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![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](https://image.slidesharecdn.com/burns-160419144753/85/Burns-Pathophysiology-Evaluation-and-Management-38-320.jpg)
![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](https://image.slidesharecdn.com/burns-160419144753/85/Burns-Pathophysiology-Evaluation-and-Management-51-320.jpg)
![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](https://image.slidesharecdn.com/burns-160419144753/85/Burns-Pathophysiology-Evaluation-and-Management-52-320.jpg)
Uploaded byAnkit Sharma
Burns Pathophysiology, Evaluation and Management
09 x 2 Genitalia - 01 Total Body Surface Area - 100 63 Evaluation History Mechanism of injury Time of injury Associated inhalational injury Past medical history Medications 64 Evaluation Examination Primary survey Airway, Breathing, Circulation Secondary survey Head to toe examination Assessment of TBSA involved Depth of burn Associated injuries 65 Evaluation Investigations Hematological
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Burns Pathophysiology, Evaluation and Management
- 1. BURNS – PATHOPHYSIOLOGY, EVALUATION & MANAGEMENT DRARUN KUMAR M GUIDE : DR S MEHROTRA DR ANKIT SHARMA MS (GEN SURG), MCH (PLASTIC SURGERY) 1
- 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. Definition Injuries that resultfrom direct contact or exposure to any physical, thermal, chemical, electrical, or radiation source are termed as Burns. 3
- 4.
- 5. Historical Perspective Firstdirect 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. Historical Perspective 1607: GF Hildanus : Pathophysiology of Burns 1797 : Edward Kentish : Chronic Burn scar Marjolin’s ulcer 6
- 7. Historical Perspective 19thcentury : Dupuytren’s classification based on depth 1842 : Curling : Gastric & Duodenal Ulceration Thomas Blizard CurlingBaron Guillaume Dupuytren 7
- 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. Historical Perspective 1951: 45% TBSA Burns 49% mortality Present : > 70 % TBSA 49 % mortality Focus of advance : Improved survival Rehabilitation of Burn survivors 9
- 10.
- 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. 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. 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.
- 15. Classification Based onCause Thermal Electrical Chemical Radiation Inhalation 15
- 16. Thermal Injuries Mostcommon 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. Thermal Injuries Flame Direct contactwith 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. Electrical Burns Usuallyfollows 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. Electrical Burns Severitydepends 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. Electrical Burns Low-tensioninjuries(<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. Electrical Burns High-tensioninjuries(>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. Electrical Burns Lightning HIGH VOLTAGE!!! Injury may result from Direct Strike Side Flash Severe injuries often result 22
- 23.
- 24. Electrical Burns Manifestations:- External Burn Internal Burn Musculoskeletal injury Cardiovascular injury Respiratory injury Neurologic injury Rhabdomyolysis and Renal injury 24
- 25.
- 26. Chemical Burns Usuallyassociated 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. 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. Chemical Burns Systemicabsorption of offending agents causing metabolic derangements Formic acid – haemolysis, Haemoglobinuria Hydrofluoric acid – hypocalcemia 28
- 29. Radiation Exposure Wavesor 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. Radiation Exposure Gammaradiation & X-rays Most dangerous penetrating radiation May produce localized skin burns & extensive internal damage 30
- 31. Classification Based onDepth I Degree - Epidermis II Degree - Epidermis+ Dermis III Degree - Epidermis+ Dermis + Subcutaneous tissue IV Degree - Above + Muscles/bone 31
- 32. Classification Degree of Burn 1st Degree2nd 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.
- 34.
- 35. Pathophysiology : LocalEffects 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. Pathophysiology : LocalEffects Zone of hyperemia Viable tissue, not at risk for further necrosis 37
- 37. Pathophysiology : LocalEffects 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. Pathophysiology : LocalEffects 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. Clinical Significance Formationof constricting eschars & requirement of emergency escharotomy 40
- 40. Pathophysiology : LocalEffects 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. Pathophysiology : LocalEffects 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. Pathophysiology : LocalEffects Mediator Local effect Systemic effect CRF Inhibitory to other factors 43
- 43. Pathophysiology : SystemicEffects 44 > 30 % Burns in adults
- 44. Pathophysiology : SystemicEffects Hemodynamic consequences Reduced cardiac output • Impaired electrical activity of muscle • Vasoconstriction of peripheral vesselsInitial phase • Hypovolemia • Reduced venous returnDelayed phase 45
- 45. Pathophysiology : SystemicEffects Hemodynamic consequences Myocardial dysfunction : O2 derived free radicals (mechanism unclear) Increased systemic vascular resistance & organ Ischemia ( Renal & GI system) 46
- 46. Pathophysiology : SystemicEffects 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. Clinical Significance Importanceof Emergency & Adequate Resuscitation 48
- 48. Pathophysiology : SystemicEffects GI system Mucosal atrophy Increased intestinal permeability Decreased absorption of glucose, amino acids & fatty acids 49
- 49. Clinical Significance Curling’sulcer : Prophylaxis 50
- 50. Pathophysiology : SystemicEffects 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. Pathophysiology : SystemicEffects Hypermetabolic response Phase I [ebb] First 48 hrs Decrease in cardiac output urine output O2 consumption BMR Impaired glucose tolerance with hyperglycemia 52
- 52. Pathophysiology : SystemicEffects 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. Clinical Significance Importance ofTechniques of early excision Nutritional support 54
- 54. Pathophysiology : SystemicEffects 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. Pathophysiology : SystemicEffects 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.
- 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. Pathophysiology : Oropharynx Heat Denaturationof 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. Pathophysiology : Tracheo-bronchialareas 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. Clinical Significance Importantto identify respiratory insult & Early Intubation in case required. 61
- 61.
- 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.
- 64.
- 65. Lund and BrowderCharts 66
- 66. Palm Method Sizeof Patient’s palm 1% of TBSA Irregular wounds with scattered distribution. 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.
- 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. 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. 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. PRE HOSPITAL MANAGEMENT PRIMARYASSESSMENT 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. PRE HOSPITAL MANAGEMENT PRIMARYASSESSMENT 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. PRE HOSPITAL MANAGEMENT PRIMARYASSESSMENT Pulse rate better monitor than BP Spinal immobilization: Explosion/ deceleration injury Cervical collar (Philadelphia collar)
- 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. 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. 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. PRE HOSPITAL MANAGEMENT SECONDARYASSESSMENT 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. PRE HOSPITAL MANAGEMENT SECONDARYASSESSMENT 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. HOSPITAL MANAGEMENT INITIAL CAREFACILITY C – A – B Establish adequate airway ET intubation – impending airway edema (post initiation of IV therapy) Maintain cervical spine immobilization
- 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. 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. 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
- 85. ESCHAROTOMY Elevate limbsabove 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
- 86. 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
- 87. RECEPTION • Resuscitation –ensureABC • 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
- 88. Respiratory Care Assessairway, 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
- 89. Cardiovascular Care Increasecapillary 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
- 90. Severity of BurnInjuries 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
- 91. OUTCOME PROGNOSIS (Baux Score) Sumof Age in years + Area of burn in % TBSA < 80 good 80-100 life threatening >100 bad
- 92. Resuscitation Phase First24-48 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
- 93.
- 94. Parkland Formula Fluidof 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
- 95. Parkland Formula Maximumapplicable TBSA – 50% Fully dilated capillaries Maximum capillary permeability No further mounting of inflammatory response
- 96. 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
- 97. 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
- 98. Pediatric age group CarvajalFormula 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
- 100. Assessment of Adequacyof 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
- 101. RESUSCITATION FAILURE Delayedresuscitation Electric burns Inhalation injury Escharotomy Carbon monoxide poisoning Elderly patients
- 102. Nutritional Support Burnwounds 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
- 103. Routes of NutritionalSupport 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
- 104. Nutritional Support Formulas toPredict 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
- 105.
- 106. Burn Wounds Risk forInfection Skin first line of defense Necrotic tissue bacterial growth Management Burn wounds are frequently monitored for bacterial colonization Wound swab cultures and invasive biopsies
- 107. Role of burnwound 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.
- 108. 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
- 109. Burn Wound Care AntimicrobialAgent 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
- 110. Burn Wound Care Antimicrobialagent Bacitracin/ Neomycin/ Polymyxin B - not broad spectrum, painless, easy to apply Nystatin(Mycostatin) - antifungal Mupirocin(Bactroban) - anti staphylococcal
- 111. 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
- 112. Soak silver dressingsand gauze in WATER (not saline). Apply the silver dressing. Wrap with moist gauze. Secure with mesh, gauze or tape.
- 113. 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
- 114. 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
- 115. Burn Wound Care Coverwith 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
- 116. Burn Wound Care Debridementof 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
- 117. Why excise theburn? 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
- 118. Timing of surgery “Ultraconservative” Conservative Early Acute 119
- 119. Urgent surgery High-tension electricalinjury Deep encircling burns - escharotomy limbs trunk 120
- 120. For small burns 121 Excisionand grafting as soon as possible clearly non-healing
- 121. Early excision ofburns 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
- 122. TANGENTIAL BURN EXCISION &EARLY SPLIT SKIN GRAFTING 123
- 123. 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
- 124. Early burn surgery Superioroutcomes where suitably equipped mortality length of hospital stay morbidity during acute burn scar quality 125
- 125. 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
- 126. 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
- 127. Burn Wound Closure PermanentSkin 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
- 128. 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
- 129.
- 130. Burn Wound Closure TemporarySkin 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.
- 131. Types of temporarySkin Grafts Biosynthetic- Homograft (cadaveric)/ Xenograft (porcine) Artificial Skins (collagen based)- Trancyte/ Integra Synthetic – Biobrane/Opsite
- 132. Burn Wound Closure BiosyntheticTemporary 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
- 133. Biosynthetic Temporary SkinGrafts 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
- 134. Biosynthetic Temporary SkinGrafts 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
- 135. Biobrane Artificial dressinghas 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
- 136. Donor Site: WoundConsiderations 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
- 137.
- 138. Burn Wound Infection Focal/ multi focal/ generalized More the area of infection ↑chances of septicemia Common org- Strep, Staph & Pseudomonas
- 139. 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
- 140. Clinical Signs ofBurn 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
- 141. Management Topical antimicrobial therapy - Mafenide acetate - Silver sulfadiazine - Silver nitrate Systemic antibiotics Eschar excision & covering with biological dressings
- 142. Burn Sepsis Host& opportunistic organism balance altered Immunologic alteration Defect in cell-mediated immunity Abnormal activation of complement pathway
- 143. Sepsis inburn 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
- 144. III. Progressivetachypnea 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
- 145. 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
- 146. Identify &document infection: Culture positive infection Pathologic tissue source identified Clinical response to antimicrobials Burn Sepsis
- 147. Clinical Manifestations Hyperthermia,Hypothermia (later) Tachycardia Increased ventilation High cardiac output Leucocytosis Thrombocytopenia Hypotension & oliguria
- 148. Treatment Definitive wound excision Antibiotics Supportive Care
- 149.
- 150. Begins dayone 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
- 151. 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
- 152. Contracture Formation Shrinkageand 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
- 153. Psychosocial Considerations Alterations inBody 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
- 154.
- 155. RAs (grafts) Liposomalgene 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
- 156. RAs (grafts) ARTIFICIALSKIN 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
- 157. 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
- 158. BURNS !!! B Breathing UUrinary output R Rule of Nines & Resuscitation with fluid N Nutrition S Shock & Silvadene
- 159. References Total BurnCare; 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
- 160.