Burns

All about burns

1. BURNS Dr Vipin V Nair 1

2. OVERVIEW Part I Historical perspective Statistics Classification of Burns Pathophysiology Evaluation 2 Part II Management Pre-hospital Care Resuscitation & Nutritional support Burn wound care Complications Rehabilitation

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. HISTORICAL PERSPECTIVE 4

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. Historical Perspective 1607 : GF Hildanus : Pathophysiology of Burns 1797 : Edward Kentish : Chronic Burn scar  Marjolin’s ulcer 6

7. Historical Perspective 19 th century : Dupuytren’s classification based on depth 1842 : Curling : Gastric & Duodenal Ulceration 7 Thomas Blizard Curling Baron Guillaume Dupuytren

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 9

10. 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) 10

11. CLASSIFICATION 11

12. Classification Based on Cause Thermal Electrical Chemical Radiation Inhalation 12

13. Thermal Injuries Most common Types : Dry & wet Contact Direct contact with hot object (pan or iron) Anything that sticks to skin (i.e. tar, grease or foods) 13

14. 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 14

15. 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 15

16. 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 16

17. 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 17

18. 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 18

19. Electrical Burns Lightning HIGH VOLTAGE!!! Injury may result from Direct Strike Side Flash Severe injuries often result 19

20. Electrical Burns 20

21. Electrical Burns Manifestations:- External Burn Internal Burn Musculoskeletal injury Cardiovascular injury Respiratory injury Neurologic injury Rhabdomyolysis and Renal injury 21

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23. 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 23

24. Chemical Burns 24

25. Chemical Burns Systemic absorption of offending agents causing metabolic derangements Formic acid – haemolysis , Haemoglobinuria Hydrofluoric acid – hypocalcemia 25

26. 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 26

27. Radiation Exposure Gamma radiation & X-rays Most dangerous penetrating radiation May produce localized skin burns & extensive internal damage 27

28. Classification Based on Depth I Degree - Epidermis II Degree - Epidermis+ Dermis III Degree - Epidermis+ Dermis + Subcutaneous tissue IV Degree - Above + Muscles/bone 28

29. 29 Classification Degree of Burn 1 st Degree 2 nd Degree Partial Thickness 2 nd Degree Deep Burns 3 rd Degree 4 th 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

30. 30 Classification Degree of Burn 1 st Degree 2 nd Degree Partial Thickness 2 nd Degree Deep Burns 3 rd Degree 4 th Degree Involvement Epidermis Epidermis + Dermis E+ D E+D+Subcut tissue E+D+S+muscles , tendons & bone Appearance Red to Pink Dry, No Blisters Red to pink, Wet and weeping wounds Thin-walled, fluid-filled blisters Mottled: Red, pink, or white area Moist Dry, leathery & rigid, Eschar (hard and in-elastic) Red, white, yellow or black Black (dry, dull and charred) Eschar tissue: hard, inelastic Symptoms & Signs Pain ++ Pain ++++ Painful - less severe Painless & insensitive to palpation, 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

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32. PATHOPHYSIOLOGY 32

33. Pathophysiology : Local Effects 33 JACKSON’s burn zones

34. Pathophysiology : Local Effects Burn wound edema Biphasic pattern Burn shock : >1/3 rd of TBSA Hypovolemia + Rapid edema formation 34 1 st Hr 12-24 Hrs Immediate & Rapid increase in edema Gradual increase

35. 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 35

36. Clinical Significance Formation of constricting eschars & requirement of emergency escharotomy 36

37. Pathophysiology : Local Effects 37 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

38. Pathophysiology : Local Effects 38 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

39. 39 Pathophysiology : Systemic Effects > 30 % Burns in adults

40. Pathophysiology : Systemic Effects 40

41. Pathophysiology : Systemic Effects Hemodynamic consequences Myocardial dysfunction Increased systemic vascular resistance & organ Ischemia ( Renal & GI system) 41

42. Pathophysiology : Systemic Effects Renal system 42

43. Clinical Significance Importance of Emergency & Adequate Resuscitation 43

44. Pathophysiology : Systemic Effects GI system Mucosal atrophy Increased intestinal permeability Decreased absorption of glucose, amino acids & fatty acids 44

45. Clinical Significance Curling’s ulcer : Prophylaxis 45

46. 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 46

47. 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 47

48. 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 48

49. Clinical Significance Importance of Techniques of early excision Nutritional support 49

50. 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) 50

51. 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) 51

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53. 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 53

54. 54 Pathophysiology : Oropharynx

55. 55 Pathophysiology : Tracheo -bronchial areas

56. Clinical Significance Important to identify respiratory insult & Early Intubation in case required. 56

57. EVALUATION 57

58. Wallace’s Rule of “9” 58

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60. Palm Method Size of Patient’s palm  1% of TBSA Irregular wounds with scattered distribution . 60

61. MANAGEMENT OF BURNS

62. PHASES OF TPT

63. PRE HOSPITAL MANAGEMENT Rescuer to avoid injuring himself Remove patient from source of injury Stop burn process

64. Burning clothing; jewelry, watches, belts to be removed Pour ample water on burnt area (not ice/ ice packs – skin injury & hypothermia) 64

65. PRE HOSPITAL MANAGEMENT

66. 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 O 2 if no obvious resp distress

67. PRE HOSPITAL MANAGEMENT PRIMARY ASSESSMENT ET intubation + assisted ventilation with 100% O 2 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)

68. PRE HOSPITAL MANAGEMENT PRIMARY ASSESSMENT Pulse rate better monitor than BP Spinal immobilization: Explosion/ deceleration injury Cervical collar (Philadelphia collar)

69. 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.

70. 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

71. PRE HOSPITAL MANAGEMENT

72. PRE HOSPITAL MANAGEMENT

73. 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

74. HOSPITAL MANAGEMENT INITIAL CARE FACILITY

75. INITIAL CARE FACILITY

76. INITIAL CARE FACILITY

77. ESCHAROTOMY Deep 2 nd & 3 rd 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

78. 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

79. 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

80. Resuscitation –ensure ABC Large gauge I.V catheter Central line Insertion Foleys catheter and NG tube placement Quick assessment of extent Tetanus prophylaxis (the only IM administered inj ) Weigh the patient

81. Respiratory Care Assess airway, respiration & breath sounds Removal of pulmonary secretions O 2 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

82. 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

83. 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

84. OUTCOME PROGNOSIS ( Baux Score) < 80 good 80-100 life threatening >100 bad Sum of Age in years + Area of burn in % TBSA

85. Resuscitation Phase

86. PARENTERAL FLUIDS

87. 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

88. Parkland Formula Maximum applicable TBSA – 50% Fully dilated capillaries Maximum capillary permeability No further mounting of inflammatory response

89. Adult Fluid Resuscitation

90. Adult Fluid Resuscitation

91. Pediatric age group

92. 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

93. RESUSCITATION FAILURE

94. Nutritional Support

95. 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

96. 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

97. BURN WOUND CARE

98. 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

99. 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 >10 6  high risk of infectious & graft failure.

100. 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

101. 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

102. Burn Wound Care Antimicrobial agent Bacitracin/ Neomycin/ Polymyxin B - not broad spectrum, painless, easy to apply Nystatin( Mycostatin ) - antifungal Mupirocin(Bactroban) - anti staphylococcal

103. 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

104. Soak silver dressings and gauze in WATER (not saline). Apply the silver dressing. Wrap with moist gauze. Secure with mesh, gauze or tape.

105. Burn Wound Care

106. 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

107. 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

108. 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

109. 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 111 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

110. Timing of surgery “Ultraconservative” Conservative Early Acute 112

111. Urgent surgery High-tension electrical injury Deep encircling burns - escharotomy limbs trunk 113

112. For small burns Excision and grafting as soon as possible Clearly non-healing 114

113. 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 115

114. TANGENTIAL BURN EXCISION & EARLY SPLIT SKIN GRAFTING 116

115. TANGENTIAL BURN EXCISION & EARLY SPLIT SKIN GRAFTING 117

116. Early burn surgery Superior outcomes where suitably equipped Mortality Length of hospital stay Morbidity during acute burn Scar quality 118

117. 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 119

118. 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

119. 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

120. 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

121. Burn Wound Closure

122. 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.

123. Types of temporary Skin Grafts

124. 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

125. 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

126. Biosynthetic Temporary Skin Grafts

127. 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

128. 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

129. Burn Wound Infection Focal/ multi focal/ generalized More the area of infection  ↑ chances of septicemia Common org- Strep, Staph & Pseudomonas

130. 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

131. Clinical Signs of Burn Wound Infection 2 nd 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

132. Management

133. Burn Sepsis Host & opportunistic organism balance altered Immunologic alteration Defect in cell-mediated immunity Abnormal activation of complement pathway

134. Burn Sepsis Sepsis in burn pt  c oncern for infection. Age-dependent definition with adjustments for children The trigger includes 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)

135. Burn Sepsis

136. Burn Sepsis

137. Burn Sepsis Identify & document infection: Culture positive infection Pathologic tissue source identified Clinical response to antimicrobials

138. Clinical Manifestations

139. Treatment

140. Rehabilitation 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

141. 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

142. Contracture Formation

143. 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

144. 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

145. Take home message - BURNS !!! B B reathing U U rinary output R R ule of Nines & R esuscitation with fluid N N utrition S S hock & S ilversulfadiazine

146. THANK YOU 150