Smoke inhalation injury

Smoke inhalation is the leading cause of death due to fires. It produces injury
through several mechanisms, including thermal injury to the upper airway, irritation
or chemical injury to the airways from soot, asphyxiation, and toxicity from carbon
monoxide (CO) and other gases such as cyanide.
Hallmarks
smoke inhalation complexed with burn injury (i.e. facial burns, carbonaceous
particles in the nasal cavity, periorbital edema, hair singeing). Early endotracheal
tube placement is necessary to secure patency of the upper airways and adequate
ventilation.
Signs and symptoms
Findings on physical examination may include the following:

Facial burns
Blistering or edema of the oropharynx
Hoarseness
Stridor
Upper airway mucosal lesions
Carbonaceous sputum

Symptoms of lower respiratory tract injury include the following:

Tachypnea
Dyspnea
Cough
Decreased breath sounds
Wheezing
Rales
Rhonchi
Retractions
Cyanosis may be present. However, cyanosis is an unreliable indicator of hypoxia
because neither carbon monoxide nor cyanide cause cyanosis.

Findings in patients exposed to asphyxiants may include the following:

CNS depression, lethargy, and obtundation
Irritability, severe temporal headache, and generalized muscle weakness
Coma (nearly always from CO poisoning)

Diagnosis
Studies may include the following:
Pulse oximetry and CO-oximetry
Arterial blood gases (ABGs)
Carboxyhemoglobin level
Lactate
CBC
Chest radiography (in patients with significant exposure or pulmonary symptoms)
ECG
Serial cardiac enzymes (in patients with chest pain)
Pulmonary function testing
Direct laryngoscopy and fiber optic bronchoscopy

Carboxyhemoglobin levels in the blood and the corresponding clinical

manifestations are as follows:
0-10% - Usually no symptoms
10-20% - Mild headache, atypical dyspnea
20-30% - Throbbing headache, impaired concentration
30-40% - Severe headache, impaired thinking
40-50% - Confusion, lethargy, syncope
50-60% - Respiratory failure, seizures
>70% - Coma, death

Blood carboxyhemoglobin levels may underestimate the degree of CO intoxication

because of oxygen administered to the patient before arrival to the hospital. The

use of nomograms to extrapolate levels to the time of rescue has been shown to
have prognostic value.

Management

When a patient presents with smoke inhalation, immediate assessment of the

patients airway, breathing, and circulation should be done. Provide IV access,
cardiac monitoring, and supplemental oxygen in the setting of hypoxia. Some
patients manifest bronchospasm and may benefit from the use of bronchodilators.
When upper airway injury is suspected, elective intubation should be considered.
Airway edema can progress over the next 24-48 hours and may make later
intubation difficult if not impossible. Studies have shown that initial evaluation is not
a good predictor of the airway obstruction that may ensue later secondary to rapidly
progressing edema.

Although controlled studies assessing the effects of steroids on various forms of

chemical pneumonitis are disappointing, steroids have been suggested as having
some value in exposure to the following:
Oxides of nitrogen (NOx)
Zinc oxide (HC)
Red phosphorus (RP)
Sulfur trioxide (FS)
Titanium tetrachloride (FM)
Polytetrafluoroethylene (PTFE; Teflon)

Patients with smoke inhalation should be monitored for 4-6 hours in the ED. Those
who are at low risk for injury and whose vital signs and physical examination
findings remain normal can usually be discharged with close follow-up and
instructions to return if symptoms develop. Patients with any of the following should
be strongly considered for hospitalization:
History of closed-space exposure for longer than 10 minutes
Carbonaceous sputum production
Arterial PO 2 less than 60 mm Hg
Metabolic acidosis
Carboxyhemoglobin levels above 15%

Arteriovenous oxygen difference (on 100% oxygen) greater than 100 mm Hg

Bronchospasm
Odynophagia
Central facial burns

Mechanical ventilation may be necessary in patients with declining lung function,

oxygenation levels, and ventilation. It is given as follows:
Positive pressure ventilation with low tidal volumes (3-5 mL/kg)
Positive end-expiratory pressure (PEEP), with plateau pressures below 30 cm
water

Neurologic abnormalities and a history of loss of consciousness are the primary

clinical features used to define severe CO toxicity and are indications for hyperbaric
oxygen (HBO) therapy. In addition, HBO use is indicated in patients with any of the
following:
Base excess lower than -2 mmol/L
CO level greater than 25% (or >15% in pregnancy, as fetal hemoglobin binds CO
more tightly)
Signs of cerebellar dysfunction
Cardiovascular dysfunction
Pulmonary edema
Extremes of age

Most often, inhalation injury results from direct damage to exposed epithelial
surfaces and causes conjunctivitis, corneal edema, rhinitis, pharyngitis,
laryngitis, tracheitis, bronchitis, bronchiolitis, and alveolitis. Systemic
absorption of toxins also occurs. Ascertaining if respiratory insufficiency is
due to direct pulmonary injury or is the result of the extensive metabolic,
hemodynamic, and subsequent infectious complications of surface burns is
difficult.
Inhalants are classified as irritants, asphyxiants, or systemic toxins. Irritants
cause extensive cell injury within the respiratory tract. Systemic toxins are
absorbed through the respiratory tract and go on to damage other organ
systems. Toxic gases are liberated during the combustion of various
substances, as listed in the table below.

Inhalants
Type

Inhalant

Irritant gases

Ammonia

Bleaching
agent,
sewage and
Chlorine
water
disinfectant,
cleansing
products
Combustion
of coal, oil,
Sulfur dioxide
cooking fuel,
smelting
Combustion
of diesel,
welding,
Nitrogen dioxide manufacturin
g of dyes,
lacquers, wall
paper
Asphyxiants
(mitochondrial
toxins)

Hydrogen
cyanideb

Hydrogen
sulfidec

Source
Injury/Mechanism
Fertilizer, refrigerant,
Upper airway
manufacturing of
epithelial damage
dyes, plastics, nylon

Lower airway
epithelial damage

Upper airway
epithelial damage

Terminal airway
epithelial damage

Competes for oxygen

sites on hemoglobin,
Carbon
Combustion of weeds,
myoglobin, hememonoxidea
coal, gas, heaters
containing
intracellular proteins
Tissue asphyxiation by
Burning of
inhibiting intracellular
polyurethane,
cytochrome oxidase
nitrocellulose
activity, inhibits ATP
(silk, nylon,
production, leads to
wool)
cellular anoxia
Sewage
Like cyanide, tissue
treatment
asphyxiants by
facility,
inhibition of
volcanic
cytochrome oxidase,

gases, coal
mines,
natural hot
springs

leads to disruption of
electron transport
chain, results in
anaerobic metabolism

CNS narcosis,
anesthetic stats,
Inhalant abuse
diffuse GI symptoms,
(toluene, benzene,
peripheral
Freon); aerosols; glue; neuropathy with
gasoline; nail polish
weakness, coma,
Systemic toxins Hydrocarbons remover; typewriter
sudden death,
correction fluid;
chemical
ingestion of petroleum pneumonitis, CNS
solvents, kerosene,
abnormalities, GI
liquid polishes
irritation,
cardiomyopathy,
renal toxicity
Blocks
acetylcholinesterase;
Organophosphat Insecticides,
cholinergic crisis with
es
nerve gases
increased
acetylcholine
Metal oxides
of zinc,
Flulike symptoms,
copper,
Metal fumes
fever, myalgia,
magnesium,
weakness
jewelry
making
a
Major
component of
smoke.

Smells like
almonds,
component of
smoke from
fires.

Smells like
rotten eggs.

Carbon monoxide
Individual cases of CO poisoning can occur under many circumstances (e.g.,
furnace malfunction, motor vehicle exhaust exposure). Multiple cases may
occur after large-scale disasters that result in widespread, long-term power
outages (e.g., major hurricanes), where the residential use of portable gas
generators in poorly ventilated areas creates the ideal situation for CO
poisoning. In a study evaluating unintentional CO poisoning of Florida state
residents from 1999-2007, 89% of all CO poisoning-related deaths were non
fire related.

Oxides of nitrogen
At ground level, NOx are produced during electric or arc welding, combustion
of fuels, detonation of nitrate-based explosives, combination of nitrogencontaining products, and decomposition of organic matter. Recently filled
farm silos have high nitrogen dioxide levels for approximately 10 days,
peaking at 4000 ppm. Significant quantities of nitrogen dioxide also are
found in diesel engine exhaust.
Any person in one of the following occupational tasks or environments is at
risk for accidental exposure to NOx:

Unventilated farm silos

Welding in confined spaces

Detonating nitrogen-based explosives in enclosed spaces (e.g., tanks,

ships)

Handling nitric acid

Resurfacing ice arenas

Using anesthetic gases

Missile fuel oxidizer spills

Zinc oxide

Since this smoke can be distributed by grenades, candles, pots, artillery

shells, and special air bombs, any military personnel engaged in the use or
activity of these tools are at risk for HC exposure. Exposure to zinc oxide also
is common among welders and those who are engaged in the smelting of
zinc.

Red phosphorus
Phosphorus smokes are used in military formulations for smoke screens,
incendiaries, smoke markers, colored flares, and tracer bullets. Workers at
phosphorus loading plants also can be exposed to phosphorus smoke.

Sulfur trioxide
Exposure to FS is an occupational hazard in the chemical and metal plating
industries. FS exposure also may occur in the production of detergents,
soaps, fertilizers, or lead-acid batteries (car batteries), in printing and
publishing, or in photography shops. With reduced use of FS by the military,
exposure in that setting has become less common.

Titanium tetrachloride
Because FM smoke breaks down so rapidly in the environment, people who
work with it in industry seem to be most at risk. Because titanium
tetrachloride is extremely irritating and corrosive in both the liquid
formulation and the smoke formulation, its use has diminished.

Oil fog
Military personnel can be exposed to fine-particle oil fog when it is used in
training or in combat. Similar exposures may occur in industrial settings
where oil mists are created, such as the following:

Metalworking

Automobile and textile industries

Pressrooms

Mining

Die and mould lubrication

Teflon particles

Exposure to these fumes is common in closed-space fires where Teflon is

pyrolyzed. In addition, polymer fume fever has been observed in persons
with occupational exposure to Teflon powder whose cigarettes became
contaminated with Teflon.

Differential Diagnoses
Acute Respiratory Distress Syndrome
Anaphylaxis
Aspiration Pneumonitis and Pneumonia
Asthma
Bacterial Pneumonia
Chronic Obstructive Pulmonary Disease (COPD) and Emphysema in
Emergency Medicine
Heart Failure
Pneumothorax
Pulmonary Embolism
Viral Pneumonia

In the workup of inhalation injuries caused by toxic smoke, the primary

investigation focuses on the pulmonary system. Other tests may be clinically
indicated based on history, physical examination, and underlying health
problems. Carbon dioxide levels also may be monitored, since patients with
prior lung disease such as asthma and chronic obstructive pulmonary
disease may be affected more severely and are at greater risk to retain
carbon dioxide.

Studies may include the following:

Pulse oximetry and CO-oximetry
Arterial blood gases (ABGs)
Carboxyhemoglobin level
Lactate
Complete blood cell count (CBC)
Chest radiography
Electrocardiogram
Serial cardiac enzymes (in patients with chest pain)
Pulmonary function testing
Direct Laryngoscopy and fiber optic bronchoscopy

Pulse Oximetry and CO-oximetry

Pulse oximetry readings can be misleading in the setting of carbon monoxide
(CO) exposure or methemoglobinemia because these devices use only 2
wavelengths of light (the red and the infrared spectrum), which detect
oxygenated and deoxygenated hemoglobin only and not any other form of
hemoglobin. Readings are falsely elevated by CO-bound hemoglobin
(carboxyhemoglobin).

In methemoglobinemia, light reflection is similar to that in reduced

hemoglobin. Pulse oximetry may show a depressed oxygen saturation, but
the decrease does not accurately reflect the level of methemoglobinemia. In
fact, as methemoglobin levels reach 30% or higher, the pulse oximetry
reading converges on approximately 85%.

CO-oximeters use 4 wavelengths of light and are capable of detecting

carboxyhemoglobin and methemoglobin as well as hemoglobin and
oxyhemoglobin. Some newer co-oximeters use 5 wavelengths and are also

able to measure sulfhemoglobin. The percent of oxyhemoglobin measured by

CO-oximetry is an accurate measure of the arterial oxygen saturation. The
difference between saturations obtained by CO-oximetry and calculated
figures is known as the saturation gap and is an indicator of
dyshemoglobinemia.

Arterial Blood Gases

Arterial oxygen tension (partial pressure of arterial oxygen [PaO2]) does not
accurately reflect the degree of CO poisoning or cellular hypoxia. The PaO2
level reflects the oxygen dissolved in blood that is not altered by the
hemoglobin-bound CO. Because dissolved oxygen makes up only a small
fraction of arterial oxygen content, a PaO2 level within the reference range
may lead to serious underestimation of the decrement in tissue oxygen
delivery and the degree of hypoxia at the cellular level that occurs when CO
blocks the delivery of oxygen to the tissues.

With most blood gas machines, the oxygen saturation is calculated on the
basis of the PaO2 level. Thus, such a reading does not give an accurate
determination of oxygen saturation, which must come from CO-oximetry.
ABG measurements are nonetheless useful to assess the adequacy of
pulmonary gas exchange. Although the presence of a PaO2 level that is
within the reference range may not exclude significant tissue hypoxia
because of CO, the presence of a low PaO2 (< 60 mm Hg in room air) or
hypercarbia (alveolar [arterial] carbon dioxide pressure [PaCO2] level of 55
mm Hg) indicate significant respiratory insufficiency. Metabolic acidosis
suggests inadequate oxygen delivery to the tissues.
The difference between the partial pressure of oxygen in the alveolus and
that measured on an ABG is the alveolar-arterial (A-a) gradient. This value,
usually less than 5-10 mm Hg, may be several hundred mm Hg in the setting
of significant pulmonary injury and can be used to assess improvement or
deterioration in lung function when measured at a stable fraction of inspired
oxygen (FiO2).

The alveolar gas equation can be used to estimate the efficiency of

pulmonary oxygen delivery to the arterial circulation in the presence of
supplemental oxygen administration. This formula determines the alveolar
oxygen pressure.

The formula is: PaO2 = (FiO2) x (PB - PH2 O) - (PaCO2/RQ).

PB represents barometric pressure
PH2 0 represents the partial pressure of water vapor (47 mm Hg at body
temperature, ambient pressure)
RQ represents the respiratory quotient (estimated at 0.8).
Carboxyhemoglobin Level
Carboxyhemoglobin levels in the blood and the corresponding clinical
manifestations are as follows:
0-10% - Usually no symptoms
10-20% - Mild headache, atypical dyspnea
20-30% - Throbbing headache, impaired concentration
30-40% - Severe headache, impaired thinking
40-50% - Confusion, lethargy, syncope
50-60% - Respiratory failure, seizures
>70% - Coma, death

Blood carboxyhemoglobin levels may underestimate the degree of CO

intoxication because of oxygen administered to the patient before arrival to
the hospital. Smokers may have baseline levels up to 5-10% and may
experience more significant CO poisoning for the same level of exposure as
nonsmokers. Finally, correlation between carboxyhemoglobin levels and
eventual neurologic outcome is poor.

Lactate and Other Blood Studies

Elevated lactate levels may result from metabolic acidosis secondary to the
following:

Hypoxia
CO
Cyanide (CN)
Methemoglobinemia
Inadequate resuscitation
Unrecognized trauma

Lactate levels associated with CN poisoning have been reported as being

above 8 mmol/L. The concentration of lactate increases proportionally with
the degree of CN poisoning, and lactate levels higher than 10 mmol/L are a
sensitive indicator of CN levels higher than 1 mg/mg. Note that in most
institutions, CN levels can take hours to days for results; therefore, one must
rely on clinical and indirect laboratory data.
Approach Considerations
Beware that patients may appear asymptomatic on arrival but may develop
significant signs and symptoms as long as 36 hours after exposure,
especially in fires, which produce small particles with low water solubility. Be
aware of pertinent historical risk factors when treating patients with potential
smoke inhalation injury. These include closed-space fires, carbonaceous
sputum, elevated carbon monoxide (CO) levels, and central facial burns.
Acute respiratory distress usually responds very well to aggressive initial
management. Normal laboratory values and imaging studies, coupled with
clinical improvement, can give the health care provider a false sense of
security. The patient then may be discharged, only to deteriorate as delayed
pulmonary edema ensues. Any patient with significant exposure to toxic
smokes should be observed for 24-48 hours and imaged with serial chest
radiographs. Difficulty arises in defining a significant exposure, since the
clinical response is so varied.
Provide intravenous (IV) access, cardiac monitoring, and supplemental
oxygen in the setting of hypoxia. A small subset of patients manifest
bronchospasm and may benefit from the use of bronchodilators, although
this is not well documented. This is especially true of patients with
underlying chronic obstructive pulmonary disease (COPD) or asthma.

Treatment of inhalation injuries caused from toxic smokes is based on clinical

presentation and involves primarily supportive care directed at the
cardiopulmonary system. In some cases (eg, cyanide [CN] poisoning,
methemoglobinemia), specific antidotes are available. Subcutaneous
epinephrine has been used in zinc oxide (HC) exposures.
Corticosteroids are attractive for suppressing inflammation and reducing
edema, but no direct data support their use in smoke inhalation. Because of
the increased risk of pulmonary infection and delayed wound healing,
prolonged use of steroids is discouraged. However, consider a brief course of
steroids in those patients with otherwise unresponsive severe lower airway
obstruction. In addition, patients receiving steroids prior to injury who may
experience adrenal insufficiency should receive stress doses of steroids.
Although controlled studies assessing the effects of steroids on various forms
of chemical pneumonitis are disappointing, steroids have been suggested as
having some value in exposure to the following:
Oxides of nitrogen (NOx)
Zinc oxide (HC)
Red phosphorus (RP)
Sulfur trioxide (FS)
Titanium tetrachloride (FM)
Polytetrafluoroethylene (PTFE; Teflon)

In a case series by Huang et al, 25% of patients presented after HC exposure

with acute lung injury requiring ventilatory support. All of these patients
survived with glucocorticoids, antibiotics and lung-protective ventilatory
management. However, there was no control group, so a causal link could
not be made between survival and steroid treatment.
Smoke inhalation injuries predispose the airways to infection because of
cellular injury, reduction of mucociliary clearance, and poor macrophage
function. Acute bacterial colonization and invasion peaks at 2-3 days after
smoke inhalation. Prophylactic antibiotics should not be used, as they are not
only ineffective but increase the risk of emergence of resistant organisms.
Discerning secondary infection from the effects of inhalation injury can be
very difficult because both may produce fever, elevated white blood cell

counts, and abnormal radiography findings. Antimicrobial therapy should be

reserved for patients with definitive microbiologic evidence of infection that
is not responding to aggressive support therapy or when clinical
deterioration occurs in the first 72 hours.
The most common organisms in secondary pneumonia after smoke
inhalation injury are Staphylococcus aureus and Pseudomonas aeruginosa.
Direct parenteral coverage with antibiotics to cover these bacteria if infection
is suspected.
Prehospital Care
As always, prehospital care providers must do everything in their power to
remove the patient from ongoing exposure without becoming casualties
themselves. Although emergency department (ED) care is mostly supportive,
prompt delivery to the ED should be a priority.
Secure the airway as needed, deliver high-flow oxygen by mask, and obtain
IV access. Cardiac monitoring also is important for any patient with
respiratory distress. Beta-agonists such as albuterol may be given as a
nebulized treatment to those who demonstrate signs of bronchoconstriction.
If respiratory failure is present, the patient should have assisted ventilation
and/or endotracheal intubation. Perform cricothyrotomy if airway obstruction
is present or impending and an airway cannot be secured orally.
Obtain a CO level at the scene if possible. In a consecutive case series of 18
patients, cardiac arrest complicating CO toxicity was uniformly fatal, despite
administration of hyperbaric oxygen (HBO) therapy after the initial
resuscitation. The prognosis of this condition should be considered when
making triage decisions for these patients.

Emergency Department Care

Presently, no specific treatment exists to ameliorate the tissue damage and
reduce the vulnerability to infection induced by smoke inhalation. Administer
100% oxygen because of the likelihood of CO inhalation in fires. Once CO
toxicity, cyanide (CN) toxicity, and methemoglobinemia have been
addressed, subsequent treatment is predominantly supportive.
The most urgent concern in patients is the patency of the upper airway and
adequacy of ventilation. Check for exposure to heat and thermal injury to the
nose, mouth, face, and singed hair. Consider smoke involvement if soot is on
the face and in sputum, although smoke inhalation is possible without

evidence of soot. The proportion of patients with an inhalation injury who

require endotracheal intubation is higher for those who also have a burn
injury: 62% with a burn versus 12% without a thermal injury and the
incidence of inhalation injury increases with the size of the burn
It is of vital importance that the magnitude of the swelling in the areas of the
face and mandible be closely scrutinized when making decisions about the
need for an artificial airway. The threshold for intubation should be lower
than in other patients due to the potential of rapid development of airway
edema. This is especially true of the pediatric patient. When upper airway
injury is suspected, elective intubation should be considered because
progression of edema over the next 24-48 hours may make later intubation
difficult if not impossible.
If systemic paralysis is necessary for intubation, succinylcholine can be used
safely in the immediate post-burn phase and up to several days afterward,
although one should be cognizant of the possibility of a rise in serum
potassium. Inflate the tube cuff to minimal levels, even allowing a small leak,
to prevent iatrogenic tracheal damage in patients with an already
compromised tracheal mucosa.
Patients whose injury involves cutaneous burns have ongoing circulatory
derangements. Fluid loss through burned areas from intense inflammation
with vasodilatation and capillary leak or from the subsequent infectious
complications necessitates large fluid volume resuscitation. Large-bore IV
catheter access may be needed to facilitate fluid resuscitation.
Use formulas (e.g., Parkland) to calculate fluid resuscitation if severe burns
are present. Even minor errors in estimation of body surface area; burned
surface area; and fluid, electrolyte, and protein requirements can produce
profound hemodynamic and respiratory compromise. Frequent evaluation of
heart rate, perfusion, and blood pressure are needed to determine stability
and guide therapy.

In mass casualty scenarios, the use of fiber optic bronchoscopy may be

beneficial to rapidly triage patients to intensive care, ward, or observation
status. Mobilization of otolaryngology and/or anesthesia resources may be
necessary to accomplish this in a timely fashion.
patients with any of the following should be strongly considered for
hospitalization:
History of closed-space exposure for longer than 10 minutes

History of syncope
Carbonaceous sputum production
Arterial PO 2 less than 60 mm Hg
Metabolic acidosis
Carboxyhemoglobin levels above 15%
Arteriovenous oxygen difference (on 100% oxygen) greater than 100 mm
Hg
Bronchospasm
Odynophagia
Central facial burns

For patients with isolated smoke inhalation, treatment in an intensive care

unit is appropriate. However, patients with significant cutaneous burns
should be transferred to a burn center when stable, if they meet the criteria
for transfer.

Carbon Monoxide Poisoning

Assume elevated levels of carboxyhemoglobin in all fire victims. CO is not
only responsible for most prehospital deaths due to smoke inhalation, it is
also the leading cause of injury/death from all poisons worldwide.
The half-life of CO is 320 minutes on room air, 90 minutes on 100% oxygen,
and 23 minutes in a hyperbaric chamber at 3 atmospheres absolute (ATA).
Elimination of CO depends primarily on the law of mass action, so alveolar
PO2, rather than alveolar ventilation, is the critical factor in its removal.
Hyperbaric oxygen therapy
In patients with CO poisoning from smoke inhalation, the main reason for use
of hyperbaric oxygen (HBO) therapy is to prevent delayed neurological
sequelae. Carboxyhemoglobin levels are poor indicators of the severity of
intoxication; patients with significant toxicity may have low levels. In fact, at

the time of the initial HBO treatment, patients enrolled in most studies have
normal or near-normal carboxyhemoglobin levels.
Prospective, randomized controlled trials have compared HBO with
normobaric oxygen (NBO) therapy for CO poisoning. Four of these studies
show a benefit for CO poisoning; two do not. The data and conclusions drawn
from these studies are conflicting and highlight the controversy surrounding
the utility of HBO.
In a prospective, double-blind study that compared HBO with NBO in patients
with symptomatic acute CO poisoning, Weaver and colleagues found that 3
HBO treatments decreased the incidence of cognitive sequelae by 46% at 6
weeks. Furthermore, a benefit continued to be seen at 12-month follow-up.
Essentially, for every 6 patients treated with HBO, one case of delayed
neurologic sequelae could be avoided. The evidence of benefit with HBO was
so strong that the study was halted before its scheduled completion.
Although there has been much debate regarding the accuracy of
neuropsychometric testing, including the fact that patients who are
depressed and who have attempted suicide with non-CO means perform as
poorly as CO-exposed patients, such testing remains an objective means to
evaluate cognitive function.
Neurologic abnormalities and a history of loss of consciousness are the
primary clinical features used to define severe CO toxicity and are indications
for HBO. In addition, HBO use is indicated in patients with any of the
following:
Base excess lower than -2 mmol/L
CO level greater than 25% (or >15% in pregnancy, as fetal hemoglobin
binds CO more tightly)
Signs of cerebellar dysfunction
Cardiovascular dysfunction
Pulmonary edema
Extremes of age

Note that the incidence of delayed neurologic sequelae increases with a

more symptomatic initial clinical picture, in older patients, and in those with
a prolonged exposure.

The American College of Emergency Physicians Clinical Policies

Subcommittee recommended in 2008 continued use of HBO in CO poisoning,
especially in children and pregnant women, due to the conflicting results of
previous studies.

Cyanide Poisoning
Individuals exposed to CN poisoning may present with a variety of symptoms
ranging from headache and altered mental status to hypotension,
arrhythmia, and cardiovascular collapse followed by shock. Management of
CN toxicity has historically involved the creation of an alternate binding site
for CN to compete with cytochrome oxidase and also to provide substrate
necessary to convert CN to a nontoxic metabolite.

Although not universally available, hydroxocobalamin (Cyanokit) is the

preferred treatment of CN toxicity. In fact, many prehospital personnel use
this product before the patient arrives if there is a high index of suspicion. It
has been used in France for more than 30 years and was approved by the US
Food and Drug Administration (FDA) in 2006.

Hydroxocobalamin is a hemelike molecule with a complexed cobalt atom that

binds directly to CN to form cyanocobalamin (vitamin B-12), which is
excreted renally. In vitro studies indicate that hydroxocobalamin penetrates
cells and can act intracellularly. Adverse effects are chromaturia and
reddening of the skin. Empiric administration to patients subsequently
confirmed to have CN poisoning has been shown to be associated with 67%
survival.
Hydroxocobalamin has a rapid onset of action, is easy to administer, does
not interfere with tissue oxygenation, is well tolerated, and is safe for smoke
inhalation patients. Additionally, it is not associated with hypotension or the
formation of a dyshemoglobinemia (as was found in previous antidote kits)
and it improves hemodynamic stability.
The traditional CN antidote kit contains amyl and sodium nitrite to create a
methemoglobin level of 3% and 20-30%, respectively, which, in turn, has a
higher affinity for CN than for cytochrome a3. Also included is sodium
thiosulfate, which provides substrate for the enzyme rhodanese; this
combines thiosulfate and CN to form a nontoxic compound, thiocyanate,
which is excreted renally.

Induction of methemoglobinemia is theoretically dangerous in a patient with

an elevated carboxyhemoglobin level because further reduces oxygencarrying capacity, so the clinician should consider withholding the nitrite
portion of the kit. Another drawback of this treatment is the delayed onset of
thiosulfate. Note that there is limited information about the efficacy of
sodium thiosulfate for CN poisoning, as there are no clinical trials of sodium
thiosulfate available. Finally, this treatment may be more preventative rather
than curative.

Though no prospective studies have conclusively demonstrated a decrease

in mortality with the use of sodium thiosulfate alone, optimal treatment at
this time is the combined use of hydroxocobalamin and thiosulfate. This is
because sodium thiosulfate has poor intracellular penetration and slow
onset. The combination of treatments allows quick extraction of cyanide
without the formation of other dyshemoglombinemias and offers a sulfurdonating drug that maximizes the function of rhodanese.

Experimental Treatments
Studies on experimental induction of smoke inhalation confirm the presence
of an acute surfactant deficiency. Instillation of artificial surfactant shortly
after injury was beneficial. Larger studies are needed before instituting such
therapy.
Oxidant injury eventually leads to cast formation of cellular debris in the
airways, thus contributing to pulmonary failure. A pediatric study has shown
that aerosolized heparin/N -acetylcysteine decreases the incidence of
atelectasis, reintubation rates, and overall mortality.
Acetylcysteine and L-3,4 dehydroproline and a combined regimen of
hydrocortisone and penicillamine have been used to treat ARDS induced by
inhalation of smoke from smoke bombs. Positive outcomes were attributed to
early treatment with penicillamine. In animal studies, acetylcysteine has also
been found effective for PTFE exposure.
In an animal model, whole-body hypothermia has been shown to suppress
oxidant bronchoalveolar damage and pulmonary inflammation.
Mechanistically, this appears to halt the progression of bronchoalveolarcapillary permeability.

Pulmonary Toilet
As with many respiratory conditions, the use of chest physiotherapy is widely
accepted in inhalation injury but remains unproven in controlled trials. The
use of percutaneous cupping and postural drainage seem reasonable to clear
airways of cellular debris and soot, thereby preventing atelectasis and
obstruction. Obviously, care must be taken in attempting this in the presence
of significant chest wall burns.
Encourage extubated patients to cough and breathe deep. In patients who
are intubated, use gentle suctioning to remove mucus, debris, and sloughed
epithelium. Fiberoptic bronchoscopy may be helpful in removing the debris
and in facilitating pulmonary toilet.
Mechanical Ventilation
Mechanical ventilation may be necessary in patients with declining lung
function, oxygenation levels, and ventilation. Use of positive pressure
ventilation with low tidal volumes (3-5 mL/kg) and positive end-expiratory
pressure (PEEP) and maintenance of plateau pressures below 30 cm water
significantly increases short-term survival and is associated with decreased
tracheobronchial cast formation. In fact, this treatment has been shown to
increase the intensive care unit (ICU) survival rate from 29% to 62%.
PEEP may assist in opening obstructed closed alveoli and help ventilation in
those patients with poor compliance by increasing functional residual
capacity. Ideally, PEEP stents alveoli open, preventing the atelectasis and
alveolar flooding that can result from surfactant dysfunction, increasing
interstitial fluid, and third-spacing.
High-frequency percussive ventilation (HFPV), while not as commonly used in
the ED, is considered standard therapy in many burn centers. HFPV
generates pulsatile flow at up to 600 cycles per minute, which entrains the
humidified gas by its effect on molecular diffusion. It can improve clearance
of airway secretions and allow continued patency of the lower airways. In
patients with inhalation injury and burns involving less than 40% of total
body surface area, HFPV decreases both morbidity and mortality.

Diet
Patients should take nothing by mouth until it becomes clear that they will
not require tracheal intubation because of significant respiratory or
hemodynamic compromise.

Even with extensive burns, most patients can tolerate enteral feedings at the
end of the first 24 hours. Begin enteral feedings as soon as possible. As
enteral intake increases, decrease intravenous fluids accordingly. Patients
may demonstrate marked hyper metabolism. Therefore, providing adequate
nutritional support is important.
n the military setting, the mission-oriented protective posture (MOPP) gear
ensemble provides adequate protection against all smokes. In the industrial
setting, guidelines have been established for the protection of the worker as
well as any person who may encounter toxic smokes. Aim preventive efforts
at decreasing the concentration of the smoke and the time of exposure and
recognizing underlying health problems that may be exacerbated by
exposure to toxic smokes.
Beta2 Agonists
These agents relieve reversible bronchospasm by relaxing smooth muscles of
the bronchi. Increased resistance from airway edema and reflex
bronchoconstriction from irritation of airway receptors contribute to airway
obstruction.
Bronchodilators are important in the treatment of bronchoconstriction and
bronchorrhea. Toxic smokes can cause bronchoconstriction, especially if the
exposed individual has underlying asthma or chronic obstructive pulmonary
disease (COPD). In patients with profound bronchoconstriction and wheezing,
subcutaneous epinephrine has been helpful in stabilizing mast cells and
halting or reversing potentially fatal bronchoconstriction.
Albuterol
Albuterol is a beta-agonist that is useful in treatment of bronchospasm
refractory to epinephrine. It relaxes bronchial smooth muscle by acting on
beta2-receptors, while having little effect on cardiac muscle contractility.
Airway resistance is decreased, and ventilation is improved.
Epinephrine racemic
Racemic epinephrine alleviates airway edema and reflex bronchospasm.
Although it has not been directly studied in smoke inhalation, inhaled
racemic epinephrine can theoretically provide relief from both airway edema
and reflex bronchospasm in this setting.
Terbutaline
Terbutaline is used for severe bronchoconstriction, especially in patients with
underlying reactive airways disease. This agent acts directly on beta2-

receptors to relax bronchial smooth muscle, relieving bronchospasm and

reducing airway resistance.
Epinephrine
Epinephrine is used for severe bronchoconstriction, especially in patients
with underlying reactive airways disease. This agent has alpha-agonist
effects that include increased peripheral vascular resistance, reversed
peripheral vasodilatation, systemic hypotension, and vascular permeability.
The beta-agonist effects of epinephrine include bronchodilation, chronotropic
cardiac activity, and positive inotropic effects.
Antidotes, Other
Several CN antidotes exist, which work by different mechanisms of action.
Hydroxocobalamin binds to CN to form cyanocobalamin. Amyl nitrite and
sodium nitrite convert a portion of circulating hemoglobin to methemoglobin.
Sodium thiosulfate allows the production of thiocyanate.
Sodium thiosulfate
After formation of methemoglobin and production of cyanomethemoglobin,
thiosulfate acts as a sulfur donor to the endogenous enzyme rhodanese. This
enzyme removes CN from the cyanomethemoglobin complex and forms
thiocyanate, which is excreted renally. CN also is removed directly from
cytochrome oxidase and is converted to thiocyanate in the presence of
thiosulfate via the enzyme rhodanese.
Methylene blue
Methylene blue is used to convert methemoglobin to oxyhemoglobin. It
contains a tetramethyl thionine chloride moiety that is reduced (it is an
electron acceptor) in the presence of nicotinamide adenine dinucleotide
phosphateoxidase (NADPH) and methemoglobin reductase to
leukomethylene blue. Leukomethylene blue then becomes available to
reduce methemoglobin to oxyhemoglobin.
Methylene blue may be ineffective in treating patients with glucose-6phosphodiesterase (G-6-PD) deficiency because, in the hexose
monophosphate shunt, G-6-PD is essential for the generation of NADPH.
Without NADPH, methylene blue cannot act as a reducing agent in the
transformation of methemoglobin to oxyhemoglobin.
Hydroxocobalamin (Cyanokit)

Hydroxocobalamin is a vitamin B-12 precursor that contains a cobalt ion,

which has greater affinity for cyanide than does cytochrome oxidase. Binding
of cyanide to the cobalt ion results in the formation of cyanocobalamin,
which is excreted renally. Hydroxocobalamin has few adverse effects and has
the following advantages over other cyanide treatments:
This agent is safe to use in victims of smoke inhalation. Cyanocobalamin is a
pigmented compound, and interferes with spectrophotometric tests. Any
necessary blood samples should be drawn prior to administration of antidote
if possible, because it will not be possible to obtain accurate results for most
blood tests afterward.
Amyl nitrite
In the presence of nitrites, hemoglobin is converted to methemoglobin,
which has a higher binding affinity for CN than does the cytochrome oxidase
complex. Administration of amyl nitrite produces a methemoglobin level of
5% and subsequent formation of cyanomethemoglobin, allowing electron
transport and cellular respiration to continue. This medication is given until
an IV line is established and sodium nitrite can be administered.
Sodium thiosulfate & sodium nitrite (Nithiodote)
In the presence of nitrites, hemoglobin is converted to methemoglobin that
has a higher binding affinity for CN than does the cytochrome oxidase
complex. Administration of sodium nitrite produces a methemoglobin level of
20-30% and subsequent formation of cyanomethemoglobin, allowing
electron transport and cellular respiration to continue.
Corticosteroids
Whether corticosteroids are beneficial in toxic smoke inhalation is a matter of some
debate, but many experts consider these agents helpful in this setting.
Corticosteroids are considered especially useful in metal fume fever, which is
believed to be mediated by an inflammatory cascade of events involving cytokines
and histamine release.
Methylprednisolone
Methylprednisolone decreases inflammation by suppressing the migration of
polymorphonuclear neutrophils (PMNs) and reversing increased capillary
permeability.

Dexamethasone

Dexamethasone decreases immune reactions. It provides a local anti-inflammatory

effect while minimizing some of the gastrointestinal and other risks associated with
systemic medications. Dexamethasone suppresses the migration of
polymorphonuclear leukocytes (PMNs) and reduces capillary permeability.