The chemical burn to the airways results in a spectrum of clinical manifestations during this period. At the very least, a mucosal irritation will persist for several days causing a bronchorrhea, increased cough, and mucus production. The damaged ciliary function of the airways lining leads to a high risk for infection manifested first (in the next 3 to 4 days) by a bacterial tracheobronchitis followed by a bronchopneumonia. Bacterial colonization is inevitable. Characteristically with a severe injury, the damaged mucosa becomes necrotic at 3 to 4 days post-injury and begins to slough. Increased viscous secretions can lead to distal airway obstruction, atelectasis, and a high risk of a rapidly developing bronchopneumonia.

As airways inflammation and bronchial blood flow increases over the next several days, a diffuse interstitial edema can develop. Even modest volume overload will markedly potentiate the edema process. The magnitude of the pulmonary infection is in large part dependent on the status of host defenses and the aggressiveness of pulmonary support. The combination of the chemical lung burn and a body burn markedly potentiate the morbidity and mortality of either process. If infection can be controlled and secretions cleared, the acute process will resolve over the next 7 to 10 days. However, the risk of infection persists for several weeks, extending well into the inflammation period.

In the first several days after injury, remaining soot continues to be present in the airways secretions. Diffuse rhonchi are usually present, once inflammation develops. Wheezing also frequently persists as a result of continued bronchospasm and bronchial edema, the latter being the more prominent cause. Continued coughing and pulmonary toilet as well as the residual airways edema and some bronchospasm increase the work of breathing, which can lead to fatigue and hypoventilation. Secretions then become tenacious and more difficult to clear. Rales compatible with an edema process will noted in the most severe airways injuries, especially with concomitant volume overload. Evidence of bacterial tracheobronchitis is common, followed by bronchopneumonia in a substantial number of patients. The characteristics of the symptom complex are as follows:

SYMPTOMS OF TRACHEOBRONCHITIS

Diagnosis of severity of injury is based on the course of the disease process than on initial findings from laryngoscopy, fiberoptic bronchoscopy, which basically only indicate that an injury is present. Chest radiographs during this period, in general, underestimate the severity of lung damage because the injury is usually initially confined to the airways.

Clinical evidence of continued respiratory compromise; namely, dyspnea, tachypnea, diffuse wheezing, and rhonchi precede radiographic changes. The first evidence on radiography of lung damage is usually that of either diffuse atelectasis, pulmonary edema, or bronchopneumonia. Altered gas exchange reflected in blood gas analysis and assessment of changes in sputum characteristics are useful parameters to monitor.