Transcript Burns in Children

Burns in Children Review
Tarek Hazwani, MD
Assistant Consultant Pediatric Intensivist
King Abdulaziz Medical City
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Burns in Children Review
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Anatomy of Skin
Pathophysiology
Critical Factors
Management
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Anatomy of Skin
Largest body organ
 More than just a passive
covering
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Anatomy
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Two layers
• Epidermis
• Dermis
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Skin Functions
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Sensation
Protection
Temperature regulation
Fluid retention
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Burn: Pathophysiology
Loss of fluids
 Inability to maintain body
temperature
 Infection
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Burn: Pathophysiology
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Patients with large burns (≥15 percent
TBSA for young children and ≥20 percent
for older children and adolescents) develop
systemic responses to these mediators.
For patients with 40 percent TBSA or more,
myocardial depression can occur .
As a result, patients with major burns may
become hypotensive (burn shock) and
edematous (burn edema).
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Burn: Pathophysiology
Metabolic response :
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Following resuscitation, children with
major burns develop a hypermetabolic
response that results in a dramatic
increase in energy expenditure and protein
metabolism .
Evidence suggests that modulation of the
hypermetabolic response with therapies
such as beta blockers and human growth
hormone may improve outcomes for
severely burned children
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Pathophysiology
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Systemic capillary leak usually
persists for 18 to 24 hours.
Protein is lost from the
intravascular space during the
first 12 to 18 hours after a burn,
after which vascular integrity
improves.
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Critical Factors
Depth
 Extent
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Burn Depth
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First Degree (Superficial)
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Involves only epidermis
Red
Painful
Tender
Blanches under pressure
Possible swelling, no
blisters
• Heal in ~7 days
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Burn Depth
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Second Degree
(Partial Thickness)
• Extends through
epidermis into dermis
• Salmon pink
• Moist, shiny
• Painful
• Blisters may be present
• Heal in ~7 to 21 days
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Burn Depth
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Burns that
blister are
second degree.
But all second
degree burns
don’t blister.
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Burn Depth
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Third Degree (Full
Thickness)
• Through epidermis,
dermis into underlying
structures
• Thick, dry
• Pearly gray or charred
black
• May bleed from vessel
damage
• Painless
• Require grafting
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Burn Depth
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Often cannot be accurately
determined in acute stage
Infection may convert to higher
degree
When in doubt, over-estimate
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Burn Extent
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Pediatric Rule of Nines
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18, Front
18, Back
For each year over 1
year of age, subtract
1% from head,
add equally to legs.
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13.5
13.5
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Burn Extent
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Rule of Palm
• Patient’s palm
equals 1% of
his body
surface area
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Burn Extent
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Burn Severity
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Based on
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Depth
Extent
Location
Cause
Patient Age
Associated Factors
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Critical Burns Need Burn centre
American Burn Association
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Age <10 years with >10 percent TBSA burn
Age ≥10 years with >20 percent TBSA burn
Full thickness burn >5 percent TBSA
Inhalational injury
Any significant burn to face, eyes, ears,
genitalia, or joints
Significant associated injuries (fractures or
major trauma)
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Associated Factors
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Patient Age
• < 5 years old
• > 55 years old
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Burn Location
• Circumferential burns of chest,
extremities
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Burn shock
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characterized by specific
hemodynamic changes
(decreased cardiac output and
plasma volume, increased
extracellular fluid, and oliguria)
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Burn Edema
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Fluid shift intravascular to extravascular
soon after a burn—persist for the first 24
hours
In small burns edema peaks early, in large
burns edema developed continue for 18-24
hours
Unburned tissue edema occurs when burn
exceeds 35-40% TBSA
Early increase vascular permeability—in
part related to histamine—mechanism is
likely related to PMN and their adhesion to
the endothelium
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Burn : Management
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Stop Burning Process
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Remove patient from source of
injury
Remove clothing unless stuck to
burn
Cut around clothing stuck to
burn, leave in place
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Assess
Airway/Breathing
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Start oxygen if:
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Moderate or critical burn
Decreased level of consciousness
Signs of respiratory involvement
Burn occurred in closed space
History of CO or smoke exposure
Assist ventilations as needed
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Assess Circulation
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Check for shock signs /symptoms
Early shock seldom results from effects of
burn itself.
Early shock = Another injury until proven
otherwise
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Obtain History
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How long ago?
What has been done?
What caused burn?
Burned in closed space?
Loss of consciousness?
Allergies/medications?
Past medical history?
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Rapid Physical Exam
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Check for other injuries
Rapidly estimate burned,
unburned areas
Remove constricting bands
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Treat Burn Wound
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Cover with DRY, CLEAN SHEETS
Do NOT rupture blisters
Do NOT put goo on burn
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Special Considerations
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In Pediatrics always
Consider possibility of abuse
As many as 10% of abuse cases
involve burns
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Burn: Management
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Parkland formula, as follows:
(2-4 cm3 of crystalloid) X (%
BSA burn) X (body weight in kg)
The Parkland formula must be
modified in pediatric patients by
adding maintenance
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Burn: Management
Fluid resuscitation
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Estimating fluid requirements : for the first
24 hours following a burn injury include:
Parkland - 4 mL/kg per percent total burn
surface area (TBSA). Add glucose
maintenance fluid for children <5 years of
age.
Galveston - 5000 mL/m2 per percent TBSA.
Add 2000 mL/m2 per day for maintenance
requirements.
Half of the fluid is given over the first 8
hours. The remaining half is given over the
next 16 hours
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Burn: Management
Fluid resuscitation
Choice of fluid:
 Ringers lactate (RL) is the
resuscitation and maintenance fluid
of choice for the first 24 hours at
most burn centers.
 Experts recommend adding D5% to
maintenance fluid for children <20
kg to prevent hypoglycemia .
 Colloid is typically added after 24
hours to restore oncotic pressure
and preserve intravascular volume
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Burn: Management
Colloid resuscitation
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The addition of plasma or albumin to resuscitation
fluids has been criticized on the assumption that
the burn-induced increase in vascular permeability
and the consequent extravasation of proteins
persist for up to 36 h post injury .
The main concern is that protein administration
during the first 24 h increases protein accumulation
in the interstitium and thus traps water .
Using 131iodine-labeled albumin and
autoradiographic techniques to demonstrate have
shown that effective transcapillary sieving of
albumin molecules into burned skin essentially
stops at approximately 8 h post injury and that
edema of injured tissues, maximal at 3 h post burn,
persists beyond24 h post injury
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Burn: Management
Fluid resuscitation
Monitoring fluid status:
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The volume status of burn patients must be carefully
monitored in order to successfully navigate the narrow
path between inadequate volume and fluid overload. The
following parameters are helpful :
 Urine output should be maintained at 1 to 2 mL/kg per
hour for children <30 kg and 0.5 to 1 mL/kg per hour for
those ≥30 kg.
 Heart rate is a better monitor of circulatory status in
children than is blood pressure. Tachycardia may
indicate hypovolemia, but pain can elevate heart rate in
euvolemic patients.
 Metabolic acidosis can be a marker for inadequate fluid
resuscitation, but also occurs with carbon monoxide or
cyanide exposure
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Burn: Management
Fluid resuscitation
Burn Children not response to large
fluid volumes to maintain adequate
perfusion :
 Volume loss from occult injuries
 Neurogenic shock as the result of a
spinal cord injury
 Myocardial depression or decreased
vascular tone from inhaled or
ingested toxins
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Burn: Management
Pain control
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Most burn centers use
morphine
Fentanyl may be a safer choice
for initial pain management for
patients whose cardiovascular
status may be unstable
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Burn: Management
Antibiotics
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Topical antibiotics have been used
to dress burn wounds:
It is : available, and reduce the risk
of infection.
The topical antibiotic is applied to
the wound which is then covered
with a nonadherent dressing.
Specific antibiotic : Silver
sulfadiazine , Mafenide , Bacitracin
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Burn: Management
Special Considerations
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Steroids have no role in treating
burn wounds
Intravenous antibiotics are not
recommended in the initial
treatment of most burn patients, as
it may increase the chance of
colonization with more virulent and
resistant organisms. They should be
reserved for those patients with
secondary infections
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Burn: Complications
Infection
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Early Infections :
Organism : GAS , S. aureus
Specific colonization of burn wounds is somewhat
predictable over time. Initially, gram-positive organisms
are present;
infection that occurs in the first 48 hours after the burn
is usually secondary to GAS.
The incidence of GAS infections in burned patients has
decreased, probably secondary to immediate use of
topical antimicrobial therapy.
Routine administration of antibiotics prophylaxis is not
recommended ( colonization and potential infection with
more resistant organisms).
S. aureus also causes early septicemia. If there is
concomitant inhalation injury.
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Burn: Complications
Bacteremia
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Bacteremia is not uncommon in the
burned patient.
Risk factors include wound
manipulation and the presence of an
intravascular catheter.
infected intravascular thrombus can
cause persistent bacteremia.
Endocarditis must be considered in
any patient with prolonged
bacteremia.
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Burn: Complications
Renal failure
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ARF in burn patients is not common. Two distinct
pictures
of ARF can be observed: early ARF, occurring
either few hours after injury or in the first few days,
and late ARF developing approximately 1 or more
weeks after burn injury. Early ARF may be due to
hypovolemia and hypoperfusion of the kidneys,
whereas late ARF is a consequence of infection,
endotoxemia,
and MODS
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Burn: Complications
Renal failure
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Renal damage can arise even
from hemoglobinuria
in burn patients with associated
hemolysis, the administration of
haptoglobin may prevent
hemoglobinuria-nduced renal
failure
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Inhalation Injury
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Inhalation Injury
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10-20% hospitalized burn patients sustained
inhalation injury.
Increased mortality
History (closed space)
P.E. (facial burn, singed nasal hairs, erythema,
carbonaceous material in back of the troat)
laboratory tests (carboxyhemoglobin>15%) and
bronchoscopy (erythema and sooty deposite in
the airway)
Treatment: supportive. Nasotracheal or
endotracheal intubation preferable to early
tracheostomy. Prophylactic antibiotics and
steroids not indicated.
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Inhalation Injury
Problems
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Hypoxia
Carbon monoxide toxicity
Upper airway burn
Lower airway burn
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Inhalation Injury
Carbon Monoxide
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Product of incomplete combustion
Colorless, odorless, tasteless
Binds to hemoglobin 200x stronger
than oxygen
Headache, nausea, vomiting,
“roaring” in ears
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Inhalation Injury
Carbon Monoxide
Exposure makes pulse
oximeter data meaningless!
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Inhalation Injury
Carbon Monoxide Measurement
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Carbon monoxide has various effects depending
upon levels
Must check levels on Blood Gas analysis
􀂄􀂄 0-10% can be seen in smokers can be seen in
smokers
􀂄􀂄 10-20% patients can have headache
􀂄􀂄 20-30% patients develop severe headache,
nausea, vomiting, CNS collapse
􀂄􀂄 30-40% patients present with syncope,
convulsions, depressed cardiac activity and
respiratory function
􀂄􀂄 40% and greater death may ensue within
hours
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Inhalation Injury
Upper Airway Burn
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True Thermal Burn
Danger Signs
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Neck, face burns
Singing of nasal hairs, eyebrows
Tachypnea, hoarseness, drooling
Red, dry oral/nasal mucosa
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Inhalation Injury
Lower Airway Burn
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Danger Signs
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Loss of consciousness
Burned in a closed space
Tachypnea (+/-)
Cough
Rales, wheezes, rhonchi
Carbonaceous sputim
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Electrical Burns
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Electrical Burns
Considerations
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Intensity of current
Duration of contact
Kind of current (AC or DC)
Width of current path
Types of tissues exposed
(resistance)
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Electrical Burns
Considerations
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Conductive injuries
• “Tip of Iceberg”
• Entrance/exit wounds may be small
• Massive tissue damage between
entrance/exit
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Electrical Burns
Management
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Make sure current is off!
Check ABCs
Assess carefully for other injuries
Patient needs hospital evaluation,
observation
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Electrical Injury
Complications
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If gross urinary pigment is present: sodium
bicarbonate and mannitol are initially given
in addition to Ringer’s lactate.
Diuretics in contraindicated.
Urine output maintained 100-125 ml/h until
it is seen to clear
Precipitate cardiac arrhythmia,routine
cardiac monitoring not necessary, unless
cardiac arrest at accident, abnormal EKG,
arrhythmia during transport
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Electrical Injury
Other Complications
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Respiratory arrest
Spinal fractures
Long bone fractures
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Chemical Burns
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Chemical Burns
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Alkaline substances such as sodium
and potassium hydroxides and
cements are most common cause of
chemical burn
Direct chemical reaction instead of
heat production
Often underestimated. Immediate
treatment—copious tap water
lavaging
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Chemical Burns
Concerns
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Damage to skin
Absorption of chemical; systemic
toxic effects
Avoiding EMS personnel exposure
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Chemical Burns
Management
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Remove chemical from skin
Liquids
• Flush with water
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Dry chemicals
• Brush away
• Flush what remains with water
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Chemical Burns
Injuries require special care
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Hydrofluoric acid: treated with a paste
made of 35 ml of 10% calcium
gluconate
in 150 gm of K-Y jelly. Applied to the
affected area and changed every hour if
needed. More severe case require
subcutaneous injection of calcium
gluconate into the painful area
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Chemical Burns
Injuries require special care
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Phenol: not soluble in water.
Absorbed
through intact skin.
Topical application of polyethylene
glycol or vegetable oil
Phosphorus: keep the areas
copiously irrigated and continuously
wet with water, early debridement
of extraneous particles
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Chemical Burns
Injuries require special care
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Cement: rinsed with water until
the soapy feeling disappear,
then dried thoroughly
Tar: respond well to application
of bacitracin or neomycin
ointment for 12 hours, then
washed off and silver
sulfadiazine applied
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Thank You
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