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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: Dec 2019. | 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
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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]. 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
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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
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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
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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
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● 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
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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,
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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
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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.
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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
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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,
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
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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
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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
13 de 25 20/01/2020 12:41 a. m.
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.)
14 de 25 20/01/2020 12:41 a. m.
● 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
16 de 25 20/01/2020 12:41 a. m.
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
17 de 25 20/01/2020 12:41 a. m.
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.
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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.
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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)
20 de 25 20/01/2020 12:41 a. m.
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
21 de 25 20/01/2020 12:41 a. m.
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.
22 de 25 20/01/2020 12:41 a. m.
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.
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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.
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25 de 25 20/01/2020 12:41 a. m.

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Inhalation injury from heat, smoke, or chemical irritants

PATHOPHYSIOLOGY AND CLASSIFICATION

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

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

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

● 1 (mild injury) – Minor or patchy areas of erythema or carbonaceous deposits in the

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

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

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

● History of closed space entrapment

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

● Pneumonia – Although the risk of nosocomial pneumonia is increased, there is no benefit

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

Supportive treatments — Supportive treatment includes the use of bronchodilators for

Bronchodilators — Aerosolized bronchodilators should be given when wheezing or

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

N-acetylcysteine (NAC) is a powerful mucolytic agent that can be useful in treatment of

Example treatment protocol for nonintubated patients — An example protocol approach

● 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

● Alternate aerosolized NAC with a bronchodilator (if wheezing) and aerosolized

● Perform nasotracheal suctioning as needed

● Encourage early ambulation

Extubation criteria — Extubation criteria include a wide variety of physiological variables

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

SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

● The evaluation and initial management of accompanying trauma or burn injuries is

● Proper airway management is critical in patients with inhalation injury. Endotracheal

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

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

Topic 105477 Version 11.0

Anatomy of the tracheobronchial tree

Graphic 104076 Version 2.0

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

Graphic 106164 Version 1.0

Carbon monoxide poisoning: Rapid overview

Assess for minor symptoms: headache, nausea/vomiting

Assess pregnancy status

Physical examination usually unremarkable

Check acid-base status using (preferably arterial) blood gas

Intubate as clinically indicated

We suggest hyperbaric oxygen (HBO) for:

CO level >25% (>20% if pregnant)

Severe metabolic acidosis (pH <7.1)

Graphic 60672 Version 11.0

Cyanide poisoning: Rapid overview

Initial symptoms are nonspecific: headache, anxiety, confusion, abdominal pain

Vital signs: initial hypertension/tachycardia/tachypnea progresses to respiratory and circulatory collapse

Skin: may be flushed with "cherry red" color