The health effects of an acute exposure to an irritant gas or vapor are dependent on the physiochemical properties of that particular gas or vapor, as well as specific host factors. The extent of exposure varies considerably and is most pronounced in subjects with preexisting airway diseases. Acid and alkaline gases such as chlorine and ammonia produce extreme alterations in pH that cause tissue damage by direct contact. Other gases produce chemical reactions that cause free radical release, inflammation, and membrane damage.
The site of pulmonary injury is most dependent on the water solubility of the gas. High-solubility gases (e.g., ammonia, sulfur dioxide, formaldehyde, or methyl iso-cyanate) can affect all exposed mucous membranes, including: ocular (irritation, erythema, and conjunctivitis, and with heavy exposure delayed-onset of cataracts), nasal (irritation, congestion, rhinorrhea, and erythema), facial burns (skin and lip), pharyn-geal (throat and tongue irritation, burns and edema), and laryngeal (burns, edema, and obstruction) injuries. Intermediate-solubility gases such as chlorine may produce upper-airway irritation, but the mucous membrane irritation is not as intense as for highly soluble gases. Because of its intermediate solubility, chlorine's effect extends more distal, producing both upper- and lower-airway injury, and pulmonary edema. Low-solubility gases, like phosgene or oxides of nitrogen, produce little in the way of upper-airway irritation, but produce intense damage to the lower airways and pulmonary edema. The low-solubility gases are more likely to produce delayed-onset symptoms and delayed-onset pulmonary edema, usually within the first 24 hours.
Several factors may influence the severity of lung injury. For the most part, pulmonary injury severity is determined by (1) gas solubility and (2) exposure duration multiplied by gas concentration. Problems in escaping the exposure due to orthopedic problems or to falling or mouth breathing due to nasal obstruction may also play important roles in determining exposure and injury severity. For example, if gas density is high (e.g., chlorine or phosgene), the gas cloud may hug the floor, thereby increasing exposure to a victim who has fallen.
Oxides of nitrogen, like nitrogen dioxide, commonly produce a triphasic illness pattern. Initial presentation may be that of cough, wheeze, dyspnea, central chest pain, fever, sweating, and weakness. Physical examination may reveal wheezes and crackles, and the patient may be hypotensive and cyanotic. The patient's x-ray may be normal or may show pulmonary edema. This phase of the illness will resolve and the patient may be relatively asymptomatic and then 2 to 8 weeks later develop symptoms of bronchiolitis obliterans. Presentation includes the late development of fevers, chills, wheeze, cough, dyspnea, and chest pain associated with wheezes and crackles on physical exam. The chest films may be normal or may show diffuse, small nodules. Chest CT scans with expiratory imaging may show air trapping, bronchial wall thickening and nodules suggestive of bronchiolitis obliterans.
The early management and treatment of acute inhalation injury from an irritant gas is summarized below and is primarily supportive, including immediately removing any contaminated clothing that might further increase the absorption of a substance through the skin.
1. Start high-flow 100% oxygen and consider arterial blood gas and co-oximetry panel.
2. Obtain history of any odors or knowledge of specific toxic agent.
3. Examine patient for eye injuries, flush eyes, and treat if inflammation is noted.
4. Examine patient for burns to face, nose, mouth, or throat.
5. If victim is hoarse, has difficulty phonating, facial burns or carbonaceous sputum, evaluate the airway with laryngoscopy or bronchoscopy and if edema is present, consider early intubation.
6. Examine chest and consider early use of bronchodilators, mucomyst, and or inhaled corticosteroids.
7. Peak flow rates and/or bedside spirometry may be helpful in diagnosing or documenting reversible bronchospasm. Full pulmonary function tests (volumes, diffusion, and/or provokability) should be reversed for a later timepoint.
8. Chest x-rays may be useful as a baseline but are generally not helpful in the acute setting unless the patient has significant hypoxemia or asymmetric breath sounds.
9. Observe patient for delayed pulmonary edema for 24 hours if the patient is hypoxemic or has been exposed to a low-solubility gas, such as phosgene.
Careful attention to the eyes is important since there may be late development of cataracts with heavy exposures. If the gas has already been identified, then knowing its solubility can help in the triage of exposed victims. For example, high-solubility gases (sulfur dioxide or ammonia) affect the upper airways and only cause lower-airway injuries when the dose effect is large. Thus, if a potential victim, exposed to ammonia, has no upper-airway signs or symptoms (watery, teary eyes, red face, rhinitis, red sore nose, erythema of the posterior pharynx or hoarseness), it is unlikely that the patient has inhaled a dose high enough to cause lower-airway injury. The patient who presents with tachypnea and stridor, particularly with some hoarseness, is at a high risk of developing progressive laryngeal edema and complete obstruction of the airway, and therefore should be considered for emergency intubation. Certainly if symptoms of upper-airway damage are present, a prompt inspection of the larynx by a laryngoscope or fiberoptic laryngoscope would be imperative, since once sufficient edema develops these patients are extremely difficult to intubate and one may have to do an emergency tracheostomy. If upper-airway edema is present, pharmacologic treatment includes nebulized racemic epinephrine and systemic corticosteroids. If edema is minimal and early intubation is not required, conservative care to maintain airflow consists of positive pressure breathing (BIPAP or CPAP) or a mixture of helium/oxygen gas that due to its lower density can improve upper-airway flow dynamics by reducing turbulence. However, in the presence of edema not immediately requiring intubation, conservative care should only be done if frequent monitoring to assess edema progression and emergent intubation is possible.
When the patient is exposed to a low-soluble gas, like phosgene, upper-airway signs and symptoms are not expected and observation is required because it may take as long as 24 hours for reactive airways dysfunction syndrome or pulmonary edema to develop. The development of reactive airways dysfunction syndrome (RADS) or asthma after exposure to irritant gases is the most common long-term complication. Early treatment with inhaled bronchodilators and inhaled corticosteroids is a well-proven treatment approach for those with symptoms and reversible bronchospasm. Reversible bronchospasm can be confirmed by documenting improvement in flow rates after treatment with either a peak flow meter or spirometry. Currently, no studies exist to determine whether early use of inhaled corticosteroids is a viable prophylactic strategy. However, the side effects of inhaled corticosteroids are minimal. Sinusitis may accompany lower-airway inflammation, and treatment with nasal corti-costeroids, decongestants, nasal anticholinergic agents, and antihistamines are typical interventions.
Observation is critical if the patient complains of dyspnea or if tachypnea is noted, as these may be the earliest signs of impending pulmonary edema after acute inhalation exposure. While chest imaging is not useful in the early detection of pulmonary injury if the patient is asymptomatic, it is valuable if the patient is in respiratory distress or if pulmonary auscultation is abnormal or asymmetrical, in which case, oxime-try (remember, not useful with chemical asphyxiants such as carbon monoxide and H2S), arterial blood gases, and chest radiographs should be immediately obtained. Treatment is supportive. Abnormal gas exchange if severe should be treated with positive pressure ventilation aiming for the lowest mean airway pressure possible while still supporting gas exchange. Intubation may also be necessary if bronchial secretions are excessive and require frequent pulmonary toilet by catheter or bronchoscopic suc-tioning. Systemic corticosteroids are controversial for the treatment of noncardiogenic pulmonary edema and there is probably no role in the acute treatment of inhalation lung injury.
In the weeks following irritant gas exposures, the patient may continue to suffer from sinusitis, RADS, and asthma. Chronic cough syndrome may also result from irritant gas exposures. When chest radiographs and/or chest CT scans are normal, chronic cough is usually due to asthma or RADS, sinusitis, and/or gastroesophageal reflux. When chest imaging is abnormal, cough may be due to pneumonia or bronchiolitis obliterans. Prophylactic antibiotics have been suggested because sloughing of the tracheal mucosa offers a good culture media for bacteria. However, there is no evidence that prophylactic antibiotics reduce the incidence of pneumonia. Instead, antibiotics should be used only if pneumonia occurs and when possible targeted to the organisms responsible. Chest physiotherapy, high-frequency percussive ventilation, bronchodila-tors, and frequent suctioning may be helpful in those patients with mucus plugs and thick secretions. Bronchiolitis obliterans is a serious complication that usually responds to oral steroids, but may be progressive or even fatal if not treated promptly. It is unlikely that early treatment with only antibiotics or inhaled steroids is preven-
tive. Some might argue that, given the possibility of bronchiolitis obliterans, early treatment with oral steroids (prednisone at 40-60 mg/daily) for 8 weeks might be a reasonable prophylaxis strategy after exposure to those gases known to cause this problem, particularly in those patients with silo-filler's disease or those exposed to high doses of NO2 or SO2. Others believe that the occurrence of severe or life-threatening bronchiolitis obliterans after inhalation injury is too rare to warrant the routine use of oral steroids. Experimental anecdotal therapy for acute inhalation injury includes nebulized sodium bicarbonate or nebulized mucomyst (N-acetylcysteine) to break up secretion and to reduce free radical damage. The long-term consequences of irritant inhalation injury are summarized below in order of most common first:
Reactive airways dysfunction syndrome (RADS) or asthma Chronic bronchitis Bronchiectasis, i.e., ammonia, SO2 Bronchiolitis obliterans, i.e., NO2, SO2 Bronchostenosis, i.e., mustard gas Restrictive interstitial fibrosis
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