Deep Tissue Injury and Pressure Ulcers: Prevention, Diagnosis, and Management, Exams of Medicine

Download Deep Tissue Injury and Pressure Ulcers: Prevention, Diagnosis, and Management and more Exams Medicine in PDF only on Docsity! wound certification exam questions and answers. what are 6 risk factor components of Braden Scale for pressure ulcer? - \sensory perception, moisture, mobility, activity, nutrition, and shear/friction What is the name of the organization that developed the pressure ulcer staging? - \NPUAP (national pressure ulcer advisory panel) pathological effect of excessive pressure on soft tissue can be attributed by 3 factors? what are they? - \tissue tolerance, duration of pressure, and intensity of pressure what are the extrinsic factors that impact pressure ulcers? - \increase in moisture, friction and shearing how does friction play a role in shearing which eventually leads to pressure ulcer? - \friction alone causes only superfical abrasion, but with gravity it plays a synergistic effect leading to shearing. When gravity pushes down on the body and resistance (friction) between the patient and surface is exerted, shearing occurs. because skin does not freely move, primary effect of shearing occurs at the deeper fascial level. what are the intrisinc factors of pressur ulcers? - \nutritional debilitation, advanced age, low BP, stress, smoking, elevated body temperature Aging skin undergoes what elements affecting risk for pressure ulcer? - \dermoepidermal junction flattens, less nutrient exchange occurs, less resistance to shearing, changes in sensory perception, loss of dermal thickness, increased vascular fragility; ability of soft tisuse to distribute mechanical load w/out comprosing blood flow is impaired What does nonblanching erythema indicate in the skin r/t PU? - \when pressure is applied to the erythematic area skin becomes white (blanched), but once relieved, erythema returns -indicating blood flow; however in nonblanching erythema, skin does not blanche-indicating impaired blood flow-suggesting tissue destructon why does sitting in a chair pose more of a risk in skin break down than lying? - \deep tissue injury or PU is likely to occur sooner sitting down because tissue offloading over boney prominences is higher Describe what you will see in deep tissue injury? - \purple or maroon localized area of discolored intact skin skinor blood filled blister; may be preceded by painful, firm, mushy, or boggy; skin may be warmer to cooler in adjacent tissue. In dark skin, thin blister or eschar over a dark wound bed may bee seen Describe stage I pressure ulcer? - \Intact skin with nonblanchable redness of localized area. Will not see blanching in dark skin, but changes in skin tissue consistency (firm vs boggy when palpated), sensation (pain), and warmer or cooler temperature may differ from surrounding area Describe stage II pressure ulcer? - \partial-thickness wound where epidermis and tip of dermis is lost with red-pink wound bed w/out slough. may also present as intact or open/ruptured serum -filled blister Describe stage III pressure ulcer? - \full-thickness wound where both epidermis and dermis is lost and subcutaneous tissue may be visible, but deeper structures such as muscle, bone, and tendon are not exposed; slough my be present but it doesn't obscure depth and tunneling and undermining may be present Describe stage IV pressure ulcer? - \full-thickness wound with exposed bone,tendon, and muscle; slough or eschar may be seen in some parts of the wound bed. you will often see tunneling and undermining. Osteomyelitis may be dxed at this stage, since bone is palpable Describe unstageble ulcers? - \full-thickness wound where base of the ulcer is covered by slough and/or eschar, obscuring depth When should eschars not be removed? - \when it's stable with dry, adherent, and intact w/out erythema on the heel; this serves as the body's natural cover and should not be removed. Therapeutic function of pressure distribution is accomplised by what 2 factors? - \immersion and envelopement Define immersion? - \depth of penetration or skining into surgace allowing pressure to be spread out over surrounding area rather than directly over boney prominence Define envelopement? - \is the ability of support surface to conform to irregularities without causing substantial increase in pressure what is bottoming out? - What is the gold standard for evaluating valve failure and extent of reflux? - \duplex ultra sound What are some methods for manaing venous ulcers and CVI - \limb elevation- >heart level for 1-2 hours/daily and during sleep, calf pump exercises or referral to PT for shuffling gait, weight control, medications (diuretics, topical corticosteroids, Pentoxifylline (Trental), and compression therapy How does Pentoxifylline work and when is it appropriate? - \reduces aggregation of platelets and WBC, reducing capillary plugging and enhances blood flow. ordered when standard therapy is not effective When are elastic or inelastic compressions indicated? - \elastic for patients who are sedenatary vs. inelastic for patients who are amublatory When are high pressure compressions (30-40mmgHg) indicated, when assessing ABI? - \ABI>0.8 can use high compressions when are compressions contraindicated? - \venous thrombosis in LE w/ulcers and uncompensated heart failure when is sustained (continuous) compression contraindicated? - \in the presene of PVD with an ABI that is < or =0.6 or when ABI is >0.5 but <0.8 is more appropriate when is IPC (intermittent pneumatic compression)-dynamic compression indicated? - \for patients with venous insufficiency and ABI< or =0.5, for those who cannot tolerate sustained compression, as an adjunct therapy to sustained therapy, those who are immobile when is modified or lower compressions appropriate (23-30mmHg)? - \when coexisting arterial disease is present all patients with leg uclers should be screened for arterial disease using what, initially? - \doppler which measures ABI; takes BP in the arm and ankle and compares ratio What are the attributes of short-stretch compression? - \it's inelastic, sustained compression and provides a modified to therapeutic level of pressure-reusable What are the attributes of long-stretch compression? - \same as short stretch except it's elastic (ex. Surepress) what are the attributes of multi-layer compression? - \sustained, elastic, disposable, and provides therapeutic to modified pressure (ex. 3M w/coban) what are the attributes of paste compression and problems associated with it? - \sustained, inelastic, disposable, and provides modified level of pressure;lacks absorptive property so skin has tendency to macerate, patients are sensitive to calamine paste, slippage, poor fit, and inablity to bathe. When are compression stockings indicated? - \only when venous insufficiency is stable and used as maintenace therapy, since compressions are for "life" to prevent venous ulcers what are the goals in treating LEAD? - \maximizing perfusion, minimizing risk of infection, using evidence-based wound care, and ongoing assessment and managment of ischemic pain What is the gold standard for revascularization of sapenous veins? - \bypass graft what are the 6 P's in assessing for acute limb ischemia? - \pulse, pallor, polar (cool), pain, paresthesia(burning and tingling sensation), and paralysis What is the general appearance of LEAD? - \thin, shiny epidermis, loss of hair growth, thickened nails, edema is variable depending on positioning and coexisting disease; pale or ischemic (purpura and petechiae secondary to blood thinners) What vacular symptoms or perfusion status will you see in LEAD during assessment? - \diminished ABI and TBI; dimished or absent pulse; delayed capillary refill time; abnormal turbulence of blood flow (aka bruit), depedent rubor or elevational pallor, cool skin What kinds of pain will the patient with LEAD experience and what is the interpretation? - \patient experiences intermittent claudication with moderate-heavy activity which is relieved by 10 minutes of rest=50% vessel occlusion; experiences nocturnal pain during sleep which is caused by leg elevation and decreased cardiac output- this is relieved by placing limb in dependent position; rest pain occurs in the absence of activity and with legs in dependent position=90% occlusion What are modifiable risk factors for LEAD? what are the lab goals for managing them? - \tobacco: stop smoking diabetes: HbA1c <7.0 and if possible for high risk patients, <6.0 dyslipidemia (elevation of cholesterol and triglycerides): HDL >40, LDL<100, TG <150 HTN: <140/90 (for DM, <130/80) In presence of arterial occlusion, refill time will be longer than what? in seconds? - \will take > 2-3 seconds. what are the ABI values and its indicator? - \>1.3=invalid 1.0-1.3=normal range 0.9 or less=LEAD 0.8-0.6=borderline 0.5 or less=severe ischemia and revascularization needed When should you obtain TcPO2 (transcutaneous partial pressure of O2)? - \when ABI or TBI cannot be performed d/t calcification or amputation of ankles or toes What are the values of TcPO2 and its interpretation? - \40 mmHg or greater=normal <40mmHg=hypoxia w/impaired wound healing When do you use SLP (segmental leg pressure)? - \used to determine location of occlusion for surgical intervention. a 30mmHg decrease in pressure between two adjacent levels indicate occlusion when should you not use TBI? - \when toes are amputated or toes are col that it's not reliable What conditions cause vasoconstrictive properties which worsens LEAD? - \smoking, pain, dehydration, cold temperature, lack of exercise, constrictive clothing when is pulsve volume recordings (PVR) and doppler waveform studies indicated? - \it is recommended when ABI >1.3; the wave forms reflect severity of occlusion what tests give you an anatomic roadmap, prior to revascularization? - \MRA, angiography, duplex angiography, or computed tomographic angiography when is HBO indicated in arterial ulcers? - \patients w/significant ischemia who are not candidates for revascularization and wound healing is impaired Describe the characteristics of a neuropathic wound and periwound? - \wounds are usually found on the planatar, dorsum of metatarsal, and lateral sides of foot; wounds are usually red , if no ischemia not present; wound edges are well defined; exudate is moderate to large; callus periwound Describe the grading system and its corresponding symptoms of Wagner Ulcer Classification system? - \there are 5 grading categories: is not recommended bc of excessive bleeding; instead autolytic or enzymatic debridement is preferred. avoid adhesive dressings and cont to keep wound moist. Describe Calciphylaxis? - \Painful, burning, and sometimes itchy lesion that's indurated, necrotic w/violacious discoloration. The skin cells die because of lack of blood supply (dry gangrene). This causes deep and often extensive ulcers. Occurs w/ESRD patients with hypercalcemia, hyperphosphatemia, and hyperparathydroidism. A distinct finding w/calciphylaxis is intact peripheral pulses bc bloo flow distal to or deeper than necrosis remains intact. Txed with normalization of calcium and phosphorous. IV Sodium thiosulfate has shown to be beneficial. What acronym is used to evaluate surgical infections, post-op for 5 days? What does each letter stand for? - \ASPSIS: A: abx S: serous discharge E: erythema P: purulent drainage S: separation of tissue I: isolation of bacteria S: stay as inpatient prolonger >14 days How are surgical wounds usually closed? - \by primary or secondary intention what solution is usually used in traumatic wounds to decrease contamination? - \Dakin's solution or sodium hypochlorite; should have limited use bc it also kills healthy cells when is TCC contraindicated in treating neuropathic ulcers? - \patient with acute deep infection, sepsis, or gangrene. may not be indicated for those who are noncompliant, would be unstable to stand or walk, exessive edema, fragile skin and who have ulcers that have depth >size of width what is used as an adjunct therapy to surgical shoe, healing shoe, or walking splint and when TCC is not warranted? - \foam felt dressing (FFD) what surgical procedure is used for those with peripheral neuropathy and equinus contractures? - \tedon-achilles lengthening (TAL) what are the clinical manifestations of incontinence associated dermatitis (IAD)? - \areas of body where incontinence will be spread to is observed; risk factors are associated w/urinary or bowel incontinence (abx, carthartics, hypoalbumina, fecal impaction, IBS, infection, radiation, fat malabsorption); blistering, shallow irregular patches that's red and denuded and/or macerated; painful what are the clinical manifestations of Candidiasis? - \occurs in skin folds where moisture is bountiful (intertrigo, pendulous breasts, groin, perineum, inner thighs -like IAD); associated w/moisture and immunosuppresion; confluent patchy rash or erythematous papules (raised discoloration) with cheesy-white exudate; pustules and satellite lesions also seen; itchy, burning discomfort; Potassium hydroxide preparation scraping (KOH) done for testing What are the clinical manifestations of Herpes Simplex? - \viral condition affecting the genitalia areas (perianal, buttocks, genitals); isolated vesicles rupture and crusts over Differentiate IAD, Cutaneous Candidiasis, and Herpes Simplex from pressure ulcer? - \types of lesions, medical hx and location of the conditions assist in diagnosing. Whereas IAD and Cadidiasis occurs in skin fold areas, Herpes is found in genitalia while PUs occur over boney prominences. IAD is incontinence related, Candidiasis is associated with moisture issues and Herpes is a STD. Uniqueness of lesions also depicts type of condition. IAD is irregular, denuded, blistering; Candidiasis is confluent, patchy, papular, pustular, cheesy-like exudate; Herpes is isolated blister which eventually ruptures into crust; PUs in stage II may be confused with the alluded conditions in that it's superficial, partial thickness wound that's red w/serous blister whys is albumin and prealbumin an important lab value to know in wound management and healing? - \lab values indicate potential risk for malnutrition. Protein is needed in growth factors to promote healing. Becasue albumin has a long half life, it foretells muscle wasting/malnourishement which has been chronic. Albumin level <3.5 is malnourished (normal is 3.5-5). Conversely, prealbumin has a short half life of 2 days and indicates acute stage. <19.5 is malnourished (19.5-35.8 normal). What does transferrin lab value a good indicator of? - \iron deficiency Are the the interpretations of BMI for underweight, normal, overweight, and obesity? - \> 18.5kg =underweight 18.5-24.9=normal 25-29.9=overweight 30 and > is obesity What % of body weight is considered significant weight loss? - \5 % or greater w/in 30 days (1 month) or 10% or greater w/in 180 days (6 months) Which nutritional element is needed for angeogenesis, collagen synthesis/remodeling, immune fx and serves as precursor to nitric oxide and wound contraction? - \protein How much protein is necessary per kg, for wound healing? - \1.25-1.5kg/body weight which vitamin assists in angiogenesis and epithealization? - \Vitamin A; this also helps with collagen synthesis which vitamin assists in collagen synthesis, immune function, fibroblast function, and enchances activation of leukocytes and macrophages and essential in cell wall integrity? - \Vitamin C which mineral is needed for protein synthesis? - \zinc how many calories are needed per kg for sufficiency? - \30-35kcal/body weight what lab values help identify patients who are malnourished and need nutritional support for wound healing? - \weight(<18.5 is underweight, need 30-35kcal/weight, significant weight loss =5% w/in 30 days or 10% w/in 180 days); prealbumin (<19.5=malnourished and 19.5- 35.8=normal), and albumin(<3.5 =malnourished and 3.5-5=normal) What the the acroynm TIME used for? - \used as principle for wound bed preparation What does TIME stand for? - \tissue, nonviable; infection/inflammation; moisture balance; edge of wound Explain the pathophysiology of moisture balance? - \dessication slows epithelial cell migration, excessive fluid causes maceration of wound margins; application of moisture-balance dressing, compressions; edema is controlled, epithelial cell migration is restored, maceration avoided Explain the pathophysiology of nonviable tissue on a wound bed? - \defective matrix and cell debris impairs healing. Debridement restores functional extracellular matrix proteins; viable wound base restored Explain the pathophysiology of infection/inflammatory process? - \high bacterial counts prolong inflammation, increases inflammatory cytokines, increases protease activity, and decreases growth factors; implementing topical/systemic antimicrobials and protease inhibitors; bacterial bioburden is diminished Explain the pathophysiology of impaired wound edges? - \In primary intention, wound edges are well approximated and heals by epithealization and connective tissue deposition. surgical incision secured w/staples, surtures, or adhesive tape explain wound healing by secondary intention and give and example? - \wound edges are not approximated and healing occurs by granulation tissue formation, contraction of wound edges, and epithelialization. chronic wounds such as PU and dehisced incisions explain wound healing by tertiary intentions and give examples? - \aka delayed primary intention. wound is kept open for several days. superficial wound eges then are approximated, and center of wound heals by granulation tissue formation. abdominla incision complicated by significant infection (deep tissue is healing by graulation and superficial layer of skin is sutured) "red islets" represent what part of the skin layer? - \basement membrance of the epidermis, which projects deep into the dermis to line the epidermal appendages. Each islets serves as a source of new epithelium why is migration in wound healing delayed when wound is covered w/ a scab? - \in order to create a moist envinroment, epithelial cells secrete enzymes knwon as MMP (metallproteinases) to lift the scab what are the major components of partial-thickness repair include? - \1. inflammatory response to injury 2. epithelial proliferation and migration (resurfacing) 3. differentiation of the epidermal layers to restore barrier fx of skin what happens in wound healing, if wound involves dermal loss - \granulation formation or connective tissue repair will precede concurrently with reepithealization when do you know complete healing has occured in epithelial resurfacing or healing by regeneration? - \when skin pigmenation matches the individual's normal skin tone what must be restored in partial dermal loss in wound healing? - \rete ridges/dermal papillae what are the key components of proliferative phase? - \epithealization, neoangiogenesis, and matrix deposition/collagen synthesis what are the 4 major phases in full-thickness repair? - \1. hemostasis (platelets degranulate and release growth factors) 2. inflammatory (leakage of neutrophils, macrophages ) 3. proliferative/rebuilding (cont recruitment of growth factors, granulation formation, contraction of wound edges, epithelial resurfacing) 4. maturation/remodeling (collagen synthesis) granulation tissue is often referred to as - \extracellular matrix (ECM) in full-thickness wounds, why is the new epidermis slightly thinner than original epidermis? - \ret pegs that normall dip into dermis is lacking In chronic wounds where wound is healing by secondary intention, why is healing delayed? - \hemostasis is absent, presence of excess of proinflammartory cells where wound bed is bioburdened, prolonged proliferative phase where granulation and wound contraction must take place before epithealization what are the characteristics of a chronic wound? - \prolonged inflammatory phase, cellular senescene, deficiency of growth factor receptor sites, absence of hemostasis phase which triggers fibrin production and growth factor release, and high level of proteases how does diabetes effect repair process? - \prolongs inflammation, reduces collagen synthesis, decreases tensile strength, impairs epithelial migration, compromises vasculature how does advance age affect wound healing? - \dimished proliferation of cells critical to repair, increased number of senescent cells, diminished production of growth factors, hormonal changes, multiple co-existing comorbidities why is nutrition critical in wound healing? - \it's important in collagen synthesis, tensile strength, immune fx