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Pressure Ulcers Jennifer E. Marks, D.O. February 25, 2004 LRI.

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Presentation on theme: "Pressure Ulcers Jennifer E. Marks, D.O. February 25, 2004 LRI."— Presentation transcript:

1 Pressure Ulcers Jennifer E. Marks, D.O. February 25, 2004 LRI

2 Definition of Pressure Ulcer An area of unrelieved pressure over a defined area, usually over a bony prominence such as the sacrum Pressure leads to ischemia, cell death, and tissue necrosis, as capillaries are compressed and the blood flow is restricted Muscle is the most sensitive tissue to pressure, skin is the most resistant

3 How do pressure ulcers usually present? 1. High pressure over bony prominence (can be a single insult) 2. At muscle and bone interface, ischemia results. 3. Affected area with erythema, induration, warmth, and skin is intact 4.Days to weeks s/p insult, EVEN WITH PRESSURE RELIEF, the wound opens, and is a depression with necrotic tissue

4 Pressure ulcers Associated with : 1. Shear forces 2. Impaired sensorium/sensation (SCI patients!) 3. Poor nutrition- serum albumin positively correlates with pressure ulcer stage, and negatively correlates with risk 4. Chronic illness 5. Elevated tissue temperature- Higher metabolic demands 6. Maceration

5 SCI patients Increased risk for pressure ulcer formation Estimated incidence 25-66%

6 Pathomechanics Shear forces- Tangential to the skin surface. Can play a major role in the formation of sacral ulcers. Axial forces- Perpendicular to the skin surface. Unrelieved axial pressure 4-6 times the systolic pressure can cause necrosis in less than 60 minutes! If tissue capillary pressure is exceeded, ulcers will form at that site.

7 How much pressure is too much? Kosiak 1961- Studied the effects of pressure and time on rat muscle. More pressure=less time for an ulcer to form Found that alternating pressure of as little as 5 minute intervals led to considerably less ulcer potential.

8 Kosiak’s research led to the current practice of turning patients every two hours. Why don’t we measure pressure/shear as clinicians? –Transducers are thick, bulky, and expensive –Shear transducers have not been modified for clinical use

9 What is a safe amount of pressure? Studies by Landis et al. have led clinicians to believe that pressures under 32 mm Hg are generally believed safe This value is influenced by tissue stiffness, tissue composition, and the patient’s body contour

10 Clinical Wound Assessment 1. Color photography- Use ruler in picture to give dimensions. Very useful when done in a serial fashion. An alternative is to draw pictures of the wound. 2.Location- Be specific. 3.Size- Be sure to include length, width, and depth measurements, in centimeters.

11 Clinical Wound Assessment 4. Describe the type of irrigation utilized, and the dressing type. 5.Drainage: –Amount(minimal, moderate, copious) –Color (serous, serosanguinous, prurulent) –Odor(present, absent)

12 Clinical Wound Assessment 6. Undermining/tunneling – Present/absent 7. Wound character- What kind of tissue? Is there granulation, slough? Stage the ulcer IF THERE IS ESCHAR PRESENT, YOU CANNOT STAGE THE WOUND!

13 Clinical Wound Assessments Stage I Nonblanchable erythema not resolved in 30 minutes, epidermis intact reversible with intervention Stage II Partial thickness loss of skin involving the epidermis, possible into dermis Stage III Full thickness destruction through dermis into subcutaneous tissue Stage IV Deep tissue destruction throgh subcutaneous tissue to fascia, muscle, bone

14 Systemic Conditions associated with chronic wounds SCIB/B alterations, contractures, spasticity,denervation atrophy,insensitivity ElderlyReduced skin elasticity, altered skin microcirculation DMInsensitivity, microangiopathy

15 Treatment Sharp debridement Mehanical nonselective debridement Enzymatic Debridement Autolytic debridement

16 Sharp debridement Removal of devitalized tissue/eschar via surgical means. Small wounds can be debrided at bedside, more extensive wounds can be addressed in the OR Most effective/quickest method of removing necrotic tissue. Debridement is done to the point where the tissue bleeds with forceps and a scalpel. Must have the clinical skill/judgement necessary to be able to discern the difference between vitalized and nonvital tissue. Cons: Can damage healthy tissue

17 Mechanical nonselective debridement Whirlpool Irrigation Wet to Dry dressing- utilize normal saline, place moist gauze on the wound, let dry. –When the dressing is removed, the necrotic tissue comes off it. –Cons: Healthy tissue can be damaged

18 Wet to Dry vs. Wet to Moist Saline wet to dry dressings are used to debride necrotic wounds Wet to moist dressings maintain a clean moist wound bed and are removed before they dry out. Wet to moist dressings have to be changed more frequently

19 Enzymatic Debridement Utilizes chemical agents (such as Accuzyme) in the form of ointments which work on the necrotic wound debris, and do not affect the viable tissue

20 Autolytic debridement The bodies own enzymes break down dead tissue.Wound cells secrete proteases, collagenases that digest eschar. Hydrocolloid dressings help to promote this type of debridement. Pros: Very effective in noninfected wounds- an occlusive dressing allows wound fluid to collect Cons: If the wound is infected, you have just created an abcess!

21 Wound dressings Gauze Transparent adhesive dressings Hydrocolloid dressings Gel dressing Calcium alginate dressings

22 Transparent adhesive dressings Ex. Tegaderm, Opsite Semipermeable, occlusive Stage I/II wounds without debris Allow gaseous exchange/water vapor transfer from the skin, prevent peri-wound maceration Do not use if wound is exudative or the patient is diaphoretic

23 Hydrocolloid dressings Ex. Duoderm Interact with wound exudate, and make a gel Keep wound surface moist. Enhances healing, protects versus secondary infection Help to minimize shear –Good for shallow stage III sacral ulcers

24 Calcium alginate dressings Made from brown seaweed (ex. Sorbsan), sterile Semi-occlusive, highly absorbable Good for treating exudative or contaminated wounds Need to be frequently changed

25 Most common pressure ulcer sites Ischium 28% Sacrum 17-27% Trochanter 12-19% (Bears weight when patient is in a sitting position) Other commonly affected sites include coccyx, heel, and malleolus

26 Treatment Proper medical care Turn patient Q 2 hours Frequent dressing changes Proper nutrition- High protein diet indicated as a high amount of protein is lost through the wound Pressure relief in wheelchair, specialty support surfaces Continued wound assessment

27 Support surfaces Include overlays (water, gel, foam, air) Specialty beds –Low air loss beds (Flexicare)have cushions filled with air that keep pressures below the capillary closing pressures –Air fluidized beds (Clinitron) use warm air forced through silicone beads to mimic a fluid medium

28 Which support surface is best? No study has shown conclusively that one surface performs better than the others! Must individualize your approach If a patient has a Stage III or IV ulcer, the patient should be utilizing a pressure relief product

29 Wound Infection Presentation: Foul odor, greenish drainage, dull white base (versus red granulation tissue). Can have cellulitis, with erythema, warmth, swelling, tenderness. Systemic bacteremia: Chills, anorexia, nausea/vomiting, fever, increased white count, mental status changes, glucose intolerance in diabetics. Signs of bacteremia/cellulitis- IV abx/possible debridement

30 Wound cultures Should not be routinely performed, as the cultures will always be positive Exception- If antiseptic such as Betadine is used prior to local debridement, and an abcess or other sequestered collection is exposed Occasionally, cultures are taken for burn wounds Greater than 10 5 CFU’s- wound will not heal

31 When are topical antibiotics indicated for pressure ulcers? If a pressure ulcer does not heal after 2-4 weeks of optimal treatment, can try silver sulfadiazine or triple antibiotic ointment x 2-3 weeks

32 Osteomyelitis Must keep in mind, especially with a Stage IV pressure ulcer or if ulcer over a bony prominence 25% of nonhealing ulcers have bone infection Gold standard- Bone biopsy Imaging- XRay, MRI

33 Xray Reactive bone formation and periosteal elevation =osteomyelitis BONE SCANS ARE A POOR STUDY TO DETECT OSTEOMYELITIS! High false positive rate.

34 MRI 95% sensitive On T2 weighted image, can demonstrate marrow edema Can reveal soft tissue abnormalities such as perirectal fistulas

35 Why don’t we just close the wound (vs. using flap)? Usually not enough soft tissue Too much tension where the incision site would be

36 Musculocutaneous flaps Why use a muscle flap when muscle is the first tissue to become ischemic? –Minimizes “deadspace”, and provide tissue with rich vasculature –NOT being used as a cushion! –In less than a year, the flap usually atrophies, but the blood supply remains intact –Also, the surgeon can put the suture line away from the maximal pressure area

37 When are flaps indicated? Better for an SCI patient, or when muscle loss will not affect ambulatory ability Not as easy a decision in an ambulatory patient, where function can be compromised

38 Best treatment for a pressure ulcer? NO ONE RIGHT ANSWER! Keep in mind: 1. PREVENTION 2. Must correct the underlying problem 3. Wounds must be cleaned/ dead tissue removed before healing can occur 4. Keep wound moist- Permits cells to perform migration/mitosis

39 What is being researched? Electrical stimulation – some studies are showing improved pressure ulcer healing rate in chronic stage III and IV ulcers –Controversial –Also small study using growth factors in SCI patients. –Both areas need more research

40 Works Cited Braddom, Randall L. Physical Medicine and Rehabilitation. Second Edition. Philadelphia, Pennsylvania. W.B. Saunders Company, 2000. O’Young, Young, et al. Physical Medicine and Rehabilitation Secrets. Second Edition. Philadelphia, PA. Hanley & Belfus Inc., 2002.

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