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Burns Rohit.pptx
- 1. BURNS – PATHOPHYSIOLOGY, EVALUATION & MANAGEMENT MAJ ROHIT KUMAR SINGH GUIDE : MAJ SUNIL NP 1
- 2. OVERVIEW Statistics Classification of Burns Pathophysiology Evaluation Management 2
- 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. 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) 4
- 5. Classification Based on Cause Flame- convection and radiation Scald – hot liquids Contact- common in elders Chemical Electrical 5
- 6. Classification Based on Depth I Degree - Epidermis II Degree - Epidermis+ Dermis III Degree - Epidermis+ Dermis + Subcutaneous tissue IV Degree - Above + Muscles/bone 6
- 7. 7 Classification Degree of Burn 1st Degree 2nd Degree Partial Thickness 2nd Degree Deep Burns 3rd Degree 4th Degree Involvement Epidermis Epidermis + Dermis Epidermis+ Dermis E+D+Subcut tissue E+D+S+muscles, tendons & bone Appearance Symptoms & Signs Painful Painful Painful to pinprick(less severe) Painless,insensitive, Severe Edema No Edema Healing 3-5 days , spontaneous No Scarring 2 weeks, min scarring, minimal discolouration and textual difference 2-6 weeks Hypertrophic scarring / formation of contractures No spontaneous healing No spontaneous healing
- 10. 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 10 JACKSON’s burn zones
- 11. Pathophysiology : Local Effects Zone of hyperemia Viable tissue, not at risk for further necrosis 11
- 12. Pathophysiology : Systemic changes Inflammation and edema First in burn wound then generalized Mechanism – Decrease in interstitial hydrostatic pressure Decrease in plasma oncotic pressure Increase in interstitial oncotic pressure Mediators induced vasoconstriction, vasodilatation and increase in capillary permeability 12
- 13. Clinical Significance Mediators – Increase capillary permeability – histamine, bradykinin, vasoactive amines, prostaglandins, leukotrienes etc. Increase vascular resistance- serotonin released from aggregated platelets High dose vit c therapy reduces resuscitation fluid requirment 13
- 15. Pathophysiology : Systemic Effects Hemodynamic consequences Reduced cardiac output Decrease cardiac contractility Loss of plasma volume Increases blood viscosity 15
- 16. Pathophysiology : Systemic Effects Renal system 16 Decreased cardiac output, decreased blood flow Stress induced hormones & mediators (angiotensin, aldosterone, vasopressin Decreased renal blood flow & GFR Oliguria & renal failure
- 17. Clinical Significance Importance of Emergency & Adequate Resuscitation Role of CRRT- reduces renal failure related death 17
- 18. 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 18
- 19. 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 19
- 20. Pathophysiology : Systemic Effects Hypermetabolic response 3 to 4 days after the injury 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 20
- 21. Pathophysiology : Systemic Effects Injury to Airway and Lungs Inhalation of hot and smoked- filled air 3 Component – Upper airway injury, Lower airway injury and metabolic poisoning Warning signs – Facial burns History Hoarseness of voice / stridor Singeing of facial and nasal hair Deep burns around mouth and Neck 21
- 22. Pathophysiology : Systemic Effects Metabolic poisoning Incomplete combustion – CO and HCN CO poisoning Most frequent cause of death in smoke induced inhalational injury Hb affinity of CO 200-250 times that of O2 Mechanism: Inactive and impasirs oxygen delivery at tissue level Competitive inhibition of Cyt P450 Impaired cellular respiration 22
- 23. Pathophysiology Hydrogen cyanide Fires involving N2 containing polymers Mechanism : Combines with FE 3+ in Cyt A3 complex Inhibition of cellular oxygenation with resultant tissue anoxia 23
- 24. Pathophysiology Changes in Gut Ischemia to Gut mucosa Reduction in Gut motility and prevents absorption of food Translocation of gut bacteria Abdominal compartment syndrome – mucosal swelling, stasis and peritoneal edema Danger to peripheral circulation Circumferential full thickness burn- limb threatening ischemia 24
- 25. Assessment of Burn Wound Assessing Size 25
- 26. Wallace’s Rule of “9” Head & Neck - 09 Upper limbs - 09 x 2 Trunk - 18 x 2 Lower limbs - 18 x 2 Perineum - 01 26
- 28. 28
- 29. 29 Lund and Browder Charts
- 30. Palm Method Size of Patient’s palm 1% of TBSA Irregular wounds with scattered distribution. 30
- 32. PRE HOSPITAL MANAGEMENT Ensure Rescuer Safety Stop the burning process Check for other injuries – Standard A- B- C check Cool the burn wound Analgesia and slows microvascular damage Min 20 min/ 15* C Avoid hypothermia Give Oxygen,elevate and analgesia
- 33. HOSPITAL MANAGEMENT Principle of ATLS followed- Airway control, breathing and ventilation Circulation, Disability- neurological status Exposure with environmental control Fluid resuscitation
- 34. 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
- 35. Severity of Burn Injuries Major determinants of outcome of burn: Depth of burns TBSA involved Presence of an inhalational injury Site - face, hands, feet, face or perineum Age and comorbidities
- 36. Criteria for admission to a burns unit Suspected airway or inhalational injury Burns likely required fluid resuscitation (>15% in adults and >10% in children) Likely to require surgery Burns of any significance to hands, face,feet or perineum Extremes of ages , non-accidental burns Burns with associated potentially serious sequelae High tension electric burns Concentrated hydrofluoric acid burns
- 37. Airway Recognition of potentially burned airway Early intubation until swelling subsides (48 hrs) Signs of laryngeal oedema are late symptoms Time frame from burn to airway occlusion – 4 to 24 hrs 37
- 38. Breathing Inhalational Injury Observe for signs of smoke inhalation Trapped in fire for couple of minutes Presence of soot in nose and oropharynx Patchy consolidation on chest x-ray Clinical features- tachypnoea, dyspnoea, tachycardia, low SPo2, confusion ( symptoms can take 24 hrs to 5 days) Treatment- Physiotherapy, nebulisers, and warm humidified oxygen Continuous or intermittent positive pressure using mask If required then intubation NAC and heparin nebulisation Bronchodilators- Albuterol 38
- 39. Thermal burn injury to lower airway Occurs with steam injuries Treatment is supportive and same as inhalational injuries Metabolic Poisoning History of altered consciousness, trapped in enclosed space Immediate blood gas measurement- metabolic acidosis Treatment – CO poisoning- high flow and high concentration Oxygen ( Carboxyhaemoglobin level more than 10%) Cyanide poisoning- Iv Vit B12(Hydroxycobalamine) 39
- 40. Mechanical blocking to breathing Full-thickness burns across chestwall Stops Rib expansion compromises respiratory function CO2 retention and high inspiratory pressure in ventilated pationts Treatment - Escharotomy 40
- 41. 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
- 42. OUTCOME PROGNOSIS (Baux Score) Sum of Age in years + Area of burn in % TBSA < 80 good 80-100 life threatening >100 bad
- 43. Fluid resuscitation IV resuscitation – Adult with >15% TBSA and Child with >10% TBSA Should commence from time of injury, delay should be avoided Additional maintenance fluid for children Judicious monitoring in elderly
- 44. Variables in calculation – Percentage of TBSA burned Initial weight of the patient Rate/type of fluid Fluid loss maximum in first 8 hrs then slows by 24-36 hrs. Initial rate of fluid estimation – Multiplying TBSA burned by 10 in adults. Should continued until formal calculation of resuscitation needs. 44
- 45. Crystalloid Resuscitation Fluid of Choice Lactated Ringer’s (RL) in Adults and 5% RL in children <2yrs NS can produce hyperchloremic acidosis Modified Parkland Formula- most commonly used 3-4 ml x % of TBSA 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 Maintenance fluid must be given in children – DNS 100ml /kg for 24 hrs for first 10 KG 50 ml/Kg for next 10 Kg 20 ml/kg for each kg over 20kg
- 46. Hypertonic Saline Produces hyperosmolality and hypernatremia Reduction in shift to intracellular fluid to extracellular space Advantage- Less tissue edema Reduction in escharotomies and intubations Disadvantage – prolonged hypernatremia need careful monitoring 46
- 47. Colloid Resuscitation Albumin – most commonly used Mechanism- counteracts outward capillary hydrostatic pressure Administered after first 12 hours post burn Most common formula- MUIR AND BARCLAY formula Estimates amount of fluid need to be infused during first 36 hrs % of TBSA burn x weight in (kg) x 0.5 = one portion Total 6 portions given over 36 hrs 47
- 48. One infusion 4 hrly for 12 hrs (3 potions ) One infusion 6 hrly for 12 hrs (2 portions) Final infusion over 12 hrs Original formula used FFP as colloid of choice Disadvantage- Expensive Additional pressure on renal system 48
- 49. Common burn resuscitation formulas 49
- 50. Monitoring of resuscitation Avoid dynamic and rigid adherence to protocol Key monitoring of resuscitation is UO UO- Adult - 0.5 ml/kg/hr Children- 1ml/kg/hr Infant – 1-2 ml/kg/hr Vital Signs Heart rate and blood pressure CVP Level of Consciousness Reduced UO- 10ml/kg bolus, High UO- >2ml/kg/hr – reduce infusion
- 51. 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
- 52. Routes of Nutritional Support High-protein & high-calorie diet Often requiring various supplements Composition – 1-2 g/kg/day of protein Carbohydrate – stimulates insulin – anabolic role Routes: Enteral – preferred Parenteral – central TPN preferred TPN increases risk of infection Anabolic agent- Oxandrolone and propranolol
- 53. 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
- 54. BURN WOUND CARE
- 55. Burn Wounds Wound dressing – Protect damaged epithelium, minimize bacterial and fungal colonization Splinting action Occlusive to reduce evaporative loss Provide comfort Risk for Infection Skin first line of defense Necrotic tissue bacterial growth
- 56. choice of dressing – Superficial epidermal wound – no dressing indicated Topical salves to keep skin moist Analgesics for pain Partial thickness burn- Daily dressing with topical antibiotics, cotton gauze and elastic wraps or Longer lasting antimicrobial dressing Deep partial thickness or full thickness burn Occlusive antimicrobial dressing Excision and grafting 56
- 57. Burn Wound Care Antimicrobial Agent Salves: requires frequent dressing change 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
- 58. Burn Wound Care Bacitracin/ Neomycin/ Polymyxin B - not broad spectrum, painless, easy to apply Nystatin(Mycostatin) - antifungal Mupirocin(Bactroban) - anti staphylococcal
- 59. Burn Wound Care Soaks Silvernitrate 0.5%,5% Mafenide acetate, Dakin’s solution, Domboro’s solution Can be added without changing dressing , underlying skin can become macerated Acticoat (antimicrobial occlusive dressing) A silver impregnated gauze that can be left in place for 5-7 days Moist with sterile water only; remoisten every 3-4 hours
- 60. 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
- 61. Synthetic and biologic dressing Allograft (cadaver skin), Biobrane, suprathel and dermal equivalent products Advantage Provides stable coverage without painful dressing change Decreases pain in wound Barrier to evaporative loss Do not inhibit epithelisation Applied with in 72 hrs of injury before bacterial colonization Used to cover second degree wound or full thickness wound 63
- 62. Biologic dressing remains for weeks without rejected in burn patients. Used in partial thickness burn >50% TBSA Disadvantages – transmission of viral diseases and residual mess Biobrane – collagen coated silicone manufactured in to sheet Adhered to burn wound with dried wound transudate with in 24- 48 hrs No antimicrobial activity Dermal equivalents – Collagen matrix ( dermal substitute) + Silicone sheet(epidermal substitute) 64
- 63. 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
- 64. 66
- 65. Full thickness and Deep burn Treatment Echarotomy Torniquet like effect of circumferential burn. Tissue pressure >30mmhg Performed bedside using scalpel or electro cautery Incision on lateral or medial aspect of extremities Whole length of eschar incised longitudinally Complication – hyperemia and edema formation Hypotension 67
- 67. 69
- 68. Excision and Grafting No advantage of unexcised eschar Early burn excision advantage- utilisation of window period Anaesthetic window Hemodynamic window (minimal blood loss) Bacterial window Staged approach – excision in first week of burn 20% burn wound per operation 70
- 69. Performed with torniquet and application of epinephrine (1:100000) Tumescence fluid injected in both donor and eschar site Deep dermal burn- tengential excision until punctate bleeding observed Full thickness burn- full excision of skin up to viable fat meshing of the graft- to reduce size of donor site 20 to 30 % TBSA- not meshed or narrow ratio(2:1) meshing Extensive burn – higher ratios ( 3:1 to 9:1 ) Mesh pattern Scarring Loss of skin graft- Inadequate excision, shearing forces, fluid accumulation, Infection Alternative to skin Graft- cultured keratinocytes 71
- 70. 72
- 71. COMPLICATIONS
- 72. Burn Wound Infection Focal/ multi focal/ generalized More the area of infection ↑chances of septicemia Common org- Strep, Staph & Pseudomonas
- 73. 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
- 74. 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
- 75. Management Topical anti microbial therapy - Mafenide acetate - Silver sulfadiazine - Silver nitrate Systemic antibiotics Eschar excision & covering with biological dressings
- 76. Burn Sepsis Host & opportunistic organism balance altered Immunologic alteration Defect in cell-mediated immunity Abnormal activation of complement pathway
- 77. 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
- 78. Burn Sepsis 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
- 79. Burn Sepsis 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)
- 80. Burn Sepsis Identify & document infection: Culture positive infection Pathologic tissue source identified Clinical response to antimicrobials
- 81. Clinical Manifestations Hyperthermia, Hypothermia (later) Tachycardia Increased ventilation High cardiac output Leucocytosis Thrombocytopenia Hypotension & oliguria
- 82. Treatment Definitive wound excision Antibiotics Supportive Care
- 83. THANK YOU 85