Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Aging Integumentary System
Transcript
6/28/2016 Jill Heitzman, PT, DPT Board Certified Geriatric Clinical Specialist Board Certified Neurologic Clinical Specialist Certified Wound Specialist Certified Exercise Expert for Aging Adults Auburn, AL FUNCTIONS OF THE SKIN Protection: Physical barrier to micro organisms and foreign matter to fight against infection and excessive loss of fluids, storage of fat and water Sensation: Nerve endings present in the skin allow ability to feel pain, pressure, heat and cold Thermoregulation: Regulates body temperature through vasoconstriction, vasodilation and sweating Excretion: Excretion of waste products such as electrolytes and water Metabolism: Synthesis of Vitamin D in skin exposed to sunlight, activates metabolism of calcium and phosphates; minerals important in bone formation, Hormonal production and synthesis Body Image: Performs cosmetic, identification and communication roles Immunologic: Resident immune cells that participate in immune processing are present in epidermis and dermis (Langerhans cells and dermal dendritic cells, respectively) Over the lifespan skin becomes drier, less elastic less perfused vulnerable to damage from pressure, friction, shear, moisture, malnutrition 3 1 6/28/2016 Appearance changes Skin tags, warts and other blemishes. Hair and nails change Hair changes: Normal Aging Reduced hormone levels result decrease in size of the hair follicle and thinning of the hair is noted. Diminished melanin results in the color transitions to gray. A thorough hair and scalp inspection can identify underlying pathologies and pathologies can impact Hair changes Hair Changes associated with Pathology Hair loss Alopecia: rapid loss that is patchy or diffuse May be associated with pharmacology or chemotherapy Heparin can produce hair loss Hair texture Changes indicate hypothyroidism Protein malnutrition can make the hair dry or course; can also change color to a reddish or bleached appearance 2 6/28/2016 Nail Changes *The nail bed is very vascular and an excellent location for assessing the adequacy of the patient’s peripheral circulation. Nail beds : bluish or purple in color may indicate cyanosis pale may indicate reduced arterial blood flow. Decreased peripheral circulation Nails grow more slowly but often thicker; brittle and split into layers. Nail Changes Nail changes can also indicate functional and nutritional status: Mobility decline and visual changes, Nails appear unkempt appearance may require podiatrist or other health care provide to reduce the risk of surrounding skin damage and wounds. Nails can indicate nutritional deficiencies. Protein deficiency: Bands across the nail Zinc deficiency: White spots across the nail Anemia: Spoon shaped nails Normal aging changes skin 80% of adults older than 65 suffer 1 or more chronic conditions Drug therapies contribute to fragility of the skin Advanced age, comorbidities, medications, environmental factors, nutrition and lifestyle contribute to the overall condition of the skin 3 6/28/2016 Risk Factors affecting Aging Skin and Wound Healing Age Stress Nutrition Bacterial Obesity Comorbidities Polypharmacy Decreased mobility Decreased mental status burden/infection Smoking Pressure Irradiation Incontinence AGE Age alone is not a risk factor for impaired integumentary The increase in comorbidities has a greater impact However, some physiological changes impact function of the integumentary system Epidermis Function is for moisture retention and protection With aging: The epidermis thins Decrease in the density of the Langerhans Cells RESULTS Less effective in protection from infection and dehydration 4 6/28/2016 Basement Membrane Functions as an interface between epidermis and dermis and composed of projections known as rete pegs to provide resistance to shearing forces With Aging: Rete pegs flatten leading to thinning of the basement membrane RESULTS Increased vulnerability to shear related injury Dermis The deeper layer of the skin that is responsible for: Structural integrity and provides nutrition, hydration and oxygen to the epidermis via diffusion Composed of: collagen which provides tensile strength Elastin which provides ability of the skin to stretch and recoil Dermis (cont.) With Aging: A decrease in fibroblasts leads to decrease in production of elastin and collagen Collagen becomes disorganized Degradation of elastin fibers Dermis layer thins and has fewer blood vessels and nerve endings; remaining blood vessels thin RESULTS Decreased sensation and blood supply The thin remaining blood vessels prone to hemorrhage Senile Purpura: discoloration of skin 5 6/28/2016 Subcutaneous Layer Composed of adipose tissue, blood, and lymphatic vessels, nerves Function is to facilitate regeneration of the dermis and to connect the dermis to underlying structures With Aging Thinning of all components of subcutaneous layer RESULTS Decreased ability to provide structural protection Decreased thermal regulation Slow regeneration Younger Older Epidermis Dermis Subcutaneous Decrease epidermal and dermal layers Decreased ground substance, elastin & collagen in dermis Reduced epidermal turnover Flattened epidermal rete pegs and dermal papillae Decreased thickness of dermis and hypodermis Decrease in pain perception Decrease number of melanocytes Decrease number of Langerhans cells Decrease mast cells Decrease sweat glands Diminished vascularity Decreased subcutaneous fat Decrease epidermal and dermal layers Decrease elastin and collagen in dermis Reduced epidermal turnover Flattened epidermal rete pegs & dermal papillae Decrease thickness of dermis and hypodermis Decrease pain perception 6 6/28/2016 Aging affects on the Phases of wound healing Hemostasis Inflammatory Proliferation Epithelialization Maturation Inflammation phase changes Decrease response/migration of cells Prolong phase Proliferative phase Decrease amounts of fibronectin Excess degradation of wound bed Maturation phase Slow wound contraction/epithelialization Reduced tensile strength Altered skin permeability Alterations of temperature regulation/ decrease insulation Increase risk for infection Decreased elasticity/durability of the scar Less scar formation 7 6/28/2016 ALTERED WOUND HEALING PROCESS Progressive loss of skin function increased vulnerability to the environment decreased homeostatic ability. The result is poor wound healing greater risk for infection altered inflammatory response. Leads to a breakdown of normal tissue impairment in acute wound healing predisposes the aging adult to chronic wounds. Delayed Slower Increased risk for infection Comorbidities Contributing to Skin Alterations and Delayed Wound Healing Long standing chronic diseases affect wound healing due to circulatory & nutritional deficits, mobility and sensation issues, and multiple pharmaceutical interventions Diabetes Vascular disease: Arterial or Venous Cardiac diseases Neurological Dementia/Cognition/depression 8 6/28/2016 PVD, COPD, anemia: Decrease oxygen and nutrients to the wound Decrease bloody supply /perfusion Diabetes: Damage to WBC and macrovascular system Immunosuppression: Affects collagen synthesis during proliferation Limits immune cells during inflammation Medications/chemotherapy increases these affects…. Neurological diseases Impaired mobility Loss of sensation Hematological diseases Anemia Leukemia Hepatic dysfunction: Decrease protein/albumin Edema Risk of infection Increase risk of dehiscence Faulty collagen deposition Alcoholism: Affects: nutritional status, liver, CV system and mental status. 9 6/28/2016 Co morbidity considerations 80% pressure ulcer-associated deaths occur in persons over 75 years Controversy regarding prevention of pressure ulcers in neurological disease and end of life Vicious cycle of chronic conditions leading to functional decline, malnutrition, deconditioning and immobility leading to open wounds which then perpetuates the cycle Steroids: (prednisone, cortisone) Decreases vascular permeability Has catabolic effect on peripheral tissue Interfere with inflammation and fibroblast growth Inhibits epidermal regeneration/epithelization Decreases tensile strength NSAIDS Topical delays re-epithelialization Oral reduces the inflammatory process Medications Contributing to Skin Alterations Corticosteroids Antibacterials Antihypertensives Analgesics Tricyclic antidepressants Antihistamines Antineoplastic agents Antipsychotic drugs Diuretics Hypoglycemic agents 10 6/28/2016 Other drug issues Nonsteroidal anti-inflammatory drugs (NSAIDS) diminished inflammatory response Impact is greater with those with diabetes Immunosuppressive agents affect duplicating cells. Warfarin increases bleeding tendency Tight control of diabetes management is needed for wound healing High blood sugar decreases the rate of collagen synthesis decreases the rate of angiogenesis decreases fibroblast proliferation decrease tensile strength inhibits re-epithelialization Sustained hyperglycemia decreases all phases of healing and the body’s ability to fight infection A1c Importance High blood glucose levels can lead to integumentary trauma Trauma/stress can lead to high blood glucose levels Need to know the history of the high blood glucose not just the current day 11 6/28/2016 FUNDAMENTAL AREA OF WOUND HEALING OFTEN OVERLOOKED Nutritional Status of NH patients 232 NH patients studied by anthropometric measurements and biochemical profiles 59% had some form of malnutrition 17 of those had pressure ulcers Gruen, 2016) Nutrition Ulcerations correlates to: Nutritional deficiencies/intake Undesired weight loss Low body mass index (<18.5) Wound healing increases the demand for calories and protein with deficiencies resulting in: Prolong inflammatory phase Inhibition of fibroplasia & proteoglycan synthesis and decrease angiogenesis (proliferative phase) Inhibiting remodeling Gruen, 2016) 12 6/28/2016 Nutrition Risk “anorexia of aging” appetite decline weight loss decreased metabolic rate Protein-Energy Malnutrition (PEM) Definition: Wasting and excessive loss of lean body mass resulting from too little energy being supplied to the body tissue that can be reversed solely by the administration of nutrients Malnutrition Independent risk factor for increased pressure ulcers Correlation between malnutrition and Loss of taste sensation Poor denture Loss of spouse/socialization GI changes Comorbidities/pharmacology (restricted diets) Stressors: Recent move, recent loss, illness Pathological State Imbalance between intake and body needs leads to: loss of body weight-10% of body wt in 6mos or 5% in 30days muscle wasting poor wound healing loss of skin integrity resulting in spontaneous wound development development of chronic wounds and infections Low protein levels associated with: increased interstitial edema decreasing the delivery of nutrients to the damaged tissue increased risk for pressure ulcers. Diagnosis: Failure to thrive 13 6/28/2016 OBESITY Adipose tissue has poor blood supply Malnutrition is common, especially protein malnutrition, Operations on people who have prolonged healing times due to: the prolonged operations greater blood loss decreased tissue perfusion and oxygenation increased intra-abdominal pressure immobility. These patients, if bed ridden for any length of time, have a greater risk for developing pressure ulcers due to easily exceeding the capillary closing pressure of 32mmHg especially if their body weight is superimposed over a bony prominence OBESITY Increase stress on the surgical site Decrease tissue perfusion Decrease in tissue oxygenation Greater risk for pressure ulcers Vasoconstriction Increase in platelet aggregation Decrease in available oxygen 14 6/28/2016 IRRADIATION Radiation Therapy causes Cellular injury to fibroblasts, endothelial cells and vascular supply in the area Can produce edema and burns The aging process results in a delayed healing process -up to 4x slower than younger populations BUT unless another co morbid factor is present, healing will be effective, just slowed. Chronic Wounds Characterized as a non healing wound with prolonged inflammation defective re-epithelialization, impaired matrix remodeling and/or harmful bacteria loads. 15 6/28/2016 BACTERIAL BURDEN/INFECTION May be systemic or local Result is a prolonged uncontrolled inflammation phase All wounds have bacteria; infection is classified as a bacterial burden of >105 organisms/gram of tissue Infection/antibiotics All chronic wounds have bacteria present 60% of patients with chronic wounds have received antibiotics, increasing the risk of ADR and affecting not only wound healing but the affect of other medications Move from wound contamination to colonization needs to be identified: The wound will show signs of distress and appear stalled in relation to the phases of healing. The infection can remain local or become systemic. Bacterial cells reaching a level of greater than 105/gram of tissue is perceived to be a key determinant in infection and delayed wound healing Early Clinical Recognition Pain and tenderness may be indicative of wound infection but pain may also present for other reasons. Other clinical signs of infection include change in quantity, color, or odor of the drainage presence of pus erythema of the wound edges local pain and/or edema increased temperature abnormal or absent granulation tissue cellulitis change in the periwound sensation Acute wound infections seem to be most associated with pain, redness, swelling, loss of function and increased temperature. Chronic wound infections are more associated with increased pain, wound breakdown, odor, and friable granulation tissue. 16 6/28/2016 Superficial or Deep Infection Superficial bacterial damage will Deep infections show signs of present with NERDS: STONES: Size increase Nonhealing Exudate increasing Temperature of periwound increases Red friable granulation Osteo structures can be probed or Debris on the surface Smell These superficial bacterial infections usually treated topically. exposed (i.e. bone) New areas of breakdown Erythema/Edema/Exudate increases Smell These deeper wound infections need to be cultured for proper systemic intervention. MRSA Potentially increasing due to the increase use of broad spectrum antibiotics Hospital Acquired Tends to lead more to systemic infection Needs antibiotics that are out of the resistant strain Community Acquired Tends to lead more to skin and soft tissue infection Can be more often treated locally with topical agents and silver impregnated dressings Yeast/Fungi Infections Superficial: Tinea pedis (athlete’s foot) Intermediate: Candida Albicans Deep: Aspergillosis: invade underlying tissues Risk for yeast and fungal infections in aging adults: Antibiotics and corticosteroids Candidiasis presents in moist skin folds and appears as erythema, a whitish pseudo membrane and peripheral papules and pustules (cottage cheese like) Oral Candidiasis, thrush appears as a white coating of the oral cavity, especially the tongue. This type of yeast infection produces fissures on the tongue and restricts oral intake, compromising the aging adult further. 17 6/28/2016 Yeast/Fungi Infections Candidiasis Presents in moist skin folds Appears Erythema Whitish pseudo membrane Peripheral papules and pustules Oral Candidiasis, thrush White coating of the oral cavity, especially the tongue. Produces fissures on the tongue Restricts oral intake, compromising the aging adult further. Immobility Leads to: Increase risk of pressure ulcers Loss of lean muscle tissue and bone density Decreased blood flow to the lower extremity Lack of use of the foot and calf pump adds to the risk for lower extremity swelling and circulatory difficulties. Decreased physical activity leads to obesity and diabetes Incontinence Incontinence is not a normal part of aging Urinary incontinence has implications for skin damage. Leading to maceration of the skin in this region occurs. This will soften and separate the epidermal layers A moist environment has been shown to increase the risk of pressure ulcers Both urinary and fecal incontinence can alter the skin’s integrity. Candidiasis often appears in the groin area further leading to skin breakdown 18 6/28/2016 Decreased Mental Status Cognitive awareness is necessary for promotion of wound healing. Inadequate understanding of proper nutrition or proper skin hygiene can increase the risk of development skin breakdown. Once a wound occurs, proper management includes the cognitive factor to perform the required care for: wound cleansing and dressing skin hygiene and nutritional management medication usage (oral and topical) positioning for pressure or edema relief Dry Skin Rash Dermatitis/eczema Herpes Infections Skin tears Scars Cancer Pressure Ulcers Chronic Venous Insufficiency Arterial Insufficiency Diabetes Skin Failure Prevalence in Aging Adults Most common in those over 90 years Skin tears Venous insufficiency ulcers Arterial insufficiency ulcers Venous Leg ulcers 3-4x higher in those 80 years than those 65-70 Pressure ulcers 5-7x higher in those over 80 than in those 65-70 Shah, et al, 2016 19 6/28/2016 Major complaints of the aging population Supplemental additions of moisture to the skin surface becomes necessary. Humidity of > 70% is required in order to draw moisture from the environment. Superficial breaks occur as a result of dry skin and the formation of deeper fissure involving the dermal base occurs Excessive washing and bathing strips away the surface lipid and induces dryness, referred to as xerosis. Humidifier Room temperature as low as comfortable Bathe in warm (not hot) water Avoid harsh soaps (those with alcohol) and drying agents (such as powders) Use skin emollients (after bath while skin damp and before bed). Reduce bathing frequency to 1-2 times/week Offering fluids to residents/patients Common appearance May indicate Infection Reaction to a pharmacological, nutrient or other environmental intervention or contact Uticaria a raised wheal-like lesion often associated with food or drug allergic reactions are often wet or oozing patient scratching may lead to further skin abrasions and localized skin infections. 20 6/28/2016 Inflammation depends on the trigger. The earliest and mildest skin changes seen as Erythema & edema which may progress to vesicles (small blisters <1cm in size). These vesicles will begin to weep Followed by Crusts consisting of dried fluid that is either serum (clear), pus (yellow and thick) or blood (red-brown). Scaling is the end result seen on the surface of the skin Lesions < 1cm in size Macule: flat Papule: raised Vesicle: blister Lesions >1 cm Patch: flat Plaque: raised Bulla: blister The chronic inflammation: skin thickening with increased surface markings (lichenification), excoriation, and a change in pigmentation. 21 6/28/2016 Dry skin (xerosis) Hypersensitivity to allergens and other irritant changes in the basal epidermis & scaling. In the aging adult, Commonly seen on the hands, eyelids and ears. Common complaint is itching-increases at night. Scratching provokes the inflammatory response. Can also result in disfiguring skin lesions. Stress and environmental conditions such as foods, dust mites, bacteria have been linked to exacerbations The typical skin changes in chronic venous disease. CVI leads to edema and capillary hyper permeability. Hemosiderin staining- classic pigmentation appearance. The deposited fibrin leads to a woody fibrosis of the skin Dryness and scaling on the legs resulting in eczematous changes characterized by red, superficial, itchy plaques and weepy crusts often mistaken as cellulitis lipodermatosclerosis. Occur during the final phase of wound repair disorganized weave to collagen fiber bundles differences in capillary density altered pigmentation of the epidermis a diminished content and organization of elastic fibers The tensile strength of the skin is reduced Affects the person’s appearance & self confidence, especially if on the hand or face 22 6/28/2016 Documentation by: Height, Vascularity, Pigmentation, Pliability Active scars are raised, red, firm and pliable Susceptible to change Hypertrophic scars Within boundaries of wound but raised above surface. Contain fibroblasts with abnormal growth factor responses Respond to skin substitutes & variety of film dressings Keloid scars Outside the boundaries of the wound Appearance of a benign tumor. Generally occur in the upper trunk, face, neck & ears Familial, especially in darker pigmented populations Skin tears Often seen as minor inconsequential wounds, yet are very painful and can often lead to more complications and chronic wounds if not properly treated. Often there is no reported cause of the skin tear. However, there have been links to bumping into objects, wheelchair or bed injuries, transfers and falls. 23 6/28/2016 Skin Tears: Risks & Prevelence In institutions: Skin tears have been shown to increase during peak activity hours of 6 to 11 AM and 3 to 9 PM. The risk for skin tears as a result of: echanical trauma when assistance is required for bathing, dressing, toileting and transferring. Adhesives from wound dressings Payne-Martin Classification System for Skin Tears Accepted since 1993 but has not been widely incorporated into practice. This classification divides skin tears into 3 categories: Category 1: A: linear skin tear w/o tissue loss & the epidermis & dermis are separated B: flat w/ an epidermal flap over the dermis to w/in 1mm of wound margin. Category 2: A: partial tissue loss of 25% of the epidermal flap gone B: partial tissue loss of >25% of the epidermal flap loss Category 3: skin tear with complete tissue loss, epidermal flap is absent More common in the 6th to 8th decade. Usually, unidermatomal on the thoracic area Rare cases on the L/E associated with taking steroids Preceded by a mild paresthesia and pruritus within a specific dermatome Contagious until the lesions have crusted Usually resolve in 4 weeks Approx. 10-20% will develop post herpetic neuralgia Pain that exists from 1-4 months after resolution of the skin lesions. Results in sensory loss and spontaneous pain due to destruction of sensory neurons. 24 6/28/2016 Shingles Vaccine CDC recommends people aged 60 and older get a onetime vaccination In 2009 only 10% of this population had received the vaccine By 2010, 14.4% In 2014, Shingles vaccine question is part of the core questionnaire for every state to use with aging adults WHY?? Shingles impacts ADLS due to intense pain, thus costs health care dollars Need to adopt corrective measures to address problems of disparities http://www.cdc.gov/aging/pdf/state-aging-health-in-america-2013.pdf Skin Cancer dx in 40-50% of those over age 65 at least 1x in their lifetime, a growing global problem Chronic vascular ulcers can degenerate into a malignancy (Marjolin’s ulcer) and many epidermal cancers can mimic venous ulcers in appearance, location and symptoms. Further eval. is needed when there is: An increase size despite appropriate treatment Increase in pain hypertrophic (excess) granulation tissue Develop irregular base or margin Wounds with excessive bleeding Any deposit that has a caviar appearance Any change in an existing growth or a new growth on the skin that ulcerates but does not heal as anticipated 25 6/28/2016 Asymmetry of one half of the mole not matching the other half Border being irregular with ragged or notched edges Color of brown, tan or black in varying degrees but uniform within the mole Diameter being >6mm or the size of a pencil eraser tip are classic signs of potential melanoma. **There is now an additional evaluation level of “E” for the evolution, enlargement or elevation of a lesion Cancer Skin cancer is estimated to be diagnosed in 40-50% of those over the age of 65 at least once in their lifetime and is a growing global problem The link between UV exposure and skin cancer has been well established and induces all 3 major forms of skin neoplasms; basal cell carcinoma, squamous cell carcinoma and malignant melanoma. Chronic vascular ulcers can degenerate into a malignancy (Marjolin’s ulcer) and many epidermal cancers can mimic venous ulcers in appearance, location and symptoms. Clark Staging System Used for determining treatment intervention. Stage 0: A nonmelanoma lesion confined to the epidermis. Stage 1: Carcinomas <2cm Stage 2: Carcinomas >2 cm Stage 3: Involves structures below the skin, i.e.., muscle/bone/cartilage/lymph nodes Stage 4: Metastasized lesions *The actual depth may vary depending upon the region of the body involved 26 6/28/2016 Types of Skin Cancer Precancerous actinic keratosis abnormal changes in keratinocytes and can become squamous cell carcinoma. Clinical features include single or multiple dry scaly adherent lesions on habitually sun exposed skin usually begin as barely perceivable rough spots of skin (sandpaper feeling); more often felt than seen progressing to erythematous, scaly plaques that flake of or are exfoliated by toweling after a shower or shaving Basal cell and squamous cell carcinoma Grouped as nonmelanoma skin cancers The recognized cause is prolonged and cumulative exposure to the sun Can be found in chronic non healing ulcers that appear similar to other types of ulcers (venous/arterial insufficiency, diabetic or pressure ulcers) however they do not appear in the more typical locations. Often is only diagnosed after several months when inflammatory changes and edema was improved, but the wound was enlarged and many times having a raised granulated edge Basal Cell Carcinoma Slow growing Rarely metastasize Can cause local skin destruction and changes in skin and body appearance They appear as lesions with pearly borders, depressed centers and rolled edges Chronic wounds will have a shiny, translucent surface typically have uniform abundance or exuberant granulation tissue extending above or even overlapping the wound margins 27 6/28/2016 Squamous Cell Carcinoma Besides UV rays, radiation and tissue damage from scars, ulcers and fistulas may also produce squamous cell carcinomas These tumors affect the skin and mucous membranes can be more invasive and malignant than basal cell carcinoma if not treated promptly Squamous cell carcinoma has a hyperkeratotic appearance may ulcerate and bleed. This should be suspected in a reddish/black non healing wound that has an appearance of caviar. Malignant Melanoma Highly metastatic lesions Worldwide, this type of cancer is growing faster than any other except for lung cancer Due to chronic sun exposure, the risk for malignant skin cancer increases with age Risk factors include fair complexion with a tendency to easily sunburn and a family history of melanoma. The most common locations are on the legs of women and trunk of men. These tumors have irregular borders, can be brown or black and are usually larger than 6mm. Melanoma: Breslow Depth Scale Stage Depth Depth of tissue involvement I < 0.75 MM Confined to epidermis II 0.75-1.55mm Invasion into the papillary dermis III 1.51-2.25mm Fills papillary dermis and compresses the reticular dermis IV 2.25-3.0 mm Invasion of reticular dermis (localized) V >3.0mm Invasion of subcutaneous tissue (regionalized by direct extension) 28 6/28/2016 Pressure Ulcers Pressure ulcers can reduce the overall quality of life because of the pain, treatment interventions, and increased length of institutional stay even contributing to premature mortality. The estimated cost for pressure ulcer care: $11 billion annually $500-$70,000.oo per individual pressure ulcer NPU Advisory Panel, 2015 Litigations regarding pressure ulcers have also added a financial burden on healthcare costs. Prevalence/incidence Despite awareness of prevention, pressure ulcer development continues to be a concern. Hospitalized patients in the United States between 1993- 2008 had a 63% increase of pressure ulcers The prevalence of pressure ulcers is widespread across all settings: 0.4-38% in acute care, 2-24% in long-term care 0-17% in home care. The incidence of new pressure ulcers is also widespread 6% in 2008 5% in 2009 US Dept. Of Health Human Services,2013 Friction/Shear The role of friction/shear is described in terms of poor lifting and handling techniques Friction: Dragging the patient instead of lifting and increases in areas of moisture. Shear: Patient sliding causing superficial to slide across the deeper tissue resulting in a shearing force 29 6/28/2016 Pressure ulcers can occur from any pressure source Pressure Ulcers Characteristics Due to pressure Over bony prominence Vary in depth Necrotic tissue often present Exudate common May be painful Associated with malnutrition Staging Pressure INJURY New staging system as of 2016 Pressure injuries are staged to indicate the extent of tissue damage Definition: Localized damage to the skin and/or underlying soft tissue over a bony prominence or related medical or other device. Can present as intact skin or open ulcer and may be painful Occurs as result of intense or prolong pressure or in combination with shear May be affected by microclimate, nutrition, perfusion, co-morbidities, and conditions of the soft tissue NPU Advisory Panel, 2016 30 6/28/2016 Stage 2: Partial Thickness skin loss; exposed dermis Wound bed is viable, pink or red, most and may present as an intact or ruptured blister Adipose tissue and deeper tissues are not visible Granulation tissue, slough or eschar are not present Often result of microclimate changes and shear over pelvis and heel. Do not use to describe moisture related damage due to incontinence, dermatitis, adhesives or trauma (skin tears, burns abrasions) Stage 3: Full thickness skin loss Adipose is visible Granulation and epibole (rolled edges) often present Slough and/or eschar may be present Depth varies by anatomical location Undermining and tunneling may occur Fascia, muscle, tendon, ligament, cartilage and/or bone is NOT exposed If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury Stage 4: Full thickness skin and tissue loss Exposed or directly palpable fascia, muscle, tendon, ligament, cartilage and/or bone Epibole, undermining, tunneling may occur Depth varies by anatomical location If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury 31 6/28/2016 Unstageable Pressure Injury: Obscured skin and tissue loss Full thickness skin and tissue loss cannot be confirmed due to being obscured by slough or eschar Once removed, a Stage 3 or 4 will be revealed Stable eschar (dry, adherent, intact without erythema or fluctuance) on an ischemic limb or the heel(s) should not be removed. Deep Tissue Injury: Persistent non blanchable deep red, maroon, or purple discoloration Intact or non intact skin or epidermal skin separation revealing a dark wound bed or blood filled blister Pain & temperature changes often precede skin color changes Discoloration may appear differently in dark pigmented skin Results from prolong or intense pressure and shear forces at bone-muscle interface May evolve rapidly to reveal actual extent of injury or may resolve without tissue loss Other Pressure Injuries Mechanical Device: Use of devices designed and applied for diagnostic or therapeutic purposes. Injury generally conforms to the pattern or shape of the device Use the staging system for documentation Mucosal Membrane Pressure Injury Injury is found on mucous membranes with history of a medical device use in the location of the injury These injuries cannot be staged 32 6/28/2016 Chronic Venous Insufficiency Most common cause of leg ulcers; 81% of all cases with the risk of ulcers increasing with age Risk increases with: Age Greater in the long term care population Idenified as: Venous hypertension >90mmHg resulting in frequent/constant ulceration Chronic Venous Insufficiency Physiological process for ulcerations: Edema physically stretches the skin causing epidermal/dermal damages-resultant skin barrier disruption. Skin Barrier disruption compounds the inflammatory reaction of the underlying tissues creating more edema worsening the epidermal damage. The skin may become hypersensitive to chemicals and allergens causing more damage to the surrounding tissues Venous Ulcers Characteristics Due to inadequate return of venous blood Superficial (dermal) Ruddy, granular tissue Irregular wound margins Leg dark, brownish hue Exudate usually present Achy pain Associated with venous disease Occur in lower leg 33 6/28/2016 Venous Wounds Classification (1-3) CEAP classification system consists of 4 elements: Clinical classification Etiologic classification Anatomic classification Pathophysiology Venous Ulcer Treatment Treatment is restoration of venous return and management of edema Elevation Wrapping Protection from injury Lifelong compression therapy Arterial Insufficiency Have also been called ischemic ulcers and occur in patients with peripheral artery disease (PAD) The primary risk factors Diet Hypertension Hyperlipidemia Hypertriglyceridemia Diabetes mellitus Obesity from a sedentary lifestyle Stress Cigarettes Family history 34 6/28/2016 Arterial Insufficiency Ulcers Characteristics Due to lack of arterial blood flow Deep, “punched out” Pale wound bed Leg cool, pulseless Necrotic tissue from embolus Minimal exudate Arterial Insufficiency Ulcers Even wound margins Cellulitis common Associated with PVD Usually painful, in absence of neuropathy Treatment is restoration of arterial flow if surgical candidate Diagnostic tests: Ankle/Brachial index (BP of ankle divided by highest BP of arm) Patients with <.45 are not going to heal. At risk if <.8 Capillary refill time Count “1001” …after pinching great toe to check refill time. Rubor of Dependency Legs are pale with elevation and increase redness with dependency 35 6/28/2016 Ankle Brachial Index Utilizing a Doppler for evaluating the ABI is the preferred method Method: Patient should lay supine for 15-20 minutes prior to measurement Measure both UE and take highest systolic measurement For Each LE: determine the highest systolic pressure between dorsal pedis and post tibialis Divide the LE systolic by the highest UE systolic Ankle Brachial Index Adequate blood supply: > 0.6 and <1.2 Borderline PAD, needs further eval: >0.6 and <0.8 A false elevation of the ABI (>1.2)can occur in patients with calcified vessels such as diabetes Elevation and compression therapy is contraindicated in patients with arterial ulcers especially if the ABI is less than 0.5. Diabetes Microvascular or macrovascular complications can lead to bruises or injuries that do not heal, gangrene, and ultimately progress to amputation Greater risk of developing repetitive ulcerations and infections due to the vascular changes Early identification of sensory loss with proper intervention could lead to a decrease in the number of wounds in this population. 36 6/28/2016 Neuropathic (Diabetic) Ulcers Characteristics Due to pressure in numb areas, such as feet Associated with diabetes Deep Painless (leg neuropathic) Even wound margins Callous surrounding ulcer Granular tissue, unless PVD Cellulitis or osteomyelitis common, MRSA common Occur on metatarsal heads, areas where shoes rub Staging Systems for Diabetic Wounds (Grade 0-III) University of Texas Diabetic Wound Classification System (Grade 0 – III) 0= Preulcerative or postulcerative lesion, completely epithelialized I = Superficial wound, not involving tendon, capsule or bone II = Wound penetrating to tendon or capsule III = Wound penetrating to bone or joint Podiatrists use the Wagner Scale 0-5 0-Pre-ulcerative lesion, healed ulcers, presence of bony deformity 1-Superficial ulcer without subcutaneous tissue involvement 2-Penetration through the subcutaneous tissue, may expose bone, tendon, ligament of the joint capsule 3-Osteitis, abscess or osteomyelitis 4-Gangrene of digit 5-Gangrene of the root requiring disarticulation 37 6/28/2016 The LEAP Risk scale is also used. Risk Category 0: Intact protective sensation Yearly follow-up foot screening Proper footwear education Risk Category 1: Loss of protective sensation (LOP), no foot deformity Follow-up every six months Patient education LEAP Risk Category 2: LOP with foot deformity Follow-up every three months Patient education and skin care Risk Category 3: LOP with foot deformity and history of previous ulceration or amputation Follow-up monthly Patient education and skin care Custom molded orthotics Prescription footwear 38 6/28/2016 Plus dorsal area of between 1st and 2nd distal metatarsal Modified from Northcoast Medical Treatment of Diabetic(neuropathic) Ulcers Treatment Removal of callous Offloading Boots Shoes Assessment for osteomyelitis MRSA common Topicals must be selective for MRSA ***Osteomyelitis is a common complication: Majority of amputations are preceded by this 39 6/28/2016 Skin Failure Langemo and Brown define “skin failure” as an event in which the skin and underlying tissue die due to hypo perfusion that occurs concurrent with sever dysfunction or failure of the organ systems. Skin Barrier Failure The skin is the largest organ of the body As with other internal organs the skin fails too Acute, chronic or end-stage skin failure Skin Deterioration In the failing individual, skin deterioration is the often the most outward manifestation of overall faltering physiology 40 6/28/2016 Acute Skin Failure Acute skin failure: Skin & underlying tissue die due to hypoperfusion concurrent with a critical illness More often seen in ICU or acute care settings Chronic Skin Failure Skin & underlying tissue die due to hypoperfusion concurrent with ongoing, chronic disease states Occurs in a more steady fashion Individuals usually older and have multiple comorbidities Internal organ systems increasingly and irreversibly lose their ability to function as the end of life nears Chronic Skin Failure Risk Factors Manifestations Chronic illness Loss of fat & muscle mass Older population Decreased mobility Multiple co-morbidities Skin & underlying tissue changes Decline in mentation Decreased functional ability Malnutrition 41 6/28/2016 Interventions for Chronic Skin Failure Well documented multidisciplinary interventions Nutritional support Hydration Medical management Hygiene Functional rehabilitation Pressure redistributing surface selection End-Stage Organ Decompensation & Failure Large and unusual presentations of skin failure Body shunts blood to vital organs Widespread deep tissue destruction over stressed areas can appear in a matter of hours or less Sacrum Heels Posterior calf muscles Arms Elbows Multiple Organ Death Reveals itself on the external skin Few interventions can lessen the external skin damage as the body actively begins to shut down Clear, honest communication of medical assessments and prognosis among: Health care providers Patient/resident Significant others Establish realistic goals for treatment of unavoidable complications, pain and suffering at the end stages of life 42 6/28/2016 SCALE Skin Changes At Life’s End Expert panel published paper in 2008 Current understanding of complex skin changes at life’s end limited Not all pressure ulcers are avoidable End of Life Phase of life when a person is living with an illness that will often worsen and may eventually cause death Kennedy Terminal Ulcer An unavoidable ulcer Those who exhibit this ulcer will be at the end stage of life Usually appears about 2 to 6 weeks before death 43 6/28/2016 Kennedy Terminal Ulcer Not a cause of a patient's death May starts out superficially as a blister or a Stage 2 Looks much like an abrasion with small black almost vasculitic spots Rapidly progresses to a Stage III or a Stage IV On sacrum in the shape of a pear, butterfly or horseshoe with irregular borders Cause remains unknown Dialogue Necessary in Presence of Chronically Ill The occurrence of skin failure in the chronically ill is a time to establish dialogue Pros and cons of future aggressive medical interventions Should this be Palliative Care? “The decision to move a patient from curative to a palliative treatment plan requires that the clinician has determined that the wound is ultimately non-healing rather than undertreated” Shah, 2016 44 6/28/2016 CONSIDERATIONS Patient preference Respect their autonomy to accept or reject treatment Beneficence The best interest of the patient and health of society Nonmaleficence Duty to do no harm to the patient Justice Impartiality/fairness Surrogate Decision Maker If patient is not competent then advance directive followed before durable power of attorney Patient/Family conferences: S-P-I-K-E-S protocol SETTING Quiet setting, sitting eye to eye PERCEPTION Ask what they know about the condition INVITATION Ask how much detail they want to know KNOWLEDGE Present in a non technical/ simple language in small pieces EMOTION/EMPATHIZE/ Listen for emotion and identify EVALUATE cause SUMMARIZE Goals for Palliative Wound Care Preventing wound from getting larger Prevent new pressure ulcers Prevent infection Managing odor, exudate, bleeding Assessing and treating pain Self image, dignity, quality of life 45 6/28/2016 Practical Pointers for Palliative Care Practice meticulous skin care Avoid soap Use a low pH-balanced cleanser, gently Apply moisturizers Use low pH skin cleanser when incontinence present Apply a moisture barrier Protect skin from maceration Practical Pointers for Palliative Wound Care Nutrition and hydration Encourage repositioning to the extent possible Encourage turning and repositioning if possible Protect heels Assess, treat, reassess wound associated pain Medications Appropriate wound care Nonadherent dressings that can stay on for several days Skin sealants Nonpharmacological techniques Practical Pointers for Palliative Wound Care Prevent infections Minimize/mask odor Minimize or eliminate friction/shear forces Minimal mechanical force during wound cleansing Autolytic/enzymatic debridement preferred if needed 46 6/28/2016 Wounds at end of life Limited studies related to end-of-life wounds End-of-life wounds prevalence for ~1-million hospice patients Millions of other frail elderly persons living with chronic diseases suffer with end-of-life wounds Awareness of residents at risk for skin failure A wound/skin care program that addresses palliative treatment can significantly enhance the quality of life for patients/residents Determining the Etiology of any open wound is a critical first step Essential Elements Wound assessment Nutrition Debridement Management of Cleansing Dressings Offloading infection Protection from pressure Documentation 47 6/28/2016 Essential Elements Site: exact location Stage, if pressure ulcer Periwound: color, edema, injury, pain, warmth, texture, maceration Tunneling, sinus tract, undermining: location, depth Pain Size: length, width, depth Type of tissue: slough, necrotic, epithelial, granulation Exudate: color, amount, odor Pain Management Factors contributing to Pain ***Dried out dressings Adherent dressings Adhesive dressings Wound cleansing Wound debridement Patient’s previous experience Fear of hurting Packed gauze When is Pain Experienced? During Dressing removal During wound Debridement During Dressing Application While dressing is in wound Other 65% 25% 3% 2% 2% -Moffatt et al, 2002 48 6/28/2016 Chronic Wound Pain Persistent pain when nothing is being manipulated. Clinical Practice Guidelines -NPUAP Document pain: During turning Dressing changes Debridement Manage pain by: Covering wounds Adjusting support surfaces Repositioning Appropriate Analgesics as needed Effective Pain management Proper assessment Appropriate dressing selection Appropriate pressure relieving surfaces Appropriate Physical Therapy Interventions Patient Centered approach Observe body language and nonverbal cues Encourage deep, rhythmic breathing Negotiate a signal for “time out” Guided Imagery 49 6/28/2016 No single dressing can provide optimum environment for healing all wounds. Proper dressing can reduce medications needed for pain Considerations: Use: Types: Absorption Protection Debridement Promotion of granulation/w ound closure Length before changing: Transparent films Daily Hydrocolloids 3-10 days Hydrofibers As drainage indicates Hydrogels Alginates Collagens Foam gauze Modalities and Interventions Debridement Autolytic Enzymatic Sharp/Surgical Mechanical Negative Pressure Wound Therapy Electrical Stimulation Ultrasound Hyperbaric Oxygen Wet to dry, pulsatile lavage, low frequency US, whirlpool Light therapy Biological Chemical Conclusion Skin’s loss of integrity due to internal and external insults that need to be recognized in order to develop proper POC The Plan of Care is dependent on goals of therapy: Healing Palliative Restorative 50 6/28/2016 REFERENCES AHQR, US Dept. HHS. Pressure Risk Assessment and Prevention. http://effectivehealthcare.ahrq.gov/index.cfm/search-forguides-reviews-andreports/?productid=1490&pageaction=displayproduct National Pressure Ulcer Advisory Panel. http://www.npuap.org/news/ Robert L; Labat-Robert J; Robert AM. Physiology of skin aging. Clin Plast Surg. 2012; 39(1):1-8. Posthauer ME, Banks M, Dorner B, Schols J. The Role of Nutrition for Pressure Ulcer Management: National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel, and Pan Pacific Pressure Injury Alliance White Paper. Advances in Skin and Wound Care: April 2015; 28(4):175-188. Sha P, Han Aung T, Ferguson R, Ortega G, Shah J. Ethical Considerations in Wound Treatment of the Elderly Patient. Journal of the American College of Clinical Wound Specialists, 2016; 6(3):46-52. Gruen D. Wound Healing and Nutrition: Going Beyond Dressings with a Balanced Care Plan. Journal of the American College of Clinical Wound Specialists, 2016; 2(3): 46-49. Hakim, E.W., Heitzman, J. (2013). Wound management in the presence of peripheral arterial disease. Topics in Geriatric Rehabilitation, 29(3):187-194. Pieper B, Langemo D, Cuddigan J. Pressure Ulcer Pain: A Systematic Literature Review and National Pressure Ulcer Advisory Panel White Paper . Ostomy Wound Management 2009;55(2):16–31. Heitzman, J. “Foot Care for Patients with Diabetes”, Topics in Geriatrics 2010, Vol 26, No 3 pp 250-263 Pieper, B, ed. Pressure Ulcers: Prevalence, Incidence and Implications for the Future. Monograph by NPUAP, Nov 2012. Obtained at http://www.npuap.org/resources/educational-andclinical-resources/prevalence-incidence-monograph Rabbia J. “Impaired Integumentary Repair”. In: Geriatric Physical Therapy, 3rd ed. Elsevier: St. Louis, 2012. Dorner B, Posthauer ME, Thomas D, and the National Pressure Ulcer Advisory Panel. The role of nutrition in pressure ulcer prevention and treatment: National Pressure Ulcer Advisory White Paper. Retrieved at http://www.npuap.org/wpcontent/uploads/2012/03/Nutrition-White-Paper-WebsiteVersion.pdf Cheung,C. Older adults and ulcers: chronic wounds in the geriatric population. Adv in Skin & Wound Car. Jan 2010; 23(1):39-44. American Academy of Dermatology. Agingskinnet. http://skincarephysicians.com/aginskinnet/bascifacts.html. 51 6/28/2016 American Cancer Society. Detecting skin cancers. www.cancer.org. Accessed March 24, 2016 Chen TM, Fife CE. Never say never: Is it realistic to declare zero tolerance on pressure ulcers? Adv for LTC Mgt. Jan/Feb 2009:18-20. Feldman J. The Challenge of Infection in Lymphedema. National Lymphedema Network. 2011; July-Sept: 23(3) Retrieved at http://www.lymphnet.org/membersOnly/dl/reprint/Vol.%2023 /Vol_23-No3_Challenge_of_Infection.pdf Nigam Y, Knight J. Exploring the anatomy and physiology of ageing: the skin. Nursing Times. Dec 2008; 104(49):24-25 American Cancer Society. Skin Cancer: Basal and Squamous Cell. Retrieved at http://www.cancer.org/cancer/skincancerbasalandsquamouscell/detailedguide/skin-cancer-basal-andsquamous-cell-treating-squamousl-cell-carcinoma Accessed July 10. 2015 Asongwed ET, Chesbro SB, Karavatas SG. Peripheral arterial disease and the ankle-brachial index: what home healthcare clinicians need to know. Home Health Nurse. 2009 Mar; 27(3):160-7 Hawkins B. Strategies for the effective management of challenges associated with negative pressure wound therapy. Retrieved at http://www.woundsource.com/sites/default/files/whitepapers/p ractical_guide_to_negative_pressure_wound_therapy.pdf Biscoe AL, Bedlow A. Warfarin-induced skin necrosis diagnosed on clinical grounds and treated with maggot debridement therapy. BMJ Case Rep. Published online 2013 Jan 28. doi: 10.1136/bcr-2012-007455 Retrieved at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3604521/ Nalamachu S, Morley-ForsterP. Diagnosing and managing post herpetic neuralgia. Drugs & Aging. 2012 Nov; 29(11):863-9 Argoff CE. Review of current guidelines on the care of post herpetic neuralgia. PubMed Commons Postgrad Med. 2011 Sep; 123(5):134-42. APTA. Online Guide to Physical Therapy Practice. Principles of Physical Therapist Patient and Client Management. Retrieved at http://guidetoptpractice.apta.org/content/1/SEC2.body Hyoseo k Kang. Current therapeutic agents and anesthetic considerations for diabetes mellitus. Korean J Anesthesiol. 2012 Sep; 63(3): 195–202. Published online 2012 Sep 14. doi: 10.4097/kjae.2012.63.3.195 Retrieved at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3460146/ Ghosh V. What is Systemic Infection? Retrieved at http://www.preservearticles.com/2012032028128/what-issystemic-infection.html Lessnau, Klaus-Dieter; Bronze M, ed. Pseudomonas aeruginosa Infections Clinical Presentation; Apr 28, 2014. Retrieved from: http://emedicine.medscape.com/article/226748-clinical#a0216 52 6/28/2016 National Hospice and Palliative Care Organization. Palliative Care: An explanation of Palliative Care. Retrieved at http://www.nhpco.org/palliative-care-0 NIH. US National Library of Medicine. Contact Dermatitis. Retrieved at http://www.nlm.nih.gov/medlineplus/ency/article/000869 .htm Young, D, Schuerman, S, Flynn K, Hartig K, Moss D, Altenburger B. Reliability and Responsiveness of an 18 Site, 10-g Monofilament Examination for Assessment of Protective Foot Sensation. Journal of Geriatric Physical Therapy 2011, April/June; 34(2):95 53
