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+ + +. No Disclosures. Center For Colon & Rectal Surgery. Center For Colon & Rectal Surgery. What do these have in common?. PRESSURE ULCERS. Sam Atallah, MD General Surgery Colon & Rectal Surgery August 11, 2009. + + +. General Considerations. Basic Principles in Wound Healing

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  1. + + +

  2. No Disclosures

  3. Center For Colon & Rectal Surgery

  4. Center For Colon & Rectal Surgery

  5. What do these have in common?

  6. PRESSURE ULCERS Sam Atallah, MD General Surgery Colon & Rectal Surgery August 11, 2009

  7. + + +

  8. General Considerations • Basic Principles in Wound Healing • Importance of Oxygen • Effect of Edema • Role of Tissue Necrosis and Exudate • Understanding the Chronic Wound

  9. Basic Principles in Wound Healing • Epithelialization is more rapid under moist conditions compared to dry conditions • Winter and Scales (Nature, 1963) • Without dressings a superficial wound with minimal devitalized tissue will scab as blood and serum coagulates • This forms a protective moisture barrier • Epithelialization occurs with controlled clot proteolysis and migration of the epithelium under the clot

  10. Basic Principles in Wound Healing • When a wound is kept moist with an occlusive dressing, the exudate does not become infected and epithelial migration is optimized • Example: skin graft donor sites will epithelialize faster under an occlusive dressing • Pain is also reduced under an occlusive dressing

  11. Basic Principles in Wound Healing • “Moist Healing” can be achieved by • occlusive dressings • occlusive ointments or creams • continually moistened dressings

  12. Basic Principles in Wound Healing • The traditional wet-to-dry dressing actually produces desiccation and necrosis on the surface layer of the wound when it’s allowed to completely dry • Wet-to-Dry dressings are effective for debridement of wound exudate, but a moist healing environment combined with water irrigation is probably more effective

  13. Importance of Oxygen • Oxygen is key for normal metabolic cellular function • Wounds are actively proliferating and have a higher metabolic demand, so oxygen is even more important

  14. Importance of Oxygen • PMNs require ambient pO2 level of 25 mmHg • At this level, superoxide radicals are formed • Important bacteriocidal properties • Enzymes that make superoxide prefer pO2 of 50mmHg • Collagen synthesis requires a high oxygen tension

  15. Importance of Oxygen • Fresh wounds are hypoxic with low oxygen tension • Fresh wounds are initially avascular and therefore hypoxic • Measurements of pO2 at the center of a fresh wound approach 0 mmHg • pO2 rises quickly with angiogenesis

  16. Importance of Oxygen • In general, wound pO2 is lower than surrounding tissues • Atherosclerosis and small vessel disease can cause impaired oxygen delivery • Local scar and fibrosis can reduce normal pO2 (40 mmHg) to 25 mmHg or lower

  17. Importance of Oxygen • Other systemic factors may contribute to wound hypoxia: • Hypovolemia • Anemia (DD O2) • Alkalosis, other causes of LEFT shift in Hb-O2 curve • Systemic vasoconstriction, sepsis, excessive catacholamines • Smoking related arteriopathy • Diabetes

  18. Importance of Oxygen • Suboptimal tissue oxygen levels correlate with post-op wound infections • Increasing FiO2 to 80% during colonic resection decreases the rate of post-op wound infections • Oxygen delivery to tissue is the primary determinant of healing • Jonsson, Jensen, Goodson, et al. Ann Surg 1991 • Vienna Sudy New England Journal 2000 • Cornell JAMA 2004

  19. Importance of Oxygen • Hyperbaric oxygen therapy does result in high oxygen levels in most wounds • Treatments 1.5 hrs; 2-2.5 Atm; 100% O2 • What happens when between treatments? • No conclusisve data to show efficacy • Lack of prospective, randomized trials • No standards for indication, length, and duration of treatment • Used especially for diabetic foot ulcers and irradiated wounds • Consider as adjunct for obligate anaerobic necrotizing soft tissue infection

  20. Effect of Edema • In tissue, cells receive oxygen by diffusion from nearby capillaries • Inflammation and venous insufficiency lead to edema, as does poor nutritional status (low serum albumin) • This increases diffusion distance and results in lower tissue pO2 • Edema control - even when tissue isn’t noticeably swollen can be very beneficial • Extremity elevation • Compression stocking (esp. venous stasis ulcers) • SCDs • Elastic wraps (athletics)

  21. Role of Tissue Necrosis and Exudate • Open wounds contain devitalized tissue • Devitalized tissue is problematic because: • It becomes super-infected with microbes • It leads to poor tissue perfusion • Exudate is made up of serum proteins and dead inflammatory cells • Exudate increases devitalized tissue mass, and therefore must be cleared

  22. Role of Tissue Necrosis and Exudate • Devitalized tissue must be surgically excised, especially dermis • Why dermis? • If necrotic dermis is left in place, the underlying subcutanous adipose tissue which is LESS vascular than overlying dermis will become infected • For small areas of devitalized tissue, simple washings, whirlpool, water irrigation are sufficient but GOLD STANDARD is surgical ‘sharp’ debridement

  23. Understanding the Chronic Wound • What is a ‘chronic’ wound? • Fails to heal after 3 months • Examples: • Pressure Sore • Leg Ulcer • Foot Ulcer

  24. Understanding the Chronic Wound • Are CHRONIC wounds intrinsically different from ACUTE wounds? • Bottom line: Chronic wounds resist healing because they lack key factors (as mentioned, oxygen tension, etc) • The goal is to correct as best as possible those systemic factors

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  26. Treatment & ManagementOf Pressure Sores

  27. Pressure Sores - Background • Common problem • 148 Hospitals • Incidence of clinically identified pressure sores is 9.2% (Meehan) • Skilled care / RN homes range (2.4% - 23%) • Expensive problem • Exceeds $ 1.3 Billion (USA)

  28. Pressure Ulcers Terminology 101

  29. Terminology • Decubitus Ulcer • Bed Sore • Pressure Sore (prefered) • Pressure Ulcer (acceptable)

  30. Pressure Sores • Not always acquired in bedridden patients • Although: “The Bed Is The Enemy” • Not always acquired while in lying in decubitus (supine) position • All pressure sores involve two things: • Prolonged pressure • Over a bony prominence • Overlying the ischium • Overlying the sacrum • Overying the trochanter • Less common: Heel, Knee, Ankle

  31. Atypical Locations • Only 1.6 % of pressure ulcers are outside of the pelvic region or lower extremities

  32. What factors determine the ability of tissue to withstand pressure? • Duration of the pressure • Amount of pressure • Related shear forces

  33. What insult is caused by prolonged pressure? • Most important: Occludes the microcirculation • This happens when tissue pressure exceeds capillary filling pressure (25mmHg) • Doesn’t take much . . . Result is ischemia • Pressure over the sacrum can reach 80mmHg in a recumbent patient • Without frequent changes in position, tissue necrosis can result in hours

  34. Dermal and Soft Tissue Properties • Skin is more resistant to pressure than the underlying subcutaneous fat and muscle • Often, this leads to the finding of a small area of skin necrosis overlying a broad area of soft tissue and fat necrosis • Like an ICEBERG

  35. Stages of Pressure Ulcers

  36. Different Standards Three classifications that are commonly used: 1.NPUAP Staging (National Pressure Ulcer Advisory Panel, 1989) 2.IAET (International Association Enterostomal Therapy, 1988) 3.WOCN Staging (Wound Ostomy and Continence Nurses Society, 1992)

  37. Stage I (NPUAP) Pressure Ulcer • Erythematous and Edematous skin • Blue or purple (like a bruise) in dark pigmented pts • Skin is intact • Often tender to touch • Skin temperature variance (warm or cool) • Changes is skin consistency (firm or boggy) • Patient may complain of itching, burning, or pain

  38. Stage I (NPUAP) Pressure Ulcer

  39. Stage II (NPUAP) Pressure Ulcer • Partial Skin loss • Varying depths into dermis • Visible, yellow debris • Shallow crater • Occasional blistering

  40. Stage II (NPUAP) Pressure Ulcer

  41. Stage III (NPUAP) Pressure Ulcer • Full-thickness skin loss • Subcutaneous soft tissue exposure • Often, associated soft tissue necrosis • Stage III does not extend beyond the underlying fascia • Undermining of adjacent tissue may be seen

  42. Stage III (NPUAP) Pressure Ulcer

  43. Stage IV (NPUAP) Pressure Ulcer • Full-thickness skin loss • Exposed subcutaneous tissue • Usually, the bony prominence is exposed • The bony cortex is typically involved • Extensive necrosis typical • Damage to deep tissues (muscle, tendon) • Undermining, sinus tracts can be seen

  44. Stage IV (NPUAP) Pressure Ulcer

  45. VAC Therapy

  46. Efficacy of VAC Therapy • Pre-treatment of pressure ulcers using subatmospheric pressure dressing enhances plastic surgical coverage (Raymond Horch, et al. European Pressure Ulcer Advisory Panel) • 2004 study, n = 89 pts • 6 weeks V.A.C. followed by fascia-cutaneous/myocutaneous flap closure • 93% of stage III and IV ulcers healed completely • 7.6% of V.A.C. treated stage III & IV sores completely healed vs. historic control of 3.5%

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