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W Burns Dr AJ Fortin Dermatology Week - Meds I Wound Healing Phases • Factors affecting healing • Technique for optimal healing • Scars • - Hypertrophic - Keloid Types of Wound Healing Primary Healing • when a wound is closed within hours of its creation • wound edges are reapproximated directly by using sutures or staples Delayed Primary Healing • A contaminated wound is left open to prevent wound infection • The wound edges are approximated following a delay of several days Lawnmower injury Types of Wound Healing Secondary Healing • an open full-thickness wound is allowed to close by both wound contraction and epithelialization • There is a direct correlation between the number of myofibroblasts and the extent of wound contraction Types of Wound Healing Healing of Partial-Thickness Wounds • Involve the epithelium and the superficial portion of the dermis, heal mainly by epithelialization • There is minimal collagen deposition and an absence of wound contraction Epithelialization • Epithelialization of an incisional wound involves the migration of cells at the wound edges over a distance of less than 1 mm, from one side of the incision to the other. Incisional wounds are epithelialized within 24-48 hours after injury. Phases of Wound Healing Rubor, Tumor, Calor, Dolor Maturation Phase • Remodeling begins approximately 21 days after injury, when the net collagen content of the wound is stable. • During remodeling, collagen becomes more organized. Collagenases and matrix metalloproteinases in the wound assist removal of excess collagen while synthesis of new collagen persists. Contraction vs Contracture • Contraction must be distinguished from contracture - a pathologic process of excessive contraction that limits motion of the underlying tissues and is typically caused by the application of excessive stress to the wound. Factors Affecting Wound Healing Idiopathic manipulation: • tissue necrosis increases with the severity of trauma, e.g.. rough tissue handling, • necrosis extends the period of inflammation and retard healing. Age: • Both tensile strength and wound closure rates decreases with age. Mechanical stress: • Abnormal tension on the skin can give rise to blanching and subsequent necrosis. Steroids: • Steroids interfere with fibrogenesis, angiogenesis, and wound contraction. Smoking: • Nicotine produces vasoconstriction and limits distal perfusion. Oxygenation/perfusion: • Oxygen is important for collagen synthesis, matrix deposition, angiogenesis, and epithelialization. Oxygen-derived free radicals: • They may cause cellular injury by 1) degrading hyaluronic acid and collagen; 2) destroying cell membranes; 3) interfering with important protein enzyme system. Hydration: • Amoistwoundwillhealfasterthan the dry one. Factors Affecting Wound Healing Infection: • Wound infection occurs when the infective threshold is >100,000 (105) organisms per gram of tissue. • Bacterial infection promotes collagenolytic activity Nutrition: • Low serum protein level is associated with a prolonged inflammatory phase and impaired fibroplasia. Denervation: • Denervated skin is more prone to ulcerate than normal skin because of high rates of collagenase activity and lack of sensory protection. Diabetes mellitus: • Microcirculation impairment due to; stiffened RBC, increased blood viscosity, susceptibility to atherosclerosis, impaired phagocytosis, which along with neuropathy and ischemia increase the risk of infection. Anti-inflammatory agents: • NSAID (Aspirin and ibuprofen) have shown to decrease collagen synthesis an average of 45% even at ordinary therapeutic doses. Chemotherapy: • When chemotherapy is begun 10-14 days postoperatively, little effect is noted on wound healing over the long term despite a demonstrable early decrease in wound healing. Radiation therapy: Vitamin C: • Ascorbic acid is essential cofactor in the synthesis of collagen. Vitamin E: Zinc: • It is a common constituent of dozens of enzymes in human tissues and is essential for wound healing. Vitamin A: • Vitamin A stimulates collagen deposition Growth factors: • They are agents promoting cell proliferation and induce the migration of the cells to the injured area. Nitric oxide: • It’s suspected of playing a role in the early phases of wound healing, possibly serving as a modulatory/demodulatory second messenger for several of the polypeptide growth factors. What Can We Do? Optimal tissue handling technique • Avoid pinching epidermis • Debride unhealthy tissue • Suturing technique • - Enter at 90º to skin - Ensure skin edges align perfectly - Appropriate tension • Protective dressing - Keep clean - Avoid shear, mechanical injury - Keep moist but avoid excessive mois • Remove sutures at appropriate time - 5-7 days for face - 7-10 days elsewhere Abnormal Scars When an imbalance occurs between the anabolic and catabolic phases of the healing process, more collagen is produced than is degraded, and the scar grows in all directions. Excessive scar tissue is classified either as a keloid or a hypertrophic scar. Abnormal Scars • Hypertrophic scars are elevated over the skin surface but limited to the initial boundaries of the injury, tends to regress spontaneously, and are generally responsive to treatment. Abnormal Scars • A keloid is an overgrowth of dense fibrous tissue that extends beyond the borders of the original wound, does not usually regress spontaneously, and tends to recur after excision. • May be tender, painful, or pruritic or they may cause a burning sensation. • Keloids tend to be present on the face (with cheek and earlobes predominating), upper extremities, chest, presternal area. Abnormal ScarsTreatments: Prevention • Silicone gel sheets • compression therapy • intralesional corticosteroid injections • Cryosurgery • Excision • radiation therapy • laser therapy • interferon therapy • imiquimod 5% cream • Burns Diagnosis & Prognosis Inhalational injury • Burn size (TBSA) • Depth or Degree • (history & mechanism of injury) Location • Circumferential • Age • Associated injuries • Comorbidities • Prognostic Indicators Depth of injury • Age • TBSA • Inhalation • Age (y) Percentage of TBSA w 50% mortality 0-14y 98% 15-44 72% 45-64 51% >65 25% Inhalational Injury Contributes heavily to morbidity and mortality in burned patients • Injuries • - Carbon monoxide intoxication (smoke inhalation) - Upper airway injury - Pulmonary inhalational injury (steam) - Circumferential chest scar Risk factor is enclosed, smoke-filled space. ie. airplane cockpit Escharotomy Fluid Resuscitation Massive fluid shifts (edema) lead to intravascular hypovolemia • Goal of resuscitation is to maintain circulation to all tissue • Choice of Fluids and Rates • • Parkland Formula 4 cc/ kg/ %TBSA burn / 1st 24 hours - 1/2 over 1st 8 hours - 1/2 over 2nd 16 hours Percent Total Body Surface Area Traditional and current CLASSIFICAION of burns. Nomenclatu Traditional Depth re Clinical findings Superficial First degree Epidermis Erythema, painful, no blisters Partial thickness (superficial) Partial thickness (deep) Second degree Superficial Dermis (papillary) Deep dermis (reticular) Blisters w clear fluid, painful Full thickness 3rd-4th degree Dermis +\underlying tissues Hard leatherlike eschar, purple fluid, insensate Second degree Whiter, less pain, diff to tell from full thick. Estimation of Burn Depth Superficial Erythematous May Form blisters Very painful, hypersensitive Blanch w pressure Wet and pink Estimation of Burn Depth Superficial Partial Thickness Erythematous May Form blisters Very painful, hypersensitive Blanch w pressure Wet and pink May blister Discomfort rather than pain Less sensitive to touch but sensate Cap refill slow or absent Dry and whitish Estimation of Burn Depth Superficial Partial Thickness Full thickness Erythematous May Form blisters Very painful, hypersensitive Blanch w pressure Wet and pink May blister Discomfort rather than pain Less sensitive to touch but sensate Cap refill slow or absent Dry and whitish Dry white Leathery Rarely blanches Coagulated vessels may be visible Estimation of Burn Size The Rule of Nines Children Indications for Transfer to a Burn Unit • Large burn • - 2° and 3° burn >20% TBSA • >10% if <10 or >50y old • - inhalational injury • Deep burn Sensitive areas - Face – Hands - Feet - Genitalia – Perineum – Overlying major joints Difficult to assess injury - Significant electric injury - Significant chemical injury - 3° burn >5% TBSA • Respiratory compromise • Significant comorbidities - DM, CVD, PVD etc. Polytrauma • Special social/emotional circumstances • Operative Treatment Excision of deep partial thickness and full thickness burns with immediate skin grafting • Improves survival, decreases hospital stay, fewer metabolic complications • Skin Grafting • Tools: - Harvesting • Knife • Dermatome - Application • Mesher • Bolster • Splinting • VAC Skin Graft Harvesting Split Thickness vs Full Thickness Split-Thickness Skin Graft Harvesting Split-Thickness Skin Graft Harvesting Split-Thickness Skin Graft Harvesting Split-Thickness Skin Graft Harvesting Graft Healing • Imbibition (0 - 2 d) - Graft held in place by fibrin • Neovascularization (2 - 3d) - New blood vessel ingrowth • Proliferation (3d - 4 m) - New collagen bridges across the wound bed • Maturation (1 - 2 y) - Revision of collagen Full-Thickness Skin Graft Harvesting • Technique: - Template - Harvest & De-fat - Apply & Bolster Full Thickness Skin Graft • Advantage: - Less contraction - Better colour match - Lower maintenance donor sit • Disadvantage: - Poorer take (thickness) - Available only for small defects Special Burns ELECTRICAL BURNS High voltage >1000 volts Low voltage <1000 volts 2 types of injury: Arc injury: thermal injury that occurs when patient is to close to electric source when the current arcs superficial burns to exposed skin usually face, hands and forearms Entry Exit Electrical Burns Current flow injury: current flows through the body entrance and exit wounds damage more extensive than surface wounds indicate often associates injuries damage depends on: 1. cross sectional diameter of the body part that current flows through … damage to tissue greatest in the limbs less in the torso 2. resistance to current Electrical Injury Cardiac arrhythmias are common in low voltage household injuries QuickTime™ and a decompressor are needed to see this picture. Associated fractures secondary to falls/muscle contracture Muscle damage may be severe & worsen • Compartment syndrome develops - Fasciotomies to prevent necrosis • Myoglobin - Acute renal failure -- 50% mortality - Alkalinize urine, high urine output Electrical Injury • • LIP & Oral Commissure 4% of burn injuries in children - Biting electrical cord/ sucking on wall socket • Bleeding (labial artery) • Scar contractures - Microstomia - Asymmetry - Splinting Special Burns CHEMICAL BURNS Alkalis & Acids: cause damage by breaking down tissue proteins Treatment: remove contaminated clothes COPIOUS IRRIGATION with extensive injuries monitor for metabolic disturbance: ABG’s, lytes renal & liver function after lavage/debridement treatment of the wound is no different from thermal burns Use of specific neutralizing agents debated most common hydrofluoric acid- calcium chloride/gluconate Chemical Burns Factors affecting severity of burn Concentration of chemical • Duration of skin contact • Manner of skin contact (occlusive garment) • Prior condition of skin • Lipid solubility of chemical • Inherent toxicity of compound • Chronic Leg Ulcers • Venous Stasis - 70% • Peripheral Vascular Disease (ischemia) - 10% • Peripheral Neuropathy (diabetes etc) • Trauma - Biopsy chronic wounds to rule out malignancy (marjolin’s ulcer) QuickTime™ and a decompressor are needed to see this picture. • Leg Ulcers Arterial Insufficiency - Feet and legs often feel cold - Whitish or bluish, and shiny - Ulcer is dry, ‘punched out’ - Distal location - Painful - Inadequate blood flow • QuickTime™ and a decompressor are needed to see this picture. Venous Insufficiency - Feet and legs are swollen - Surrounding skin is brownish, dry, scaley - Medial malleolus - Ulcer is weepy - Painless - Inadequate drainage Neuropathic - Feet are insensate - Dry, callused skin - Often sinus tract & deep abscess -Ulcer over pressure point QuickTime™ and a decompressor are needed to see this picture. Venous Stasis • Incompetent valves - Pericapillary fibrin deposition - Barrier to O2 diffusion - White cell plugging of capillary loops - Lipodermosclerosis • Clinical Signs: - Edematous, hyperpigmented - Varicosities/ thrombophlebitis - Ulcerations often around ankles/lower legs Hemosiderin Staining & Edema Venous Stasis • Treatment: - Bedrest, leg elevation - Compression garments • Up to 7 in 10 venous ulcers heal within 12 weeks if treated with compression bandaging Nutrition - Debride devitalized tissue - Dressings - Ligation of incompetent perforating veins - Resistant ulcers may need complete excision & reconstruction/coverage (skin grafting) Vasculopaths Beware the comorbidities • - Diabetes - Coronary artery disease - AAA – Smoking - Pulmonary disease - Anticoagulation • Contraindication for compression therapy! • 50% of patients with arterial insufficiency also have chronic venous stasis