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Pathophysiology of the burn wound

Pathophysiology of the burn wound. Skin biology Pathophysiologic changes with thermal injury. Skin biology Epidermis. Multifunctionality: Barrier function UV protection Immune responses Five keratinocyte layers

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Pathophysiology of the burn wound

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  1. Pathophysiology of the burn wound • Skin biology • Pathophysiologic changes with thermal injury

  2. Skin biologyEpidermis • Multifunctionality: • Barrier function • UV protection • Immune responses • Five keratinocyte layers • Stratum basalis (regenerative), stratum spinosum, stratum granulosum, stratum lucidum, stratum corneum (barrier function) • Melanocytes • Produce melanin for ultraviolet protection • Langerhans cells • BM derived antigen presenting cells with phagocytic capability • Sensory nerves

  3. Skin biologyBasement membrane • Basement membrane • Connects epidermis to dermis via epidermal projections • Keratinocyte-derived collagen VII anchoring fibrils anchor epidermis to dermis • Following epithelialization, fibril formation may take weeks to months to mature with increased risk for shearing and blistering • Rete ridges and dermal papillae also contribute to epidermal-dermal adhesion

  4. Skin biologyDermis • Heterogeneous layer of skin with multiple functions: • Mesenchymal elasticity and durability • Vascularity • Immunity • Two basic layers separated by a vascular plexus • Superficial papillary dermis • Deep reticular dermis

  5. Pathophysiologic changes of thermal injury • Jackson’s zones of Injury • Zone of coagulation (center of wound) • Zone of stasis (‘at risk’ for conversion) • Zone of hyperemia (outer periphery)

  6. Jackson’s 3 zones of injury on an ankle burn: (a) the zone ofcoagulation; (b) the zone of stasis, and (c) the zone of hyperemia.

  7. Assessment of burn depth1st-degree burn • Superficial burn • Epidermis only • Heals in 3–4 days • e.g. sunburn

  8. Assessment of burn depth2nd-degree burn • Superficial dermal burn • extends into the papillary dermis • pink/moist wound, hypersensitive and blanching • heals in 2–3 weeks • e.g. scald burn or flash burn • Deep dermal burn • extends into reticular dermis • pale/dry wound, decreased sensation, and sluggish capillary refill • if not healed by 3 weeks grafting usually indicated • e.g. grease burn, flash burn, prolonged scald exposure

  9. Lower extremity burn having components of a superficialdermal burn (a) with a wet, pink and moist appearance, as well as a deeperdermal burn; (b) with mottled pink and white areas.

  10. Assessment of burn depth≥ 3rd-degree burn • Full thickness burn • Extends through the skin to the SQ or deeper • Black or charred, leathery, insensate • Excise and graft early to reduce risk of infection and scarring • e.g. flame burns, contact burns

  11. Deep contact burn in an elderly patient who was unconsciousnext to a space heater. Arrows denote the imprints of the space heater grill on his lateral thigh.

  12. Assessment of burn depthAdjuncts to clinical judgment • Experienced burn surgeon 46–67% accurate in determining which burns will heal on PBD 1 • Additional techniques proposed to identify non-healing wounds: • laser Doppler imaging • thermography • MRI • biopsy • ultrasound • light reflectance • No technique has proven superior to serial exams

  13. Mechanisms of thermal injury • Flash and flame burns • Scalds • Contact burns • Chemical burns • Electrical burns

  14. Mechanisms of thermal injuryFlash and flame burns • Responsible for more than half of burn injuries • Etiology • House fires • Outdoor fires with use of accelerants • propane, gasoline, and kerosene • 28% related to alcohol use • Flash burn • Typically superficial to partial dermal burns with preservation of skin covered by clothing • Flame burn • Typically deep dermal or full thickness burns • Inhalation injury likely with gasoline fire and/or house fire

  15. Mechanisms of thermal injuryScalds • Second most common burn injury-related admission • Depth of scald injury depends on • Water temperature (>110ºF) • Duration of contact • consistency of liquid (i.e. soup vs coffee vs grease) • Skin thickness • based on age and anatomical location • Clothed areas may have deeper burns due to retention of heat and longer contact with skin • e.g. diapers or socks • Other sources of scald burns • Grease/oil • typically deep dermal or full thickness burns

  16. Mechanisms of thermal injuryContact burns • Typically small areas due to hot metal, plastic, glass or coals • Burn depth related to • Temperature of material • Duration of contact • Patient-related disabilities (e.g. neuropathy) • Commonly responsible for pediatric palm burns • Grafting of palm can lead to life-long disability and timing of surgery is controversial • Early grafting restores function quickly but destroys unique palmar nerve endings and palmar fasciocutaneous ligaments

  17. Mechanisms of thermal injuryChemical burns • Acids cause tanning with impermeable barrier limiting deep penetration • e.g. cleaning solvents • Hydrofluoric acid burns unique in need for calcium treatment • Topical • Intravenous – for life-threatening hypocalcemia • Intra-arterial – for comfort and hypocalcemia • Alkalis combine with lipids (saponification) and dissolve tissue • e.g. cement or drain openers • Etiologies • Work-related • Assault • Improper use of household products and harsh solvents • Progressive damage diluted with copious H20 irrigation • 15–20 minutes • pH test of skin until neutral • Attempts to neutralize causes exothermic reaction and thermal injury

  18. Mechanisms of thermal injuryElectrical burns • Due to very high intensity localized heat as body becomes an ‘accidental’ resistor • High voltage injuries (>1000 volts) • many work-related • deep tissue necrosis • arrhythmia (typically atrial fibrillation) • cognitive deficits • acute and delayed neuromuscular degeneration • carpal tunnel injuries • compartment syndromes • early surgical intervention indicated for acidosis ± signs of rhabdomyolysis or deterioration of neuro-sensorimotor exam • cataract formation • Low voltage injuries (<440 volts) • Typically small deep burns at contact points with rare systemic injury, • Classic pediatric injury involves oral commissure with risk of delayed oral artery bleed

  19. Criteria for transfer of a burn patient to a burn center • Second-degree burns greater than 10% total body surface area • (TBSA) • • Third-degree burns • • Burns that involve the face, hands, feet, genitalia, perineum, and • major joints • • Chemical burns • • Electrical burns including lightning injuries • • Any burn with concomitant trauma in which the burn injuries • pose the greatest risk to the patient • • Inhalation injury • • Patients with pre-existing medical disorders that could complicate • management, prolong recovery, or affect mortality • • Hospitals without qualified personnel or equipment for the care of • critically burned children.

  20. Guidelines for referral to a burn center • Partial-thickness burns greater than 10% TBSA • Burns involving the face, hands, feet, genitalia, perineum, or • major joints • Third-degree burns in any age group • Electrical burns, including lightning injury • Chemical burns • Inhalation injury • Burn injury in patients with complicated pre-existing • medical disorders • Patients with burns and concomitant trauma in which • the burn is the greatest risk. If the trauma is the greater • immediate risk, the patient may be stabilized in a trauma • center before transfer to a burn center. • Burned children in hospitals without qualified personnel for • the care of children • Burn injury in patients who will require special social, • emotional, or rehabilitative intervention

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