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Chronic Ulcers
Integ 3 exam
| Question | Answer |
|---|---|
| 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
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