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Dr. Robert P Casola, DO Ken Miller, PAC Basics of wound care management.

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Presentation on theme: "Dr. Robert P Casola, DO Ken Miller, PAC Basics of wound care management."— Presentation transcript:

1 Dr. Robert P Casola, DO Ken Miller, PAC Basics of wound care management

2 Introduction to wound care  Tremendous advances have been made in our understanding of wounds and the wound healing process. The knowledge is a powerful tool for clinical success when used by a wound care professional to develop a management plan.  Wound care must go far beyond standard dressing techniques. All major local and systemic factors, affecting the healing process, must be recognized and controlled.  The vast majority of wound healing problems can be corrected, assuming as physician, the abnormality can be identified. The objective of this lecture is to present some of the basic concepts of wound healing and wound care to allow the physician to handle this rapidly growing field.

3 Wounds that fail to heal  Problem wounds are those that fail to respond to established medical and surgical management in a reasonable time period.  Most commonly located in the lower extremity  A major health issue  Frustrate medical profession  The most important issue in wound management is determining the underlying etiology.  Then: identifying any risk factors disrupting the wound healing process.

4 Advanced age  Inhibits tissue regeneration

5 Nutritional deficiency  Decreases wound repair  Increases susceptibility to infection  Prealbumin  Albumin  Protein  Iron stores

6 Circulatory defects  Arterial vascular insufficiency ● decreases oxygen delivery impairing inflammatory. response and lowers resistance to infection. ●Hypoxia inhibits leukocyte killing functions.  Venous insufficiency ● compromise inflammatory response. ●engorgement of tissues.

7 Diabetes mellitus  Atherosclerosis compromising fluid  Selective cellular and humoral  Immunity inhibition  Insulin deficiency  Depresses inflammatory response.  Inhibits cellular proliferation.

8 Renal insufficiency (diabetes)  Increased risk of infection and wound dehiscence.  Secondary to delayed granulation and compromised collagen deposition.

9 Infection  Impairs leukocyte function, wound contraction, and epithelialization.

10 Immunosuppression  Chemotherapy  impairs healing by suppression of inflammation on protein synthesis and cell replication.  Steroids  Suppresses inflammatory phase, collagen synthesis, and inhibits contraction.

11 Radiation  Tissue ischemia secondary to progressive endarteritis  Suppresses cellular proliferation and causes tissue hypoxia.

12 Foreign Bodies  Increases risk of aiding infection (suture)

13 Local Factors  Desiccation  Inhibits inflammatory stage  Moisture  Maceration  Inhibits epithelialization

14 Cornerstone of Treatment  Is a systemic approach to identifying the underlying etiologic and risk factors which initiate or prolong the effects of delayed healing.  A multidisciplinary approach is needed to optimize the treatment of wounds.  Wound repair includes a complex interaction between:  Cells  Biomedical mediators  Extracellular matrix molecules  Cellular microenvironment

15  Body consists of an  Outer covering- the epidermis  Middle layer- the dermis  Inner lining- subcutaneous tissue

16 Basic Mechanism of Repair  Formulation of vascularized collagen.  Fibroblastic tissue (granulation).  Recovering of the granulation tissue with epithelium and mucosa.  The manner in which cutaneous wounds heal depends on the extent of the injury.

17 Three Major Categories of Cutaneous Wounds  Partial  Full  complex

18 Partial Thickness  Defect that removes the epidermis to the keratin layer.  Keratinocytes migrate to the wound then divide to reform the epidermis and mature to produce keratin.

19 Full Thickness Wounds  Complete skin coverage is lost, exposing the subcutaneous tissue, fascia, or muscle.  New connective tissue grows from the wound edge. Fibroblasts move to the wound and produce collagen and glycosaminoglycan.

20 Complex  Extensive penetration of the tissues and organs with major compromise of neurovascular, deep muscles or osseous structures. Not part of discussion today.

21 Simplification of a Wound  Wound Space  Microvascular disruption.  Clot form closest to the nearest capillary loop.  Tissue death  Amount of death depends on physical, cellular, or enzymatic trauma.

22 Goal  To shrink space by primary closing with removal of non usable tissue  Or to provide the best environment for repair.

23  The wound space is the regulatory compartment, and the vascularized tissue around is the responder, O2 is the critical factor.  O2 conducts macrophages and growth factors.  O2 controls collagen synthesis.  O2 controls neutrophil phagocytosis.  O2 tension controls epithelization.

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25 Angiogenesis New capillaries on wound surface

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31 Systemic Components of Wound Healing 1. Adequate Wound Blood Flow  Oxygenation  Neutrophils require O2 for bacterial killing.  Fibroblast require O2 for collagen deposition and matrix deposition.  Epithelial cells require O2 for proliferation and wound contracture.

32 2.Maintenance of body protein stores, especially muscle  Protein makes up collagen and all the elements included in healthy growth factors.

33 3.Optimal nutrition  Healing requires a higher utilization of calories, amino acids, and micronutrients.

34 4.Aggressive Treatment of Infection  Infection causes a metabolic drain and impedes wound healing  Shunts blood away from wound  Decreases deposition collagen

35 5.Minimize Stress Response  Increase cortisol release  Peripheral vasoconstriction Necessary to manage pain and anxiety

36 Local Factors Impeding Healing

37 1.Tissue hypoxia  Decrease in O2 delivery  Decrease in O2 saturation hemoglobin  Eschar on wound surface  Surface exudate

38 Correction on Hypoxia  Correction of cardiovascular function  Resolution of large vessel obstruction  Aggressive wound debridement  Removal exudate  Control infection

39 2.Local Infection  Water soluble topical agents (sulfadiazine)  Antibiotic solution/ ointments  Systemic antibiotics  Localized debridement  Adequate tissue oxygenation

40 3.Wound Exudate  An excess of white cells at the surface can consume O2 and cause local wound hypoxia  Clean wound- adherent dressing occlusive  Non clean wound- non adherent occlusive dressing

41 4.Wound Desiccation  Impairs epithelial migration  Decreases local wound defenses  Increase surface necrosis Collagen/ Fibrin dressings Hydrocolloid dressing

42 5.Mechanical Trauma  Dressing changes too frequent or adherent

43 Amputations  The average cost of amputation, rehabilitations, and prosthetic fitting  $90,000-$120,000

44 Scary Statistics  65,000 major lower extremity amputations a year.  ● Diabetic Amputations  10% morbidity< 1st year  10% contralateral amputation after 1st year  30% morbidity by 3rd year  >50% reamputation by 5th year  65% of all nondramatic amputations are caused by complications of diabetes  ● Diabetes is the 4th leading cause of death in the U.S.  6% of the adult population in U.S.  16 million people in U.S.  >7.5% of all hospitalizations  20% of all admissions related to PVD (peripheral vascular disease)

45 ● Of All Diabetic Amputation  9% foot  31% BKA (below knee amputation)  30% AKA (above knee amputation)  Contralateral limb amputation increases 10% a year  After 5 years 50% end up being a bilateral amputee ● At any given time  1 million diabetics are currently under treatment for wounds associated with their disease. There has been no significant change in the statistics over the last 10 years.

46 to treat or not to treat, that is the question:

47 Prevention is Better Than Treatment.  Reposition the patient every 2 hours.  Over head trapeze.  Overlays to beds.  Air mattress.  Clinitron bed.  Oscar boots/ E-Z boots

48 Debridement  Mechanical: loop/ blade/ scissors whirl pool  Chemical: wet-to-dry GCP Santyl

49 Dressings  Transparent: opsite to open, dry wounds. change every 3-7 days can place: Bactroban Gentamicin Silvadene  Hydrogels  Xerofoam  Xeroform To shallow wounds/ no exudate Autolytic Debridement  Hydrocolloids To: wet wounds with moderate exudate promote autogenesis (granulation) Iodoflex/ Aquacel- AJ

50 Dressings  Foam dressings Promote protection Flap/Graft sites i.e.: Lyoform  Iodosorb Heavy exudate  Wound Vac

51 Surgery 3 types of flap closure  Simple: Skin and subcutaneous  Fasciocutanous: Above (+) fascia  Myocutaneous: Above (+) muscle

52 Infection Management  Local: Topical antibiotics Keep slough and colonization down  Systemic: Soft tissue- oral/ IV 2-4 weeks Deep tissue- IV 4-8 weeks

53 Nutritional Support  Wound healing needs protein and O2  Malnutrition <80% IBW Albumin<3.5 Causes: Muscle wasting/ xerosis/ dependent edema

54 Treatment Plan  Off load patients problem  Improve nutritional state  Vascular improvement  Connect anemia  Wet-to-dry/ dry-to-wet  Wound vac  Debridement of wounds  Stop incontinence  Wound monitoring

55 Cellulitis Vs. Vasculitis C vs V  ESR/CRP  Edema  Varicosity  CHF

56 Treatment for:  Vasculitis: Compression of edema Diuretics Steroids topical cream IV/ oral  Cellulitis: antibiotics IV/ oral

57 Arterial/ Venous Wounds  Arterial wound: dry sharp edges slough  Venous wound: wet uneven edges slough

58 Treatment For:  Arterial wounds- Santyl Bactroban Gentamycin Silvadene  Venous wounds- Iodosorb Iodiflex Aquacel AG Compression/ schantz wrap/ unna boot

59 Wound Vac Use on wounds:  Needing debridement  Deep wounds  Granulation tissue Can use for:  Draining wounds  Seroma/ serosanguinous  Lipodermalysis

60 Wound Care Costs:  A lot of money  A lot of time  A lot of energy See handout for your cost.


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