Wounds & Wound Management PDF

WOUNDS & WOUND MANAGEMENT By AHMED Elshora  Definition & phases of wound healing.  Factors affecting wound healing.  Types of wound healing.  Classification & types of wounds.  Management of open  WOUNDS “A cut or break in the continuity of any tissue, caused by...

WOUNDS & WOUND MANAGEMENT By AHMED Elshora  Definition & phases of wound healing.  Factors affecting wound healing.  Types of wound healing.  Classification & types of wounds.  Management of open  WOUNDS “A cut or break in the continuity of any tissue, caused by injury or operation which may be associated with disruption of the structure and function.”  Wound healing All wounds heal following a specific sequence of phases which may overlap These phases are: Inflammatory phase Proliferative phase Remodelling or maturation phase  Haemostasis & inflammation phase Day 0 – 5 Starts at the moment of injury – the clotting cascade is initiated Platelets aggregate, release cytokines & growth factors that stimulate: 1. Chemotaxis of macrophages which help phagocytosis & wound debridement 2. Activation of fibroblasts & endothelial cells. Haemostasis & inflammation phase The inflammatory phase is characterised by heat, swelling, redness, pain and loss of function at the wound site This phase is short lived in the absence of infection or contamination  Proliferation phase Characterized by proliferation of : Fibroblasts: Derived from surrounding tissues and secrete collagen fibers. Endothelial cells: Derived from intact venules and form new capillary buds which together with fibroblasts form the granulation tissue. Epithelial cells: Derived from wound edges and migrate to close the epithelial defect.  Maturation and remodeling phase Deposition of collagen in the wound: Collagen III 1st then over the next weeks it decreases while collagen I increases. Collagen fibers become thicker, arranged along lines of stress and increase the tensile strength of the wound. Remodeling continues for about 1 year. Wound never attains its full original tensile strength.  Wound contraction Helps to diminish the size of the wound. Starts immediately and continues for the next 2-3 weeks. Special myofibroblasts.  Factors affecting wound healing General factors Local factors  Factors affecting wound healing General factors Age: Slow in elderly due to decreased protein turnover. Debilitating diseases: as ureamia, jaundice, cirrhosis, diabetes and malignancy. Irradiation: inhibit wound contraction and granulation tissue formation. Prior irradiation causes ischemia due to end arteritis obliterans.  Factors affecting wound healing General factors Nutrition:  Proteins: essential for synthesis of collagen.  Vit. C: essential for maturation of protocollagen.  Vit. A: essential for epithelialization.  Calcium, Zinc, Copper and Manganese. Drug intake:  Steroids: inhibit the inflammatory response and the formation of fibroblasts.  Factors affecting wound healing Local factors Vascularity: good blood supply in face & scalp helps rapid healing while poor blood supply below knee causes delayed healing: (time of suture removal). Immobilization: wounds over joints or weight bearing areas. Tension: sutures under tension, haematoma increase wound tension causing ischemia & delayed healing.  Factors affecting wound healing Local factors Infection: bacteria compete with fibroblasts for oxygen and nutrition & secrete collagenolytic enzymes that destroy collagen. Foreign bodies and necrotic tissue: impair wound healing. Adhesion to a bony surface: prevents wound contraction as over the shin of the tibia & chronic venous ulcers.  CLASSIFICATION OF WOUNDS (Rank and Wakefield) classification. a. Tidy Wounds  like surgical incisions and wounds caused by sharp objects.  Usually primary suturing is done. Healing is by primary intention.  b. Untidy Wounds  They are due to: Crushing, Tearing , Avulsion , Devitalised injury , Vascular injury, multiple irregular wounds and Burns.  Fracture of the underlying bone may be present.  Wound dehiscence, infection, delayed healing are common.  Types of wounds Closed Open wounds wounds Haema Incised Lacerated Missile Contusions toma Abrasions wounds wounds Penetrating wounds wounds Bites Contusion Blow with blunt object. Extravasation of blood from injured capillaries. Painful & swollen. Bluish, brownish then green. TTT:Elevation & anti-infl. Oint.  Haematoma Excessive bleeding. 1st cystic then clot within hours and later liquefies. TTT: Absorption Organization by fibrosis Abscess Liquifaction and cyst formation Calcification (myositis ossificans) False aneurysm Abrasions Scraping of the superficial layers of the skin due to friction with a hard rough surface. Very painful due to exposure of sensitive nerve endings. TTT: Cleaning with antiseptic & non adherent dressing. Incised wounds Sharp cutting instruments as razors, glass pieces or knives. Longer than deep, edges are clean cut & usually extensive hge. Tendons & nerves are liable to be cut.  Lacerated wounds Severe violence with blunt objects, (RTA or falling from height). Irregular in shape, severely traumatized, devascularized & contaminated.  Lacerated wounds Degloving injury Lacerated wound are Commonly accompanied by degloving injury of skin & s.c. tissue from deep fascia. Skin devascularization become apparent in few days.  Penetrating wounds Penetration by a pointed object as a knife. More deep than long, so may injure deep important structures that can be missed. Small external opening & poor drainage encouraging infection. Bites Either animal or human bites Lacerated wounds with involvement of bones, joints, tendons, vessels, nerves. Puncture wounds (difficult to irrigate and decontaminate) with high risk of infection.  Types of wound healing Primary intension: clean wounds immediately closed by sutures or clips. Minimal scar  Types of wound healing Secondary intension:  Edges not approximated or gaping due to haematoma or infection.  Filling with granulation tissue & ugly scar.  Types of wound healing Tertiary intension:  Contaminated wounds may be left open for about 5 days.  If there are no signs of infection delayed primary sutures can be done.  Classifying wounds Wounds may be classified according to the number of skin layers involved: Superficial Involves only the epidermis Partial Thickness Involves the epidermis and the dermis Full Thickness Involves the epidermis, dermis, fat, fascia and exposes bone CLASSIFICATION OF SURGICAL WOUNDS 1. Clean wound Herniorrhaphy. Excisions. Surgeries of the brain, joints, heart, transplant. Infective rate is less than 2%. 2. Clean contaminated wound Appendicectomy. Bowel surgeries Gallbladder, biliary and pancreatic surgeries. Infective rate is 10%. 3. Contaminated wound Acute abdominal conditions. Open fresh accidental wounds. Infective rate is 15-30%. 4. Dirty infected wound Abscess drainage. Pyocele. Empyema gallbladder. Faecal peritonitis. Infective rate is 40-70%.  Management of open wounds Bleeding: control by direct local compression (clean dressing & tight bandage).No tourniquet except as a temporary measure. Suspcted fracture: splint & arrange for X-ray Thorough cleaning of the wound: saline irrigation & removal of foreign bodies then antiseptics as povidine iodine. Inspection: of all structures within the wound and dealing with them:  Management of open wounds Arteries & veins either large (repaired) or small (ligated). Nerves or tendons (repaired). Muscles are repaired by mattress sutures if cleanly incised, while ischaemic or necrotic muscles should be completely excised (dark red or gray in colour, does not contract if pinched and does not bleed if incised). Bones : no internal fixation if there is possibility of infection, better external fixation. Deep fascia should be left open in contaminated wounds or extensive tissue destruction.  Complications of wounds General Shock Crush syndrome (traumatic anuria) Compartmental syndrome Local Infection: Pyogenic or Specific Gangrene vascular or infective Complications of healing  Complications of Wound Healing Dehiscence: partial or total separation of wound layers due to general or local factors. Dehiscence of abdominal wound is called burst abdomen. Evisceration: With total separation of wound the visceral organ protrudes through the wound opening  Complications of wound healing Stretching of the scar.  Complications of wound healing Contracture: Shortening of the scar tissue. KELOID: ‘Like a claw’ Keloid is common in blacks. Common in females. Genetically predisposed. Often familial. There is defect in maturation and stabilization of collagen fibrils  Keloid continues to grow even after 6 months, may be for many years. It extends into adjacent normal skin. It is brownish black/pinkish black (due to vascularity) in colour, painful, tender and sometimes hyperaesthetic. Keloid may be associated with Ehlers – Danlos syndrome or scleroderma. When keloid occurs following an unnoticed trauma without scar formation is called as spontaneous keloid, commonly seen in Negros.  Some keloids occasionally become non- progressive after initial growth.  Pathologically keloid contains proliferating immature fibroblasts, proliferating immature blood vessels and type III thick collagen stroma. Site: Common over the sternum. Other sites are upper arm, chest wall, lower neck in front. Differential diagnosis: Hypertrophic scar.  Treatment: Controversial. 1. Excision and skin grafting. 2. Irradiation. 3. Excision and irradiation. 4. Steroid injection—Intrakeloidal triamcinolone, is injected at regular intervals, may be once in 7-10 days, of 6-8 injections. 5. Steroid injection—Excision—Steroid injection. 6. Methotrexate and vitamin A therapy into the keloid. 7. Silicone gel sheeting. 8. Laser therapy. 9. Vitamin E/palm oil massage. 10. Intralesional excision retaining the scar margin may prevent recurrence. It is ideal and better than just excision. Recurrence rate is very high—more than 50%. HYPERTROPHIC SCAR Occurs anywhere in the body. Not genetically predisposed. Not familial. Growth usually limits up to 6 months. It is limited to the scar tissue only. It will not extend to normal skin. HYPERTROPHIC SCAR It is pale brown in colour, not painful, nontender. Often self limiting also. It responds very well for steroid injection. Recurrence is uncommon. It is common in wounds crossing tension lines, deep dermal burns, wounds healed by secondary intention. Complications Often this scar breaks repeatedly and causes infection, pain. After repeated breakdown it may turn into Marjolin’s ulcer. It is controlled by pressure garments or often revision excision of scar and closure, if required with skin graft. Reference SRB’s Manual of Surgery 3rd ed. Thank You