Transcript 幻灯片 1 - shsmu.edu.cn

Topics to be Covered
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Definition
Initial management
Emergent or shock phase
Assessment of inhalation injury
Assessment of burn severity and extent
Wound management
Burn infection
Electrical burn
Chemical burns
Summary
Definition
 Burn
- Thermal
- Scald
- Contact
- Electrical
- Chemical
- Radiation
Initial Management I
 STOP THE BURNING PROCESS
- Water for smoldering clothing
- Water for chemical burns
- Remove clothing - keep warm
- Cool water for small 2° burns only
Initial Management II
 ASSURE ADEQUACY OF VENTILATION
AND OXYGENATION
- Provide oxygen for all burns to treat carbon
monoxide
- Consider early endotracheal intubation with
smoke inhalation injury
Initial Management III
 Initiate restoration of HEMODYNAMIC
stability systemically & locally
- Isotonic crystalloid infusion
- Remove any constricting items
- Consider escharotomy for circumferential burns
Initial Management IV
 Look for other traumatic injuries
Initial Management V
 Burn wound last priority
Skin
Burn Wound Depth
First degree
Superficial second
Deep second
Third degree
Burn Wound Depth
DEGREE
CAUSE
APPEARAN
CE
PAIN
HEALIN
G
SCAR
Superficial
second
hot liquid,
short
exposure
wet, pink,
blisters
severe
10-14
days
minimal
Deep
second
chemicals,
direct
contact
flames
less wet, red
blisters
red with
patchy white
areas
dry, white
Moderate
minimal
2-6
weeks
moderate or
severe
chemicals,
flames,
explosion,
with very
high
temperature
dry, white, or
char
none
need
graft
mild to severe,
depending on
timing and type
of graft
Third
Burn Wound Depth
DEGREE
CAUSE
APPEARAN
CE
PAIN
HEALIN
G
SCAR
Superficial
second
hot liquid,
short
exposure
wet, pink,
blisters
severe
10-14
days
minimal
Deep
second
chemicals,
direct
contact
flames
less wet, red
blisters
red with
patchy white
areas
dry, white
Moderate
minimal
2-6
weeks
moderate or
severe
chemicals,
flames,
explosion,
with very
high
temperature
dry, white, or
char
none
need
graft
mild to severe,
depending on
timing and type
of graft
Third
Superficial second degree burn
Burn Wound Depth
DEGREE
CAUSE
APPEARAN
CE
PAIN
HEALIN
G
SCAR
Superficial
second
hot liquid,
short
exposure
wet, pink,
blisters
severe
10-14
days
minimal
Deep
second
chemicals,
direct
contact
flames
less wet, red
blisters
red with
patchy white
areas
dry, white
Moderate
minimal
2-6
weeks
moderate or
severe
chemicals,
flames,
explosion,
with very
high
temperature
dry, white, or
char
none
need
graft
mild to severe,
depending on
timing and type
of graft
Third
Deep second degree burn
Burn Wound Depth
DEGREE
CAUSE
APPEARAN
CE
PAIN
HEALIN
G
SCAR
Superficial
second
hot liquid,
short
exposure
wet, pink,
blisters
severe
10-14
days
minimal
Deep
second
chemicals,
direct
contact
flames
less wet, red
blisters
red with
patchy white
areas
dry, white
Moderate
minimal
2-6
weeks
moderate or
severe
chemicals,
flames,
explosion,
with very
high
temperature
dry, white, or
char
none
need
graft
mild to severe,
depending on
timing and type
of graft
Third
Third degree burn
Animation of burn wound depth
Estimating Burn Extent
Rule of Nine's - in increments of 9% BSA
- entire upper limb
- anterior or posterior surface of one lower limb
- 1/2 of the anterior or posterior surface of the trunk
- total head and neck (adult)
 Lund & Browder Chart emphasizes the relatively larger
head size in:
- in infancy (largest)
- childhood (larger)
- adulthood (normal)
 Patient's palm size in children represents 1 - 1.25%
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Notes of Nine’s
sites
% of TBSA
Child
Head & neck
9
9 +[12- X (Age)]
Both upper limbs
9X2
9X2
Trunk
9X3
9X3
Buttocks
Both lower limbs
9X5+1
9 X 5 + 1- [12- X( Age)]
Chinese nine’s
Calculation%
Surface area%
part
9
6
head
3
neck
3.5x2
arm
3x2
fore arm
2.5x2
hand
13
trunk front
13
trunk back
1
perineum
2.5x2
buttock
10.5x2
thigh
6.5x2
leg
3.5x2
foot
2x9
3x9
5x9+1
Emergent or Shock Phase
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Increased Vascular Permeability
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Altered microcirculation from direct heat injury and
inflammation
Time course:
Peak shift 3-8 hrs
- Continuous 2 days
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increased proteins permeability leading to large plasma
leak
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Hypovolemia
Edema formation
Edema increases tissue pressure (need for escharotomy)
Resorption over next 5-7 days (can cause hypervolemia)
Body fluid
blood volume
Leakage
other
third gap
After thermal injury
4%
40%
40%
52%
48%
4%4%
8%
Hypovolemia → Fluid resuscitation
Crystalloid
Crystalloid & colloid
Formula for Fluid Resuscitation I
Crystalloid
ml/%TBSA/kg BW
Colloid
ml/%TBSA/kg BW
G5W
First 24 hours
1.00
0.50
2000 ml
Second 24 hours
½ of above
½ of above
Same as above
For adult
Formula for Fluid Resuscitation II
Crystalloid
ml/%TBSA/kg BW
Colloid
ml/%TBSA/kg BW
G5W
First 24 hours
0.75
0.75
2000 ml
Second 24 hours
½ of above
½ of above
Same as above
For adult with extensive deep burn
Formula for Fluid Resuscitation III
Crystalloid
ml/%TBSA/kg BW
Colloid
ml/%TBSA/kg BW
G5W
First 24 hours
1.00
1.00
70-80 ml/kg
Second 24 hours
½ of above
½ of above
Same as above
For child
Monitoring Guidelines
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Pulse: young patient
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Electrocardiogram
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0.5 to 1 cc/kg/hr is adequate in absence of diuretic such as alcohol
Exception: Myoglobin or hemoglobinuria where over 1cc/kg/hr is indicated
Base deficit
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particularly important for patient more than 45 years old
Urine output
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Pulse less than 120, reasonable perfusion; pulse > 130, increase fluid
Elderly or with heart disease : pulse not accurate reflection of perfusion
> 5 meq / liter reflects decreased tissue oxygenation. Look for progressive
decrease in base deficit as marker of adequacy of resuscitation.
Peripheral perfusion
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For systemic circulation
For circumferential arm, leg burns
Vital signs
Fluid infusion
1.5ml for adult
1.75ml for children
2.0ml for infant
X % burn X kg BW
Circulation
Renal
Urine
Output
0.5-1.0ml/kg BW/hr
Adjustable
Wound management I
 Superficial second degree burns
- Do not move the blisters and do try to keep
the outer of the blisters intact.
- Do not change the dressing too frequently
unless the dressing is odor the wound is
infected
Wound management II
 Deep second degree burns
Apply 1% silver sulfadiazine cream to the wound
- Change dressing daily
- Apply the 10% sulfamylon cream to the infected
wound
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Wound management III
 Third degree burns
during the early stage
Admit as edema process may require escharotomies
- apply 1% silver sulfadiazine cream with dressing
- Change dressing daily
- Apply 10% sulfamylon cream to the infected wound
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Operation
Tangential excision
- Fascia excision
- Skin grafting
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Special Area
 Apply topical antibiotic ointment or
cream followed by soft gauze dressing
 Face treat open
 Perineum treat open
 Meets criteria for Burn Center due to
high risk location
Burn Infection I
 Wound infection
 Invasive infection
 Burn wound sepsis: the quantity of bacteria in
the tissue underneath eschar ≥ 105/g
 Systemic infection
Burn Infection II
 Irritable, disorienting, hallucinating,
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persecutory delusion, apathy
Shivering High fever or hypothermia
Tachycardia
Tachypnea
Deterioration of the burn wound
The count of WBC higher or lower than that in
normal range
Burn Infection III
 Excision of deep burn wounds and covering
the excised wound during early stage
 Antibiotics
 Nutrition and systemic support
Electrical Burn I
 Resistance
- Resistance is a measure of how difficult it
is for electrons to pass through a material
and is expressed in a unit of measurement
termed an ohm.
- The amount of heat developed by a
conductor varies directly with its resistance.
Ohm’s Law
 The relationship between current flow
(amperage), pressure (voltage), and
resistance is described in Ohm’s law,
which states that the amount of current
flowing through a conductor is directly
proportional to voltage and inversely
related to resistance.
 Current (I) = Voltage (E)/Resistance (R)
Joule’s Law
 Power (watts) lost as a result of the
current passage through a material
provides a measure of the amount of
heat generated and can be determined
by Joule’s law
 Power (P) = Voltage (E) x Current (I)
Body Resistance I
 The callused palm may reach 1,000,000
ohms/cm2, while the average resistance of
dry normal skin is 5000 ohms/cm2 decrease
to 1000 ohms/cm2 if hands are wet.
 The stratum corneum that serves as an
insulator for the body Exposure of the skin to
50 volts for 6-7 seconds results in blisters that
have a considerably diminished resistance.
Body Resistance II
 The dermis offers low resistance, as do
almost all internal tissues except bone,
which is a poor conductor of electricity.
 Bone has a high resistance, thus
readily transforms current to heat
production, which may result in
periosteal necrosis or even melting of
the calcium phosphate matrix.
Electric Arc
 Contact with high-voltage current may be
associated with an arc or light flash
 Temperature of the ionized particles and
immediately surrounding gases of the arc can
be as high as 4000°C (7232°F) and can
melt bone and volatilize metal. As a general
guide, arcing amounts to several centimeters
for each 10,000 volts.
Effects of Electricity On the Body
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Effects of electricity on the body are determined by 7 factors:
(1) type of current, (2) amount of current, (3) pathway of
current, (4) duration of contact, (5) area of contact, (6)
resistance of the body, and (7) voltage. Low-voltage electric
currents that pass through the body have well-defined
physiologic effects that are usually reversible. For a 1-second
contact time, a current of 1 milliampere (mA) is the threshold
of perception, a current of 10-15 mA causes sustained
muscular contraction, a current of 50-100 mA results in
respiratory paralysis and ventricular fibrillation, and a current
of more than 1000 mA leads to sustained myocardial
contractions.
Tetanizing Effect
A level of alternating current is
reached for which the subject cannot
release the grasp of the conductor.
This tetanizing effect on voluntary
muscles is most pronounced in the
frequency range of 15-150 Hz.
Factors Found To Be of Primary
ventricular fibrillation is inversely proportional to the square root of
the importance are duration of current flow and body weight. The
threshold for shock duration and directly proportional to body weight.
When the heart is exposed to currents of increasing strength, its
susceptibility to fibrillation first increases and then decreases with
even stronger currents. At relatively high currents (1-5 amps), the
likelihood of ventricular fibrillation is negligible with the heart in
sustained contraction. If this high current is terminated soon after
electric shock, the heart reverts to normal sinus rhythm. In cardiac
defibrillation, these same high currents are applied to the chest to
depolarize the entire heart.
High-voltage Accidents
In high-voltage accidents, the victims
usually do not continue to grasp the conductor.
Often, they are thrown away from the electric
circuit, which leads to traumatic injuries (eg,
fracture, brain hemorrhage). The infrequency
with which sustained muscular contractions
occur with high-voltage injury apparently
occurs because the circuit is completed by
arcing before the victim touches the contact.
Low-voltage Electric Burns
Low-voltage electric burns almost
exclusively involve either the hands or oral
cavity. In either injury, hospitalization is
recommended to treat the local burn injury
and monitor for systemic sequelae.
Current Pathways I
Low-voltage current generally follows the path of least
resistance (ie, nerves, blood vessels), yet high-voltage
current takes a direct path between entrance and ground.
The volume of soft tissue through which current flows
behaves as a single uniform conductor, thus is a more
important determinant of tissue injury than the internal
resistance of the individual tissues. Current is concentrated
at its entrance to the body, then diverges centrally, and
finally converges before exiting.
Current Pathways II
Consequently, anatomic locations of the contact sites
are critical determinants of injury. Most of this
underlying tissue damage, especially muscle, occurs at
the time of initial insult and does not appear to be
progressive. Microscopic studies of electric burns
demonstrate that this initial destruction of tissues is not
uniform. Areas of total thermal destruction are mixed
with apparently viable tissue. Between the entrance
and exit points of the electric current, widespread
anatomic damage and destruction may be seen. An
electric current can injure almost every organ system.
Entry and Exit Wounds
Between the entrance and
exit points of the electric
current, widespread anatomic
damage and destruction may
be seen.
Initial Management of Electrical Burn
If disconnecting the victim from
the electric circuit does not restore
pulses, the first responder must
start cardiopulmonary resuscitation
to restore breathing and circulation.
Systemic Complications
 Peripheral nerve injury
 cardiac injury
 Vascular damage
 Eye injuries
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A wide range of voltages, from 220-50,000 volts,
results in a cataract in 6% of electric injuries. Time
of onset of the symptoms ranges from 3 weeks to 2
years. Lesions of the cornea, fundus, and optic
nerve, without alteration of the lens, also have been
reported.
Systemic Complications
Severe potassium deficiency is an
unexplained manifestation of highvoltage electric injury. This problem was
identified in patients with normal renal
function who were eating well 2-4 weeks
after injury. In these patients, respiratory
arrest and severe cardiac arrhythmias
may lead to the diagnosis.
Chemical Burns I
Chemical injuries are commonly encountered
following exposure to acids and alkali, including
hydrofluoric acid, formic acid, anhydrous
ammonia, cement, and phenol. Other specific
chemical agents that cause chemical burns
include white phosphorus, elemental metals,
nitrates, hydrocarbons(烃）, and tar.
Chemical Burns II
Chemical burns continue to destroy tissue until
causative agent is inactivated or removed. For example,
when hydrotherapy is initiated within 1 minute after skin
contact with either an acid or alkali, severity of the skin
injury is far less than when treatment is delayed for 3
minutes. When contact time exceeds 1 hour, pH of a
sodium hydroxide (NaOH) burn cannot be reversed.
Similarly, brief washing of a hydrochloric acid (HCl) burn
more than 15 minutes after exposure does not
significantly alter acidity of damaged skin.
Water is the Agent of Choice
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Water is the agent of choice for decontaminating acid and alkali skin
burns.
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Deleterious effects of attempting to neutralize acid and alkali burns
were first noted in experimental animals in 1927. In every instance,
animals with alkali or acid burns that were washed with water
survived longer than animals treated with chemical neutralizers.
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The additional trauma of the heat generated by the neutralization
reaction superimposed on the already existing burn accounts for the
striking difference between the results of these two treatment
methods.
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The same effect may occur when certain chemicals contact water,
yet large volumes of water tend to limit this exothermic reaction.
Notes Of Hydrotherapy
Because contact time is a critical determinant of
severity of injury, for skin exposed to a toxic liquid
chemical, an exposed person or a witness to the injury
must initiate hydrotherapy immediately.
 When workers clothes are soaked with such agents,
valuable time is lost if their clothing is removed before
copious washing commences.
 Gentle irrigation with a large volume of water under low
pressure for a long time dilutes the toxic agent and
washes it out of the skin.
 During hydrotherapy, rescuer should remove the
patient’s clothes; the rescuer should wear rubber
gloves to prevent hand contact with chemical.
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Hydrofluoric Acid
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Significant local and systemic toxicity can result from
exposures of eye, skin, or lung to HF
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Inhalation of HF vapor is rare and usually involves explosions that produce
fumes or high concentrations of liquid HF (>50%) that soak the clothing of
the upper body. Patient outcomes vary considerably depending on
concentration and duration of exposure to HF.
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Inhalation and skin exposure to 70% HF has caused pulmonary edema
and death within 2 hours.
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Pulmonary injuries that are not evident until several days after exposure
also can occur. The patient has no respiratory symptoms and a normal
chest radiograph initially, yet massive purulent tracheobronchitis that is
refractory to treatment may develop.
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HF binds calcium and magnesium with strong affinity. Systemic fluoride
toxicity, including dysrhythmias and hypocalcemia, can occur from
ingestion, inhalation, or dermal exposure to HF.
Treatment of HF burn
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all patients with significant HF exposure should be hospitalized
and monitored for cardiac dysrhythmias and electrolyte status
for 24-48 hours.
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If left untreated, a burn caused by 7 mL of 99% HF can
theoretically bind all available calcium in a 70-kg man.
Prolonged QT interval on electrocardiogram is a reliable
indicator of hypocalcemia.
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Hypocalcemia can occur after significant exposures to HF and
should be corrected with 10% calcium gluconate administered
IV.
Phosphorus Burn
White phosphorus is a yellow, waxy,
translucent solid element that burns in
air unless preserved in oil.
Tissue Injury
Tissue injury from exposure to white
phosphorous appears to be caused
primarily by heat production, The
ultimate result of this thermal injury is
often a painful partial or full-thickness
burn
Prehospital Care
 Immediate removal of contaminated clothing
 Submersion of phosphorus-contacted skin in
cool water (Avoid warm water because white
phosphorous becomes liquid at 44°C
 Remove phosphorus particles from victims
skin and submerge in water.
 Cover burned skin with towels soaked in cool
water during transport to the ED.
Treatment Of White Phosphorus Burns
 Wash burned skin with a suspension of 5%
Sodium bicarbonate and 3% copper sulfate in
1% hydroxyethyl cellulose (This mixture must be
made by hospital pharmacies )
- For easy identification
- Decreases the rate of oxidation of phosphorus
particles to limit their damage to underlying tissue
- Remove blackened particles
Systemic Complications
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Metabolic derangements have been identified in
white phosphorous burns.
Postburn serum electrolyte changes consist of
depression of serum calcium and elevation of serum
phosphorus. Also identified are postburn ECG
abnormalities, including prolongation of QT interval,
bradycardia, and ST-T wave changes. These ECG
changes may explain early sudden death
occasionally seen in patients with apparently
inconsequential white phosphorous burns.
After hydrotherapy and treatment with appropriate
antidote, definitively manage skin burns in the
hospital intensive care unit setting as with any other
burn wound.