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 oxime (which also affect the skin) as well as military smokes, products of combustion, and many toxic industrial chemicals. Most of these compounds are gases or highly volatile liquids.
(See also Overview of Chemical-Warfare Agents.)
Toxic chemical-warfare agents that affect the respiratory tract are divided into 2 types depending on which part of the tract is predominantly affected (see table Representative Type 1, Type 2, and Mixed-Effect Chemicals With Acute Local Effects on the Respiratory Tract):
Type 1 agents usually are those with inhaled particles (eg, smoke), which tend to settle out before reaching the alveoli, or highly water-soluble and/or highly reactive chemicals, which dissolve into respiratory mucosa before reaching the alveoli. Type 1 agents cause necrosis and sloughing of the respiratory epithelium in the large airways, which may cause partial or total airway obstruction. Chemical pneumonitis and secondary bacterial pneumonitis may occur as a consequence of type 1 local damage. High doses of type 2 agents also can cause type 1 (large-airway) effects, although the type 1 effects are more likely to be transient.
Type 2 agents usually are lower-solubility and/or less-reactive chemicals, which travel to the alveoli before dissolving. These agents damage pulmonary capillary endothelium, causing fluid leakage into interstitial spaces and alveoli; pulmonary edema may result. With some type 2 agents (eg, oxides of nitrogen and HC smoke [hexachloroethane plus zinc oxide]), acute pulmonary edema may be followed days to weeks later by progressive and potentially irreversible pulmonary fibrosis. The mechanism is presumed to be immunologic. High doses of type 1 agents can also cause pulmonary edema.
Mixed-effect agents include most inhaled chemicals with local effects on the respiratory tract. Mixed-effect agents lie in the middle of the spectrum of aqueous solubility and chemical reactivity and have both type 1 and type 2 effects. They act in both large airways and alveoli although one effect or the other usually predominates except at high doses.
Representative Type 1, Type 2, and Mixed-Effect Chemicals With Acute Local Effects on the Respiratory Tract
Type 1 agents initially cause sneezing, coughing, and laryngospasm (eye irritation can also occur). Patients with airway obstruction have hoarseness, wheezing, and inspiratory stridor. With a high dose of a type 1 agent, chest tightness or shortness of breath may subsequently develop as a herald of pulmonary edema.
With type 2 agents, symptoms and signs are usually delayed several hours following exposure. Patients initially complain of chest tightness or shortness of breath. Physical findings may be minimal except for rare expiratory crackles and dullness to percussion. Time of onset is shorter with higher doses; development of dyspnea within 4 hours of exposure suggests a potentially lethal dose.
Clinical diagnosis is used to recognize exposure and distinguish type of damage (not necessarily the precise agent). Patients with an initially noisy chest and prominent symptoms are presumed to have type 1 involvement (large airways). Delayed onset of shortness of breath with a relatively quiet chest suggests type 2 damage. Although a high dose of type 2 agent may initially cause coughing, sneezing, and wheezing, these signs typically decrease over time; the patient then appears well until developing progressive shortness of breath.
Chest x-ray may be normal initially. Scattered opacities due to chemical or secondary pneumonitis may develop with type 1 damage. Eventually, as pulmonary edema becomes radiographically evident, Kerley B lines and fluffy interstitial infiltrates due to type 2 damage will become visible.
Bronchoscopy can confirm type 1 damage but may miss early type 2 damage.
Laboratory testing is not helpful in initial diagnosis, but pulse oximetry and/or arterial blood gas (ABG) measurements can help monitor for clinical deterioration.
Severe signs of type 1 damage (eg, severe wheezing, inspiratory stridor, soot around the nose or mouth due to smoke inhalation) should lower the threshold for early intubation. With a type 2 agent, it is important to re-triage patients frequently. Initially asymptomatic patients also require monitoring for deterioration; even mild symptoms are grounds for prompt transport to a medical facility because such patients often deteriorate further. Most patients with shortness of breath due to early pulmonary edema can be triaged as delayed for medical treatment; they can usually tolerate a short delay if more immediate casualties require treatment. However, such patients should have highest priority (urgent) for evacuation because they may require definitive, life-saving treatment in a pulmonary intensive care unit.
For type 1: Early intubation and bronchodilators, sometimes inhaled corticosteroids, and antibiotics for documented secondary bacterial infection
For type 2: Oxygen and positive-pressure ventilation (continuous positive airway pressure in conscious patients; positive end-expiratory pressure in ventilated patients), bronchodilators, and rarely corticosteroids
It is important to treat the damage rather than the agent because some agents cause both type 1 and type 2 effects even at low doses, and high doses of either agent cause both types of damage. Decontamination of vapor or gas exposure is not indicated, and there are no specific antidotes for these agents.
For type 1 effects, give warm, humidified 100% oxygen by face mask. Bronchoscopy may be both diagnostic and therapeutic, via the removal of necrotic debris from the large airways. Early intubation and assisted ventilation may be needed. Bronchodilators may help by increasing the caliber of airways. Inhaled corticosteroids may decrease the inflammation that often accompanies large-airway damage. For management of smoke inhalation, see Smoke Inhalation.
For type 2 effects, patients should be admitted to an intensive care unit (ICU). Oxygen should be given via continuous positive airway pressure (CPAP) in conscious patients or via positive end-expiratory pressure (PEEP) in intubated patients. Positive-pressure ventilation may help force fluid from the alveolar spaces back into the pulmonary capillaries (see also Treatment of Acute Hypoxemic Respiratory Failure). A central line may help monitor pulmonary pressures so that they can be controlled without inducing hypovolemic shock. Although bronchodilators are indicated mainly to dilate large airways in cases of type 1 damage, recent evidence suggests that they act via independent pathways to alleviate type 2 damage as well. Corticosteroids do not relieve pulmonary edema but oral corticosteroids may be indicated early for patients exposed to HC smoke or to oxides of nitrogen in an effort to prevent late-onset pulmonary fibrosis.
Prophylactic antibiotics do not help either type of injury. Antibiotics should be given only after diagnosis of bacterial infection is made, including isolating an organism and determining antibiotic sensitivities.
The views expressed in this article are those of the author and do not reflect the official policy of the Department of Army, Department of Defense, or the US Government.