Wound Healing PDF

WOUND Objectives By the end of this session, the students should be able to: Define a wound Enlist the factors affecting wound healing Discuss normal and abnormal wound healing Classify types of wounds Manage acute and chronic wounds Discuss scars and its types WHAT IS WOUND...

WOUND Objectives By the end of this session, the students should be able to: Define a wound Enlist the factors affecting wound healing Discuss normal and abnormal wound healing Classify types of wounds Manage acute and chronic wounds Discuss scars and its types WHAT IS WOUND A break in skin or other body tissues caused by injury or surgical incision. What is wound healing? A mechanism by body to restore the integrity of the injured part. Local and systemic factors influencing wound healing LOCAL: SYSTEMIC: Skin tension Advancing age Hypoxia and ischemia Obesity Vascular insufficiency Malnutrition Lymphoedema Smoking Contamination Diseases (e.g. diabetes mellitus, Infection connective tissue diseases) Presence of foreign bodies Immunocompromised (e.g. AIDS) Radiotherapy Medications (e.g. steroids, immunosuppressants, chemotherapy) NORMAL WOUND HEALING HAEMOSTATSIS: ( following injury) INFLAMMATORY PHASE: ( from wound to 1-2days) PROLIFERATIVE PHASE:(3rd day to 2-4 weeks) REMODELLING PHASE: ( maturation, from 2-3 weeks up to a year or more) Haemostasis Platelet adhesion causes activation Thrombin and release of formation occurs Vasoconstriction alpha granules( which generates and platelet TGFB, PDGF, FGF, the fibrin and plug formation EDF, VEGF), leads thus stabilize the to platelet platelet plug aggregation INFLAMMATORY PHASE Platelet activation cause Increase vascular Macrophage as scavenger, influx of inflammatory permeability( by histamine on day 2-3. cells i.e., leukocytes and and serotonin) & It is the phase of rubor, neutrophils inflammatory cell infiltrate tumor, calor, dolor PROLIFERATIVE PHASE Fibroblast Angiogenesis Collagen type III Re-epithelialisation Granulation tissue New small vessels formation(pink and formation wound contraction, granular) increase tensile strength REMODELLING PHASE Wound contraction Collagen from III to => inc. tensile Decrease I (stronger)and strength(80%) max. vascularity realignment in 12th week  PRIMARY INTENTION: wound edges opposed, minimal tissue trauma, least inflammation, normal healing, minimal scar ABNORMAL WOUND SECONDARY INTENTION: wound left open, HEALING heals by granulation, contraction & re- epithelialisation, inc. inflammatory & proliferative phases, poor scar TERTIARY INTENTION: ( delayed primary healing)wound left open initially (untidy or contaminated wounds) edges opposed later when favourable, less satisfactory scar Classification of wound:  Surgical wound infection risk factors: Contaminated or dirty wound American Society of Anaesthesiologists (ASA) score ≥3 Operative time longer than the expected duration for similar procedures TYPES OF WOUND TYPES OF TIDY UNTIDY WOUND Incised Crushed/avulsed Clean Contaminated Healthy tissue Devitalised tissue Seldom tissue loss Often tissue loss ACUTE WOUNDS Bites Puncture wounds Haematoma Degloving Compartment syndrome High pressure injection injuries MANAGING ACUTE WOUNDS Preparation: Antibiotics, analgesia or anaesthesia, tetanus cover Wound: debridement and irrigation Exploration Repair of structures and hemostasis Closure: skin close (without tension), reconstruction, suture choice, consider drains, type of dressing Follow up: suture removal, physiotherapy, monitor complications and scar management  Wounds that fails to heal in expected time for a wound of that type. Delays in healing mostly prolonged inflammatory phase and persistent infection CHRONIC WOUNDS TYPES: Leg ulcers Pressure sores  ULCER: a break in epithelial continuity Mechanism: a prolonged inflammatory phase=> LEG ULCERS overgrowth of granulation tissue and heals by scarring and leaves fibrotic margins. SLOUGH: necrotic tissue at the centre of the ulcer Aetiology of leg ulcers Venous: varicose veins( venous hypertension) Arterial: a. Large vessel ( atherosclerosis) b. Small vessel ( diabetes) Infection (bacterial, fungal, mycobacterial, syphilis) Autoimmune disorders ( vasculitis, RA, SLE) Trauma( bites, self–inflected, burns) Metabolic disorders( diabetes mellitus, gout, calciphylaxis) Neoplasm: squamous cell, basal cell, sarcoma MANAGEMENT Assess arterial, venous circulation and sensation of lower limbs If unresponsive to simple treatment=> biopsy( Marjolin’s ulcer) Treat underlying cause Surgery: only when non-operative treatment fails or intractable pain Meshed skin grafts In venous ulcers: recurrence is high so hygiene, elevation & elastic compression  Tissue necrosis with ulceration due to prolonged pressure PRESSURE/ BED SORES In paraplegic, elderly, severely ill patients (PRESSURE/ DECUBITUS Mechanism: if external pressure> capillary ULCERS) occlusive pressure(>30mmHg), Dec blood to skin , necrosis, ulceration Pressure injury Common sites: ischium, greater trochanter, sacrum, heel, malleolus, occiput  Staging of pressure sores I. Only erythema( non-blanchable) intact skin II. Partial- thickness skin loss( only epidermis & dermis) III. Full-thickness skin loss ( subcutaneous tissue but not underlying fascia) IV. Full-thickness skin loss ( through fascia with extensive tissue loss) Deep tissue pressure: Persistent non- blanchable, deep red, injury maroon or purple discoloration MANAGEMENT Prevention is best treatment by good skin care, pressure dispersion cushion or foam, air mattresses, urinary or faecal diversion if needed. Turn the patient every 2-4 hourly. Wheelchair- bound should lift themselves for 10 sec every 10 mins  Good nutrition Surgical management: Adequate debridement Vacuum-assisted closure(VAC) to fill dead space and to provide sensate skin Large skin flaps with muscles SCAR Immature scar: first pink, hard, raised & itchy often During maturation: paler, softer, flatter, & itchiness diminishes TYPES OF SCAR Atrophic scar: pale, flat, stretched, easily traumatized, thin epidermis & dermis, on back and tension areas. Treatment excision & resuturing ( rarely improve) Hypertrophic scar Keloid scar  Hypertrophic scars Keloids scars Size stay within the area of the initial wound grow beyond the initial wound begin within a month or two after the initial begin a few months or several years after Onset wound and continue to grow for many months the wound and grow over time Outlook shrink after a year do not shrink in size Color may be a lighter pink or red color may be a darker purple-red color can stiffen joint movement because the scar Effect on movement do not affect joint movement shortens tissues Incidence more common less common can develop anywhere on the body but often develop on certain areas of the body, Location near sites where a wound is infected, irritated, including the upper torso, earlobes, and or untreated or where a joint moves the skin cheeks HYPERTROPHIC SCAR KELOID SCAR  TREATMENT Hypertrophic scar: Silicone sheeting or gel is widely accepted as the first-line prophylactic and treatment option for hypertrophic and keloid scars. Intralesional steroids injection( triamcinolone) Fractional laser therapy ( dec. redness) Pressure/ compression therapy (moulds, elastic garments) Surgical excision & steroid, 5-FU Keloid: Silicone sheeting or gel + Intralesional steroids injection, 5-FU Fractional laser therapy Patient counselling regarding expectation, Intralesional excision( keloid only) Radiotherapy Alternative: Bleomycin, mitomycin C, imiquimod) Vit E/ palm oil massage  https://www.youtube.com/watch?v=cnkhLMQJUPw  Reference: Bailey & Any question love Short Practice of Thank you surgery, 28th edition