3. Burn its types and explanation about it.ppt

Topic about burn

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BURN
MANAGEMENT

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I. INTRODUCTION
A burn is a coagulative destruction of
the surface layers of the body caused by
heat, chemicals or irradiation.
For optimal outcome
multidisciplinary team approach
Burn center mx

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II. EPIDEMIOLOGY
More than 90 % of burns are caused by
carelessness or ignorance & are completely
preventable
Nearly half are smoking-or alcohol-related
Most affected groups are children & young
adults

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III. ETIOLOGY
A.SCALD BURNS
Scalds from hot water are the most common cause
of burn
Depth is proportional to temperature,
duration of contact & thickness of skin
eg. Water at 60
o
c for 3 sec
water at 69
o
c for 1 sec cause deep dermal or
full-thickness burn
Burns by thick soup
Immersion scalds are always deep, severe burns

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B. FLAME BURNS
Next most common
House fires, smoking related fires,
improper use of flammable liquids,
automobile accidents, ignition of clothing
from stoves or space heaters ,fall into
open fire

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C.FLASH BURNS
Explosion of natural gas,propane,gasoline
& other flammable liquids cause intense heat for
a brief time`
Depth depends on the amount and type of fuel
Clothing, unless it ignites, is protective against
flash burns
May be associated with thermal damage to the
upper airway

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D. CONTACT BURNS
Result from contact with hot metals,
plastic, glass or hot coals
Limited in extent & very deep

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E.CHEMICAL BURNS
Caused by strong acids or alkalis
Occurs as a result of industrial accidents,
assaults or improper use of harsh solvents
& drain cleaners
Cause progressive damage until they are
inactivated by reaction with the body
tissue or diluted with water

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Acid burns may be more self-limiting than
alkali burns
Chemical burns should be considered deep
dermal or full-thickness until proven
otherwise
Neutralizing agent shouldn’t be used

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F. ELECTRICAL BURNS
may be low-voltage or high-voltage
3 mechanisms of injury :
1.Electrical current injury
2.Electrothermal burns from arcing current
3.Flame burns caused by ignition of
clothes
Deep destruction of muscles ,nerves &
vessels –myoglobinuria --ATN
The entry & exit wound is only the tip of
the iceberg

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IV. BURN PREVENTION
More than 90 % of all burns are preventable by
using common sense & taking ordinary
precautions
Other measures
Flame-resistant sleepwear for children
Smoke detector in the house
Maximum temp. for home & public hot water
heaters be set below 60
o
c
Public announcements on TV regarding hot
water,carburetorflashes,cooking,scalds etc
Teaching at school for childern“stop drop & roll”

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V.PATHOPHYSIOLOGY OF BURN
Pathology
Three zones
Zone of coagulation :irreversible vessel
coagulation & no capillary blood flow
Zone of stasis :sluggish capillary blood flow
Zone of hyperemia :the usual inflammatory
response of healthy tissue to non-lethal injury

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Burn shock:
Tissue trauma release of mediatorsincrease
in vascular permeability or increase in
hydrostatic pressureincrease fluid
,electrolytes & plasma into the interstitial space
This process is maximum in the 1
st
8 hrs
Changes at the cellular level
Decrease ATPase activityincrease Na
+
&
water into the cell
Hypoproteinemia

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Clinical response
Decrease BV decrease COreflex
compensation by increase PR ,increase
cardiac work & decrease capacitance of
big veins
If not corrected early selective vc to the
skin ,muscle and gut and kidney
Irreversible shockdeath

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Metabolic response to burn injury
Hypermetabolism
Due to neuro-endocrine mediator response
(catecholamines are the major hormones)
Causes :increased heat loss from the burn
wound
increased B-adrenergic stimulation
Metabolic changes :
Increase gluconeogenesis esp from alanine
Increased glycogenolysis
Increased proteolysis

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Immune response to burn injury
1.Decrease cell-mediated immunity
2.Decrease humoral immunity
3.Decrease neutrophil activity (chemotaxis,
IC killing)

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VI. BURN SEVERITY &
CLASSIFICATOION
Depending on site, size, depth, associated
inhalational injury, associated Trauma ,comorbid
illness , age
MILD: 2
O
burn <15 % in adults

2
O
burn <10 % in children
3
0
burn < 2 %
MODERATE: 2
O
burn 15-25 % in adults
2
O
burn 10-20 % in children
3
0
burn < 10 %

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MAJOR: 2
O
burn >25 % in adults & > 20 % in
children
3
0
burn > 10 %
most burns involving hands, face,
eyes, ears, feet, perineum
most pts with inhalational injury,
electrical injury, complicated by other
major trauma
poor risk pts with burns

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Size of burn
Determined by
rules of 9 & 7
palm of the pt as 1 %
Lund & Browder (see fig.)

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Name--------Age--------Wt----------

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Classification by Depth of burn
First degree burn
involve only the epidermis
don’t blister
erythematous b/c of dermal Vasodilation
quite painful
the erythema & pain subside over 2 or 3
days
day 4 ,injured epithelium desquamates

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Second degree burn
Superficial dermal burns
include the upper layer of dermis
blisters
pink & wet when blisters are removed
painful
blanches with pressure
heal spontaneously in less than 3 wks
less scar
color mismatch in pigmented individuals

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Deep dermal burns
extend into the reticular layer of the
dermis
a mottled pink & white color
discomfort rather than pain
heal in 3 –9 wks
hypertrophic scarring

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Third degree burns (full-thickness burns)
involve all layers of the dermis
heal only by wound contracture, epithelization
from the edges or by skin grafting
appear white, cherry red or black
leathery
painless
doesn’t blanch
develop a classic burn eschar

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The assessment of burn depth
Standard technique ---clinical

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VII. RESPIRATORY INJURY
Smoke or thermal damage to respiratory
tree occurs in 30 %
3 types :
1.Carbon monoxide poisoning
2.Thermal injury
3.Smoke poisoning

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1.Carbon monoxide poisoning
60 –70 % of deaths from house fires
Pathophysiology
co has affinity for Hb 200x greater than
oxygen
co + Hb coHb
coHb interferes with oxygen delivery to
tissues

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Grading [co %] sxs
Mild < 20 .headache, mild dyspnea,
visual changes,
confusion
Moderate 20-40 .irritability, diminished
judgement, dim
vision, nausea, easy
fatigability
Severe 40-60 .hallucinations,
confusion,
ataxia, collapse, coma
Treatment :100 % oxygen

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2.Thermal airway injury
limited to the upper airway (above the
v.cords ) & trachea

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Risk pts for upper airway obstruction
.those injuries in an explosion with burns of
the face & upper torso
.those who have been unconscious in a fire
.mucosal burns of mouth, nasopharynx,
Larynx
oEarly endotracheal intubation for 3-5 days
until the edema subsides

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3.Smoke poisoning
Mechanism of injury :
-direct epithelial injury
-interference with aerobic respiration

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Diagnosis of inhalational injury:
Hx :fire in enclosed space,
burn in the face, wheezing ,
air hunger, excessive sputum
P/E :soot in the mouth & pharynx ,singed
nasal hair ,hoarseness ,wheeze,
carbonaceous sputum, acrid smell of
smoke in victims clothes
Lab :bronchoscopy ,CXR ,[CO], arterial o
2

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VIII. TREATMENT OF BURN
Care at the scene
-rescue of the burned victim
-remove the clothing
-airway mx
-CPR (if there is cardiac arrest)
-R/o other major trauma & give first aid
-application of cold water

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-keep the pt warm
-cover the wound with clean sheet
-transport to the nearby health facility

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Emergency room care
-ABC
-Fluid management
Indications :-children > 10 %
-adult >15 %
Formulae ( fig. )
1. Parkland : 4ml x wt(Kg) x % TBSA
burn
-Ringer’s lactate
2. Evans
3. Brooke
4. Modified Brook

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Pertinent Hx: -circumstance of burn
-medical Hx
-type of burn
-when & where the burn
occurs
Physical Exam : -a full P/E
-size of burn
Lab. Tests :Hct, glucose ,BUN, electrolyte,
blood gas, [co]
Patient monitoring during resuscitation:
-clinical : skin, uop
-laboratory :Hct

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-Tetanus prophylaxis
-Pain control with i.v. opiates
-Care of the burn wound:
Escharotomy (fig)
-chest escharotomy at the anterior axillary
line
-extermity escharotomy
.can be done as a bedside procedure
without local anesthesia

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Blister mx
Orthodox way of mx of wound
Daily washing
Removal of loose dead tissue
Topical application of saline-soaked dressings
until they heal by themselves or granulation
tissue appear in the base of the wound
Skin graft over the granulating wound after 3-8
wks after injury

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-Nutritional support
.Neuroendocrine response to burn ---
hypermetabolism ----exaggerated energy
expenditure & massive nitrogen loss
.depends on the burn size
.pt with major burn needs high calorie in the
form of CHO , protein and fat
.add vitamins & minerals

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oRoute of administration
-oral
-NG tube feeding
-parentral
Ancillary nutritional support measures
-metabolic expenditure can be minimized by
blunting stressful stimuli
oWarming burn pts
oPain control
oPrevent sepsis ,hypovolemia ,DHN

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IX. COMPLICATIONS of Burn
I. INFECTION
Most morbidity & mortality in severely burned pts are
related to infections
Predictors of infection :
Burn size
Age
Inhalation injury
Site of infection in burn pts :
1. Wound infection
-the essential pathological feature of burn wound sepsis
is invasion of organisms into viable tissue

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Treatment : .expeditious excision of
the wound
.topical antimicrobial
therapy (silver nitrate,
silver sulphadiazine, mafenide)
.systemic antibiotics after
culture and sensitivity test

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2. Pneumonia
Most common
Bronchopneumonia has replaced
hematogenous pneumonia as the most
common form o pulmonary infections in
burn pts
3. Suppurative thromophelebitis
Occurs in 5 % of major burns
Ass with use of i.v. catheters esp by cut-down
technique
Incidence increases with duration of
catheterization
4. UTI

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II. Curling ulcer
III. Seizures
-unique to childeren
-result from electrolyte imbalance,hypoxemia,
infection & drugs (penicillin, phenothiazine,
diphenhydramine, aminophylline)
IV. Fecal impaction
-from immobilization, DHN, narcotic analgesics
V.Hypertrophic scar, keloid, contracture,
Marjolin’s ulcer

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VI. Ileus & acute gastric dilation
PREVENTION OF CONTRACTURE
-early excision and grafting
-splintage
-elevation of extremity
-early physiotherapy
-prevention of infection