BURNS

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BURNS
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Topics to be Covered

• 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

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Definition

• Burn
• Thermal
• Scald
• Contact
• Electrical
• Chemical
• Radiation

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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

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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

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Initial Management III

• Initiate restoration of HEMODYNAMIC stability
  systemically locally
• Isotonic crystalloid infusion
• Remove any constricting items
• Consider escharotomy for circumferential burns

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Initial Management IV

• Look for other traumatic injuries

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Initial Management V

• Burn wound last priority

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Skin
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Burn Wound Depth
First degree
Superficial second
Deep second
Third degree
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Burn Wound Depth
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Burn Wound Depth
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Superficial second degree burn
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Burn Wound Depth
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Deep second degree burn
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Burn Wound Depth
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Third degree burn
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Animation of burn wound depth
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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 Nines
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Chinese nines
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Emergent or Shock Phase

•  Increased Vascular Permeability
• Altered microcirculation from direct heat injury
  and inflammation
• Time course 
• Peak shift 3-8 hrs
• Continuous 2 days
• increased proteins permeability leading to large
  plasma leak
• Hypovolemia
• Edema formation 
• Edema increases tissue pressure (need for
  escharotomy) 
• Resorption over next 5-7 days (can cause
  hypervolemia)

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After thermal injury
Edema

• Hypovolemia ? Fluid resuscitation
• Crystalloid
• Crystalloid colloid

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Formula for Fluid Resuscitation I
For adult
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Formula for Fluid Resuscitation II
For adult with extensive deep burn
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Formula for Fluid Resuscitation III
For child
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Monitoring Guidelines

• Pulse young patient
• Pulse less than 120, reasonable perfusion pulse
  gt 130, increase fluid
• Elderly or with heart disease pulse not
  accurate reflection of perfusion
• Electrocardiogram
• particularly important for patient more than 45
  years old
• Urine output
• 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
• gt 5 meq / liter reflects decreased tissue
  oxygenation. Look for progressive decrease in
  base deficit as marker of adequacy of
  resuscitation.
• Peripheral perfusion
• For systemic circulation
• For circumferential arm, leg burns

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Vital signs
Fluid infusion 1.5ml for adult 1.75ml for
children 2.0ml for infant X burn X kg BW
Renal
Circulation
Urine Output 0.5-1.0ml/kg BW/hr
Adjustable
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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

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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 burnsduring 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
• 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

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Burn Infection I

• Wound infection
• Invasive infection
• Burn wound sepsis the quantity of bacteria in
• the tissue underneath eschar 105/g
• Systemic infection

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Burn Infection II

• Irritable, disorienting, hallucinating,
  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

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Burn Infection III

• Excision of deep burn wounds and covering the
  excised wound during early stage
• Antibiotics
• Nutrition and systemic support

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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.

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Ohms Law

• The relationship between current flow
  (amperage), pressure (voltage), and resistance is
  described in Ohms 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)

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Joules 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 Joules law
• Power (P) Voltage (E) x Current (I)

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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.

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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.

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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 4000C (7232F) and can melt bone and
  volatilize metal. As a general guide, arcing
  amounts to several centimeters for each 10,000
  volts.

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Effects of Electricity On the Body

• 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.

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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.

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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.

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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.

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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.

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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.

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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.

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Entry and Exit Wounds

• Between the entrance and exit points of
  the electric current, widespread anatomic damage
  and destruction may be seen.

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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.

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Systemic Complications

• Peripheral nerve injury
• cardiac injury
• Vascular damage
• Eye injuries
• 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.

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Systemic Complications

• Severe potassium deficiency is an
  unexplained manifestation of high-voltage
  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.

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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(?), and tar.

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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.

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Water is the Agent of Choice

• Water is the agent of choice for decontaminating
  acid and alkali skin burns.
• 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.
• 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.
• The same effect may occur when certain chemicals
  contact water, yet large volumes of water tend to
  limit this exothermic reaction.

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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
  patients clothes the rescuer should wear rubber
  gloves to prevent hand contact with chemical.

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Hydrofluoric Acid

• Significant local and systemic toxicity can
  result from exposures of eye, skin, or lung to HF
• Inhalation of HF vapor is rare and usually
  involves explosions that produce fumes or high
  concentrations of liquid HF (gt50) that soak the
  clothing of the upper body. Patient outcomes vary
  considerably depending on concentration and
  duration of exposure to HF.
• Inhalation and skin exposure to 70 HF has caused
  pulmonary edema and death within 2 hours.
• 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.
• 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.

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Treatment of HF burn

• all patients with significant HF exposure should
  be hospitalized and monitored for cardiac
  dysrhythmias and electrolyte status for 24-48
  hours.
• 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.
• Hypocalcemia can occur after significant
  exposures to HF and should be corrected with 10
  calcium gluconate administered IV.

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Phosphorus Burn

• White phosphorus is a yellow, waxy,
  translucent solid element that burns in air
  unless preserved in oil.

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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

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Prehospital Care

• Immediate removal of contaminated clothing
• Submersion of phosphorus-contacted skin in cool
  water (Avoid warm water because white phosphorous
  becomes liquid at 44C
• Remove phosphorus particles from victims skin and
  submerge in water.
• Cover burned skin with towels soaked in cool
  water during transport to the ED.

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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

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Systemic Complications

• 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.