B- Grade 2 infected
Stage C- Grade 2 ischemic
Stage D- Grade 2 infected and ischemic
Stage A- Grade 3 wound penetrating to bone or joint
Stage B- Grade 3 infected
Stage C- Grade 3 ischemic
Stage C- Grade 3 infected and ishemic
Wagner Dysvascular scale; grade 0 pre-ulcerative, healed ulcer or bony deformity
wagner dysvascular scale; grade 1 superficial with subcutaneous tissue involvement
wagner dysvascular scale; grade 2 entire subcutaneous, may have exposed bone, ligament, tendon, joint capsule
wagner dysvascular scale; grade 3 osteitis, abscess, osteomyelitis
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
diagnosis of osteomyelitits lab values=erythrocyte sedimentation> 120mml/hr (elevated WBC); x-ray; positive bone scan (MRI, Bone Biopsy)
Neuropathic ulcers: GOLD STANDARD Tx there is no single and agreed upon standard of care
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
prevention (offloading) patella-tendon brace with custom-molded footwear
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
Qualifying conditions (DM) (medicare coverage) peripheral neuropathy with callus; pre-ulcerative calluses, previous foot ulceration, foot deformity, foot or partial foot amputation, poor circulation
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)
growth factors in diabetic ulcers topical application of growth factor may be of limited benefit
neuropathic ulcers debridement
neuropathic ulcers grafts, local flaps, or free-tissue transfers with microvascualr surgery may be needed to salvage an extremity
skin substitutes some evidence that graft skin (Apligraft) may be useful
Created by: drewtimo@msu.edu