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Superficial thickness burns

Superficial Thickness Burns: Pathogenesis and clinical findings Author: Amanda Eslinger Elise Hansen Illustrator: Amanda Eslinger Reviewers: Alexander Arnold Sunawer Aujla Yan Yu* Duncan Nickerson* * MD at time of publication Epidermis (Penetrated by superficial burns) Dermis Sub-cutaneous tissue Erythema Radiation Sunlight (most common), x-ray, nuclear emission/explosion Specific to sunlight radiation, UV rays reach keratinocytes in the epidermis p53 tumor suppressor protein is induced in keratinocytes Transient cell cycle arrest Apoptotic pathway is Fire Contact Scald Chemical Electrical Direct damage to keratinocytes Skin erosion and sloughing of skin cells Direct stimulation of nociceptive nerve endings in the epidermis DNA repair mechanisms are activated Mistakes in repair process Malignancy (See ‘Basal Cell Carcinoma’ Slide & ‘Squamous Cell Carcinoma’ Slide) Fluid leaves vasculature and enters interstitial tissues of the skin, causing it to swell Edema Triggers release of endothelin A proalgesic protein Selective excitement of nociceptive nerve ending in epidermis Pain initiated in keratinocytes Keratinocytes apoptose Prostaglandins, arachidonic acid metabolites, substance P & proinflammatory cytokines are released into surrounding tissue ↑ Vascular permeability ↑ bloodflow carries warmth to body area Irritation of endothelial cells in the dermal vascular plexus Release of endothelium derived vasodilators such as nitric oxide Vasodilation, ↑ blood flow through vessels ↑ blood under skin leads to skin appearing red Warmth Pressing on skin occludes blood vessels temporarily, making skin Blanchable underneath appear white immediately after pressure is lifted Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Dec 2, 2013, updated Aug 25, 2023 on www.thecalgaryguide.com