Wound Care Protocol

1. Wound Care Protocol Stanojka Lipovac MD, MPT, CWS CP of NYS

2. PRESSURE ULCERS • Pressure ulcer is a localized area of tissue necrosis that develops when soft tissue is compressed for a period of time between bony prominence and outside surface that body is positioned on. • Without identification and early intervention of causative factors, blood flow will cease and cause cell death. • Successful treatment of pressure begins with maintaining adequate blood flow to the tissue and by correctly selecting pressure-relieving devices. DDNA Conference 2007

3. PRESSURE ULCERS BODY AREAS AT RISK PositionPrimary areasSecondary areas Seated ischial tuberosities, sacrum, coccyx, heels greater trochanter, elbows, thigh Side-lying greater trochanter, shoulder, ear, elbow, knees and ankles, thigh heels Supine sacrum, coccyx, back, elbows, occiput heels * heels are at risk in all position DDNA Conference 2007

4. PRESSURE ULCERS • Pressure ulcers are defined using AHCPR (Agency for Health Care Policy and Research) recommended staging system. A new Stage I definition was adapted by the NPUAP (National Pressure Ulcer Advisory Panel) that is more inclusive of the range of skin pigmentation. They are staged as follows: DDNA Conference 2007

5. PRESSURE ULCERS • Stage I is an observable pressure related alteration of intact skin whose indicators as compared to the adjacent or opposite area on the body may include changes in one or more of the following: skin temperature (warmth or coolness), tissue consistency (firm and boggy feeling) and/or sensation (pain and itching) The ulcer appears as a define area of persistent redness in lightly pigmented skin, whereas in darker skin tones, the ulcer may appear with persistent red, blue or purple hues. DDNA Conference 2007

6. PRESSURE ULCERS Stage I DDNA Conference 2007

7. PRESSURE ULCERS Stage I DDNA Conference 2007

8. PRESSURE ULCERS • Stage II is partial thickness skin loss involving epidermis, dermis or both. The ulcer is superficial and presents clinically as an abrasion, blister or shallow crater. DDNA Conference 2007

9. PRESSURE ULCERS Stage II DDNA Conference 2007

10. PRESSURE ULCERS Stage II DDNA Conference 2007

11. PRESSURE ULCERS • Stage III is full thickness skin loss involving damage to, or necrosis of subcutaneous tissue that may extend down to, but not trough underlying fascia. The ulcer presents clinically as a deep crater with or without undermining of adjacent tissue. DDNA Conference 2007

12. PRESSURE ULCERS Stage III DDNA Conference 2007

13. PRESSURE ULCERS Stage III DDNA Conference 2007

14. PRESSURE ULCERS • Stage IV is full thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (e.g. tendon, joint capsule). Undermining and sinus tracts also may be associated with stage IV pressure ulcers. DDNA Conference 2007

15. PRESSURE ULCERS Stage IV DDNA Conference 2007

16. PRESSURE ULCERS Stage IV DDNA Conference 2007

17. PRESSURE ULCERS Limitations in stage definition: • When eschar is present, pressure ulcer cannot be accurately staged until the eschar has been removed. • Assessment of Stage I pressure ulcer may be difficult in patients with darkly pigmented skin. DDNA Conference 2007

18. PRESSURE ULCERS A. Mechanical factors • Moisture • Friction • Pressure • Shear DDNA Conference 2007

19. PRESSURE ULCERS • Moisture a. Causes- excessive perspiration, incontinence, drainage, tube leakage b. Tissue injury- macerates epidermis, promotes bacterial growth, viral and fungal growth DDNA Conference 2007

20. PRESSURE ULCERS • Friction • Cause- rubbing of epidermis on external surface • Tissue injury-abrasions and erosions DDNA Conference 2007

21. PRESSURE ULCERS • Pressure • Cause- sustained externally applied pressure over bony prominence that impedes blood flow • Inversed relationship between pressure and duration • Reactive hyperemia is a warning sign of PU development DDNA Conference 2007

22. PRESSURE ULCERS • If pressure increases, time before ischemia occurs decreases. Only two hours at 200mm Hg. Low pressure applied over longer periods of time are thought to be more significant in the development of pressure ulcers than higher pressure of shorter duration. Clinically, most small, deep ulcers are the result of very high pressures acting on the skin for very short time periods, whereas large, deep ulcers, are the results of lower amounts of pressure maintained over longer time periods. DDNA Conference 2007

23. PRESSURE ULCERS • Critical Vascular Occlusion time (CVOT) • That is time, which causes cell death. • Normal CVOT is 2 hours • May be less in compromised pt DDNA Conference 2007

24. PRESSURE ULCERS • Shear • Cause- Layer of the skin moving over one other • Tissue damage- superficial, blistering, undermining, tunneling DDNA Conference 2007

25. PRESSURE ULCERS B.Contributing factors decreasing tissue tolerance • Nutrition • Age • Edema • Underlying disease • Temperature • Anemia DDNA Conference 2007

26. PRESSURE ULCERS • Nutrition Patients that are underweight and have poor nutrition with inadequate intake of proteins, vitamins and minerals are at higher risk of developing PU DDNA Conference 2007

27. PRESSURE ULCERS • NUTRIENT FUNCTION RESULTS OF DEFICIENCY ________________________________________________________________________ Proteins Wound repair Poor healing Clotting factor production Edema White blood cell (WBC) Lymphopenia production and migration Impaired cellular immunity Cell-mediated phagocy tosis Fibroblast proliferation Neovascularization Collagen synthesis Epithelial synthesis Wound remodeling ________________________________________________________________________ DDNA Conference 2007

28. PRESSURE ULCERS Albumin Controls osmotic equilibrium Hypoalbuminemia, with generalized edema thereby slowing oxygen diffusion and transport mechanisms from the capillaries metabolic and cell membrane ________________________________________________________________________ Carbohydrates Supply cellular energy Body uses visceral and muscle proteins for energy Spare protein ________________________________________________________________________ Fats Supply cellular energy •Inhibited tissue repair Supply essential fatty acids Cell membrane manufacture Prostaglandin production ________________________________________________________________________ DDNA Conference 2007

29. PRESSURE ULCERS Vitamin A Collagen synthesis Poor healing Epithelialization __________________________________________________________________________________ Vitamin C Membrane integrity Scurvy Poor healing Capillary fragility and bleeding __________________________________________________________________________________ Vitamin K Coagulation Increased risk of hemorrhage/ hematoma formation __________________________________________________________________________________ Pyridoxine •Antibody and WBC formation Decreased resistance to infection Riboflavin •Cofactors in cellular development Thiamine •Promote enzyme activity __________________________________________________________________________________ DDNA Conference 2007

30. PRESSURE ULCERS Copper Collagen cross-linkage Decreased collagen synthesis ________________________________________________________________ Iron Collagen synthesis Anemia, leading to increased risk of local tissue ishemia Enhances leukocytic Impaired tensile strength bacterial activity Impaired collagen cross- linkage ________________________________________________________________ Zinc Cell proliferation Slow healing Cofactor for enzymes Alteration in taste Anorexia DDNA Conference 2007

31. PRESSURE ULCERS • Age Skin changes with age Slower metabolism Decreased mobility Incontinence DDNA Conference 2007

32. PRESSURE ULCERS • Edema Internal pressure on tissue combined with external pressure over bony prominences Diminished tissue perfusion DDNA Conference 2007

33. PRESSURE ULCERS • Temperature Increased caloric requirement Diaphoresis DDNA Conference 2007

34. PRESSURE ULCERS • Anemia Diminished O2 and CO2 exchange that results in instable collagen formation and decreased tensile strength DDNA Conference 2007

35. PRESSURE ULCERS • Underlying disease • PVD- diminished tissue perfusion • DM -microvascular damage, impaired inflammatory response • Renal- altered maintenance of BP, Electrolyte balance • Cardiac- diminished tissue perfusion DDNA Conference 2007

36. PRESSURE ULCERS C. Skin risk factor identification • Population at risk • Skin risk assessment tools • Norton scale • Braden scale • Selecting skin assessment tool • How easy is to use • How frequently DDNA Conference 2007

37. Braden Scale • Prevention starts with risk assessments of all consumers. Braden scale is a tool used to determine the likelihood of pressure ulcer development that takes in consideration mobility, moisture status, and nutrition as well as consumers mental status. The Braden Scale is a summated rating scale made up of six subscales scored from 1-3 or 4, for total scores that range from 6-23. The subscales measure functional capabilities of the patient that contribute to either higher intensity and duration of pressure or lower tissue tolerance for pressure. A lower Braden Scale Score indicates lower levels of functioning and, therefore, higher levers of risk for pressure ulcer development. Every consumer gets score that determines the need of starting prevention protocol. DDNA Conference 2007

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39. Risk assessment and skin assessment form Predisposing factors. * Pressure * Poor circulation * Friction * Systemic illness * Shear * Moisture DDNA Conference 2007

40. Risk assessment and skin assessment form High risk category: • Immobilized • Edema • Malnutrition • Cast • Incontinence • Radiation/steroid therapy • Multiple trauma • Healed pressure ulcers • Chronic disease DDNA Conference 2007

41. Wound Care Protocol Wound care protocol is comprised of prevention and intervention standards of care: • Prevention: Identification of patients at risk for skin break down using assessment tolls and applying early intervention strategies. • Intervention: Applying standards of care for all wound types. DDNA Conference 2007

42. Implementing the Protocol: • Education of all involved • List assessment of all consumers • Identification of team members: • Physician • Nurse • Rehab Team • Nutritionist • Direct Care • Residential Coordinator • Consumer DDNA Conference 2007

43. Implementing the Protocol: • Nursing and PT to review all consumers who scored <17 on the Braden Scale • Communicate regularly to review appropriateness of dressing and PRD’s. • Direct care staff should report to nurse any redness noted and the nurse will inform nutritionist about any pressure ulcer. • Inform primary care physician about any PU. DDNA Conference 2007

44. Responsibilities of Team Member • Physician: • Treatment orders • History and physical of consumers DDNA Conference 2007

45. Responsibilities of Team Member • Nurse: • monitor lab values • keeping documentation (risk assessment tools, body check reports) • coordinate other team members • carry out skin care treatment orders • monitor nutritional intake • accountable for implementation of wound care protocol • inform rehab about any pressure ulcer DDNA Conference 2007

46. Responsibilities of Team Member • Direct care staff: • consumer activity • consumer nutritional intake and reporting it to nurse • reporting to nurse of any change in skin integrity • diaper change DDNA Conference 2007

47. Responsibilities of Team Member • Dietary: • nutritional assessment including intake • monitor weight • monitor lab values • provide with nutritional supplements DDNA Conference 2007

48. Responsibilities of Team Member Rehab: • PT/OT: • assessment of consumer’s positioning • provide appropriate PRD’s • positioning of splinting devices • SLP: • assessment of swallowing status • diet consistency DDNA Conference 2007

49. Responsibilities of Team Member • Residential Coordinator: • monitor direct care staff • provide re-in servicing in positioning and use of PRD • report any information to nurse DDNA Conference 2007

50. Prevention Protocol • Policy: Braden scale will be done on every consumer to determine his or her risk of developing pressure ulcer. • All consumers will be assessed at the beginning of protocol implementation • Consumers with the score of 18 or higher will be reassessed semi-annually and with every change in medical condition. • Consumers will be reassessed after every hospitalization. • Consumers with the score of 17 or less will be started on prevention protocol and re- assessed quarterly and PRN. • Braden scale will be done by a nurse and it will be a filed in consumers medical record. • Consumers on prevention protocol will be reported to primary care practitioner and to dietary department DDNA Conference 2007