Inhalation Injury From Heat, Smoke, or Chemical Irritants

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Inhalation injury from heat, smoke, or chemical irritants

Author: Ronald P Mlcak, PhD, MBA, RRT, FAARC
Section Editors: Eileen M Bulger, MD, FACS, Marc G Jeschke, MD, PhD, Jess Mandel, MD
Deputy Editors: Kathryn A Collins, MD, PhD, FACS, Geraldine Finlay, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Mar 2020. | This topic last updated: Feb 28, 2018.
INTRODUCTION
Inhalation injury is a nonspecific term that refers to damage to the respiratory tract or lung tissue
from heat, smoke, or chemical irritants carried into the airway during inspiration [1]. The term is
often used synonymously with smoke inhalation injury. Inhalation injury resulting from fire remains
one of the leading causes of death [2]. The pathophysiology, clinical features, diagnosis, initial
management, subsequent management, and special considerations of inhalation injury are
reviewed here. The emergency care of thermal burns is discussed separately. (See "Emergency
care of moderate and severe thermal burns in adults" and "Moderate and severe thermal burns in
children: Emergency management".)
EPIDEMIOLOGY
Annually in the United States, an estimated 372,900 fires in residential buildings result in an
average of 2530 deaths, 13,125 injuries, and $7 billion (USD) in property loss [3]. Pulmonary
complications following burns and inhalation injury are responsible for up to 77 percent of the
deaths, among which the majority are due to carbon monoxide poisoning [4,5]. Inhalation injury is
common following burn injury and increases in incidence with the size of the burn injury and age of
the patient [6,7]. In addition, inhalation injury has been shown to be an independent predictor of
mortality in burn patients [8].
PATHOPHYSIOLOGY AND CLASSIFICATION
Inhalation injury can affect the airways as well as result in systemic toxicity [9]. The location and
severity of injury depends on several factors, including the ignition source, the size and diameter
of the particles in the smoke, the duration of the exposure, and the solubility of the gases [10,11].
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Direct toxin damage is caused by the lower-molecular-weight constituents of smoke because of

their pH, ability to form free radicals, and ability to reach the distal airways and alveoli [12-15].
Based upon the primary localization of the insult, inhalation injury is classified into injuries of the
upper airway, the tracheobronchial system, or the lung parenchyma [9,16].
Upper airway injury — The leading injury in the upper airway (above the vocal cords) is thermal
injury due to the efficient heat exchange in the oro- and nasopharynx. The immediate injury results
in erythema, ulcerations, and edema. In combined burn and inhalation injury, aggressive fluid
administration required to treat burn shock promotes early edema formation [17]. In addition,
burns to the face and neck may cause anatomic distortion or external compression of the upper
airway, complicating airway management [18]. In addition to the acute inflammation, damage of
ciliary function impairs physiological clearance processes of the airway, leading to an increased
risk of bacterial infection for several weeks. Furthermore, the increased production of thick
secretions can cause distal airway obstruction, atelectasis, and impaired gas exchange [11,18,19].
Tracheobronchial injury — With the exception of inhalation of steam, injury to the

tracheobronchial tree (figure 1) is usually caused by chemicals in smoke. However, toxic inhalation
of noxious gases (eg, chlorine), liquids (eg, acid), and direct airway fire (eg, intraoperative) can
also be associated with a similar process. Clinical symptoms include persistent coughing and
wheezing, soot-containing airway secretions (ie, melanoptysis), increased work of breathing
resulting in hypoventilation, erythema, hyperemia, and increased pulmonary shunting from lobar
collapse or atelectasis [11,18].
The tracheobronchial area is richly innervated by vasomotor and sensory nerve endings [11,20].
Smoke inhalation stimulates these nerves to release neuropeptides. These neuropeptides then
induce bronchoconstriction and nitric oxide synthase (NOS) to generate reactive oxygen species
(ROS) [11,21-23]. These neuropeptides can function as tachykinins, inducing an inflammatory
response with the downstream effects of bronchoconstriction, increased vascular permeability, and
vasodilation [23]. These factors potentiate local cellular damage and the loss of hypoxic
pulmonary vasoconstriction, which causes bronchial blood flow to increase manyfold. In addition,
the increased bronchial blood flow delivers activated polymorphonuclear leukocytes and cytokines
to the lung, increasing the host inflammatory response [23]. Furthermore, the loss of an intact
bronchial epithelium and the effects of ROS result in a loss of plasma proteins and fluid from the
intravascular space into the alveoli and bronchioles [23,24]. The transvascular shift of protein
results in exudate and cast formation within the airways, leading to alveolar collapse [23,24].
These processes contribute to ventilation-perfusion mismatch as a primary mechanism of
hypoxemia following the inhalation injury [24,25].
Parenchymal injury — Damage to the lung parenchyma is delayed. The time difference from the
initial injury to the occurrence of a decrease in arterial oxygen tension to inspiratory oxygen
fraction ratio (PaO2:FiO2 ratio) is correlated with the severity of the lung injury [11,16]. A faster
time is associated with more severe injury. Injury to the lung parenchyma is characterized by
atelectasis and alveolar collapse resulting in increased transvascular fluid flux, a decrease in
surfactant, and a loss of hypoxic vasoconstriction and therefore impaired oxygenation.
Furthermore, a severe imbalance in alveolar hemostasis and decreased fibrinolytic activity, with
massive fibrin deposition in the airways, causes a ventilation-perfusion mismatch [11,26].
Airway obstruction and atelectasis increases the risk for pneumonia. The risk for pneumonia is
increased because of the impaired function of alveolar macrophages, polymorphonuclear
leukocytes, and mucociliary clearance mechanisms [27-29].
Systemic toxicity — Direct systemic effect of inhalation injury is caused by breathing toxic
substances formed via combustion or pyrolysis. The two most relevant gases associated with
increased morbidity and mortality are carbon monoxide and hydrogen cyanide [11].
● Carbon monoxide poisoning – Carbon monoxide is one of the most frequent immediate
causes of death following inhalation injury [11,30]. Carbon monoxide is a colorless, odorless
gas with an affinity for hemoglobin more than 200 times higher than that of oxygen [31].
Carboxyhemoglobin shifts the oxyhemoglobin dissociation curve to the left, impairing release
of oxygen at the tissues and utilization of oxygen in mitochondria, leading to tissue hypoxia
[32]. The table shows signs and symptoms at various concentrations of carboxyhemoglobin
(table 1).
Carbon monoxide poisoning should be suspected in all patients who present following
inhalation injury or house fires until it is excluded by a normal blood carboxyhemoglobin level.
Pulse oximetry cannot screen for carbon monoxide exposure, as it does not differentiate
carboxyhemoglobin from oxyhemoglobin. Carboxyhemoglobin levels are measured with CO-
oximetry on arterial or venous blood. Treatment indications are given in the table (table 2).
(See "Carbon monoxide poisoning" and "Pulse oximetry", section on 'Co-oximetry'.)
● Hydrogen cyanide – Hydrogen cyanide is the gaseous form of cyanide (CN), which is a
colorless gas with the odor of bitter almonds [11]. Cyanide poisoning is difficult to confirm
during the initial postburn period because the symptoms are nonspecific and cyanide levels
cannot be measured soon enough to be clinically meaningful. Given the high probability of its
presence at a fire scene, cyanide toxicity should be considered in every patient with an
inhalation injury. Treatment for cyanide poisoning should be considered in any patient being
treated for smoke inhalation (table 3). Treatment can be initiated in those at risk who display
depressed level of consciousness, cardiac arrest, or cardiac decompensation in the absence
of laboratory confirmation. (See "Cyanide poisoning".)
CLINICAL FEATURES
History and physical — Inhalation injury should be suspected based on a history of exposure to
heat, smoke, or chemicals, and supporting clinical features. When presented with a patient with a
suspected inhalation injury, the clinician should first review the history and reported mechanism of
injury. Pertinent information includes exposure to flame, smoke, or chemicals; duration of
exposure; exposure in an enclosed space; and a history of loss of consciousness [23,33].
Generalized symptoms such as dizziness, nausea, or vomiting may be reported. Carbon

monoxide poisoning should be presumed in any patient who presents following smoke inhalation
until it is excluded by a normal carboxyhemoglobin level as measured by CO-oximetry. The
physical signs and symptoms of various concentrations of carboxyhemoglobin are given in the
table (table 1). (See "Carbon monoxide poisoning" and "Pulse oximetry", section on 'Co-oximetry'.)
Clinical symptoms of upper airway injury, such as difficulty breathing, might not be immediately
obvious until edema is severe enough to significantly impair airway diameter [11,16]. Symptoms of
lower respiratory tract injury may include shortness of breath and productive cough.
Physical findings include burns to the face, singed nasal vibrissae, soot in the oropharynx, nasal
passages, proximal airways, and carbonaceous sputum [9,23,34,35]. Other signs of upper airway
injury include hoarseness and stridor, which increase the work of breathing and may lead to
respiratory fatigue with sub- and suprasternal retractions. Signs of lower respiratory tract injury
may include any or all of the following: tachypnea, decreased breath sounds, wheezing, rales,
rhonchi, or use of accessory respiratory muscles [2].
Laboratory findings — Standard laboratory studies should be obtained, including a complete

blood count, electrolytes, blood urea nitrogen, creatinine, lactate level, and toxicology screen. An
arterial blood gas (ABG) should be sent for CO-oximetric measurement of the oxyhemoglobin
saturation, carboxyhemoglobin concentration (table 1), and methemoglobin concentration. The
reason for measuring the oxyhemoglobin saturation via CO-oximetry is that standard pulse
oximetry cannot distinguish oxyhemoglobin from carboxyhemoglobin. (See "Carbon monoxide
poisoning" and "Pulse oximetry", section on 'Co-oximetry'.)
Chest imaging — Chest radiography is typically obtained in the initial evaluation of the injured
patient but has low sensitivity for inhalation injury [12]. Most patients with inhalation injury have a
normal chest radiograph at presentation, and for those with abnormal findings, the degree of injury
is usually underestimated [11,36]. The presence of pulmonary opacities on initial chest films has
been implicated as a marker of severe injury and a poor prognosis [37].
Some have suggested that computed tomography of the chest may be helpful as an early
predictor of smoke inhalation severity [38,39]. In these studies, the airway wall thickness to total
bronchial diameter (T/D) ratio is measured. In a study of 40 patients, the number of days of
mechanical ventilation correlated with the T/D ratio.
DIAGNOSIS

The diagnosis of inhalation injury may be suspected based upon clinical findings in the setting of
smoke exposure, but a definitive diagnosis relies upon direct examination of the airways.
Direct airway examination — Once the airway is secured and the patient is hemodynamically
stabilized, a suspected diagnosis of inhalation injury should be confirmed with visual inspection of
the airways [2]. Direct laryngoscopy can be used for a limited direct examination of the upper
airways for obvious signs of smoke inhalation. However, fiberoptic bronchoscopy allows
examination of the airways from the oropharynx to the lobar bronchi and is the standard for
confirming a diagnosis of inhalation injury [1,2,9,35]. Clinical signs of inhalation injury include
mucosal erythema and edema, blistering, ulceration, or bronchorrhea, fibrin casts, or evidence of
charring [23].
Injury severity scoring — Findings on bronchoscopy can help predict the risk and severity of
acute lung injury, which aid in subsequent management (eg, fluid therapy, treatment of
tracheobronchitis) [23]. Multiple studies have shown that inhalation injury is a graded phenomenon
with increasing severity correlating with worse outcomes [23,40,41]. Several scoring systems have
been proposed, but the standardization and validity of these are controversial [1,23]. The
Abbreviated Injury Score (AIS) grading scale using bronchoscopy correlates well with mortality as
well as gas exchange (table 4) [23,42-44]. Increasing severity of injury as reflected in increasing
AIS also correlates with a greater need for supportive treatment.
AIS grading of inhalation injury by bronchoscopy is as follows [42]:
● 0 (no injury) – Absence of carbonaceous deposits, erythema, edema, bronchorrhea, or

obstruction
● 1 (mild injury) – Minor or patchy areas of erythema or carbonaceous deposits in the proximal
or distal bronchi
● 2 (moderate injury) – Moderate degree of erythema, carbonaceous deposits, bronchorrhea, or

bronchial obstruction
● 3 (severe injury) – Severe inflammation with friability, copious carbonaceous deposits,

bronchorrhea, or obstruction
● 4 (massive injury) – Evidence of mucosal sloughing, necrosis, endoluminal obliteration
MANAGEMENT OVERVIEW
Initial care and disposition — The first priority in the prehospital setting is to rescue the victim
from the source of fire and to limit time of exposure. Assessment of the patient's airway, breathing,
and circulation should be performed expeditiously. The initial diagnosis and management of
accompanying traumatic or burn-related injuries is based upon Advanced Trauma Life Support

(ATLS) protocols. Immediately life-threatening injuries take precedence [11,18]. For patients with
suspected inhalation injury who are not intubated initially, the adequacy of breathing as assessed
by respiratory rate, chest wall motion, and auscultation of air movement should be frequently
reevaluated [11,18]. If possible, information about comorbidities should be obtained [11]. (See
"Prehospital care of the adult trauma patient" and "Pediatric considerations in prehospital care"
and "Emergency care of moderate and severe thermal burns in adults", section on 'Initial
assessment and treatment'.)
Patients with an appropriate history (eg, escaped a fire) but a low risk for inhalation injury based
on clinical findings (listed below) and without cutaneous burns need to be monitored for a
minimum of four to six hours. If the vital signs remain stable, the patient can usually be discharged
with instructions to return if any symptoms develop.
Patients with any of the following clinical findings should be hospitalized, typically in a monitored
setting [2]:
● History of closed space entrapment

● History of syncope
● Carbonaceous sputum
● Arterial PaO2 <60 mmHg
● Metabolic acidosis
● Carboxyhemoglobin levels greater than 15 percent
● Bronchospasm/wheezing
● Facial burns
If any of the criteria listed in the table are met (table 5), the patient should be referred to a regional
burn center [45]. The patient may require interim care at the hospital to which he/she presented
until transfer can be arranged. (See "Overview of the management of the severely burned patient",
section on 'Emergency burn care'.)
Patients who typically require intubation are described below. (See 'Securing the airway' below
and 'Ventilator management' below.)
Patients who do not require intubation should receive humidified 100 percent oxygen by face
mask to displace carbon monoxide, if not already initiated [46,47]. For those at risk of developing
oxygen-induced hypercapnia (eg, patients with a history of chronic obstructive pulmonary disease
or obstructive sleep apnea), a low threshold to treat the patient with noninvasive ventilation or
mechanical ventilation is prudent. Tissue hypoxia is multifactorial and can quickly lead to death.
Hypoxia is due, in part, to the inspiration of air with an FiO2 <15 percent during the fire (fire
consumes ambient oxygen) and is also related to impaired delivery and utilization of oxygen by
the tissues from carbon monoxide and cyanide poisoning [46,48]. Carbon monoxide poisoning
should be presumed in any patient who presents following smoke inhalation until it is excluded by

a normal carboxyhemoglobin. (See 'Systemic toxicity' above and "Cyanide poisoning" and
"Carbon monoxide poisoning".)
Securing the airway — Proper airway security and management is critical in patients with
inhalation injury. Loss of an airway in patients with burns and inhalation injury can be catastrophic.
The anesthesiologist, surgeon, and/or critical care physician should decide the most appropriate
method of airway management either by endotracheal intubation or placement of a tracheostomy.
The proper size (preferably >7.5 cm outer diameter to allow secretion clearance and the passage
of a bronchoscope), tube placement, and stabilization technique are all important considerations.
The most experienced provider available should establish and secure the airway. The security of
the tube needs to be checked frequently as airway edema increases or decreases. (See "Direct
laryngoscopy and endotracheal intubation in adults" and "Rapid sequence intubation for adults
outside the operating room".)
Endotracheal intubation is frequently used as a supportive therapy in the management of

inhalation injury. In one reported series, up to 80 percent of patients with inhalation injury required
intubation for at least short-term management [49]. Some patients will ultimately require
tracheostomy. (See 'Tracheostomy' below.)
A decision for early intubation should be based upon any of the following signs: deep burns to the
face or neck, blisters or edema of the oropharynx, stridor, use of accessory muscles, respiratory
distress, sub- and suprasternal retractions, or hypoventilation. Intubated patients with concern for
carbon monoxide poisoning should also be placed on humidified 100 percent oxygen until
carboxyhemoglobin levels normalize. Humidified oxygen helps to avoid the development of
inspissated secretions. The American Burn Association's Advanced Life Support protocol
suggests that if there is any question about the security of the patient's airway, the patient should
be intubated prior to transfer to a trauma or burn center [50,51]. The endotracheal tube can be
removed, if indicated, once the patient has been safely transported.
Intubation for altered mental status, imminent airway obstruction, or respiratory failure may be
indicated subsequently during the hospital course since the development of upper airway
inflammation and edema may be delayed by 24 hours and lower airway edema delayed by 36
hours [52]. Other reasons for needing intubation include complications that develop during the
hospital course, such as sepsis, acute respiratory distress syndrome, pneumonia, pulmonary
toilet, and for operative procedures. Changing the endotracheal tube and reintubation for
unplanned extubation are dangerous in the presence of upper airway edema, and aggressive
monitoring to ensure airway security is essential to avoid problems [53].
Subsequent care — After initial stabilization and transfer to the intensive care unit, treatment for
inhalation injury is mainly supportive. Patients are monitored during the subsequent one to five
days for the following:

● Airway inflammation and systemic toxicity – In the early phase (<36 hours), treatment is
focused on treating systemic toxicity (carbon monoxide, hydrogen cyanide) and managing
early airway edema and bronchospasm. After inhalation injury, upper and lower airway
inflammation may result in increased airway edema, mucosal slough, and cast formation,
which result in impaired gas exchange. These are managed with aggressive pulmonary toilet
and may require therapeutic bronchoscopies. (See 'Example treatment protocol for
nonintubated patients' below and 'Pulmonary care' below.)
● Pneumonia – Although the risk of nosocomial pneumonia is increased, there is no benefit for
prophylactic antimicrobial therapy for inhalational injury. (See "Overview of the management
of the severely burned patient", section on 'Antimicrobial therapy'.)
● Fluid balance – What constitutes appropriate fluid resuscitation for patients with inhalation
injury is still subject to debate. It has been demonstrated that inhalation injury increases fluid
requirements in burn patients over and above that calculated based upon the severity of
burns [11,23,54]. (See "Emergency care of moderate and severe thermal burns in adults",
section on 'Fluid resuscitation'.)
● Altered metabolism – Patients with inhalation injury may also demonstrate marked
hypermetabolism [55]. An increased production of carbon dioxide requires a high minute
ventilation to maintain a normal pCO2 and may require ventilatory support to achieve. Enteral
nutrition formulas with a low respiratory quotient may help limit carbon dioxide production,
improving the patient's ability to keep up with respiratory demands. (See "Hypermetabolic
response to moderate-to-severe burn injury and management".)
● Acute respiratory distress syndrome – Acute respiratory distress syndrome (ARDS) may also
develop several days after the exposure [37]. The presentation, diagnosis, and management
of ARDS caused by smoke inhalation are similar to those for ARDS due to other etiologies.
(See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in
adults" and "Acute respiratory distress syndrome: Supportive care and oxygenation in adults"
and "Ventilator management strategies for adults with acute respiratory distress syndrome".)
PULMONARY CARE
Treatment of inhalation injury is supportive and aimed at relieving bronchospasm, reducing

pulmonary secretions, and clearing the airways of fibrin casts and sloughed, necrotic bronchial
epithelium, which can cause airway obstruction and atelectasis leading to pneumonia. (See
'Pathophysiology and classification' above.)
Supportive treatments — Supportive treatment includes the use of bronchodilators for wheezing
and airway clearance measures such as administration of aerosolized mucolytic agents alternating
with aerosolized heparin, chest physiotherapy, and postural drainage. Intubation and therapeutic
bronchoscopy may be necessary to control secretions, which should diminish within 7 to 10 days
in the absence of pulmonary infection.
The routine administration of corticosteroids does not appear to confer any benefit following
smoke inhalation [56].
Bronchodilators — Aerosolized bronchodilators should be given when wheezing or

bronchospasm occurs. Bronchodilators relax bronchial muscle, stimulate mucociliary clearance,
decrease airflow resistance, and improve dynamic compliance [23,57]. Bronchodilators that are
useful in the treatment of inhalation injury include albuterol, levalbuterol, and racemic epinephrine,
usually administered every four hours [57].
Mucolytic agents — Clearing the airways is an essential component of the management of

patients with inhalation injury. This can be achieved with a combination of inhaled pharmacologic
agents (eg, N-acetylcysteine) and mechanical means, such as therapeutic coughing, chest
physiotherapy, airway suctioning, early ambulation, and, if necessary, intubation with suctioning or
therapeutic bronchoscopy [58].
N-acetylcysteine (NAC) is a powerful mucolytic agent that can be useful in treatment of inhalation
injury. N-acetylcysteine contains a thiol group and is a strong reducing agent that breaks the
disulfide bonds that give stability to the mucoprotein network of molecules in mucus [57]. However,
NAC is also an airway irritant and may produce bronchoconstriction. A bronchodilator should be
added if wheezing or bronchospasm occurs with NAC treatment. Generally a NAC dose of 3 mL of
a 20% solution every four hours is used.
The combination of NAC and aerosolized heparin has been shown to be effective for the treatment
of inhalation injury in animal studies [59]. Inhaled anticoagulants decrease the formation of fibrin
casts following inhalation injury but do not alter systemic markers of clotting and anticoagulation
[60]. A systematic review identified five retrospective studies using inhaled anticoagulants for the
treatment of inhalation injury in children and adults [59,61-64]. A placebo-controlled clinical trial
(NCT01773083) is pending [65]. In some, but not all, studies, inhaled anticoagulants have reduced
morbidity or were associated with increased survival. Nebulized heparin/NAC significantly reduced
reintubation rates and the incidence of atelectasis and improved mortality in one study [61], and, in
another, the two agents resulted in better lung compliance, less pulmonary edema, and less
airway obstruction compared with controls [62]. In a separate retrospective study, nebulized
heparin in conjunction with a beta-agonist and mucolytic significantly decreased the duration of
mechanical ventilation and increased the number of ventilator-free days in patients with inhalation
injury [66]. When used, we dose inhaled heparin at 5000 to 10,000 units in 3 mL normal saline,
every four hours. Of note, one randomized trial comparing differing doses of inhaled heparin found
no significant differences between 5000 and 10,000 units [60].

Example treatment protocol for nonintubated patients — An example protocol approach used
by the author to treat inhalation injury in nonintubated patients is given below. Individual aspects of
pulmonary care are discussed in more detail below. (See 'Pulmonary care' above.)
● Titrate humidified high-flow oxygen to maintain oxygen saturation >90 percent
● Supervise the patient performing coughing and deep breathing exercises every two hours
● Turn the patient side to side every two hours
● Administer chest physiotherapy every two hours
● Alternate aerosolized NAC with a bronchodilator (if wheezing) and aerosolized heparin/saline
● Perform nasotracheal suctioning as needed
● Encourage early ambulation
● Educate the patient and family about the disease process and prognosis
Ventilator management — Patients with inhalation injury and concomitant burn injury frequently
require mechanical ventilator support. An estimated 33 percent of burn patients require
mechanical ventilation, and the incidence increases significantly in the presence of inhalation
injury [67]. However, the optimal ventilator strategy for patients with burns and inhalation injury is
not well defined [68]. A survey of mechanical ventilator practices across burn centers in North
America has shown no single ventilator mode is used consistently in the management of burn
patients, regardless of their insult [68]. (See "Overview of initiating invasive mechanical ventilation
in adults in the intensive care unit".)
Tidal volumes — Based upon the Acute Respiratory Distress Syndrome (ARDS) Network
Study, low tidal volumes and limiting plateau pressures are the currently accepted lung-protective
practices for mechanical ventilation [69]. However, burn patients and patients with inhalation injury
were not included in the studies that led to the widespread acceptance of these mechanical
ventilation strategies [49,70]. The tidal volume selected for burn patients with inhalation injury
varies between 6 to 8 mL/kg of predicted body weight [57]. However, a large retrospective study
suggests that the use of higher tidal volumes decreases ARDS, atelectasis, and ventilator days
when compared with low tidal volumes in pediatric burn patients with inhalation injury [71]. The
exact tidal volumes needed for a patient with burns and inhalation injury still needs to be
determined. A good rule of thumb would be to limit tidal volumes and plateau pressures to the
lowest level tolerated by the patient's compliance, airway resistance, and work of breathing. (See
"Ventilator management strategies for adults with acute respiratory distress syndrome".)
Modes of ventilation — Pulmonary management of patients with burns and inhalation injury
may deviate from typical ventilator management practices in the general intensive care unit (eg,
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larger-than-typical tidal volumes). Clinical trials identifying the best strategies for burn patients are
lacking. From observational studies, no single ventilator mode prevails. In one survey, pressure
support ventilation and volume-assist control modes were the most commonly reported initial
modes used in burn patients with or without inhalation injury [70]. Open lung techniques of
mechanical ventilation, including high-frequency percussive ventilation, high-frequency oscillatory
ventilation [72], and airway pressure release ventilation, have also been used in the management
of patients with inhalation injury [70]. (See "Modes of mechanical ventilation".)
Extubation criteria — Extubation criteria include a wide variety of physiological variables that
have been proposed to aid in discontinuing mechanical ventilation in burn patients with inhalation
injury. Additional extubation criteria for burn patients with inhalation injury suggest the use of the
rapid shallow breathing index, evaluation of the work of breathing, Glasgow coma scale,
Richmond Agitation Sedation Scale, and the Confusion Assessment Method for the intensive care
unit [70]. Furthermore, a daily sedation vacation and daily weaning trial is suggested to determine
success of weaning from mechanical ventilation and a successful extubation. Importantly, patients
should show signs of resolving airway edema and inflammation with minimal secretions and/or an
ability to cough and clear secretions when they develop. (See "Extubation management in the
adult intensive care unit" and "Methods of weaning from mechanical ventilation" and "Weaning
from mechanical ventilation: Readiness testing" and "Weaning from mechanical ventilation: The
rapid shallow breathing index".)
Suggested criteria include [4]:
● PaO2/FiO2 ratio >250 mmHg

● Maximal inspiratory pressure >60 cm H2O
● Vital capacity at least 15 to 20 mL/kg
● Spontaneous tidal volume 5 to 7 mL/kg
● Maximal voluntary ventilation two times the minute volume
● Resolution of the need for intubation
● Audible leak around the endotracheal tube
Tracheostomy — Some burn centers elect to place a tracheostomy tube in all patients with burns
and inhalation injury. However, although one trial found improved patient comfort and security with
early tracheostomy, there were no significant differences in length of stay, incidence of pneumonia,
survival, or duration of intubation for early compared with later tracheostomy. We typically proceed
with tracheostomy after three failed extubation attempts or after 21 days [73]. In the setting of
anterior neck burns, tracheostomy should be delayed until five to seven days after skin grafting
[74]. Tracheostomy is reviewed separately. (See "Overview of tracheostomy", section on 'Timing of
tracheostomy'.)
SPECIAL POPULATIONS
Children — In pediatric patients, airway compromise is the most common cause of severe
morbidity and mortality, likely due to the small size of the airway. It is essential that the clinician
frequently evaluate the magnitude of swelling in the face and neck to prevent airway compromise.
In addition, pediatric patients with burns and inhalation injury are tachypneic and can exhibit an
increased work of breathing. Vigilance and frequent clinical assessments are warranted.
The threshold for intubation needs to be lower in pediatric patients due to the potential for rapid
development of airway edema [2]. Endotracheal tube size needs to be specifically tailored for the
pediatric patient with inhalation injury. Due to their anatomy, the chance of accidental extubation is
higher in pediatric patients than adults. Endotracheal tube security is essential to maintaining a
patent airway. Loss of an airway in this population can result in airway compromise and potentially
be fatal. An emergency airway box with appropriate-sized equipment is recommended to be kept
at the bedside.
Older adults — Adults over 65 years of age have a mortality from burns that is six times the
national average [75]. Due to lower physiological reserves and comorbidities, treatment of this
patient population presents a unique challenge. A number of existing risk factors are present in
older adults. These include increased risk of infections, pulmonary diseases, and comorbidities.
Older adults have a decrease in pulmonary reserve, lung mechanics, and a decreased lean body
mass, as well as coronary artery disease. Additionally, pneumonia and urinary tract infections are
the most prevalent complications in older adult burn patients. Treatment options are identical to
younger patients, keeping in mind the physiological differences due to aging and comorbidities. No
evidence supports changing treatment protocols [75].
Inhalation injury other than smoke — While the optimal management strategy is unknown,
patients with inhalation injury due to agents other than smoke are typically managed in the same
fashion as for smoke in inhalation, with the exception of monitoring for carbon monoxide
poisoning.
MORBIDITY AND MORTALITY
Inhalation injury is an independent predictor of mortality in burn patients. Pulmonary-related

complications following burns and inhalation injury are responsible for up to 77 percent of the
deaths, most of which are related to carbon monoxide poisoning. In a review that identified 769
patients with smoke inhalation-related acute lung injury, the in-hospital mortality rate was 26
percent, and among those with associated severe burns (>20 percent total body surface area
[TBSA]), it was 50 percent [76]. In addition to severe associated burns, other clinical factors
associated with in-hospital mortality included burn age >60 years and vasopressor use.
The National Burn Repository of the American Burn Association found that patients with inhalation
injury had a higher case fatality for a given Baux score (age+total burn surface area) compared

with those with no inhalation injury, but the added risk was not constant [77]. As an example, the
presence of inhalation injury increases mortality nearly 24-fold for burn patients under the age of
60 with a total burned surface area <20 percent. From another study, the mortality of burn patients
increased by 20 percent in the presence of smoke inhalation [35]. The need for mechanical
ventilation and severe inhalation injury on bronchoscopy predict increased mortality in patients
with inhalation injury due to burns [78].
Long-term sequelae — Most patients do not suffer long-term functional impairment following
smoke inhalation. In one study of 23 patients with a history of severe smoke inhalation, there were
no changes in spirometry, nonspecific airway hyperresponsiveness, or cardiac or pulmonary
variables when measured during maximal exertion approximately four years after the exposure
[79]. However, one review reported pulmonary function changes up to 10 years post-injury in a
group of severely burned children with inhalation injury [57]. Rare long-term sequelae include
tracheal stenosis, bronchiectasis, interstitial fibrosis, reactive airways dysfunction syndrome, and
bronchiolitis obliterans [80,81], although most of these cases appear to have followed severe
chemical bronchitis or nosocomial pneumonia at the time of injury. One study showed that
inhalation injury did not appear to significantly impact the quality of life of pediatric patients with
inhalation injury eight years after follow-up [82]. (See "Clinical presentation, diagnostic evaluation,
and management of central airway obstruction in adults".)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Care of the patient with
burn injury".)
SUMMARY AND RECOMMENDATIONS
● Inhalation injury is a nonspecific term that refers to damage to the respiratory tract or
pulmonary parenchyma by heat, smoke, or chemical irritants. Inhalation injury also causes
systemic toxicity owing to toxic gases (eg, carbon monoxide, hydrogen cyanide). About one-
third of patients with burn injuries have a concomitant inhalation injury. Pulmonary-related
complications following burns and inhalation injury are responsible for up to 77 percent of
deaths related to burn injury. (See 'Introduction' above and 'Epidemiology' above and
'Morbidity and mortality' above.)
● Carbon monoxide poisoning should be presumed in any patient who presents following
smoke inhalation until it is excluded by a normal carboxyhemoglobin level on CO-oximetry.
The initial approach to presumed carbon monoxide poisoning involves administering

supplemental oxygen at FiO2 of 100 percent. (See 'Initial care and disposition' above and
'Systemic toxicity' above.)
● Early intubation is justified for any patient with suspected inhalation injury and signs of
respiratory distress (stridor, use of accessory respiratory muscles), hypoxemia,
hypoventilation, deep burns to the face or neck, or blistering or edema of the oropharynx.
(See 'Securing the airway' above.)
● The evaluation and initial management of accompanying trauma or burn injuries is prioritized
using Advanced Trauma Life Support protocols. Transfer to a burn center should be initiated
for patients with inhalation injury and burns who meet the American Burn Association referral
criteria (table 5). (See 'Initial care and disposition' above.)
● For patients with clinical features suspicious for inhalation injury, such as a history of smoke
exposure in an enclosed space, and physical findings (eg, facial burns, singed nasal
vibrissae, soot in the oropharynx, nasal passages, and proximal airways), we use
bronchoscopy to confirm the diagnosis of inhalation injury. (See 'Diagnosis' above.)
● Proper airway management is critical in patients with inhalation injury. Endotracheal intubation
is frequently used as a supportive therapy in the management of inhalation injury. Loss of an
airway in patients with burns and inhalation injury can be catastrophic. The most experienced
practitioner available should establish and secure the airway. Tube security needs to be
checked frequently as swelling increases or decreases. (See 'Initial care and disposition'
above.)
● The inpatient management of patients with inhalation injury treatment is mainly supportive
and consists of monitoring the patient for subsequent development of airway compromise.
Upper airway problems tend to occur within 24 hours of inhalation injury and are managed by
intubation until the upper edema subsides, while lower airway compromise tends to occur
later (one to three days after injury). (See 'Supportive treatments' above.)
• Aerosolized bronchodilators are effective in several ways and should be given when
wheezing or bronchospasm occurs (table 6). Bronchodilators relax bronchial muscle,
stimulate mucociliary clearance, decrease airflow resistance, and improve dynamic
compliance.
• Clearing the airways is an essential component in the management of patients with

inhalation injury. This can be achieved with a combination of inhaled pharmacologic
agents (N-acetylcysteine, heparin) and mechanical means, such as therapeutic
coughing, chest physiotherapy, airway suctioning, early ambulation, and, if necessary,
intubation with suctioning or therapeutic bronchoscopy.

● Mechanical ventilation of patients with inhalation injury should begin with low tidal volumes (6
to 8 mL/kg), adjusting them based upon the patient's condition, compliance, airway
resistance, and tolerance. There is no consensus on the optimal mode of mechanical
ventilation, but if the patient develops acute respiratory distress syndrome, a lung-protective
strategy should be used. Assessing readiness for extubation and daily weaning trials should
be evaluated every morning, and the patient should be removed from mechanical ventilation
as soon as he/she meets criteria. (See 'Ventilator management' above.)
● Most patients do not suffer long-term respiratory impairment following smoke inhalation;
however, although rare, residual long-term sequelae may include tracheal stenosis,
bronchiectasis, interstitial fibrosis reactive airway disease, and bronchiolitis obliterans. These
are usually associated with severe injury. (See 'Morbidity and mortality' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
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Topic 105477 Version 11.0

GRAPHICS
Anatomy of the tracheobronchial tree
The pulmonary artery and its branches follow the same course as the tracheobronchial
tree.
Graphic 104076 Version 2.0

Signs and symptoms of various concentrations of carboxyhemoglobin levels
CO-Hb, % Signs and symptoms
0-10 None
10-20 Tightness across forehead, slight headache, dilation of the cutaneous blood vessels
20-30 Headache and throbbing in the temples
30-40 Severe headache, weakness, dizziness, dimness of vision, nausea, vomiting, collapse
40-50 Same as above, greater possibility of collapse; syncope, increased pulse and respiratory
rates
50-60 Syncope, increased respiratory and pulse rates, coma, intermittent convulsions, Cheyne-
Stokes respiration
60-70 Coma, intermittent convulsions, depressed heart action and respiratory rate, possible death
70-80 Weak pulse, slow respiration leading to death within hours
80-90 Death in less than 1 hour
>90 Death within minutes
Reproduced from: Einhorn IN. Physiological and toxicological aspects of smoke produced during the combustion of
polymeric materials. Environ Health Perspect 1975; 11:163.

Carbon monoxide poisoning: Rapid overview
To obtain emergent consultation with a medical toxicologist, call the United States Poison Control Network at 1-800-
222-1222, or access the World Health Organization's list of international poison centers
(www.who.int/gho/phe/chemical_safety/poisons_centres/en/index.html).
History
Duration and mechanism of exposure
Assess for major symptoms: loss of consciousness, confusion, symptoms consistent with hypoxia (ie, chest pain)
Assess for minor symptoms: headache, nausea/vomiting
Assess pregnancy status
Physical examination
Careful evaluation of mental status
Physical examination usually unremarkable
Diagnostic evaluation
Check CO level with co-oximetry of arterial or venous blood
Check acid-base status using (preferably arterial) blood gas
Obtain ECG in all patients; measure cardiac biomarkers in patients ≥65, patients with significant cardiac risk
factors, and younger patients with chest pain or symptoms suggestive of ischemia
Consider CNS imaging (head CT) in patients with altered mental status to rule out other etiologies
Measure blood cyanide concentration; consider empiric treatment for cyanide poisoning in patients with smoke
inhalation
Treatment
Secure airway, breathing, and circulation:
Intubate as clinically indicated
Apply high-flow oxygen to ALL CO poisoned patients regardless of pulse oximetry or arterial pO 2
Direct fire department to assess for environmental exposure and remove victims
We suggest hyperbaric oxygen (HBO) for:
CO level >25% (>20% if pregnant)
Loss of consciousness
Severe metabolic acidosis (pH <7.1)
Concern for end-organ ischemia (chest pain, ECG changes, altered mental status)
CNS: central nervous system; CO: carbon monoxide; CT: computed tomography; ECG: electrocardiogram; HBO:
hyperbaric oxygen.

Cyanide poisoning: Rapid overview
To obtain emergent consultation with a medical toxicologist, call the United States Poison Control Network at 1-800-
222-1222, or access the World Health Organization's list of international poison centers
(www.who.int/gho/phe/chemical_safety/poisons_centres/en/index.html).
General information
Cyanide poisoning is rapidly lethal unless treated with antidote
Clinical features
History
Ascertain if patient has access to cyanide, or if patient was part of a high-risk event (eg, fire, industrial exposure)
Initial symptoms are nonspecific: headache, anxiety, confusion, abdominal pain
Physical examination
Vital signs: initial hypertension/tachycardia/tachypnea progresses to respiratory and circulatory collapse
Skin: may be flushed with "cherry red" color
Neurologic: seizures and coma as poisoning progresses
Laboratory evaluation
Obtain the following:
Fingerstick glucose, acetaminophen and salicylate levels, electrocardiogram, and pregnancy test (when
appropriate)
Basic chemistries and serum lactate

Elevated anion gap acidosis, with elevated lactate, expected in cyanide poisoning
Venous blood appears bright red
Central venous blood gas with concomitant arterial blood gas

Narrowed venous-arterial PO2 gradient supports cyanide toxicity
Carboxyhemoglobin and methemoglobin levels

Rule out dyshemoglobinemias
Use nitrites (see below) cautiously or not at all in presence of dyshemoglobinemias
Cyanide poisoning can cause: renal failure, hepatic failure, rhabdomyolysis, pulmonary edema; obtain relevant
studies as indicated
General treatment
Secure airway, breathing, and circulation. Intubation is usually required. Administer high-flow oxygen by
nonrebreather face mask regardless of pulse oximetry reading.
Do NOT perform mouth to mouth resuscitation in cases of suspected cyanide toxicity. Patients with dermal
exposure must be decontaminated using proper precautions.
Give a single dose of activated charcoal if the airway is adequately protected (50 g in adults; 1 g/kg in children
with maximum dose of 50 g)
Treat hypotension with rapid IV boluses of isotonic fluid and vasopressors as needed. Treat seizures with a
benzodiazepine (eg, diazepam 5 mg IV).
Obtain assistance from medical toxicologist or poison control center
Antidotal treatment
Administer cyanide antidote when cyanide poisoning is clinically suspected. Hydroxocobalamin is the preferred
antidote.
If hydroxocobalamin is available, give the following:

Hydroxocobalamin 70 mg/kg up to 5 g IV (5 g is standard adult dose)
Sodium thiosulfate (25 percent): 1.65 mL/kg up to 50 mL IV; may repeat once (maximum dose 12.5 g)
If hydroxocobalamin is not available, cyanide toxicity is known or strongly suspected, and there are no
contraindications to nitrites, give the following:
Sodium nitrite 10 mg/kg - up to 300 mg - by slow IV infusion; may repeat once
Sodium thiosulfate (25 percent) 1.65 mL/kg up to 50 mL IV; may repeat once
If hydroxocobalamin is not available and cyanide toxicity is possible but not certain, or the patient has
contraindications to nitrites, give the following:
Sodium thiosulfate (25 percent) 1.65 mL/kg up to 50 mL IV; may repeat once
Refer to topic for details about nitrite treatment for children and patients with anemia, and for treatment in cases
of unlikely cyanide poisoning

Abbreviated injury score (AIS) for bronchoscopic gradation of inhalation injury
Grade Class Description
0 No injury Absence of carbonaceous deposits, erythema, edema, bronchorrhea

or obstruction
1 Mild injury Minor or patchy areas of erythema, carbonaceous deposits in

proximal or distal bronchi*
2 Moderate injury Moderate degree of erythema, carbonaceous deposits,

bronchorrhea, or bronchial obstruction*
3 Severe injury Severe inflammation with friability, copious carbonaceous deposits,

bronchorrhea or obstruction*
4 Massive injury Evidence of mucosal sloughing, necrosis, endoluminal obliteration*
*Any or a combination of the findings.
From: Endorf FW, Gamelli RL. Inhalation injury, pulmonary perturbations, and fluid resuscitation. J Burn Care Res 2007;
28:80. DOI: 10.1097/BCR.0B013E31802C889F. Copyright © 2007 American Burn Association. Reproduced with
permission from Lippincott Williams & Wilkins. Unauthorized reproduction of this material is prohibited.

Burn center referral criteria*
Partial-thickness burns greater than 10% of TBSA
Burns that involve the face, hands, feet, genitalia, perineum, or major joints
Third-degree burns in any age group
Electrical burns, including lightning injury
Chemical burns
Inhalation injury
Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or
affect mortality
Any patient with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk
for morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be
stabilized initially in a trauma center before being transferred to a burn unit. Physician judgment will be necessary
in such situations and should be in concert with the regional medical control plan and triage protocols.
Burned children in hospitals without qualified personnel or equipment for the care of children
Burn injury in patients who will require special social, emotional, or rehabilitative intervention
TBSA: total body surface area.

* A burn center may treat adults, children, or both. Burn injuries that should be referred to a burn center include any of
the criteria listed.
Copyright © American Burn Association. Advanced Burn Life Support Provider Manual. Chicago. 2011. 25-27. Print.

Example of inhalation injury treatment protocol in nonintubated adults
Titrate humidified high-flow oxygen to maintain SaO 2 >90%
Cough, deep breathing exercises every two hours
Turn patient side to side every two hours
Chest physiotherapy every two hours
Alternate mucolytic and heparin/saline nebulization:*
Nebulize 3 mL of 20% N-acetylcysteine every four hours; add a bronchodilator if wheezing or bronchospasm
occurs
Alternate with nebulized unfractionated heparin ¶ 5000 to 10,000 units in 3 mL of normal saline every four
hours
Nasotracheal suctioning, as needed
Early ambulation
Sputum cultures for intubated patients every Monday, Wednesday, and Friday
Pulmonary function studies at discharge and at outpatient visits
Patient/family education about the disease process
PT: prothrombin time; PTT: partial thromboplastin time.

* This alternating regimen provides a nebulizer treatment every two hours and is usually continued for seven days.
¶ Preservative-free heparin is not required. Nebulized heparin typically does not affect systematic coagulation parameters;
however, most clinicians managing burn patients monitor PT and PTT on a routine basis.
Adapted from: Mlcak RP, Hegde SD, Herndon DN. Respiratory Care. In: Total Burn Care, 4th ed, Herndon DN (Ed),
Saunders Elsevier, Philadelphia 2012.

Contributor Disclosures
Ronald P Mlcak, PhD, MBA, RRT, FAARC Nothing to disclose Eileen M Bulger, MD,
FACS Grant/Research/Clinical Trial Support: Atox Bio [Necrotizing soft tissue infections (AB103)]; Potrero
Medical [Critical care (Advanced urine output monitor)]. Consultant/Advisory Boards: Opticyte [Shock (Direct
cellular oximeter)]. Equity Ownership/Stock Options: Opticyte [Shock (Direct cellular oximeter)]. Marc G
Jeschke, MD, PhD Nothing to disclose Jess Mandel, MD Nothing to disclose Kathryn A Collins, MD, PhD,
FACS Nothing to disclose Geraldine Finlay, MD Consultant/Advisory Boards: LAM Board of directors, LAM
scientific grant review committee for The LAM Foundation.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.
Conflict of interest policy

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Inhalation injury from heat, smoke, or chemical irritants

PATHOPHYSIOLOGY AND CLASSIFICATION

Direct toxin damage is caused by the lower-molecular-weight constituents of smoke because of

Tracheobronchial injury — With the exception of inhalation of steam, injury to the

Generalized symptoms such as dizziness, nausea, or vomiting may be reported. Carbon

Laboratory findings — Standard laboratory studies should be obtained, including a complete

https://nebulosa.icesi.edu.co:2104/contents/inhalation-injury-from-heat-smoke-or-chemical-irritants/print?search=inhalación de humo&source=se… 4/29

AIS grading of inhalation injury by bronchoscopy is as follows [42]:

● 0 (no injury) – Absence of carbonaceous deposits, erythema, edema, bronchorrhea, or

● 2 (moderate injury) – Moderate degree of erythema, carbonaceous deposits, bronchorrhea, or

● 3 (severe injury) – Severe inflammation with friability, copious carbonaceous deposits,

● 4 (massive injury) – Evidence of mucosal sloughing, necrosis, endoluminal obliteration

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● History of closed space entrapment

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Endotracheal intubation is frequently used as a supportive therapy in the management of

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Treatment of inhalation injury is supportive and aimed at relieving bronchospasm, reducing

Bronchodilators — Aerosolized bronchodilators should be given when wheezing or

Mucolytic agents — Clearing the airways is an essential component of the management of

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● Titrate humidified high-flow oxygen to maintain oxygen saturation >90 percent

● Turn the patient side to side every two hours

● Administer chest physiotherapy every two hours

● Perform nasotracheal suctioning as needed

● Encourage early ambulation

Suggested criteria include [4]:

● PaO2/FiO2 ratio >250 mmHg

MORBIDITY AND MORTALITY

Inhalation injury is an independent predictor of mortality in burn patients. Pulmonary-related

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SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

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• Clearing the airways is an essential component in the management of patients with

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Use of UpToDate is subject to the Subscription and License Agreement.

2. emedicine.medscape.com/article/771194-overview (Accessed on November 23, 2015).

3. www.cdc.gov/HomeandRecreationalSafety/Fire-Prevention/index.html (Accessed on January

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11. Rehberg S, Maybauer MO, Enkhbaatar P, et al. Pathophysiology, management and

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Antonio, TX, USA on 28 March 2006. Burns 2007; 33:681.

38. Yamamura H, Kaga S, Kaneda K, Mizobata Y. Chest computed tomography performed on

39. Yamamura H, Morioka T, Hagawa N, et al. Computed tomographic assessment of airflow

45. www.ameriburn.org/BurnCenterReferralCriteria.pdf (Accessed on November 23, 2015).

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77. www.ameriburn.org/NBR.php (Accessed on November 23, 2015).

82. Rosenberg M, Ramirez M, Epperson K, et al. Comparison of long-term quality of life of

Topic 105477 Version 11.0

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Anatomy of the tracheobronchial tree

Graphic 104076 Version 2.0

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Signs and symptoms of various concentrations of carboxyhemoglobin levels

CO-Hb, % Signs and symptoms

20-30 Headache and throbbing in the temples

70-80 Weak pulse, slow respiration leading to death within hours

80-90 Death in less than 1 hour

>90 Death within minutes