BURN

(Dr. James Taclin Banez)

Etiology
Cutaneous burns caused by application of:
1.
2.
3.
4.

Heat
Cold
Caustic chemical
Electricity

Depth of injury is proportional to:

1. Temperature applied
2. Duration of contact
3. Thickness of skin
Types of Burn wounds
1.
2.
3.
4.

Scald
Flame burns
Flash burns
Contact burns

Scald
- Most common cause of burn from
hot water
- >140 F or >160 C in 3 secs.
- >156 F or >69 C in 1 sec
- Thin skin in children & elderly
deeper burns

Flame burns
- 2nd most common mechanism of
thermal injury
- Usually victims from house fires/
assoc. with resp. injury

Flash burns
- Due to explosion of natural gas &
electrical arch
- Depth depends on the amount and
kind of fuel that explodes and the
amplitude of current.
- Often full thickness and require
grafting

Contact burns
- Contact with hot metals, plastic,
glass, or hot coals
- Against iron, ovens, and wood
burning stoves, motor vehicle and
motor collisions may leave victims
In contact with hot engine part

Burn Severity
Severity is related to:
1. Burn size (>20%)
2. Burn depth (deep partial thickness to
stage IV)
3. Part of the body burned (face, hands,
and perineum)

Burn Size

Rule of Nine (for Adult)

Burn depth

The thickness of skin varies with age, sex and

area of the body
-

Epidermis is thicknest (0.5 cm) o n

palm & sole, then (1mm) back,

thinness (1mm) on the eyelids and

genitalia
- Adult and children same thickness,
but infant skin thickness in each
specific area may be less than one
half that of adult skin
- Over 50 years of age, dermal
atrophy, all areas of skin become
thin in elderly patients, and the skin
appendages are far less active
Burns not extending all the way through
the dermis leave behind epitheliumlined skin appendages
When dead dermal tissue is removed,
epithelial cells swarm from the surface
of each appendage to meet swarming
cells from neighboring appendages,
forming a new, fragile epidermis on top
of a thinned and scarred dermal bed.

The less dermis remains:

1. The longer the burns takes to heal
2. The greater the inflammatory response
3. The more severe the scarring
Burns that heal w/in 3 weeks usually do so:
1. w/out hypertrophic scarring
2. no functional impairment
3. w/ long term pigmentary changes are
common

Burn Depth

1. Shallow burns
2. Deep burns
Classification of burn according to increasing
depth
A. Shallow Burns:
1. Epidermal Burn:

(1st degree)
- No blister
- Erythema due to dermal
vasodilation
- Quite painful
- 4th day injured epithelium
desquamate peeling (sunburn)
2. Superficial Partial thickness:
- Second degree
- Includes upper layer of dermis
- Characteristically forms blisters
(fluid accumulation between
epidermis and dermis).
- If blisters are removed the wound is
pink, wet, painful and blanch w/
pressure
- Heal spontaneously < 3wks w/o
functional impairment
B. Deep Burns:
1. Deep Partial Thickness: (second
degree)
- Extends into the reticular
layer of the dermis
- w/ blisters but wound
surface mottled pink and
white color
- Complains of discomfort
rather than pain
- Pressure applied -->
capillary refill is slow or
absent.
- 2nd day wound is white and
dry
- If not excised & grafted
heals in 3 to 9 wks w/
scarring
- Joint function can be
impaired
2. Full Thickness: (third degree)
- All layers of the dermis
- Appear white, cherry red
or black and may or may
not have deep blisters

Leathery, firm and

depressed compared w/
adjoining normal skin
Insensate
Develop a classic burn
eschar, an intact dead and
denatured dermis that
separates after days or wks.
Heal only by wound
contracture,
epithelialization from the
wound margin or skin
grafting

3. Fourth Degree:
- Involves also the
subcutaneous fat and deeper
structures
- Almost always have
charred appearance
- Electrical burns, contact
burns, immersion burns
and patients who are
unconscious at time of burn

Those that will heal w/in 3wks are better

treated by nonoperative wound care:

1. Ability to detect dead cells or

denatured collagen (biopsy,
ultrasound, vital dyes)
2. Assessment of changes in blood
flow (fluorometry, laser
doppler & thermography)
3. Analysis of the color of the
wound (light reflectance
methods)
4. Evaluation physical changes,
such as edema (MRI)

Physiologic Response to Burn Injury

Burn inflammatory process involving

the entire organism

Systemic Inflammatory Response

Syndrome (SIRS):
Alterations of the metabolic,
cardiovascular, gastrointestinal
and coagulation systems
resulting to:

Shallow burns

1.
2.

Hypermetabolism
increased cellular,
endothelial and
epithelial permeability
(classic hemodynamic
alteration)
3. Often extensive
microthrombosis

State-of-the-art burn care involves early

excision and grafting (E&G) of all burns
that will not heal w/in 3wks:
Deep burns

Assessment of Burn Depth

Standard technique for determining burn

depth: clinical observation of the
wound
Other techniques to qualify burn
depth:

Burn Shock:

Complex process of circulatory

and microcirculatory
dysfunction that is not easily or
fully repaired by fluid
resuscitation.

Tissue trauma & hypovolemic

shock releases local & systemic
mediators ---> increase
vascular permeability and
microvascular hydrostatic
pressure ---> burn edema.

Mediators released:
1. Histamine inc. permeability
2. Serotonin platelet aggregation, inc.
vascular resistance
3. Eicosanoids (arachidonic &
prostacyclin), inc. hydrostatic pressure
and blood flow edema
4. Kinins (bradykinin) inc. permeanility
5. Vasoactive amines inc. vascular
pressure

Pathophysiology of Burn shock

Burn shock is both hypovolemic and

cellular in etiology
1. Hemodynamic changes includes:
a. Inc. extracellular fluid
b. Dec. plasma volume
c. Dec. Cardiac output
d. Oliguria

The primary goal is to restore and

preserved tissue and end organ
prefusion.
Maximal edema formation occurs b/w:
8 -12 hrs in small burns
12 -24 hrs in major burns
2. Changes at cellular level: (>30%
burn)
a. Systemic decrease in cell trans
membrane potential. Dec. in Na
K ATPase activity.
b. Defective ATP metabolism in
burn

Metabolic Response to Burn Injury

1. Hypermetabolism:
- Inc. catabolism of CHO,
lipids, and CHON
- Recommended protein
intake is 2g/kg per day
- >100% REE (1.3x BMR)
due to:
a. Increased heat loss from
the burn wounds
Due to increased
blood flow and skin
loss
b. Increased betaadrenergic stimulation
Basal Energy Expenditure can be
estimated by Harris and Benedict
Equation:
- BEE (Men) = 66.47 +
(13.75 x weight in kg) +
(5.0 x height in cm) (6.76
x age in years) kcal/day
- BEE (Women) = 65.51 +
(9.56 x weight in kg) +
(1.85 x height in cm)
(4.68 x age in years)
kcal/day

Constant po yung mga given na

number

2. Neuroendocrine Response:
- Catecholamine massively elevated
and major endocrine mediator of
hypermetabolism in burn
- Giving propranolol diminish
REE and O2 consumption
Emergency Room:
Burn wound not the 1st concern
1. AIRWAY and BREATHNG
Careful inspection of the mouth and
pharynx

Presence of stridor, hoarseness and

expiratory wheezes are signs of
potentially serious airway edema
or inhalation injury
Copious mucus production and
carbonaceous sputum
Carboxyhemoglobin levels should
be obtained

LR solution at a rate of 1000

ml/h in adults and 20 ml/kg/hr
in young children
Foley catheter placed and urine
output monitored hourly, the
goal being 30 ml/hr in adults
and 1.0 ml/kg/hr in young
children
Once the extent of the burn is
ascertained, resuscitation should
be tailored to the injury using
the Parkland formula

Emergency care of Burn wounds

At the scene:
1. Aiway:
Exposed to smoke CO
poisoning
100% O2 inhalation (mask)
If unconscious or resp. distress
intubate

CONSEQUENCES OF LOW
CARDIAC OUTPUT
1. Depress CNS function
RESTLESSNESS
LETHARGY COMA
2. Heart failure
3. Acute Renal Failure
4. Ischemia of GIT

Emergency assessment of inhalation injury:

Decreased P:F ratio (Pao2:FIO2), is one

of the earliest indicators of smoke
inhalation.

400-500 is normal
< 300 = impending pulmonary
problem
< 250 = indication for
endotracheal intubation

Fiberoptic bronchoscopy can

accurately assess edema of upper airway.

Central Venous Pressure (CVP) placed:

1. Pts. w/ burns >50% TBSA
2. Those who have assoc. medical
problems
3. At the extremes of age
4. Those with concomitant inhalation
injuries
Fluid Resuscitation after 24 hrs

2. CIRCULATION:
Fluid resuscitation:
Burn shock and Myocardial injury
Due to proinflammatory
cytokines released causing
microvascular leak dec.
Cardiac output (burns approach
20% TBSA)

Put 2 large bore IVF

Better use upper ext. even if w/
burn than lower ext. for high
septic thrombophlebitis

Total maintenance fluid = (1500ml/m2)

+ evaporated water loss [(25 + %TBSA
burn) x m2 x 24]
Pt will require approximately 1.5 times
their normal maintenance fluids
following successful resuscitation from
major thermal injury
Bcos. of the loss of intracellular K
during burn shock, the k requirement in
adults w/ normal renal function is
approximately 120 mEq/d

safest course is usually to decompress

the stomach w/ a NGT.

Care of Burn wounds

ESCHAROTOMY

Bed side, observe sterility, (-) local

anesthesia, IV opiates, done up to
subcutaneous layer
Resp. distress could be due to
inelasticity of chest wall

FASCIOTOMY

Compartment syndrome can

developed up to 72 hrs following
injury
Cutting through deep fascia
Anterior axillary line & transverse
incision along costal margin

Pain Control
-

Pain control is best managed w/ small

intravenous doses of an opiate until
analgesia is adequate w/o inducing
hypotension

INHALATION INJURY
1. Carbon Monoxide Poisoning:

Extremities: done if
1. Cyanosis
2. Deep tissue pain
3. Progressive paresthesia
4. Progressive decrease or absence of
pulses
5. The sensation of cold extremities
Doppler to assess arterial flow

Tetanus Prophylaxis
-

Previous immunization w/in 5 yrs

requires no tx, immunization w/in 10
yrs requires tetanus booster, and
unknown immunization status
requires hyperimmune serum

Gastric Decompression
-

Many burn centers begin enteral

feeding on admission to reduce the
risk of gastric ulceration (Curlings
ulcer), prevent ileus, and blunt
catabolism.
If pt transport is via air ambulance or is
going to take more than a few hrs, the

Majority of house fire deaths

CO2 is colorless, odorless and
tasteless gas w/ affinity to Hgb
200x that of 02.
Mechanisms of interfering O2
delivery:
a. Prevents reversible
displacement of O2 on
the Hgb molecule
b. COHg shifts the O2-Hg
dissociation curve to the
left.
c. CO2 binds to reduced
cytochrome a3, causing
less effective intracellular
respiration
d. CO bind to cardiac and
skeletal muscle, direct
toxicity
e. CO act in CNS causing
demyelination causing
neurologic symptoms.

Signs and Symptoms: (Level of COHb)

Treatment:

<10% COHb asymptomatic

20% COHb headache,
nausea/vomiting, loss manual
dexterity
30% COHb weak, confused &
lethargy
40 60% COHb lapses of coma
>60 % - usually FATAL

100% oxygen via a nonbreather face

mask while waiting for measurement
of COHb levels

UPPER AIRWAY:

2. Thermal Airway Injury:

Most of the heat in burning

room is dissipated in the
oropharynx, nasopharynx and
proximal tracheobronchial
tree due to:
1. Oropharynx and
nasopharynx provide an
effective mechanism of
heat exchange due to:
-

large surface
area
associated air
turbulence
mucosal fluid
lining that acts
as a heat
reservoir.

2. Sudden exposure to hot

air typically triggers
reflex closure of the
vocal cords

Greatest risk:
a. Explosion
b. Burns of face and
upper thorax
c. Unconscious in a fire
Edema ---> upper airway
obstruction
Presence of intraoral and
pharyngeal burns indication --->
endotracheal intubation
Tube is placed until edema
subsides
Steroid has no role in tx upper
airway edema in burns.

Treatment of Airway injury

Endotracheal intubation if indicated

A soft cuffed endotracheal tube should
be inserted and left in place until the
edema subside
An adult pt ability to breath around the
tube w/ the cuff deflated is an indication
for removal of the tube

LOWER AIRWAY:

Tracheobronchitis
Supplemental O2
Bronchodilators

Early Excision and Grafting (E&G):

For deeper burns (deep partial

thickness and full thickness burns),
rather than wasting for spontaneous
separation, the eschar is surgically
removed and the wound closed via
grafting techniques and/or immediate
flap produces tailored to the individual
pt.
E&G is be done w/in 3 7 days, and
certainly by 10 days, following injury
appears prudent
Excision can be performed to include
the burn and SQ fat to the level of the
investing fascia (fascial excision)
Tangentially removing thin slices of
burned tissue until a viable bed remains
(tangential excision)
Dec. in hospital stay, costs, and time
away from work or school
Early E&G dramatically dec. the
number of painful debridement required
Pts w/ burns of 20% - 40% TBSA will
have fewer infectious wound
complications if treated with early E&G

In animal models, the

immunosuppression and
hypermetabolism assoc. w/ burns can be
ameliorated by early burn wound

TANGENTIAL (SEQUENTIAL) EXCISION

The principle of tangential excision is to

excise layers of the eschar at a tangential
angle to the surface until viable tissue is
reached. The burn can be removed w/ a
variety of instruments, usually hand
dermatomes

FASCIAL EXCISION

Fascial excision is typically reserved for

pts w/ deep full thickness burns, or w/
large, life threatening full thickness
burns

3. The presence of an inhalation injury

strongly correlates w/ infection,
particularly pneumonia
4. Premorbid diabetes significantly inc.
infection rates following thermal injury,
especially when coupled w/ poor
glycemic control

Abrupt onset of a) hyperglycemia, b)

fall in BP, and c) dec. in urinary output
should suggest the possibility that the pt
is becoming unstable
If these findings are assoc. w/
development of hypothermia, feeling
intolerance, and/or a falling platelet
count, the pt is probably developing
sepsis. It is important to do an
immediate infection work up and
administer the appropriate
antimicrobials

Advantages:
1. It results in a reliable bed of known
viability
2. Tourniquets can routinely be used for
extremities
3. Operative blood loss is less than w/
tangential excision
4. Less experience is required to ensure an
optimal bed

INFECTION
RISK FACTORS:
1. The incidence of infection correlates
with burn severity (TBSA).
- Burns involving <20% TBSA in
otherwise healthy individuals are rarely
assoc. w/ life threatening infection
2. Children appear to be more susceptible
to systemic infection than adults for any
given size burn.

PNEUMONIA
Inhalation injury inc. the risk of
developing pneumonia. However, this
may be more r/t endotracheal
intubation than the actual inhalation
injury
The dx of pneumonia is confirmed by
the presence of characteristic infiltrates
on the chest radiographs and positive
sputum cultures
Following inhalation injury, early
infiltrates usually represent chemical
pneumonitis and not infection, although
this injured pulmonary tissue may
become infected
Broad spectrum antibiotics
VASCUALAR CATHETER RELATED
INFECTION

 all vascular access modalities carry risk

of infectious complication
catheter related blood stream infection
(CRBSI) is inversely related from the
distance of the burn wound
Dx of CRBSI, should be appropriately
treated w/ systemic antimicrobials and
immediate removal of the catheter
ELECTRICAL INJURY AND BURNS
Injury severity depends:
1. Amperages of the current
(determined by the voltage of the
source and the resistance of the
victim)
2. Pathway of current through the
victims body
3. Duration of contact w/ the source

Electrical current sources are typically

classified as either low or high
voltage, w/ 1000 volts (V) being the
dividing line, and distinct injuries are
assoc w/ each type.
The smaller the size of the body parts
through w/c the electricity passes, the
more intense the heat and the less the
heat is dissipated into the surrounding
tissue.
Disruption of muscle cells release
cellular debris and myoglobin into the
circulation to be filtered by the kidney.
If this condition is untreated, the
consequences can be irreversible renal
failure
The most devastating injury w/ frequent
brain dmg occurs when current passes
through the head, but the spinal cord
dmg is possible whenever current passes
from one side of the body to the other
Schwann cells are quite susceptible, and
delayed transverse myelitis can occur
days or weeks after injury

Cataracts are well recognized sequela

of high voltage electrical burns. They
occur in 5 7% of pts, frequently are
bilateral, occur even in the absence of
contact points on the head, and typically
manifest w/in 1 2 yrs of injury.

CHEMICAL BURNS

Strong acids or alkalia cause most

chemical burns. In contrast to thermal
injury, chemical burn cause progressive
dmg and injury until the chemicals are
inactivated by reaction with tissues or
diluted by therapeutic irrigation.
Acid burns typically are more self
limiting than alkali burns> alkalis
combine w/ cutaneous lipids to create
soap, and are thus able to continue
dissolving the skin until they are
neutralized.
Irrigating for at least 15 min under a
running stream of tepid water limit the
overall severity of the burn
Neutralizing agents or antidotes are
contraindicated, except w/ hydrofluoric
acid burns
Hydrofluoric acid may cause death from
hypocalcemia even after moderate
exposure. HFA burns are unique
chemical burn in that they should be
acutely treated w/ an antidote, Ca
gluconate
Chemical burns should be considered
deep partial thickness or full
thickness until proven otherwise. As
such, they are best treated by early E&G
after full demarcation of injury

PAIN CONTROL

The mainstays of pharmacologic pain

control are analgesics, principally
opioids and NSAIDs.
Anesthetic agents, namely ketamine
and NO, are quite useful for extremely
painful procedures such as dressing
changes

HYPERTHROPIC SCARS

Burn scar hyperthropy classically

develops in deeper partial thickness
and full thickness injuries that are
allowed to heal by primary intention.
Delayed excision is more likely to result
in hyperthrophic scarring, and
pigmented individuals are at an inc. risk
Donor sites also can become
hyperthrophic, and this propensity
appears to be r/t graft thickness, donor
site infection, and pt characteristics
Pressure applied directly to a
hypertrophic scar has been the most
widely used tx modality

COMPRESSION GARMENTS
quickly reduces the mass of
hypertrophic scars
Triamcinolone commonly used
steroids
Prevented:
1. Early E&G of burn
wound
2. w/ used of splint, ROM
exercises in joint areas
and pressure garments
3. intralesional injection of
triamcinolone
4. surgical correction (Z
plasty, flap
reconstruction)

MARJOLINS ULCERS

Chronic ulceration of old burn

scars was noted by marjolin to
predispose malignant
degeneration. Squamous cell
carcinoma is most common.