WOUNDS - SURGERY.pptx very nice and educative for all

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1. TOPIC:SURGICAL WOUNDS,WOUND HEALING AND SCARS BY: KASENDWA ALLAN FACILITATOR : DR OCEN WILLIAM LIRA UNIVERSITY FACULTY OF MEDICINE DEPARTMENT OF SURGERY

2. SURGICAL WOUNDS,WOUND HEALING AND SCARS Learning objectives To understand normal healing and how it can be affected To know how to manage wounds of different types ,of different structures and at different sites To know aspects of disordered healing that lead to chronic wounds The variety of scars and their treatments To differentiate between acute and chronic wounds

3. WOUND HEALING Wound healing is a mechanism where by the body attempts to restore the integrity of the injured part. Several factors may influence healing : Site of wound Structures involved Mechanism of wounding Contamination Loss of tissue Local factors e.g. pressure and vascular insufficiency Systemic factors e.g. malnutrition,diseases,steroids,smoking etc.

4. NORMAL WOUND HEALING Normal wound healing occurs in three or four phases The inflammatory phase The proliferative phase The remodeling phase(maturation) T he destructive phase may follow the inflammatory phase consisting of cellular cleansing of the wound by macrophages.

5. Inflammatory phase Inflammatory phase begins immediately after wounding and lasts for 2-3 days, bleeding is followed by vasoconstriction and thrombus formation to limit blood loss Platelets stick to the damaged endothelial lining of vessels, releasing ADP which causes thrombolytic aggregates to fill the wound When bleeding stops, platelets then release several cytokines from their alpha granules. These include platelet derived growth factor(PDGF), platelet factor IV and transforming factor beta(TGFB), these attract polymorph nuclear leukocytes(PMN) and macrophages. Platelets and the local injured tissue release vasoactive amines such as histamines, serotonin and prostaglandins which increase vascular permeability for infiltration of PMN Macrophages remove devitalized tissue and microorganisms. Support of cells is provided by fibrin from fibrinogen. Phase is described in four words- redness,swelling,pain and heat.

6. Proliferative phase It lasts from third day to the third week, consisting mainly of fibroblasts activity with the production of collagen and ground substance. Fibroblasts need vitamin C to produce collagen. Growth of new blood vessels such as capillary loops. The wound tissue formed earlier in this phase is called granulation tissue. Later in this phase, there is increase in tensile strength due to increased collagen type III deposition hence the phase is characterized by wound contraction reducing the surface area of wound over the first three weeks of healing.

7. Remodeling phase It is characterized by maturation of collagen . There is re alignment of collagen fibers along the lines of tension, decreased wound vascularity and wound contraction due to fibroblast and myofibroblast activity. This maturation of collagen leads to increased tensile strength in the wound which is maximal at twelfth week post injury.

8. Phases of healing

9. Normal wound healing at specific tissues Bone: phases are as above but periosteal and endosteal proliferation lead to formation of callus which consists of osteoid, callus forming is minimal and primary healing occurs, if there is gap then secondary healing occurs. Nerve: distal to the wound , wallerian degeneration occurs, proximally the nerve suffers traumatic degeneration as far as the last node of Ranvier, regenerating nerve fibers are attracted to there receptors by neurotropism followed by profuse growth of new nerve fibers from the cut proximal end. Tendon: here healing follows two mechanism, intrinsic consisting of synovial diffusion and vincular blood flow and extrinsic which depends on formation of fibrous adhesions between the tendon and tendon sheath.

10. Classification of wound closure and healing Primary intention : Wound edges opposed Normal healing Minimal scar Secondary intention: Wound left open Heals by granulation, contraction and epithelialization Increased inflammation and proliferation Poor scar Tertiary intention: Wound initially left open Edges later opposed when healing conditions are favorable

11. Types of wounds There are two types of wounds i.e. Tidy Untidy surgeons aim is to convert all untidy to tidy wounds by removing all contaminated and devitalized tissue. Appropriate tests for hepatitis viruses and immunodeficiency virus are required.

12. TIDY WOUND

13. UNTIDY WOUND

14. differences Tidy wounds; Incised Clean Healthy tissues Seldom tissue loss Untidy wounds: Crushed or avulsed Contaminated Devitalized tissues Often tissue loss

15. Managing acute wounds Cleansing Exploration and diagnosis Debridement Repair of structures Replacement of lost tissue where indicated Skin cover if required Skin closure without tension

16. Facial trauma but none found after careful matching

17. Some specific wounds Bites :bites from small animals are common in children, these wounds have high bacterial virulent counts hence prophylaxis is required. Injuries to the ear, tip of nose and lower lip are most common in victims of human bites. Puncture wounds: wounds caused by sharp objects should be explored to to the limit of tissue blood staining Hematoma: it may require release by incision or aspiration, untreated hematoma may also calcify and therefore require surgical exploration if symptomatic. Degloving : occurs when the skin and subcutaneous fat are stripped by avulsion from the underlying fascia leaving the bone exposed. It may be open or closed , an example is a ring avulsion injury with loss of finger skin.

18. Dog bite in a child

19. Degloving hand injury

20. Degloving buttock injury

21. Chronic wounds Can be defined as a wound that fails to heal in usually three weeks. Delays may occur in any phase but usually the inflammatory phase. Leg ulcers : most common, an ulcer is defined as a break in the epithelial continuity. A prolonged inflammatory phase leads to overgrowth of granulation tissue which heals by scarring leaving a fibrotic margin. Necrotic tissue at ulcer Centre is called a slough.

22. Pressure sores These can be defined as tissue necrosis with ulceration due to prolonged pressure. Pressure sore frequency in descending order : ischium, greater trochanter,sacrum,heel,malleolus, occiput. Stage 1; no breach in the epidermis Stage 2: partial thickness skin loss involving epidermis abnd dermis Stage 3: full thickness skin loss extending into the subcutaneous tissue but not through fascia Stage 4: full thickness skin loss through fascia , extensive tissue destruction involving muscle, bone, tendon or joint.

23. Pressure ulcer

24. Necrotizing soft tissue infections These are commonly poly microbial infections with gram positive aerobes and gram negative anaerobes and beta hemolytic streptococcus. There is usually a history of trauma or wound contamination. There are two types of necrotizing infections; clostridial( gas gangrene) and non clostridial(streptococcal gangrene and necrotizing fascilitis)

25. Necrotizing fascilitis of anterior abdominal wall

26. Signs and symptoms of necrotizing infections Unusual pain Oedema Crepitus Skin blistering Fever Pink skin staining Focal skin gangrene Shock and multi organ failure

27. SCARS The maturation phase discussed earlier represents the formation of scar. The immature scar becomes mature over a period lasting a year or more Scars are often described as being atrophic, hypertrophic and keloid. Atrophic scar is pale , flat and stretched in appearance and easily traumatized as epidermis and dermis is thin Hypertrophic scar is an excessive scar tissue that doesn’t extend beyond the boundary of the original wound. Its just due to prolonged inflammatory phase. A keloid is an excessive scar tissue that extends beyond the boundaries of the original tissue due to elevated levels of growth factor Treatment: excision, silicon gel, vitamin E etc.

28. Multiple keloid scars

29. CONTRACTURES When scars cross joints or flexion creases, a tight web may form restricting the range of movements at the joint called contracture. It may cause hyperextension or hyper flexion deformity, in the head it affects head extension. Treatment may be simple involving multiple Z- plasties or more complex requiring the onset of grafts or flaps. Splintage and intensive physiotherapy are often required post operatively.

30. Burn contractures showing hyperextended fingers and hyper flexed elbow

31. Post traumatic midline neck contracture

32. Multiple Z plasty release of finger contracture

33. REFRENCES Bailey and love textbook of short practice of surgery 27 th edition Lippincott textbook of surgery 2004 An introduction to the use of vacuum assisted closure .world wide wounds, 2001 END.