PRESSURE ULCER PREVENTION & TREATMENT Prepared by Linda Kennedy-Mull
All SCI individuals are atrisk for developingpressure ulcers (PU).
Pressure Ulcers occur more frequently in people with: More extensive Irresponsible paralysis & behavior – completeness of SCI smoking/ETOH/drug Longer duration of abuse SCI Poor nutrition Less functional Those who won’t independence assume (para’s vs. quad’s) responsibility for skin care
Incidence: 32-40% of individuals admitted to SCI units in the USA develop pressure ulcers during initial hospitalization: 37% of ulcers were sacral ulcers & of those, 50% were Stage III or IV.
Recurrence ’97 study – 176 veterans with SCI had 35% recurrence rate; smoking, diabetes & coronary / vascular disease all associated with highest risk of recurrence.
Costs: ’94 study – total cost of treatment was ~ $1,335 Billion / year. 69% of this provided in hospitals ’92 study – cost was: ~ $70,000 to treat full thickness ulcer ~ $20-30,000 to treat less serious ulcers
RISK FACTORS Standard Risk Factors: Malnutrition Friction Incontinence Moisture Shearing Loss of Sensation Immobility
RISK FACTORS Assess Degree of Risk Use Braden Scale: Admission Every time patient’s condition changes Monthly in NHCU * Use clinical judgment as well
RISK FACTORS Assess Demographic & Psych/social Risk Factors Age Ethnicity, Cultural Values Sex Cognition Marital Status Substance Abuse Education Psychological Health
RISK FACTORS Normal Skin Largest single organ of the body Main function is to isolate & protect the body from environment Skin insulates the body & helps maintain core body temp Skin consists of 2 layers: Epidermis, Dermis
RISK FACTORS Neurologically Impaired Skin SCIs have altered autonomic nervous system Degree of alteration varies with level of injury SCI above T6 changes functional properties of the skin-sweating reflex is lost SCIs are unable to maintain constant body temp in early stages following injury
RISK FACTORS Neurologically Impaired Skin Changes that occur in skin: Increase in collagen catabolism Decrease in amino-acid metabolites in skin Decrease in Type I & II collagen, which robs the skin of elasticity & strength Skin is more fragile below injury Decrease blood flow & supply below injury, which affects delivery of nutrients, etc. * Takes 3-5 years for changes to stabilize
RISK FACTORSMuscle Atrophy Caused by Paralysis Produces loss of muscle bulk: Less cushioning Less protection Less absorption of mechanical forces
PHYSIOLOGY of WOUND HEALING Two Mechanisms of Repair Regeneration: replacement of lost tissue with more of the same tissue Connective Tissue Repair: lost tissue is replaced by scar formation Type of Repair: determined by the tissue layer involved
PHYSIOLOGY of WOUND HEALING Partial Thickness Wounds: Dermal Repair: Epidermal Repair: Concurrent with Inflammatory response epithelialization Epithelial Angiogenesis proliferation Fibroblasts Migration become (resurfacing) plentiful– 7 days Re-establishment Collagen fibers of epidermal are visible – 10 layers days
PHYSIOLOGY of WOUND HEALING Full Thickness Wounds (continued) Proliferative Phase (3-20 days) Granulation tissue develops Wound contracts Collagen is produced to give strength & elasticity Maturation Phase (up to 2 years) Begins when the wound has closed Tensile strength of scar tissue =/<80%
PRESSURE ULCERS Most pressure ulcers can be prevented, but sometimes even VIGILANT nursing care will not prevent the development or worsening of ulcers in some high-risk individuals. Improving Nutrition Managing Incontinence Activating Prevention Measures Frequent turning Use of overlays, low air loss, etc.
PRESSURE ULCERS (CONTINUED) Four Goals for Protection Identify at risk individuals & factors placing them at risk Maintaining & improving tissue tolerance to pressure Protecting against adverse effects of external mechanical forces Reducing incidence through education
Severe Pressure Ulcer withBone Loss
PRESSURE ULCERS Staging of Pressure Ulcers: WOCN Staging Stage I: non-blanching Stage III: full thickness skin loss erythema of intact skin involving damage or necrosis of subcutaneous tissue that may extend down to, but not through, Stage II: partial thickness skin the fascia. Presents as a deep loss involving epidermis &/or crater with or without dermis. Ulcer is superficial & undermining. presents as an abrasion, blister, or shallow crater Stage IV: full thickness skin loss with extensive damage, * Staging Limitations: destruction,or necrosis of muscle, Echar/slough prevents staging bone or supporting structures. Identifying Stage I is difficult in Undermining & sinus tracts may be dark skin present No reverse staging as wound heals
Stage I Pressure Ulcer
Stage II Pressure Ulcer
Stage III Pressure Ulcer
Stage IV Pressure Ulcer
PRESSURE ULCERS Ulcer Assessment Stage the Ulcer Drainage: exudate, transudate Location (serosanguinous), amount Size – measure weekly or more Undermining, often,if dramatic Tunneling, Sinus change Tract
PRESSURE ULCERS Ulcer Assessment (continued) Tissue Type: viable/non-viable, describe as red, yellow, tan, black, etc. Surrounding Skin: Pain/sensation or lack of in SCI Edema Induration Color Maceration Fungus Hair present
ULCER TREATMENT Goals Treatment / Intervention Evolve as the patient’s wound progresses Pressure Relief Dressings change from absorbent, to debriding, REPOSTIONING to maintaining moist Overlays, mattress wound environment replacement, static or Patient & family dynamic, low air loss, air education fluidized
ULCER TREATMENT Electrical Stimulation Appropriate Dressing Increases oxygen & nutrient Choice is based on 3 aspects: transport Color of wound Decreases edema Depth of wound Increases fibroblastosis Exudates Increases collagen development Other considerations: • Indication: chronic wounds not Infection responding to conservative tx Tissue surrounding wound • Contraindicated: in osteo, malignancy, pacemakers, over Fragility of skin pregnant uteruses, over heart or Medical conditions impacting carotid sinuses, or over laryngeal healing musculature Change Tx if wound has not Surgical improved after 2-4 wks or Immediately, if negative Flap Repair outcome Skin Graft
FACTORS IMPACTING WOUND HEALING Infection Infection vs. Contamination All chronic wounds are contaminated, but can still heal Infection prolongs the Inflammation Phase & delays healing Obtain appropriate cultures: superficial swab, needle aspiration, tissue biopsy. Culture Technique: 10 point method
FACTORS IMPACTING WOUND HEALING Treatment Systemic antibiotics Topical antiseptics, antimicrobial, antibiotic agents NPUAP – do not use topical antiseptics to reduce Bacterial load. If used, limit to 2-3 days Cytotoxic topical agents: Betadine Dakins (bleach) Acetic Acid (vinegar) Hydrogen Peroxide
PREVENTION MEASURES Reposition at lease q2 hrs. using Prevent moisture accumulation pillows or foam wedges Use lifting devices to move Keep bony prominences from patient; friction injuries can be direct contact from one another prevented by using linen to move Provide total heel pressure relief patient, using lotion & films for patients who are immobile At risk patient should be Side-to-side turning of no more automatically placed on a than 30 degrees rotation pressure reducing device: Keep head of bed at lowest Zone-Aire Beds degree of elevation consistent RIK Gel Flotation Mattresses with condition Alternating Pressure Mattress Water Mattress Limit amount of time HOB is elevated to prevent shearing
PREVENTION MEASURES Chair bound patients need pressure relieving cushions – consult O.T. Chair bound patients need repositioning q 1 hr or taught to shift weight q 15 minutes Positioning of chair bound patients should include consideration of postural alignment, distribution of weight, balance, stability, & pressure relief Conduct DAILY comprehensive skin inspections Education of patient, family / significant other