BURNS

Mechanisms of Injury
and Biomechanics
• Energy Agents
– Thermal: Heat
– Chemical: Acid, alkali
– Electrical (includes
lightening injuries)
– Ultraviolet radiation
– Ionizing radiation
Concurrent Injuries

• Pulmonary system: Inhalation

injury
• Other trauma-related injuries
– Fractures
– Head injuries
– Abdominal injuries
– Chest injuries
 Pathophysiology

• Skin and soft tissue injury (zones)

• Plasma loss and other vascular responses
• Hypoxemia and asphyxia
• Carbon monoxide poisoning
• Pulmonary injury
• Hypermetabolism
 HEAT INJURY
• The most immediate and obvious injury is that due to
heat.
• Excess heat causes rapid protein denaturation and cell
damage.
• The depth of heat injury is
dependent on the depth of heat
penetration.
• Wet heat (scald) travels
more rapidly into tissue than
dry heat (flame).
 HEAT INJURY

• A surface temperature of over

60' C produces immediate cell
death as well as vessel thrombosis.
• Dead skin tissue on the surface is known as eschar.
• Depth of burn is dependent on the temperature of the heat insult,
the contact time and the medium (air-water).
• Depth of the skin layer is critical as the thinner the skin, the deeper
the burn.
• The inflammatory response initiated by the heat injury is responsible for further early
tissue damage, increased capillary permeability and in large part responsible for the
later wound conversion if inflammation becomes excessive.
 BURN EDEMA

• A layer of protein-rich edema fluid develops between

the eschar (zone of coagulation) and the perfused,
heat-injured micro vessels as a result of increased
(heat and mediator-induced) micro vascular
permeability.
 BURN EDEMA

• The leak is most prominent in the first 8-12 hours but can
persist for days.
• In superficial burns, the edema actually physically separates
viable and non-viable tissue, producing blisters, so that
mechanical cleaning can remove the dead tissues.
• In deep second-degree and third-degree burns, the edema
occurs throughout the injured tissue.
 BURN EDEMA

• However, the necrotic dermis remains physically adherent

to the sub dermal space and requires sharp dissection
(debridement) to remove the dead tissue or the process
of necrolysis must occur. This process is deleterious due to
the risk of infection and degree of tissue inflammation, as
well as absorption of dead tissue.
• The degree of tissue edema is dependent on the amount
of resuscitation fluid given and the vascular pressures
perfusing the area.
INFLAMMATION INDUCED WOUND INJURY

• Protease Release Injuring Healing Tissue and

Deactivating Growth Factors
• Oxidants Release Injuring Cells, Denaturing Proteins,
and Activating Inflammation
• Consumption of Wound Oxygen by Neutrophils
Leading to Tissue Hypoxia
• Increasing Stimulus to Fibrosis
 ISCHEMIA INDUCED INJURY

• Instant surface vascular thrombosis occurs along with cell death

from the heat insult.
• Ischemia does not play a role in the initial surface necrosis.
• However, the injured capillaries below the surface, where tissue is
still viable, can continue to thrombose due to initial heat and
subsequent mediator injury, to endothelial cells, causing further
ischemia and further tissue necrosis.
• Systemic hypovolemia or local impairment in perfusion due to
constricting eschar or edema will produce the same effect.
 Impaired Breathing from deep chest wall
burn
• The restriction to ventilation is further compromised
by the abdominal burn diminishing the movement of
the diaphragm.
•
Tissue Damage
Zone of Injury
 Pathophysiology

• ZONE OF COAGULATION
– This zone is comprised of the surface tissue necrosis of
the initial burn eschar.
– The surface injury is caused mainly by the heat or
chemical insult.
– Obviously this zone has an irreversible injury.
– Tissue not viable
 ZONE OF INJURY
(STASIS)

• Deep and peripheral to the zone of coagulation,

there is a sizable area of tissue injury where cells
are viable but can easily be further damaged.
• The terms "stasis" or "ischemia" were used
because the progressive injury in this area was
thought to be due to capillary thrombosis from
injured endothelium, leading to ischemia-
induced cell death.
 ZONE OF INJURY (STASIS)
• Fibrin deposition, vasoconstriction, and thrombosis indeed do
occur, most likely as a result of continued release of mediators.
• However, early epithelial cell death in this area, unrelated to
blood flow, is reported to be quite high, leading to slowing of
healing.
• Epithelial cells are particularly prone to environmental insults
such as desiccation- and inflammation-induced injury.
• This zone is most prominent in mid-to-deep-dermal burns
where there is less reserve in the remaining viable cells and
less blood flow.
 ZONE OF
HYPEREMIA

• Peripheral to and below the zone of stasis is the zone of

hyperemia.
• The area is characterized by minimal cell injury but with
vasodilatation due to neighboring inflammation-induced
mediators.
• Completed recovery of this tissue is expected unless there
is an additional severe insult such as an invasive infection
or profound tissue inflammation.
• Increased blood flow
 ZONES OF INJURY IN TWO BURN DEPTHS

• THE ZONES OF STASIS OR INJURY AND HYPEREMIA (reaction)

are much larger in a mid dermal burn compared to a
superficial burn.
• This larger zone of injury exceeds the increase in size of
the zone of coagulation (necrosis) between the two
depths.
 Factors Increasing Zone of Injury

• lower blood flow with a deeper

burn
• increased risk of infection with
deeper burn
• presence of surface necrotic tissue
 CONTINUING BURN WOUND INJURY

• ongoing inflammation caused by

- neurotic tissue
- bacteria on surface
- caustic topical agents
- surface exudate
• excess wound proteolytic activity MID-DERMAL BURN (Admission)
- activated by surface insults
- continued damage to viable cells and new tissue growth
- damage to wound surface and matrix denaturation of growth
factors
• excess oxidant release
- injuring viable cells
 Pathophysiology - Plasma Loss and Other
Vascular Responses
• Increased capillary permeability
– Decreased colloid osmotic pressure
– Plasma loss leads to hypovolemia

• Rate of fluid loss from intravascular spaces

depends on:
– Age
– Burn size and depth
– Intravascular pressures
– Time elapsed since the burn
 Pathophysiology -
Vascular System Changes
• Hemoconcentration of blood
• Increased blood viscosity
• Increased peripheral resistance
• Actual number of red blood
cells is diminished
 Pathophysiology - Hypoxemia/Asphyxia

• Reduction in fraction of inspired oxygen leads to

arterial hypoxemia
• Asphyxia occurs when the blood has a decreased
amount of oxygen and an increase in carbon dioxide in
the blood and tissues
 Pathophysiology -
Carbon Monoxide Poisoning
• Carbon monoxide is a tasteless, odorless, colorless gas that is
present in the smoke of combustion of organic materials
• Carbon monoxide binds to oxygen binding sites on hemoglobin
molecules; oxygen carrying capacity reduced
• Carbon monoxide also affects the cardiac muscle since it binds
with myoglobin
 Pathophysiology -
Pulmonary Injury
• Occurs when inhaled particles enter the lung
• Accumulation of debris and secretions results in:
– Airway obstruction
– Atelectasis
– Impaired ciliary clearance
• Sequelae: Pulmonary edema, pneumonia
Pathophysiology - Hypermetabolism
• Increased basal metabolic rate due to
autonomic nervous system response
• Influences
– Age
– Ambient temperature
– Anxiety
– Activity
– Infection (late)
Pathophysiology - Hypermetabolism
Signs and Symptoms
• Tachypnea
• Tachycardia
• Low-grade fever
 Electrical Burns

• Sources
– Lightning (direct exposure: DC)
– Alternating current (AC): Tetany
 Electrical Burns
• Assess
– Voltage
– Type of current
– Location of electrical source
– Duration of contact
 Electrical Burns

Signs and Symptoms

• Two wounds (entrance and exit)
• Altered level of consciousness
• Cardiac dysrhythmias
• Presence of hemoglobinuria or myoglobinuria
 Chemical Burns

Sources
• Acid
• Alkali
• Petroleum-based
Chemical Burns
Assess
• Identify causes
• Contact poison
center
• Extent of injury
progression
Chemical Burns

Influenced by:
• Length of contact
• Concentration of chemical
• Amount of chemical
 Chemical Burns
Signs and Symptoms
• Erythema
• Edema
• Blisters
• Tissue necrosis
• Pain
 Nursing Care - Assessment

History
• What was the causative
agent/mechanism of burn?
• Does the agent pose a threat to the team?
• Any clothing or jewelry to be removed?
• Patient complaints?
• Is the patient hoarse?
 Nursing Care - Assessment

History (continued)
• Where was the patient located?
• What was the patient’s weight?
• Has the patient consumed alcohol or taken
drugs?
• Is the mechanism of injury/pattern of burn
suspicious?
• Is the patient a smoker?
 Nursing Care -
Physical Assessment
Inspection
• Determine airway patency and breathing
effectiveness
• Nasopharynx and oropharynx
• Singed nasal, facial, and eyebrow hairs
 Nursing Care -
Physical Assessment
Inspection (continued)
• Burns and edema
• Count respiratory rate, determine breathing pattern,
watch expansion of chest during inspiration
 Nursing Care -
Physical Assessment
Determine Severity of the Burn
• Based on depth, extent, and
location
• Age, pre-existing health
status, presence of other
injuries, and mechanism of
injury
 Nursing Care -
Physical Assessment
• Superficial: First degree
burn
• Partial thickness:
Second degree burn
• Full thickness:
Depth of the Burn
 MID-DERMAL BURN
• Necrosis to mid-dermis
• Large zone of injury (potential conversion)
• Eschar separated from viable tissue by edema layer
 Third degree burn
(Deep Dermal Burn)
• Full thickness:
– Necrosis involving majority of skin layers
– Zone of necrosis adherent to zone
– Smaller edema layer

–
In a full thickness burn, the zone of injury can
readily extend below the skin into subcutaneous
tissues. The zone of hyperemia develops in the
subeschar area being most evident beginning about
7 days post burn.
 Visually Deceiving Burn

• Some burns usually caused by

contact with flames or extremely hot temperature, like
explosion, have the destroyed epidermis
still present on the wound.
• The depth can be underestimated unless the wound is
gently washed and debrided after which the size and
depth is more clearly defined.
 FLAME BURN (DIRECT CONTACT)
• Looks superficial with blisters but mechanism suggests
deep burn

• When gently cleaned, wound is noted to be a

combination of deep second and third degree burn
 Nursing Care -
Physical Assessment
Determine Extent of Burn Injury
• Percent of total body surface area (TBSA) burned
• Rule of Nines
• Lund and Browder chart
• To measure the extent of irregular burns, percent
burned surface can be estimated by considering the
palm of the patient’s hand, which is equivalent to 1%
 Nursing Care -
Physical Assessment
The Rule of Nines
 Determine Location of the Burn
• Circumferential burns of the chest or neck may lead to
respiratory compromise
• Certain locations of thermal burns present specific patient
problems
– Face and neck
– Hands
– Feet
– Perineum
 Nursing Care -
Physical Assessment

Auscultation
• Breath sounds
• Pulses in burned digits with
a Doppler Ultrasonic Flow Meter
 Nursing Care -
Physical Assessment
Palpation
• Peripheral pulses
• Extremities to determine sensory function and
neurovascular compromise
• Feel temperature of the skin to determine peripheral
perfusion status
 Diagnostic Procedures
• Radiographic Studies
– Chest
• Laboratory Studies
– Arterial blood gases, carboxyhemoglobin, pH, and SaO2
– Urinalysis, hemoglobin, myoglobin
• Other
– Pulse oximetry
– Fiberoptic, flexible bronchoscopy
 Planning and Implementation
History of smoke exposure or
exposure to high temperature e.g.
explosion
Direct laryngoscopic evidence of
injury
Symptoms of stridor, dyspnea (often
delayed in onset)

• Stop the burning process

• Ensure patent airway
• Administer oxygen via a nonrebreather mask at a flow
rate sufficient to keep the reservoir inflated to 12 to
15 L/min
 Planning and Implementation

• Assist ventilation (positive end expiratory pressure or

continuous positive airway pressure)
• Cannulate 2 veins with large bore 14- or 16-gauge catheters
and initiate infusion of a warmed intravenous solution
• Infuse 2 to 4 ml/kg x % of TBSA burned
– Give within the first 24 hours
– Give 1/2 in the first 8 hours postburn
 Fluid Resuscitation Protocol
• Establish and maintain adequate
• Circulation
• Burns >20% TBS require initial fluid resuscitation
• Use at least one large bore intravenous catheter.
• Begin Ringer’s Lactate.
• Estimate initial rate according to the estimated percent of total
body skin surface burned (%TBS).
• Estimated body weight
• 2cc-4cc/kg/%TBS burn in 24 hours giving half of the estimate in
first 8 hours, remaining last 16 hours
 Practice Math Formula

• 80 gms patient got burned at 10AM

• IV started at 11AM
• TBSA burned =?
– Full face
– Full trunk
– Both arms
• MD writes for 4cc/kg/%TBS
 Fluid Resuscitation Protocol
• Foley catheter- Nasogastric tube
• Maintain: Blood Pressure>90 systolic
• Urine output 0.5-1.0ml/kg/hr
• Pulse <130Temperature >37°C
• Modify protocol in the presence of massive burns,
inhalation injury, shock, and in elderly patients:- Fluid
requirements are greater to prevent burn shock- Include
colloid: either Hespan or Albumin in the patients from the
beginning
 Planning and Implementation

• Administer analgesic medications

• Insert an indwelling catheter
• Insert a gastric tube
• Apply cool, saline-moistened, sterile dressings to
TBSA burns < 10%
• Cover burns > 10% TBSA with a clean, dry sheet
• Keep the patient warm
 Planning and
Implementation

• Assist with escharotomies of chest wall and/or extremities

• Elevate burned extremities
• Treat or assist with burn wound care
• Care for localized burn wound
• Provide psychosocial support
• Prepare for operation, admission, or transfer
 Planning and Implementation
• If severely burned, transfer to a burn center and
consult with the receiving facility
• Hyperbaric oxygen therapy (HBO)
• Administer medications, especially for cyanide
poisoning
 Nursing Interventions
for an Electrical Burn
• Monitor pH, PaO2, PaCO2, SpO2, bicarbonate
• Infuse intravenous fluids at 70 to 100 ml/hr
• Observe color of urine for myoglobin
• Monitor cardiac rate and rhythm
• Monitor for signs and symptoms of compartment
syndrome
 Nursing Interventions
for a Chemical Burn
• Assure protection of trauma team
• Irrigate burned area
• Do not waste time identifying agent
• Phenol should be irrigated with water
• Hydrofluoric burns: Topical application of 5% calcium
gluconate-based gel
• Cool tar/asphalt burns and use petroleum products
 Eye Injury (Prevention & Treatment)

• Permanent eye damage con be prevented if copious,

continuous irrigation with water, saline or Ringer’s
Lactate
• Remove contact lenses
• Hold eyelids apart and begin gentle, continuous
irrigation
• Use if IV bag and tubing provides continuous
controlled irrigation
Evaluation and Ongoing Assessment

• Monitor pulmonary status

• Monitor urinary output
• Assess peripheral circulation
• Assess progression of edema formation
 Burn injuries that should be referred to a
burn unit includes the following:

• Partial thickness burns greater than 10% total body surface area
(TBSA).
• Burns that involve the face, genitalia, perineum or major joints
• Third degree burns in any age group.
• Electrical burns including lightening injury
• Chemical burns including lightening injury Inhalation injury.
• Children with any of the above burn injuries.
 Burn injuries that should be referred to a burn
unit includes the following:

• pre-existing medical disorders that could complicate

management.
• traumatic injury (such as fractures) in which the burn injury
poses the greatest risk of morbidity or mortality. If the
trauma poses the greater immediate risk, then the patient
must be initially stabilized in the nearest appropriate facility
before being transferred to a burn unit.
• Any burned children if the hospital initially receiving the
patient does not have qualified personnel or equipment for
children.