This aspect of inhalation injury is often an extension of the upper airways injury just described but is generally much more serious than that produced by heat alone. Toxic gases contained in smoke as well as carbon particles coated with irritating aldehydes and organic acids can result in injury to both upper and lower airways. The location of injury will depend on the duration of exposure, the size of the particles, and the solubility of the gases.

Breath holding and laryngospasm, as a result of airway irritation, are protective mechanisms against excessive exposure in the conscious patient. The unconscious patient, however, loses this protection, resulting in a more severe injury to the lower airways. Information as to status of consciousness at the scene should be sought in the history.

Water-soluble gases found in smoke from burning plastics or rubber, such as ammonia, sulfur dioxide, and chlorine, react with water in the mucous membranes to produce strong acids and alkalies that lead to irritation, bronchospasm and mucous membrane ulceration, and edema. Severe impairment of the ciliary mechanism of the mucosa occurs, leading to impairment of the removal of particles and mucus. Lipid-soluble compounds, such as nitrous oxide, phosgene, hydrogen chloride, and various toxic aldehydes, are transported to the lower airways on carbon particles that, in turn, adhere to the mucosa. All these agents produce cell membrane damage. There is also marked early increases in bronchial blood flow, which accentuates the edema formation.

Alveolar edema is not a major component of the early disease state.

A body burn markedly potentiates the inhalation-induced lung dysfunction caused by chemical injury. Mortality rate for patients with severe inhalation injury alone is 5 to 8%. Mortality rate of the combination of a major burn and smoke inhalation far exceeds that of either injury alone.

Small airways injury from smoke. ( Broncho constriction caused by the mucosal injury)

Fatal Smoke inhalation injury (Note: Airway and alveolar  collapse with massive atelectasis. Note also the mucosal cast in the opened airway

Closer view of mucosal slough found in massive injuries. However, removal of mucosal plugs is a common finding in any significant smoke inhalation

Symptoms may well be absent on admission, with the true magnitude of the degree of injury only becoming evident after 24 to 48 hours. Early symptoms usually consist of bronchospasm manifested as wheezing and bronchorrhea. An intense initial bronchorrhea caused by the irritation of the airway mucosa in combination with increased oral and nasal secretions can give the appearance of fulminant pulmonary edema. The sources of these secretions, however, is not the pulmonary circulation in the vast majority of cases. Injury at the alveolar level is usually fatal. The presence of soot in the lung secretions is certainly evidence off smoke exposure but is not a necessary finding. Early bronchospasm and bronchiolar edema initiated by the irritant gases causes a marked decrease in lung compliance and increased work of breathing. Impaired clearance of secretions will accentuate the problem. The resulting ventilation-perfusion (V/Q) mismatch will create impaired gas exchange with an increasing alveolar-arterial oxygen gradient and minute ventilation. In summary, the symptom complex is as follows:

Diagnostic aids are history of closed space exposure, physical findings (soot, presence of symptoms), increased carboxyhemoglobin, direct visualization of injury (laryngoscopy, fiberoptic bronchoscopy), and indirect visualization, V/Q xenon scan).

A history of confinement in a closed space during the burning process is a good indicator of potential lung damage. However, single breath exposures to toxic chemicals are sufficient to produce major airways damage. An absence of a history, especially by transferring medical personnel, often means a lack of detailed information about the circumstances of injury. The true story often takes hours or days to determine. Physical findings on admission that suggest smoke exposure include a facial burn, soot in the sputum, dyspnea, coughing, wheezing, and bronchorrhea. If present, these findings are helpful. However, many patients demonstrate minimal symptoms early after injury and only when airways edema develops do symptoms become evident. An elevated carboxyhemoglogin level indicates an exposure to the elements in smoke. Often, considerable displacement of the carbon monoxide has occurred before arrival due to standard institution of oxygen at the scene.

Laryngoscopy will demonstrate the presence of mucosal irritation at and above the cords and provide information about the need for endotracheal intubation. Absence of upper airways changes almost always means absence of lower airways injury. Visualization of the upper and lower airways by fiberoptic bronchoscopy can provide information on the anatomic extent of injury but initial findings have not been found to prognosticate accurately the magnitude of injury to allow anticipation of the subsequent course.

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Chest roentgenogram upon admission of a 36 year old patient with extensive burns, undergoing resuscitation.
NOTE: Absence of parenchymal involvement despite a severe airways injury.

Initial treatment of a chemical burn consists of an aggressive approach to upper airway maintenance and pulmonary support, which includes maintenance of small airways patency and removal of soot and the mucopurulent secretions. Careful well-monitored fluid resuscitation is necessary to avoid accentuation of the process. Under volume resuscitation will aggravate the pulmonary dysfuntion as much as will over-resuscitation. The addition of positive end-expiratory pressure (PEEP) is frequently necessary to maintain small airway patency and an adequate functional residual capacity by assisting in holding the edematous airway open until edema resolution. Early endotracheal intubation and PEEP have been reported to decrease pulmonary deaths after severe burns and smoke inhalation. Prevention of airway closure is much more readily accomplished than is the reopening of collapsed airways. A large enough tube, i.e. at least a 7mm internal diameter, should be used in adults because very thick secretions develop as a result of the lung injury. If the initial tube is too small, it will be very dangerous to change once massive facial and airway edema develops. Although the nasotracheal route may be more comfortable to the patient, the size of the tube may need to be compromised and lead to later problems for secretion clearance. The continued use of additional humidified oxygen to maintain adequate oxygen delivery as well as to assist in the clearance of secretions is indicated. Elevation of the patient’s head and chest 20 to 30⁰ is also helpful.

Bronchospasm is a frequent component of the chemical injury. However, diagnosis can be complicated by rhonchi and upper airways noises, caused by increased secretions. A helpful clue to determining the magnitude of increased airways resistance is the difference between dynamic and static compliance. The difference between the two reflects increased resistance to airflow, which will, of course, also include the endotracheal tube. Bronchospasm can be treated with bronchodilators, either parenteral or via aerosol. The beta₂ sympathomimetic agents, metaproterenol (Allupent) or isoetharine (Bronkosol), are effective bronchodilators. Intravenous aminophylline, although a good bronchodilator, is frequently limited in its use because of the tachycardia seen in the early postburn period.

Beginning about 18 to 24 hours after a burn, increasing airway resistance is often due to bronchiolar edema and airway plugging rather than bronchospasm. The impaired gas exchange often responds to further increases in PEEP in addition to bronchodilators. PEEP in excess of 10 cm H₂O will produce some impairment in cardiac output if hypovolemia is also present. Prophylactic antibiotics are not indicated. The injured airways mucosa will frequently become colonized with bacteria, especially if an endotracheal tube is present. Prophylactic antibiotics will only select for the more resistant organisms. It is now well-demonstrated that corticosteroids in the presence of a body burn increase rather than decrease the smoke inhalation morbidity and mortality. Steroids are therefore contraindicated in the presence of a burn. With inhalation injury in the absence of a burn, no benefit has been demonstrated.

Close monitoring of the adequacy of gas exchange is necessary, particularly during the early evolution of the inhalation injury. An indwelling arterial line or a pulse oximeter is required. The pulse oximeter indicates arterial oxygen saturation using a photosensor that detects the color of the blood flowing beneath the probe.

ASSESS FOR LOWER AIRWAYS INJURY ( to Ventilate or Not to Ventilate With Positive Pressure)