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Thermal and Inhalation Injury

Chapter 39
Written by : Melissa Dearing LSC-Kingwood
Epidemiology

In the U.S.
Results in 60,000 hospitalizations
annually
6000 deaths annually
Mortality the highest in
Young children
elderly
Epidemiology

In pediatric thermal injuries:


Less than 5% are the result of
chemical or electrical burns
10-15% result from flame burns
When associated with smoke inhalation
are the most deadly
Scalding burns account for 75-80%
Prevention

Smoke detectors that work


Keep matches out of reach
Lower the temp on hot water heaters
Cover electrical outlets
Buy flame resistant childrens clothing
Use fire-safe cigarettes
Mortality Rate

Highest when:
Burn exceeds 30% body surface area.
See figure 39-1
Associated with smoke inhalation
Child younger than 4 years old
Pathophysiology

Disruption of the protection provided


by skin:
Protects body from infection and injury
Prevents fluid loss
Regulates body temp
Provides sensory input from environment
Pathophysiology

Composed of 2 layers
Epidermis thin outer layer
Dermis deeper, thick inner layer
Dermis contains:
Hair follicles
Sweat glands
Sebaceous glands
Sensory fibers for touch, pain, pressure and temp
Beneath the dermis
Subcutaneous tissue composed of connective
tissue and fat
Classification of Burn

1st Degree
Superficial
Involves only the dermis
Skin is red
No blisters
Painful and sensitive to touch
Classification of Burn

2nd Degree
Involve the epidermis and part of the
dermis
Very painful due to nerve endings that
survive the insult
Blistering is common
Healing occurs quickly
Classification of Burn

3rd Degree
Full thickness burns
Involve injury and necrosis below the
hair follicles thru the entire thickness of
skin and into subcutaneous tissue
Area swells slowly and appears blanched
Sensory nerves are destroyed causing
local anesthesia
Management

1st degree usually heals by itself


2nd and 3rd degree may require
grafting, excision and antimicrobial
therapy such as Silva dine
Management

Important to initiate accurate fluid


resuscitation ASAP
Careful: overaggressive fluid
resuscitation may result in high
extravascular hydrostatic pressure,
pulmonary edema and soft tissue
swelling
Urine output is a good indicator of
hydration
Inhalation Injury

Mortality from smoke injury alone is


0-11%
Mortality from smoke injury and burns
is 30-90%
Smoke inhalation that results in
pneumonia has a mortality rate of
60%
Physiologic Consequences of
Inhalation Injury
Box 39-1
Upper Airway Injury

Results in obstruction from:


Edema
Hemorrhage
Ulceration of mucosa
Mild pharyngeal edema can lead to
complete upper airway obstruction
and asphyxia in only a few hours
Inflammation can be the result of
ammonia, hydrogen chloride and
chemical irritants found in smoke
Lung Parenchyma Injury

Only steam is capable of


overwhelming the upper airway
defenses and transmitting heat to the
subglottic airways
Direct cellular injury results in
inflammatory response
Leads to bronchoconstriction
Increase in tracheobronchial blood flow
with edema
Leukocyte infiltration
Lung Parenchyma Injury

Sloughing of necrotic tissue plugs up


the airways
Can cause partial or complete airway
obstruction
Can be fatal
Lung Parenchyma Injury

Pulmonary parenchyma shows:


Varying degrees of congestion
Interstitial and alveolar edema
Hyaline membranes
Dense atelectasis
Lung Parenchyma Injury

Systemic effects:
Increase in RAW
V/Q mismatch
Increase in oxygen consumption
Decrease in compliance
Decrease in oxygenation
Decreased surfactant production
Carbon Monoxide Poisoning

Smoke inhalation from all types of


fires result in significant CO exposure.
Pulse oximeter do not reflect the true
oxygen saturation in the presence of
COHB.
Symptoms- Table 39-1
Clinical Manifestations

Smoke inhalation injury more likely in


individuals with:
History of burn injury in an enclosed space
Appearance of facial burns
Singed nose and facial hair
Erythema of the oropharynx
Carbonaceous sputum
Debris around the nose, mouth and pharynx
Bronchoscopy

Gold standard for diagnosis of


inhalation injury
Provides direct visualization of airway
Soot
Charring
Mucosal erythema
Ulceration
Hemorrhage
Edema
inflammation
Management

Oxygen Therapy
Airway Maintenance
Bronchial Hygiene Therapy
Pharmacologic Management
Mechanical Ventilation
Conventional
High frequency
Management

Oxygen Therapy
Initially give 100%
Wean by blood gas values
Analyze COHB with co-ox
Management

Airway maintenance
Intubation by most skilled clinician
Nasalintubation is easier for securing a tube
to a burned face
Burns to the neck can cause tightening of
the tissue causing restriction to the airway
Escharotomies to reduce the pressure exerted
to the area
Management

Bronchial Hygiene Therapy


Retained secretions can be life threatening
Early ambulation
Therapeutic coughing
Chest PT
Airway suctioning
Therapeutic bronchoscopy
Pharmacologic agents for retained secretions
Management

Pharmacological Management
Inhalation
injury creates intense
bronchospasm and wheezing
Manage with B2 agonists
Racemic epinephrine to promote vasoconstriction
(trx edema), bronchodilation, and breaking up of
secretions
Mucomyst to break down mucus in the airway
Heparin/mucomyst nebulizer may reduce pts
mortality
Management

Mechanical Ventilation
Forresp failure associated with inhalation
injury
Ptswith this type of injury are at increased
risk of ventilator associated injury
Management

Conventional Mechanical Ventilation


Start with Vt of 12-15 ml/kg
Better
outcomes with non conventional
modes of ventilation such as:
Pressure limited ventilation
Reduced rate of death with this type of injury
High Frequency Ventilation

Provides o2 at lower concentrations


and adequate ventilation at reduced
airway pressures.
Reduces barotrauma
Less incidence of pneumonia
Improved PaO2/FiO2 ratio
Complications

Most common complications are


infection and resp failure
Barotrauma due to MV
Late complications due to
inflammatory responses of the body
Bronchiectasis
Bronchial stenosis
ETT cuffs erosion
Long Term Outcomes

Most patients have normal lung


parenchyma return within 5 months
Children heal slowly
PFT changes for up to 8 years
Altered lung mechanics
Impaired gas exchange
Chest wall scarring
Weak resp muscles
Some children never regain normal lung
function

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