Joyce Black Joyce Black, PhD, RN, DNP (Hon), CWCN, FAAN University of Nebraska Medical Center, Omaha

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1 Joyce Black, PhD, RN, DNP (Hon), CWCN, FAAN University of Nebraska Medical Center, Omaha Pressure Perpendicular force in excess of capillary flow to tissues, hypoxia develops and tissue dies Shear Pull and stretch blood vessels as tangential force is applied to tissue, tissue becomes hypoxic Friction is no longer seen as an etiology No pressure component Heat builds up and leads to blistering Pressure leads to deformation of cells Cells can die When combined with ischemia, resulting injury is faster When combined with shear (leading to ischemia) same result Shear deep in tissues HOB at 45 degrees is worst combination of shear and pressure Can patients be turned when HOB up 45 degrees? Do we understand shear injury to tissue? Nonblanchable erythema once pressure off Pallor until hyperemic Torn edges on wound This dyspneic patient sat up to breathe and developed significant shear injuries Skin temperature and humidity in the space between the bed surface Relatively ignored until recently Increases risk of pressure ulcers Temperature increases metabolic need 10% increased need for each 1 degree rise These substrates cannot be delivered if the skin is under pressure Moisture decreases tolerance Differential diagnosis needed Is this a pressure ulcer? Or another wound? Just because the skin is open does not make the ulcer a pressure ulcer However, if it is staged, the presumption will be that the wound was due to pressure Skin tear Arterial ulcer IAD Pressure Ulcer 1

2 Nursing owns the skin Skin wounds present on admission (POA) cannot be considered facility acquired Therefore, essential to develop a plan of care to promote healing or prevent worsening And, crucial to limit liability by finding any and all wounds at the time of admission Deep tissue injury is a unique ulcer and will require reassessment to find those POA Assessment of the heel has long been a nursing role but you have to look and not feel for stage Is Documentation to collect data Obvious entries Not mixed in with bathing documentation Methods to obtain needed detail We collect more on pulmonary (respiratory rate, 5 lobes, sound types, type of breathing, etc) than on skin Expect that all skin be assessed Admission with no exceptions Every shift following CQI for complete assessments TEDs, sequentials, devices removed? Use structured approach to risk assessment that includes a comprehensive skin assessment (SOE = C) Policy should include timing for skin assessments Skin assessments must be done daily on all patients Look closely at areas subjected to pressure of any kind Deep tissue injury does not present for 48 hours, if patient has been immobile for any reason, check the skin closely for 3 days following that time Skin inspection should include assessment for localized heat, edema or induration, especially in individuals with darkly pigmented skin. (SOE = C) Research on techniques to identify stage I ulcers in darkly pigmented skin needed. More than one person to move and lift Potential for injury with movement 12 2

3 Locations Tissue on tissue pressure Bed trash in skin folds Under medical devices Bilateral hip ulcers from sitting in undersized chairs, wheelchairs, and commodes Remain about 33-50% of HAPU s High risk patients are those in ICU All patients with devices are at risk Reducing the incidence Fit and refit device after admission Move or remove device to examine skin Making a greater impact Provide feedback to manufacturer about device ulcers from their products Observe the skin for pressure damage caused by medical devices (SOE = C) Considered a pressure ulcer Mucous membrane ulcers are not staged See NPUAP for poster on MDRs SAWC Black 2015 IAD Blistering DTI ITD Ulcerated Scar A shallow stage III One open shiny wound with normal skin around it, this is on the hip No granulation tissue or slough Painful, but heal quickly Microclimate lesions Shear 3

4 Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment. Copyright 2007: NPUAP Copyright 2007: NPUAP Early presentation of purple-maroon tissue Blistered phase Necrotic phase Koziak s model shows ulcers developing in 2 hours at 600 mmhg pressure And ulcers developing after 10 hours at 200 mg Hg pressure Are these ulcers different? OR cases over 3 hours are very high risk 21 Confinement > 3 hrs (Black) OR cases, ER/IR stays Found down at the scene ICU position in Semi-Fowlers ICU turning via the bed Anemia (Baharestani) Anticoagulant Use (Richbourg) Anemia and AC (Honaker) Develops on skin subjected to pressure HOB up = sacral, upper buttocks at sacrum Flat = Buttocks tissue Sitting erect = ischium Can develop under medical devices Developed while HOB up Developed while flat 4

5 Bruising Traumatic events History of trauma Skin injury in pelvis Ischemic events Arterial or venous Drug induced End of life Skin diseases Pyoderma Calciphylaxis End of Life Ischemia Calciphylaxis Depending on the hue, DTI may be difficult to see Is it easier to see DTI in wet skin? Could thermography work? Pyoderma Epidermal loss with skin slippage Red blistered skin visible Commonly called a skin tear Breakdown between skin folds Common sites Under breasts Under panniculi Under other skin folds Due to friction of skin folds rubbing together Often colonized with Candida and other organisms Satellite Lesions History Heavy or immobile patient who is pulled over onto the side or onto carts Assessment Skin is damp/maceration of skin within cleft Burn-like slit in skin Risk factors History of incontinence with exposure of the skin to urine Use of briefs or pads that increase exposure Skin looks denuded in multiple areas with flaring on the edges Skin may also smell of ammonia * Photos courtesy Linda Bohacek 5

6 Dry, intact, not blistered Pink or red with diffuse (not sharply defined), often irregular borders Mild Shiny and moist skin with weeping Pinpoint areas of bleeding Raised areas/blisters Angry bright red color Small areas of skin loss Painful Moderate 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 Severe Important distinction IAD is usually not a reportable condition IAD may not be fully preventable IAD seldom, if ever, evolves into full thickness ulceration However, it can be prevented and healed if managed well Stage II may have depth if it extends Into the reticular dermis Partial thickness pressure ulcers heal by reepithelialization. The epithelial cells are nearby on the edge of the ulcer. Therefore, no scar is produced. Full thickness pressure ulcers close by first clearing slough and eschar and then producing scar tissue to pull the ulcer edges closer together. The edges of the ulcer roll because there is no surface for epithelial cells to slide over. Partial Thickness heal by reepithelialization and also seen at edges of early healing in full thickness Full thickness heals with granulation and scar Superficial multiple lesions in moist skin Moisture weakened skin leading to traumatized skin with in bed movement versus pressure 6

7 Seen in full thickness ulcers Commonly healed with NPWT rather than surgery Repeated trauma leads to new ulcer No stage for this ulcer yet It is full thickness You cannot feel a stage I or DTI pressure ulcer and you can t see them through stockings How can the first citation of a pressure ulcer on the heels be a stage III or IV? Etiology Pressure Time frame may be shorter High Risk Groups Immobile legs Peripheral vascular disease impairs reperfusion Diabetic Neuropathy Immobility Leg Whole Body Short and long term Neuropathic Disease Lack of usual cues to move Arterial Inflow Disease Lack of usual reactive hyperemia Malnutrition -weakness End stage renal disease Systemic infection Ischemic tissue prone to infection Shunting to maintain BP Campbell, 2010; Clegg, 2009; Edwards, 2006; Lyman, 2009; Okura, 2006; Senturan, 2009 Heel trapped on bed as patient slides down Hammock effect Agitated or confused patients rubbing their heels or digging in to the bed Friction no longer an etiology of pressure ulcers Serum blisters are from trauma Blood blisters are DTI (or unstageable in LTC) 7

8 Wheel chair injury Friction/agitation Dragging foot on floor Direct trauma Lawn mower injury Pressure ulcers from traumatic injury look the same as other pressure ulcers DM accelerates arteriosclerosis DM leads to neuropathy with loss of protective awareness Ulcers usually from footwear Pressure ulcer on the heel of a DM, looks the same Inability to see all the skin For obese patients, get adequate help For immobile patients, look whenever being moved for any reason For patients with medical devices, remove the device and look beneath it Lack of knowledge of what common wounds look like Leads to all open wounds being classified as pressure ulcers See attachment on wound identification We ll review the usual and not so usual issues 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 Immobility Prior injury to the skin Stage I Deep Tissue Injury Prior healed ulcer with scar tissue Perfusion problems From Coleman, 2013 Recurrent ulcer in a Spinal Cord Injured patient 8

9 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 patients are at risk Do they direct care? Facilities with care bundles have the lowest incidence of pressure ulcers Padula, 2013 Or is the care so routine and risk so similar from patient to patient that they are simply recorded Use of Braden subscales Immobility is the biggest predictor of risk in general Shear is high risk factor in sacral ulcers Sedation is high risk factor for device ulcers Nothing has been specifically studied Any program to reduce pressure ulcers will reduce DTI Consider your high risk residents Renal failure patients on dialysis who come back exhausted and having not eaten Neuropathic residents who cannot tell the staff that a device is too tight their heel is on the bed the wheelchair or chair cushion is worn or deflated Sedated residents who cannot tell the staff that They need to be repositioned Education of nurses spends little time on bedside care Do not expect new grads to be able to see when a patient can be turned or how to actually turn the patient Same is true for other personal cares If hospital pillows are thin, when combined with inadequate turning Leads to stripe appearance to pressure ulcers along buttocks cleft Long striped ulcers may be developing from pinch injury Inadequate turning angles? Edges of pillows/wedges? Striped pressure ulcer of low back Study of residents in long term care on foam mattresses Well designed RCT, well powered Residents turned randomly Q 2,3 and 4 hrs Instructions for aides Compliance with turning measured Outcomes Pressure ulcer formation was the same at all frequencies of turning on viscoelastic foam Can we now get to a turning schedule we can live with? Bergstrom, et al, 2014 JAGS 9

10 Start with high density foam (memory foam) for residents who turn themselves Add low air loss overlay For residents who have moist skin Dyspnea, obese, in pain, terminally ill Change to alternating pressure For residents who do not move themselves or require a lot of help to be moved Place bariatric beds (with LAL overlay) For residents over pounds Over 39 inches of girth Heel elevation from the bed with pillow if bedrest short-term Pillows do not work for long term prevention (Heyeman, 2009) Boots if bedrest long term Over 6 hours (Cuddigan, 2009) Weak residents slide down and sit on the sacrum Bed pillows are not designed for pressure redistribution Need a seat cushion under the buttocks! Repositioning hourly if not moving Far from ideal placement of seat cushion 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. (SoE = B; SoE = ) Evidence includes 4 studies, one RCT Where are those patients in your facility? Santamaria: N = 440 admitted in ED went to ICU (2013) 13.1% vs 3.1% Kalowes: N = 397 patients in ICU 7 ulcers vs 1 Park: N = 102 patients in ICU 46% vs 6% 939 patients in 3 Trials of Mepilex Brindle: N = 93 PrU rate lower in ICU (2010) Brindle: N = 105 PrU rate lower in cardiac surgery (2012) Chaiken: N = 273 PrU rate fell from in ICU (2012) Castelano; N = 71 PrU in cardiac OR fell from 16.7 to 0% (2012) Walsh: N = 62 PrU in ICU rate fell from 12.5 to 7% (2010) 604 patients in Pre and Post Studies Role of nutrition fairly well described New ideas Liberalize the diet for residents at risk, with ulcers and at end of life Vitamin C, zinc and iron are not needed if resident is eating Albumin and prealbumin are not predictive of nutritional risk They are inflammatory markers, so if the patient has an inflammatory disease, blood levels are low 10

11 Process to determine why a problem happened in the first place, so it wont happen again Correcting the symptom alone is a waste of resources Be aware of bias Intentional and unintentional Finding the root of the problem is not easy work But if the latent source of the problem can be found you can get rid of the problem 2015 National Pressure Ulcer Advisory Panel National Pressure Ulcer Advisory Panel 63 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? 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 11

12 Pressure ulcers skin on top of buttocks cleft Patient was supine at time of pressure This is a DTI that occurred in the OR This patient s head was elevated when pressure applied DTI nearer to sacrum This patient was lying on his side when DTI developed Ulcer on the side of heel If due to pressure, what preventive practices were carried out? Turning? How often? What angle was the patient off the surface? If the patient could not be turned was the surface upgraded? Were heels elevated? Was elevation continuous? Was the surface upgraded due to high risk? Was the patient turned regardless of the surface? Is the surface working? Was the resident repositioned hourly in a chair? Was a chair cushion used? Was the cushion working? If due to microclimate Was the skin kept clean and dry? Was incontinent urine and stool quickly removed? Was the method of skin cleansing nonabrasive? Was the skin protected against next exposure? Was the skin moisturized? Was an incontinent brief removed for several hours each day? Was a low air loss or microclimate surface used? If due to shear Was the body areas subjected to shear protected? Dressings on sacrum in HOB up patients? Padding in chair if patient slouches or is in recliner chair 12

13 If due to protein calorie malnutrition Was the patient hydrated and fed at the dietician s recommendations? Were supplements consumed? Was swallowing addressed? If not, was the deviation explained? E.g., Advanced Directives Difficult aspect beware of bias Consider competing priorities What is the unit of origin Predominately in ICU? How many actually started in OR? ER? Is the ICU bed designed for prevention? Examine training/competencies Are skin care/pressure ulcer competencies done annually? 74 If the patient is aware of the ulcer Does he know when it started? Does he know why it happened? Did he tell anyone? This patient's DTI was discovered when her stockings were removed What does she know about this ulcer? Pressure ulcer prevention must become a lifestyle for some patients Find ways to help them adapt If nonadherence is present Document it factually Document what you told them and what they did Be certain your awareness of nonadherence and the documentation appears in the record before the ulcer starts 75 Classify as quality improvement to reduce discovery Use the location and stage at discovery to find the timing of the ulcer What was happening to patient at that time? Was pressure ulcer prevention possible? If yes, was it carried out? Documented? Over reliance on beds Creating narrow ulcers along gluteal cleft PrU prevention not a priority Under appreciation for seriousness of ulcers Resident has the right to refuse to turn Lack of expectation for complete skin assessment Ulcers beneath medical devices Ulcers found at more advanced stages 78 13

14 Lack of awareness and accountability for Policies and guidelines Prevention bundle Braden scale scoring Proper staging of ulcers Availability of supplies/devices Documentation issues Insufficient EMR issues Communication issues Nurse to nurse Nurse to others From Prince, 2010 Fishbone diagram helps to examine Performance and Feedback Are your unit pressure ulcer rates posted? Skills and knowledge Are you including skin in yearly competencies? Motivation Are staff recognized for a job well done? Job expectations Are policies and procedures current? Accessible? Environment and tools How old are your beds on the units? Organizational support 2015 National Pressure Ulcer Advisory Panel National Pressure Ulcer Advisory Panel 80 Ishikawa (1985; 1990) 2015 National Pressure Ulcer Advisory Panel 82 Pressure Relief/Reduction Offloading Upscaled beds/mattress, chair cushions Teaching pressure redistribution Wound care Dressings, packing, topicals Nutrition Increased protein and calories 3 legged stools tip over when any one leg is missing National Pressure Ulcer Advisory Panel 14

15 Assess ulcer with each dressing change (SOE = C) Is ulcer improving? Less necrotic tissue, less slough, less pain More granulation tissue Smaller size or depth Pain manageable with less intense medications Or is ulcer deteriorating? Greater size, depth, odor, drainage, pain From NPUAP Guidelines Formally assess the ulcer at least weekly Measure length, width, depth Tissue type in deepest portion of ulcer Allows staging Periwound appearance Odor, type and volume of drainage Draw conclusions from data If ulcer is improving, are all the treatments needed? If ulcer is deteriorating, what new treatments are needed? 9/5 (NN) buttocks ulcer found, treated using protocols 9/6 (NN) stage III on right buttock, 5 x 3 cm, 85% red, 10% yellow, 5% black 9/7 (NN) MD office notified of 9 x 7 cm decube on right buttocks, area has progressive from ½ cm on Thursday. Is a stage III ulcer now. 9/9 (PT) ischial ulcer is 6.5 x 5.5 cm, 100% slough and eschar covered, heel is dry, black eschar 9/10 (Wound nurse): Right ischium 8 x 5 x 0.2 cm, with 4.5 x 2.2 area of slough Right?? 2.5 x 2.2 cm partially covered with avascular tissue Left heel mushy Left shin 1.2 x 1.0 cm Consider using baseline and serial photographs to monitor pressure ulcer healing over time (SOE = C) Good photos are invaluable Evidence of true condition for comparison to documents of wound status Evidence of presence of ulcer at time of admission Poor photos don t help much Cannot determine ulcer location, date of photo If family has taken photos of ulcers, you need to do so also 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? Week 1 Week 3 Week 6 Week 12 15

16 Be honest and discuss Does this wound have the capability to heal? Is blood flow adequate to the legs? Is the wound getting infected from stool? Is nutrition adequate to support healing? Will the resident stay off of the ulcer? If any of these are no Create a care plan for palliation and expect the patient to die of sepsis from the ulcers Do not debride the wound 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 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, boggy eschar, septic patients Ischemic limbs lack blood flow for healing Exposed bone increases risk of osteomyelitis Monitor for development of unstable eschar Trim loose eschar with small scissors Plan on 6 months for healing Osteomyelitis Stable eschar removed exposes necrotic tissue Staging Terminology Focus of 2016 NPUAP Conference There have been some good studies in pressure ulcers, however it remains one of the most serious and poorly researched conditions in the world! 16