Irritant gases are those which, when inhaled, dissolve in the water of the respiratory tract mucosa and cause an inflammatory response, usually due to the release of acidic or alkaline radicals. Irritant gas exposures predominantly affect the airways, causing tracheitis, bronchitis, and bronchiolitis. Other inhaled agents may be directly toxic (eg, cyanide Systemic Asphyxiant Chemical-Warfare Agents , carbon monoxide Carbon Monoxide Poisoning Carbon monoxide (CO) poisoning causes acute symptoms such as headache, nausea, weakness, angina, dyspnea, loss of consciousness, seizures, and coma. Neuropsychiatric symptoms may develop weeks... read more ) or cause harm simply by displacing oxygen and causing asphyxia (eg, methane, carbon dioxide).
The effect of inhaling irritant gases depends on the extent and duration of exposure and on the specific agent.
Chlorine, phosgene, sulfur dioxide, hydrogen chloride, hydrogen sulfide, nitrogen dioxide, ozone, and ammonia are among the most important irritant gases. Hydrogen sulfide is also a potent cellular toxin, blocking the cytochrome system and inhibiting cellular respiration. A common exposure involves mixing household ammonia with cleansers containing bleach; the irritant gas chloramine is released.
(See also Pulmonary Chemical Warfare Agents Pulmonary Chemical-Warfare Agents Pulmonary agents include traditional chemical-warfare “choking” agents such as chlorine, phosgene, diphosgene, and chloropicrin and some vesicants such as sulfur mustard, Lewisite, and phosgene... read more and Overview of Environmental Pulmonary Disease Overview of Environmental Pulmonary Disease Environmental pulmonary diseases result from inhalation of dusts, allergens, chemicals, gases, or environmental pollutants. The lungs are continually exposed to the external environment and... read more .)
Acute exposure to high concentrations of toxic gas over a short time is characteristic of industrial accidents resulting from a faulty valve or pump in a gas tank or occurring during gas transport. Many people may be exposed and affected. The release of methyl isocyanate from a chemical plant in Bhopal, India in 1984 killed > 2000 people.
Respiratory damage is related to the concentration and water solubility of the gas and the duration of exposure.
More water-soluble gases (eg, chlorine, ammonia, sulfur dioxide, hydrogen chloride) dissolve in the upper airway and immediately cause mucous membrane irritation, which may alert people to the need to escape the exposure. Permanent damage to the upper respiratory tract, distal airways, and lung parenchyma occurs only if escape from the gas source is impeded.
Less soluble gases (eg, nitrogen dioxide, phosgene, ozone) may not dissolve until they are well into the respiratory tract, often reaching the lower airways. These agents are less likely to cause early warning signs (phosgene in low concentrations has a pleasant odor), are more likely to cause severe bronchiolitis, and often have a lag of ≥ 12 hours before symptoms of pulmonary edema develop.
The most serious immediate complication is acute respiratory distress syndrome Acute Hypoxemic Respiratory Failure (AHRF, ARDS) Acute hypoxemic respiratory failure is defined as severe hypoxemia (PaO2 (See also Overview of Mechanical Ventilation.) Airspace filling in acute hypoxemic respiratory failure (AHRF) may result... read more (ARDS), which usually occurs acutely but can be delayed as long as 24 hours. Patients with significant lower airway involvement may develop bacterial infection.
Ten to 14 days after acute exposure to some agents (eg, ammonia, nitrogen oxides, sulfur dioxide, mercury), some patients develop bronchiolitis obliterans progressing to ARDS. Bronchiolitis obliterans with organized pneumonia Cryptogenic Organizing Pneumonia Cryptogenic organizing pneumonia is an idiopathic condition in which granulation tissue obstructs alveolar ducts and alveolar spaces with chronic inflammation occurring in adjacent alveoli.... read more can ensue when granulation tissue accumulates in the terminal airways and alveolar ducts during the body’s reparative process. A minority of these patients develop late pulmonary fibrosis.
Symptoms and Signs of Acute Exposure to Irritant Gas
Soluble irritant gases cause severe burning and other manifestations of irritation of the eyes, nose, throat, trachea, and major bronchi. Marked cough, hemoptysis, wheezing, retching, and dyspnea are common. The upper airway may be obstructed by edema, secretions, or laryngospasm. Severity is generally dose-related. Nonsoluble gases cause fewer immediate symptoms but can cause dyspnea or cough.
Patients who develop ARDS have worsening dyspnea and increasing oxygen requirements.
Diagnosis of Acute Exposure to Irritant Gas
History of exposure
Spirometry and lung volume testing
Diagnosis is usually obvious from the history. Patients should have a chest x-ray and pulse oximetry. Chest x-ray findings of patchy or confluent alveolar consolidation usually indicate pulmonary edema. Spirometry and lung volume testing are done. Obstructive abnormalities are most common, but restrictive abnormalities can predominate after exposure to high doses of chlorine.
CT is used to evaluate patients with late-developing symptoms. Those with bronchiolitis obliterans that progresses to respiratory failure manifest a pattern of bronchiolar thickening and a patchy mosaic of hyperinflation.
Inhalational injury can occur anywhere along the airway passages and can be classified based on the primary area of injury such as upper airway, the tracheobronchial system, or lung parenchyma. Direct visualization of the airways will help confirm diagnosis. The Abbreviated Injury Score is a grading scale used to determine clinical severity of injury (1 Diagnosis reference Irritant gases are those which, when inhaled, dissolve in the water of the respiratory tract mucosa and cause an inflammatory response, usually due to the release of acidic or alkaline radicals... read more ):
0. No injury—Absence of carbonaceous deposits, erythema, edema, bronchorrhea or obstruction
1. Mild injury— Minor or patchy areas of erythema, carbonaceous deposits in proximal or distal bronchi
2. Moderate injury—Moderate degree of erythema, carbonaceous deposits, bronchorrhea, or bronchial obstruction
3. Severe injury—Severe inflammation with friability, copious carbonaceous deposits, bronchorrhea or obstruction
4. Massive injury—Evidence of mucosal sloughing, necrosis, endoluminal obliteration
1. Albright JM, Davis CS, Bird MD, et al: The acute pulmonary inflammatory response to the graded severity of smoke inhalation injury. Crit Care Med 40(4):1113–1121, 2012. doi: 10.1097/CCM.0b013e3182374a67
Prognosis for Acute Exposure to Irritant Gas
Treatment of Acute Exposure to Irritant Gas
Removal from exposure and 24-hour observation
Bronchodilators and supplemental oxygen
Sometimes inhaled racemic epinephrine, endotracheal intubation, and mechanical ventilation
Sometimes corticosteroids, depending on the specific chemical exposure
With a few exceptions, management is based on symptoms rather than the specific agent. Patients should be moved into fresh air and given supplemental oxygen. Treatment is directed toward ensuring adequate oxygenation and alveolar ventilation.
Bronchodilators and oxygen therapy may suffice in less severe cases.
Severe airflow obstruction is managed with inhaled racemic epinephrine, endotracheal intubation Tracheal Intubation Most patients requiring an artificial airway can be managed with tracheal intubation, which can be Orotracheal (tube inserted through the mouth) Nasotracheal (tube inserted through the nose)... read more or tracheostomy, and mechanical ventilation Overview of Mechanical Ventilation Mechanical ventilation can be Noninvasive, involving various types of face masks Invasive, involving endotracheal intubation Selection and use of appropriate techniques require an understanding... read more .
Because of the risk of ARDS, any patient with respiratory tract symptoms after toxic inhalation should be observed for 24 hours. High-dose corticosteroids should not be routinely used for ARDS induced by inhalational injury; however, a few case reports suggest efficacy in severe ARDS following zinc chloride smoke inhalation.
After the acute phase has been managed, physicians must remain alert to the development of reactive airways dysfunction syndrome, bronchiolitis obliterans with or without organized pneumonia, pulmonary fibrosis, and delayed-onset ARDS.
Prevention of Acute Exposure to Irritant Gas
Care in handling gases and chemicals is the most important preventive measure. The availability of adequate respiratory protection (eg, gas masks with a self-contained air supply) for rescuers is also very important; rescuers without protective gear who rush in to extricate a victim often succumb themselves.
Low-level continuous or intermittent exposure to irritant gases or chemical vapors may lead to chronic bronchitis, although the role of such exposure is especially difficult to substantiate in smokers.
Chronic inhalational exposure to some agents (eg, bis[chloromethyl]ether, certain metals) causes lung and other cancers (eg, liver angiosarcomas after vinyl chloride monomer exposure).
Irritant gas exposures predominantly affect the airways, causing tracheitis, bronchitis, and bronchiolitis.
Complications of acute exposure may include acute respiratory distress syndrome, bacterial infections, and bronchiolitis obliterans (sometimes leading to pulmonary fibrosis).
Diagnosis of acute exposure is usually obvious by history, but do pulse oximetry, chest x-ray, spirometry, and lung volume assessment.
Treat acute exposure supportively and observe patients for 24 hours.
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