Inhalation injury from heat, smoke, or chemical irritants
- Ronald P Mlcak, PhD, MBA, RRT, FAARC
Ronald P Mlcak, PhD, MBA, RRT, FAARC
- Associate Professor Respiratory Care
- School of Health Professions
- UTMB Health
- Administrative Director of Ancillary Services
- Shriners Hospitals For Children, Galveston, TX
- Section Editors
- Eileen M Bulger, MD, FACS
Eileen M Bulger, MD, FACS
- Section Editor — Trauma Surgery
- Professor of Surgery
- University of Washington
- Marc G Jeschke, MD, PhD
Marc G Jeschke, MD, PhD
- Section Editor — Burn Surgery
- Director Ross Tilley Burn Centre
- Sunnybrook Health Sciences Centre
- Professor, Department of Surgery and Plastic Surgery
- University of Toronto
- Jess Mandel, MD
Jess Mandel, MD
- Section Editor — Pulmonary Vascular Disease
- Professor of Medicine
- University of California, San Diego
Inhalation injury is a nonspecific term that refers to damage to the respiratory tract or lung tissue from heat, smoke, or chemical irritants carried into the airway during inspiration . The term is often used synonymously with smoke inhalation injury. Inhalation injury resulting from fire remains one of the leading causes of death . The pathophysiology, clinical features, diagnosis, initial management, subsequent management, and special considerations of inhalation injury are reviewed here. The emergency care of thermal burns is discussed separately. (See "Emergency care of moderate and severe thermal burns in adults" and "Emergency care of moderate and severe thermal burns in children".)
Annually in the United States, an estimated 372,900 fires in residential buildings result in an average of 2530 deaths, 13,125 injuries, and $7 billion (USD) in property loss . Pulmonary complications following burns and inhalation injury are responsible for up to 77 percent of the deaths, among which the majority are due to carbon monoxide poisoning [4,5]. Inhalation injury is common following burn injury and increases in incidence with the size of the burn injury and age of the patient [6,7]. In addition, inhalation injury has been shown to be an independent predictor of mortality in burn patients .
PATHOPHYSIOLOGY AND CLASSIFICATION
Inhalation injury can affect the airways as well as result in systemic toxicity . The location and severity of injury depends on several factors, including the ignition source, the size and diameter of the particles in the smoke, the duration of the exposure, and the solubility of the gases [10,11]. Direct toxin damage is caused by the lower molecular weight constituents of smoke because of their pH, ability to form free radicals, and ability to reach the distal airways and alveoli [12-15]. Based upon the primary localization of the insult, inhalation injury is classified into injuries of the upper airway, the tracheobronchial system, or the lung parenchyma [9,16].
Upper airway injury — The leading injury in the upper airway (above the vocal cords) is thermal injury due to the efficient heat exchange in the oro- and nasopharynx. The immediate injury results in erythema, ulcerations, and edema. In combined burn and inhalation injury, aggressive fluid administration required to treat burn shock promotes early edema formation . In addition, burns to the face and neck may cause anatomic distortion or external compression of the upper airway, complicating airway management . In addition to the acute inflammation, damage of ciliary function impairs physiological clearance processes of the airway, leading to an increased risk of bacterial infection for several weeks. Furthermore, the increased production of thick secretions can cause distal airway obstruction, atelectasis, and impaired gas exchange [11,18,19].
Tracheobronchial injury — With the exception of inhalation of steam, injury to the tracheobronchial tree (figure 1) is usually caused by chemicals in smoke. However, toxic inhalation of noxious gases (eg, chlorine), liquids (eg, acid), and direct airway fire (eg, intraoperative) can also be associated with a similar process. Clinical symptoms include persistent coughing and wheezing, soot-containing airway secretions (ie, melanoptysis), increased work of breathing resulting in hypoventilation, erythema, hyperemia, and increased pulmonary shunting from lobar collapse or atelectasis [11,18].To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- PATHOPHYSIOLOGY AND CLASSIFICATION
- Upper airway injury
- Tracheobronchial injury
- Parenchymal injury
- Systemic toxicity
- CLINICAL FEATURES
- History and physical
- Laboratory findings
- Chest imaging
- Direct airway examination
- Injury severity scoring
- MANAGEMENT OVERVIEW
- Initial care and disposition
- - Securing the airway
- Subsequent care
- PULMONARY CARE
- Supportive treatments
- - Bronchodilators
- - Mucolytic agents
- Example treatment protocol for nonintubated patients
- Ventilator management
- - Tidal volumes
- - Modes of ventilation
- - Extubation criteria
- SPECIAL POPULATIONS
- Older adults
- Inhalation injury other than smoke
- MORBIDITY AND MORTALITY
- Long-term sequelae
- SUMMARY AND RECOMMENDATIONS