PRESSURE ULCER INJURY

PRESSURE ULCER INJURY

Background Epidemiology Cost Definition Classification Etiology Risk assessment Skin assessment on admission Prevention Wound healing assessment Management and treatment

BACKGROUND Care of pressure ulcers is interdisciplinary and involves nursing, nutrition, rehabilitation,and surgical subspecialties. A vexing of treatments are available with few studies to prove efficacy of one over the other. The standard of care for pressure ulcers is evolving All primary care providers, particularly geriatricians and hospitalists, need to be aware of prevention strategies, documentation standards, and treatment choices avoid unnecessary and futile procedures improve quality of life curtail health care costs

BACKGROUND Pressure ulcers: Pain Decreased quality of life Longer hospital stay(4.8 vs 11.2) Increased chance of readmission within 30 days after hospital discharge (17.6% vs 22.6%) Increased chance of admission to a long term facility Increased risk of death (2.6% vs 11.6%) Increased risk of death within 30 days of discharge (4.4% vs 15.3%) Infectious complications include : Cellulitis Abscess Sepsis Osteomyelitis

BACKGROUND Pressure ulcers are a designated quality measure in hospitals, Long term care, and home care settings. As a result of their association with quality of care, pressure ulcers have become a major risk management issues Pressure ulcer data for skilled nursing facilities is currently published by CMS on the Nursing Home Compare website, but as yet there is no federal mandate for publication of pressure ulcer statistics for hospitals and home care

BACKGROUND In addition, pressure ulcers have been spotlighted in value-based purchasing and pay-for-performance initiatives. In 2008 the CMS introduced a policy to decline payment to hospitals for certain hospital acquired conditions that include stage 3 or 4 pressure ulcers. It is considered a never event

2.5 million patients develop Pressure injury annually, and their incidence and prevalence varies greatly depending on stage, setting National incidence rate of 2.5% in hospitals UC Irvine Health point prevalence for June 2016= 3.6% 13.1% Critical care 6.9% Step down Higher rates are consistently reported in older populations Long term care,prevalence ranges from 8.5 %to 32.2% Nursing Home residents 11-24% One study reported that up to 54.7 percent of terminally ill nursing home residents have pressure ulcers EPIDEMIOLOGY

EPIDEMIOLOGY Most pressure ulcers develop during acute hospitalization, usually during first 2 weeks of hospitalization Incidence rate vary by clinical setting 0.4%-38% for hospital 2.3%-23% for long term care 0%-17% for home care 54% in patients 70-89 years old In-hospital deaths for persons with pressure ulcers 11.6% compared to those without, 2.6% 60,000 persons die from pressure ulcer complications each year

COSTS Average hospital-associated costs for 1 stage 4 ulcer $129,248 National health care costs estimated at $22 billion dollars for 2016 Average length of hospital stay nearly 3 times longer with a pressure ulcer Care of pressure ulcer is costly with estimates of 3500$ to more than 151,700 $ per patient, depending on the stage Increases nurse s work load by 50% As of Oct 2008, Medicare and CMS no longer pay for the costs associated with a pressure ulcer that develops while in the hospital. It is considered a never event Estimated daily cost for prevention 54.66$,daily cost of treatment for stage I/II 2,770$ and stage III/IV 5,622$ More than 17000 lawsuit annually. It is second most common claim after wrongful death $250,000+ per settlement

Pressure injury definition

PRESSURE ULCER INJURY AKA Pressure sore, decubitus ulcer, bed sore A localized area of tissue necrosis that tend to develop when soft tissue is compressed between a bony prominence and an external surface for a prolonged period of time. NPUAP, 1989 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/or 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, comorbidities and condition of the soft tissue. NPUAP 2016 New Terminology: Pressure Injury

Etiology and Pathophysiology

PRESSURE INJURY ETIOLOGIES Extrinsic factors Pressure Shear Friction Heat and moisture as contributors (microclimate) Intrinsic factor Immobility Incontinence Malnutrition Decreased skin perfusion Age > 75

PRESSURE Three elements lead to the development of a pressure ulcer: 1.Duration of the pressure 2.Tissue tolerance 3.Intensity of pressure and vascular occlusion

PRESSURE Compression of soft tissue between bony prominences and an external surface (chair or bed) Normal capillary blood pressure = 20-40 mmhg, average 32mmHg Higher pressure on bony prominences Tissue damage was thought to be caused by compression of capillaries, known as Capillary Closing Pressure.. Pt lying on standard hospital mattress has 50-95 mmhg over greater trochanters and heels, sitting generates 300-500 mmhg over ischial tuberosities Pressure ulcer can develop within 2-6 hours: pressure >70 mmhg for 2 hours result in irreversible tissue damage in animal models Cone shaped distribution-more extensive damage deeper than appears superficially, the subcutaneous tissue, including muscles, are more sensitive to ischemia than epidermis and dermis

PATHOPHYSIOLOGY If pressure is relieved within a few hours, a brief period of reactive hyperemia (redness) occurs with no lasting tissue damage If pressure continues unrelieved, the endothelial cells lining the capillaries become disrupted with platelet aggregation, forming microthrombi that block blood flow and cause anoxic necrosis of surrounding tissue

ADDITIONAL PATHOPHYSIOLOGY Since muscle is more sensitive to pressure and hypoxia than skin, underlying tissue may be necrotic by the time you see a lesion on the skin surface Shearing forces reduce the ability of tissue to withstand pressure (tissue subjected to shear force can suffer ischemia at only half the pressure than without shear)

SHEAR Force acting tangentially on an area of an object. Skin remains stationary and the tissues below the skin (fat/muscle) are deformed/distorted Causing angulation and stretching of blood vessel Leads to reduced blood supply to the skin Gravity often plays a role Occurs when a patient is in bed or chair or placed in incline and gradually slides downward deeper tissues pulled down by gravity,while superficial epidermis and dermis fixed through contact with external surface Shear stresses on a tissue decrease the tissues ability to withstand normal loads

FRICTION Occurs when patient pulled/dragged across a surface The resistance to motion in a parallel direction relative to the common boundary of two surfaces. Damaging superficial layer of skin Can cause abrasions, damage to dermis. Usually associated with skin/bedding or skin/seating cushion interfaces Occurs during transferring and repositioning Results in Stage 2 pressure ulcer

MICROCLIMATE Heat and moisture balance. Increased humidity at the skin/bedding interface, the skin softens, reducing its ability to withstand shear and friction forces. Temperatures >95 degrees causes increased perspiration, increasing maceration risk and increasing skin ph.

INTRINSIC FACTORS Immobility Decreased spontaneous nocturnal movements correlate highly with pressure ulcer development Healthy sleeping subjects make spontaneous movements or changes of position q 15 min Geriatric patients with <20 spontaneous nocturnal movements at higher risk. Nocturnal movements tended to decrease as length of hospital stay increased Patients with neurological compromise or decreased level of consciousness may lack or be unable to respond to early warnings of prolonged ischemia(discomfort) that normally result in adjustments of position Malnutrition Often coexist with pressure ulcer though causal relationship not well established

INTRINSIC FACTORS Incontinence, altering skin ph, moisture gets trapped and macerates the skin, allowing for entrance of bacteria. normal ph of 4-6.5, provides the acid mantle which is protective against most bacteria urine (4.5-8) and feces (7-7.5) tend to be closer to a neutral ph, although wide variations can occur due to health status Up to 5 fold increased risk in some studies, but high correlation between incontinence and immobility so may not necessarily be an independent predictor

INTRINSIC FACTOR Decreased skin perfusion Hypotension, dehydration, vasoconstriction secondary to shock, CHF Age >75 years Changes in epidermal turnover, dermal thickness, collagen and elastin production and vascularity with aging

COMMON SITE OF OCCURRENCE Ischium 29% Sacrum17-27% Trochanter 12-19% Heel 9-18% Occiput, elbow, and scapula Other body parts as well

Intact skin STAGE 1 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 pressure injury

Partial-thickness loss of skin with exposed dermis. STAGE 2 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. This stage should not be used to describe moisture associated skin damage including incontinence associated dermatitis, intertriginous dermatitis, medical adhesive related skin injury, or traumatic wounds

Full-thickness loss of skin STAGE 3 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 and/or bone are not exposed. If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury.

STAGE 4 Full-thickness skin 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

UNSTAGEABLE PRESSURE INJURY 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.

Intact skin or blood filled blister DEEP TISSUE PRESSURE INJURY localized area of persistent non-blanchable 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. 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)

DTI BACKGROUND Highest in ICU (14% of all ulcers) Coccyx, sacral, buttocks, heels Comorbidities: anemia, DM, fecal incontinence, PVD, malnutrition Risk: orthopedic & respiratory Time of injury precedes DTI 3-5 days 84% ICU & incontinent, 40% sacrum; 30% heels; 90% present as maroon, purple 66% resolved; 9% deteriorated.

MEDICAL DEVICE RELATED PRESSURE INJURY: Medical device related pressure injuries result from the use of devices designed and applied for diagnostic or therapeutic purposes. The resultant pressure injury generally conforms to the pattern or shape of the device. The injury should be staged using the staging system. Some are Unavoidable

Conduct standardized risk assessment and skin assessment on admission

WOUND ASSESSMENT Pressure ulcers must be detected early can usually heal quickly if discovered in early stages and treated properly. can deteriorate quickly, particularly in patients with severe immobility in conjunction with multisystem disease. As a result, timely examination and documentation is an important component of management. consistent and compete documentations.

WOUND ASSESSMENT Wound documentation includes diagnosis, stage, location, length,width, depth, presence of odor and or drainage, presence of undermining and tunneling, as well as characteristics of the wound bed, margins, and surrounding skin. Supplemental information include warmth, capillary refill, and presence of pulses, edema, anasarca, and lymphedema. Measurement is an important component of wound assessment, particularly for determining the effectiveness of clinical interventions. Measurement involves head to toe length, width, and depth and should be both consistent and accurate. The simplest method uses a centimeter ruler to measure length and width, and a cotton tipped swab to measure depth, tunneling and undermining

Pressure Ulcer Prevention

PRESSURE ULCER PREVENTION The standard of care for pressure ulcer prevention includes risk assessment appropriate pressure redistribution/pressure relief interventions if the patient is deemed at risk Patient positioning Positioning devices Support surfaces

SCREENING AND POPULATION AT RISK Female, African American, over 75 years old Limited mobility Admitted from nursing home Admitted to critical care from ED Re-admitted to nursing home from hospital Critical care: sepsis, surgery > 8 hrs, long term vasopressor therapy Over 65: surgery >4 hrs. Intraoperative hypotension Previous pressure ulcer Skin diagnoses: gangrene, nutritional deficiencies, DM, anemia System failure: paralysis, senility, resp failure, ARF, CVA, and CHF Infection: sepsis, osteomyelitis, pneumonia, bacterial infections, UTI

SCREENING AND POPULATION AT RISK SCI (approx 80% will develop a pressure ulcer in their lifetime, and approx 30% will develop more than one.) 30-50% will develop an ulcer in their first month post injury Thought to be due to hypotension secondary to sympathetic nerve dysfunction, overall lower perfusion states. Loss of muscle mass over bony prominences over time. Any patient with impaired sensation, no feedback loop to alter their position (diabetic, SCI, CVA) impaired cognitive status Incontinent of bowel or bladder (compromising the skin s integrity) Nutritionally compromised (TPN, tube feeds, dysphasia, NPO, burns) Hypoalbuminemia <3.4g/dL

ASSOCIATED RISKS IN THE ACUTE CARE SETTING Immobilization, restraints Medical devices (catheters, foreign objects, C-collars, nasal cannulas, splints, casts, etc) Debilitation/ Sedation Hemodynamically unstable, patients on vasopressors with MAP <60mmHg, hypotensive (shunting of blood to vital organs)(2) Lying for hours on hard imaging and operating tables patient turning by dragging, which produces a friction force, or by positioning too far superiorly in the bed thereby causing increased shear forces

several validated instruments are available that quantify risk. RISK ASSESSMENT The most widely used tool is the Braden scale which has been validated in home, skilled nursing facilities and hospital settings but not in ICU. Sensitivity 70-90%, specifity60-80% Unclear whether scales perform better than clinical judgement However other studies have noted that risk assessment tools can be weak predictors of which patients are more likely to develop pressure ulcer. current scales also do not contain information related to organ system failure or physiologic factors such as hypoxia and hypotension which may engender increased pressure ulcer risk. Therefore, clinical judgment should be relied on to determine at risk status in addition to the formalized risk assessment scale

Assess patient s risk of developing pressure ulcer Score range 6-23; Low score=high risk 18 or below indicates risk 10 or below indicates HIGH risk Risk of breakdown below a score of 18, or a score of 2 in any category subset. Determine increased risk and trigger alternate mattress, heel float boot, turning and lift team initiation, and/or other nursing interventions USE the same tool for Acute care, LTC, Home care & communicate findings during transitions NHs: Assess on admission and weekly for 4 weeks, then quarterly Acute Care: Assess daily/q shift BRADEN SCALE

NUTRITIONAL ASSESSMENT Serum albumin < 3.5 TLC < 1,800 Weight < 80% ideal 5% weight loss/30 days <75% food intake at most meals Body mass index <20 10% weight loss/180 days

30-40 cal & 1.2-2.1 gms protein/kg/day NUTRITION SUPPORT Vitamin A & E No evidence Vitamin C RDA supplements if deficiencies exist 2 RCTs with flaws making interpretation difficult Arginine Evidence to support supplementation Zinc No evidence 200-220mg/day, if risk for deficiencies exist Part of MVI ok over use can cause damage when determining nutritional needs, it is important to consider other factors such as preexisting protein calorie nutrition and comorbidities.

PRESSURE RELIEF Patient positioning Turning every 2 hours, remember seated patients as well!!!!! Post a turning schedule as appropriate Keep head of the bed <45 degrees Avoid positioning directly on trochanter Avoid dragging, use lifting device and draw sheets Inspect skin over bony prominences and other pressure points with repositioning whenever you treat a patient who is at risk Positioning devices Position pillows to elevate pressure points off the bed, floating the heels or use heel float boots. Pillows and foam wedges can help keep pressure off bony prominences

PRESSURE RELIEF Support surfaces Static Devices distribute local pressure over wider body surface are. Lower cost Pads, cushion, most mattress overlays (gel,foam,air,water) Use in low risk for pressure development and in patients with ulcer who are able to assume variety of positions without bearing weight on ulcer Dynamic devices: uses a power source to alternate air currents to regulate or redistribute pressure against the body.higher cost Alternating air mattress Low air mattress Air fluidized (high air loss) Use of dynamic support surfaces in high risk patients has been shown to improve outcomes and cost savings Use in patients at moderate high risk for pressure ulcer development or in patients with full thickness pressure ulcers, non heling ulcers or ulcers on multiple sites making positioning difficult

How to Assess Wound Healing

WOUND ASSESSMENT FOR HEALING NPUAP Pressure Ulcer Scale for Healing (PUSH) Size 10 categorical ratings Exudate None, Minimal, Moderate, Large Tissue Appearance Healed, Epithelial, Granulation, Slough, Necrotic Sum all 3 for total score www.npuap.org

WOUND ASSESSMENT FOR HEALING Bates-Jensen Wound Assessment Tool 13 items rated 1-5 scale 1=best 5=worst for the item Sum for total score (13-65 range) Available from author Size & Depth Edges & Undermining Necrotic tissue type & amt. Exudate type & amt. Surrounding Tissue Characteristics Color Induration Edema Granulation Epithelialization

WOUND HEALING ASSESSMENT Do the Math How to make size more meaningful: Measure weekly Length x Width Use same reference points Surface area change at 1 week predictive of 50% healing (P=.0001) Bates- Jensen (1998) retrospective 143 ulcers

ASSESS YOUR MANAGEMENT Full Thickness Improve q 2-4 weeks Most heal within 1 year Healing fastest in first 3 months Partial Thickness Improve q 1-2 weeks Heal 60 days In one study all pressure ulcers that healed had a percentage area reduction of more than 47% at 2 weeks, which provide reliable predictor of healing Best practice recommends that pressure ulcers that do not decrease in size within two weeks of active treatment should be reassessed and treatment modified accordingly

Use principle of Wound Bed Preparation to guide management

WOUND BED MANAGEMENT Wound management to increase body s own ability to heal and to improve effectiveness of treatments. Change the molecular and cellular environment of a chronic wound to that of an acute healing wound The foundation of this concept is an orderly approach to accelerate endogenous healing and facilitate the effectiveness of therapeutic measures. The goal is to reestablish the balance of growth factors, cytokines, proteases, and their natural inhibitors as found in acute wounds, thereby stimulating the healing process. Wound bed preparation focuses on critical components of management, including moisture and exudate, bacterial balance, and debridement.

WOUND BED PREPARATION

T-I-M-E T Tissue Debridement Remove Non-Viable or Deficient Tissue. Types of Debridement: 1.Autolytic 2.Mechanical 3.Enzymatic 4.Biological 5.Sharp Goal: remove necrotic tissue, micro debris, reduce bacterial burden Pain management and control of bleeding are important components of mechanical and sharp debridement.

DIFFERENCES: INFECTION & COLONIZATION All chronic wounds are contaminated or colonized with bacteria but may not be infected. Contamination and /or colonization of wound will not elicit host reaction and does not interfere with healing. Challenge is to distinguish colonization vs Infection

INFECTION I -- Infection or Inflammation Reduce Microorganisms & Inflammatory Cells Infection & inflammation lead to increased cytokines, proteases and reactive oxygen species in the wound Surface swab cultures reflect colonization and are not clinically useful Deep tissue culture or blood culture more clinically useful

INFECTION managing underlying conditions, including diabetes, anemia, poor nutritional status, cardiopulmonary disease, and any cause of edema Wound infections can be treated locally, systemically, or both depending on the clinical situation. Local treatments include dressings containing antimicrobial compounds such as gentian violet, methylene blue, silver, cadexomer iodine. topical antibiotics include mupiricin, neomycin, polymyxin b, and bacitracin. multiple topical antifungal are available, including the imidazl, tiazole, and thiazol compounds. Systemic treatment depends on the suspected organisms an clinical setting

CHRONIC WOUNDS & INFECTION Chronic wounds contaminated with skin flora Enterococcus, Staphylococcus, Bacillus Heal in presence of bacteria More likely to develop MRSA Treat with Bactroban or silver dressings topically Signs of infection: Increasing pain, friable, edematous, pale dusky granulation tissue, foul odor, & wound breakdown, pocketing at base, or delayed healing little consensus on definition of wound infection in a chronic wound. Sign and symptoms include fever, increased drainage, pain, warmth, edema, erythema, slough, odor, cessation of healing, or worsening of the wound. Many of these may not be present in older patients, people with diabetes, or patient with malnutrition or immunocompromise. Diagnosis is based on clinical evaluation of local and systemic symptoms in concert with laboratory studies. Increased WBC count may be found when the infection is acute but is an unreliable indicator of chronic infection. Critical level of colonization or BIOFILMS can delay healing

BIOFILMS-SESSILE MICROBIAL COMMUNITIES Initiated by surface attachment of bacteria & Cell-cell interactions Colonies grow in an elaborate 3-D structure Glycocalyx matrix: extracellular polysaccharide matrix encasing the bacterium Exhibit up to 1000 times more resistance than plain, ordinary bacteria in a planktonic state. Biofilms Identified in 60% of Biopsies of Chronic Wounds but in Only 6% of Acute Wound

ULCER CARE: CLEAN All wounds should be protected from contamination with urine and feces At dressing changes, with low pressure What to clean with? 1)Clean wounds 1)NS 2)Water and Soap 2) Necrotic, infected wounds 1)Commercial cleaners a. povidine-iodine b. hypochlorite (Dakin's)--staph, strep, dissolves necrotic tissue, controls odor c. acetic acid--pseudomonas aeruginosa in superficial wounds Antiseptic solutions 10-14 days then stop Broad spectrum of effectiveness cytotoxic antimicrobial control

MOISTURE M Moisture Balance E Epithelial Edge Goal is maintaining a moist but not wet wound environment If it s dry,wet it; if it s wet, dry it Moisture Retentive dressings 1) Physiologically favor cell migration and matrix formation 2) Accelerates healing of wounds by promoting autolytic debridement 3) Reduces pain

MOISTURE Alternatively, excess moisture inhibits wound healing through maceration that impairs both the wound bed and peri-wound area. Exudate contains elevated level of matrix metalloproteinases MMP which can degrade the extracellular matrix, impairing cell migration and connective tissue deposition. Growth factor also inhibited by MMP Several products promote moist wound healing such as hydrocolloids, hydrogels, and other bio-occlusives. The exudate of chronic wounds contains heightened proteolytic activity, matrix metalloproteases, and macromolecules that inhibit growth factors Foams Hydro fibers Alginates Collagen containing product : inactivates harmful cytokines and factors that inhibit healing.

DRESSINGS OVERVIEW

DRESSING SELECTION

DRESSING DEAD SPACE Light packing Prevent abscess formation Treatment of choice 1)Calcium alginates 2)impregnated gauze 3)Negative pressure wound therapy