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Burns - Pathophysiology, Evaluation and Management

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Burns pathophysiology, evaluation and management.

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Burns - Pathophysiology, Evaluation and Management

  1. 1. BURNS – PATHOPHYSIOLOGY, EVALUATION & MANAGEMENT DR ARUN KUMAR M GUIDE : DR S MEHROTRA DR ANKIT SHARMA MS (GEN SURG), MCH (PLASTIC SURGERY) 1
  2. 2. OVERVIEW  Part I  Historical perspective  Statistics  Classification of Burns  Pathophysiology  Evaluation  Part II  Management  Pre-hospital Care  Resuscitation & Nutritional support  Burn wound care  Complications  Rehabilitation 2
  3. 3. Definition Injuries that result from direct contact or exposure to any physical, thermal, chemical, electrical, or radiation source are termed as Burns. 3
  4. 4. HISTORICAL PERSPECTIVE 4
  5. 5. Historical Perspective  First direct evidence of treatment for burns - Cave paintings of Neanderthal man  1500 BC : Egyptian Smith Papyrus – Resin & Honey  Ambroise Pare ( AD 1510 – 1590) : Technique of early excision of burn wounds 5
  6. 6. Historical Perspective  1607 : GF Hildanus : Pathophysiology of Burns  1797 : Edward Kentish : Chronic Burn scar  Marjolin’s ulcer 6
  7. 7. Historical Perspective  19th century : Dupuytren’s classification based on depth  1842 : Curling : Gastric & Duodenal Ulceration Thomas Blizard CurlingBaron Guillaume Dupuytren 7
  8. 8. Historical Perspective  1947 : Texas city disaster  Truman G. Blocker Jr: Multidisciplinary team approach of Burns.  First Burn Institute for children in Galveston 8
  9. 9. Historical Perspective  1951 : 45% TBSA Burns  49% mortality  Present : > 70 % TBSA  49 % mortality  Focus of advance : Improved survival  Rehabilitation of Burn survivors 9
  10. 10. STATISTICS 10
  11. 11. Problem Statement : Global  An estimated 265000 deaths every year are caused by burns.  One of leading causes of disability-adjusted life-years (DALYs) lost in low- and middle-income countries.  In 2004, nearly 11 million people worldwide were burned severely enough to require medical attention. WHO Apr 14 11
  12. 12. Problem Statement: US  Burn Injuries Receiving Medical Treatment : 486,000  Fire/Smoke Inhalation Deaths : 3,275  Hospitalizations Related to Burn Injury : 40,000  Survival Rate : 96.8% American Burn Association, 2016 12
  13. 13. Problem Statement : India  70 lakh burn injury cases annually  Over 10,00,000 people are moderately or severely burnt every year  1.4 lakh people die of burn every year.  Around 70% of all burn injuries occur in most productive age group (15-35 years).  Around 4/5 are women & children.  As many as 80% of cases admitted are a result of accidents at home (kitchen- related incidents) 13
  14. 14. CLASSIFICATION 14
  15. 15. Classification  Based on Cause  Thermal  Electrical  Chemical  Radiation  Inhalation 15
  16. 16. Thermal Injuries  Most common  Types : Dry & wet Contact Direct contact with hot object (i.e. pan or iron) Anything that sticks to skin (i.e. tar, grease or foods) 16
  17. 17. Thermal Injuries Flame Direct contact with flame (dry heat) structural fires / clothing catching on fire Scalding Direct contact with hot liquid / vapours (moist heat) Cooking, bathing or car radiator overheating Single most common injury in the paediatric pt 17
  18. 18. Electrical Burns  Usually follows accidental contact with exposed object conducting electricity  Electrically powered devices  Electrical wiring  Power transmission lines  Can also result from Lightning  Damage depends on intensity of current 18
  19. 19. Electrical Burns  Severity depends upon:  what tissue current passes through (Low voltage/ High voltage)  width or extent of the current pathway  AC or DC  duration of current contact  Tissues with the lowest resistance eg. nerves, blood vessels & muscles  Heat generation during passage of the current injures the tissues  Skin has a relatively high resistance, hence is mostly spared 19
  20. 20. Electrical Burns  Low-tension injuries(<1000 V)  Low energy burns  Minimal damage to subcutaneous tissue  Entry & Exit points – fingers  small deep burns  AC  Tetany within muscles, cardiac arrest due to interference with normal cardiac pacing 20
  21. 21. Electrical Burns  High-tension injuries(>1000V)  Flash/ Flame / Current  Earthed high tension lines  Arc over the patient  Flash burn  Heating of the surrounding air  Explosion  Flame burn  Direct contact  patient acts as conduction rod huge subcutaneous damage 21
  22. 22. Electrical Burns  Lightning  HIGH VOLTAGE!!!  Injury may result from Direct Strike Side Flash  Severe injuries often result 22
  23. 23. Electrical Burns 23
  24. 24. Electrical Burns  Manifestations:-  External Burn  Internal Burn  Musculoskeletal injury  Cardiovascular injury  Respiratory injury  Neurologic injury  Rhabdomyolysis and Renal injury 24
  25. 25. 25
  26. 26. Chemical Burns  Usually associated with industrial exposure  Accidental mishandling of household cleaners  Degree of tissue damage determined by - Chemical nature of the agent - Concentration of the agent - Duration of skin contact 26
  27. 27. Chemical Burns  Acids  Immediate coagulation necrosis creating an eschar; self-limiting  Bases (Alkali)  Liquefactive necrosis with continued penetration into deeper tissue resulting in extensive injury Eg. Lime, potassium hydroxide, cement 27
  28. 28. Chemical Burns  Systemic absorption of offending agents causing metabolic derangements  Formic acid – haemolysis, Haemoglobinuria  Hydrofluoric acid – hypocalcemia 28
  29. 29. Radiation Exposure  Waves or particles of energy that are emitted from radioactive sources  Alpha radiation  Large, travel a short distance, minimal penetrating ability  Can harm internal organs if inhaled, ingested or absorbed  Beta radiation  Small, more energy, more penetrating ability  Usually enter through damaged skin, ingestion or inhalation 29
  30. 30. Radiation Exposure  Gamma radiation & X-rays  Most dangerous penetrating radiation  May produce localized skin burns & extensive internal damage 30
  31. 31. Classification  Based on Depth  I Degree - Epidermis  II Degree - Epidermis+ Dermis  III Degree - Epidermis+ Dermis + Subcutaneous tissue  IV Degree - Above + Muscles/bone 31
  32. 32. Classification Degree of Burn 1st Degree 2nd Degree Partial Thickness 2nd Degree Deep Burns 3rd Degree 4th Degree Involvement Epidermis Epidermis + Dermis E+ D E+D+Subcut tissue E+D+S+muscles, tendons & bone Appearance Symptoms & Signs Pain ++ Pain ++++ Painful -less severe Painless,insensitive, Severe Edema No Edema Healing 3-5 days , spontaneous No Scarring 2 weeks, min scarring, minimal discolouration 2-6 weeks Hypertrophic scarring / formation of contractures No spontaneous healing No spontaneous healing 32
  33. 33. 34
  34. 34. PATHOPHYSIOLOGY 35
  35. 35. Pathophysiology : Local Effects  Zone of coagulation  Necrotic area with cellular disruption  Irreversible tissue damage  Zone of stasis  Moderate insult with decreased tissue perfusion  Can survive or go on to coagulative necrosis depending on wound environment 36 JACKSON’s burn zones
  36. 36. Pathophysiology : Local Effects  Zone of hyperemia  Viable tissue, not at risk for further necrosis 37
  37. 37. Pathophysiology : Local Effects  Burn wound edema  Biphasic pattern  Burn shock : >1/3rd of TBSA Hypovolemia + Rapid edema formation 1st Hr 12-24 Hrs Immediate & Rapid increase in edema Gradual increase 38
  38. 38. Pathophysiology : Local Effects  Edema in non-burned tissue  Loss of capillary endothelial integrity  Reduced transmembrane potentials of skeletal muscle at the site of injury as well as away from the site of damage [-90mv -70 to -80mv]  Increase in intracellular Na & water leading to edema 39
  39. 39. Clinical Significance  Formation of constricting eschars & requirement of emergency escharotomy 40
  40. 40. Pathophysiology : Local Effects  Inflammatory Mediators Mediator Local effect Systemic effect Histamine Increased microvascular permeability Arteriolar dilatation & Venular contraction Reduced BP Hypovolemia Prostaglandins (PGE2) Local Vasodilatation (increased blood flow & increased permeability) Reduced systemic & pulmonary arterial BP Prostacycline (PGI2) Increased capillary permeability Reduced BP Leukotrienes (LB4 & LD4) Pulmonary HTN Thromboxane A2 & B2 Vasoconstriction  Ischaemia of wound Increasing depth of burn GI Ishcaemia Pulmonary HTN Kinins (Bradykinin) Increased microvascular permeability Vasodialatation Reduced BP Hypovolemia 41
  41. 41. Pathophysiology : Local Effects Mediator Local effect Systemic effect Serotonin Increased permeability of large blood vessels Catecholamines Epinephrine Nor-epinephrine Vasoconstriction (a1 receptors) Vasodialatation (b1 receptors) Antiistaminic & Bradykinin Reduce permeability Increased PR, BP, Metabolism O2 Radicals O2-, H2O2, OH-, ONOO- Tissue damage & Increased permeability Cardiac dysfunction PAF Increased permeability Angiotensin II & Vasopressin Vasoconstriction GI Ishcaemia Increased BP 42
  42. 42. Pathophysiology : Local Effects Mediator Local effect Systemic effect CRF Inhibitory to other factors 43
  43. 43. Pathophysiology : Systemic Effects 44 > 30 % Burns in adults
  44. 44. Pathophysiology : Systemic Effects  Hemodynamic consequences  Reduced cardiac output • Impaired electrical activity of muscle • Vasoconstriction of peripheral vesselsInitial phase • Hypovolemia • Reduced venous returnDelayed phase 45
  45. 45. Pathophysiology : Systemic Effects  Hemodynamic consequences  Myocardial dysfunction : O2 derived free radicals (mechanism unclear)  Increased systemic vascular resistance & organ Ischemia ( Renal & GI system) 46
  46. 46. Pathophysiology : Systemic Effects  Renal system Decreased cardiac output, decreased blood flow Stress induced hormones & mediators (angiotensin, aldosterone, vasopressin) Decreased renal blood flow & GFR Oliguria & renal failure 47
  47. 47. Clinical Significance  Importance of Emergency & Adequate Resuscitation 48
  48. 48. Pathophysiology : Systemic Effects  GI system  Mucosal atrophy  Increased intestinal permeability  Decreased absorption of glucose, amino acids & fatty acids 49
  49. 49. Clinical Significance  Curling’s ulcer : Prophylaxis 50
  50. 50. Pathophysiology : Systemic Effects  Immune system  Global depression in immune function  Diminished production of macrophages  Increased neutrophil count (dysfunctional) followed by decrease after 48- 72 hrs  Impaired cytotoxic T cell activity  Increase risk of infections  Depressed Th function 51
  51. 51. Pathophysiology : Systemic Effects  Hypermetabolic response  Phase I [ebb]  First 48 hrs  Decrease in cardiac output urine output O2 consumption BMR  Impaired glucose tolerance with hyperglycemia 52
  52. 52. Pathophysiology : Systemic Effects  Hypermetabolic response  Metabolic variables gradually increase within first five days post injury to reach a plateau  Phase II [flow]  Increase in metabolic rate  Urine cortisol  Serum catecholamines  Basal energy expenditure  Serum cytokines  Hyperdynamic state – increase in cardiac output  Insulin resistance  Persists for upto 3 years 53
  53. 53. Clinical Significance Importance of Techniques of early excision Nutritional support 54
  54. 54. Pathophysiology : Systemic Effects  Inhalational Injury  80% of fire-related deaths due to inhalation of toxic gases  Synergestic effect of inhaled toxic gases (CO + HCN)  Agents:  Carbon Monoxide  Hydrogen Cyanide  Hydrogen chloride (PVC)  Nitrogen oxides  Aldehydes & Acrolein (Wood & Kerosene) 55
  55. 55. Pathophysiology : Systemic Effects  Carbon Monoxide  Most frequent cause of death in smoke induced inhalational injury  Pathology : 0.1% of CO  50% Carboxy Hb  Hb affinity of CO  200-250 times that of O2  Mechanism: Competitive inhibition of Cyt P450 Free radical formation (Xanthine dehydrogenase Xanthine Oxidase) 56
  56. 56. Carbon Monoxide 57
  57. 57. Pathophysiology  Hydrogen cyanide  Fires involving N2 containing compounds  Mechanism : Inhibition of cellular oxygenation with resultant tissue anoxia Reversible inhibition of Cyt oxidase (Fe 3+) by CN 58
  58. 58. Pathophysiology : Oropharynx Heat Denaturation of proteins Complement Activation Histamine release Formation of Xanthine Oxidase Converts Uric acid to urea Release of O2 free radicals Edema formation Release of Eicosanoids Attract PMNs to the site (Amplify effects) Massive Edema 59
  59. 59. Pathophysiology : Tracheo-bronchial areas Chemical Injury to airway Seperation of ciliated epi-cells from BM Increased Circulation to lung & bronchial circulation Edema formation Diffuse transudate in early changes Bronchoconstriction Fibrin casts Obstruction of smaller airways Culture media for infections Pneumonia , Sepsis & Death 60
  60. 60. Clinical Significance  Important to identify respiratory insult & Early Intubation in case required. 61
  61. 61. EVALUATION 62
  62. 62. Wallace’s Rule of “9”  Head & Neck - 09  Upper limbs - 09 x 2  Trunk - 18 x 2  Lower limbs - 18 x 2  Perineum - 01 63
  63. 63. 18 4.5 9 1 9 4.5 18 4.5 4.5 9 9 4.5 9 4. 7 4.5 7 18 1 64
  64. 64. 65
  65. 65. Lund and Browder Charts 66
  66. 66. Palm Method  Size of Patient’s palm  1% of TBSA  Irregular wounds with scattered distribution. 67
  67. 67. OVERVIEW  Part I  Historical perspective  Statistics  Classification of Burns  Pathophysiology  Evaluation  Part II  Pre-hospital Care  Resuscitation & Nutritional support  Burn wound care  Complications  Rehabilitation 68
  68. 68. MANAGEMENT OF BURNS
  69. 69. PHASES OF TPT  Phase 1: Treatment at the scene and tpt to initial care facility  Phase 2: Assessment and stabilization at initial care facility and tpt to burn ICU.
  70. 70. PRE HOSPITAL MANAGEMENT  Rescuer to avoid injuring himself  Remove patient from source of injury  Stop burn process  Burning clothing; jewelry, watches, belts to be removed  Pour ample water on burnt area (not ice/ ice packs – skin injury & hypothermia)
  71. 71. PRE HOSPITAL MANAGEMENT  Chemical burns:  Remove saturated clothing  Brush skin if agent is powder  Irrigation with copious amount water to be started and continued in hospital  Electrical burns:  Turn off the current  Use non-conductor item to separate from source
  72. 72. PRE HOSPITAL MANAGEMENT PRIMARY ASSESSMENT  A – B – C – Cervical spine immobilization  Respiratory tract:  Edema of upper airway sets in very fast  Upper airway obstruction  100% humidified O2 if no obvious resp distress
  73. 73. PRE HOSPITAL MANAGEMENT PRIMARY ASSESSMENT  ET intubation + assisted ventilation with 100% O2 if:  Overt signs and symptoms of airway obstruction (Progressive hoarseness)  Suspected inhalational injury (smoke/ carbon monoxide intoxication)  Unconscious patient/ rapidly deteriorating patient  Acute respiratory distress  Burns of face & neck  Extensive Burns (> 40% TBSA)
  74. 74. PRE HOSPITAL MANAGEMENT PRIMARY ASSESSMENT  Pulse rate better monitor than BP  Spinal immobilization:  Explosion/ deceleration injury  Cervical collar (Philadelphia collar)
  75. 75. PRE HOSPITAL MANAGEMENT  Ice/ice cold water causes numbness, intense vasoconstriction, hypothermia causing further damage.  Do not break blisters.  Do not apply lotions, powders, grease, ghee, gentian violet, calamine lotion, toothpastes, butter and other sticky agents over the burn wound.  Prevent contamination: Wrap burn part in clean dry sheet /cloth.  Assess for life threatening injuries.
  76. 76. PRE HOSPITAL MANAGEMENT  NO I/M or S/C inj (Capillary leakage results in unpredictable absorption)  I/V morphine to allay anxiety  Pain relief and reassurance  Withhold oral intake
  77. 77. PRE HOSPITAL MANAGEMENT  Co-morbid conditions/ pre-existing illness  Initiate rapid transfer to hospital  Secure and protect the airway  Cervical spine immobilization; if necessary
  78. 78. PRE HOSPITAL MANAGEMENT SECONDARY ASSESSMENT  Performed only if no immediate life threatening injury/ hazard present  Thorough head to toe evaluation  Medical history, medication, allergies, mechanism of injury  Start IV line (not reqd in hospital <60 min away)
  79. 79. PRE HOSPITAL MANAGEMENT SECONDARY ASSESSMENT  RL infusion:  ≥ 14 yrs – 500mL/hr  6-14 yrs – 250mL/hr  ≤ 5yrs – 125mL/hr  Apply clean dressing/ sheet to protect area and minimize heat loss  IV Tramadol to relieve pain  No topical antimicrobial
  80. 80. HOSPITAL MANAGEMENT INITIAL CARE FACILITY  C – A – B  Establish adequate airway  ET intubation – impending airway edema (post initiation of IV therapy)  Maintain cervical spine immobilization
  81. 81. INITIAL CARE FACILITY  History  Mechanism of injury  Time of injury  Surroundings (closed space/ chemicals)  Physical examination  Head to toe assessment  Careful neurological examination (cerebral anoxia)  Corneal fluorescent examination in facial burns  Labs: CBC, electrolytes, BUN  Pulmonary assessment: ABG, CXR, carboxyhemoglobin
  82. 82. INITIAL CARE FACILITY  Pulse in extremities: manual/ doppler  Loss of distal circulation Pallor/coolness/absent pulse/loss capillary refill/decreased oxygen saturation  Pain on passive extension  Deep pain at rest  Absent pulse: emergency escharotomy to release constrictive, unyielding eschar
  83. 83. ESCHAROTOMY  Deep 2nd & 3rd degree circumferential burns  Chest: To allow respiratory movement  Limb: To restore circulation in limb with excess swelling under rigid eschar  Bedside, IV sedation, cautery  Midaxial incision into eschar, Across joints  Caution at elbow, wrist, fibular head, medial ankle, neck  Not in SC tissue  Exposes SC fat
  84. 84. ESCHAROTOMY  Elevate limbs above level of heart  Monitor pulses for 48 hrs  Chemical escharotomy if pulses +nt but feeble.  Useful in hand burns.  Enzyme – collagenase  Complications : bleeding, infection  Antimicrobial prophylaxis must to prevent sepsis
  85. 85. INDICATIONS FOR ADMISSION  >15% burns in adults  10% burns in children  Airway and inhalation injury.  Significant burn involving face, hands, feet and perineum.  Extremes of age.  Suspected non-accidental burns.  Burns that require early surgery (deep partial thickness / full thickness)  Patients deficient of nursing care by attendants at home  Severe electric and acid burns that is likely to have serious sequelae
  86. 86. RECEPTION • Resuscitation –ensure ABC • Large gauge I.V catheter • Central line Insertion • Venesection • Foleys catheter and NG tube placement • Quick assessment of extent • Tetanus prophylaxis (the only IM administered inj) • Weigh the patient
  87. 87. Respiratory Care  Assess airway, respiration & breath sounds  Removal of pulmonary secretions  O2 Humidification  Chest physiotherapy, deep breathing & coughing  Frequent position changes and suction  Pharmacologic Considerations:  Bronchodilators and mucolytics  Circumferential chest burns can impair ventilation  Escharotomy may be required
  88. 88. Cardiovascular Care  Increase capillary permeability  “Capillary Leakage Syndrome”  Fluid shift  intravascular to interstitial space  blistering and massive edema  Excessive insensible loss via burn wound 3-5 lit/d !!  Finally  hypovolemia  untreated BURNS’ SHOCK
  89. 89. Severity of Burn Injuries  Treatment of burns as per severity of injury  Severity is determined by:  Depth of burns  TBSA involved  Site - face, hands, feet, face or perineum  Age  Associated injuries N Engl J Med 1996;335:1581 J Trauma 1994;36;59
  90. 90. OUTCOME PROGNOSIS (Baux Score) Sum of Age in years + Area of burn in % TBSA < 80 good 80-100 life threatening >100 bad
  91. 91. Resuscitation Phase  First 24-48 hours after initial burn injury or until spontaneous diuresis occurs.  Resuscitation phase characterized by:  Life-threatening airway problems  Cardiopulmonary instability  Hypovolemia  Goal:  Maintain vital organ function and perfusion
  92. 92. PARENTERAL FLUIDS
  93. 93. Parkland Formula  Fluid of Choice  Lactated Ringer’s (RL)  NS can produce hyperchloremic acidosis  4 ml x % of burn x weight (Kg) in 24 hours  First ½ of total volume given in the first 8 hours  Remaining ½ of total volume given over following 16 hours  NEXT 24 HRS  Total volume ½ of first day  Colloids ( 0.5 ml / kg / % )  5 % glucose to make up the rest
  94. 94. Parkland Formula  Maximum applicable TBSA – 50%  Fully dilated capillaries  Maximum capillary permeability  No further mounting of inflammatory response
  95. 95. Adult Fluid Resuscitation  Evan’s formula:  Requirement for first 24 hrs  Colloids : 1ml/kg/% burn  Saline : 1ml/kg/% burn  D5 : 2000ml  Requirement for second 24 hrs  ½ of first 24 hrs
  96. 96. Adult Fluid Resuscitation  Brooke formula  Requirement for first 24 hrs Colloids : 0.5ml / kg /% burn RL : 1.5ml / kg / %burn D5 : 2000ml in adults  Requirement for second 24 hrs  ½ of first 24hrs
  97. 97. Pediatric age group Carvajal Formula  5000cc x m2 x % BSA initial + 2000cc x m2 maint /d  Change to 5%D+RL with albumin after 6 hrs  Urine output 1-2 cc/ kg/h
  98. 98. Assessment of Adequacy of Fluid Resuscitation  Monitor  Urinary Output Adult: > 1 ml/ kg/ hr  Daily Weight  Vital Signs Heart rate and blood pressure CVP Level of Consciousness  Laboratory values
  99. 99. RESUSCITATION FAILURE  Delayed resuscitation  Electric burns  Inhalation injury  Escharotomy  Carbon monoxide poisoning  Elderly patients
  100. 100. Nutritional Support  Burn wounds consume large amounts of energy:  Requires massive amounts of nutrition to promote wound healing  Monitoring Nutritional Status  Weekly albumin levels  Daily weight  EMR (Estimated metabolic requirement) (Curreri formula) =25kcal x body weight (kg) + 40 kcal x % BSA
  101. 101. Routes of Nutritional Support  High-protein & high-calorie diet  Often requiring various supplements  Routes: ORAL (BEST) Enteral  Gut is the preferred alternative route  G-tube or J-tube (Head injury/ surgery/ unconscious) Parenteral  TPN and PPN  Associated with an increased risk of infections
  102. 102. Nutritional Support Formulas to Predict Caloric Needs in Severely Burned Children Age group Maintenance needs Burn wound needs Infants (0-12 mo) 2100 KCal/ %TBSA/ 24hr 1000 KCal/ %TBSA/ 24hr Children (1-12 yr) 1800 KCal/ %TBSA/ 24hr 1300 KCal/ %TBSA/24 hr Adolescents (12-18 yr) 1500 KCal/ %TBSA/ 24hr 1500 KCal/ %TBSA/ 24hr
  103. 103. BURN WOUND CARE
  104. 104. Burn Wounds Risk for Infection  Skin  first line of defense  Necrotic tissue  bacterial growth  Management Burn wounds are frequently monitored for bacterial colonization Wound swab cultures and invasive biopsies
  105. 105. Role of burn wound cultures  Early cultures positive/ high counts  early contamination of the burn wound  Routine cultures  aid in empiric antimicrobial coverage if the patient subsequently becomes ill  Increasing colony counts  change topical antimicrobial agents.  Colonization by virulent or resistant organisms  predictor of impending invasive burn wound infection.  Wound colony counts >106  high risk of infectious & graft failure.
  106. 106. Burn Wound Care Hydrotherapy Shower, bed baths or clear water spray Maintain appropriate water and room temperature Limit duration to 20-30 minutes Don’t burst blisters, aspirate them!!! Trim hair around wound; except eyebrows Dry with towel; pat dry, don’t rub! Clean unburned skin and hair
  107. 107. Burn Wound Care Antimicrobial Agent  Silvadene (silver sulfadiazine)  Broad spectrum; the most common agent used  Painless & easy to use  Doesn’t penetrate eschar  Leaves black tattoos from silver ion  Sulfamylon (mafenide acetate)  Penetrates eschar  Painful for approximately 20 minutes after application  Metabolic acidosis
  108. 108. Burn Wound Care Antimicrobial agent  Bacitracin/ Neomycin/ Polymyxin B - not broad spectrum, painless, easy to apply  Nystatin(Mycostatin) - antifungal  Mupirocin(Bactroban) - anti staphylococcal
  109. 109. Burn Wound Care  Betadine  Drying effect makes debridement of the eschar easier  Acticoat (antimicrobial occlusive dressing)  A silver impregnated gauze that can be left in place for 5 days  Moist with sterile water only; remoisten every 3-4 hours
  110. 110. Soak silver dressings and gauze in WATER (not saline). Apply the silver dressing. Wrap with moist gauze. Secure with mesh, gauze or tape.
  111. 111. Burn Wound Care Antimicrobial (SOAKS)  0.5% Silver nitrate  Effective against all micro-organism  Stains contacted area, leaches sodium from wound  Methemoglobinemia  5% Mafenide acetate  Painful  metabolic acidosis  0.025 Sodium hypochlorite - Gram Positive organism  0.25% Acetic acid - Gram Negative organism
  112. 112. Closed Dressing  Advantages • Less wound desiccation • Decreased heat loss • Decreased cross contamination • Debriding effect • More comfortable • Disadvantages • Time consuming • Expensive • Increase chances of infection if not changed frequently
  113. 113. Burn Wound Care Cover with a Sterile Dressing  Most wounds covered with several layers of sterile gauze dressings.  Special Considerations:  Joint area lightly wrapped to allow mobility  Facial wounds may be left open to air  Circumferential burns: wrap distal to proximal  All fingers and toes should be wrapped separately  Splints over dressings
  114. 114. Burn Wound Care Debridement of the wound  May be completed at the bedside or as a surgical procedure.  Types of Debridement: Natural  Body & bacterial enzymes dissolve eschar; takes a long time Mechanical  Sharp (scissors), Wet-to-Dry Dressings or Enzymatic Agents Surgical
  115. 115. Why excise the burn?  Burn wound is a focus for sepsis  Burn stimulates inflammatory mediators  Deep burns cannot heal without grafts  Possible effect on future scar quality 118  Non full-thickness burns may heal spontaneously  Superficial burns heal with acceptable scars  Excised burn wound must be closed  Major burn surgery is hazardous but
  116. 116. Timing of surgery  “Ultraconservative”  Conservative  Early  Acute 119
  117. 117. Urgent surgery High-tension electrical injury Deep encircling burns - escharotomy  limbs  trunk 120
  118. 118. For small burns 121 Excision and grafting as soon as possible clearly non-healing
  119. 119. Early excision of burns  Tangential excision to viable tissue on day 2-3  Janzekovic (1970) Jackson & Stone (1972)  Current concept – within hours  Hardly any bleed  Upto 60% burns 122
  120. 120. TANGENTIAL BURN EXCISION & EARLY SPLIT SKIN GRAFTING 123
  121. 121. TANGENTIAL BURN EXCISION & EARLY SPLIT SKIN GRAFTING 124  Early wound closure; shorter hospital stay  No increase in morbidity  Significant ↓ in mortality  Reduced bacterial colonization  Tissue preservation  Maintenance of function  Less scaring
  122. 122. Early burn surgery Superior outcomes where suitably equipped  mortality  length of hospital stay  morbidity during acute burn  scar quality 125
  123. 123. Desirable surgical management  Excision of all non-shallow burns as soon as practicable in as few stages as possible  Closure of excised wounds with autograft, allograft or artificial material  Definitive wound closure 126
  124. 124. Surgical Management Skin Grafting  Closure of burn wound  Spontaneous wound healing would take months for even a small full-thickness burn  Eschar is removed as soon as possible to prevent infection  Wound needs to be covered to prevent infection, loss of heat, fluid and electrolytes  Therefore, skin grafting is done for most full-thickness burns.  Can be permanent or temporary
  125. 125. Burn Wound Closure Permanent Skin Grafts  Two types: Autografts and Cultured Epithelial Autografts (CEA)  Autograft  Harvested from pt  Non-antigenic  Less expensive  Decreased risk of infection  Can utilize meshing to cover large area  Disadvantage : lack of sites and painful
  126. 126. Burn Wound Closure  Cultured Epithelial Autografts (CEA) A small piece of pt’s skin is harvested and grown in a culture medium (PDGF impregnated) Takes 3 weeks to grow enough for the first graft Very fragile; immobile for 10 days post grafting Useful for limited donor sites Disadvantage : very expensive; poor long term cosmetic results and skin remains fragile for years
  127. 127. Burn Wound Closure
  128. 128. Burn Wound Closure Temporary Skin Grafts  Why temporary ??  Available donor sites are used first, but in large burns  not enough donor sites. While waiting for donor site to heal it can be reused as a temporary covering.
  129. 129. Types of temporary Skin Grafts  Biosynthetic- Homograft (cadaveric)/ Xenograft (porcine)  Artificial Skins (collagen based)- Trancyte/ Integra  Synthetic – Biobrane/Opsite
  130. 130. Burn Wound Closure Biosynthetic Temporary Skin Grafts  Homograft  Allograft  Live or cadaver human donors  Fairly expensive/ all the function of skin  Best infection control of all biologic coverings  Disadvantage :  Disease transmission (HBV & HIV)  Antigenic: body rejects in 2 weeks  Not always available  Storage problems
  131. 131. Biosynthetic Temporary Skin Grafts  Heterograft  Xenograft  Graft between 2 different species  Porcine most common  Fresh, frozen or freeze-dried (longer shelf life)  Amenable to meshing & antimicrobial impregnation  Antigenic: body rejects in 3-4 days  Fairly inexpensive  Disadvantage : Higher risk of infection
  132. 132. Biosynthetic Temporary Skin Grafts  Artificial Skins Transcyte: A collagen based dressing impregnated with newborn fibroblasts. Integra: A collagen based product that helps to form a “neodermis” no anti-microbial property  Synthetic Any non-biologic dressing that will help prevent fluid & heat loss Biobrane, Xeroform, OpSite or Beta Glucan collagen matrix
  133. 133. Biobrane  Artificial dressing has elastic property  Bilayer fabric  Inner layer - knitted nylon threads coated with porcine collagen  Outer layer - rubberized silicone  Pervious to gases but not to liquids and bacteria  Epithelialization takes place under the dressing in partial thickness wound in 1-2 wks
  134. 134. Donor Site: Wound Considerations  The donor site is often the most painful aspect for the post-operative pt  brand new wound !!  Variety of products are used for donor sites Most are left in place for 24 hours and then left open to air  Donor sites usually heal in 3 wks
  135. 135. COMPLICATIONS
  136. 136. Burn Wound Infection  Focal/ multi focal/ generalized  More the area of infection  ↑chances of septicemia  Common org- Strep, Staph & Pseudomonas
  137. 137. Monitoring Wound Infection  Definite diagnosis  wound biopsy  More than 100,000 organisms is highly suggestive of burn wound infection  Concomitant positive blood culture is a reliable indicator  Children & burns > 30% TBSA are more likely to develop burn sepsis
  138. 138. Clinical Signs of Burn Wound Infection  2nd degree burn  full-thickness necrosis  Focal dark-brown or black discoloration  Wound degeneration  “neo-eschar” formation  Unexpectedly rapid eschar separation  Hemorrhagic discoloration of sub-eschar fat  Erythematous or violaceous edematous wound margin  Septic lesions in unburned tissue  Crusted serrations of wound margin
  139. 139. Management  Topical anti microbial therapy - Mafenide acetate - Silver sulfadiazine - Silver nitrate  Systemic antibiotics  Eschar excision & covering with biological dressings
  140. 140. Burn Sepsis  Host & opportunistic organism balance altered  Immunologic alteration  Defect in cell-mediated immunity  Abnormal activation of complement pathway
  141. 141.  Sepsis in burn pt  concern for infection.  Age-dependent definition with adjustments for children.  The trigger includes at least three of the following:  I. Temperature >39° or <36.5°C  II. Progressive tachycardia  Adults >110 bpm  Children >2 SD above age-specific norms (85% age-adjusted max heart rate) Burn Sepsis
  142. 142.  III. Progressive tachypnea  Adults >25 /min not ventilated Minute ventilation >12 L/min ventilated  Children >2 SD above age-specific norms (85% age- adjusted max respiratory rate)  IV. Thrombocytopenia (only 3 days after initial resuscitation)  Adults <100 000/mcl  Children <2 SD below age-specific norms Burn Sepsis
  143. 143.  V. Hyperglycemia (in the absence of pre-existing diabetes mellitus)  Untreated plasma glucose >200 mg/dL or equivalent mM/L  Insulin resistance – examples include  >7 units of insulin/h intravenous drip (adults)  Resistance to insulin (>25% increase in insulin requirements over 24 hours)  VI. Inability to continue enteral feedings >24 hours  Abdominal distension  Enteral feeding intolerance (residual >150 mL/h in children or 2× feeding rate in adults)  Uncontrollable diarrhoea (>2500 mL/d for adults or >400 mL/d in children) Burn Sepsis
  144. 144.  Identify & document infection:  Culture positive infection  Pathologic tissue source identified  Clinical response to antimicrobials Burn Sepsis
  145. 145. Clinical Manifestations  Hyperthermia, Hypothermia (later)  Tachycardia  Increased ventilation  High cardiac output  Leucocytosis  Thrombocytopenia  Hypotension & oliguria
  146. 146. Treatment  Definitive  wound excision  Antibiotics  Supportive Care
  147. 147. REHABILITATION PHASE
  148. 148.  Begins day one and may last several years  Nursing care  Meticulous asepsis continues to be important  Major areas of focus:  Support for adequate wound healing  Prevention of hypertrophic scarring & contractures  Psychosocial Support  Patient and family  Promotion of maximal functional independence Rehabilitation
  149. 149. Hypertrophic Scar Formation  Excessive scar formation, which rises above the skin  Management: Pressure Garments  Elasticized garments that are custom fitted  Maintains constant pressure on the wound  Result: smoother skin & minimized scar appearance  Pt Considerations:  Must be worn 2-3 hours a day  Up to 1-2 years  Jobst garments, foam sponge, foam tape, silicon gel sheet
  150. 150. Contracture Formation  Shrinkage and shortening of burned tissue  Results in disfigurement  Especially if burn injury involves joints  Management is application of opposing force:  Splints, proper positioning, mobilisation Must begin at day one Multidisciplinary approach is essential
  151. 151. Psychosocial Considerations Alterations in Body Image  Loss of Self-Esteem  Returning to community, work or school  Sexuality  Supports Services  Psychologist, social work & vocational counselors  Local or national burn injury support orgs  Psy Considerations  Encourage pt & family to express feelings  Assist in developing positive coping strategies
  152. 152. RECENT ADVANCES
  153. 153. RAs (grafts)  Liposomal gene transfer Branski L, Pereira CT, Herndon DN, Jeschke MG. Gene therapy in wound healing: Present Status and Future Directions. Gene Therapy, 2006 Aug 24  cationic cholesterol-containing liposomal constructs  (best so far)  Naked DNA application,  Viral transfection,  High-pressure injection  Liposomal delivery
  154. 154. RAs (grafts)  ARTIFICIAL SKIN SUBSTRATES  Dermal matrices with epidermal components Boyce ST, Kagan RJ, Yakuboff KP, Meyer NA, Rieman MT, Greenhalgh DG, Warden GD. Cultured skin substitutes reduce donor skin harvesting for closure of excised, full-thickness burns. Ann surg, 2002 Feb; 235(2):269-279  Amniotic wound coverage devices . Branski LK, Herndon DN, Masters OE, Celis M, Norbury WB, Jeschke MG. Amnion in the treatment of pediatric partial-thickness facial burns. Burns, 2007 Oct 4.  Dermal component matrices Schulz JT 3rd, Tompkins RG, Burke JF. Artificial skin. Ann Rev Med, 2000; 51:231-244
  155. 155. CONCLUSION  Early, aggressive, controlled fluids  Monitor urine output as a guide to resuscitation  Prevent extension of injury  Maintain high suspicion for inhalation injury & low thresh hold for intubation  Always rule out co-incident trauma  Frequent reassessment of extremities  Seek out & treat CO poisoning  Liberal use of analgesia  Prevent hypothermia  Provide for increased metabolic demands
  156. 156. BURNS !!! B Breathing U Urinary output R Rule of Nines & Resuscitation with fluid N Nutrition S Shock & Silvadene
  157. 157. References  Total Burn Care; David N Herndon 4th Ed  Bailey And Love's Short Practice of Surgery 26th Ed 2013  Schwartz’s Principles of Surgery, 10th Ed  Sabiston Textbook of Surgery 19th ed 2012 160
  158. 158. THANK YOU 161

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