burns classification and management

1. BURNSBURNS
 Dr BINU K JOHN
 JR1
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2. BURNSBURNS
Destruction of skin by heat severe
local and systemic physiological alterations
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3. BURNSBURNS
Results in 10-20 thousand deaths
annually
Survival best at ages 15-45
Children, elderly, and diabetics
Survival best burns cover less than 20%
of TBA
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4. TYPES OF BURNSTYPES OF BURNS
Thermal
exposure to flame or a hot object
Chemical
exposure to acid, alkali or organic substances
Electrical
result from the conversion of electrical energy into heat.
Extent of injury depends on the type of current, the pathway of
flow, local tissue resistance, and duration of contact
Radiation
result from radiant energy being transferred to the body
resulting in production of cellular toxins
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5. Chemical BurnChemical Burn
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6. ElectricalElectrical BurnBurn
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7. BURN WOUNDBURN WOUND
ASSESSMENTASSESSMENT
Classified according to depth of injury and
extent of body surface area involved
Burn wounds differentiated depending on the
level of dermis and subcutaneous tissue
involved
1. superficial (first-degree)
2. deep (second-degree)
3. full thickness (third and fourth degree)
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8. Depth of burnsDepth of burns
First degree : limited to epidermis
Second degree : (Partial thickness)
 superficial partial thickness- epidermis and
superficicial dermis(superficial to papillary
dermis)
 deep partial thickness- through epidermis and
into deep dermis(deep dermal)
Third degree : Full thickness
Fourth degree: fascia,muscle or bone is involved
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9. 9

10. SUPERFICIAL BURNSSUPERFICIAL BURNS
(FIRST DEGREE)(FIRST DEGREE)
Epidermal tissue only affected
Erythema, blanching on pressure, mild
swelling
no vesicles or blister
Not serious unless large areas involved
Eg; sunburn
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11. SECOND DEGREESECOND DEGREE
*Involves the epidermis and deep layer of
the dermis
Fluid-filled vesicles –red, shiny, wet, severe
pain
Hospitalization required if over 20% of
body surface involved
i.e. tar burn, flame
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13. FULL THICKNESS (THIRD/FOURTHFULL THICKNESS (THIRD/FOURTH
DEGREE)DEGREE)
Destruction of all skin layers
Requires immediate hospitalization
Dry, waxy white, leathery, or hard skin,
no pain
Exposure to flames, electricity or
chemicals can cause 3rd
degree burns
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14. 4/1/2011 14

15. 4/1/2011 15

16. 07/16/16 16
Extent of BurnsExtent of Burns
 Wallace’s rule of nines
◦ Easy to remember, quick method

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19. 07/16/16 19
Lund & Browder
More accurate, more time spent
calculating TBSA burned

20. Lund Browder Chart used forLund Browder Chart used for
determining BSAdetermining BSA
4/1/2011 20Evans, 18.1,

21. Pathophysiology of burnsPathophysiology of burns
Burn coagulative necrosis of
epidermis and underlying tissues
Depth depends on temperature,duration of
exposure and specific heat of the
causative agent
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22. Zones of injuryZones of injury
Zone of coagulation – irreversibly
damaged tissue
Zone of stasis – moderately damaged
with decreased tissue perfusion
Zone of hyperaemia – area of
vasodilatation from which healing process
begins
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23. 23

24. Local burn injuryLocal burn injury
Cytological damage due to protein
denaturation by rising temperature
Temp in excess of 45 degree C
blockage of thermolabile enzymes
 When enzymatic activity to 50% of
normal, cell death occurs
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25. Local injury (cont’d)Local injury (cont’d)
Factors which determine the extent of
injury other than thermal insult are
Blood supply
Additional trauma
Oedema
Microbial invasion
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26. Local inflammatory responseLocal inflammatory response
Both immediate & delayed vascular & cellular
immune response
Mediators – histamine, bradykinin, vasoactive
amines, prostaglandins, leukotrienes, activated
compliment & catecholamines etc.
Thermal injury vasoconstriction of arterioles
& venules and dilatation of capillaries
Capillaries & venules become permeable
leakage of fluid, electrolytes and proteins
Most rapid fluid loss occurs in the first 12 hours
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27. Systemic responseSystemic response
Drop in cardiac ouput of upto 50%
Increased interstitial pressure and injured
basement membrane massive oedema
Direct toxic effect
Nearly total body capillary permeability occurs
in pts. With >30% burn
Fluid enters a functional third space
Burn shock
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28. Cardiovascular responseCardiovascular response
(cont’d)(cont’d)
Besides the fluid portion cellular elements also have
predictable response
Progressive anaemia- due to direct destruction of
RBCs by heat, malfunction of normal hypoxic
response, red cell trapping by RE system and losses
through increased capillary permeability
Initial thrombocytopenia followed by
thrombocytosis and hypofibrinogenaemia
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29. Renal responseRenal response
High levels of ADH maximal water
reabsorption
Maximum Na reabsorption due to aldosterone
release from adrenals
Increased amounts of myoglobin ,haemoglobin
and toxic products acute tubular necrosis
unless adequate GFR is maintained.
This results in acute renal failure
Myoglobin is the most injurious agent
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30. Pulmonary responsePulmonary response
Heat can cause damage to upper airway
 oedema and obstruction
Hypoxia can lead to release of injurios free oxygen
radicals and arachidonic acid metabolites
When cardiac output falls, vascular space contracts
ventilation-perfusion imbalance
During resuscitation large volumes of salt containing
fluids can make chest wall heavy and difficult to
move or even pulmonary oedema
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32. Gastrointestinal responseGastrointestinal response
Splanchnic vasoconstriction
Acute gastric dilatation, vomiting, gastric
mucosal ulceration curling’s ulcer
Translocation of gut bacteria
Liver function is altered in major burns
Early enteral feeding serves to protect
the GIT
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33. Neuroendocrine responseNeuroendocrine response
Adrenaline and noradrenaline as a protective
mechanism
But catecholamine mediated hypermetabolism,
tachycardia and hyperdynamic cardiac activity
may lead to postburn cardiac dysfunction and
death
Glucocorticoids and mineralocorticoids are also
elevated
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34. Metabolic-nutritional responseMetabolic-nutritional response
Metabolic rate of burn victim is greatly accelerated
Oxygen consumption
Nitrogen losses
Proteolysis Lipolysis Gluconeogenesis
Evaporative water losses increase at tremendous
energy expense body cooling and shivering
which adds to energy demands
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35. Immune responseImmune response
In burns both cellular & humoral immunity is
depressed
Overall lymphopenia, decrease in IL-2, delayed
rejection of allograft skin suggest impaired
cellular immunity
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36. Cellular immune deficiencyCellular immune deficiency
Lymphocyte depressor substances
 arachidonic acid metabolites
 interferons
 bactrial endotoxin
 cutaneous burn toxin
denatured protein
Corticosteroids
Histamine
Immunoglobulins,immune complexes
Antibiotics 36

37. TreatmentTreatment
Prehospital
Remove from the source of injury
Ensure rescuer safety
Cool the burn wound, avoid hypothermia
All rings, jewelry,watches and belts
should be removed
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38. Evaluation of burn victimEvaluation of burn victim
Airway
Breathing and ventilation
Circulation
Disability
Fluid resuscitation
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39. AirwayAirway
Burned airway creates symptoms by
swelling
Early intubation in suspected airway burn
is safest
Clues of airway burn- blisters on hard
palate, burned nasal mucosa, loss of hair
in the nose and deep burns around the
mouth and in neck
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41. BreathingBreathing
Inhalational injury-due to smoke inhalation
Suspect in those trapped in fire, presence of
soot in nose
C/F-increasing respiratory effort and rate, rising
pulse, anxiety and confusion and decreasing O2
saturation
Symptoms develop as late as 24 hrs to 5 days
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42. Treatment of inhalational injuryTreatment of inhalational injury
Physiotherapy
Nebulisers
Warm humidified O2
Blood gas measurements
PPV if condition deteriorates
COHb of > 10% high inspired O2
Mechanical block to breathing from FTB
escharotomy
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44. Major determinants of outcome ofMajor determinants of outcome of
burnburn
Percentage of surface area involved
Depth of burns
Presence of an inhalational injury
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45. Fluid resuscitationFluid resuscitation
Sufficient volume to be infused to maintain perfusion
not only to vital organs but also to damaged skin
I/V resucitation is indicated in burns of > 10%in
children and > 15% in adult
Types of fluid used – Ringer lactate(Hartman’s
solution),Human albumin or FFP, and hypertonic
saline
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46. Contd..Contd..
 The principle is to maintain IV vol. at a state
sufficient to perfuse all vital organs.
 Fluid loss depends on BSA involved.
 Replacement should be started if 10-15% BSA is
involved.

47. PARKLAND FORMULAPARKLAND FORMULA
 Dr.Charles Baxter of PARKLAND Hospital
 Total vol. in first 24 hrs=
4ml/Kg Body Weight/% of burn TBSA
 Half in first 8hrs
 Next half in next 16 hrs
 Area more than 50% is taken as 50%

48. TIME DEPENDENT VARIABLES SHOULD BETIME DEPENDENT VARIABLES SHOULD BE
CALCULATED FROM TIME OF BURNSCALCULATED FROM TIME OF BURNS

49. MAINTANENCEMAINTANENCE
 For next 24 hrs
 up to 10 kg-100ml/kg
 10-20kg-50ml/kg
 more than 20kg-20ml/kg

50. MonitoringMonitoring
 B.P, Pulse
 URINE OUTPUT
 b/w 0.5-1 ml/Kg/Hr
if below this-increase by 50%
below this+signs of hypoperfusion -10ml/Kg
Bolus

51. WHY RINGER LACTATE?WHY RINGER LACTATE?
 Composition
 Isotonic
 Low sodium
 High pH-6.5
 Buffering effect of lactate

52. Role of COLLOIDSRole of COLLOIDS
 Usually in 2nd 24 hr
 After capillary leak has subsided
 Mostly in
burns >40%
heart diseases
inhalational injuries
geriatric age group

53. COLLOIDSCOLLOIDS
 ALBUMIN-5%

54. Muir and BarclayMuir and Barclay FormulaFormula
 estimates the amount of fluid that needs to be infused during
the first 36 hours after a major burn.
 It divides up the total time into six periods of varying duration.
Each period requires the same volume of fluid.
 The volume for each period is calculated from the following
formula: (weight in kilograms multiplied by the percentage total
body surface area of the burn) divided by two.

55. Each infusion volume is given as follows:
first 12 hours - 3 infusions at 4 hour intervals
second 12 hours - 2 infusions at 6 hour intervals
third 12 hours - 1 infusion
The Muir and Barclay Formula was described for
albumin as the resuscitation fluid. It tends to give
less fluid per unit time than the Parkland Formula
favoured by the British Burns Association.
55

56. BROOKE FORMULABROOKE FORMULA
FIRST 24 HOURS
RL 1.5ml/kg/%burn
COLLOID – 0.5ml/kg/%
GLUCOSE IN WATER – 2000ml
SECOND 24 HOURS
RL - .5ml/kg/%burns
Colloids 0.25ml/kg/%burns
Glucose in water same as first 24hour

57. EVANS FORMULAEVANS FORMULA
 FIRST 24 HOURS
 N.S. – 1ml/kg/%burns
 COLLOID – 1ml/kg/%burns
 GLUCOSE IN WATER – 2000ml
 SECOND 24 HOURS
 HALF OF FIRST HOUR REQUIREMENT

58. Treatment of the burn woundTreatment of the burn wound
Tetanus prophylaxis
Escharotomy- in circumferential FTB
FTB and obvious deep dermal burn – require
operative treatment for excision and skin grafting
Till then managed by antibacterial dressing to
prevent or delay bacterial colonisation
Most common dressings for FTB and
contaminated burns -1% silver sulfadiazine cream,
silver nitrate solution(0.5%),Mafenide acetate,
bacitracin ,neomycin, polymyxin B,mupirocin etc
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59. Superficial partial thickness andSuperficial partial thickness and
mixed depth woundsmixed depth wounds
Superficial PTB heal irrespective of the dressing
Borderline deep dermal burns may heal without
scar if properly dressed with suitable dressing
 Topical antimicrobial dressing,synthetic and
biological dressings like allograft(cadaver skin),
xenograft (pig skin), amniotic membrane,
Transcyte, Biobrane,Integra are different
options available
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60. Other aspects of treatmentOther aspects of treatment
Analgesia- Oral or Intravenous
Can range from Paracetamol and NSAID
to opiates depending on the severity of
pain
Powerful short acting analgesia before
dressing changes
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61. NutritionNutrition
Hypermetabolism occurs after severe burn as high as
200% the BMR
High demand is met by mobilisation of carbohydrate, fat
and protein stores muscle wasting and wt. Loss
Malnutrition leads to functional impairment of many
organs and delayed wound healing
Diet may be given either enterally or parenterally
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62. Control of infectionControl of infection
Burns patients are immunocompromised
Burn wound,oedematous lungs and gut, monitoring lines
and catheters provide portals for infection
Temp>38.5deg.C, leukocytosis,thrombocytosis
Increasing signs of catabolism are indicative of infection
Control of infection is guided by regular swab cultures,
cultures from catheter tips and sputum
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63. Multiorgan failureMultiorgan failure
Most of the deaths in severe burns are
attributable to MOF
MOF is the sequela of systemic inflammatory
response syndrome caused by variety of severe
clinical insults like infection, burns, pancreatitis,
shock, trauma, ischemia, immune mediated organ
injury
Carries high mortality
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64. Hubbard TankHubbard Tank

65. Moist Wound HealingMoist Wound Healing
 A landmark study in1962 proved that partial thickness wounds re-
epithelialized more rapidly under occlusive dressings with the reason being
that occlusive dressings maintained a moist wound surface.
 Wound bacterial colonization which can occur in a moist healing
environment did not appear to retard healing or cause sepsis
 Fluid layer on wound surface increases not only the rate of re-
epithelialization, but all aspects of healing

66. Burn ScarBurn Scar
 PREVENTION OF HYPERTROPHIC SCAR
Early wound closure
- Temporary skin substitutes
- Skin grafting
- Permanent skin substitutes
- Wound protection

TREATMENT OF HYPERTROPHIC SCAR
Surgery Therapies
- excision- laser- cryotherapy
Biophysical Therapies
- compression- ultrasonic, scar massage
Pharmacologic Therapy
- corticosteroids- interferon - protein kinase C inhibitors

67. Wound CareWound Care
 SUPERFICIALTO MID-DERMAL BURNS
 Inspect daily
 If gauze adherent and no exudates, simply change outer dry gauze
 Change dressing, wash surface and reapply if exudates present
 Use topical antibiotic if infection considered

68. Wound CareWound Care
AREAS TREATED OPEN WITH BACITRACIN
 Reapply ointment two to three times daily
 Gently wash off crusts, exudates, especially on face and neck
AREAS COVERED WITH TEMPORARY SKIN SUBSTITUTES
 Change outer dry gauze daily to remove collected exudates
 Roll out small pockets of exudates from beneath substitute
 Can leave open without dressing once drainage has ceased if substitute well
adhered
 Remove skin substitute if exudate extensive or if nonadherent with topical agent
and change to grease gauze method

Remove once wound reepithelialized

69. Wound CareWound Care
DEEP BURNS

70. Wound Care
Why is Surgery Preferred for Deep Dermal Burns?
Primary healing of a deep dermal burn often leads to
hypertrophic scar or skin breakdown, especially if the burn
takes over 6 weeks to heal.

71. SURGICAL EXCISION & GRAFTINGSURGICAL EXCISION & GRAFTING
MANAGEMENTMANAGEMENT
GENERAL PRINCIPLES FOR BURN EXCISION AND GRAFTING
 The patient must be thermodynamically stable before considering excision
 The potential for significant blood loss must be recognized
 Pulmonary problems clearly present & require a plan of management in the
OR
 Hypothermia must be avoided during surgery
 The stress induced by anesthesia and surgery must be limited to that which
the patient can safely tolerate
 Significant blood loss in a major burn should be replaced with blood
products
Consists of Tangential Excision, Excision to fascia (Escharectomy),
escharotomy etc

72. Excision to FasciaExcision to Fascia

73. Skin substitutesSkin substitutes
INTEGRA®
Dermal Regeneration Template is a
two-layer skin regeneration system. The outer
layer is made of a thin silicone film that acts as
your skin's epidermis. It protects the wound from
infection and controls both heat and moisture
loss. The inner layer is constructed of a complex
matrix of cross-linked fibers. This porous
material acts as a scaffold for regenerating dermal
skin cells, which enables the re-growth of a
functional dermal layer of skin. Once dermal skin
has regenerated, the silicone outer layer is
removed and replaced with a thin epidermal skin
graft. This completes the procedure and leaves
you with flexible, growing skin.
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75. TranscyteTranscyte

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78. CURRENT USE OF ANTIBACTERIAL AGENTS INCURRENT USE OF ANTIBACTERIAL AGENTS IN
BURNSBURNS
Use of
Prophylactic
Topical
Antibiotic Cream

79. CURRENT USE OF ANTIBACTERIAL AGENTS IN BURNS
Use of Topical Antibiotics to Treat
Infection

80. Itch TreatmentItch Treatment
PHYSICAL APPROACH
 skin moisturizers
 compression garments
 cool baths
 massage therapy
PHARMACOLOGICAL APPROACH
 Oral Antihistamines
 Topical Anesthetic Agents
 Pain Medication
 Topical Doxepin Cream

81. RehabilitationRehabilitation
Goals: to limit loss of motion, prevent/minimize anatomical deformity, return
patient to work ASAP.

82. 83
Reconstructive Surgery
Early aggressive excision and skin grafting will decrease the requirement
for late secondary reconstructions
Usually deferred till hypertrophic scars mature except when there is
compromise of vital functions

83. Horizons in Burn CareHorizons in Burn Care
 Cultured epithelial grafts (CEA)

84. Stage A: Identify appropriate patient for
CEA (>50 percent total body surface area
(TBSA) limited donor sites)
Stage B: Obtain biopsy and send to
laboratory
Stage C: Wound preparation Total
excision completed by post-burn day five
to seven. All wounds covered with thick
cryo-preserved allograft.
Stage D: CEA Remove allograft epidermis85

85. Stage E: Postoperative care CEA exposed
to air two or more times a day.
Stage F: CEA takedown (Performed at
the bedside (POD seven to 10)
Stage G: Post-takedown resume
hydrotherapy. If wound cultures are
negative, use dry dressings. If wound
cultures are positive, then use topical
antimicrobials.
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