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Abdul Aziz Assaigh FRCS, FACS. Professor of Surgery.

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Presentation on theme: "Abdul Aziz Assaigh FRCS, FACS. Professor of Surgery."— Presentation transcript:

1 Abdul Aziz Assaigh FRCS, FACS. Professor of Surgery.
Wound Healing Abdul Aziz Assaigh FRCS, FACS. Professor of Surgery.

2 Intended learning objectives
At the end of this presentation students will be able to: Describe the process of wound healing, primary, secondary and tertiary intention wound healing & factors which affect it. Summarize the management of different types of wound & the consequences of adverse healing.

3 Wounds Definition: Disruption of normal continuity of bodily structures due to trauma.

4 Introduction Major part of work load for surgeons
Responsible for creation of some wounds Knowledge of wound healing will rationalize the approach to wound management

5 Phases of wound healing
Three phases of wound healing: Inflammatory Phase Proliferative Phase Remodeling Phase

6 Inflammatory Phase Lasting up to 72 hours
Characterized by hemostasis and inflammation Fibrin -platelet clot entrapping red cells Release of platelet-derived growth factor (PDGF), transforming growth factor (TGF-β), & other biologically active proteins PMN entry (Polymorphonuclear leukocytes) kill bacteria, phagocytose clot, and release inflammatory cytokines

7 Inflammatory Phase (continued)
Monocyte migrate from capillary & differentiate into macrophages within hours. Release of several factors-PDGF, TGF-β, keratinocyte growth (KGF), vascular endothelial growth (VEGF), fibroblast growth (FGF) and many others. VEGF and other growth factors stimulate angiogenesis KGF- stimulate epithelium migration & proliferation. FGF attract fibroblasts

8 Inflammatory Phase

9 Proliferative Phase 72 hours to 3 weeks.
Granulation tissue formation (inflammatory cells, fibroblast, neovasculature, matrix of collagen, fibronectin and proteoglycans). Fibroblasts migrate & proliferate in fibrin, fibronectin and proteoglycans matrix Fibroblast produce collagen and other matrix molecules. Collagen- Type III in early stages of healing , Type I most abundant in adult tissues Epithelialization from basement membrane/ wound edges

10 Proliferative Phase

11 Remodeling Phase 3 weeks – 2 years
Inflammatory cells & new capillaries resolve by apoptosis Type III collagen replaced by adult type I (4:1 ratio) Fibroblasts differentiate into myofibroblasts-wound contraction. Collagen reorganizes along line of tension giving strength to the wound ( eventually 80%)

12 Wounds terminology Acute wounds: < 4-6 weeks.
Chronic wounds: present for > 6 weeks.

13 Factors affecting wound healing
Advanced age (7-8th decade): Reduced cell proliferation, motility, collagen synthesis and inflammation. Clinical: Leave sutures longer Better scar (reduced inflammatory reaction) Ischemia: impairs collagen synthesis, cell proliferation, ability of PMN to kill bacteria. Clinical: elderly affected most, smoking , pain (vasoconstriction) Examples: chronic ulcers ( diabetic foot, venous ulcers, pressure sores)

14 Factors affecting wound healing
Malnutrition: Low albumin(˂3G/L) ↓ cell proliferation. Vit C- ↓ collagen synthesis. Vit A- protects from steroid induced repair problems. Zinc & copper- cofactors for enzymes in wound healing. Vit E- anti-inflammatory ? Better scar Clinical: Vitamins & nutritional supplements do not improve healing in well nourished patients. Oedema: Increased diffusion distance for O₂ & nutrition Pericapillary cuffing trapping growth factors Clinical: Oedema control helps healing

15 Factors affecting wound healing
Radiation: fibrosis, loss of small vessels, reduced proliferative & synthetic response Clinical: Spontaneous ulcer may develop many years later. Surgical intervention with well vascularized tissue. Steroid: depress collagen synthesis Chemotherapy: ↓ inflammatory response Clinical: Rarely a sever problem in wound healing Systemic diseases: diabetes, vascular, anemia Foreign body Malignancy

16 Wound Types Abrasions Friction damage resulting in superficial bruising and loss of varying skin thickness

17 Wound Types Incised (Tidy) Clean cut, inflicted by a sharp object (knife, glass), no devitalized tissue.

18 Wound Types Lacerated (Untidy)
Irregular margin. Caused by crushing, tearing. Contains devitalized tissue.

19 Wound Types Degloving wounds
Result from shearing forces Skin is completely torn off the underlying tissue, Severing its blood supply. Skin remain intact but deprived of blood supply due to rupture of feeding vessels.

20 Wound Types Penetrating wounds
An injury that occurs when an object pierces the skin & enters a tissue of the body, creating an open wound Knife & guns. High velocity wounds are associated with extensive deeper tissue injuries.

21 Types of wound healing Primary healing: Closure of a wound within hours of its creation. Epithelium may cover such wounds in 24 hours Secondary healing: No formal wound closure; the wound closes spontaneously by contraction and reepithelialization. Tertiary healing (delayed primary): Initial wound debridement and dressing for few days (5-7) and then formal closure with suturing.

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23 Wound Management Incised (Tidy): Clean cut, inflicted by sharp object (knife, glass), no devitalized tissue. Management: Wound haemostasis Immediate wound closure (Primary closure).

24 Wound management Lacerated (Untidy): Caused by crushing, tearing or burn. Irregular margin. Contains devitalized tissue. Management: Wound “debridement”- removing dead or devitalized tissue and foreign body If made clean- primary closure If uncertain- delayed primary closure in few days If tissues are bruised, swollen, uncertain vascularity- leave open for secondary healing.

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26 Late presented wounds Wound presented between 6-18 hours after injury (incised or lacerated) Management: Wound debridement Mild contaminated wounds – delayed primary closure and antibiotic cover Grossly contaminated wounds – leave open for secondary healing.

27 Infected wounds Wounds presenting later than 18-24 hours.
Almost always infected. Management: Debridement Systemic antibiotic Wound heal by secondary healing or skin grafting ( secondary closure)

28 Degloving injuries Management: Excision
Degloving injuries Management: Excision. Skin grafting or skin flap closure.

29 Puncture: Standing over nail or sharp object.
Puncture & Bites Puncture: Standing over nail or sharp object. FB or bacteria carried deep into tissue. Management : X-ray- for FB Wound irrigation, antibiotic, tetanus prophylaxis ± FB removal Bites: Animal, human Small or large wounds High incidence of infection from mouth organisms Management: Wound irrigation, debridement, antibiotics, left open to heal.

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31 Skin "graft“: All the vessels nourishing the graft are cut.
Wounds with skin loss Small skin defect at aesthetically or functionally unimportant site- left to heal by secondary intention. Skin "graft“: All the vessels nourishing the graft are cut. Skin "flap“: Some blood supply remain intact during transfer.

32 Split skin (Thiersch) grafts
Epidermis with a portion of the dermis. Electric dermatome. Donor site: Heal by epithelialization from skin appendages. Graft can be expanded by ‘meshing’ to cover larger area. Thinner graft take more easily on imperfect vascular bed. Used for covering granulating areas and burns. Do not take on bare bone, cartilage and tendons. Appearance not as good as full thickness graft. Grafts shrink.

33 Dermatome Skin graft

34 Management of non-healing wounds
Complete evaluation of the patient: -Systemic illness- diabetes, anemia, heart failure, COPD, hypothyroidism etc. -Nutritional status Examination of the wound: -Site (pressure points, lower leg) -Size -Surface appearance (necrotic/ devitalized tissue) -Foreign body -Surrounding area (pigmentation, atrophy, cellulitis, osteomyelitis) Biopsy -

35 Management of non-healing wounds
Ensure adequate oxygenation (anemia) Treat underlying systemic disease e.g. diabetes Improve nutritional status Treat infection Surgical debridement- dead, devitalized tissue Wound irrigation Dressing

36 Ideal dressing materials
Ideal dressing materials should be: Non- adherent Permeable to gases (oxygen) Permeable to water vapour Impermeable to micro-organisms Absorbent Minimizing injury to surrounding skin

37 Common dressing materials
Moist gauze- limited absorptive capacity, needs frequent dressing change Polyurethane films (Opsite)- used as an external dressing Hydrocolloids (Duoderm) - absorptive, adhesive Alginates (Kaltostat)- absorptive, non-adhesive Foams- absorptive, non-adhesive Absorptive powders ( Debrisan, Duoderm granules) Non-adherent gauze

38 Adverse healing Poor alignment: Lips vermilion border.
Stretched scar: Wounds closed with tension. Contracture: Linear scar across a flexor surface. Common with burn. Pigment alteration: Hyper or hypopigmented scars. Stitch marks: If skin sutures left for longer period. Hypertrophied scar: More cellular, collagen and vascularity Raised, red, itchy and tender. Keloid: Over growth of scar tissue beyond the limit of scar Common over chest, back, shoulder and ear lobes.

39 Poor alignment

40 Stretched scar

41 Contracture

42 Pigment alteration

43 Keloid

44 Thank you!


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