Irritant gas inhalation injury: symptoms, diagnosis and patient care

Irritant gases are those which, when inhaled, dissolve in the mucosal water of the respiratory tract and cause an inflammatory response, usually due to the release of acid or alkaline radicals

Exposures to irritant gases mainly affect the airways, causing tracheitis, bronchitis and bronchiolitis

Other inhaled drugs may be directly toxic (e.g. cyanide, carbon monoxide) or cause harm by simply replacing oxygen and causing asphyxia (e.g. methane, carbon dioxide).

The effect of inhalation of irritant gases depends on the magnitude, duration of exposure and the specific agent.

Chlorine, phosgene, sulphur dioxide, hydrochloric acid, hydrogen sulphide, nitrogen dioxide, ozone and ammonia are among the most important irritant gases.

Hydrogen sulphide is also a potent cellular toxin, blocking the cytochrome system and inhibiting cellular respiration.

A common exposure involves domestic mixing of ammonia with detergents containing bleach; chloramine, an irritant gas, is released.

Acute exposure to irritant gases

Acute exposure to high concentrations of toxic gas in a short period is characteristic of industrial accidents, due to a faulty valve or pump in a gas cylinder, or accidents occurring during gas transportation.

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 (e.g. chlorine, ammonia, sulphur dioxide, hydrochloric acid) dissolve in the upper respiratory tract and immediately cause irritation of the mucous membranes, alerting people to the need to avoid exposure.

Permanent damage to the upper respiratory tract, distal airways and lung parenchyma only occurs if escape from the gas source is prevented.

Less soluble gases (e.g. nitrogen dioxide, phosgene, ozone) cannot dissolve until they enter the respiratory tract, often reaching the lower airways.

These agents are less able to cause early warning signals (phosgene at low concentrations has a pleasant odour), are more likely to cause severe bronchiolitis, and often have a delay of ≥ 12 h before symptoms of pulmonary oedema develop.

Complications of irritant gas inhalation

The most severe and immediate complication is acute respiratory distress syndrome, which usually occurs acutely but may be delayed up to 24 h.

Patients with significant lower airway involvement may develop a bacterial infection.

10 to 14 days after acute exposure to certain agents (e.g., ammonia, nitrogen oxide, sulphur dioxide, mercury), some patients develop bronchiolitis obliterans that evolves into acute respiratory distress syndrome.

Obliterative bronchiolitis evolving into pneumonia can occur when granulation tissue accumulates in the terminal airways and alveolar ducts during the body’s reparative processes.

A minority of these patients develop late-onset pulmonary fibrosis.

Symptomatology of acute irritant gas exposure

Soluble irritant gases cause severe burns and other irritant manifestations in the eyes, nose, throat, trachea and main bronchi.

Severe coughing, haemoptysis, wheezing, retching and shortness of breath are common. The upper airways may be obstructed by oedema, secretions or laryngospasm.

Severity is generally dose-related. Non-soluble gases cause fewer immediate symptoms, but may cause dyspnoea or coughing.

Patients who develop acute respiratory distress syndrome have worsening dyspnoea and increased oxygen demand.

Diagnosis of acute exposure to irritant gases

  • Exposure history
  • Chest X-ray
  • Spirometry and lung volume assessment

From the history, the diagnosis is usually obvious.

Patients should undergo chest X-ray and pulse oximetry.

A chest X-ray finding of spotty or confluent alveolar thickening usually indicates pulmonary oedema.

Spirometry and lung volume assessment are performed.

Obstructive abnormalities are more common, but restrictive abnormalities may predominate after exposure to high doses of chlorine.

CT scan is used to evaluate patients with symptoms developing late after exposure.

Those with bronchiolitis obliterans, which develop into respiratory failure, show a picture of bronchiolar thickening and irregular mosaic hyperinflation.

Inhalation lesions can occur anywhere along the airway tracts and can be classified according to the primary area of injury, such as the upper airway, the tracheobronchial system or the lung parenchyma.

Direct visualisation of the airway can help confirm the diagnosis.

The Abbreviated Injury Score is a rating scale used to determine the clinical severity of injury (1):

  • No injury: absence of coal dust deposits, erythema, oedema, bronchorrhoea or obstruction
  • Mild injury: small or irregular areas of erythema, coal dust deposits in proximal or distal bronchi
  • Moderate lesion: moderate degree of erythema, coal dust deposits, bronchorrhoea or bronchial obstruction
  • Severe lesion: severe inflammation with friability, abundant coal dust deposits, bronchorrhoea or obstruction
  • Massive lesion, evidence of mucosal desquamation, necrosis and endoluminal obliteration

Diagnosis reference

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 of acute exposure to irritant gases

Most people recover completely, but some have persistent lung injury with reversible airway obstruction (reactive airway dysfunction syndrome) or restrictive abnormalities and pulmonary fibrosis; smokers are at high risk.

Treatment of acute exposure to irritant gas

Removal from exposure and 24 h observation

  • Bronchodilators and supplemental oxygen
  • Sometimes racemic inhaled adrenaline, endotracheal intubation and mechanical ventilation
  • Sometimes corticosteroids, depending on the specific chemical exposure

With few exceptions, management is based on symptoms rather than the specific agent.

Patients should be moved to fresh air and given supplemental oxygen.

Treatment is directed towards ensuring adequate oxygenation and alveolar ventilation.

Bronchodilators and oxygen therapy may be sufficient in less severe cases.

Severe airflow obstruction is managed with inhaled racemic adrenaline, endotracheal intubation or tracheotomy and mechanical ventilation.

Because of the risk of acute respiratory distress syndrome, any patient with respiratory tract symptoms after toxic inhalation should be kept under observation for 24 h.

High-dose corticosteroids should not routinely be used for acute respiratory distress syndrome induced by inhalation injury; however, some clinical cases suggest efficacy in severe acute respiratory distress syndrome following inhalation of zinc chloride smoke.

After treating the acute phase, the clinician should pay attention to the development of reactive airway dysfunction syndrome, obliterative bronchiolitis with or without pneumonia, pulmonary fibrosis and delayed-onset acute respiratory distress syndrome.

Prevention of acute exposure to irritant gas

The most important prophylactic measure is to be careful when working with gases and chemicals.

The availability of suitable respiratory protection (e.g. gas masks with self-contained air supply) is also of great importance to rescuers; rescuers who rush to free the victim without protective equipment often succumb themselves.

Chronic exposure

Continuous or intermittent exposure to low doses of irritant gases or chemical vapours can cause chronic bronchitis, although it is particularly difficult to establish the role of such exposures in smokers.

Chronic inhalation exposure to certain agents (e.g., bis[chloromethyl]ether or certain metals) causes lung or other neoplasms (e.g., liver angiosarcoma after exposure to vinyl chloride monomers).

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