This document provides information on the pathophysiology and treatment of burns. It discusses the local and systemic effects of burns including cardiovascular, renal, pulmonary, gastrointestinal and immune responses. It describes methods of assessing burn severity including depth of burn and percentage of total body surface area burned. Treatment involves fluid resuscitation according to the Parkland formula, wound care, infection control, nutrition and management of complications like multiorgan failure.
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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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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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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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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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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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
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
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.
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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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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
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
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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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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