Toxic Inhalational Lung Injury

What every physician needs to know:

Given the continuous exposure of the upper and lower airways and lung parenchyma to the environment, the possibility that we may inhale any of a broad array of toxic substances is not surprising. Whether exposure to any of these materials translates into a clinically significant disorder depends on a variety of physiologic and pathologic responses. While the number of potentially toxic, respirable substances is almost limitless, the pulmonary and systemic effects of a variety of agents have been well characterized, and they constitute the basis for this discussion of toxic inhalational lung injury.

Several factors are important in determining the location and magnitude of toxic lung injury that arises from inhalation of smoke, aerosols, vapors, or fumes, including the size and water solubility of the inhaled material.

The size of the inhaled particle (Figure 1) is a critical determinant of pathogenesis in inhaled toxin exposure. Larger particles deposit in the nasopharynx through impaction and have limited penetration to the lower respiratory tract and alveoli. Smaller particles penetrate more easily to the level of the bronchioles and alveoli, producing respiratory toxicity at those sites. Particles larger than about 80 µ are usually not inspirable through the nose, and those larger than 5 µ do not usually penetrate to the level of the alveoli. Very small particles–such as those smaller than 0.1 µ in diameter, penetrate deeply into the distal airways and lung parenchyma.

Figure 1

The water solubility of the inhaled material (Figure 2) is another important determinant of the effect of inhaled toxins. Materials with high water solubility, such as hydrochloric acid, ammonia, and sulfur dioxide, are readily deposited in the moist mucosal surfaces of the conjunctivae, nose, and oropharynx. Once dissolved in the water phase of the mucous membrane lining, these agents form acidic and alkaline moieties, leading to noxious symptoms that tend to prompt exposed individuals to flee from the toxic environment.

Figure 2

The same compounds may also stimulate specific irritant receptors of the upper airways, resulting in reflex bronchoconstriction, which limits further exposure. However, agents with low water solubility, such as phosgene, fail to elicit an immediate noxious reaction so continued exposure to the toxin is possible. Agents with intermediate water solubility, such as chlorine gas, may affect the respiratory tract diffusely and at multiple levels.

Other factors that influence the effect of toxic inhalations include the atmospheric concentration of the inhalant, the duration of exposure, the environment’s level of ventilation, and various attributes of the individual who inhales the toxin, including their use of respiratory protective devices, level of minute ventilation, age, comorbidities, smoking status, and genetic susceptibility.

Several important determinants shape the clinical presentation of toxic inhalation injury, including where the toxin is deposited in the respiratory system. Inhaled toxins with high water solubility tend to localize to the upper airways, including the nose, pharynx, larynx, and trachea. These agents may produce direct tissue injury in the upper airway, with the magnitude of the injury dependent upon the dosage and duration of exposure.

Clinical findings include eye irritation, discomfort in the nasal passages and pharynx, cough, and upper respiratory secretions. Nonspecific symptoms of headache and lightheadedness are also seen. The upper airways may be compromised by the formation of airway edema, increased airway secretions, and denuded epithelium. An inflamed, denuded upper airway epithelium not only compromises the integrity of the upper airway but also predisposes the patient to reduced tracheal clearance mechanisms and secondary infection.

Induction of laryngospasm by inhaled irritants further potentiates airway compromise.

Inhaled toxins that affect the conducting airways also induce airway edema, inflammation, and airway obstruction, in part because of bronchoconstriction. Persistent bronchial hyper-responsiveness may be noted several days following the initial exposure. Clinical findings include dyspnea, wheezing, obstructive findings on spirometry, and hypoxemia due to ventilation-perfusion mismatch.

Reactive airways dysfunction syndrome (RADS) is defined as a persistent asthma-like disorder precipitated by a single acute exposure to an inhaled irritant.

RADS is characterized by the absence of a latent period for sensitization that is typical of occupational asthma. RADS may persist for months or years following exposure, and pathogenesis likely includes airway epithelial injury, airway inflammation, and subsequent structural changes in the airways (airway fibrosis). Symptoms include the acute onset of asthma within 24 hours of exposure; spirometry shows airway obstruction, which is usually at least partially bronchodilator-responsive. While the disorder typically resolves (within weeks to months), it may be permanent. Animal data suggest that systemic corticosteroids may be beneficial; however, this has yet to be validated in human studies.

Agents with low water solubility, such as nitrogen dioxide or phosgene, can penetrate into the lower respiratory tract and pulmonary parenchyma, causing pulmonary edema following a latent period of several hours. Failure to observe patients exposed to these agents closely for at least 24 may result in significant morbidity and mortality as a result of the subsequent development of pulmonary edema and hypoxemia.

Agents that penetrate into the distal airways and lung parenchyma are also characterized by the onset of persistent, chronic injury, including bronchiolitis obliterans (BO) and bronchiolitis obliterans organizing pneumonia (BOOP). BO is characterized by narrowing and obstruction of distal airways, with shortness of breath and obstructive spirometry developing several weeks after exposure. Hyperinflation may be noted on CXR, and airway pathology reveals granulation tissue, small airway lumens, and bronchiolar obliteration. The onset of BOOP may also be delayed by several weeks following acute exposure. Cough, dyspnea, fever, and malaise are noted, and the CXR or CT scan typically shows diffuse, patchy, ground-glass opacifications. The pulmonary function test pattern is restrictive. BOOP usually, but not invariably, responds well to systemic corticosteroids.

Classification:

A vast number of potential respiratory toxins exist in the environment. Several have been well characterized and described extensively in the literature. Representative examples of agents associated with acute toxic inhalation injury are described here.

Ammonia

Environmental Sources of Exposure

Ammonia is a water-soluble compound that is prevalent in a variety of industrial settings, in fertilizers, in a variety of polymers and explosives, and as a coolant in refrigeration. It is also commonly used as a household cleaner. Its pungent odor is readily recognized.

Mechanism of Tissue Injury

Because of its high water solubility, ammonia dissolves readily in the mucosa of the proximal airways, forming ammonium hydroxide, which is caustic to respiratory tissues. Intracellular water is liberated as tissue is damaged, potentiating further dissolution of inhaled ammonia gas. The ammonium hydroxide induces alkaline burns, enhanced by the exothermic reaction associated with the compound’s formation. The edema, mucosal hemorrhage, and denudation of airway tissue may produce upper airway obstruction and result in death.

Spectrum of Respiratory Disorders Associated with Toxic Exposure

The broad range of respiratory disorders associated with ammonia exposure includes tracheobronchitis, bronchiolitis, bronchopneumonia, pulmonary edema, RADS, and obstructive airways disease. Isolated cases of interstitial lung disease and bronchiectasis have also been reported.

Fatal cases following significant exposure are associated with laryngeal edema, airway obstruction, noncardiogenic pulmonary edema/ARDS, and secondary infection in the setting of diffuse airway and pulmonary parenchymal damage. The initial acute pneumonia may resolve over several days, only to be followed by the gradual onset of airways obstruction.

Cadmium

Environmental Sources of Exposure

Cadmium is a metal found in multiple industrial applications, including production of nickel-cadmium batteries. It is used extensively in the paint industry and in the production of plastics and rubber. Workplace exposure is usually related to soldering or smelting.

Mechanism of Tissue Injury

The pathogenesis of acute respiratory injury due to cadmium inhalation has not been well elucidated. Pathologic findings following fatal inhalation include diffuse tracheobronchitis characterized by consolidation, alveolar hemorrhage, and extensive epithelial damage throughout the airways.

Spectrum of Respiratory Disorders Associated with Toxic Exposure

Patients with cadmium exposure may be asymptomatic for several hours following exposure. Subsequently, fever, body aches, and malaise develop, similar to the findings in metal fume fever (described below). Cough and dyspnea follow. In fatal cases, progression of pulmonary infiltrates to ARDS has been described.

Chlorine

Environmental Sources of Exposure

Chlorine gas is a yellow-green substance that has intermediate water solubility. Its toxicity was first described with use as an agent of warfare in World War I. More recently, exposures have been reported in the industrial setting. A recent validation study evaluating triage systems in chlorine spills determined that oxygen saturation measured by pulse oximetry is an early indicator of injury severity and eventual outcomes in toxic inhalation with chlorine.

Approximately 15 million tons of the gas are produced each year in the US. Chlorine is used to bleach wood pulp derivatives and to disinfect water supplies. Chlorine toxicity has been reported in households, primarily related to the formation of chloramines derived from household bleach when it is mixed with ammonia or other products that contain hydrochloric or phosphoric acid. Chlorine gas exposure has also been described around swimming pools as a result of the use of calcium hypochlorite and other related agents used in water purification. Because chlorine exposure may result in delayed irritation of the upper airway mucosal surfaces, exposure to the gas may be more prolonged than with other more noxious agents.

Mechanism of Tissue Injury

Chlorine gas reacts with water to form hydrochloric and hypochlorous acids. These agents are highly water-soluble and are capable of producing significant tissue damage in the upper airways. Reactive oxygen and nitrogen species may also be generated. Most toxicity associated with chlorine exposure is localized to the upper airways. Fatal exposures may occur over a broad range of concentrations, from 50-2000 ppm.

Spectrum of Respiratory Disorders Associated with Toxic Exposure

The findings are those of conjunctivitis, rhinitis, and tracheobronchitis. Pathologic findings include diffuse tracheobronchitis, desquamation of airway epithelium, and pulmonary edema. Long-term sequelae may include both restrictive and obstructive pulmonary disorders, most of which resolve within two years of initial exposure.

RADS has been reported. Residual effects appear to be related to the intensity of exposure, the victim’s minute ventilation during exposure, and their prior baseline respiratory status, smoking history, and allergic background. Development of RADS appears more likely in those who are current or former smokers or who have an atopic history.

Mercury

Environmental Sources of Exposure

Mercury has been used extensively in a variety of industries, including ore smelting, cement production, extraction of gold from mercury amalgams in mining, fur and felt hat-making, and dentistry. Isolated reports of intense industrial exposure to mercury vapor have been reported in Japanese zinc refinery workers.

Mechanism of Tissue Injury

Mercury vapor is thought to disrupt sulfhydryl-based enzyme systems. Coagulation of protein and disruption of cellular metabolic activity occur. Pathologic findings include diffuse capillary damage, pulmonary edema, and widespread injury to airway epithelium. Exposure to more than 1-2 mg per mm³ of elemental mercury vapor for several hours produces diffuse bronchiolitis and pneumonitis. Several hours following exposure, acute diffuse alveolar damage and hyaline membrane formation may be noted. Systemic absorption produces kidney and liver damage, as well as central nervous system disease.

Spectrum of Respiratory Disorders Associated with Toxic Exposure

Upon exposure to mercury vapor, little in the way of upper airway irritation is likely to be noted at first. Victims may be unaware of their exposure and continue to work in the contaminated environment. However, over 24-48 hours, widespread pulmonary infiltrates and ARDS may occur. While most respiratory findings resolve within a few days, there have been reports of progression to pulmonary fibrosis.

Nitrogen Dioxide

Environmental Sources of Exposure

Nitrogen oxides are prevalent in air pollution, primarily from automobile engine exhaust, burning coal, and other organic products, but also cigarette smoke. Acute, high-intensity exposure may be seen in mining, welding, and in the manufacture of explosives. A classic form of toxic exposure is known as “silo fillers’ disease,” an occupational risk for farmers who are exposed to high concentrations of nitrogen dioxide gas that develops in silos that are filled with degenerating biological materials.

Mechanism of Tissue Injury

When hydrolyzed in the water content of the airway mucosa, nitrogen dioxide generates toxic nitrous and nitric acid species. Also, nitrogen dioxide promotes free radical activity. Airway and lung injury may occur anywhere along the respiratory tract, but the principal site of damage is the terminal bronchioles and more distal airways.

Spectrum of Respiratory Disorders Associated with Toxic Exposure

Initial clinical manifestations of nitrogen dioxide exposure include cough, chest tightness, dyspnea, headache, and nausea. After a period of several hours of clinical stability or improvement, progressive shortness of breath occurs in concert with the development of pulmonary edema because of an increase in pulmonary capillary permeability and pulmonary vascular damage. Patients who survive the episode of pulmonary edema may develop bronchiolitis obliterans (BO) or bronchiolitis obliterans organizing pneumonia (BOOP) several weeks following the acute exposure.

Phosgene

Environmental Sources of Exposure

Phosgene (COCl₂), also known as carbonyl chloride or carbonic acid dichloride, is a colorless gas at room temperature and a colorless liquid when cooled or pressurized. The gas, which is present in minute concentrations as an atmospheric pollutant, is used extensively in the chemical industry, primarily in the production of dyes, foams, resins, and chemicals used in agriculture. It is also used in the development of polymers and polycarbonates. Five million metric tons are produced annually. While accidental exposures may affect individuals or larger populations, the agent’s notoriety is based on its use as a chemical weapon during World War I which led to tens of thousands of deaths.

Mechanism of Tissue Injury

Phosgene induces tissue damage in at least two ways: hydrolysis and acylation. Hydrolysis of the gas produces hydrogen chloride and carbon dioxide, but only small amounts of hydrogen chloride are produced in the airways because of the gas’s poor solubility. Deposition in mucous membranes in the upper airway and eyes may produce irritation but typically only when phosgene exposure is intense. Because of a general lack of symptoms from upper airway irritation and little protective reflex bronchoconstriction induced, exposure duration may be longer than it would be otherwise.

Acylation appears to be the principal mode of tissue injury. Acylation arises when phosgene loses reactive carbon and oxygen atoms that generate hydroxyl, thiol, amine, and sulfhydryl moieties in proteins, lipids, and carbohydrates. The resulting reactions produce injury to lung surfactant and peroxidation of lipids, including the phospholipids that are present in cell membranes. Subsequent damage from the release of leukotrienes and up-regulation of oxidative enzyme systems ensues.

Spectrum of Respiratory Disorders Associated with Toxic Exposure

The onset of clinical symptoms may be either immediate or delayed. Development of immediate symptoms, including cough, chest tightness, and wheezing, appears to be related to the concentration of the gas and development of HCl in mucosal water. At a concentration of greater than 3 ppm, throat irritation occurs, and eye irritation, cough, and chest tightness occur at higher concentrations.

Delayed symptoms may follow a symptom-free period of 48 hours. The duration of the symptom-free interval appears to be inversely proportional to the level of exposure. Following the symptom-free period, cough, dyspnea, and respiratory distress from fulminant pulmonary edema may be observed. Chances of survival from pulmonary edema are good, but prolonged sequelae, including chronic bronchitis and emphysema, have been reported.

Sulfur dioxide

Environmental Sources of Exposure

Sulfur dioxide is a dense, colorless gas that has the pungent odor of burning matches. It arises from the burning of coal and petroleum products. It is used industrially as a preservative in the food industry. Toxic exposures have occurred in ore smelting, the sugar refining industry, and in industrial settings in which bleaching of wood pulp and wool occurs. It is also released into the atmosphere during volcanic eruptions.

Mechanism of Tissue Injury

Sulfur dioxide reacts with the water component of airway epithelium to generate sulfuric acid. Sulfuric acid coagulates tissue and generates hydrogen ions, sulfites, and bisulfites–moieties that then react with oxygen to produce reactive oxygen species. The resulting lipid peroxidation may contribute to the injury.

Spectrum of Respiratory Disorders Associated with Toxic Exposure

Clinical manifestations include nose, eye, and throat irritation and cough. Obstructive airway physiology arises, and the proximal airway mucosa may be damaged extensively. Lower respiratory tract involvement is evident as ARDS. With high-level exposures, death may occur in minutes from hypoxemia arising from alveolar hemorrhage and pulmonary edema. RADS has been described following a single exposure, and bronchitis has also been reported. Development of bronchiolitis obliterans weeks after the initial exposure has been described.

Zinc chloride

Environmental Sources of Exposure

Zinc chloride, or hexite, is a component of smoke-generating devices, including smoke bombs. Zinc chloride is formed through the reaction of zinc oxide with hexachloroethane.

Mechanism of Tissue Injury

Deposition of zinc chloride on airway and alveolar surfaces results in the compound’s reacting with water to generate HCl and zinc oxychloride. Direct irritation of airway surfaces ensues, resulting in tracheobronchitis and pneumonia.

Spectrum of Respiratory Disorders Associated with Toxic Exposure

Patients with toxic zinc chloride exposure have nonspecific symptoms of cough and dyspnea and are at risk for progression to development of ARDS.

Metal Fume Fever/Polymer Fume Fever

Environmental Sources of Exposure

First described in the early 19th century, metal fume fever, also known as brazier’s disease or “Monday morning fever,” is a disorder characterized by fever, chills, body aches, and malaise following exposure to fumes containing a metal oxide. A number of metals, including copper, magnesium, nickel, silver, zinc, beryllium, and cadmium, have been implicated. Although the disorder has been reported in a variety of metal workers, welders appear to be at highest risk.

Most of the welding fumes are generated by the electrode or wire rod used during the welding process. Additional contributors to the fumes include electrode coatings, fluxes, and painted services of the material being welded. The particles generated are ultrafine, ranging in diameter from 0.01 to 0.10 microns.

A similar syndrome, “polymer fume fever,” has been reported following exposure to fluorocarbon polymers.

Mechanism of Tissue Injury

The pathogenesis of metal fume fever is thought to be based on production of the inflammatory cytokines induced by exposure to metal oxide. Bronchoalveolar lavage findings are consistent with a pulmonary influx of polymorphonuclear leukocytes.

Spectrum of Respiratory Disorders Associated with Toxic Exposure

Metal fume fever is characterized by a flu-like illness. Symptoms at onset include upper airway irritation and are followed by fever, chills, and body aches two to four hours following exposure. Cough and dyspnea may also be observed. Symptoms resolve over the course of two days. Repeated exposure leads to a diminution in the effects (tachyphylaxis), so “Monday morning fever” reflects recurrence of symptoms upon re-exposure following two weekend days away from the work environment.

CXR findings in asymptomatic welders may demonstrate numerous airspace opacities. Pathologic examination of the opacities reveals iron oxide deposits, a disorder known as siderosis, which is considered a benign pneumoconiosis. The characteristic tachyphylaxis of metal fume fever is not seen with polymer fume fever.

Are you sure your patient has toxic inhalational lung injury? What should you expect to find?

The symptoms and signs of exposure to inhaled toxins depend upon the primary site in the airways where the toxin is deposited and the degree to which the toxin forms irritants that either minimize or prolong exposure to the agent. For example, exposure to ammonia results in the acute onset of highly noxious upper airway and conjunctival symptoms, prompting the person to flee from the environment, which minimizes exposure. On the other hand, exposure to chlorine gas may be more prolonged because of the lack of severe irritation in the upper airways and eyes.

Ammonia

The spectrum of respiratory disorders includes tracheobronchitis, bronchiolitis, bronchopneumonia, pulmonary edema, RADS, and obstructive airways disease. There have also been isolated reports of interstitial lung disease and bronchiectasis.

Fatal cases following significant exposure occur in the setting of laryngeal edema, airway obstruction, and noncardiogenic pulmonary edema, along with secondary infection in the setting of diffuse airway damage. The initial acute syndrome of pneumonia may resolve over several days, only to be followed by the gradual onset of airways obstruction.

Cadmium

Patients with cadmium exposure may be asymptomatic for several hours following exposure. Subsequently, fever, body aches, and malaise may develop, similar to the clinical findings in metal fume fever. Cough and dyspnea follow. In fatal cases, progression of diffuse pulmonary infiltrates to ARDS has been described.

Chlorine

Clinical manifestations include conjunctivitis, rhinitis, cough, wheezing, and dyspnea. Pathologic findings include diffuse tracheobronchitis, desquamation of airway epithelium, and pulmonary edema. Long-term sequelae may include both restrictive and obstructive disorders though many cases resolve within two years of initial exposure. A large cohort study of mill workers exposed to chlorine at a textile factory demonstrated an increase in the proportion of workers with an accelerated FEV1 annual decline and decreased FEV1/FVC ratio in the 18 months following toxic exposure. RADS may also occur. Those most predisposed to the development of RADS are current or former smokers or those with allergic backgrounds.

Mercury

After one is exposed to mercury vapor, little in the way of upper airway irritation is noted at first. Victims may be unaware of their exposure and continue to work in the contaminated environment. However, approximately 12-24 hours following exposure, cough, and shortness of breath develop, occasionally accompanied by nonspecific symptoms of fever, vomiting, and diarrhea. As symptoms progress, widespread pulmonary infiltrates and potential ARDS may occur. While most respiratory symptoms usually resolve within a few days following exposure, there are reports of progression to pulmonary fibrosis.

Nitrogen dioxide

Initial clinical manifestations of toxic nitrogen dioxide exposure include cough, chest tightness, dyspnea, headache, and nausea. After a period of several hours of clinical stability or improvement, progressive shortness of breath occurs in concert with the development of pulmonary edema because of increased capillary permeability and pulmonary vascular damage. Patients who survive the pulmonary edema may develop BO or bronchiolitis obliterans organizing pneumonia (BOOP) several weeks following the acute exposure.

Patients must be monitored carefully following exposure, as they may progress within hours to ARDS. Similarly, post-acute event follow-up is important to evaluate for progressive development of respiratory impairment that is due to BO, although administration of systemic corticosteroids may mitigate its development.

Phosgene

Onset of clinical symptoms may be either immediate or delayed. Development of immediate symptoms, including cough, chest tightness, and wheezing, appear to be related to the concentration of the gas and development of HCl in mucosal water. With a concentration greater than 3 ppm, throat irritation develops, and eye irritation, cough, and chest tightness occur at higher concentrations.

Delayed symptoms may follow a symptom-free period of 48 hours. The duration of the symptom-free interval appears to be inversely proportional to the exposure dose. Following the symptom-free period, cough, dyspnea, and respiratory distress that are due to fulminant pulmonary edema may be observed. Chances of survival from pulmonary edema are good, but prolonged sequelae, including chronic bronchitis and emphysema, have been reported.

Sulfur dioxide

Clinical manifestations include nose, eye, and throat irritation, along with cough. Obstructive airway physiology arises, and the proximal airway mucosa may be damaged extensively. Lower respiratory tract involvement is evident as ARDS. With high-level exposures, death may occur in minutes from hypoxemia arising from alveolar hemorrhage and pulmonary edema. RADS has been described following a single exposure, and bronchitis has been reported. Development of BO weeks after the initial exposure has been described.

Zinc chloride

Patients with toxic zinc chloride exposure have nonspecific symptoms of cough and dyspnea and are at risk for progression to ARDS.

Metal fume fever/polymer fumes fever

Metal fume fever is characterized by a flu-like illness. Symptoms at onset include upper airway irritation and are followed by fever, chills, and body aches two to four hours following exposure. Cough and dyspnea may also be observed. Symptoms resolve over the course of two days. Repeated exposure leads to a diminution in the effects (tachyphylaxis), so “Monday morning fever” reflects recurrence of symptoms upon re-exposure following two weekend days away from the work environment.

CXR findings in asymptomatic welders may demonstrate numerous opacities that are due to iron oxide deposits (siderosis, a benign pneumoconiosis).

Beware: there are other conditions that can mimic toxic inhalational lung injury:

Not applicable.

How and/or why did the patient develop toxic inhalational lung injury?

Discussed above.

Which individuals are at greatest risk of developing toxic inhalational lung injury?

See section on Classification.

What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?

Not applicable.

What imaging studies will be helpful in making or excluding the diagnosis of toxic inhalational lung injury?

CXR and CT scan findings in toxic inhalations include a number of patterns (Figure 3). Patchy focal infiltrates may develop initially and, in some cases, progress to ARDS. Virtually any of the agents discussed may produce pulmonary infiltrates, but particularly noteworthy are phosgene, chlorine, sulfur dioxide, and nitrogen dioxide. Metal fume fever is usually associated with a clear CXR, but patchy infiltrates are sometimes seen.

Figure 3

When exposure results in either acute or chronic airways obstruction, CXRs may reveal hyperinflation. Subacute or chronic fluctuating pulmonary infiltrates, noted as ground-glass opacifications on chest CT, suggest bronchiolitis obliterans organizing pneumonia (BOOP).

What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of toxic inhalational lung injury?

Pulmonary function test findings include obstructive, restrictive, and mixed patterns (Figure 3). Obstructive physiology has been reported with many of the agents described, but most notably chlorine and cadmium. A number of agents, including nitrogen dioxide, sulfur dioxide, mercury, and ammonia, may produce small airways narrowing and obstructive physiology consistent with BO.

Development of partially reversible airways obstruction due to RADS has been reported with ammonia and chlorine exposures.

A restrictive pattern is expected in patients who develop bronchiolitis obliterans organizing pneumonia (BOOP), and either an obstructive or a restrictive pattern may occur in cases of metal fume fever, although these patterns are uncommon.

What diagnostic procedures will be helpful in making or excluding the diagnosis of toxic inhalational lung injury?

Not applicable.

What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of toxic inhalational lung injury?

Not applicable.

If you decide the patient has toxic inhalational lung injury, how should the patient be managed?

General Principles of Management

General management for virtually all toxic exposures begins with immediate removal of the individual from the toxic environment and ensuring an adequate airway. In many instances, particularly following exposure to highly water-soluble compounds that have local irritant effects on the upper airways, management should include copious irrigation of mucosal surfaces with water. Close observation for development of upper respiratory tract complications, including upper airway edema and airway obstruction, is critical. Use of inhaled bronchodilators may also be helpful.

Additional Interventions

Additional interventions may be warranted for some exposures. For example, nebulized sodium bicarbonate may be useful in chlorine exposure, although clinical trials have not been performed. Use of corticosteroids in the setting of nitrogen dioxide exposure may be helpful in mitigating the subsequent development of bronchiolitis obliterans. However, robust data are lacking to support the routine use of corticosteroids. With inhalational mercury poisoning, the use of chelating agents that are often employed following mercury ingestion has not been demonstrated to be of benefit. Patients who continue to deteriorate clinically despite optimal therapies may ultimately require lung transplantation.

What is the prognosis for patients managed in the recommended ways?

See section on Classification.

What other considerations exist for patients with toxic inhalational lung injury?

Not applicable.

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