Joyce Black Sept 2016

Transcription

1 Implementing the 2014 Pressure Ulcer Prevention Guidelines In Long Term Care, PhD, RN CWCN, FAAN University of Nebraska npuap.org A = direct evidence from well designed controlled trials N = 6 B = direct evidence from clinical series N = 71 C = indirect evidence (other wounds, healthy humans, animal models) and or expert opinion N = 498 Strength of Evidence Labeled A, B, C here Strong positive recommendation N = 247 Weak positive recommendation N = 294 No specific recommendation N = 34 Strength of Recommendation Labeled 2, 1, 0 here 2015 National Pressure Ulcer Advisory Panel Reduce the intensity of the pressure Support surfaces Dressing the skin to reduce the pressure Reduce the duration of the pressure Turning and repositioning Reduce the effect of shear Keeping the head of the bed low Dressing the skin to provide a barrier Improve the health of the skin Giving nutrition and hydration Keeping the skin clean and dry Protecting damaged skin Use a rigorous method to conduct P&I studies Be clear on which residents (C/2) Educate the assessors and check reliability Two assessments per skin inspection Compare findings to data sets using similar methods (C/1) Many studies of P&I included in guideline Use facility acquired rates rather than prevalence rates to evaluate pressure ulcer prevention programs (C/1) Be clear on whether Stage 1 was included Present data by level of risk for risk adjustment Braden Score Unit ulcer acquired 1000 patient days (C/1) Report by common anatomical locations Include data on medical device ulcers and mucous membrane ulcers Perform root cause analysis to determine avoidability Identify unavoidable ulcers Is this wound a pressure ulcer? Was it due to pressure? Was it due to shear? Is this wound on a previously healed PrU? When was this wound discovered? What size, stage, location? Due to a medical device? On mucous membrane? What was risk score Was it accurate? Did a prevention plan stem from the score? 1

2 Differential diagnosis needed Is this a pressure ulcer/injury? Or another wound? Just because the skin is open does not make the ulcer a pressure ulcer/injury However, if it is staged, the presumption will be that the wound was due to pressure Skin tear IAD Arterial ulcer Pressure Injury Stage at time of initial discovery Stage I --- likely began in last hours DTI --- purple tissue without epidermal loss likely began 48 hours ago Important because you might not have had this patient 48 hours ago Turning may have been impossible OR cases Stage II --- likely began in last 24 hours Stage III-IV --- began at least 72 hours ago SEATED HOB UP FLAT HOB UP HEELS ON BED Conduct structured risk assessment as soon as possible, but within a maximum of 8 hours (C/2) Repeat based on residents acuity or change in condition (C/1) Several comments on this statement Why wait 8 hours? What about 12 hour shifts? Do not rely on total risk assessment score alone, use subscales to plan preventive care (C/2) Use clinical judgement to refine risk assessment No risk scale is perfect (C/2) Braden most common in US Key Risk Factors of mobility/activity limitations and skin status Perfusion is not included Key issue is what is done with the score? Does it direct care? Or is the Braden done just to achieve paper compliance? Consider bedfast or chair-fast residents to be at risk (B/1) The most significant risk factor Elders with significant comorbidities do not ulcerate until they are bedbound or chairfast Easily understood by all providers Consider these aspects of immobility (B/2) Mobility related ADLs Factors affecting mobility Friction and shear within mobility Interface pressures 2

3 Consider Stage 1 pressure ulcers to be a risk factor for progression to higher stages or development of new ulcers (B/1) Consider existing pressure ulcers to be a risk factor (B/2) Consider the general status of the skin (B/1)? Scar formation over prior healed full thickness ulcer Consider the impact of impaired perfusion and oxygenation on risk (C/1) Use proxy variables to indicate risk Peripheral arterial disease Diabetic neuropathy Stroke Renal disease CV instability, hypotension requiring vasopressors History of smoking Food intake Low weight/low body mass index Arm measurements Malnutrition diagnosis Weight loss Nutrition screening / dietician referral Nutrition assessment scale scores Albumin and prealbumin are not predictive In the acutely ill, these proteins are low when inflammation is present Oregon Wound Conference 2015 Dual urinary and fecal incontinence. Skin moisture. Moisture subscale of a risk assessment tool. Fecal incontinence. Urinary catheter in use Urinary incontinence. Increased body temperature Advanced age Sensory perception Hematological measures Abnormal urea and electrolytes Low WBC, albumin, hemoglobin Elevated C-reactive protein (inflammatory marker) General health status Dependent in ADLs DNR status IAD is not a pressure ulcer 3

4 In individuals at risk of pressure ulcers, conduct a comprehensive skin assessment: as soon as possible but within eight hours of admission (or first visit in community settings) Consider the process of skin assessment in the evening and on weekends and holidays Is the policy clear enough to direct care during those times? as part of every risk assessment ongoing based on the clinical setting and the individual s degree of risk prior to the individual s discharge (C/1) More than one person to move and lift Potential for injury with movement 20 Use the finger or disc method to assess (C/1) Differentiate the cause and extent of erythema -blanchable or nonblanchable? (C/2) Blanchable erythema Normal reactive hyperemia and should disappear in several hours May be inflammatory erythema Nonblanchable erythema Indicates structural damage to the capillary bed/microcirculation Nonblanching erythema shown to be an independent predictor of Stage 2 pressure ulcer development Inspect the skin under and around medical devices at least twice daily (C/2) Include skin assessment in handoff Conduct more frequent skin assessments at the skindevice interface in individuals vulnerable to fluid shifts and/or exhibiting signs of localized/generalized edema (C/2) Lip ulceration after a 45 minute intubation with tube taped in place Avoid positioning the individual on an area of erythema whenever possible (C/2) A carry over from 2009, but a crucial message Keep the skin clean and dry (C/2) Yes, this is new to the 2014 guideline! Use a ph balanced skin cleanser (C/2) Yes, this is new to the guideline! Cleanse the skin promptly following episodes of incontinence (C/2) Yes, this is new to the 2014 guideline! Microclimate is local tissue temperature and moisture at body/support surface interface Metabolic rate rises with increased temperature and without increased perfusion due to pressure tissue will die Consider the need for additional features such as ability to control moisture and temperature when selecting a support surface and or surface cover (C/1) Do not apply heating devices directly on skin surfaces or pressure ulcers (C/1) 4

5 Consider using silk-like fabrics rather than cotton or cotton-blend fabrics to reduce shear and friction (B/1) Four studies examining effect of reduced friction from linen on pressure ulcer formation Consider applying a polyurethane foam dressing to bony prominences (e.g., heels, sacrum) for the prevention of pressure ulcers in anatomical areas frequently subjected to friction and shear (B/1) Lack of clarity in discussion about actual structure of dressing Not all studies cited used polyurethane foam Many polyurethane foam dressings on the market Important to know how they work and if they can reduce pressure, shear or microclimate Dressings do not replace the rest of prevention! (C/1) ability to manage microclimate ease of application and removal ability to regularly assess the skin anatomical location where the dressing will be applied the correct dressing size Must be larger than area at risk Pressure and shear forces are transmitted through the dressing For muscle contraction in SCI residents (C/0) Subjects used shorts with ES in them to cause contraction of gluteus and hamstrings May have gotten a neutral response due to respondents not focusing on SCI Assess the weight status of each individual to determine weight history and identify significant weight loss 5% in 30 days or 10% in 180 day (C/1) Assess the individual s ability to eat independently (C/2) Assess the adequacy of total nutrient intake Food, fluid, oral supplements and enteral/parenteral feeds (C/2) Adjust energy intake based on weight change or level of obesity. Adults who are underweight or who have had significant unintended weight loss may need additional energy intake (C/2) Revise and modify/liberalize dietary restrictions when limitations result in decreased food and fluid intake (C/1) 5

6 1.25 to 1.5 grams protein/kg per day for both residents at risk and with ulcers (B-C/1) Assess renal function to ensure that high levels of protein are appropriate (C/2) Provide/encourage consumption of a balanced diet that includes good sources of vitamins and minerals. (C/2) Provide/encourage vitamin and mineral supplements when dietary intake is poor or deficiencies are confirmed or suspected. (C/1) Provide and encourage adequate daily fluid intake for hydration consistent with the individual s comorbid conditions and goals. (C/2) Monitor for signs and symptoms of dehydration (C/1) Provide additional fluid for individuals with dehydration, elevated temperature, vomiting, profuse sweating, diarrhea, or heavily exuding wounds. (C/2) Reposition all individuals at risk of pressure ulcers, unless contra-indicated. (A/2) 3 RCTs discussed in the guideline Bergstrom s RCT was after the cut off date A repeat from the 2009 guideline with changed wording, 2009 addressed duration and magnitude Consider the condition of the individual and the pressure redistribution support surface in use when deciding if repositioning should be implemented as a prevention strategy. (C/1) When residents cannot be moved, change the mattress Study of residents in long term care on foam mattresses 942 Residents at moderate to high risk for PI Turned randomly Q 2,3 and 4 hrs Compliance with turning measured Outcomes Pressure injury formation was the same at all frequencies Q 2 hr = 2.5% Q 3 hr = 0.6% Q 4 hr = 3.1% Pressure injury formation did not differ by risk High risk = 1.8% Moderate risk = 2.1% Bergstrom, et al, 2013 JAGS If turning take 5 minutes per turn x 12 turns a day = 1 hour In acute care, RN = $38/day per patient In a 200 bed hospital, turning half the residents= $3800 for salary if alone How many residents can be turned alone? Adding in back injury Dept of labor lists CNA as the number 1 highest risk for back injuries (LPN = #4, RN = #6) Bates-Jensen, 2011 Consider the pressure redistribution support surface in use when determining the frequency of repositioning. (A/1) Appeared in 2009 guideline stated differently Establish pressure relief schedules that prescribe the frequency and duration of weight shifts. (C/1) Teach individuals to do pressure relief lifts or other pressure relieving maneuvers as appropriate. (C/2) Do not leave the individual on a bedpan longer than necessary. (C/2) Yes, this statement is in the guidelines! 6

7 Use a split leg sling mechanical lift when available to transfer an individual into a wheelchair or bedside chair when the individual needs total assistance to transfer. Remove the sling immediately after transfer. (C/1) Do not leave moving and handling equipment under the individual after use, unless the equipment is specifically designed for this purpose. (C/2) New NPUAP position on the breathability of slings Use the 30 tilted side-lying position (C/1) No discussion of the efficacy of this position in bariatric residents Encourage residents who can reposition themselves to sleep in a 30 to 40 sidelying position or flat in bed (C/1) Be certain the patient is actually turning Avoid HOB elevation that places patient in a slouched position Maximal shear forces at 45 HOB elevation When turned to left side be certain that the sacrum clears the bed. Move patient off of shoulder No support surface replaces turning/repositioning They may help with turn assist features They may lengthen the time interval Select a support surface that meets the individual s needs, based on: (C/2) level of immobility and inactivity; need for microclimate control and shear reduction; size and weight of the individual; risk for development of new pressure ulcers Identify and prevent potential complications of support surface use. (C/1) Entrapment Falling with an overlay higher than side rails High air loss leading to fluid loss Review the characteristics of foam mattresses to ensure they are high specification. (C/2) Depth = 6 inches thick Density = density hardness Support factor = Inflection Density: (IFD) 1.75 to 2.4 Cover MVTR = minimum 300 g/m²/24hrs Other features to consider Multi layering alters the design Memory foam may increase skin temperature Cross cut foam may reduce shear Stiffer side walls can facilitate transfers Concave shape may prevent falls, but difficult to lift patient Hinging system may improve ability to sit up in bed without shearing Choose positioning devices and incontinence pads, clothing and bed linen that are compatible with the support surface. Limit the amount of linen and pads placed on the bed. (C/2) 7

8 Support surfaces don t last forever About 5-7 years per most manufacturers Based on average use. How old are your hospital beds? Work with maintenance to find out the age of the mattress fleet Purchase new mattresses for some units yearly Write the date of purchase on the surface Use a pressure redistributing seat cushion for individuals sitting in a chair whose mobility is reduced. (B/2) Examine your hospital bedside chairs for pressure redistribution and use chair cushions Limit time sitting in a chair without pressure relief (B/2) Not a new statement, but very important now with progressive mobility programs Interface pressures on ischial tuberosities can become very high in the chair Individualize the selection and periodic reevaluation based on: (C/1) body size and configuration; the effects of posture and deformity on pressure distribution; and mobility and lifestyle needs. Select a stretchable/breathable cushion cover that fits loosely on the top surface to dissipate heat and moisture (C/1) Inspect seating surface daily for wear Use a pressure redistributing seat cushion for individuals sitting in a chair with reduced mobility (SOE = B) Limit the time an individual spends seated in a chair without pressure relief (SOE = B) Develop a decision tree on seat cushion selection for residents not seen by PTs Consider both air cell and foam cushions residents with neurological disease or injury who will mobilize by wheelchair need to be seen and evaluated by seating specialists Air Cell Foam Gel Air Columns Develop a schedule for progressive sitting according to the individual s tolerance and pressure ulcer response. (C/1) Commonly done after flap repair, this statement appears in the general guidelines Increase activity as rapidly as tolerated. (C/1) One study found increased PrU with progressive mobility program that included HOB elevation to 45 degrees as part of the mobility intervention 8

9 Risk factors for heel ulcers are not clearly identified Apply heel suspension devices per manufacturers instructions (C/1) Remove heel suspension device periodically to assess skin integrity (C/1) Check skin more frequently in residents at higher risk due to PVD and neuropathy Do not use IV bags to float heels (C/2) Posterior prominence of the calcaneus Lack of subcutaneous tissue Average heel pad thickness is 18 mm Average skin thickness is 0.64 mm No direct arterial inflow From peroneal and posterior tibial arteries NDNQI reports that 17 was average Braden for persons with heel ulcers Other findings Average Braden was =/ in heel ulcered residents (Clegg) Braden Range was in heel ulcered residents (Walsh) By Braden: Cognitive-sensory scale of 3 or below Immobility subscale score of 3 or below Friction/shear subscale score of 2 or below if rubbing heels into bed By other Risk Factors Diabetes with neuropathic change Peripheral vascular disease with impaired inflow Low ABI Poor capillary refill Systemic infection leading to low BP ESRD End stage respiratory disease Does the patient move legs independently? Does the patient have normal or delayed capillary refill? Palpable pulses? Does the patient have normal sensation? Does the patient wear TEDs? When these factors are present residents are at risk Pillows for short term risk Pillows for nonmoving residents If the resident kicks the pillow off the bed it is not going to work! 9

10 Pillows Don t stay under the calf Migrate to under the knee Fall off of the bed Don t fully elevate the heel Are placed under the heel Difficult due to boots designed to be worn in supine position Consider more circular boot Use pillows to float heels off of recliner leg rest Be cautious resident does not push feet into leg rest Result from the use of devices designed and applied for diagnostic or therapeutic purposes ulcer generally closely conforms to the pattern or shape of the device Mucous membrane is very vulnerable to pressure from medical devices These ulcers are not staged Cuddigan, Janet E., Elizabeth A. Ayello, and. "Saving heels in critically ill patients." JWECT 28.2 (2008). Print. Consider adults with medical devices to be at risk for MDR-pressure ulcers. (B/2) 34.5% of ulcers in ICU were from Medical Devices Consider children with medical devices to be at risk for pressure ulcers. (B/2) Rates very by type of device and age of child Review and select medical devices based on the devices ability to induce the least degree of damage from the forces of pressure and/or shear. (B/2) A root cause analysis will identify the device and changes in device or practice may be needed Ensure that medical devices are correctly sized and fit appropriately (C/2) Edema post application increases pressure Apply all medical devices following manufacturer s specifications. (C/2) Return faulty devices How can you, if you aren't tracking them? Ensure that medical devices are sufficiently secured to prevent dislodgement without creating additional pressure. (C/2) Dressings may be needed for padding 10

11 Inspect the skin under and around medical devices at least twice daily for the signs of pressure related injury on the surrounding tissue. (C/1) Device will need to be moved Include in handoff? Increase assessment frequency in edematous residents (C/2) Reposition or rotate and support device to change pressure points (C/2) Remove device as soon as feasible (C/2) Keep skin clean and dry under device (C/2) Ulcers from Foley From trach ties Assess all skin folds regularly. (C/2) Access adequate assistance (C/2) Differentiate intertriginous dermatitis from Stage 1 and 2 pressure ulcers. (C/1) Ensure the individual is provided with a bed of appropriate size (width) and weight capacity specifications. (C/2) Consider enhanced pressure redistribution, shear reduction and microclimate control (C/1) Avoid pressure on skin from tubes, other medical devices and foreign objects. (C/2) Use pillows or other positioning devices to offload the pannus or other large skin folds and prevent skin-on-skin pressure. (C/1) Check the bed for foreign objects. (C/1) Assessments and Care Planning Consider the individual s cognitive status when conducting a comprehensive assessment and developing prevention or treatment plan. (C/2) Incorporate the individual s cognitive ability into the selection of a pain assessment tool. (C/2) Differentiate from other skin injuries, particularly incontinence-associated dermatitis or skin tears. (C/1) Set goals consistent with the values and goals (C/1) Engage the family or legal guardian when establishing goals of care and validate their understanding of these goals. (C/1) Educate the individual and his or her significant others regarding skin changes in aging and at end of life. (C/2) 11

12 Regularly reposition the older adult who is unable to reposition independently. (A/2) Same evidence as was used for repositioning Exercise caution in position selection and manual handling technique when repositioning. (C/1) Frequently reposition the head of older adults who are sedated, ventilated or immobile. (C/1) Send overlay with residents to dialysis If possible, ask dialysis nurses to glide residents into different positions during the run If using a turn and position system Place residents on the side following dialysis Examine dialysis in your root cause analysis Work with dieticians to increase protein in those with ulcerations Upscale mattresses to microclimate management with alternating pressure Use turn and position systems to aid in turning without patient effort Dress high risk areas with foam dressings Liberally medicate for pain Use small shifts of body weight to supplement turns Two prevention recommendations are an A level Consider support surface when planning Repositioning using data from European studies Using Electrical stimulation for prevention was the lowest rated item at C/0 Greater majority of statements are C/1 level The National Pressure Ulcer Advisory Panel (NPUAP) serves as the authoritative voice for improved patient outcomes in pressure ulcer prevention and treatment through public policy, education and research. npuap.org, PhD, RN, CWCN, FAAN University of Nebraska Medical Center Amboise Pare: I only dressed the wound, God healed it National Pressure Ulcer Advisory Panel 12

13 Treat the disease that caused the wound Sometimes many things, sometimes few Burns versus trauma Minimize edema and inflammation Provide adequate blood flow and oxygen to the wound Provide adequate protein and carbohydrate to promote cellular repair Prevent infection in the wound bed Not fixing the problem that caused the wound Continued pressure No improvement in arterial flow No control of venous hypertension Not providing enough protein and calories to promote healing Body becomes catabolic Not reducing risk of infection in wound bed Prolonged inflammation The cells in the open wound become senescent Biofilm develops 3 legged stools tip over when any one leg is missing Controlling or curing the cause Pressure redistribution Arterial bypass Compression garments Protective clothing for skin tears Wound care (From 2014 Guidelines) Debridement, dressings/packing, topicals Do not debride ischemic tissue or malnourished pts Nutrition (from 2014 Guidelines) Increased protein and calories Vitamin and zinc supplement if low Principles guiding care Devitalized tissue must be removed to decrease inflammation and reduce risk of infection Exception today is the heel in an ischemic limb Principles Match debridement type to condition of ulcer and patient Autolytic for stable slough Hydrogels, hydrocolloids Enzymatic for stable slough in stable patient that can tolerate 2 or more weeks of therapy Collagenase/Santyl Mechanical for stable slough in stable patient in whom pain can be managed Gauze dressings, whirlpool, ultrasound Biologic Fairly rapid Sharp or surgical Infected ulcers, slough, boggy eschar, septic patients Techniques 13

14 Stage 3 or 4 with slough Enzymatic debrider on slough Moisture retentive wound bed filler Alginate if highly exudative Foam if mildly exudative No hydrocolloids or films Silver, honey or cadexomer iodine for biofilm control Cover dressing Absorptive Window area if dressing change frequent Silicone contact layer November 2015 Return to form and function Seen best in acute wound healing Scar prevents form and function in large wounds and chronic wounds Wound closure in patients at end of life or end stage disease is not the priority for care Patient engagement Management of condition Management of wound These ischial ulcers have little hope for closure without a comprehensive plan and patient engagement Inability to control underlying disease Diabetes Malnutrition Venous hypertension Arterial inflow Pressure loading Infection Cancer Paralysis We will examine several acute and chronic wounds and look at the unique aspects of their care Are All Pressure Injuries the Same? Staging and Care, PhD, RN, CWCN, FAAN University of Nebraska Medical Center Omaha, NE 14

15 Pressure Injury Definition A pressure injury is localized damage to the skin and/or underlying soft tissue usually over a bony prominence or related to a medical or other device. The injury can present as intact skin or an open ulcer and may be painful. The injury occurs as a result of intense and prolonged pressure or pressure in combination with shear. The tolerance of soft tissue for pressure and shear may also be affected by microclimate, nutrition, perfusion, co-morbidities and condition of the soft tissue. Soft tissue is compressed between bone/cartilage and external surface Tissue deformation Tissue destruction Ischemia Visible presentation begins in the skin, but damage is more extensive National Pressure Ulcer Advisory Panel Stage 1 Pressure Injury: Non-blanchable erythema of intact skin Shear forces damage the skin Direct damage Decrease tolerance for pressure Microclimate Direct damage of superficial layers Decreases tolerance for pressure Intact skin with a localized area of non-blanchable erythema, which may appear differently in darkly pigmented skin. Presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes. Color changes do not include purple or maroon discoloration; these may indicate deep tissue 2016 National Pressure Ulcer Advisory Panel pressure injury. 88 Stage 1 in Darkly Pigmented Skin Intact skin with a localized area of non-blanchable erythema, which may appear differently in darkly pigmented skin. The pigmentation of the skin may prevent seeing the reactive hyperemia in the pressure injury Moistening the skin will often aid in seeing color change Ask about pain in the area Palpate the skin for induration 2016 National Pressure Ulcer Advisory Panel Examine all skin subjected to pressure Remove stockings, splints, braces and clothing Move oxygen tubing and face masks Inspect the heels by looking at them Use a mirror if needed Determine blanche response Moisten darkly pigmented skin 89 15

16 Stage 1 Pressure Injury Image Darkly pigmented skin does not have a visible blanche response Examine the skin for other changes indicating pressure injury Discoloration compared to surrounding skin Pain in the area Palpate for Induration Skin is intact Skin is purple or maroon Epidermolysis develops Epidermal lift Epidermal separation Epidermal lift Epidermal separation 2016 National Pressure Ulcer Advisory Panel 91 Offload pressure from the area Turn side to side Elevate heels from bed Sleeves with foam inside do not relieve pressure Usually no need to upgrade sleeping surface Do not rub tissue Continue to assess skin on each shift Use moisturizing and skin protecting cleansers Keep skin cleaners at bedside Reposition hourly in w/c Sleep flat at night Boggy or true Stage I Stage as Stage I Elevate heels Flex knee gatch to reduce hammock effect Topical vasodilators? Water filled gloves? (Adejumo, 2010) Clinical issues with pressure relief Abduction pillows with hip replacement Buck s traction Stage 2 Pressure Injury: Partial-thickness skin loss with exposed dermis Partial-thickness skin loss with exposed dermis. The wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister. Adipose (fat) is not visible and deeper tissues are not visible. Granulation tissue, slough and eschar are not present. These injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel National Pressure Ulcer Advisory Panel

17 Stage 2 Definition, continued This stage should not be used to describe moisture associated skin damage (MASD) including incontinence associated dermatitis (IAD), intertriginous dermatitis (ITD), medical adhesive related skin injury (MARSI), or traumatic wounds (skin tears, burns, abrasions) National Pressure Ulcer Advisory Panel IAD Skin Tear 97 ITD Viability of the dermis Viable dermis appears Shiny Red Visible blood vessels in reticular layer Edge may be distinct in thick tissue or beveled in thin tissue Painful May have serous drainage May have a thin layer of nonremovable fascia visible 2016 National Pressure Ulcer Advisory Panel Visible blood vessels and fascia (thin ivory layer). Distinct edge due to thick skin Beveled edge 98 Stage 2 Pressure Injury Images Inspect skin for shallow wounds or shiny areas of skin loss Normal surrounding skin Do not include wounds covered with slough They are full thickness Do not include ulcers healing with granulation tissue Stage 2 of the lateral heel Stage 2 of the thigh and scrotum from medical device Stage 2 of the anterior chest from prone position 2016 National Pressure Ulcer Advisory Panel Stage 2 Pressure Injury Healing Epithelialization The presence of epithelial cells in hair follicles and sweat glands in the dermis promotes healing without scar and contracture Pigmentation seldom returns Deep tissue injury develops a thin blister The wound bed remains dark 2016 National Pressure Ulcer Advisory Panel

18 History of urine or fecal incontinence Skin has urine odor Skin is red Small open wounds where urine or stool has been in contact with skin Look in folds of skin Incontinence associated dermatitis is due to prolonged exposure to caustic fluids Skin fold breakdown Associated with sweating Common skin folds include breasts, groin, beneath skin folds May have bacteria and Candida present in skin fold Axilla: Proteus mirabilis Enterococcus faecalis Staphylococcus coag neg Candida albicans VRE Pannus: Staphylococcus coag neg Proteus mirabilis Enterococcus faecalis Candida albicans Escherichia coli From Edwards, Black, Unpub data Breast: Proteus mirabilis Staphylococcus coag neg Diphtheroids Groin: Staphylococcus coag neg Candida albicans Diphtheroids Proteus mirabilis Enterococcus faecalis Knee: Proteus mirabilis Staphylococcus coag neg Only 33% of the organisms cultured were Candida Albicans History of exposure to burning substance Burns can be due to Hot liquids Caustic fluids Very painful wounds Blisters form This burn was from Betadine that pooled beneath the patient Known traumatic event Most common locations are hands, shins and forearms May occur during transfers or falls Common in paper-thin skin Elderly with loss of skin bulk Chronic cortisone use Off load Do not position supine Limit sitting to 1 hr and put feet on footstool Use chair cushion 4 inches of foam Air cell cushions Protect with skin Hydrocolloid Tends to roll, melt and be difficult to remove Skin ointments better Increase calories and protein intake 18

19 Blister Protection Offloading Dressings? Or topicals? No shoes that rub Open ulcers Hydrocolloids, gels, honey, foams effective Offloading Deep Tissue Pressure Injury: Persistent non-blanchable deep red, maroon or purple discoloration Intact or non-intact skin with localized area of persistent nonblanchable deep red, maroon, purple discoloration or epidermal separation revealing a dark wound bed or blood filled blister. Pain and temperature change often precede skin color changes. Discoloration may appear differently in darkly pigmented skin. This injury results from intense and/or prolonged pressure and shear forces at the bone-muscle interface National Pressure Ulcer Advisory Panel DTPI Definition Continued The wound may evolve rapidly to reveal the actual extent of tissue injury, or may resolve without tissue loss. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle or other underlying structures are visible, this indicates a full thickness pressure injury (Unstageable, Stage 3 or Stage 4). Do not use DTPI to describe vascular, traumatic, neuropathic, or dermatologic conditions. Vasopressor Ischemia Traumatic Bruising Coumadin Necrosis Evolution of DTPI Day 1 DTPI Day 3 DTPI Day 10 Unstageable Classify this pressure injury as a Deep Tissue Pressure Injury while it is intact discolored skin (Day 1) or discolored skin with epidermal blistering (Day 3). If the DTPI becomes necrotic, it is classified as unstageable (Day 10) 2016 National Pressure Ulcer Advisory Panel National Pressure Ulcer Advisory Panel Evolution of DTPI in darkly pigmented skin Images of Deep Tissue Pressure Injury Due to the thickness of the skin, the epidermal separation will remain intact for a longer period of time. This phase can be mistaken for skin tears National Pressure Ulcer Advisory Panel National Pressure Ulcer Advisory Panel

20 Traumatic events History of trauma in the body area now purple Skin injury in pelvis Hematoma with loss of overlying skin (Morel- Lavalee Lesion) Pelvic Hematoma Bruising Ischemic events Arterial or venous Vasoactive drug induced End of life Little known, may be a shallower eschar Venous congestion Ischemia End of Life Hematoma Skin diseases with purple hues or rapid eschar formation Pyoderma Calciphylaxis Lymphedema Coumadin necrosis Coumadin Necrosis Lymphedema Calciphylaxis Pyoderma Offload, offload, offload Turn side to side only On back 3 times per day to eat Boots for heels If unstable, change surface and turn slowly Maintain perfusion Therapies being tested Noncontact low freq US Data from Honaker shows resolution if started early Topical balsam of peru Anecdotal Treatments in the future? HBO? Antioxidants? Honaker JS, Effects of non-contact low-frequency ultrasound on healing of suspected deep tissue injury: a retrospective analysis. Int Wound J Feb;10(1): Stage 3 Pressure Injury: Full-thickness skin loss Stage 3 Pressure Injury with Epibole Full-thickness loss of skin, in which adipose (fat) is visible in the ulcer and granulation tissue and epibole (rolled wound edges) are often present. Slough and/or eschar may be visible. The depth of tissue damage varies by anatomical location; areas of significant adiposity can develop deep wounds. Undermining and tunneling may occur. Fascia, muscle, tendon, ligament, cartilage or bone is not exposed. If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury. Epibole (EE-pibb-ohlee) The rolling of the outer rim of the ulcer onto itself Due to lack of tissue in the wound bed to support the epidermal cells to cross the wound bed Needs to be removed 2016 National Pressure Ulcer Advisory Panel National Pressure Ulcer Advisory Panel

21 Wound bed in a Stage 3 Pressure Injury Ulcer surface appearance Full thickness pressure injury heals via Granulation tissue Capillary buds Contracture May create epibole Epithelialization over the scar Is fragile for at least a year Slough (sluf) Dried inflammatory fluids that is moist, stringy, and yellow, tan, gray, green or brown Eschar (ES-car Necrotic tissue that is leathery or thick and black, brown or tan 2016 National Pressure Ulcer Advisory Panel National Pressure Ulcer Advisory Panel Images of Stage 3 Pressure Injury Stage 4 Pressure Injury: Full-thickness loss of skin and tissue. Ischium Sacrum Heel Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone in the ulcer. Slough and/or eschar may be visible. Epibole (rolled edges), undermining and/or tunneling often occur. Depth varies by anatomical location. If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury National Pressure Ulcer Advisory Panel National Pressure Ulcer Advisory Panel Images of Stage 4 Pressure Injury Muscle Bone Tendon Granulation tissue Epibole (rolled edge) Slough inflammatory byproduct, not tissue Eschar Necrotic tissue Heals by scar and contraction Of course, the question often is what if I don t know the history of the wound? Stage it as you see it today 2016 National Pressure Ulcer Advisory Panel

22 Necrotic wounds in distal tissue in limbs with poor perfusion Painful Punched-out Pressure ulcers can develop quickly in ischemic limbs Heal slowly, if at all Arterial ulcer DFU- ulcers on the walking surfaces of the foot in an ambulatory neuropathic diabetic Calloused Deep (r/o osteo) DFU Pressure ulcer in ischemic foot Offload Turn side to side Not reposition Upscale bed Do not count turn assist beds and lateral rotation beds as turning Débride slough Increase protein and calories Offload, offload Turning, upscale bed if patient cannot be placed side to side Control shear Control diarrheal exposure Increase protein/calories Consider tube feeding/tpn even if short term Use exudate absorbing dressings/packing protect periwound Unstageable pressure injury: Obscured full-thickness skin and tissue loss Unstageable Images Full-thickness skin and tissue loss in which the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar. If slough or eschar is removed, a Stage 3 or Stage 4 pressure injury will be revealed. Stable eschar (i.e. dry, adherent, intact without erythema or fluctuance) on an ischemic limb or the heel(s) should not be removed. Nose Heel Sacrum 2016 National Pressure Ulcer Advisory Panel National Pressure Ulcer Advisory Panel

23 Characteristics Intact, hard eschar Normal, non-fluctuant surrounding tissue No pain in wound No drainage No odor Leave this skin intact There is nothing underneath it! Trim as it sloughs Open wound edges Drainage, odor Fever, other signs of cellulitis, sepsis Debridement needs to be sharp for cellulitic wounds This stable eschar was debrided and created an unstable ulcer bed Limit sitting to as little as possible We prefer bedrest Patient prefers being up Check function of w/c cushion Débride quickly Rule out osteomyelitis Increase intake of protein and calories Reteach program for continued offloading and skin inspection Turn side to side only Upscale bed Start chemical debridement as long as eschar is thin and tissues or patient show no infection Sharp debridement if infected or thick Increase calories and protein Medical Device Related Pressure Injury Definition Offload side to side Upscale bed Surgical debridement or excision Pack with single rolled gauze Do not apply occlusive dressing Increase protein and calories Medical device related pressure injury results from the use of devices designed and applied for diagnostic or therapeutic purposes. The resultant pressure injury generally closely conforms to the pattern or shape of the device. These ulcers should be staged unless on mucous membrane. Unstageable Stage 1 Stage 2 Stage 3 Deep tissue pressure injury Stage National Pressure Ulcer Advisory Panel 23

24 Mucosal Membrane Pressure Injury Images of Mucous Membrane Ulcers Mucosal membrane pressure injury is found on mucous membranes with a history of a medical device in use at the location of the injury. These ulcers cannot be staged. There is no epidermis or dermis in this tissue Upper layer is epithelium Columnar cells produce mucus Laminar layer provides support 2016 National Pressure Ulcer Advisory Panel National Pressure Ulcer Advisory Panel When more than one stage is present Stage the wound using the most severe stage this ulcer is an unstageable ulcer 2016 National Pressure Ulcer Advisory Panel 3 legged stools tip over when any one leg is missing Pressure Relief/Reduction Offloading (from 2014 Guidelines) Upscaled beds/mattress, chair cushions Teaching pressure redistribution Limit sitting on ulcer to 1 hour 3 times per day Wound care (From 2014 Guidelines) Debridement, dressings/packing, topicals Do not debride ischemic tissue or malnourished pts Nutrition (from 2014 Guidelines) Increased protein and calories Vitamin and zinc supplement if low Principles guiding care Devitalized tissue must be removed to decrease inflammation and reduce risk of infection Exception today is the heel in an ischemic limb Principles Match debridement type to condition of ulcer and patient Autolytic for stable slough Hydrogels, hydrocolloids Enzymatic for stable slough in stable patient that can tolerate 2 or more weeks of therapy Collagenase Mechanical for stable slough in stable patient in whom pain can be managed Gauze dressings, whirlpool, ultrasound Sharp or surgical Infected ulcers, slough, boggy eschar, septic patients Techniques Screen all patients with pressure ulcers for nutritional deficits (SOE = C) When nutritionist is not available: Can the staff estimate caloric needs? Fluid needs? Can the staff provide adequate calories/protein/fluids? Patient needs to eat more calories and protein to heal a wound than that did prior to wounding. Is the tube feeding that is not infused when held for meds, treatments, and so on replaced? 24

25 Encourage consumption of a balanced diet that includes good sources of vitamins and minerals (SOE = B) Are patients with ulcers eating inadequately and being supplemented with vitamin C, zinc and iron? Scurvy uncommon today Zinc treatments over 2 weeks can alter copper status Do not routinely order these supplements and allow patients to eat poorly Assess pain with appropriate pain scales (SOE = B) Pressure ulcers are ischemic wounds They hurt all the time If baseline pain is mild, use nonopioid If baseline pain is more intense, consider why infection, pressure etc and treat pain Do not assume cognitively impaired patients have no pain Pain input tracks working, response to pain tracts are not Important to reevaluate the current surface in use However, for the most part the surface that the patient developed the ulcer on will not suffice for healing Decision on surface is primarily based on: Sensation, Spontaneous Movement Ability to be positioned off of ulcer Who can order them? and how? They do not replace turning or repositioning They can fail and need to be assessed The surface needs to be cleaned Consider changing them every 30 days Document the name of the actual bed in use on pressure ulcer cases Try to get wounds to heal early Remove biofilm with frequent dressing changes Debride wounds aggressively Use antiseptics However, no matter what you do the biofilm reforms in hours 25

26 Surgical- now Sharp- now Mechanical- days A. Autolytic B. Enzymatic C. Mechanical D. Sharp E. None Enzymatic-weeks Autolytic many weeks A. Autolytic B. Enzymatic C. Mechanical D. Sharp E. None A. Autolytic B. Enzymatic C. Mechanical D. Sharp E. None A. Autolytic B. Enzymatic C. Mechanical D. Sharp E. None A. Autolytic B. Enzymatic C. Mechanical D. Sharp E. None 26

27 Prevent contamination of the wound Retard growth of pathogens Remove cellular and tissue debris Absorb drainage Promote healing from the base of the wound Protect granulation tissue by keeping wound bed moist (not wet) Supply the wound bed with missing cellular elements Control symptoms of unhealable wounds Stage 3 or 4 with slough Enzymatic debrider on slough Moisture retentive wound bed filler Alginate if highly exudative Foam if mildly exudative No hydrocolloids or films Silver, honey or cadexomer iodine for biofilm control Cover dressing Absorptive Window area if dressing change frequent Silicone contact layer Cover dressing needs to be securely adhered to the skin Without damaging skin on removal Skin prep helps protect skin Cover dressings include Gauze Hydrogels Hydrocolloids Gauze/hydrocolloid/ foam impregnated with Antiseptics Silver Honey Cadexomer Iodine Not Betadine Xeroform (bismuth) Hibiclens? Approved for open wounds Antibiotics Antibiotic Solutions Use silver dressings on wounds with loose slough Adherent or thick slough needs debridement, silver does not penetrate Wounds with delays in healing Granulation tissue pale or fragile (easily bleeds) Local signs of infection Systemic infection needs antibiotics high risk patients Bactroban for MRSA in DM Do not use as a long term dressing Cellular debris (slough) develops from inflammation Biofilm Exposure to fecal matter Continued pressure Maintenance debridement for biofilm control Few dressings to prevent exposure Better to divert fecal stream 27

28 Tissue debris is eschar Develops from continued pressure frank infection Treatment of eschar Sharp removal if on pelvis Stable eschar on ischemic limbs should be left in place Enzymes seldom penetrate Eschar needs debridement Stable heel eschar Leave dry, trim as it lifts Blood is best absorbed by gauze Needs to be changed when wet Serous drainage is inflammatory by-product Absorb high volumes with alginate Longer dressing change intervals Becomes gel when filled with drainage Use petrolatum or foam as cover dressing Absorb high volumes with gauze Shorter dressing change intervals Absorb lower volumes with foams Prevent injury to normal skin and healed skin around the wound Hydrocolloids, films as window frame Alginates come in ropes and dressings to conform to wound spaces Fill entire wound space Called dead space Prevents pockets of unhealed tissue within wound bed Prevents anaerobic growth Options Pack with one long dressing Paste or gel Alginate Once granulation tissue is present throughout the wound bed Change dressing to gel to retain moisture Use dressings with long wear time Foam, gel, some hydrocolloids Avoid wet to dry dressings and wet to moist dressings do not maintain wound bed moisture injure new tissue when removed Therefore are used only when debridement is needed Debridement of nonviable tissue Antiseptic dressings Silver Iodine Honey Antibiotics if patient is septic or bacteremic Increase nutrition and pressure relief Dressings can provide A matrix for cellular growth Collagen Growth factors Commonly considered as advanced therapies May be tested as primary treatments to speed healing 28

29 Composite dressings to prevent shear injury in ventilator dependent patients who need HOB elevated Effect of foam on shear Ohura, Takahashi from Japan Composite dressings prevented sacral ulcers in ICU patients by Brindle, patients in 2 groups No ulcers in dressing group 6 in control group Occlusive dressings on contaminated wounds Leads to local invasion and sepsis Packing deep wounds with multiple dressings Leads to retained packing and abscess Use of one dressing until healed Wet to dry dressings until healed can t happen Prolonged use of cellular toxins in clean wounds Use iodine, silver and Dakin s for short times Lack of pain control before removing dressings Nothing Silicone/Foam dressing Hydrocolloid dressing Film dressing Nothing Silicone-foam dressing Hydrocolloid Hydrogel MIST Hydrocolloid without packing Dry packing and cover dressing Moist packing and cover dressing Dilute Betadine packing and cover dressing Skin protection Antifungal Hydrocolloid Siliconefoam 29

30 All pressure ulcers must be assessed daily If dressing is on (and 3-5 day dressing) note if it is intact If wound visible, note if it is stable Monitoring system must be easy to follow Use single page in paper chart PUSH tool At the first sign of deterioration, plan must change Increasing drainage Change in nature of drainage Drainage becoming more bloody or purulent Increasing pain, odor Failure to heal When healing, debriding dressings need to be stopped There is no such thing as wet to dry dressings until healed! Evidence is modest Mostly clinical case series Clinical experience with NPWT for most of us Perhaps with newer models of NPWT we can get some RCTs Evidence on electrical stimulation Evidence on noncontact low frequency ultrasound Wound science is really beginning to focus on cellular healing cellular determents to healing Biofilms Treatments needed by chronic wounds, by acute wounds and by complex wounds I dressed the wound, God healed it (Ambroise Pare, ) Today I optimized the patient, God healed the wound is still true, PhD, RN, CWCN, FAAN Associate Professor Nursing University of Nebraska Medical Center 30

31 Peripheral Arterial Disease is noncardiac disease of blood vessels that slow blood flow to the peripheral tissues Today often called Lower Extremity Arterial Disease (LEAD) 2 Forms Chronic limb ischemia Progressive, often leads to ulceration Acute limb ischemia Sudden loss of limb perfusion that threatens the limb Can be critical limb ischemia Rest pain, ulceration/gangrene Arteriosclerosis Begins with arterial injury that leads to production of plaque Plaque eventually obstructs the flow of blood Further injury to the artery can lead to clot formation Process more rapid in diabetes At age 55, 10-25% of people have arteriosclerosis 70-80% of them are asymptomatic They don t stress the demand on the blood flow Patients with arterial disease are 4 times more likely to die within 10 years than nondiseased patient Patients with critical limb ischemia 50% alive at 2 years 25% have amputations 25% have died from cardiac disease Intermittent claudication From the Latin word to limp Reproducible pain on exercise which is relieved by rest A supply demand problem Pain also occurs when leg is elevated Pain is relieved when leg is lower than the heart Other symptoms Burning or aching pain in feet and leg Cold feet Nonhealing ulcers Smoking Diabetes mellitus Hypertension Homocysteinemia Hypercholesterolemia Stenosis becomes so occlusive that blood flow is severely impaired Pain at rest supply cannot meet demand at rest Ischemia Ulceration or gangrene 6 P s of acute limb ischemia Vascular Pallor Pulselessness Persistent coldness Neurological Pain Paresthesias Paralysis 31

32 Thin shiny skin Loss of hair Thick nails Slow capillary refill Absent or weak pulses Abnormal ABI Pallor or pain when leg raised Redness (rubor) when leg down Necrotic wounds in distal tissue in limbs with poor perfusion Painful Punched-out Pressure ulcers can develop quickly in ischemic limbs Heal slowly, if at all Pressure ulcer Ankle Brachial Index Compare blood pressure in arm to that taken in the foot Cuff on lower leg Doppler on dorsalis pedis and posterior tibial to hear systolic ABI = systolic/ankle Interpretation ABI over 1.3 = abnormal, noncompressible vessels ABI of = normal ABI 0.5 to 0.8 impaired flow with demand ABI < 0.4 impaired flow at rest Measuring the flow of blood into the leg by assessing the levels of oxygen in the tissues Values over 40 mmhg usually indicate ability to heal Healing unlikely with values > 25 mmhg 32

33 The ulcer is a symptom, how can the cause be treated? Improving Arterial Flow to the Limb Surgical revascularization Antiplatelet aggregates (aspirin, Trental) Vasodilators Slow the disease progression Stop smoking, no nicotine in vapors or patches Smoking cessation tough Dropped from 41% to 17% (Alhadad, 2013) Walking program Walk to point of pain Hyperbaric oxygen therapy Improve dietary intake of fruits, vegetables, fish, fiber Limit intake of red meat These changes are not to aid healing but slow the disease Glucose control if diabetic Skin care Apply emollients after bathing to prevent cracking and fissures Dry toe space well Use lamb s wool or stockings to keep warm Place in boots if bedridden Remove on every shift to assess skin/heels Avoid injury Do not go barefoot Wear closed toed shoes Inspect shoes before wearing Wear protective material when outdoors Get professional foot care Wear socks during the winter Do not use heating devices Do not use chemicals on limbs Promptly treat minor injures Assess for infection Erythema halo around wound Begin antibiotics DM often have MRSA Betadine paint Dress foot ulcer with dry dressings Use topical lidocaine Do not debride stable eschar or dry gangrene No perfusion to aid healing Will develop wet gangrene Unstable eschar Indications Nonhealing Irreversible ischemia Level of amputation determined by TCOMs Begin as low as possible due to morbidity Many operations are palliative Survival at 3 years 57% of BKA 39% of AKA 33

34 Arterial disease is progressive Patient and family may come to help to cure this when cure is not possible Have a plan for those discussions The most common chronic wound, PhD, RN CWCN University of Nebraska Prolonged elevations in blood sugar leads to deposits of glucose in the cell as sorbitol and fructose The deposits slow nerve conduction and allow oxygen free radicals to accumulate and slow production of nitric oxide Tightens ligaments in foot Injures the nerves Constricts the arteries Accelerated small vessel atherosclerosis Tibial and peroneal arteries commonly affected Arteries narrow due to formation of plaque and cannot dilate when needed Extent of disease is worse than age of patient would predict 20 year old DM Sensory Loss Increased sorbitol in blood binds to nerves Initially painful Then numb and unable to feel hot and cold pressure from shoes Injury from blunt or sharp objects Repeated injury from pressure and shear Wounds go unnoticed 34

35 Reduced sweat and oil in skin leads to dry skin that cracks Susceptible to tears and infections in open wounds Increased capillary blood flow (if no macro PVD) > false sense of security about foot circulation But these vessels are permanently open Cardiac disease Digestive disease Loss of function in the intrinsic (originating in the foot) muscles of the foot Claw toe deformity Convex foot with a rocker bottom appearance Charcot deformity Dynamic plantar foot pressures are elevated Atrophy of intrinsic foot muscles Primarily plantar flexors of toes clawing of toes subluxation at M-P joints Loss of arch of foot More than flat feet Limitation of ankle joint mobility Shortened Achilles tendon The foot has a Called Charcot changes rocker deformity Fractures and dislocations of bones and joints that occur with minimal or no known trauma May require surgery to reconstruct the bones Cracks & Fissures Dermatophyte fungi Bacteria causing microthrombi MRSA very common Probing a DFU to determine the actual depth of the wound 35

36 Wounds in ambulatory diabetics due to injury in neuropathic limbs Callous formation around the wound Located on walking pressure points on plantar surface Metatarsal heads Tops of toes Duration of DM Usual methods of control Presence of Retinopathy Nephropathy Autonomic Neuropathy Slow digestion Orthostatic hypotension Vascular disease Smoking history and current use Ulcer history Prior ulcers and methods used for treatment Amputations? Try to determine compliance with routine care How often is skin inspected? Who does it? And how is it done? Examine both feet without shoes or socks in all patients with DM Note claw deformities Check pulses Ascend the leg until you find them Doppler Ankle-brachial index Check between the toes for ulcers Attempt to put the foot through ROM Check for protective sensation Assess shoes Wide toe box Padded sole Custom shoe if Charcot present Ankle Brachial Index Compare blood pressure in arm to that taken in the foot Cuff on lower leg Doppler on dorsalis pedis and posterior tibial to hear systolic ABI = systolic/ankle Interpretation ABI of 1 = normal ABI 0.5 to 0.8 impaired flow with demand ABI < 0.4 impaired flow at rest Monofilament testing Failure to sense 5.07 gm indicates lack of protective sensation Test multiple sites with patient s eyes closed Wagner Ulcer Classification Scale Grade 1 Superficial ulcer Appearance 2 Ulcer extension into ligament, tendon, joint capsule or fascia, with no abscess or osteomyelitis 3 Deep ulcer with abscess or osteomyelitis 4 Gangrene to portion of forefoot 5 Extensive gangrene of foot 36

37 Treating the DM Getting BG in control Daily BG/HgbA1C No smoking or nicotine patches Improving nutrition Consider impact of kidney disease on ability to metabolize proteins Wound care Debride callous Debride wound Offload Shoe Total contact casting Growth Factors TGF- approved for the DFU patient Very delayed with increased risk for infection Poorly functioning white blood cells WBC do not kill bacteria when BG is >200 Decreased signals in wound to stimulate healing Decreased levels of TGF- in wound and in skin near wound Inadequate blood supply to wound Nonulcerated Broad flat shoes Daily skin inspection No home surgery Consider the issue of nonadherence Ulcerated Complete off loading shoes or bedrest Debridement Packing WBC scan vs bone scan vs MRI to r/o osteomyelitis Often progressive amputation 80,000 lower limb amputations yearly in the US 60% are in patients with DM Check skin daily (you or spouse) Always wear shoes (that fit) even at night Esp in the toe area Trim nails carefully (avoid short nails) Be careful with new shoes (even custom shoes) Avoid home remedies Avoid heat (e.g. no hot soaks, heating pads) Don t smoke Seek treatment early; if no progress, see specialist early 37

38 Shoe size and fit Take the shoe off of the patient and trace the patient s foot on paper Place the shoe on the tracing and trace it Show the patient how the foot does not fit in the shoe Expect to see DM patients Plan for preventive care Skin inspection Callous removal Plan for ulcer care Early care has better outcomes Up to 70% of all leg ulcers are venous leg ulcers., PhD, RN, CWCN, FAAN University of Nebraska Medical Center 2.5 million people in the US have chronic venous insufficiency About 20% of those patients will develop VLU That is 500,000 patients over their lifetime VLU costs reach 2.5 billion to treat 6 million patients with current VLUs About $2500 per month per patient Chronic insufficiency of the venous valves Following DVT Venous hypertension from weak vein valves or high pressures Distention and varicosity of veins 38

39 Spider veins Varicose veins Edema when legs dependent Aching in legs Lipodermosclerosis Inflammation of fat Stasis of blood in lower leg Escapes from the vessels Erythema Hemosiderin deposits Eczema History Venous disease, DVT Hours upright in one position Use of support hose Previous ulceration Atrophie Blanche Clinical assessment Edema Lipodermatosclerosis Pain relieved with elevation Dermatitis Hemosiderin deposits Doppler to assess competency of veins Ulcer in gaiter area Control the cause venous hypertension Compression Limb elevation Antiplatelet aggregates Improve nutrition and control weight Treat the wound and dermatitis Debridement Antiseptics silver common Steroids and moisturizers to periwound skin Tissue replacement Elastic example stockings Used in bedridden patients Fibers with stretch to more than 100% of their size Effective in reducing edema, but do not always support the venous pumping function Inelastic example Unna boot Used in ambulatory patients Fibers that stretch some to little Often well tolerated due to the dramatic reduction in edema and support venous pumping function 39

40 Provide maximal pressures at the lower leg in the standing position and less when supine Lower pressures going up the leg Measured by compression at the ankle Class 1 light support (14-17 mmhg) Used to treat varicose veins Class 2 medium support (18-24 mmhg) Used to treat more severe varicosities Class 3 strong support (25-35 mmhg) Used to treat severe venous hypertension and ulcers Can be removed for showering Can be difficult to put on Compression with wraps (not TEDs) 4 inch ACE at ankle 6 inch ACE for leg Need to be rewrapped BID Risk of error in application Can be removed for bathing Inelastic Medium to high stiffness Can be bulky Can be removed for bathing Can be applied fairly easily and adjusted 40

41 Don t always fit Can lead to ulcers Can lead to tourniquet injury Inelastic wraps that cannot be reapplied for moderate level of pressure Paste can be zinc, glycerin, gelatin or calamine Covered with elastic wrap High compression - sub-bandage pressure 35-40mmHg ABI 0.8: Four-Layer bandaging (4LB - orthopaedic wool, crepe, elastic layer, cohesive layer) Reduced compression - sub-bandage pressure 17-25mmHg ABI 0.7: three-layer bandaging (orthopaedic wool, crepe, cohesive layer) AB1 0.6: three-layer bandaging (orthopaedic wool, crepe, long-stretch elastic layer) ABI <0.5: avoid compression except with medical supervision Can assist healing of VLUs When other compression systems have not worked Work while patient is resting Legs should be elevated to aid compression (and patients should not sit on wooden stairs!) High risk for recurrence without maintenance compression (elastic stockings) therapy When compliant with compression recurrence is around 28% 41

42 About 30% of leg ulcers have an arterial component Compression can worsen arterial inflow and lead to distal gangrene and limb loss Use ABI as a guide for compression ABI of (adequate) can have high compression therapy ABI between reduced strength compression ABI <0.5, compression therapy is contraindicated conduct a comprehensive vascular assessment Joyce M. Black, PhD, RN, CWCN, FAAN University of Nebraska Medical Center Omaha, NE Skin damage associated with excessive exposure to moisture Incontinence Associated Dermatitis Irritant contact dermatitis from exposure to caustic fluids (urine, stool), use of absorptive containment device Intertrigo or Intertriginous Dermatitis inflammation in skin folds related to non-caustic fluids (perspiration), friction and bacterial/ fungal bioburden Periwound maceration skin breakdown from wound exudate, associated with volume of exudate, its constituents and bacterial bioburden IAD Prevalence % IAD Incidence % Stage 2 pressure ulcers 22-30% Fungal infections 10-18% Combination injuries 21% Data from Bliss, 2006 & 2007; Peterson, 2006, Junkin, 2007; Gray 2012; Campbell, 2014; NPUAP

43 Skin ph 5.5 This acid mantle keeps our skin healthy and resists bacterial invasion Some body fluids are not caustic Sweat ph is 5.5 Exposure leads to maceration Some body fluids are caustic Diarrhea ph is acidic to alkaline Urine ph depending on disease and diet Exposure leads to IAD Water in urine or stool is absorbed into corneocytes Overhydrated cells swell and disrupt barrier leading to maceration and injury from friction Irritants pass more easily through cells to stimulate irritation and inflammation Skin becomes more alkaline and promotes bacterial growth Liquid feces contain digestive enzymes that damage skin 25 3 All incontinent patients/residents Fecal and urine combined Fecal or urine individually Use of occlusive undergarments Fragile skin condition Immobile Confused, comatose, paralyzed Unable to perform personal hygiene Pain On antibiotics or immunosuppressants Poor nutritional status, tube feeding Critically ill White soft skin Serous drg from wound Periwound maceration Level 4 -- Rarely moist Skin is usually dry; linen only requires changing at routine intervals Level 3-- Occasionally moist Skin is occasionally most, requiring an extra linen approximately once a day Level 2 - Very moist Skin is often but not always moist. Linen must be changed at least once a shift Level 1 -- Constantly moist Skin is kept moist almost constantly by perspiration, urine etc. Dampness is detected every time patient is moved or turned. Determine cause of incontinence Acute, often Urinary Tract Infection High risk groups post menopausal women patients with a history of instrumentation women recently sexually active Sometimes urgency due to caffeine Chronic, urine may be colonized High risk groups are elders with cognitive or mobility problems

44 Mild Dry, intact, not blistered Pink or red with diffuse (not sharply defined), often irregular borders Moderate Shiny and moist skin with weeping Pinpoint areas of bleeding Raised areas/blisters Angry bright red Small areas of skin loss Painful Severe Red with areas of denudement Oozing/bleeding Skin layers may be stripped off as the oozing protein is sticky and adheres to any dry surface Periwound maceration IAD, mirrored wound Unstageable ischial ulcer Unstageable ischial ulcer Not certain Keep the skin clean and dry Use a ph balance skin cleanser Clean the skin promptly following episodes of incontinence Protect the skin from exposure with skin barriers Disposable barrier cloth recommend by IHI & IAD consensus group Use a skin moisturizer to hydrate the skin Other recommendations Use an incontinence pad and/or briefs that wick away Consider pouching device or a bowel management system Ensure an appropriate microclimate & breathability < 4 layers of linen Wick away material under y Panel; adipose and breast tissue Control the cause/exposure Increase fluids and protein for healing Skin care much like prevention Clean promptly Protect the skin from next exposure Barriers with zinc oxide, dimethicone Monitor for deterioration Infection Increasing Pain Bleeding Partial thickness wounds Epithelialization Healed IAD visible in darkly pigmented skin Cleanse don t clean Use soft clothes Use ph balanced soap No Dial, Irish Spring etc Alkali based Lead to skin erosion No alcohol-based products Products can be liquid, emulsion, foam, or impregnated into wipes Don t rub to clean off debris No rinse products ideal Pat dry, don t rub 44

45 While the skin is damp apply a moisturizing lotion Lotion needs to have no fragrance, no alcohol, no preservatives Fragrance can be inhaled and can be nauseating Some compounds purposely contain alcohols to dry the skin, so that you use more product Preservatives are absorbed by fragile skin Highly allergenic Benzyl alcohol, butylated hydroxytoluene, chlorocresol, imidurea, parabens, sodium metabisuphite, sorbic acid Absorbed by very young skin (prior to 44 days of life) and very old skin and damaged skin Also called skin barriers or moisture barriers Apply product liberally to prevent skin damage from urine or stool Try to use products that contain blocking agents Dimethicone Petrolatum Zinc oxide (not by itself) Consider how you will get the product off! Liquid barrier films also available Applied to the skin and after evaporation leaves of film barrier Underpads or absorbant briefs Should wick urine away from skin not trap against the skin Pads/briefs create heat and can lead to maceration if left in place Recommendations Use when ambulating for dignity Open or remove when at bedrest Perineal odor from urine common even after bathing Only when skin cells shed, does the odor from those cells leave Important to do good skin care and change pads when soiled Deodorizers available Exposure to pressure Immobile Usually a single ulcer Ulcer not in areas of exposure to urine/stool Edge is not discrete Seldom is periwound inflamed Pressure ulcers Exposure to urine or stool Skin looks denuded in multiple open areas with flaring on the edges Skin is inflamed Ulcers are in areas that have been exposed to fluid may be mirrored or kissing Skin smells of ammonia Incontinence Associated Dermatitis 45

46 Consider history and presentation Burning sensation, worse with cleaning Red angry skin in areas exposed to urine and stool, often mirrored Maceration of skin, PhD, RN, CWCN, FAAN Associate Professor Nursing University of Nebraska Medical Center Intertriginous dermatitis (ITD) is inflammatory dermatosis of opposing skin folds Arndt & Bowers; Janniger A form of dermatitis from noncaustic body fluid (sweat) verses caustic fluids (urine and stool) (Black) 11.2% of 1116 women reported inframammary ITD (McMahon) 63% of 100 obese patients (Brown) Unknown in hospitalized patients Skin moisture is common in patients in the ICU Sweat gland found in dermis Controlled by nerve from sympathetic nervous system (fight or flight) Body temperature regulation Profuse sweating leads to water and sodium loss 46

47 Moisture from sweat is trapped in the skin fold Normally, skin fold is dry due to body movement and air flow Obese patients sweat excessively due to large body mass and relatively small skin surface to convect heat Excess moisture is absorbed by the keratinocytes Cells become boggy and do not glide easily Small open areas develop Sometimes self neglect listed as etiology Obesity alters skin barrier function Increased transepidermal water loss and erythema Increased sweat gland activity Decreased blood flow in adipose tissue Skin ph increased in inguinal skin folds in obese women Diabetes, steroid use and broad spectrum antibiotic's also contribute to ITD Our study of skin fold cultures* Culture of skin fold on admission No prior treatment with InterDry On no antibiotics or antifungals Original treatment was antifungal powders towels, pillowcases etc Could skin fold contamination be contaminating our surgical sites? Axilla: Proteus mirabilis Enterococcus faecalis Staphylococcus coag neg Candida albicans VRE Pannus: Staphylococcus coag neg Proteus mirabilis Enterococcus faecalis Candida albicans Escherichia coli Breast: Proteus mirabilis Staphylococcus coag neg Diphtheroids Groin: Staphylococcus coag neg Candida albicans Diphtheroids Proteus mirabilis Enterococcus faecalis Knee: Proteus mirabilis Staphylococcus coag neg Only 33% of the organisms cultured were Candida Albicans * Edwards, Cuddigan, Black, 2008 No relationship found between the type or quantity of microorganism cultured and the location or the severity of the erythema, odor or skin temperature. Bedridden hospitalized patients increased exposure to moisture Increased sweat production with diseases, fever, meds skin on skin contact while in bed friction with movement in bed lack of air flow associated with the restriction of movement presence of nosocomial bacteria Hahler,2006 This patient, usually mobile can keep the skin fold dry. Once confined to bed, it rests on her thighs 47

48 Consider normal folds of tissue as skin folds when at bedrest Redundant tissue in breast Groin Consider skin beneath braces and splints as skin folds The devices keeps the sweat from evaporating Consider the toe webspace in diabetics a skin fold Itching, burning type pain from the raw skin folds Usually a mirrored image Aggravated by sweating or washing the skin Inflamed skin in the skin fold Open skin lesions 283 Janninger,2005 Candidiasis? Cellulitis Odor/embarrassment Pain Surgical site infection? Reversing the cause dry the skin fold Textile designed to Wick fluid/sweat to a dry area on the fabric Called translocation Silver woven into fabric to kill bacterial and Candidal overgrowth Designed to be placed in skin fold with 1 inch exposed fabric for wicking Designed to be worn for 5 days (duration of silver) Control hyperhidrosis Keep skin folds dry by wearing light weight clothes Dry skin folds well after bathing Avoid using Antiperspirants Bed linens, shop towels, paper towels, baby blankets Individual dressings can get lost in deep skin folds 48

49 Treating Candidiasis Avoid zinc oxide due to difficulty with removal Use antifungal powder (thin dusting) Restore bowel flora OTC products Use InterDry with silver dressings in skin folds difficult to reach (obese) ITD is common but fortunately easily treated, PhD, RN University of Nebraska Medical Center Omaha, NE Skin injury due to shearing and friction forces or a blunt trauma, causing the epidermis to separate from the dermis (partial thickness wound) or both the epidermis and the dermis to separate from the underlying structures (full thickness wound). Skin tears are perceived by some to be minor injuries. Estimates of 1.5 million cases in institutionalized adults yearly 49

50 Atrophy of skin Aging thins the rete pegs loosening the connection of epidermis to dermis Corticosteroid use History of skin tears in last 90 days More than one skin tear presently Impairments in Decision making Vision, balance, hearing Self care ability Mobility Gait Physically abusive or resists care Agitated Mechanical lifts needed for movement Contracture Senile purpura/bruising White, 1994 Type 1 Type 2 Type 3 Skin flap can Less than Complete completely 25% of tissue loss cover the exposed skin missing wound Deep tissue injury Blistering skin (bullous disease, burns) Protect the skin on arms and legs with sleeves and stockings Use moisturizer on skin Use gait belts (and not the arms) for moving Avoid adhesives on thin skin Soft silicone foam dressings with atraumatic adhesives Remove tape by pushing skin away from the tape Prevent injury/falls/sharp corners Stop bleeding (elevate/pressure) Irrigate tissue gently to remove large clots Use wet cotton applicator to gently pull skin flap back into place without pulling on it Secure Adhesive wound closure strips Space apart to allow for drainage Avoid tension over flexion sites Foam dressings with mild adhesive Hold in place with tubular bandages Use an arrow to indicate direction of pull during removal Do not use staples, sutures or Steri-Strips Do not use film dressings Confirm tetanus status Baranoski, 2003; LeBlanc, 2009; 50

51 Designed for intact skin Made with strong adhesives Faster healing per RCT of 34 patients followed for 21 days Foam dressing healing = 94% Film dressing healing = 65% Thomas, 1999 Skin tears are painful Skin tears in edematous tissue will have more drainage Change the dressing to one with absorptive capabilities Skin tears can become infected Topical antibiotics will usually work Be certain your staff have a plan to prevent and treat these injuries 51