1 / 42

BURN INJURY

BURN INJURY. Joseph Hardwicke SpR Burns & Plastic Surgery West Midlands Deanery. TIMELINE OF BURN CARE. THEN. GREAT WAR. WWII. FALKLANDS. NUTRITIONAL SUPPORT. ANTI-SEPSIS. FLUID RESUSCITION. BURN EXCISION. "BURN TOXINS". SKIN GRAFTS. MESHED GRAFTS. MULTI-DISCIPLINARY

orson-gilliam
Download Presentation

BURN INJURY

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. BURN INJURY Joseph Hardwicke SpR Burns & Plastic Surgery West Midlands Deanery

  2. TIMELINE OF BURN CARE THEN GREAT WAR WWII FALKLANDS NUTRITIONAL SUPPORT ANTI-SEPSIS FLUID RESUSCITION BURN EXCISION "BURN TOXINS" SKIN GRAFTS MESHED GRAFTS MULTI-DISCIPLINARY APPROACH

  3. TIMELINE OF BURN CARE ? REHABILITATION NOW ORGAN SUPPORT SKIN CELL CULTURE SKIN SUBSTITUTES SCAR MANAGEMENT PSYCHOLOGICAL SUPPORT

  4. FIRE DISASTER

  5. AIMS • Causes of burns and the demographics of UK burn injury • The anatomy of the skin, depth of burn and the Jackson burn wound model • Estimation of burn % total body surface area (%TBSA) and fluid resuscitation • Inhalation injury

  6. CAUSES OF BURNS AND THE DEMOGRAPHICS OF UK BURN INJURY

  7. CAUSES OF BURNS • THERMAL • Hot or cold • HOT  COLD • Liquid - scald - Freezing - frostbite / nip • Solid - contact - Non-freezing - trench foot • Gas - flame • Direct cellular destruction  Freeze-thaw  Embolic/thrombotic

  8. CAUSES OF BURNS • ELECTRICAL • Low voltage < 1,000V • High voltage > 1,000V • Superhigh voltage > 10,000V • Conduction through tissues

  9. CAUSES OF BURNS • Deep tissue destruction • Myoglobinuria • Compartment syndrome • Cardiac dysrhythmias

  10. CAUSES OF BURNS • CHEMICAL • Acid • Alkali • ACID  ALKALI • Coagulative necrosis - Liquifactive necrosis • Painful - Non-painful tissue destruction • IRRIGATION • Copious water to correct pH

  11. CAUSES OF BURNS • RADIATION • UVB • Ionising radiation

  12. UK BURN DEMOGRAPHICS 250,000 burns/year 175,000 A&E attendances 13,000 hospital admissions 1,000 resuscitation burns 50% < 16 yrs 300 deaths/year Majority > 60 yrs

  13. KEY POINT • BURNS FIRST AID • Stop the burning process • Cool the burn • Cool running water • 10-30 minutes • Cover the burn • A&E if area of SKIN LOSS bigger than palm of hand CAUSES OF BURNS • THERMAL • ELECTRICAL • CHEMICAL • RADIATION • Extremes of age • Non-accidental injury • Psychiatric co-morbidity • Industrial / workplace

  14. THE ANATOMY OF THE SKIN, DEPTH OF BURN AND THE JACKSON BURN WOUND MODEL

  15. ANATOMY OF THE BURN • Functions of the skin SENSORY BARRIER METABOLIC PSYCHO- SOCIAL THERMO- REGULATION

  16. DEPTH OF BURN • SUPERFICIAL ERYTHEMA • No skin loss • Not included in burn %TBSA • PARTIAL THICKNESS • Superficial • Deep • FULL THICKNESS

  17. BURN ZONE OF STASIS • Adequate fluid resuscitation may preserve zone of stasis • Infection may cause burn extension • Early burn excision reduces necrotic load • Prognosis determined by the size of the burn unburnt skin zone of coagulation zone of hyperaemia

  18. INITIAL BURNS MANAGEMENT KEY POINT A : AIRWAY + C-SPINE CONTROL OXYGEN B : BREATHING + VENTILATION C : CIRCULATION IV ACCESS, STOP BLEEDING D : DISABILITY GCS E : EXPOSURE TEMPERATURE CONTROL %TBSA F : FLUID CALCULATION

  19. ESTIMATION OF BURN % TOTAL BODY SURFACE AREA (%TBSA) AND FLUID RESUSCITATION

  20. ESTIMATION OF %TBSA BURN • Average adult TBSA 1.7m2 • Distribution changes with age

  21. Under 10 yrs (age + 4) x 2 = kg Over 10 yrs age x 3 = kg BODY WEIGHT • Important to calculate fluid requirements • Measure or estimate MEASURE ESTIMATE

  22. FLUID RESUSCITATION • Hartman's solution / Ringer's lactate • Then titration of fluids depending upon urine output etc. KEY POINT Higher value for: Inhalation injury Electrical burns Paediatric burns 2 - 4 mls/kg/%TBSA From time of burn Half given in first 8h Half given in next 16h

  23. INHALATION INJURY

  24. INHALATION INJURY • Mortality increased by 40% • Early airway management KEY POINT POINTERS TO INHALATION INJURY Enclosed space Delayed extraction Facial burns Singed facial hair Carbonaceous sputum Hoarse voice / stridor

  25. SITE OF INJURY • Supraglottic • Thermal injury from inhaled gases • Airway spasm • Infraglottic • Chemical burns from products of combustion • Bronchoalveolar lavage

  26. TOXINS • Products of combustion • CARBON MONOXIDE • Preferential binding to Hb (200x) • Arterial blood gas • <10% normal >60% fatal • HYDROGEN CYANIDE • Synthetic rubber, polyurethane • Inhibits cytochrome C oxidase • Antidote and oxygenate Oxygen-dissociation curve shifts to the left

  27. OVERVIEW • Causes of burns and the demographics of UK burn injury • The anatomy of the skin, depth of burn and the Jackson burn wound model • Estimation of burn % total body surface area (%TBSA) and fluid resuscitation • Inhalation injury

  28. WOUND HEALING

  29. BASICS OF WOUND HEALING • Sequential process • Driven by cellular and matrix components

  30. BURN WOUNDS • Superficial partial thickness wounds heal by re-epithelialisation • Keratinocyte reserve in "epidermal derivatives" • Hair follicles • Sweat glands • Should heal by 2 weeks • Minimal scarring

  31. DEEPER BURNS • Loss of keratinocyte reserve • Loss of epidermal derivatives • Hair follicles • Oil / sweat glands • May heal by contraction from wound edge • Myofibroblasts • New matrix formed • Fibroblasts • SCAR FORMATION

  32. contracture hypertrophic keloid SCARS • End stage of normal wound healing NORMAL PATHOLOGICAL

  33. PATIENT FACTORS Medications Nutrition Mobility Systemic disease Continence Smoking LOCAL FACTORS Infection Skin loss Pressure necrosis Wound tension Tissue maceration IMPAIRED WOUND HEALING

  34. WOUND DRESSINGS • …don't need to be confusing • Adequate cleaning or surgical debridement • Aim for: • Controlled wound environment • Moist wound healing • Infection control • Analgesia

  35. THREE COMPONENTS • When putting a dressing on, consider who will be taking it off (and when)…. • All (nearly!) are made of 3 things: • A NON-ADHERENT LAYER ± antimicrobials • AN ABSORBANT LAYER depending on exudate • AN ADHESIVE LAYER depending on anatomy • Tailor-made for each patient

  36. BURN DRESSINGS • After initial assessment and stabilisation • If the burn is suitable for treatment in primary care • Clean wound, deroof large blisters • Definitive dressing • Review at 48h • If transfer is needed to burns centre • Temporary wound cover • Minimal interference • Reduce need for analgesia

  37. SKIN GRAFTS • The ideal wound dressing? • Supplies cellular and matrix components and is incorporated into the wound • Speeds up wound healing • Reduces pathological scarring in large burn wounds • BUT… • Limited resource • Donor site

  38. SPLIT THICKNESS SKIN GRAFT

  39. QUESTIONS? Joseph.Hardwicke@uhcw.nhs.uk

  40. FURTHER READING

More Related