1. Wound Healing M K Alam MS; FRCS (Ed) Professor of Surgery

2. Intended learning objectives At the end of this presentation students will be able to:  Understand the process of wound healing.  Recognize factors which affects wound healing.  Differentiate between primary and secondary intention healing.  Identify the differences between clean and contaminated wounds.  Describe management of different types of wound.  Describe the management of chronic wounds.  Understand the consequences of adverse healing

3. 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

4. Phases of wound healing Three phases of wound healing: Inflammatory Phase Proliferative Phase Remodeling Phase

5. 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 Polymorphonuclear leukocytes (PMN) entry- kill bacteria, phagocytose clot, and release inflammatory cytokines

6. Inflammatory Phase (continued) Monocyte migrate from capillary & differentiate into macrophages within 48- 72 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

7. 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

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

9. Wounds terminology Acute wounds: wound occurred within 4-6 weeks. Chronic wounds: wound had been present for longer than 6 weeks.

10. Factors affecting wound healing Advanced age (7-8 th 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)

11. 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 and 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

12. Factors affecting wound healing Radiation: progressive fibrosis, loss of small vessels, reduced proliferative and 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

13. 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.

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

15. Types of wound 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.

17. 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.

18. 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)

19. 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.

21. 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)

22. 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

23. 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

24. 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

25. 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.

26. Poor alignment

27. Stretched scar

28. Contracture

29. Pigment alteration

30. Keloid

31. Thank you!