Smoke Inhalation Injury

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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 (CN). See the image below.

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 CN 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)

See Clinical Presentation for more detail.

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 fiberoptic bronchoscopy

Carboxyhemoglobin levels in the blood and the corresponding clinical manifestations are as follows ^[1] :

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.

See Workup for more detail.

When a patient presents with smoke inhalation, immediate assessment of the patient’s airway, breathing, and circulation should be done. ^[2] 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. ^[2]

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 ^[3] :

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 PO₂ 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

See Treatment and Medication for more detail.

Smoke inhalation injury was described as early as the first century CE, when Pliny reported the execution of prisoners by exposure to the smoke of greenwood fires. Smoke—the vaporous colloidal system formed when a material undergoes combustion or pyrolysis—comprises a collection of noxious gases, airborne solid particles, and airborne liquid particles. The distribution of those particles in the respiratory tract after inhalation is determined by their size and by the person’s breathing mechanics and tidal volume.

During fires, smoke inhalation victims are unable to efficiently breathe through the nasopharynx, thereby decreasing inspiratory air filtration and enabling a greater amount of particle distribution in the airway. This subsequently leads to nasopharyngeal irritation and severe lung injury.

Inhalation injury from smoke in fires may account for as many as 60-80% of fire-related deaths in the United States, many of which are preventable. ^{[4, 5]} Excellent care rendered at today’s burn centers has greatly reduced the mortality from surface burns, ^[6] while the mortality from pulmonary injury has been increasing.

Many victims of fire accidents have both smoke inhalation and thermal injury. In fact, the co-presence of bronchopulmonary injury with cutaneous burns that exceed 30% of the total body surface area causes the mortality rate to increase more than 70%. ^[7] Other studies have shown that the incidence of inhalation injury increases with increasing burn size. ^[2]

Smoke inhalation may produce injury through several mechanisms. Heated air from a fire can cause significant thermal injury to the upper airway. Particulate matter produced during combustion (soot) can mechanically obstruct and irritate the airways, causing reflex bronchoconstriction. Noxious gases released from burning materials include carbon monoxide (CO) and hydrogen cyanide (CN).

Smoke may also contain aldehydes from combustion of furniture and cotton, and a variety of chemicals released by burning of rubber and plastics, including the following:

Chlorine gas

Ammonia

Hydrocarbons

Various acids

Ketones

Smokes and obscurants long have been used by the military as a means of hiding troops, equipment, and certain areas from view of the opposing forces and from engagement by weapons with electro-optical control systems. Although smokes typically are not used as direct chemical agents, they may produce toxic injury to skin, eyes, and all parts of the respiratory tract. ^[8] Smokes are also produced inadvertently in industry by explosion, by mechanical generation, or as a by-product of a chemical interaction.

Smokes associated with the military, industry, or both, include the following:

Oxides of nitrogen (NOx)

Zinc oxide (HC)

Red phosphorus (RP)

Sulfur trioxide (FS)

Titanium tetrachloride (FM)

Oil fog (eg, Smoke Generator Fog 2 [SGF2])

Pyrolysis of polytetrafluoroethylene (PTFE; Teflon)

The chemical property of smoke combined with burn injury induces a complex pathophysiologic process that results in hypoxic insult, early airway edema, and bronchoconstriction. ^[9]

Diagnosis of inhalation injury is not always straightforward, owing to poorly sensitive screening tests and, in many cases, the delay in manifestation of clinically significant symptoms until 24-72 hours after injury. In treatment of smoke inhalation, the most immediate concern is reversing cellular asphyxia and carbon monoxide (CO) and CN toxicity (see Treatment).

Although children are less likely than adults to experience significant smoke inhalation, it remains a serious and life-threatening problem in the pediatric population. Management of a child with burns and a coexistent inhalation injury requires a cohesive team of pediatric intensive care physicians, nurses, and burn specialists.

Children with burns have traditionally been cared for in adult burn units, but the increased availability of physicians, nurses, and ancillary staff trained in the care of severely ill pediatric patients makes the pediatric intensive care unit a superior environment. Understanding that children are not merely small adults is critical to preventing therapeutic errors and disastrous iatrogenic complications.

Exposure to metal fumes and fluorocarbons—systemic toxins typically released during industrial fires—is rare in the pediatric population. Children are less likely to be affected by systemic toxins than by toxins from household products and products of smoke, including CO and CN poisoning.

The 3 primary mechanisms that lead to injury in smoke inhalation are thermal damage, asphyxiation, and pulmonary irritation. The combination of these mechanisms can explain the pathophysiologic responses that alter the airway microenvironment with parenchymal damage and predispose smoke inhalation victims to respiratory insufficiency.

Thermal damage is usually limited to the oropharyngeal area, in part due to the poor conductivity of air. In addition, heat dissipation in the upper airways and laryngeal reflexes help protect the lower lung areas from direct thermal injury. Animal experiments have shown that 142°C inhaled air cools to 38°C by the time it reaches the carina. Steam, volatile gases, explosive gases, and the aspiration of hot liquids provide some exceptions, as moist air has a much greater heat-carrying capacity than dry air.

Tissue hypoxia can occur via several mechanisms. Combustion in a closed space can consume significant amounts of oxygen, decreasing the ambient concentration of oxygen to as low as 10-13%. For victims in that setting, the decrease in fraction of inspired oxygen (FIO₂) leads to hypoxia, even if they have adequate circulation and oxygen-carrying capacity. If sufficiently severe, hypoxia can lead to multiorgan dysfunction, which substantially raises morbidity and mortality.

Carbon monoxide

Carbon monoxide (CO) is a colorless, odorless gas produced by the incomplete combustion of carbon-containing compounds, such as wood, coal, and gasoline. It is a major component of the smoke produced in open fires.

CO causes tissue hypoxia by decreasing the oxygen-carrying capacity of the blood. Hemoglobin binds CO with an affinity more than 200 times greater than the affinity for oxygen. Other mechanisms contribute, as well. ^[10] CO causes a left shift in the oxyhemoglobin saturation dissociation curve, which reduces the ability of hemoglobin to unload oxygen.

The heart is particularly affected because CO binds with the heme molecules in myoglobin, decreasing facilitated diffusion of oxygen into muscle. Interaction of CO with myocardial myoglobin results in decreased myocardial contractility.

A classic study demonstrated that dogs breathing 13% CO died within 1 hour after carboxyhemoglobin (CO-Hgb) levels reached 54% to 90%. However, exchange transfusion with blood containing 80% CO-Hgb to otherwise healthy dogs resulted in no toxic effects, despite resultant CO-Hgb levels of 57-64%. This further supports the notion that CO toxicity is not dependent on CO-Hgb formation or, in other words, solely upon a relative anemia. ^[11]

The literature suggests that hypoxic encephalopathy secondary to CO poisoning results from a reperfusion injury in which the products of lipid peroxidation and free radical formation contribute to morbidity and mortality. The therapeutic effect of hyperbaric oxygen therapy in these patients is attributed to improvement in mitochondrial oxidative metabolism, impairment of adherence of neutrophils to cerebral vasculature (decreases inflammation), and preservation of adenosine triphosphate activity.

Cyanide

CN gas can be produced by combustion of the following:

Plastics

Polyurethane

Wool

Silk

Nylon

Nitriles

Rubber

Paper products

The incomplete combustion of nitrogen-containing materials releases hydrogen CN (HCN), a colorless gas with a bitter almond odor that is detectable by 40% of the population. The burning of cotton generates 130 µg HCN/g; of paper, 1100 µg HCN/g; and of wool, 6300 µg HCN/g. ^[12] CN is 20 times more toxic than CO and can cause immediate respiratory arrest.

CN directly stimulates chemoreceptors of carotid and aortic bodies, leading to a brief period of hyperpnea. ^[12] CN is a small lipophilic molecule and a chemical asphyxiant that interferes with cellular metabolism by binding to the ferric ion on cytochrome a₃, subsequently halting cellular respiration. Affected cells convert to anaerobic metabolism, and lactic acidosis ensues.

The organs most sensitive to cellular hypoxia are the central nervous system (CNS) and the heart. The CNS reacts to low concentrations of CN by promoting hyperventilation, thereby increasing exposure.

Consider CN toxicity in all patients with smoke inhalation who have CNS or cardiovascular findings. CN toxicity is difficult to confirm but is frequently concomitant with CO toxicity. Its presence can be inferred by the presence of lactic acidosis in the right clinical setting. Even mild degrees of CN poisoning can cause delayed neurological sequelae in survivors and permanent disability including the following:

Seizures

Various extrapyramidal syndromes

Dystonia

Postanoxic coma

Methemoglobinemia occurs in fire due to heat denaturation of hemoglobin, oxides produced in fire, and methemoglobin-forming materials such as nitrites. Methemoglobinemia is less common in smoke inhalation injury than CN and CO toxicity. The pathophysiologic consequences of methemoglobin formation are a decrease in the oxygen-carrying capacity of the blood and a shift of the oxyhemoglobin dissociation curve to the left, similar to carboxyhemoglobin.

Pulmonary injury from smoke inhalation is characterized by both hyperinflation and atelectasis. Debris from cellular necrosis, inflammatory exudate, and shed epithelium combine with carbonaceous material to narrow airways that are already compromised by edema. Reflex bronchoconstriction further exacerbates the obstruction.

Both inspiratory and expiratory resistance are increased, and the premature closure of small airways occurs, producing hyperinflation and air trapping. Surfactant production and activity are both impaired, leading to alveolar collapse and segmental atelectasis.

Low-pressure pulmonary edema plays an important role in the development of lung injury from smoke inhalation. Damage to the alveolar capillary membrane increases its permeability, and intravascular leakage into the pulmonary interstitium ensues. Eventually, increased lymphatic flow may be overwhelmed, resulting in alveolar edema. Alveoli fill with thick, bloody fluid. Loss of compliance, further atelectasis, and increasing edema can result in severe ventilation-perfusion mismatch and hypoxia.

Pulmonary injury may also occur as a direct result of hypoxia. The decrease in ambient oxygen tension that occurs during fires in closed spaces depends on the substances that are burned. Gasoline self-extinguishes when oxygen concentrations fall below 15%. Other substances may continue to undergo thermal decomposition, further decreasing ambient oxygen tension. Even small decrements in oxygen tension have a potentiating effect on inhaled asphyxiant gases, such as CO and HCN, resulting in severe lactic acidosis and a high fatality rate.

Inhalation of toxic products triggers a cascade of effects in the lower lung areas, such as the following ^[13] :

Activation of the body’s inflammatory response system

Direct tissue injury

Mucus oversecretion

Acute bronchospasm or bronchorrhea

Activation of polymorphonuclear neutrophils (PMNs), resident alveolar macrophages, increased activity of systemic interleukin (IL)–1, IL-6, IL-8, and tumor necrosis factor alpha (TNF-α) and neutrophilic infiltration are suggested to mediate the physiopathologic changes that subsequently lead to atelectasis and impaired mucociliary function. ^[7] In addition, humoral mediators such as prostanoids and leukotrienes produce reactive oxygen species and proteolytic enzymes, which contribute to the development of pulmonary edema and the formation of airway fibrin clots and hypoxemia.

Supporting the importance of the inflammatory response in tissue destruction, some studies have shown that administration of the cyclooxygenase inhibitor ibuprofen reduced the lung lymph flow in animals with smoke inhalation. ^{[14, 15]}

The direct injury is a consequence of the size of the particle, its solubility in water, and its acid-base status. Ammonia produces alkaline injury, while sulfur dioxide and chlorine gas cause acid injuries. Other chemicals act via different mechanisms; for instance, acrolein causes free radical formation and protein denaturation. ^[16]

The solubility of the substance in water determines the location of injury and timing of symptoms. Highly soluble substances such as acrolein, sulfur dioxide, ammonia, and hydrogen chloride cause injury to the upper airway and cause immediate symptoms. Substances with intermediate solubility, such as chlorine and isocyanates, cause both upper and lower respiratory tract injury with more delayed symptoms. Phosgene (a colorless gas with oxidant properties) and oxides of nitrogen have low water solubility and cause diffuse parenchymal injury, with symptoms sometimes delayed up to a day or more.

Days after the injury, the risk of bacterial infection increases markedly. Ciliary function is impaired, leading to accumulation of airway debris. Macrophages within the alveoli are destroyed, allowing bacteria to proliferate. Disruption of the epithelial barrier by ulcerations and necrosis further facilitates the development of pneumonia.

Smokes and obscurants long have been used by the military as a means of hiding troops, equipment, and certain areas from view of the opposing forces and from engagement by weapons with electro-optical control systems. Although smokes typically are not used as direct chemical agents, they may produce toxic injury to skin, eyes, and all parts of the respiratory tract. ^[8] Smokes also are produced in industry by explosion, by mechanical generation, or as a by-product of a chemical interaction.

Smokes associated with the military, industry, or both, include the following:

Oxides of nitrogen (NOx)

Zinc oxide (HC)

Red phosphorus (RP)

Sulfur trioxide (FS)

Titanium tetrachloride (FM)

Oil fog (eg, SGF2)

Teflon particles

Oxides of nitrogen

NOx are components of photochemical smog, usually approximately 0.053 ppm. Nitrogen dioxide exists as a mixture of nitrogen dioxide, a reddish brown gas, and nitrogen tetroxide, a colorless gas. Other forms of nitrogen oxide include nitrous oxide, which is a common anesthetic or (when inhaled without oxygen) asphyxiant, and nitric oxide, which quickly decomposes to nitrogen dioxide in the presence of moisture.

Inhalation of nitric oxide causes the formation of methemoglobin. Inhalation of nitrogen dioxide results in the formation of nitrite, which leads to a fall in blood pressure, production of methemoglobin, and cellular hypoxia. Inhalation of high concentrations causes rapid death without the formation of pulmonary edema.

More severe exposures result in production of yellow frothy fluid in the nasal passages, mouth, and trachea and marked pulmonary edema, which may be fatal. The symptoms following the inhalation of NOx are mostly due to nitrogen dioxide.

Zinc oxide

Zinc oxide is a constituent of HC smoke, also termed “white smoke,” which was developed by the French and US Chemical Warfare Service after World War I. A number of reports have been published on various lung abnormalities occurring in military personnel and firefighters exposed to smoke from HC smoke bombs during training drills.

HC smoke is created by combustion of a mixture of equal amounts of hexachloroethane, zinc oxide, and approximately 7% grained aluminum or aluminum powder. When ignited, these release zinc chloride, and the pyrotechnic mixture of zinc chloride and hexachloroethane rapidly absorbs moisture from the air to form a grayish white smoke.

Other chemicals also are released in the combustion process, such as chlorinated hydrocarbons (eg, phosgene and carbon tetrachloride), chlorine gas, CO, and several other compounds. These most likely contribute to the observed respiratory effects.

HC has a sweetish acrid odor, even at moderate concentrations. HC exposure can produce a gradual decrease in total lung capacity, vital capacity, and diffusion capacity of carbon monoxide (DLCO). It also is associated with the development of pulmonary edema, increased airway resistance, and decreased compliance. These changes were found to be reversible with cessation of episodic exposure. ^[17]

While upper respiratory tract damage can occur from HC, the mean diameter of the primary smoke particles is approximately 0.1 micrometers, allowing them to reach the alveoli. In a retrospective cohort study of 20 patients, Hsu et al reported significant impairment of pulmonary function within 3-21 days following acute exposure. ^[18] Follow up in 1-2 months showed significant improvement with mild-to-moderate exposures, whereas severe exposures led to interstitial fibrosis and continued functional limitation.

In a study by Conner et al performed with guinea pigs, exposure to ultrafine HC particles (0.05 µm) in increasing degrees was associated with a dose-response elevation in protein, neutrophils, and angiotensin-converting enzyme found in lavage fluid. ^[19] A direct relationship also was observed with alkaline phosphatase, acid phosphatase, and lactate dehydrogenase in lavage fluid. Centriacinar inflammation was seen histologically, indicating evidence of pulmonary damage.

An interesting study by Marrs et al involving mice, rats, and guinea pigs demonstrated a positive association of alveologenic carcinoma in a dose-response trend to HC smoke as well as a variety of inflammatory changes. ^[20] These researchers concluded that hexachloroethane and zinc, as well as carbon tetrachloride (which may be present in HC smoke), may be animal carcinogens in certain circumstances. This raises the suspicion of HC as a potential human carcinogen.

Hepatotoxicity has also been described in humans exposed to HC smokes in enclosed spaces during military training. ^[21] The toxic effects appear to be primarily due to the chlorinated compounds produced by combustion: tetrachloromethane, tetrachloroethylene, hexachlorobenzene, and carbon tetrachloride. This last compound is well known for its hepatotoxicity. Acute exposure causes elevated liver enzyme levels by day 1 or 2, with a peak around day 18-21. Liver function test results should normalize by 6 weeks.

Metal fume fever

Metal fume fever (MFF) is a well-documented acute disease induced by intense inhalation of metal oxides. MFF is primarily associated with the inhalation of zinc oxide fumes that are produced when zinc-oxide coated steel (galvanized) or zinc containing alloys (eg, brass) is exposed to high temperatures. Keyes found that 1 in 5 welders has experienced MFF by age 30 years. ^[22]

MFF is a self-limited syndrome characterized by fever, myalgias, headache, and nausea. Symptoms develop 4-12 hours after exposure and typically last several hours; severe cases generally resolve in 1-2 days. Observation is usually all that is necessary.

The exact pathology of MFF is not well understood but likely involves the deposition of fine metal particulates in the alveoli. A study by Kuschner et al on human volunteers showed that pulmonary cytokines such as tumor necrosis factor (TNF), interleukin 6 (IL-6), and interleukin 8 (IL-8) may play important initial roles in mediating metal fume fever. ^[23]

Red phosphorus

After World War II, RP smoke was developed in an attempt to avoid the toxicity associated with the manufacturing of white phosphorus. RP is 95% phosphorus in a 5% butyl rubber base and provides an adequate tank screen on the battlefield.

When RP is oxidized, it forms a mixture of phosphorous acids. When these acids are exposed to water vapor, they in turn form polyphosphoric acids, which may be responsible for the toxic injuries to the upper airways. Most of these injuries are mild irritations. No human deaths have been reported from exposure to either white phosphorus or RP smokes.

Most of the pathologic consequences associated with phosphorus are from elemental white phosphorus fumes or vapor. Contact with elemental phosphorus can cause burns to body surfaces.

A well-described condition termed phossy jaw is associated with longer-term occupational exposures to airborne phosphorus fumes. This disease is a degenerative condition affecting the entire oral cavity including soft tissue, teeth, and bones. Massive necrosis of teeth, bone, and soft tissue can lead to life-threatening infections. Treatment typically consists of soft tissue and bone debridement, abscess drainage, and reconstructive surgery.

White phosphorus and RP smokes may cause respiratory tract irritation after 2-15 minutes of exposure. This probably is caused by the polyphosphoric acids that react with moist mucosal membranes. Respiratory tract irritation has been observed at concentrations of 187 mg phosphorus pentoxide equivalents per cubic meter for 5 minutes or longer. Intense congestion, edema, and hemorrhages were observed in lung tissue following a 1-hour exposure at varying concentrations in studies using rats, mice, and goats.

Sulfur trioxide

The smoke-producing agent FS, also known as sulfuric oxide, chlorosulfonic acid, or sulfuric anhydride, is typically a colorless liquid, which can exist as ice, fiberlike crystals, or gas. When it is exposed to air, it rapidly takes up water and forms white fumes. The smoke consists of 50% sulfur trioxide and 50% chlorosulfonic acid.

FS usually is dispersed by spray atomization. The sulfur trioxide evaporates from spray particles, reacts with surrounding moisture, and forms sulfur acid. The sulfur acid condenses into droplets that produce a dense white cloud. FS is extremely corrosive, which led to its disuse in by the military. However, it has industrial use as an intermediate in the production of sulfuric acid, as well as other chemicals and explosives. ^[24]

Toxicity from FS is that of an acidic irritation to mucosal membranes and even skin. The corrosive effect of acid on mucosa and keratinized skin causes significant irritations and chemical burns.

Titanium tetrachloride

Titanium tetrachloride, known as FM, is a colorless-to–pale yellow liquid that has fumes with a strong odor. Upon contact with water, it rapidly forms hydrochloric acid and titanium compounds. It is used to make titanium metal, white pigment in paints, and other products. It breaks down rapidly in the environment.

FM readily hydrolyzes in the presence of water or moist air via an exothermic reaction that occurs in 2 stages. First, FM reacts to form a highly dispersed particulate smoke. This smoke reacts with more moisture in the air to form hydrolytic products of FM such as hydrochloric acid, titanium oxychlorides, and titanium dioxide. Generation of the smoke has been used as screens in military operations. The formation of hydrochloric acid makes it irritating and corrosive.

When FM liquid is exposed to the air, it produces white fumes. These white fumes can come into contact with skin, resulting in a mild epithelial irritation that usually subsides within 24 hours. When mixed with water, FM produces both heat and hydrochloric acid, which can work synergistically to produce deep thermal burns.

The same pathophysiologic effects that occur with FS smoke occur with FM smoke, since both generate corrosive and irritating acids.

Oil fog

SGF2 is another type of chemical smoke obscurant used in the military. SGF2 is generated by injecting a light petroleum-based lubricating oil onto a heated engine exhaust manifold, causing the oil to vaporize and eventually recondense in the atmosphere. Any industry that generates an oil mist also may produce similar exposures. Petroleum oil smokes are the least toxic smokes. They seldom produce ill effects even after prolonged or multiple exposures.

Concentrations of oil mists in industrial settings range widely (0.8-50 mg/m³), with most at 3 mg/m³. The particle sizes also vary more than 1-5 µm in median diameter. They typically have a high molecular weight and are saturated hydrocarbons derived from distilled petroleum. Exposures to such smoke are likely to last for many hours in a single day or repeatedly over consecutive days.

Animal studies have demonstrated that chronic exposure to oil fog had no effect on pulmonary function endpoints such as total lung capacity, vital capacity, residual volume, D_LCO, compliance, and end-expiratory volume. One exception exists; male rats exposed at 1.5 mg/L had decreased end-expiratory volume. Bronchiolar lavage and histopathology showed changes consistent with a mild inflammatory edema (ie, increased protein content, total cells, PMNs, macrophages).

Teflon particles

Teflon is used widely, for a variety of purposes (eg, as lubricants, insulators, nonstick coatings), in a range of industrial, commercial, and military settings. Closed-space fires in such settings have prompted studies of the toxicity of exposure to the by-products created from incinerated organofluorines. Pyrolysis of Teflon produces a particulate smoke that, if inhaled, produces a constellation of symptoms termed polymer fume fever (PFF).

Pyrolysis of Teflon occurs at approximately 450°C. Among the particles produced by pyrolysis is perfluoroisobutylene (PFIB), which appears to be the main cause of toxicity in PFF. The ultrafine particles initiate a severe inflammatory response at low inhaled particle mass concentrations, which suggests an oxidative injury. PMNs may regulate the inflammatory process with cytokine and antioxidant expression.

PFIB particles have an extremely rapid toxic effect on pulmonary tissues. Evidence of microscopic perivascular edema is observed within 5 minutes. Less intense exposures are followed by a latent period during which normal physiologic compensatory measures to control developing pulmonary edema ensue. Once these mechanisms are overcome, the time frame of which depends on the degree of exposure, the clinical syndrome of PFF follows.

More intense exposures also may produce a chemical conjunctivitis. Hemorrhagic inflammation of the lungs also can occur.

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.

Table. Inhalants ^{[1, 25]} (Open Table in a new window)

Type

Inhalant

Source

Injury/Mechanism

Irritant gases

Ammonia

Fertilizer, refrigerant, manufacturing of dyes, plastics, nylon

Upper airway epithelial damage

Chlorine

Bleaching agent, sewage and water disinfectant, cleansing products

Lower airway epithelial damage

Sulfur dioxide

Combustion of coal, oil, cooking fuel, smelting

Upper airway epithelial damage

Nitrogen dioxide

Combustion of diesel, welding, manufacturing of dyes, lacquers, wall paper

Terminal airway epithelial damage

Asphyxiants (mitochondrial toxins)

Carbon monoxide^a

Combustion of weeds, coal, gas, heaters

Competes for oxygen sites on hemoglobin, myoglobin, heme-containing intracellular proteins

Hydrogen cyanide (CN)^b

Burning of polyurethane, nitrocellulose (silk, nylon, wool)

Tissue asphyxiation by inhibiting intracellular cytochrome oxidase activity, inhibits ATP production, leads to cellular anoxia

Hydrogen sulfide^c

Sewage treatment facility, volcanic gases, coal mines, natural hot springs

Similar to CN, tissue asphyxiant by inhibition of cytochrome oxidase, leads to disruption of electron transport chain, results in anaerobic metabolism

Systemic toxins

Hydrocarbons

Inhalant abuse (toluene, benzene, Freon); aerosols; glue; gasoline; nail polish remover; typewriter correction fluid; ingestion of petroleum solvents, kerosene, liquid polishes

CNS narcosis, anesthetic stats, diffuse GI symptoms, peripheral neuropathy with weakness, coma, sudden death, chemical pneumonitis, CNS abnormalities, GI irritation, cardiomyopathy, renal toxicity

Organophosphates

Insecticides, nerve gases

Blocks acetylcholinesterase; cholinergic crisis with increased acetylcholine

Metal fumes

Metal oxides of zinc, copper, magnesium, jewelry making

Flulike symptoms, fever, myalgia, weakness

^a Major component of smoke.

^b Smells like almonds, component of smoke from fires.

^c Smells like rotten eggs.

Individual cases of CO poisoning can occur under many circumstances (eg, furnace malfunction, motor vehicle exhaust exposure). Multiple cases may occur after large-scale disasters that result in widespread, long-term power outages (eg, 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. ^[26]

At ground level, NOx are produced during electric or arc welding, combustion of fuels, detonation of nitrate-based explosives, combination of nitrogen-containing 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 (eg, tanks, ships)

Handling nitric acid

Resurfacing ice arenas

Using anesthetic gases

Missile fuel oxidizer spills

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.

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.

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.

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.

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 mold lubrication

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. ^[27]

Estimates for fatal residential building fires reported annually to US fire departments are 1,800 incidents, 2,635 deaths, 725 injuries, and $196 million in property loss. The death rate has decreased in the past 3 decades, from 30 deaths per million population to 11 deaths per million population. ^[28] Fire death rates in the United States and Canada are twice as high as in Western Europe and Japan. ^[29] Burns and fires are the third leading cause of nontransport-related accidental death in all age groups in the United States. They comprise the second leading cause of death in the home for all ages and the leading cause of death in the home for children and young adults. ^[29]

In 2011, an estimated 484,500 structure fires—370,000 of them residential—occurred in the United States. Overall, fires resulted in 3,005 nonfirefighter deaths, 17,500 injuries, and $11.7 billion in property loss. ^[30] These figures do not include the estimated 90% of fires not reported to fire departments. More than half of all fatal residential fires started between the hours of 11 pm and 7 am. ^[29]

The incidence of smoke inhalation increases from less than 10% in patients with a mean total body surface area (TBSA) burn size of 5% to more than 80% in patients with a mean TBSA burn size of 85% or more. Smoke inhalation is present in one third of patients treated at burn centers. The magnitude of smoke inhalation is devastating, as the presence of an inhalation injury has a greater effect on mortality than either patient age or surface area burned.

One study in New Jersey reports on the demographics of fire fatalities and notes that victims who perished did not parallel the ethnic census of the time. ^{[5, 29]} Whites accounted for 53% of fatalities and comprised 49% on the census. African Americans accounted for 38% of fatalities and 13% of the census.

The male-to-female ratio in fire fatalities is about 3:2.

The New Jersey study also showed that children and the elderly represented a disproportionate percentage of people injured by fire. ^[29] People younger than 11 years or older than 70 years constituted 22% of the population but accounted for 40% of all fire fatalities. These statistics closely match national figures.

Small children are especially vulnerable because they are less likely to escape a confined space and they also have a higher minute ventilation, which increases exposure to smoke and other toxins released during pyrolysis. In addition, their relatively smaller airways are more severely affected by airway edema and obstructing material.

Burns in children are 2.5 times more likely to occur by scalding rather than flame exposure. Hence, the percentage of children who experience respiratory symptoms after burns is less than that of adults, who are more often exposed to smoke-producing flames. About 50% of all burn deaths are related to inhalation injuries. Early hypoxemia is a contributor to over 50% of smoke inhalation deaths, with CO intoxication accounting for as much as 80% of the fatalities.

A comprehensive study in Dallas, Texas looked at all house fires from 1991-1997. ^[31] Many of the findings parallel those of the New Jersey study. Relative risk of injury was 1.8 for men, 1.4 for boys, 2.8 for blacks, and 2.6 for elderly persons. In addition, among the injured, the proportion of injuries that were fatal was higher in persons older than 65 years (53%) and in those younger than 10 years (67%) compared with those aged 10-64 years (30%).

The lowest income tracts had the highest rate of injury. The rate of injury in households with a median income below $20,000 per year was 8 times that of tracts with a median income greater than $80,000 per year. In fact, tracts with extremely low incomes, less than $10,000 per year, had rates of injury 20 times that of the above.

Houses built in the 1950s and 1960s were somewhat more likely to burn than houses built before this time. This may be a case of “selection of the fittest” houses, with those houses most prone to burn having already done so, leaving the most structurally sound ones still standing.

Fires caused by arson occurred predominately in census tracts with lower median incomes. Eighty percent of fires occurred in homes with median incomes of less than $40,000 per year.

Causes of the house fires were as follows:

Arson (25.5%)

Electrical wiring/equipment (16.6%)

Heating equipment (15.8%)

Cooking (11.4%)

Smoking (5.5%)

Children playing with fire (4.5%)

Unknown/other (20.6%)

The rate of fire-related injury in houses in Dallas without a functioning smoke detector was 8.7 times that of homes with functioning smoke detectors. Houses that are most likely to have fires were least likely to have functioning smoke detectors. As a result of this study, a program in Dallas now provides and installs smoke detectors in census tracts with the highest rates of injuries and deaths related to house fires. ^[31]

Most inhalation injuries are self-limited and resolve within 48-72 hours. The severity of direct pulmonary parenchymal injury depends on the extent of exposure and the type of inhaled toxins produced during combustion. Most patients do not manifest spirometry changes. Rare long-term sequelae include tracheal stenosis, bronchiectasis, interstitial fibrosis, and bronchiolitis obliterans.

The prognosis for mild-to-moderate exposures of toxic smokes is generally very good, with the usual outcome return to full recovery without sequelae. Metal fume fever is self-limited and usually resolves after a short period of observation. Exposure to white smoke (HC) in a military setting can lead to acute lung injury and in severe cases to ARDS. With more severe exposures, lungs may become severely damaged and develop chronic pulmonary fibrosis.

Children with acute pulmonary injury from toxic inhalations generally do well once supported through the initial period of inflammation and damage. Most of the pulmonary damage is self-limited and resolves within 2-3 days. The degree of recovery depends on the extent of the pulmonary parenchymal injury and subsequent hypoxic damage to the organs.

Complications may include the following:

Subglottic stenosis

Bronchiectasis

Pulmonary edema (4-9%)

Pneumonia (3-23%)

Atelectasis (1-5%)

Bacterial pneumonia often complicates inhalation injury within 4-5 days of presentation. This additional cellular damage can cause significant mortality days to weeks after the initial injury.

Exacerbation of pre-existing respiratory disease (eg, asthma, chronic obstructive pulmonary disease) is a potential sequela. ^[32] A study of firefighters showed certain subgroups to have an exaggerated decline in postexposure forced expiratory volume in 1 second (FEV₁) that was not predicted by age, smoking history, intensity of exposure, or the use of self-contained breathing apparatus. ^[33] Some of these patients, who had no family history of reactive airway disease, went on to need long-term beta-agonist therapy. Exposures to some smokes, such as isocyanates, can cause asthma in people with no history of the disease.

Airway hyperreactivity generally improves over several months following inhalation injury. However, some authors documented long-term respiratory symptoms such as cough, wheeze, and shortness of breath even after mild inhalation injury. The long-term effects of inhaled toxins on pulmonary function are not yet determined.

Concurrent CO poisoning and inhalation of other products of combustion can cause hypoxemia, end-organ injury, and morbidity. CO intoxication is a particularly serious consequence of smoke inhalation and may account for as much as 80% of fatalities from inhalation injury.

Most patients who arrive alive to the emergency department make a full recovery. However, up to one third of patients with significant CO exposure develop a secondary syndrome of long-term neurologic or neuropsychiatric dysfunction within 1-3 weeks after exposure. Higher cortical functions seem most severely affected. Whether the use of hyperbaric oxygen (HBO) therapy alters the outcome of delayed-onset neurologic dysfunction from CO poisoning remains controversial.

Severe pulmonary injury, edema, and the inability to oxygenate or ventilate can result in death. A study of the characteristics of survivors and casualties of fire fatalities found that the following specific risk factors seem to elevate the rate of mortality ^[34] :

Age: Elderly persons (>64 y) and young children (< 10 y) are the most likely to die as a result of a fire

Persons having a physical or cognitive disability have a higher mortality rate than matched controls, as do persons under the influence of alcohol or other drugs; for these vulnerable populations, if a nonvulnerable potential rescuer was present, the fatality rate dropped from 49% to 39%

The absence of a functioning smoke detector increases the risk of death in a fire by about 60%

The combination of cutaneous burn and smoke inhalation results in far higher mortality rates than occur with either injury in isolation. In patients with a burn and no associated smoke inhalation or respiratory failure, the mortality rate is less than 2%. In patients with smoke inhalation alone and no burn or respiratory failure, the mortality rate is 7%. For patients with both a burn and smoke inhalation, the mortality rate increases to 29%, suggesting that the burn wounds themselves put an additional stress on the compromised lung. ^[35]

In a study by Chou et al of 150 children with CO poisoning who were referred for hyperbaric oxygen therapy, none of the children with CO poisoning alone died, compared with 22.6% of those with the combination of CO poisoning and smoke inhalation. Among children who died, 60% had the following combination of risk factors ^[36] :

Smoke inhalation

Low body temperature on arrival in the emergency department

High initial carboxyhemoglobin level

Respiratory and cardiac arrest in the field

Clinicians should encourage the use of smoke and CO detectors in the home, which can decrease the risk of injury by permitting early escape. Regular checks to ensure that the detectors are functioning should be part of the household routine. In one study, the presence of a functioning smoke detector lowered the risk of death in a residential fire by over 60%. ^[31]

Programs aimed at educating young children about the dangers of playing with lighters and matches and programs teaching families how to safely escape from burning buildings should be used to further limit the number of children experiencing inhalation and burn injury. Anticipatory guidance during well child visits should include fire safety instructions.

For patient education resources, see the Lung and Airway Center, First Aid and Injuries Center, Procedures Center, and Poisoning Center, as well as Smoke Inhalation and Carbon Monoxide Poisoning.

Rorison DG, McPherson SJ. Acute toxic inhalations. Emerg Med Clin North Am. 1992 May. 10(2):409-35. [Medline].

Dries DJ, Endorf FW. Inhalation injury: epidemiology, pathology, treatment strategies. Scand J Trauma Resusc Emerg Med. 2013 Apr 19. 21:31. [Medline]. [Full Text].

de Lange DW, Meulenbelt J. Do corticosteroids have a role in preventing or reducing acute toxic lung injury caused by inhalation of chemical agents?. Clin Toxicol (Phila). 2011 Feb. 49(2):61-71. [Medline].

Bizovi KE, Leikin JD. Smoke inhalation among firefighters. Occup Med. 1995 Oct-Dec. 10(4):721-33. [Medline].

Hall AH, Dart R, Bogdan G. Sodium thiosulfate or hydroxocobalamin for the empiric treatment of cyanide poisoning?. Ann Emerg Med. 2007 Jun. 49(6):806-13. [Medline].

Buyantseva LV, Tulchinsky M, Kapalka GM, et al. Evolution of lower respiratory symptoms in New York police officers after 9/11: a prospective longitudinal study. J Occup Environ Med. 2007 Mar. 49(3):310-7. [Medline].

Thai A, Xiao J, Ammit AJ, Rohanizadeh R. Development of inhalable formulations of anti-inflammatory drugs to potentially treat smoke inhalation injury in burn victims. Int J Pharm. 2010 Apr 15. 389(1-2):41-52. [Medline].

Urbanetti JS. Toxic inhalational injury. Medical Aspects of Chemical and Biological Warfare. 1997. 260-267. [Full Text].

Belli S, Basaran O, Ozdemir BH, et al. Protective role of simvastatin on lung damage caused by burn and cotton smoke inhalation in rats. J Surg Res. 2011 May 15. 167(2):e283-90. [Medline].

Kao LW, Nanagas KA. Toxicity associated with carbon monoxide. Clin Lab Med. 2006 Mar. 26(1):99-125. [Medline].

Goldbaum LR, Ramirez RG, Absalon KB. What is the mechanism of carbon monoxide toxicity?. Aviat Space Environ Med. 1975 Oct. 46(10):1289-91. [Medline].

Lawson-Smith P, Jansen EC, Hyldegaard O. Cyanide intoxication as part of smoke inhalation–a review on diagnosis and treatment from the emergency perspective. Scand J Trauma Resusc Emerg Med. 2011 Mar 3. 19:14. [Medline]. [Full Text].

Choi WI, Syrkina O, Kwon KY, Quinn DA, Hales CA. JNK activation is responsible for mucus overproduction in smoke inhalation injury. Respir Res. 2010 Dec 7. 11:172. [Medline]. [Full Text].

Stewart RJ, Yamaguchi KT, Knost PM, Mason SW, Roshdieh BB, Samadani S. Effects of ibuprofen on pulmonary oedema in an animal smoke inhalation model. Burns. 1990 Dec. 16(6):409-13. [Medline].

Kimura R, Traber L, Herndon D, Niehaus G, Flynn J, Traber DL. Ibuprofen reduces the lung lymph flow changes associated with inhalation injury. Circ Shock. 1988 Mar. 24(3):183-91. [Medline].

Hill IR. Particulate matter of smoke inhalation. Ann Acad Med Singapore. 1993 Jan. 22(1):119-23. [Medline].

Chian CF, Wu CP, Chen CW, et al. Acute respiratory distress syndrome after zinc chloride inhalation: survival after extracorporeal life support and corticosteroid treatment. Am J Crit Care. 2010 Jan. 19(1):86-90. [Medline].

Hsu HH, Tzao C, Chang WC, Wu CP, Tung HJ, Chen CY, et al. Zinc chloride (smoke bomb) inhalation lung injury: clinical presentations, high-resolution CT findings, and pulmonary function test results. Chest. 2005 Jun. 127(6):2064-71. [Medline].

Conner MW, Flood WH, Rogers AE, Amdur MO. Lung injury in guinea pigs caused by multiple exposures to ultrafine zinc oxide: changes in pulmonary lavage fluid. J Toxicol Environ Health. 1988. 25(1):57-69. [Medline].

Marrs TC, Colgrave HF, Edginton JA, Brown RF, Cross NL. The repeated dose toxicity of a zinc oxide/hexachloroethane smoke. Arch Toxicol. 1988. 62(2-3):123-32. [Medline].

Loh CH, Chang YW, Liou SH, Chang JH, Chen HI. Case report: hexachloroethane smoke inhalation: a rare cause of severe hepatic injuries. Environ Health Perspect. 2006 May. 114(5):763-5. [Medline]. [Full Text].

Keyes DC. Metal fume fever. Dart RC. Medical Toxicology. 3rd ed. Philadelphia, Pa: Lippincott, Williams & Wilkins; 2004. 88-89.

Kuschner WG, D’Alessandro A, Wong H, Blanc PD. Early pulmonary cytokine responses to zinc oxide fume inhalation. Environ Res. 1997 Oct. 75(1):7-11. [Medline].

Agency for Toxic Substances & Disease Registry. Sulfur Trioxide & Sulfuric Acid. Toxic Substances Portal. Available at http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=256&tid=47. Accessed: May 9, 2013.

Weiss SM, Lakshminarayan S. Acute inhalation injury. Clin Chest Med. 1994 Mar. 15(1):103-16. [Medline].

Harduar-Morano L, Watkins S. Review of unintentional non-fire-related carbon monoxide poisoning morbidity and mortality in Florida, 1999-2007. Public Health Rep. 2011 Mar-Apr. 126(2):240-50. [Medline]. [Full Text].

Duclos P, Sanderson LM, Lipsett M. The 1987 forest fire disaster in California: assessment of emergency room visits. Arch Environ Health. 1990 Jan-Feb. 45(1):53-8. [Medline].

US Fire Administration’s (USFA’s) National Fire Incident Reporting System (NFIRS). Fatal Fires in Residential Buildings. US Department of Homeland Security, US Fire Administration. August 2010. Available at http://www.usfa.fema.gov/downloads/pdf/statistics/v11i2.pdf.

Barillo DJ, Goode R. Fire fatality study: demographics of fire victims. Burns. 1996 Mar. 22(2):85-8. [Medline].

Karter MJ Jr. Fire Loss in the United States during 2011. National Fire Protection Association, September 2012. Pediatrics. Available at http://www.nfpa.org/assets/files/pdf/os.fireloss.pdf. Accessed: May 14, 2013.

Istre GR, McCoy MA, Osborn L, Barnard JJ, Bolton A. Deaths and injuries from house fires. N Engl J Med. 2001 Jun 21. 344(25):1911-6. [Medline].

Large AA, Owens GR, Hoffman LA. The short-term effects of smoke exposure on the pulmonary function of firefighters. Chest. 1990 Apr. 97(4):806-9. [Medline].

Hoyert DL, Xu. Deaths: Preliminary Data for 2011. National Vital Statistics Reports. Available at http://www.cdc.gov/nchs/data/nvsr/nvsr61/nvsr61_06.pdf. Accessed: May 14, 2013.

Marshall SW, Runyan CW, Bangdiwala SI, Linzer MA, Sacks JJ, Butts JD. Fatal residential fires: who dies and who survives?. JAMA. 1998 May 27. 279(20):1633-7. [Medline].

Muller MJ, Pegg SP, Rule MR. Determinants of death following burn injury. Br J Surg. 2001 Apr. 88(4):583-7. [Medline].

Chou KJ, Fisher JL, Silver EJ. Characteristics and outcome of children with carbon monoxide poisoning with and without smoke exposure referred for hyperbaric oxygen therapy. Pediatr Emerg Care. 2000 Jun. 16(3):151-5. [Medline].

Whitelock-Jones L, Bass DH, Millar AJ, Rode H. Inhalation burns in children. Pediatr Surg Int. 1999. 15(1):50-5. [Medline].

Roney N, Smith CV, Williams M. Toxicological Profile for Zinc (Update). US Dept of Health & Human Services. 2007. Available at http://www.atsdr.cdc.gov/toxprofiles/tp60.html#bookmark07.

Baud FJ, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med. 1991 Dec 19. 325(25):1761-6. [Medline].

Lahn M, Sing W, Nazario S, Fosberg D, Bijur P, Gallagher EJ. Increased blood lead levels in severe smoke inhalation. Am J Emerg Med. 2003 Oct. 21(6):458-60. [Medline].

Chou CH, Kao TW, Liou SH, Chen HI, Ku HY, Chuang HJ, et al. Hematological abnormalities of acute exposure to hexachloroethane smoke inhalation. Inhal Toxicol. 2010 May. 22(6):486-92. [Medline].

Koljonen V, Maisniemi K, Virtanen K, Koivikko M. Multi-detector computed tomography demonstrates smoke inhalation injury at early stage. Emerg Radiol. 2007 Jun. 14(2):113-6. [Medline].

Agee RN, Long JM 3rd, Hunt JL, Petroff PA, Lull RJ, Mason AD Jr, et al. Use of 133xenon in early diagnosis of inhalation injury. J Trauma. 1976 Mar. 16(3):218-24. [Medline].

Carr JA, Phillips BD, Bowling WM. The utility of bronchoscopy after inhalation injury complicated by pneumonia in burn patients: results from the National Burn Repository. J Burn Care Res. 2009 Nov-Dec. 30(6):967-74. [Medline].

Huang KL, Chen CW, Chu SJ, Perng WC, Wu CP. Systemic inflammation caused by white smoke inhalation in a combat exercise. Chest. 2008 Mar. 133(3):722-8. [Medline]. [Full Text].

Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002 Oct 3. 347(14):1057-67. [Medline].

Wolf SJ, Lavonas EJ, Sloan EP, Jagoda AS. Clinical policy: Critical issues in the management of adult patients presenting to the emergency department with acute carbon monoxide poisoning. Ann Emerg Med. 2008 Feb. 51(2):138-52. [Medline].

Kung SW, Chan YC, Lau FL. Hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med. 2008 Jan. 51(1):108; author reply 108-9. [Medline].

Borron SW, Baud FJ, Barriot P, Imbert M, Bismuth C. Prospective study of hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med. 2007 Jun. 49(6):794-801, 801.e1-2. [Medline].

Huzar TF, George T, Cross JM. Carbon monoxide and cyanide toxicity: etiology, pathophysiology and treatment in inhalation injury. Expert Rev Respir Med. 2013 Apr. 7(2):159-70. [Medline].

Oremus M, Hanson MD, Whitlock R, Young E, Archer C, Dal Cin A, et al. A systematic review of heparin to treat burn injury. J Burn Care Res. 2007 Nov-Dec. 28(6):794-804. [Medline].

Desai MH, Mlcak R, Richardson J, Nichols R, Herndon DN. Reduction in mortality in pediatric patients with inhalation injury with aerosolized heparin/N-acetylcystine [correction of acetylcystine] therapy. J Burn Care Rehabil. 1998 May-Jun. 19(3):210-2. [Medline].

Huang PS, Tang GJ, Chen CH, Kou YR. Whole-body moderate hypothermia confers protection from wood smoke-induced acute lung injury in rats: the therapeutic window. Crit Care Med. 2006 Apr. 34(4):1160-7. [Medline].

Cancio LC. Airway management and smoke inhalation injury in the burn patient. Clin Plast Surg. 2009 Oct. 36(4):555-67. [Medline].

Nieman GF, Cigada M, Paskanik AM, et al. Comparison of high-frequency jet to conventional mechanical ventilation in the treatment of severe smoke inhalation injury. Burns. 1994 Apr. 20(2):157-62. [Medline].

Hall JJ, Hunt JL, Arnoldo BD, Purdue GF. Use of high-frequency percussive ventilation in inhalation injuries. J Burn Care Res. 2007 May-Jun. 28(3):396-400. [Medline].

Jones WG, Madden M, Finkelstein J, Yurt RW, Goodwin CW. Tracheostomies in burn patients. Ann Surg. 1989 Apr. 209(4):471-4. [Medline]. [Full Text].

DiGuiseppi C, Roberts I, Wade A, Sculpher M, Edwards P, Godward C, et al. Incidence of fires and related injuries after giving out free smoke alarms: cluster randomised controlled trial. BMJ. 2002 Nov 2. 325(7371):995. [Medline]. [Full Text].

Type

Inhalant

Source

Injury/Mechanism

Irritant gases

Ammonia

Fertilizer, refrigerant, manufacturing of dyes, plastics, nylon

Upper airway epithelial damage

Chlorine

Bleaching agent, sewage and water disinfectant, cleansing products

Lower airway epithelial damage

Sulfur dioxide

Combustion of coal, oil, cooking fuel, smelting

Upper airway epithelial damage

Nitrogen dioxide

Combustion of diesel, welding, manufacturing of dyes, lacquers, wall paper

Terminal airway epithelial damage

Asphyxiants (mitochondrial toxins)

Carbon monoxide^a

Combustion of weeds, coal, gas, heaters

Competes for oxygen sites on hemoglobin, myoglobin, heme-containing intracellular proteins

Hydrogen cyanide (CN)^b

Burning of polyurethane, nitrocellulose (silk, nylon, wool)

Tissue asphyxiation by inhibiting intracellular cytochrome oxidase activity, inhibits ATP production, leads to cellular anoxia

Hydrogen sulfide^c

Sewage treatment facility, volcanic gases, coal mines, natural hot springs

Similar to CN, tissue asphyxiant by inhibition of cytochrome oxidase, leads to disruption of electron transport chain, results in anaerobic metabolism

Systemic toxins

Hydrocarbons

Inhalant abuse (toluene, benzene, Freon); aerosols; glue; gasoline; nail polish remover; typewriter correction fluid; ingestion of petroleum solvents, kerosene, liquid polishes

CNS narcosis, anesthetic stats, diffuse GI symptoms, peripheral neuropathy with weakness, coma, sudden death, chemical pneumonitis, CNS abnormalities, GI irritation, cardiomyopathy, renal toxicity

Organophosphates

Insecticides, nerve gases

Blocks acetylcholinesterase; cholinergic crisis with increased acetylcholine

Metal fumes

Metal oxides of zinc, copper, magnesium, jewelry making

Flulike symptoms, fever, myalgia, weakness

^a Major component of smoke.

^b Smells like almonds, component of smoke from fires.

^c Smells like rotten eggs.

Keith A Lafferty, MD Adjunct Assistant Professor of Emergency Medicine, Temple University School of Medicine; Medical Student Director, Department of Emergency Medicine, Gulf Coast Medical Center

Keith A Lafferty, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Keisha Bonhomme, MD Resident Physician, Department of Internal Medicine, St Vincent’s Medical Center

Disclosure: Nothing to disclose.

Claudia V Martinez, MD Resident Physician, Department of Emergency Medicine, State University of New York Downstate College of Medicine

Claudia V Martinez, MD is a member of the following medical societies: American Academy of Emergency Medicine, Emergency Medicine Residents’ Association

Disclosure: Nothing to disclose.

Sage W Wiener, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Denise Serebrisky, MD Associate Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director, Division of Pulmonary Medicine, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center/North Central Bronx Hospital; Director, Jacobi Asthma and Allergy Center for Children, Jacobi Medical Center

Denise Serebrisky, MD is a member of the following medical societies: American Thoracic Society

Disclosure: Nothing to disclose.

Rachel Dillinger Lewis Katz School of Medicine at Temple University

Disclosure: Nothing to disclose.

Joe Alcock, MD, MS Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Joe Alcock, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Michael R Bye, MD Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children’s Hospital of New York Presbyterian, Columbia University Medical Center

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Charles Callahan, DO Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center

Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic Society, Association of Military Surgeons of the US, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center

Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Robert G Darling, MD, FACEP Adjunct Clinical Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Associate Director, Center for Disaster and Humanitarian Assistance Medicine

Robert G Darling, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Telemedicine Association, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Harry J Goett, MD Assistant Professor of Emergency Medicine, Department of Emergency Medicine, Temple University Hospital

Harry J Goett, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Mark Keim, MD Senior Science Advisor, Office of the Director, National Center for Environmental Health, Centers for Disease Control and Prevention

Mark Keim, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Emily B Nazarian, MD Assistant Professor of Pediatrics, Fellowship Director, Pediatric Critical Care, Golisano Children’s Hospital at Strong

Emily B Nazarian, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Girish D Sharma, MD Professor of Pediatrics, Rush Medical College; Senior Attending, Department of Pediatrics, Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush University Medical Center

Girish D Sharma, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

James Steven Walker, DO, MS Clinical Professor of Surgery, Department of Surgery, University of Oklahoma College of Medicine

James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Smoke Inhalation Injury

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