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Wound Healing and The Problem Wound Manal E. Alotaibi.

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Presentation on theme: "Wound Healing and The Problem Wound Manal E. Alotaibi."— Presentation transcript:

1 Wound Healing and The Problem Wound Manal E. Alotaibi

2 Contents Definition Types of wound closure Phases of Wound HealingPhases of Wound Healing Impaired Wound Healing: Local factors &systemic factors Excessive Healing Definition Types of wound closure Phases of Wound HealingPhases of Wound Healing Impaired Wound Healing: Local factors &systemic factors Excessive Healing

3 Definition A complex integrated sequence of cellular, physiologic, and biochemical events initiated by the stimulus of injury to tissue

4 Types of wound closure Primary closure  All Layers are closed.  Approximation of acutely disrupted tissue with sutures, staples or tape.  The incision that heals by first intention does so in a minimum amount of time.  with no separation of the wound edges, and with minimal scar formation.

5 Primary closure

6 Delayed primary closure  Approximation of wound margin delayed for several days.  Prevents wound infection in cases of contamination/foreign bodies/tissue trauma.  Less bacterial colonization in open wound.  Normal healing progress occurs.  Left open initially.  Edges approximated 4-6 days later.

7 Delayed primary closure

8 Secondary wound closure  Open wound margins approximate by biologic contraction  Surfaces not approximated  Defect filled by granulation  Deep layers are closed but superficial layers are left to heal from the inside out.  Healing by second is appropriate in cases of infection, excessive trauma, tissue loss, or imprecise approximation of tissue.

9 Secondary closure



12 WOUND HEALING PHASES  Inflammatory phase  Proliferative phase  Maturational phase











23 Inflammatory Phase  Hemostasis and Inflammation  Key components of this phase are increased vascular permeability, and cellular recruitment  Days 4 - 6  Exposed collagen activates clotting cascade and inflammatory phase  Fibrin clot = scaffolding and concentrate cytokines and growth factors

24 At the initial time of tissue disruption, platelets release coagulation factors and cytokines to initiate the healing process

25 Within the first day following tissue injury, neutrophils attatch to surrounding vessel walls and then move through the vessel walls to migrate to the wound site

26 Inflammatory Phase

27 Proliferative phase 1.angiogenesis 2.fibroplasia 3.Epithelization.  Production of collagen is hallmark  7 days to 6 weeks

28 Angiogenesis  The process of new blood vessel formation to support a healing wound environment.  tissue hypoxia – major stimulus  TNF-α, heparin, VEGF, FGF-1, FGF-2

29  The fibroplasia phase is characterized by movement of wound macrophages into the site of injury, which in turn attract fibroblasts. The fibroblasts then repair the site by producing new connective tissue matrix.

30 Wound Contraction  Actual contraction with pulling of edges toward center making wounds smaller  Myofibroblast: contractile properties  Surrounding skin stretched, thinned  Original dermal thickness maintained  No hair follicles, sweat glands

31 Epithelialization  Basal epithelial cells at the wound margin flatten (mobilize) and migrate into the open wound  Basal cells at margin multiply (mitosis) in horizontal direction )  Basal cells behind margin undergo vertical growth (differentiation )

32 Epithelialization/Contraction

33 Epithelialization

34 Proliferative Phase

35 Maturation Phase  Day 8 through years  Type III replaced by type I  Wound may increase in strength for up to 2 years after injury  Collagen organization  Cross linking of collagen

36 Maturation Phase



39 Systemic factors The most common nonhealing wounds affecting the lower extremities are associated with peripheral artery disease, diabetes and chronic venous insufficiency.  Peripheral artery disease  Diabetes  Chronic venous insufficiency  Aging  Sickle cell disease  Cancer therapy  Spinal cord disease and immobilization  Malnutrition  Smoking.

40 Excessive Healing hypertrophy and keloid formation are an overactive response to the natural process of wound healing.

41 Hypertrophic Scars  raised and thickened.  does not extend beyond the boundary of the incision/scar.  this process is exacerbated by tension lines on the area of surgery.  incisions over the knee and elbow have a higher incidence of hypertrophic reaction.  Treatment: nearly all hypertrophic scars undergo a degree of spontaneous resolvement. if still present after six months, surgical excision is indicated.

42 Hypertrophic Scars

43 Keloids  Raised and thickened.  This process extends beyond the boundary of the incision.  Continues weeks to months past the initial insult.  Higher incidence in African Americans.  Treatment: Pressure applied early may decrease the extent of keloid formation.  corticosteroid injection may be helpful.  Excision with intramarginal borders is reserved for intractable keloids.

44 Keloids

45  A wound is a disruption of the normal structure and function of the epidermis.  Wounds may be caused by a variety of mechanisms including acute injury (abrasion, puncture, crush), surgery or other factors that cause breakdown of previously intact skin (eg, ischemia, pressure).  After hemostasis has been achieved, acute wounds normally heal in an efficient manner characterized by four overlapping phases: inflammation, epithelialization, fibroplasia, and maturation.  Many disease states alter the process of wound healing, the most common of which are peripheral artery disease, diabetes, and chronic venous disease.

46  UpToDate  Wound-Healing-student-lecture- May-2011, Abigail E. Chaffin, M.D. Assistant Professor of Plastic Surgery;Tulane University School of Medicine.

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