Medical Comorbidities and their impacto on wound healing

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Medical Comorbidities and their impacto on wound healing

  1. 1. MEDICAL COMORBIDITIES AND THEIR IMPACT ON WOUND HEALING Lee C. Ruotsi, MD, CWS, UHM
  2. 2. “CARE FOR THE WOUND IS ONLY PART OF THE STORY. SUCCESS DEPENDS ON HOW YOU MANAGE THE REST OF THE PATIENT’S PROBLEMS”2
  3. 3. NORMAL WOUND HEALING3
  4. 4. HEMOSTASIS4
  5. 5. PROLIFERATIVE5
  6. 6. INFLAMMATORY6
  7. 7. REMODELING7
  8. 8. ABNORMAL WOUND HEALING  Failure to progress through normal orderly stages of wound healing.  Chronicity typically defined by failure to progress normally over a 30 day period.  Most common “hangup” appears to be in the inflammatory phase.  Visually; inadequate granulation, persistent or excessive exudate, deficient wound contraction and/or absence of neo-epithelialization.8
  9. 9. 9
  10. 10. “A chronic wound is an acute wound with an impediment” T.K Hunt, M.D. “The impediment may be the treating physician” Harriett Hopf, M.D.10
  11. 11. 11
  12. 12. SYSTEMIC FACTORS Diabetes Rheumatoid Disease Scleroderma Lupus SMOKING Vasculitis Renal Failure Chemotherapy Radiation Unusual
  13. 13. A GOOD H & P Past Medical History Past Surgical History Past Wounding History; location, timing, treatment Medications Family History Review of Systems Thorough Exam
  14. 14. GENERAL APPEARANCE Cushingoid (puffy) appearance Rheumatoid joints Cachexia Scleroderma face Abnormal affect and behavior Focal neurologic deficit Tobacco
  15. 15. DIABETES MELLITUS  20.8 mil (7% of pop.) 6.2 mil undiagnosed!  800,000 new cases per year (120,000 DFU’s)  Lifetime risk of ulceration 15%  Complex multifactorial effect of DM on micro and macro-vascular complications  Reduced flexibility and resistance of tissues to tensile compression and shear forces  Strong evidence through DCCS and UKPDS that tight control delays onset of both primary and secondary complications15
  16. 16. NEUROPATHY MOTOR  Anterior tibial weakness  Pedal muscle atrophy  Fat pad atrophy  Digital instability and deformities  Increased peak pressures due to deformities  Ulcerations over deformities16
  17. 17. NEUROPATHY SENSORY  Diabetic sensory polyneuropathy  Peri-nerve edema  Increased wounding risk due to loss of protective sensation (L.O.P.S.)  Unable to feel pressure or pain over prominences or with trauma17
  18. 18. NEUROPATHY AUTONOMIC  Faulty sweat gland activity  Dry, fissured skin leads to infection and ulceration  Uncontrolled vasodilatation due to decreased arteriolar tone18
  19. 19. RHEUMATOID DISEASE Systemic autoimmune disorder of unknown etiol. Leg ulcerations in 8 – 9% of patients Ulcer is smooth, irregularly shaped and painful Felty’s Syndrome; Combination of RA, splenomegaly, granulocytopenia and leg ulcers Systemic Treatment: High dose steroids, cyclophosphamide, Dapsone, disease modifying agents Wound treatment: Standard wound care, bioengineered skin
  20. 20. RHEUMATOID LEG ULCERS20
  21. 21. SYSTEMIC LUPUS (SLE) Systemic autoimmune disease of unknown etiology Incidence of leg ulcers 2 – 8% Ulcers typically over pre-tibial areas and extremely painful Characterized by well defined wound margins, purulent bed and varying amount of granulation Surrounding skin may be normal or erythematous with evidence of atrophie blanche Treatment is challenging; topical retinoic acid, intralesional steroids
  22. 22. LUPUS RELATED LEG ULCERS22
  23. 23. SCLERODERMA  Autoimmune disorder of unknown etiology  Ulcers usually over digits and bony prom.  Epithelialization usually difficult  C.R.E.S.T. Syndrome  Occlusive dressings23
  24. 24. RAYNAUDS  Intermittent, severe ischemia of fingers/toes  May be precipitated by cold or localized trauma  Sympathetic mediation  Soft tissue atrophy and non-healing ulcerations  Vasodilators, platelet agents, Pentoxyfilene,24 PD-5’s, nitrates
  25. 25. VASCULITIS  Inflammation of blood vessel of ? Etiology  Male = Female  Prevalent in elderly  Flat, red nodules macules or purpura  Lesions frequently ulcerate and are difficult to heal25
  26. 26. FACTOR V LEYDEN  Protein C resistance  Increased risk of thrombosis, venous > arterial  Progressive thrombotic occlusion leads to poor blood supply and wounding  Difficult to heal26
  27. 27. RENAL FAILURE  Foot ulceration 5x higher in stage 4 & 5 CKD  2x higher prevalence of amputation, PAD, neuropathy  Dialysis is independent risk factor for ulceration  Multifactorial proposed etiologies27
  28. 28. PROTEIN ENERGY MALNUTRITION  Rapid and insidious onset  Populations at risk – elderly and poor  Albumin, fibrinogen and globulin all important  Indices: albumin, transferrin, TLC, pre-albumin  Hyperglycemia delays wound healing  Variety of supplements available  B & C vits: immunity, inflammation and collagen  D,E,A,K vits: clotting, healing and anti-oxidants  Fe, Zn, Cu: small amounts but critical28
  29. 29. ABC’S OF NUTRITION ASSESSMENT A) Anthropometrics: Ht, wt, skinfolds B) Biochemical: alb, pre-alb, transferrin, TLC, minerals, BUN/Cr, hgb, hct C) Clinical signs: skin – pale, dry, scaly, swollen hair – thin, dull, changed texture eyes – sunken, scleral yellowing mouth – cheilosis, tongue color, missing teeth, gums29D) Dietary: calorie counts, % consumption
  30. 30. MEDICATIONS  Systemic Steroids  Topical Steroids  NSAIDS  Amlodipine/Nifedipine  Methotrexate  Warfarin  Heparin30
  31. 31. CHEMOTHERAPY  49 pts with stage II – III breast cancer received 3 drug chemo with vinorelbine, cisplatin and 5-FU for up to 6 cycles and up to 30 minutes pre-op. No wound infections or delays in healing noted Colleoni, et al, 2003  100 pts treated with multi-agent platinum based chemo following surgery for ovarian ca had no increase (11%) in wound complications compared to those receiving no chemo Kolb, et al, 199231
  32. 32. CHEMOTHERAPY  Bevacizumab (Avastin) - Monoclonal antibody against VEGF inhibits angiogenesis in tumor and healthy tissue alike  Cetuximab (Erbitux) - Monoclonal antibody against EGFR. Led to slightly prolonged hospital stays and drain removals Harari, et al, 200332
  33. 33. RADIATION THERAPY  Impairs vascularity and depletes cell lines Hypoxic  Impacts all phases of wound healing  Progressive over time  Good response to HBOT Hypovascular Hypocellular  Radiation Proctitis Clark, Cone et al, 200833
  34. 34. RADIATION RELATED WOUNDS34
  35. 35. PYODERMA GANGRENOSUM  Non-infectious neutrophilic dermatosis  Painful ulcers of varying depth and size  Violaceous borders  Most commonly associated with underlying disease  Pathergy !35
  36. 36. FACTITIOUS DISORDER  Accompanies various psychiatric disorders  Lesions in various stages of healing  Usually sharp borders  Tend to be in accessible areas, usually sparing mid- back36
  37. 37. ETOH INDUCED LIMO DISEASE37
  38. 38. SMOKING  Impairs wound healing via local hypoxia, endothelial and vasomotor dysfunction, atherosclerosis, platelet activation and inhibition of collagen synthesis  Increased risk of post-op infection and wound rupture compared to non-smokers38
  39. 39. 39
  40. 40. SUMMARY  Careful H&P  History of prior wounding  Lifestyle and mobility questions  Nutritional assessment  Wound characteristics  Prior treatment; successes and failures  Pay attention:40
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