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PROBLEM 2

By: Varla S. G (405090215)

TYPES OF BURN
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CUTANEOUS BURNS
Injuries to the skin caused by the application
of heat, cold, or caustic chemicals.
When heat is applied to the skin, the depth of
injury is proportional to the contact
temperature, duration of contact, and the
thickness of the skin.
The depth of the injury largely determines
healing potential and the need for surgical
intervention such as skin grafting.

COLD EXPOSURE (FROSTBITE)

Damages the skin and underlying tissues
when ice crystals puncture the cells or when they
create a hypertonic tissue environment.
Blood flow can be interrupted, causing
hemoconcentration and intravascular
thrombosis with tissue hypoxia.

CHEMICAL BURNS
Cause injury to tissues via a wide range of
caustic reactions, including radical alteration
of pH, disruption of cellular membranes,
and direct toxic effects on metabolic
processes.
In addition to duration of exposure, the
chemical nature of the injurious agent will
determine injury severity.

ELECTRICAL
Injury to cell membranes (electroporation)
disrupts membrane potential and function.
The magnitude of injury depends on the
pathway the current follows, the resistance to
current flow of the tissues involved, and the
strength and duration of current flow.

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PATHOGENESIS
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PATHOGENESIS OF BURN INJURY

Initial Injury
Heat

injury

Excess heat causes rapid protein denaturation and cell

damage.
The depth of heat injury is dependent on the depth of heat
penetration wet heat (scald) travels more rapidly into
tissue than dry heat (flame).
The depth of burn is dependent on the temperature of the
heat insult, the contact time and the medium (air-water)
The depth of the skin layer is critical as the thinner the
skin, the deeper the burn.

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INFLAMMATORY MEDIATOR
INJURY (FIRST TO THIRD DAY)
Much of the tissue damage is caused by toxic
mediators of inflammation which are
activated with the burn.
Excess production of mediators especially
oxidants and proteases will cause more
capillary endothelial and skin cell damage.

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INFLAMMATION INDUCED
WOUND INJURY
Protease Release Injuring Healing Tissue and
Deactivating Growth Factors
Oxidants Release Injuring Cells, Denaturing
Proteins, and Activating Inflammation
Consumption of Wound Oxygen by
Neutrophils Leading to Tissue Hypoxia
Increasing Stimulus to Fibrosis

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ISCHEMIA INDUCED INJURY

Instant surface vascular thrombosis occurs along
with cell death from the heat insult.
The injured capillaries below the surface,
where tissue is still viable, can continue to
thrombose due to initial heat and subsequent
mediator injury, to endothelial cells, causing
further ischemia and further tissue necrosis

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DELAYED INJURY
Continued tissue damage can occur in the burn
wound after the initial heat and mediator
damage.
The common element is ongoing inflammation
perpetuated by surface eschar, bacterial
colonization, mechanical trauma or that
caused by topically applied antibacterial
agents

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Increased neutrophils, especially in exudate

on the surface, results in increased damage to
viable tissue by both neutrophil proteases and
oxidants and neutrophil consumption of oxygen.
Wound surface protease activity, particularly
metalloprotease, has been noted to be
markedly increased on open burn wounds

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CONTINUING BURN WOUND

INJURY
ongoing inflammation caused by
- neurotic tissue
- bacteria on surface
- caustic topical agents
- surface exudate
excess wound proteolytic activity
- activated by surface insults
- continued damage to viable cells and new tissue
growth
- damage to wound surface and matrix
denaturation of growth factors
excess oxidant release
- injuring viable cells

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BURN WOUND ASSESSMENT

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HISTOLOGICAL ASSESSMENT OF
THE BURN WOUND
Zone of coagulation (necrosis)
Zone of stasis (injury)
Zone of hyperemia

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ZONE OF COAGULATION
This zone is comprised of the surface tissue
necrosis of the initial burn eschar.
The surface injury is caused mainly by the heat
or chemical insult.
Obviously this zone has an irreversible injury.

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ZONE OF INJURY
Deep and peripheral to the zone of coagulation,
there is a sizable area of tissue injury where cells
are viable but can easily be further damaged.
The terms "stasis" or "ischemia" were used
because the progressive injury in this area
was thought to be due to capillary
thrombosis from injured endothelium,
leading to ischemia-induced cell death

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ZONE OF HYPEREMIA
Peripheral to and below the zone of stasis is
the zone of hyperemia.
The area is characterized by minimal cell
injury but with vasodilatation due to
neighboring inflammation-induced mediators.
Completed recovery of this tissue is expected
unless there is an additional severe insult such
as an invasive infection or profound tissue
inflammation.

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Early epithelial cell death in this area,

unrelated to blood flow, is reported to be quite
high, leading to slowing of healing
This zone is most prominent in mid-to-deepdermal burns where there is less reserve in the
remaining viable cells and less blood flow.

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WOUND CONVERSION
This term refers to the dynamic process
whereby the Zone of Injury progresses to
the Zone of Tissue Necrosis thereby deepening
the wound.
Conversion is more likely with a mid to deep
dermal injury because of less blood flow,
longer time to healing and increased risk of
excess inflammation and infection.

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ZONES OF INJURY IN TWO BURN

DEPTHS
THE ZONES OF STASIS OR INJURY AND
HYPEREMIA (reaction) are much larger in a
mid dermal burn compared to a superficial
burn.
This larger zone of injury exceeds the increase
in size of the zone of coagulation (necrosis)
between the two depths.

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The reason is that:

The

best blood flow is present in the superficial

dermis and ischemia is a greater risk beyond that
point
Once through the epidermis, the heat transfer
increases into the dermis such that a deeper area of
heat and inflammatory injury results.

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FACTORS INCREASING ZONE OF

INJURY
Lower blood flow with a deeper burn
Increased risk of infection with deeper burn
Presence of surface necrotic tissue

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PRIMARY SURVEY &

SECONDARY SURVEY
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PRIMARY SURVEY
A airway maintenance
B breathing & ventilation
C circulation & haemorrhage control
D disability (neurological status)
E exposure with environmental control
F fluid resuscitation

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AIRWAY MAINTENANCE
open and clear the airway; in case of a
suspected injury to the cervical spine keep
movement of the neck to a minimum and never
hyperflex or hyperextend the head and neck.
If smoke inhalation is suspected intubate
before oedema makes this difficult or even
impossible

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BREATHING & VENTILATION

Expose the chest and make sure that chest
expansion is adequate
Always provide O2 in severe burns or when
inhalation injury is suspected give 4-8 L/minute
Perform escharotomy (decompression) in full
thickness circumferential burns of the chest

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CIRCULATION & HAEMORRHAGE

CONTROL

Check pulse

the radial pulse is palpable the systolic BP is 100

or more
if the femoral pulse is felt the systolic BP is 80 or
more
if the carotid pulse is felt the systolic BP is 60 or
more
if the carotid pulse is not felt immediately start CPR
if

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Stop bleeding with direct pressure

Check capillary refill, if > 2 sec it means
hypovolaemia or the need for escharotomy on that
limb; check the other limb to compare
Pallor occurs with 30% loss of blood volume
In severe burns (>20% TBSA) insert 2 large bore
peripheral IV lines

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DISABILITY NEUROLOGICAL
STATUS

Check the level of consciousness (LOC)

= Alert
V = response to Vocal stimuli
P = response to Painful stimuli
U = Unresponsive
A

Examine the pupils for light reaction

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EXPOSURE WITH ENVIRONMENTAL

CONTROL
Keep patient warm
Keep environment warm
Check for any adherent clothing, cut around it,
when removing clothing

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FLUID RESUSCITATION
Estimate TBSA, use the Lund & Browder chart
or use the palmar surface of the patients own
hand = 1%
Weigh the patient, if not possible use the
following formula: 2 x (age in years + 4)= kg,
use only in children < 12 years
Give IV fluids in burns >10% TBSA in
children and >15% TBSA in adults
Use Ringers Lactate or sodium chloride
0.9% (NS)

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Formula to be used is 4 cc x wt in kg x % TBSA

burn
Give half of the calculated deficit in the first
8 hours starting from the time of burn and
not from the time the IV drip has been
commenced
Monitor adequacy of resuscitation by measuring
the urine output, children 1 cc/kg/hr, adults
(from 30-40 kg body wt) 0.5 cc/kg/hr ~ 30-50
cc/hr, accurate measurement is only possible with
an indwelling catheter

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Insert a NGT in burns > 20% TBSA in

children and > 30% TBSA in adults
Give adequate analgesia, preferably morphine
(not in neonates) or pethidine

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HOW TO GIVE
Give half of the calculated deficit in the first
8 hours starting from the time of the burn (tob).
At the same time in children start maintenance.
Give the other half of the deficit over the
next 16 hours and in children continue to give
maintenance fluids

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For the second 24 hour period after the burn

both adults and children must be given
maintenance fluids (adults 2500 - 3000 cc/24
hrs)

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SECONDARY SURVEY
Mechanism of injury
AMPLE

Allergies

Medications

medical history
Last meal
Events/Environment related to injury
Past

Head to toe physical examination

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ASSESS EXTENT OF BURN

The extent of a burn is expressed as % of

Total Body Surface Area(%TBSA)

Use theWallace Rule of Ninesto assess burns in

adults.
Use theLund Browder Chartto assess paediatric
burns.

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ANALGESIA

Adults:
2

5mg Morphine IV repeated every 5 minutes.

Titrate to clinical picture.

Children:
Initial

dose of IV Morphine 0.1mg/kg. Repeat

according to pain score to a maximum of 0.3mg/kg

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(NASO)GASTRIC TUBE INSERTION

A nasogastric tube should be inserted in

Adult

burns >20% TBSA burn

Children >15%TBSA burn

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MEASURE URINE OUTPUT

Desired urine output:

Adults:

0.5 - 1.0 ml/kg/hr

Children <30kgs: 1ml/kg/hr

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INVESTIGATIVE TEST
Urea & Electrolytes
Full Blood Examination
Blood group
Cardiac enzymes
Arterial Blood gases
Carboxyhaemoglobin
ECG
Chest X - ray
Other tests as indicated by additional
trauma/disease

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PREVENT HYPOTHERMIA
Cover wounds to exclude air and prevent
evaporative cooling with cling film.
Use a space blanket with normal blankets over
the top
Heat room
Use warming air blankets
Warm intravenous fluids

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CHECKLIST FOR TRANSIT

Airway secure
O2 insitu
IV access established and secure
Fluid resuscitation commenced
Urinary catheter inserted and secure
Pain controlled
Wounds covered
Patient is warm
Elevate burnt area as appropriate
Tetanus status determined and appropriate prophylaxis
Nasogastric insitu as necessary
Next of kin aware
Retrieval service and receiving hospital aware
History and relevant documentation copied

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TRANSFER CRITERIA TO A BURN

CENTER
Partial thickness burns greater than 10%
total body surface area (TBSA)
Burns that involve the face, hands, feet,
genitalia, perineum or major joints
Third degree burns in any age group

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Electrical burns, including lightening injury

Chemical burns
Inhalation injury
Children with any of the above burn injuries
Burn injury in patients with preexisting
medical disorders that could complicate
management
Any patients with traumatic injury (such as
fractures) in which the burn injury poses the
greatest risk of morbidity or mortality.

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Any burned children if the hospital initially

receiving the patient does not have qualified
personnel or equipment for children.

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PROCEDURES BEFORE REFFERALS

Keep the patient warm
Wash wounds with Hibicet (Savlon) or
normal saline and cover with a clean sheet
Provide pain relief, paracetamol or morphine /
pethidine if possible
Give tetanus prophylaxis

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EMERGENCY MANAGEMENT OF
SEVERE BURNS
A. Airway maintenance with cervical spine
control
B. Breathing and ventilation
C. Circulation with haemorrhage control
D. Disability neurological status

Alert/voice/Pain/Unresposive

= AvPU

E. Exposure and environmental control

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BURN WOUND
MANAGEMENT
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SUPERFICIAL SECOND DEGREE

(PARTIAL THICKNESS BURN)
Second-degree burns are defined as those burns
in which the entire epidermis and variable
portions of the dermis layer are heat
destroyed.
A superficial second-degree (partial thickness)
burn is characterized by heat injury to the
upper third of the dermis leaving a good blood
supply

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Cause: usually hot water

Appearance:

The

micro vessels perfusing this area are injured

resulting in the leakage of large amounts of plasma,
which in turn lifts off the heat-destroyed epidermis,
causing blister formation.
A light pink, wet appearing very painful wound is
seen as blisters are disrupted.
Frequently, the epidermis does not lift off the dermis
for 12 to 24 hours and what appears initially to be a
first degree is actually a second degree burn.

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TREATMENT
Clean, remove small blisters; apply grease gauze
and soft gauze dressing (occlusion, absorbent
dressing, changed daily).
On face, perineum, apply bacitracin or
neomycin ointment, applying several times a
day.
Excellent alternative is the use of a synthetic
adhesive dressing which seals the wound and
decreases pain.

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Use a water-soluble topical antibiotic if the

wound is grossly contaminated or if one is unsure
if the wound is superficial or deep.
Prophylactic systemic antibiotics are not needed.

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OUTCOME

Healing Rate:
Despite

loss of the entire basal layer of the

epidermis, a burn of this depth will heal in seven
to fourteen days if non-infected due to
repopulation of the epithelial cells that are also
present in skin appendages, anchored deep in the
dermis.
There is a relatively small zone of injury and
conversion is uncommon except at extreme of age or
chronically ill.
Most antibiotic creams will slow the healing
rate.
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HOT WATER (SUPERFICIAL

DERMAL BURN)

TREATMENT
Transfer

to Burn center due to size, i.e., > 15% TBS

Too big to use cold dressings except for a very brief
initial period
Use topical antibodies in view of age, high risk of
conversion, infection
Alternative: temporary skin substitute to generate
wound closure

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TREATMENT
Cold water to control pain
Gently cleanse
Grease gauze, plus gauze dressing (closed
technique)
Antibiotic ointment is optional but a silver
cream not needed
Apply dressing to allow for mobility of hand

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MID-PARTIAL THICKNESS BURN

Definition:
A

mid second degree extends to the mid portion of the

dermis.
Longer exposure to hot liquids (5-10 seconds) or flash
flames (not direct contact of flames with skin) are the
most common causes.

Cause:Brief exposure to flames or flash

explosion: hot water in infant or elderly.

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Appearance:
The

burn surface may have blisters but is more red, less

wet and only moderately painful.

Treatment:
In

patients six years to 60 years, without diabetes,

chronic illness, etc., treatment is grease gauze and
occlusive dressing. A topical antibiotic ointment such as
bacitracin can also be used daily.
In very young, and very old patients, or those with
chronic illness, contaminated wounds or perineal
wounds, the traditional choice is a topical antibiotic.
First choice is silver sulfadiazine or a silver dressing
with closed dressing technique.
NewApproach: (a temporary skin substitute) which
could increase healing and decrease conversion.
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OUTCOME
These burns usually heal in about two to four
weeks.
The exception is the very young and elderly
where the dermis is thin and dept of burn is
invariable deeper.
However, there is a large zone of injury and
risk of conversion.

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DEEP PARTIAL THICKNESS (DEEP

SECOND DEGREE) BURN
A deep partial thickness or deep second-degree
burn extends well into the dermal layer and
fewer viable epidermal cells remain.
Therefore, re-epithelialization is extremely
slow, sometimes requiring months.

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APPEARANCE
In these patients, blister formation does not
characteristically occur because the dead tissue
layer is sufficiently thick and adherent to
underlying viable dermis that it does not readily
lift off the surface.
The wound surface may be red and dry in
appearance with white areas in deeper parts (dry
since fewer blood vessels are patent).
There is a marked decrease in blood flow making
the wound very prone to conversion to a deeper
injury and to infection.
Direct contact with flames is a common cause.

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TREATMENT
After initial cleaning and removal of dirt and
loose dead tissue, a topical antibiotic is
required.
A silver based dressing or cream is the first
choice.

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OUTCOME
A deep dermal burn will require 4-10 weeks or
longer to heal.
Since the new epidermis is very thin and not
adhered well to dermis (no rete pegs), wound
breakdown is common.
Excision and grafting is the preferred treatment.
Dense scarring is usually seen if the wound is
allowed to heal primarily.

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THIRD DEGREE (FULL

THICKNESS BURN)
A full thickness or third degree burn occurs with
destruction of the entire epidermis and
dermis, leaving no residual epidermal cells to
repopulate.
This wound will therefore not re-epithelialize
and whatever area of the wound is not closed
by wound contraction will require skin
grafting.

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APPEARANCE
A characteristic initial appearance of the
avascular burn tissue is a waxy white color.
If the burn produces char or extends into the fat
as with prolonged contact with a flame source, a
leathery brown or black appearance can be
seen along with surface coagulation veins.
Direct exposure with a flame is the usual
cause of a third degree burn.
The burn wound is also painless and has a
coarse non-pliable texture to touch.
This burn is termed an indeterminate burn

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TREATMENT
Gentle wash, removing loose tissue, char.
Eschar penetrating antibodies, silver cream
or dressing first choice, using closed dressing.
Early surgical excision and grafting.
Prophylactic parenteral antibiotics are not
indicated.

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OUTCOME

Except for a very small wound, e.g. 2x2 inches,

the burn wound will require excision and a
skin graft.

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CHEMICAL BURNS
Common strong acids and alkali used in
industry cause the majority of injuries.
The burn injury is typically caused by
coagulation necrosis of tissue rather than by
direct heat production.
The degree of tissue injury is dependent on the
toxicity of the chemical and the exposure
time.

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The burn wound is characteristically gray to

brown in color due to the chemically denatured
protein.
Persistent burning pain is commonly
described as the burning in process continuous as
long as the chemical is in contact with the skin.

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WOUND MANAGEMENT

Continuous water irrigation of the area

should be initiated
use

of showers in the workplace is optimum

irrigation for strong acid or alkali exposure is 30-60
minutes
continuous irrigation if eye is exposed to chemicals
do not attempt to neutralize acids with alkali or vice
versa, just use copious water

Solid chemicals should be brushed off first

prior to irrigation using safety gloves
Consider transfer
Willneed topical antibiotic as burn is
invariably deep

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FACTORS AFFECTING WOUND

HEALING

Both the very young and the elderly have

very thin skin that makes them more
susceptible to significant burn injury
Other factors that affect wound healing include:
Nutrition
Infection

Associated

illnesses such as diabetes mellitus.

Cytotoxic treatments
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BURN ITCH

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NUTRITION
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Early feeding is important because the passage

of food through the intestines
the small bowel mucosa from damage that
occurs after starvation and trauma and so
Prevents translocation of bacteria through the bowel
wall, which may lead to gram-negative sepsis.
Protects

Due to a rise in the metabolic rate in severe

burns provision of approximately 2 to 3x the
usual amount of energy is required
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At the burn site, where the blood flow may

increase tenfold, the O2 concentration remains
low and the wound tissues use anaerobic
glycolytic pathways; in other words large
amounts of glucose are consumed
There is an increased breakdown of protein
with 80 to 90% of the nitrogen lost in the urine as
urea; there is a concomitant loss of lean body
mass.

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A burn of 40% TBSA can cause weight loss

of 30% within a few weeks
There is also loss of vitamins and minerals
due to skin loss and muscle breakdown

Give extra feeds high in calories and proteins.

Supplement with Vitamins A and C, Iron and
Zinc

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Give extra feeds twice daily in burns up to

20%; increase the frequency when TBSA is > 20%
Preferably feed by mouth, if this is not
possible feed by the smallest possible nasogastric
tube
Weigh patients at least once a week

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PAIN ASSESSMENT

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SEPSIS
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Sepsis syndrome is clinically heralded by the

onset of hypothermia or hyperthermia,
hypotension, decreased urinary output,
hyperglycemia, neutropenia or
neutrophilia, and thrombocytopenia.
Teplitz and colleagues studied an experimental
model ofPseudomonasburn wound sepsis and
showed that bacteremia originated from the
junction of the burn wound and the
unburned hypodermis

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Burn patients with sepsis from invasive burn

wound infection have transient or intermittent
bacteremia or fungemia from seeding of
microorganisms into the bloodstream, but
positive blood cultures are a late sign of infection
Bacteremia also occurs from endogenous
intestinal flora because of the decreased blood
flow and gut perfusion that occur following
thermal injury

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Full-thickness burn size, age, and

inhalation injury were associated with the
development of multiple-organ dysfunction
syndrome, sepsis, and death
Burn patients with sepsis should be examined
immediately to determine the site and source
of infection, including inspection of the entire
burn wound surface

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Diagnostic tests should be done to identify the

site and source of infection, including blood,
urine, and sputum cultures
Empirical broad-spectrum antibiotic
therapy directed at the most recent bacteria
isolated from burn wound cultures and other
sources should be instituted promptly

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