Oleh : Dr. Mgs. Roni
Saleh,
SpB-SpBP(K)
I.
Phatophysiology
A.The severity of the burn is
determined by temperatur and length of exposure to the heat
source.
B.Skin has a large water conten; therefore, it overheats slowly
and cools slowly.
C.Heat continues to penetrate deeper
tissue layers even after the external heat source is removed. Immediate cooling
may reduce underlying tissue temperature, but it has a limted role in large burns because it may
reduce the patient’s core temperature.
D. Three areas of injury
1.Central
“zone of coagulation”: Nonviable, irreversibly injured tissue.
2.Middle
“zone of stasis”: Initially characterized by dilated blood vessels and
capillary diffusion. After 24 to 28 hours, dilated capillaries become occluded,
with resulting conversion of this zone of tissue to coagulation. Injury in this
zone may be reversible with appropriate treatment (cooling, fluid
resuscitation, critical care).
Outer
“zone of hyperemia”: Composed mostly of viable, edematous tissue.
E.Progressive changes in
microcirculation
1.There
is an initial, sudden decrease in blood flow.
2.Arteriolar
vasodilation follows.
3.Increase
capillary permeability leads to edema formation, which is greatest at 8 to 12
hours.
4.Endogenous
mediators (histamine, serotonin, kinins)
increase capillary permeability, leaking protein into the intersitial
space.
5.Hypoproteinemia
decreases intravascular oncotic pressure, resulting in a shift of fluid into
the interstitium
(i.e., “third spacing”)
II. Initial management
A.History
1.Identity the source: Hot liquid,
chemicals, flame, superheated air/steam, explosion, etc.
2.Duration and location of exposure:
Closed space; potential for smoke inhalation
3.Concomitant drug or alcohol
ingestion
4.Associated injury mechanism: Esplosion,
jump/fall, motor vehicle crash, etc.
B. Airway and breathing
1.Early
intubation
a.Frequently necessary to prevent
airway obstruction due to progressive airway edema.
b.Most patients with extensive
(>50%) burns requre
intubation
c.Use humidified oxygen.
2.Chest
and abdominal wall burns can severely limit chest wall excursion and impair
ventilation. Escharotomies
may be necessary
C.Circulation
1.Intravenous
access: Ideally, several peripheral
large-bore intravenous lines should be place through nonburned
tissue. Central lines are the next best
option.
2.Intravenous
fluid administration
a.Isotonic salt solutions are used
for resuscitation and maintenance.
b.Glucose should be avoided. Burn patients are frequently glucose intolerant and hyperglycemic due to
the stress response. The resulting osmotic diuresis can lead to spuriously high
urine output.
D.Disability : A rapid, thorough
baseline neurologic examination should be performed. This is especially important in the setting
of blunt trauma, head injury, carbon monoxide exposure, and/or the need for
sedation.
E.Initial wound care
1.Stop
the burning process
a.Flame burns: smoldering or burning
materials must be extinguished and removed, since they can retain heat and
exacerbate the burn injury. Irrigate the
wounds with normal saline if any foreign material remains.
b.Chemical burns: Remove all clothing
and begin gentle, copious irrigation with warm normal saline. Avoid the use of neutralizing solutions.
2.Cover:
Clean, dry, nonadherent
dressings are used to protect the wound and prevent hypothermia.
3.Analgesia.
4.Tetanus
prophylaxis.
5.Prophylactic
intravenous antibiotics are not
indicated.
6.Criteria
for admission to a burn center.
a.If 10 to 40 years old: Greater than
15% total body surface area (TBSA) second-degree burns or greater than 3%. TBSA
third-degree burns should be treated on an inpatient basis.
b.If younger than 10 years or older
than 40 years: Greater than 10% TBSA second-or third-degree burns.
c.Burns involving the face, hands
feet and/or perineum
d.Circumferential extremity burns.
e.Electrical burns
III.
Inhalation Injury
A.Etiology
1.Chemical
irritants in smoke affect the distal airways, resulting in an intense
inflammatory response, which can lead to adult respiratory distress syndrome
(ARDS) and/or systemic inflammatory response syndrome (SIRS).
2.Direct
thermal injury: inhalation of superheated air or water vapor can cause a
thermal burn to the airway mucosa.
3.Oropharyngeal
and supraglottic
edema caused by thermal injury can progress to airway obstruction
B.Evaluation
1.Maintain
a high index of suspicion.
2.Signs
and symptoms
a.History of burn in a closed space
b.Presence of facial burns and/or
oral carbon deposits.
c.Singed facial hair/nares,
hoarseness, or wheezing.
d.Unconsciousness.
3.Nasopharyngoscopy:
Can be used to directly evaluate the larynx and vocal cords for injury.
4.Bronchoscopy:
Via the endotracheal tube, if symptoms warrant.
C.Treatment
1.Intubation,
mechanical ventilation
a.Early intubation is essential.
Patients with inhalation injury often present as conscious, awake, and
comfortable initially. Upper airway
edema can progress rapidly to complete airway obstruction.
b.Ventilator management goals:
Maximize oxygenation while avoiding oxygen toxicity (keep FiO2
<0.7) and barotrauma.
2.Bronchodilators:
Useful in treating bronchospasm associated with smoke inhalation.
3.Steroids:
Have not been shown to be beneficial in avoiding pulmonary complications with
burns
D.Carbon Monoxide (CO) poisoning
1.CO
is generated by fire. When inhaled and
absorbed, it preferentially binds with hemoglobin, displacing oxygen and
blocking oxygen binding sites, causing a substantial reduction in oxygen
delivery.
2.Signs
and symptoms
a.Pulse oximetry
is unreliable
b.Cherry red skin
c.Hypoxemia
d.Mental status changes or a history
of a loss of consciousness
e.Persistent acidosis in the presence
of normovolemia
3.CO
level
a.May be normal or minimally
elevated, even with significant exposure.
b.20% to 40% Associated with severe
neurologic symptoms.
c.Greater than 60% Commonly fatal
4.Treatment
a.100% oxygen administration:
Displaces CO from hemoglobin
b.Hyperbaric therapy: Consider if the
patient is at risk for CO exposure and has mental status changes
